Hazardous metals in mineral processing plants in South Africa

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Hazardous metals in mineral processing plants in South Africa
Facilitating safety and health research in the South African mining industry
Hazardous metals in mineral processing
plants in South Africa
The risk of occupational exposure
SIMRAC Project Support Services
September 2000
SIMRAC Project Health 603
Executive Summary
The presence of heavy metals and exposure of employees thereto in mineral processing plants
in South Africa have not been studied and described in a format that can be used as a general
reference document. This document provides a review of different process steps in mineral
processing and the associated health hazards from heavy metals. It should be particularly
useful for those who are new in the field, and for the relatively uninformed who have to perform
duties that require some understanding of the processes and background to health risk
assessment. In providing these perspectives, the following aspects were considered to be of
primary importance:
•
•
•
•
•
To provide an understanding of the paradigm of human health risk assessment in the
occupational environment;
To identify heavy metals that would be of interest in mineral processing plants;
To review the context of target-organ toxicity of heavy metals in the quantification of
exposure and health risks, taking into account the concepts of speciation and bioavailability;
To provide information on the elements of occupational health risk management, providing
general principles for survey design, sampling philosophies, and interpretation methods.
To put the principles listed above in context with selected mineral processing plants in
South Africa.
The overall paradigm of health risk assessment was followed in the investigations, i.e.
according to the steps of hazard assessment, dose-response assessment, exposure
assessment, and risk characterisation.
The first step in the investigation was to select those metals that could be placed in the
category of "heavy metals". A list was compiled on the basis of toxicological properties of the
elements, and comprised of 33 elements. The elements were chosen with the objective of
health risk management in mind, rather than on the basis of the classical definition of "metals".
To assess the potential for exposure to heavy metals, the various industries must be well
understood. This study therefore reviewed fifteen selected industrial processes to identify unit
operations, potential toxicants, and exposure zones where hazards might be posed. The
information is presented in generic flow diagrams. The diagrams were developed to represent
the general process steps, rather than detailed descriptions that were not essential for
understanding the basic concepts and associated hazards. The process information was
verified by means of visits to typical plants and discussions with specialists in the various fields.
This work formed the hazard assessment part of the investigation.
The following types of mineral processing plants were studied:
• Carbon steel process with blast and basic oxygen furnace;
• Carbon steel process with direct reduced iron and electric arc furnace;
• Typical copper recovery circuit;
• Typical ferrochromium production process;
• Typical ferromanganese production process;
• Bacterial oxidation circuit for the pre-oxidation of refractory gold ores;
• Carbon-in-pulp circuit for gold recovery;
• Nickel, copper, and cobalt refining process;
• Typical phosphate rock production process;
• Platinum group metal refining;
• Typical stainless steel process;
• Typical titanium dioxide production process;
• Vanadium pentoxide production: the salt-roast process;
• Vanadium slag production process; and
• Typical circuit for zinc recovery from concentrate.
The dose-response assessment (toxicological assessment) was based on literature
information reviewed for the various metals. The primary routes of exposure to toxicants in the
occupational environment are via inhalation, ingestion, and dermal contact. Most metallic
compounds occur as solids, fumes, or in mists, and are frequently associated with particulates in
the occupational exposure scenario. Particle size determines where in the respiratory tract
inhaled particles are deposited and hence can exert their toxic effects. Metals seldom interface
with biological systems in the elemental form. They occur as compounds that vary with the ease
with which they can pass through biological membranes. An extensive literature review was
conducted, covering surveys of the most prominent international publications on the subject.
The large volume of data is summarised in tables. To place the information in context, concise
descriptions of the target organs of the body that are relevant to metal toxicity are also
presented. Because several of the metals are present in more than one processing plant,
toxicological information is presented together in one section of the report. The most relevant
information is however highlighted in the sections that deal separately with each plant.
The exposure assessment part of the studies is also handled in the descriptions of the 15
selected mineral processing plants. The approach however does not follow the conventional
occupational hygiene process of sampling and chemical analysis. It is limited to the
identification of zones of exposure, and recommendations for monitoring. Because the
protocols for occupational exposure monitoring are more related to the substances of interest
than the particular processing plants, the methodologies for monitoring are presented together
in one section in the report. Reference has however been made to appropriate monitoring in
the sections that deal separately with each plant.
Risk characterisation is presented in the paradigm for quantitative human health risk
assessment. Risks were not quantified for the various exposure scenarios, but the overall
approach to risk assessment is presented. It indicates in which areas the highest risks might
be expected, and consequently, where risk management should be applied. Human health risk
characterisation is generally divided into the evaluation of carcinogenic and non-carcinogenic
risks. Carcinogenic risks are interpreted in terms of excess lifetime cancer risks. In the
occupational exposure range the estimated cancer risk is assumed to be linear and proportional
to dose. Risks are assumed to be additive per target organ across chemicals and pathways,
unless data are available that would support synergistic or antagonistic effects. Risks are
expressed as excess cancer risk, i.e. risk not taking into account any existing risk as a result of
background exposure to substances that have the same carcinogenic properties.
Noncarcinogenic risks are evaluated by comparison with reference concentrations. If the ratio
of the air concentration to the reference concentration (hazard quotient) exceeds one, there is a
potential that adverse health effects may occur. For multiple chemical exposures, hazard
quotients are summed per target organ, unless data are available to demonstrate synergistic or
antagonistic effects. This is based on the assumption that the response of a target organ to
multiple toxic agents is additive in a linear relationship. It is measured in terms of a hazard
index, which is the sum of the hazard quotients for the individual substances.
Table of contents
Page
Executive Summary ...................................................................................................... 1
List of Figures .......................................................................................................................11
List of Tables ........................................................................................................................13
Glossary of abbreviations, symbols and terms ................................................................. 17
1
Introduction ....................................................................................................23
1.1
1.2
Research problem statement .....................................................................23
Objectives and aims of this study .............................................................24
1.2.1
1.2.2
Main objective.......................................................................................................24
Goals .....................................................................................................................24
1.3
Research context and design .....................................................................24
1.3.1
1.3.2
Research context .................................................................................................24
Research design ..................................................................................................25
1.4
Deployment of the study...............................................................................25
2
Research methodology...........................................................................27
3
Literature review .........................................................................................29
3.1
3.2
Principles of health risk assessment .......................................................29
Hazard assessment .......................................................................................29
3.2.1
Criteria for selection .............................................................................................29
3.2.1.1
3.2.1.2
The classification of heavy metals .......................................................................... 29
Regulatory classification ......................................................................................... 30
Use of the list of hazardous metals .................................................................... 31
Dose-response assessment .......................................................................31
Basic concepts in toxicology ............................................................................... 31
Mechanisms of metals toxicity ............................................................................ 33
Target organ systems and toxic responses....................................................... 36
Renal system ..........................................................................................................36
Nervous system ......................................................................................................36
Liver........................................................................................................................37
Gastrointestinal tract ............................................................................................... 37
Respiratory tract .....................................................................................................38
Haematopoietic system .......................................................................................... 39
Bone .......................................................................................................................39
Endocrine system ...................................................................................................40
Muscle ....................................................................................................................40
Eye .........................................................................................................................40
Skin ........................................................................................................................40
Cardiovascular system ........................................................................................... 41
Immune system ......................................................................................................41
Reproductive system .............................................................................................. 42
Toxicology of the elements ................................................................................. 43
Antimony (Sb) .........................................................................................................43
Arsenic (As) ............................................................................................................45
Barium (Ba) ............................................................................................................48
Beryllium (Be) .........................................................................................................50
3.2.2
3.3
3.3.1
3.3.2
3.3.3
3.3.3.1
3.3.3.2
3.3.3.3
3.3.3.4
3.3.3.5
3.3.3.6
3.3.3.7
3.3.3.8
3.3.3.9
3.3.3.10
3.3.3.11
3.3.3.12
3.3.3.13
3.3.3.14
3.3.4
3.3.4.1
3.3.4.2
3.3.4.3
3.3.4.4
3.3.4.5
3.3.4.6
3.3.4.7
3.3.4.8
3.3.4.9
3.3.4.10
3.3.4.11
3.3.4.12
3.3.4.13
3.3.4.14
3.3.4.15
3.3.4.16
3.3.4.17
3.3.4.18
3.3.4.19
3.3.4.20
3.3.4.21
3.3.4.22
3.3.4.23
3.3.4.24
3.3.4.25
3.3.4.26
3.3.4.27
3.3.4.28
3.3.4.29
3.3.4.30
3.3.4.31
3.3.4.32
3.3.4.33
Bismuth (Bi) ............................................................................................................52
Cadmium (Cd) ........................................................................................................54
Calcium (Ca)...........................................................................................................57
Chromium (Cr) ........................................................................................................59
Cobalt (Co) .............................................................................................................61
Copper (Cu) ............................................................................................................63
Indium (In) ..............................................................................................................65
Iron (Fe)..................................................................................................................67
Lead (Pb) ................................................................................................................69
Manganese (Mn).....................................................................................................71
Mercury (Hg)...........................................................................................................74
Molybdenum (Mo) ...................................................................................................76
Nickel (Ni) ...............................................................................................................78
Osmium (Os) ..........................................................................................................80
Platinum (Pt) ...........................................................................................................82
Rhodium (Rh) .........................................................................................................84
Selenium (Se) .........................................................................................................86
Silver (Ag) ...............................................................................................................88
Tantalum (Ta) .........................................................................................................90
Tellurium (Te) .........................................................................................................92
Thallium (Tl) ...........................................................................................................94
Tin (Sn)...................................................................................................................96
Titanium (Ti) ...........................................................................................................98
Tungsten (W) ....................................................................................................... 100
Uranium (U) .......................................................................................................... 102
Vanadium (V)........................................................................................................ 104
Yttrium (Y) ............................................................................................................ 106
Zinc (Zn) ............................................................................................................... 108
Zirconium (Zr) ....................................................................................................... 110
3.4
Exposure assessment: General guidelines for occupational
health risk assessment and management. .......................................... 112
3.4.1
3.4.2
Context ................................................................................................................ 112
The relationship between dust and heavy metals in exposure
assessment......................................................................................................... 112
Physical monitoring of the workplace............................................................... 114
3.4.3
3.4.3.1
3.4.3.2
3.4.3.3
3.4.3.4
3.4.3.5
3.4.3.6
3.4.4
3.4.4.1
3.4.4.2
3.4.4.3
3.4.4.4
3.5
3.6
Direct-reading instruments .................................................................................... 114
Detector-tube measurements ............................................................................... 114
Air sampling and analysis ..................................................................................... 114
Selection of appropriate positions for monitoring .................................................. 115
Personal sampling ................................................................................................ 118
Sampling and analytical methods for exposure assessment ................................. 120
Medical evaluation ............................................................................................. 124
Medical surveillance.............................................................................................. 124
Biological effect monitoring ................................................................................... 125
Biological monitoring............................................................................................. 125
Medical evaluation summary: procedures relevant to the various heavy metals ... 127
Risk characterisation ................................................................................... 134
References ...................................................................................................... 134
4
Carbon steel process with blast furnace and basic
oxygen furnace ..........................................................................................141
4.1
Introduction...................................................................................................... 141
4.2
Process description ...................................................................................... 141
4.2.1
4.2.2
4.2.3
4.2.4
4.2.5
4.2.6
Coke preparation................................................................................................ 141
Sintering .............................................................................................................. 142
Storage/blending/material handling.................................................................. 143
Blast furnace treatment ..................................................................................... 143
Basic oxygen furnace treatment ....................................................................... 144
Further refining, casting, rolling, pickling, galvanising .................................... 145
4.3
4.4
Process diagram ........................................................................................... 146
Process assessment.................................................................................... 146
4.4.1
4.4.2
4.4.3
4.4.4
Hazard identification .......................................................................................... 146
Toxicological assessment ................................................................................. 148
Exposure assessment ....................................................................................... 148
Risk quantification .............................................................................................. 148
4.5
References ...................................................................................................... 148
5
Carbon steel process with direct reduced iron and
electric arc furnace .................................................................................. 151
5.1
5.2
Introduction...................................................................................................... 151
Process description ...................................................................................... 151
5.2.1
5.2.2
5.2.3
5.2.4
5.2.5
Grinding............................................................................................................... 151
Pelletisation ........................................................................................................ 152
Direct reduction .................................................................................................. 152
Electric arc furnace ............................................................................................ 153
Casting, rolling, pickling, galvanising ............................................................... 154
5.3
5.4
Flow diagram .................................................................................................. 154
Process assessment.................................................................................... 156
5.4.1
5.4.2
5.4.3
5.4.4
Hazard identification .......................................................................................... 156
Toxicological assessment ................................................................................. 156
Exposure assessment ....................................................................................... 156
Risk quantification .............................................................................................. 157
5.5
References ...................................................................................................... 157
6
Typical copper recovery circuit ........................................................ 159
6.1
6.2
Introduction...................................................................................................... 159
Process description ...................................................................................... 159
6.2.1
6.2.2
6.2.3
6.2.4
6.2.5
Crushing and milling .......................................................................................... 159
Flotation and magnetic separation ................................................................... 159
Liquid/solid separation/drying ........................................................................... 160
Smelting and converting .................................................................................... 160
Refining and rod casting.................................................................................... 161
6.3
6.4
Flow diagram .................................................................................................. 161
Process assessment.................................................................................... 162
6.4.1
6.4.2
6.4.3
6.4.4
Hazard identification .......................................................................................... 162
Toxicological assessment ................................................................................. 162
Exposure assessment ....................................................................................... 162
Risk quantification .............................................................................................. 164
6.5
References ...................................................................................................... 164
7
Typical ferrochrome production process ................................... 165
7.1
7.2
Introduction...................................................................................................... 165
Process description ...................................................................................... 165
7.2.1
7.2.2
7.2.3
7.2.4
7.2.5
Beneficiation ....................................................................................................... 165
Material Handling ............................................................................................... 166
Smelting .............................................................................................................. 167
Alloy casting and sizing ..................................................................................... 169
Metal recovery from slag ................................................................................... 169
7.3
7.4
Flow diagram .................................................................................................. 170
Process assessment.................................................................................... 170
7.4.1
7.4.2
7.4.3
7.4.4
Hazard identification .......................................................................................... 170
Toxicological assessment ................................................................................. 170
Exposure assessment ....................................................................................... 170
Risk quantification .............................................................................................. 170
7.5
References ...................................................................................................... 172
8
Typical ferromanganese production process.......................... 173
8.1
8.2
Introduction...................................................................................................... 173
Process description ...................................................................................... 173
8.2.1
8.2.2
8.2.3
8.2.4
8.2.5
8.2.6
Beneficiation ....................................................................................................... 173
Sintering .............................................................................................................. 174
Material handling ................................................................................................ 174
8.2.4 Smelting .................................................................................................... 175
Alloy casting, crushing and sizing..................................................................... 176
Metal recovery from slag ................................................................................... 177
8.3
8.4
Flow diagram .................................................................................................. 177
Process assessment.................................................................................... 177
8.4.1
8.4.2
8.4.3
8.4.4
Hazard identification .......................................................................................... 177
Toxicological assessment ................................................................................. 177
Exposure assessment ....................................................................................... 179
Risk quantification .............................................................................................. 179
8.5
References ...................................................................................................... 179
9
Bacterial oxidation circuit for the pre-oxidation of
refractory gold ores ................................................................................. 181
9.1
9.2
Introduction...................................................................................................... 181
Process description ...................................................................................... 181
9.2.1
9.2.2
9.2.3
9.2.4
9.2.5
Crushing, Screening and Milling ....................................................................... 181
Gravity concentration ......................................................................................... 181
Flotation .............................................................................................................. 181
Bacterial oxidation and gold recovery .............................................................. 182
Bioliquor neutralisation/thickening and disposal ............................................. 183
9.3
9.4
Flow diagram .................................................................................................. 184
Process assessment.................................................................................... 184
9.4.1
9.4.2
9.4.3
Hazard identification .......................................................................................... 184
Toxicological assessment ................................................................................. 184
Exposure assessment ....................................................................................... 184
9.4.4
Risk quantification .............................................................................................. 186
9.5
References ...................................................................................................... 186
10
Carbon-in-pulp circuit for gold recovery ..................................... 187
10.1
10.2
Introduction...................................................................................................... 187
Process description ...................................................................................... 187
10.2.1
10.2.2
10.2.3
10.2.4
10.2.5
10.2.6
10.2.7
10.2.8
10.2.9
Crushing .............................................................................................................. 187
Milling .................................................................................................................. 187
Thickening........................................................................................................... 188
Leaching.............................................................................................................. 188
Adsorption ........................................................................................................... 189
Stripping and carbon regeneration ................................................................... 190
Electrowinning .................................................................................................... 191
Smelting .............................................................................................................. 192
Residue disposal ................................................................................................ 192
10.3
10.4
Flow diagram .................................................................................................. 192
Process assessment.................................................................................... 194
10.4.1
10.4.2
10.4.3
10.4.4
Hazard identification .......................................................................................... 194
Toxicological assessment ................................................................................. 194
Exposure assessment ....................................................................................... 194
Risk quantification .............................................................................................. 194
10.5
References ...................................................................................................... 194
11
Nickel, copper, cobalt refining processes ................................. 195
11.1
11.2
Introduction...................................................................................................... 195
Process description: option 1 ................................................................... 195
11.2.1
11.2.2
11.2.3
11.2.4
11.2.5
Matte grinding ..................................................................................................... 195
Atmospheric Pressure Leach and Nickel Sulphate Crystallisation ............... 196
Pressure leach ................................................................................................... 197
Selenium removal .............................................................................................. 198
Copper electrowinning ....................................................................................... 198
11.3
11.4
Flow diagram: option 1 ................................................................................ 198
Process assessment: option 1 ................................................................. 200
11.4.1
11.4.2
11.4.3
11.4.4
Hazard identification .......................................................................................... 200
Toxicological assessment ................................................................................. 200
Exposure assessment ....................................................................................... 200
Risk quantification .............................................................................................. 201
11.5
11.6
References: option 1.................................................................................... 201
Process description: option 2 ................................................................... 202
11.6.1
11.6.2
11.6.3
11.6.4
11.6.5
11.6.6
11.6.7
11.6.8
Slow cool/crush/mill/magnetic concentration .................................................. 202
Copper cementation .......................................................................................... 202
Primary pressure leach...................................................................................... 203
Secondary pressure leach ................................................................................ 203
Copper electrowinning ....................................................................................... 203
Cobalt removal ................................................................................................... 204
Nickel electrowinning ......................................................................................... 204
Sulphur removal ................................................................................................. 205
11.7
Flow diagram: option 2 ................................................................................ 205
11.8
Process assessment: option 2 ................................................................. 205
11.8.1
11.8.2
11.8.3
11.8.4
Hazard identification .......................................................................................... 205
Toxicological assessment ................................................................................. 205
Exposure assessment ....................................................................................... 207
Risk quantification .............................................................................................. 207
11.9
References: option 2.................................................................................... 207
12
Typical phosphate rock production process ............................ 209
12.1
12.2
Introduction...................................................................................................... 209
Process description ...................................................................................... 209
12.2.1
12.2.2
12.2.3
12.2.4
12.2.5
12.2.6
Crushing and Milling .......................................................................................... 209
Flotation of copper sulphide .............................................................................. 209
Magnetic separation of magnetite .................................................................... 210
Phosphate flotation ............................................................................................ 210
Phosphate rock concentrate treatment ............................................................ 210
Phosphoric acid production............................................................................... 211
12.3
12.4
Flow diagram .................................................................................................. 212
Process assessment.................................................................................... 212
12.4.1
12.4.2
12.4.3
12.4.4
Hazard identification .......................................................................................... 212
Toxicological assessment ................................................................................. 214
Exposure assessment ....................................................................................... 214
Risk quantification .............................................................................................. 214
12.5
References ...................................................................................................... 214
13
Platinum group metal refining........................................................... 215
13.1
13.2
Introduction...................................................................................................... 215
Process description ...................................................................................... 215
13.2.1
13.2.2
13.2.3
13.2.4
13.2.5
13.2.6
13.2.7
Leaching.............................................................................................................. 215
Gold extraction ................................................................................................... 216
Palladium extraction .......................................................................................... 216
Base metal separation ....................................................................................... 217
Ruthenium separation ....................................................................................... 217
Rhodium/iridium/osmium separation................................................................ 217
Platinum recovery .............................................................................................. 218
13.3
13.4
Flow diagram .................................................................................................. 218
Process assessment.................................................................................... 218
13.4.1
13.4.2
13.4.3
13.4.4
Hazard identification .......................................................................................... 218
Toxicological assessment ................................................................................. 220
Exposure assessment ....................................................................................... 220
Risk quantification .............................................................................................. 222
13.5
References ...................................................................................................... 222
14
Typical stainless steel process ........................................................ 225
14.1
14.2
Introduction...................................................................................................... 225
Process description ...................................................................................... 225
14.2.1
14.2.2
Raw material receipts and charge preparation ............................................... 225
Furnace charging and melting .......................................................................... 227
14.2.3
14.2.4
14.2.5
14.2.6
14.2.7
14.2.8
14.2.9
14.2.10
Stainless steel refining....................................................................................... 228
Continuous casting ............................................................................................ 229
Hot rolling ............................................................................................................ 230
Annealing and pickling....................................................................................... 230
Cold rolling and bright annealing ...................................................................... 231
Cutting to length, slitting, packing and despatching ....................................... 231
Effluent treatment plant ..................................................................................... 232
Water treatment/handling.................................................................................. 232
14.3
14.4
Flow diagram .................................................................................................. 232
Process assessment.................................................................................... 235
14.4.1
14.4.2
14.4.3
14.4.4
Hazard identification .......................................................................................... 235
Toxicological assessment ................................................................................. 235
Exposure assessment ....................................................................................... 235
Risk quantification .............................................................................................. 237
14.5
References ...................................................................................................... 237
15
Typical titanium dioxide production process ........................... 239
15.1
15.2
Introduction...................................................................................................... 239
Process description ...................................................................................... 239
15.2.1
15.2.2
15.2.3
15.2.4
15.2.5
15.2.6
Milling .................................................................................................................. 239
Digestion/production of digester residue byproduct ....................................... 239
Hydrolysis/leaching/washing ............................................................................. 240
Production of gypsum byproduct ...................................................................... 241
Calcining ............................................................................................................. 242
Pigment finishing ................................................................................................ 242
15.3
15.4
Flow diagram .................................................................................................. 243
Process assessment.................................................................................... 243
15.4.1
15.4.2
15.4.3
15.4.4
Hazard identification .......................................................................................... 243
Toxicological assessment ................................................................................. 243
Exposure assessment ....................................................................................... 245
Risk quantification .............................................................................................. 245
15.5
References ...................................................................................................... 246
16
The salt-roast process for vanadium pentoxide
production .....................................................................................................247
16.1
16.2
Introduction...................................................................................................... 247
Process description ...................................................................................... 247
16.2.1
16.2.2
16.2.3
16.2.4
16.2.5
Crushing and milling .......................................................................................... 247
Magnetic separation and de-watering .............................................................. 247
Roasting .............................................................................................................. 248
Leaching.............................................................................................................. 248
Precipitation and vanadium pentoxide production .......................................... 249
16.3
16.4
Flow diagram .................................................................................................. 250
Process assessment.................................................................................... 250
16.4.1
16.4.2
16.4.3
16.4.4
Hazard identification .......................................................................................... 250
Toxicological assessment ................................................................................. 250
Exposure assessment ....................................................................................... 252
Risk quantification .............................................................................................. 252
16.5
References ...................................................................................................... 253
17
Vanadium slag production process............................................... 255
17.1
17.2
Introduction...................................................................................................... 255
Process description ...................................................................................... 255
17.2.1
17.2.2
17.2.3
17.2.4
Crushing, screening and magnetic separation................................................ 255
Pre-reduction ...................................................................................................... 255
Electric arc smelting ........................................................................................... 256
Shaking ladles/vanadium slag upgrading ........................................................ 257
17.3
17.4
Flow diagram .................................................................................................. 258
Process assessment.................................................................................... 260
17.4.1
17.4.2
17.4.3
17.4.4
Hazard identification .......................................................................................... 260
Toxicological assessment ................................................................................. 260
Exposure assessment ....................................................................................... 260
Risk quantification .............................................................................................. 261
17.5
References ...................................................................................................... 261
18
Typical circuit for zinc recovery from concentrate ............... 263
18.1
18.2
Introduction...................................................................................................... 263
Process description ...................................................................................... 263
18.2.1
18.2.2
18.2.3
18.2.3
18.2.4
Roasting .............................................................................................................. 263
Leaching and precipitation ................................................................................ 264
Purification .......................................................................................................... 265
Electrowinning .................................................................................................... 266
Effluent treatment............................................................................................... 266
18.3
18.4
Flow diagram .................................................................................................. 267
Process assessment.................................................................................... 267
18.4.1
18.4.2
18.4.3
18.4.4
Hazard identification .......................................................................................... 267
Toxicological assessment ................................................................................. 269
Exposure assessment ....................................................................................... 269
Risk quantification .............................................................................................. 271
18.5
References ...................................................................................................... 271
List of Figures
Figure 3.2.1.1
Figure 3.4.4.3
Figure 4.3
Figure 5.3
Figure 6.3
Figure 7.3
Figure 9.3
Figure 10.3
Figure 11.3
Figure 11.7
Figure 12.3
Figure 13.3
Figure 14.3.1
Figure 14.3.2
Figure 15.3
Figure 16.3
Figure 17.3
Figure 18.3
Page
Periodic table of the elements, showing those elements that were
selected for investigation........................................................................... 30
Types of monitoring in occupational health protection (after
Lauwerys and Hoet, 1993: 9) .................................................................. 126
Process diagram for the carbon steel process with blast furnace
and basic oxygen furnace. ...................................................................... 147
Process diagram for the carbon steel process with with direct
reduced iron and electric arc furnace. ..................................................... 155
Process diagram for the copper recovery circuit ..................................... 163
Process diagram for the ferrochrome recovery circuit ............................. 171
Process diagram for the bacterial oxidation circuit for the preoxidation of refractory gold ores .............................................................. 185
Process diagram for the carbon-in-pulp circuit for gold recovery ............. 193
Process diagram for the Ni, Cu, Co refining process – option 1 .............. 199
Process diagram for the Ni, Cu, Co refining process – option 2 .............. 206
Process diagram for the phosphate rock production process .................. 213
Process diagram for a platinum group metal refining process ................. 219
Process diagram for a typical stainless steel process, sheet 1 of 2 ......... 233
Process diagram for a typical stainless steel process, sheet 2 of 2 ......... 234
Process diagram for a typical titanium dioxide production process ......... 244
Process diagram for the vanadium pentoxide production circuit.............. 251
Process diagram for the vanadium slag production process ................... 259
Process diagram for a typical circuit for zinc recovery from
concentrate ............................................................................................. 268
List of Tables
Table 3.2.1.2
Table 3.3.1
Table 3.3.4.1
Table 3.3.4.2
Table 3.3.4.3
Table 3.3.4.4
Table 3.3.4.5
Table 3.3.4.6
Table 3.3.4.7
Table 3.3.4.8
Table 3.3.4.9
Table 3.3.4.10
Table 3.3.4.11
Table 3.3.4.12
Table 3.3.4.13
Table 3.3.4.14
Table 3.3.4.15
Table 3.3.4.16
Table 3.3.4.17
Table 3.3.4.18
Table 3.3.4.19
Table 3.3.4.20
Table 3.3.4.21
Table 3.3.4.22
Table 3.3.4.23
Table 3.3.4.24
Table 3.3.4.25
Table 3.3.4.26
Table 3.3.4.27
Table 3.3.4.28
Table 3.3.4.29
Table 3.3.4.30
Table 3.3.4.31
Table 3.3.4.32
Table 3.3.4.33
Table 3.4.2
Table 3.4.3.2
Table 3.4.3.4a
Table 3.4.3.4b
Table 3.4.3.5
Table 3.4.3.6
Table 3.4.4.3
Table 3.4.4.4
Table 4.2.1
Table 4.2.2
Page
List of elements selected for assessment ................................................. 31
The IARC classification for carcinogenicity ............................................... 32
Antimony: Toxicological properties and target-organ effects ..................... 44
Arsenic: Toxicological properties and target-organ effects ........................ 46
Barium: Toxicological properties and target-organ effects ........................ 49
Beryllium: Toxicological properties and target-organ effects ..................... 51
Bismuth: Toxicological properties and target-organ effects ....................... 53
Cadmium: Toxicological properties and target-organ effects..................... 55
Calcium: Toxicological properties and target-organ effects ....................... 58
Chromium: Toxicological properties and target-organ effects ................... 60
Cobalt: Toxicological properties and target-organ effects ......................... 62
Copper: Toxicological properties and target-organ effects ........................ 64
Indium: Toxicological properties and target-organ effects ......................... 66
Iron: Toxicological properties and target-organ effects.............................. 68
Lead: Toxicological properties and target-organ effects ............................ 70
Manganese: Toxicological properties and target-organ effects ................. 72
Mercury: Toxicological properties and target-organ effects ....................... 75
Molybdenum: Toxicological properties and target-organ effects................ 77
Nickel: Toxicological properties and target-organ effects .......................... 79
Osmium: Toxicological properties and target-organ effects ...................... 81
Platinum: Toxicological properties and target-organ effects ...................... 83
Rhodium: Toxicological properties and target-organ effects...................... 85
Selenium: Toxicological properties and target-organ effects ..................... 87
Silver: Toxicological properties and target-organ effects ........................... 89
Tantalum: Toxicological properties and target-organ effects ..................... 91
Tellurium: Toxicological properties and target-organ effects ..................... 93
Thallium: Toxicological properties and target-organ effects ...................... 95
Tin: Toxicological properties and target-organ effects ............................... 97
Titanium: Toxicological properties and target-organ effects ...................... 99
Tungsten: Toxicological properties and target-organ effects ................... 101
Uranium: Toxicological properties and target-organ effects .................... 103
Vanadium: Toxicological properties and target-organ effects .................. 105
Yttrium (and rare earth elements): Toxicological properties and
target-organ effects ................................................................................. 107
Zinc: Toxicological properties and target-organ effects ........................... 109
Zirconium: Toxicological properties and target-organ effects .................. 111
Maximum concentrations of heavy metals that can be tolerated at
the maximum permissible dust loads in the occupational
environment ............................................................................................ 112
Some detector tubes for screening assessment of exposure .................. 114
Size of partial sample for the top 10 % potential release points at a
confidence level of 90 % ......................................................................... 116
Table of random numbers after NIOSH (1977) ....................................... 117
Size of partial sample for the top 10 % exposure subgroup at a
confidence level of 90 % ......................................................................... 119
List of NIOSH and OSHA sampling and analytical methods for air
monitoring ............................................................................................... 120
Analytical methods for biological monitoring............................................ 127
Summary of medical surveillance, biological effects monitoring, and
biological monitoring ............................................................................... 129
Coke preparation .................................................................................... 142
Sintering .................................................................................................. 142
Table 4.2.3
Table 4.2.4
Table 4.2.5
Table 4.2.6
Table 5.2.1
Table 5.2.2
Table 5.2.3
Table 5.2.4
Table 5.2.5
Table 6.2.1
Table 6.2.2
Table 6.2.3
Table 6.2.4
Table 6.2.5
Table 7.2.1
Table 7.2.2
Table 7.2.3
Table 7.2.4
Table 8.2.1
Table 8.2.2
Table 8.2.3
Table 8.2.4
Table 8.2.5
Table 8.2.6
Table 9.2.1
Table 9.2.3
Table 9.2.4
Table 9.2.5
Table 10.2.1
Table 10.2.3
Table 10.2.3
Table 10.2.4
Table 10.2.5
Table 10.2.6
Table 10.2.7
Table 10.2.8
Table 10.3.9
Table 11.2.1
Table 11.2.2
Table 11.2.3
Table 11.2.4
Table 11.2.5
Table 11.6.1
Table 11.6.4
Table 11.6.5
Table 11.6.6
Table 11.6.7
Table 12.2.1
Table 12.2.2
Table 12.2.3
Table 12.2.5
Table 12.2.6
Table 13.2.1
Table 13.2.2
Table 13.2.3
Table 13.2.4
Storage, blending and material handling ................................................. 143
Blast furnace treatment ........................................................................... 144
Basic oxygen furnace treatment .............................................................. 144
Further refining, casting, rolling, pickling, galvanising ............................. 146
Grinding .................................................................................................. 151
Pelletisation............................................................................................. 152
Direct reduction ....................................................................................... 152
Electric arc furnace ................................................................................. 153
Casting, rolling, pickling, galvanising ....................................................... 154
Crushing and milling................................................................................ 159
Flotation and magnetic separation .......................................................... 160
Liquid/solid separation/drying .................................................................. 160
Smelting and converting .......................................................................... 161
Refining and rod casting ......................................................................... 161
Beneficiation ........................................................................................... 166
Material handling ..................................................................................... 166
Smelting .................................................................................................. 168
Alloy casting and sizing ........................................................................... 169
Beneficiation ........................................................................................... 174
Sintering .................................................................................................. 174
Material handling ..................................................................................... 175
Smelting .................................................................................................. 176
Alloy casting, crushing and sizing ........................................................... 177
Metal recovery from slag ......................................................................... 177
Crushing, screening, wet milling.............................................................. 181
Flotation .................................................................................................. 182
Bacterial oxidation and gold recovery ...................................................... 183
Bioliquor neutralisation/thickening and disposal ...................................... 184
Crushing ................................................................................................. 187
Milling ...................................................................................................... 188
Thickening .............................................................................................. 188
Leaching ................................................................................................. 188
Adsorption ............................................................................................... 190
Stripping and carbon regeneration .......................................................... 191
Electrowinning ......................................................................................... 191
Smelting .................................................................................................. 192
Residue disposal ..................................................................................... 192
Matte grinding ......................................................................................... 196
Atmospheric pressure leach and nickel sulphate crystallisation .............. 197
Pressure leach ........................................................................................ 197
Selenium removal ................................................................................... 198
Copper electrowinning ............................................................................ 198
Slow cool/crush/mill/magnetic concentration ........................................... 202
Secondary pressure leach....................................................................... 203
Copper electrowinning ............................................................................ 204
Cobalt removal ........................................................................................ 204
Nickel electrowinning .............................................................................. 205
Crushing and milling................................................................................ 209
Flotation of copper sulphide .................................................................... 210
Magnetic separation of magnetite ........................................................... 210
Phosphate rock concentrate treatment ................................................... 211
Phosphoric acid production ..................................................................... 211
Leaching ................................................................................................. 216
Gold extraction ........................................................................................ 216
Palladium extraction ................................................................................ 217
Base metal separation ............................................................................ 217
Table 13.2.5
Table 13.2.6
Table 13.2.7
Table 14.2.1
Table 14.2.2
Table 14.2.3
Table 14.2.4
Table 14.2.5
Table 14.2.6
Table 14.2.7
Table 14.2.8
Table 15.2.1
Table 15.2.2
Table 15.2.3
Table 15.2.4
Table 15.2.5
Table 15.2.6
Table 16.2.1
Table 16.2.2
Table 16.2.3
Table 16.2.4
Table 16.2.5
Table 17.2.1
Table 17.2.2
Table 17.2.3
Table 17.2.4
Table 18.2.1
Table 18.2.2
Table 18.2.3
Table 18.2.4
Table 18.2.5
Ruthenium separation ............................................................................. 217
Rhodium/iridium/osmium separation ....................................................... 218
Platinum recovery ................................................................................... 218
Raw material receipts and charge preparation ........................................ 225
Furnace charging and melting ................................................................. 228
Stainless steel refining ............................................................................ 229
Continuous casting ................................................................................. 229
Hot rolling ................................................................................................ 230
Annealing and pickling ............................................................................ 231
Cold rolling and bright annealing ............................................................. 231
Cutting to length, slitting, packing and despatching ................................ 232
Milling ...................................................................................................... 239
Digestion ................................................................................................. 240
Hydrolysis/Leaching/Washing ................................................................. 241
Production of Gypsum Byproduct ............................................................ 241
Calcining ................................................................................................. 242
Pigment Finishing ................................................................................... 242
Crushing and milling................................................................................ 247
Magnetic separation and de-watering ..................................................... 248
Roasting .................................................................................................. 248
Leaching ................................................................................................. 249
Precipitation and V2O5 production ........................................................... 250
Crushing, screening and magnetic separation ........................................ 255
Pre-reduction .......................................................................................... 256
Electric arc smelting ................................................................................ 256
Shaking ladles......................................................................................... 257
Roasting .................................................................................................. 263
Leaching and precipitation ...................................................................... 264
Purification .............................................................................................. 265
Electrowinning ......................................................................................... 266
Effluent treatment ................................................................................... 266
Glossary of abbreviations, symbols and terms
Abbreviations
American Conference of Governmental Industrial Hygienists
Atomic absorption spectrometry
Atomic absorption spectrometry, flame
Atomic absorption spectrometry, graphite furnace
Atomic emission spectrometry
Biological exposure index
Biological limit value
Chronic beryllium disease
Electro-cardiography
Gravimetric analysis
Inductively coupled plasma
International Agency for Research on Cancer
National Institute for Occupational Safety and Health
Occupational exposure limit - control limit
Occupational exposure limit - recommended limit
Occupational exposure limit - time-weighted average
Occupational Safety and Health Administration
Polarography
Threshold limit value
US Environmental Protection Agency
X-ray diffraction
ACGIH
AA
AA-F
AA-GF
AES
BEI
BLV
CBD
ECG
GR
ICP
IARC
NIOSH
OEL-CL
OEL-RL
OEL-TWA
OSHA
POL
TLV
USEPA
X DIF
Symbols
Exposure concentration
Hazard index
Hazard quotient
Original equal risk group size.
Sample size or subgroup size.
Unit risk factor
Ci
HI
HQi
N
n
URFn
Terminology
Air sparge
A technique used to add air in a distillation process.
Asthenia
Want of strength.
Atherosclerosis
A form of arterio-sclerosis, in which there is fatty degeneration of the middle coat of the arterial
wall.
Autoimmunity
A reaction to an individual’s own tissues (self-antigens) to which tolerance has been lost.
Bioaccumulation
The retention and concentration of a chemical by an organism. It is a build-up of a chemical in
a living organism, which occurs when the organism takes in more of the chemical than it can rid
itself of in the same length of time and stores the chemical in its tissue, etc.
Bioavailability
The proportion of a substance reaching the systemic circulation after a particular route of
exposure.
Cardiomyopathy
Disease of the heart muscle of unknown cause.
Centrilobular
Term used to indicate the central part of soft tissues, for example in the hepatic system.
Compartmentalisation
Separation into different compartments, for example different organs or tissue, or
environmental systems.
Cortex
The outer layer of an organ or other body structure, as distinguished from the internal
substance.
Cortical cells
Cells pertaining to or of the nature of a cortex.
Cyanosis
A bluish discoloration, especially of the skin and mucous membranes due to excessive
concentration of deoxyhemoglobin in the blood.
Dartos
Also called musculus dartos or dartos muscle, the subcutaneous tissue underlying the skin of
the scrotum.
Enterohepatic
Reabsorption instead of excretion by the liver cells into the small intestine.
Euchromatin
The condensed form of chromatin in which it stains lightly, is genetically active, and is partially
of fully uncoiled, being the interphase form of the chromosome or the material of most
chromosome arms during metaphase.
Fume
Aerosol of solid particles resulting from condensation of the vapour given off from the heating of
metals.
Glomerulus
A cluster composed of blood vessels or nerve fibres.
Glycoproteins
A conjugated protein containing one or more covalently linked carbohydrate residues.
Granuloma
An imprecise term applied to an aggregation of inflammatory cells, initiated by various
infectious or noninfectious agents.
Haematopoietic
Referring to the blood system.
Haemosiderin
An intracellular storage form of iron, found in the form of pigmented yellow to brown granules
consisting of a complex of ferric hydroxides, polysaccharides, and proteins.
Hazard index (HI)
The sum of several hazard quotients for multiple substances and/or multiple exposure.
pathways.
Hazard quotient (HQ)
The ratio of a single substance exposure level for a specified time period to a reference dose of
that substance derived from a similar exposure period.
Heavy metals
Members of a group of metallic elements which are recognized as toxic and generally
bioaccumulative. The term arises from the relatively high atomic weights of these elements.
Hepatotoxic
Toxic to the liver.
Homeostatically
Controlled by the level in the human body.
Idiotope
An antigenic determinant on a variable domain of an immunoglobulin molecule.
Idiotype
A set of one or more idiotopes that distinguish a clone of immunoglobin-producing cells from
other clones.
Immunoglobulins
Any of the structurally related glycoproteins that function as antibodies.
Immunoregulatory
Control of the immune response by mechanisms such as suppressor and contrasuppressor
lymphocyte circuits and the immunoglobulin idiotype-anti-idiotype network.
Immunosuppression
The suppression of harmful immune responses.
Ischaemia
Deficiency of blood in a part, usually due to functional constriction or actual obstruction of a
blood vessel.
Lacrimation
Production of tears.
Languor
Faintness, fatique.
Lymphocytes
A variety of white blood corpuscle produced in the lymphoid tissues and lymphatic glands of the
human body.
Lymphocytosis
An increase in the number of lymphocytes in the blood.
Medulla
General term for the most inner portion of an organ or structure.
Metabolic activation
Activated by the physical and chemical processes by which the body is maintained, and those
by which energy is made available for various forms of work.
Metaphase
The second stage of cell division during which the contracted chromosomes are arranged in the
equatorial plane of the spindle prior to separation.
Midzonal
Term used to indicate the intermediate part of soft tissues, for example in the hepatic system.
Mist
Finely divided liquid droplets suspended in air, formed by bubbling, boiling, foaming, spraying,
splashing or otherwise agitating a liquid that contains heavy metals.
Mutagenic
The property of a substance to increase the rate of mutation among cells.
Neoplasia
The formation of a neoplasm.
Neoplasm
Any new and abnormal growth, specifically a new growth of tissue in which the growth is
uncontrolled and progressive.
Nephrotoxic
Toxic or destructive to kidney cells.
Nephrotoxin
A toxin which has a specific destructive effect on kidney cells.
Neuroendocrine
Pertaining to interactions between the nervous and endocrine systems and to hormones such
as vasopressin and gastrin that are elaborated in the neurons and neuron-like cells.
Neurons
Any of the conducting cells of the nervous system.
Neurotoxic
Toxic or destructive to cells of the neurosystem.
Oocyte
A developing egg cell.
Oogenesis
The process of formation of female egg cells.
Osteodystrophy
Defective bone formation.
OVM badges
Passive samplers to measure exposure to hazardous chemicals, under the label OVM.
Periportal
Situated around the portal vein
Portal
Pertaining to a porta, or entrance, especially to the portal hepatis (liver).
Radiographically
Using radiology, X-rays.
Reference concentration (RfC)
A concentration of a chemical substance in an environmental medium to which exposure can
occur over a prolonged period without an expected adverse effect. The medium in this case is
3
usually air, with the concentration expressed in mg of chemical per m of air.
Reference dose (RfD)
The maximum amount of a chemical that the human body can absorb without experiencing
chronic health effects, expressed in mg of chemical per kg body weight per day. It is the
estimate of lifetime daily exposure of a noncarcinogenic substance for the general human
population (including sensitive receptors) which appears to be without an appreciable risk of
deleterious effects, consistent with the threshold concept.
Response
The reaction of a body or organ to a chemical substance or other physical, chemical, or
biological agent.
Reticulo-endothelial system
Highly specialised cells scattered throughout the body, but mostly in the spleen, bone marrow,
liver, and lymph glands. Their main function is the ingestion of red blood cells and the
conversion of haemoglobin to bilirubin.
Rhinitis
Inflammation of the mucous membrane of the nose.
Seminiferous
Producing or conveying semen.
Sensitisers
Term used for substances that cause a higher-than-normal response when repeatedly exposed
to.
Sertoli cells
Elongated cells in the seminiferous tubules to which the spermatids become attached.
Speciation
The chemical form in which a substance exists, relating to its oxidation state.
Spermatogonia
Plural of spermatogonium.
Spermatogonium
An undifferentiated germ cell of a male.
Teratogenesis
The production of birth defects in embryos and fetuses.
Threshold
The lowest dose or exposure of a chemical at which a specified measurable effect is observed
and below which such effect is not observed. Threshold dose is the minimum exposure dose of
a chemical that will evoke a stipulated toxicological response. Toxicological threshold refers to
the concentration at which a compound exhibits toxic effects.
Threshold limit
The concentration of a chemical above which adverse health and/or environmental effects may
occur.
Toxic
Harmful, or deleterious with respect to the effects produced by exposure to a chemical
substance.
Toxicant
Any synthetic or natural chemical with an ability to produce adverse health effects. It is a
poisonous contaminant that may injure an exposed organism.
Toxicity
The harmful effects produced by a chemical substance. It is the quality or degree of being
poisonous or harmful to human or ecological receptors. It represents the property of a
substance to cause any adverse physiological effects (on living organisms).
Toxicity assessment
Evaluation of the toxicity of a chemical based on all available human and animal data. It is the
characterization of the toxicological properties and effects of a chemical substance, with special
emphasis on the establishment of dose-response characteristics.
Toxic substance
Any material or mixture that is capable of causing an unreasonable threat to human health or
the environment.
Transduction
The transforming of one form of energy to another, such as by sensory mechanisms of the
body.
Transient histological changes
Episodes of changes in the minute structure of tissues, followed by complete recovery.
Tunica albuginea
A dense, white fibrous sheath, enclosing a part or organ.
Vapour
The gaseous form of a substance that is normally in the liquid or solid state at room
temperature and pressure.
Vascularised
To supply with vessels.
Xenobiotics
A chemical foreign to the biologic system.
1
Introduction
The toxicology and therapeutic properties of metals have been subjects of interest for centuries.
For example, mercury has been used for medicinal purposes since early civilisations, yet
mercury is also one of the most toxic substances known to man. Manganese is an essential
element that has been shown to be important for growth and reproduction in animals and
humans. However, manganese is also neurotoxic, and sustained occupational exposures
above certain levels have been shown to lead to a condition known as manganism, with
symptoms that resemble Parkinson's disease. Lead is also neurotoxic, but the manifestation of
effects is not the same as for manganese. The uptake of manganese in the human body is
influenced by the body burden of iron, and there are differences between the health effects
associated with inhalation and ingestion. Several human hereditory diseases have been related
to imbalances in metal metabolism. Hexavalent chromium compounds are believed to be
carcinogenic, but no evidence exists that has linked trivalent chromium compounds to cancer.
Many other examples exist to illustrate the complexity of metal toxicology. The toxic outcomes
of exposure to metals cover virtually every adverse effect from the cellular to the whole body
level. Effects vary from sensory irritation to disabling systemic disease, including cancer of
virtually every organ of the body. As one of the oldest areas of study, metal toxicology is also
one of the most rapidly developing disciplines.
Epidemiological studies of occupational exposure to metals over many years have formed the
basis for setting exposure guidelines for the protection of employees, and also to develop
tolerable exposure levels for the public at environmental levels. In the absence of human data,
animal studies form the basis for toxicological assessment. A whole new discipline has evolved
in health risk management over the past three decades, involving many branches of science.
Generally, occupational hygiene measurements to quantify exposure to metals are interpreted
in a relatively simplistic manner. What is referred to as a "health risk assessment" in
occupational hygiene terms is often better described as a hazard assessment, because the
actual risk is not quantified. Air concentrations of toxic substances are compared to some
guideline concentrations that represent a "safe" dose concept.
The ratio of the air
concentration of an occupational toxicant to its guideline or threshold concentration is
expressed as a hazard quotient. If the hazard quotient for a particular substance exceeds one,
the exposure may lead to an unacceptable health risk and requires further investigation. In the
case of multiple chemical exposure, hazard quotients are added to get an overall hazard index,
which also should not exceed one. Various agencies in the world use different terminology, but
all these guideline values are based on the same philosophy. The underlying assumption is
that nearly all employees may be repeatedly exposed to concentrations up to the threshold
levels without developing health effects. Because of the wide variation in susceptibility of
people to environmental toxicants, it may however be possible that a small percentage of the
individuals could experience some discomfort or aggravation of a pre-existing condition, or may
develop an occupational illness in exceptional cases.
1.1
Research problem statement
The presence of heavy metals and exposure of employees thereto in mineral processing plants
in South Africa have not been studied and described in a format that can be used as a general
reference document. The intention has been to provide a concise review of different process
steps in mineral processing and the associated health hazard for those who are new in the field,
and for the relatively uninformed who have to perform duties that require some understanding
of the processes and background to health risk assessment. In providing these perspectives,
the following aspects were considered to be of primary importance:
•
•
To provide an understanding of the paradigm of human health risk assessment in the
occupational environment;
To identify heavy metals that would be of interest in mineral processing plants;
23
•
•
•
To review the context of target-organ toxicity of heavy metals in the quantification of
exposure and health risks, taking into account the concepts of speciation and bioavailability;
To provide information on the elements of occupational health risk management, providing
general principles for survey design, sampling philosophies, and interpretation methods.
To put the principles listed above in context with selected mineral processing plants in
South Africa.
1.2
1.2.1
Objectives and aims of this study
Main objective
The main objective of the studies was to acquire and document all the background information
that is necessary for an understanding of health risks associated with heavy metals in various
mineral-processing plants. This involves descriptions of unit processing steps and operational
parameters, identification of sources of chemical hazards, descriptions of toxicology, guidelines
for sampling and chemical analysis for exposure assessment, and a framework for health risk
management. This information should assist persons who are not specialists in the field in
recognising health hazards relating to heavy metals, and should facilitate the review,
implementation and management of appropriate monitoring and medical health surveillance
programmes.
1.2.2
Goals
Process descriptions and exposure assessment
Process flow sheets were developed to show the unit operations, materials, identified heavy
metals, and potential exposure locations in the mineral processing plants.
Toxicological reviews
All the metals of interest were reviewed for their toxic effects on target organs, to put exposures
and health risks into context.
Guidelines for health risk management
Guidelines for health risk management included consideration of regulatory requirements, as
well as criteria for monitoring and medical surveillance.
1.3
1.3.1
Research context and design
Research context
The study was not intended to provide a manual with step-by-step guidance that could be used
for health risk management in the various industries. Specialists in health risk management in
the industries have many such reference documents to assist in the implementation and control
of occupational health risk management programmes. It was the intention to develop a
document that would be useful for persons who are not familiar with all the industries, but have
functions or an interest relating to occupational health across several of the industries. The
document may also be useful for persons who are specialists in some of the mineral processing
plants, but wish to get an idea of the health risk status in other facilities. Whilst the research in
certain respects has been generic, it provided specialist information on metal toxicology and
target organ effects, which are not always considered in detail in the interpretation of
occupational hygiene information. In this respect, it may assist in adding some scientific depth
to health risk interpretations.
24
1.3.2
Research design
There is no universal definition of heavy metals. It appears that the concept of "heavy metals"
did not have its origin only in molecular weight classification, but more in the fact that the metals
that are relatively more toxic to humans and animals also have relatively high molecular
weights. The first step in the current investigation was to select those metals that could be
placed in the category of "heavy metals". A list was compiled on the basis of toxicological
properties of the elements, and comprises 33 elements. The elements were chosen with the
objective of health risk management in mind, rather than on the basis of the classical definition
of "metals". For example, antimony and arsenic are classified as semi-metals, and selenium is
not a metal, but it does have some suggestion of metallic behaviour. These elements are
however of toxic concern and were included in the overall assessment of human exposure.
In order to understand target organ effects of heavy metals, the studies included a review of the
target organ systems of the body, and how these systems are affected by exposure to heavy
metals. The toxicology of the metals and metal compounds is covered in a subsequent section.
This information was used to identify health hazards in mineral processing plants.
To assess the potential for exposure to heavy metals, the various industries must be well
understood. This study therefore reviewed fifteen selected industrial processes to identify unit
operations, potential toxicants, and exposure zones where hazards may be posed. The
information is presented in generic flow diagrams. The diagrams were developed to represent
the general process steps, rather than detailed descriptions that were not essential for
understanding the basic concepts and associated hazards.
The following types of mineral processing plants were studied:
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Carbon steel process with blast furnace and basic oxygen furnace;
Carbon steel process with direct reduced iron and electric arc furnace;
Typical copper recovery circuit;
Typical ferrochromium production process;
Typical ferromanganese production process;
Bacterial oxidation circuit for the pre-oxidation of refractory gold ores;
Carbon-in-pulp circuit for gold recovery;
Nickel, copper, and cobalt refining process;
Typical phosphate rock production process;
Platinum group metal refining;
Typical stainless steel process;
Typical titanium dioxide production process;
Vanadium pentoxide production: the salt-roast process;
Vanadium slag production process; and
Typical circuit for zinc recovery from concentrate.
1.4
Deployment of the study
The project focussed on the characterisation of occupational exposure to heavy metals in 15
types of mineral processing plants. Many of the substances of interest occur in more than one
process, and similar health effects may be observed in the various plants. To avoid duplication
in the assessment of the 15 production plants, the rationale for selection of the 33 elements of
interest and general toxicological aspects are presented together in one section. Exposure
assessment, which covers monitoring and certain aspects of health risk management, is also
common to the various processes, and is therefore, presented in one section. These sections
were grouped into the literature review section, according to the logical steps of health risk
assessment, i.e. hazard assessment, dose-response (toxicological) assessment, and exposure
assessment. The basis for health risk characterisation is also presented in this section. The 15
25
processing plants are discussed separately in subsequent sections. Literature references are
given in the sections pertinent to the information.
Section 1:
Section 2:
Section 3:
Sections 4 to 18:
Introduction and background.
Research methodology
Literature review.
Discussion of the mineral processing plants.
26
2
Research methodology
The overall paradigm of health risk assessment was followed in the investigations, i.e.
according to the steps of hazard assessment, dose-response assessment, exposure
assessment, and risk characterisation.
As a first step, the 15 selected mineral processing plants were described in generic format,
using documented information on the processes, materials, and products. Engineers who were
familiar with the processes compiled process flow diagrams. The diagrams show process
steps, reagents, process conditions, discharge streams, hazard identification, and positions
where it would be appropriate to quantify human exposure. More information is presented in
process descriptions. The process information was verified through visits to typical plants and
discussions with specialists in the various fields. This work covers the hazard assessment
part of the investigation.
The dose-response assessment (toxicological assessment) was based on literature
information reviewed for the various metals. An extensive literature review was conducted,
covering searches of the most prominent international publications on the subject. The large
volume of data is summarised in tables. To place the information in context, concise
descriptions of the target organs of the body that are relevant to metal toxicity are also
presented. Because several of the metals are present in more than one processing plant,
toxicological information is presented together in one section of the report. The most relevant
information is however highlighted in the sections that deal separately with each plant.
The exposure assessment part of the studies was also handled in the descriptions of the 15
selected mineral processing plants. The approach did however not follow the conventional
occupational hygiene process of sampling and chemical analysis. It was limited to the
identification of zones of exposure, and recommendations for monitoring. Because the
protocols for occupational exposure monitoring are more related to the substances of interest
than the particular processing plants, the methodologies for monitoring have been presented
together in one section in the report. Reference has however been made to appropriate
monitoring in the sections that deal separately with each plant.
Risk characterisation was limited to descriptions of the paradigm for quantitative human
health risk assessment.
27
28
3
Literature review
3.1
Principles of health risk assessment
The term risk assessment in general describes the process of data interpretation in order to
assess the potential consequences of risks from human activities and natural events. In the
occupational and environmental protection context, risk assessment examines the potential
environmental and human health consequences related to the release of chemicals to the
environment. It is an interdisciplinary process that encompasses such diverse fields as
environmental chemistry, statistics, toxicology, air physics and chemistry, analytical technology
and engineering.
There are three basic concepts that are important in understanding the risk assessment
process:
Risk can be defined as the probability that a given hazard will cause harm of a specific nature
to a human population or an ecosystem.
A hazard is a source of risk and refers to the inherent capacity of heavy metals to cause harm.
Exposure is defined as the amount of chemical or physical agent available for adsorption or
interaction at the exchange boundaries of the organism at risk.
As outlined above, environmental and occupational health risk assessments include the steps
of hazard identification, dose-response assessment, exposure assessment, and health risk
characterisation. These are followed by a statement of risk options for decision-making on the
basis of financial, political or other relevant factors. Risk assessment provides the input data
for the implementation of a risk management programme.
3.2
Hazard assessment
The project terms of reference did not specify a particular list of hazardous heavy metals for
investigation. It was therefore necessary to develop a list of metals of interest to use as a
guideline in the review of potential health hazards in the selected mineral processing plants.
The rationale for selection of metals for assessment is presented below.
3.2.1
3.2.1.1
Criteria for selection
The classification of heavy metals
Heavy metals are defined as:
Members of a group of metallic elements which are recognised as toxic and generally
bioaccumulative. The term arises from the relatively high atomic weights of these elements.
[Asante-Duah, 1996]. Elements in Period 4 onwards in the Periodic Table are considered in the
category “heavy”. Beryllium is not a heavy element, but was nevertheless included because of
its carcinogenicity. Potassium is not relevant, because it is not toxic. Any toxicity of the salts of
potassium is due to the anion thereof, for example where it is associated with cyanide. Cyanide
is of prominent interest in certain mineral processing plants, but as a result of its association
with many metals, also those that are not classifiable as heavy metals, it was not included in
this investigation. The occurrence and health consequences of cyanides should be considered
in a separate study, not only in the context of exposure to heavy metals.
Calcium compounds should be considered toxic only when they contain toxic compounds (such
as arsenic), or as calcium oxide or hydroxide. For completeness, however, calcium is included
for possible exposures to calcium oxide or hydroxide. The other elements to consider are from
Sc and the higher molecular weights under Transition Elements, and Group III onwards.
29
Period
Antimony and arsenic are classified as semi-metals, and selenium is not a metal, but it does
have some suggestion of metallic behaviour. These elements are however of toxic concern
and should be included in the overall assessment of human exposure. Uranium should be
included for reasons of its heavy-metal toxicity. Radioactivity does not form part of the current
project.
1
2
3
4
5
6
7
1
H
1
Li
3
Na
11
K
19
Rb
37
Cs
55
Fr
87
2
Be
4
Mg
12
Ca
20
Sr
38
Ba
56
Ra
88
*
**
Figure 3.2.1.1
3.2.1.2
Group
Sc
21
Y
39
*
3
Ti
22
Zr
40
Hf
72
V
23
Nb
41
Ta
73
Cr
24
Mo
42
W
74
Mn
25
Tc
43
Re
75
Fe
26
Ru
44
Os
76
Co
27
Rh
45
Ir
77
Ni
28
Pd
46
Pt
78
Cu
29
Ag
47
Au
79
Zn
30
Cd
48
Hg
80
B
5
Al
13
Ga
31
In
49
Tl
81
Ce
68
Th
90
Pr
59
Pa
91
Nd
60
U
92
Pm
61
Np
93
Sm
62
Pu
94
Eu
63
Am
95
Gd
64
Cm
96
Tb
65
Bk
97
Dy
66
Cf
98
Ho
67
Es
99
4
5
6
7
C
6
Si
14
Ge
32
Sn
50
Pb
82
N
7
P
15
As
33
Sb
51
Bi
83
O
8
S
16
Se
34
Te
52
Po
84
F
9
Cl
17
Br
35
I
53
At
85
Er
68
Fm
100
Tm
69
Md
101
Yb
70
No
102
Lu
71
Lr
103
8
He
2
Ne
10
Ar
18
Kr
36
Xe
54
Rn
86
**
La
57
Ac
89
Periodic table of the elements, showing those elements that were
selected for investigation
Regulatory classification
Table 3.2.1.2 lists toxic elements that are regulated by different agencies for the control of
environmental and occupational exposures of humans.
The US Environmental Protection Agency (USEPA) classification [Patrick, 1994] lists elements
that are of general environmental concern in ambient air. On the basis of general abundance,
occupational environments can be expected to contain a wider range of elements at levels that
are of health significance. The ACGIH list [ACGIH, 2000] has been compiled by the American
Conference of Governmental Industrial Hygienists, for use in the practice of occupational
hygiene. Occupational exposure limits listed in the Regulations for Hazardous Chemical
Substances [Department of Labour, 1995] under the South African Occupational Health and
Safety Act (No. 85 of 1993) are based on the OEL’s published by the Health and Safety
Executive in the UK. It is concluded that the lists of heavy metals as compiled by the ACGIH
and the RSA Department of Labour are relevant and essential to consider in the assessment of
exposures in mineral processing plants.
30
Table 3.2.1.2
List of elements selected for assessment
USEPA hazardous air
pollutants (HAPs)
Antimony
Arsenic
Beryllium
Cadmium
Chromium
Cobalt
Lead
Manganese
Mercury
Nickel
Selenium
3.2.2
List of metals assigned TLV’s
by the ACGIH
Antimony
Arsenic
Barium
Beryllium
Bismuth
Cadmium
Calcium
Chromium
Cobalt
Copper
Indium
Iron
Lead
Manganese
Mercury
Molybdenum
Nickel
Osmium
Platinum
Rhodium
Selenium
Silver
Tantalum
Tellurium
Thallium
Tin
Titanium
Tungsten
Uranium
Vanadium
Yttrium
Zinc
Zirconium
List metals assigned OEL’s
according to South African
regulations
Antimony
Arsenic
Barium
Beryllium
Bismuth
Cadmium
Calcium
Chromium
Cobalt
Copper
Indium
Iron
Lead
Manganese
Mercury
Molybdenum
Nickel
Osmium
Platinum
Rhodium
Selenium
Silver
Tantalum
Tellurium
Thallium
Tin
Titanium
Tungsten
Uranium
Vanadium
Yttrium
Zinc
Zirconium
Use of the list of hazardous metals
It can be expected that different elements will be relevant in the various processes, and some
of the elements listed in the table may not be present in significant concentrations in any of the
mineral processing plants. Furthermore, some of the elements may not be in a chemical form
that would be toxic. It is not inferred that sampling and chemical analyses would include all the
elements in the table. Nevertheless, the entire list of elements in the table above had to be
considered in the description and assessment of each mineral processing plant, and the overall
hazard identification.
3.3
3.3.1
Dose-response assessment
Basic concepts in toxicology
Dose-response assessment is based on the toxicological response to a dose in target tissues
to predict, for example, the non-cancer health risks resulting from human inhalation of an air
pollutant, or the level of exposure associated with a one-in-a-million risk of cancer. Risk
estimation in the low-dose region where human exposures normally occur, often depends on
31
extrapolation of dose-response information from studies using high-dose exposures in
laboratory animals.
Acute toxicity refers to the development of symptoms of poisoning or the occurrence of adverse
health effects after exposure to a single dose or multiple doses of a chemical within a short period
of time. Sensory irritation may be considered in short-term exposures, because it is
concentration-dependent rather than time-dependent.
Chronic toxicity refers to the occurrence of symptoms, diseases, or other adverse health effects
that develop and persist over time, as a result of exposure to a single dose or multiple doses of a
chemical over a relatively long period of time (months to years).
Carcinogenicity describes the ability of a chemical to cause cancer in a living organism. The
classification of carcinogens according to the International Agency for Research on Cancer
(IARC) was used in this report. This is presented in Table 3.3.1.
Table 3.3.1
The IARC classification for carcinogenicity
Group 1
Human carcinogen
Sufficient evidence of carcinogenicity in humans.
Group 2A
Probable human carcinogen
Limited human data and sufficient animal data.
Only limited human data, or only sufficient animal data in the presence of other supporting data.
Group 2B
Possible human carcinogen
Limited human data in the absence of sufficient evidence in animals.
Sufficient animal data with inadequate or no human data.
Limited animal data with other supporting data, and inadequate or no data in humans.
Group 3
Not classifiable
Data do not fit into any of the above groups.
Group 4
Probably not a human carcinogen
Evidence suggests lack of carcinogenicity in humans and animals.
Developmental toxicity refers to adverse effects on the developing organism that may result
from exposure prior to conception (either parent), during prenatal development, or postnatal to the
time of sexual maturation. Adverse developmental effects may be detected at any point in the life
span of the organism.
Sensitisation is the result of exposure to substances that have the ability to sensitise the
organism to subsequent exposures. This leads to severe responses at exposure concentrations
that are normally below the threshold for manifestation of the typical effects.
Bioavailability is a term generally used to describe the extent and rate of absorption for a toxic
substance that enters the systemic circulation in the unaltered form from the exposure site. The
concept is more complex, however, because a substance may not be bioavailable in its parent
form, but after metabolism may be converted into a form that can enter the systemic circulation.
32
Reproductive toxicity is divided into male and female reproductive toxicity. Male reproductive
toxicity is defined as the occurrence of adverse effects on the male reproductive system that
may result from exposure to toxic substances. It may be expressed as alterations to the male
reproductive organs and/or the related endocrine system, manifested as alteration in sexual
behaviour, fertility, pregnancy outcomes or modifications in other functions that are dependent
on the integrity of the male reproductive system. Female reproductive toxicity refers to adverse
effects observed in the female reproductive system that may result from exposure to toxic
substances. It includes, but is not limited to, adverse effects in sexual behaviour, onset of
puberty, fertility, gestation, parturition, lactation or premature reproductive senescence.
3.3.2
Mechanisms of metals toxicity
The primary routes of exposure to toxicants in the occupational environment are via inhalation,
ingestion, and dermal contact. Most metallic compounds occur as solids, fumes or in mists, and
are frequently associated with particulates in the occupational exposure scenario. Particle size
determines where in the respiratory tract inhaled particles are deposited and hence can exert their
toxic effects. Only a few metals and metal compounds are liquids at room temperature and
pressure, e.g. mercury (Hg), nickel tetracarbonyl [Ni(CO)4], and arsenic trichloride (AsCl3).
Liquids are in equilibrium with vapours above them, characterised by the vapour pressure of the
liquid phase. If not contained, liquid metals and compounds release vapours to which employees
may be exposed. A limited number of metal compounds exist as gases at room temperature and
pressure, e.g. arsine (AsH3) and stibine (SbH3). Metals seldom interface with biological systems
in the elemental form. They occur as compounds that vary in the ease with which they can pass
through biological membranes.
Metabolism of metals refers to all the processes by which the body handles metals. Absorption,
distribution, biochemical modification, storage, and excretion are the most important processes
in the metabolism of metals.
Absorption refers to the process where xenobiotics cross body boundaries and reach the
systemic circulation.
Distribution is the process whereby the absorbed xenobiotics are transported by the blood
circulation system to various organs and tissues.
Biochemical modification includes processes in the human body where chemical properties of
substances are modified, such as changes in oxidation state and complex and radical formation.
Storage of toxicants refers to the deposition and retention of toxicants in different organs of the
body.
Excretion is the process whereby xenobiotics are eliminated from the body through such routes
as urine, faeces and the lungs.
Organ-specific toxicity reflects the principle of compartmentalisation. The target organ receiving
the exposure is highly susceptible to injury. Both uptake and toxicity may be linked to unique
metabolic processes. For example, cadmium is known to accumulate in the kidneys as a result of
its association with the cadmium-scavenging protein metallothionin. On the other hand, lead is
distributed as a systemic toxicant throughout the entire body before being deposited in the bone.
There is often little correlation between the reaction of a target organ to the toxic effects of a metal
and the concentration of the metal in that tissue. For example, 90 per cent of the lead in the
human body is found in the skeleton, but its toxic effects are manifested primarily in the nervous
system, renal system, and haematopoietic system. It is not possible to generalise principles that
govern the mechanisms of action of toxic metals. A variety of biological effects are produced in
different organ systems, and in no case can the multiple manifestations of toxicity be assigned to
33
a single biochemical process. The mechanisms of metals toxicity can be classified into the
following categories:
Enzyme inhibition
Toxic metals normally have a high affinity for amino-acid side chains such as sulphydryl, histidyl,
or carboxyl groups, and can react directly with proteins to alter enzymatic or structural function.
Indirect effects
Metals may bind to cofactors, vitamins, and substrates, thereby altering the availability of these
essential cell constituents for biological function.
Substitution for essential metals
Several metals are essential to the human body, playing a role in protein structure, enzyme
catalysis, osmotic balance, and transport processes. Toxic metals that are chemically and
physically similar to some of the essential metals may replace the essential metals, thereby
exerting toxic effects through alteration of biological processes.
Table 2.3.2 shows an overview of target-organ toxicity of metals and metalloids.
Metal imbalance
Excessive exposure to a particular metal may lead to depletion or repletion of an essential
metal in biological systems. For example, large exposures to zinc may lead to copper
deficiency. On the other hand, sufficient zinc prevents cadmium intoxication that is manifested
as necrosis in the intestine. Lead alters tissue levels of many essential elements, including
iron, zinc, copper, and calcium.
34
Table 2.3.2
Overview of target-organ toxicity of metals and metalloids
Beryllium
Bismuth
Cadmium
•
•
•
Calcium
Chromium
•
•
Cobalt
Copper
Indium
•
Iron
Lead
•
Manganese
Mercury
•
•
•
•
•
•
•
•
•
Molybdenum
Nickel
Osmium
Platinum
•
Rhodium
•
Selenium
Silver
Tantalum
Tellurium
Thallium
•
•
•
Tin
•
•
•
•
•
•
•
•
Titanium
Tungsten
Uranium
•
Vanadium
Yttrium
•
Zinc
Zirconium
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
35
Cardiovascular
system
Skin
Eye
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Reproductive
system
•
Muscle system
Endocrine system
•
•
•
•
Barium
•
•
Immune system
Arsenic
•
•
•
•
Bone
Gastrointestinal tract
•
•
•
Haematopoietic
system
Liver
•
•
•
Antimony
Respiratory system
Nervous system
SUBSTANCE
Renal system
TARGET ORGAN SYSTEM
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
3.3.3
Target organ systems and toxic responses
After a toxic substance has entered the human body, it is distributed to target sites of action,
i.e. sites of metabolic change and excretion. This section provides short descriptions of organ
systems that respond to the toxicological impacts of occupational pollutants.
3.3.3.1
Renal system
The kidney is a very efficient filter organ and plays a crucial role in the elimination of toxicants
from the body. Anatomically the kidney is a complex arrangement of vascular endothelial cells
and tubular epithelial cells, the blood vessels and tubules being intertwined.
Excretion into the urine involves one of the following three mechanisms:
•
•
•
Filtration from the blood through the pores in the glomerulus.
Diffusion from the blood stream into the tubules.
Active transport into the tubular fluid.
The kidney is a target organ for metals toxicity for the following reasons:
•
•
•
•
•
The kidney receives 25 per cent of the blood of the cardiac output. Therefore, the exposure
of kidney tissue to foreign compounds in the bloodstream, especially the cortex that
receives more blood than the medulla, is relatively high.
One of the functions of the kidney is its concentrating ability. After glomerular filtration,
many substances are re-absorbed from the tubular fluid. Hence, the concentration of
foreign substances in the tubular lumen is considerably higher than that in the blood. The
tubular-to-blood ratio may reach values of 500:1.
Compounds that are actively transported from the blood into the tubular fluid often
accumulate in the proximal tubular cells, even more so where saturation of the transport
system occurs. This again leads to much higher concentrations than in the blood stream, to
which tubular cells are exposed.
Although to a lesser degree than the liver, the kidney has sufficient activity to be responsible
for metabolic activation.
Exposure to most heavy metals results in renal toxicity. Lead, mercury, platinum, cadmium
and chromium are amongst the most prominent nephrotoxins.
3.3.3.2
Nervous system
The nervous system consists of cells and fibre, each of which is an extension of the nerve cell.
The brain and spinal cord is known as the central nervous system and nerves proceeding from
them are named cerebrospinal or peripheral nerves. The third division, situated in the neck,
thorax and abdomen is known as the autonomic nervous system.
The central nervous system is protected from toxicants by the blood-brain-barrier. This barrier
is a functional concept based on the observation that some substances that enter and affect
other soft tissue such as the liver and kidney are excluded from the brain. Not all substances
are preferentially excluded from the brain and non-polar, lipid-soluble compounds usually
penetrate the blood-brain-barrier. The nervous system, both peripheral and central, is a
common target for toxic substances for the following reasons:
•
•
The cells making up the nervous system are particularly susceptible to changes in the
environment such as pH changes.
The distribution of blood capillaries in the brain is not uniform, in as much that white matter
is less vascularised than grey matter, resulting in a higher sensitivity to foreign compounds
in the grey matter.
36
•
•
•
It has been proposed that excitatory amino acids may damage hypothalamic neurons by
excessive stimulation and thus metabolic exhaustion of the cells.
Quantitative differences in essential cell components may make one cell type more
sensitive to toxicants than other cells. For example, small neurons are preferentially killed
when the whole brain is exposed to methyl mercury.
Certain large cells such as the cortical and hippocampal pyramidal cells and others have
unusually large nuclei and the DNA is largely present as euchromatin. These cells often
have several nucleoli. All these structural differences point to high metabolic activity in
these cells and thus increased susceptibility to anoxic damage.
Mercury, lead and manganese are among the most prominent neurotoxic substances.
3.3.3.3
Liver
The liver is the largest visceral organ and is exposed to many potentially toxic substances via
the gastrointestinal tract. The structural and functional unit in the liver is the lobule. In the
centre of this lobule is the terminal hepatic venule and at the periphery the portal space,
containing a branch of the portal vein, an hepatic arteriole and a bile duct. Based on this
configuration, pathologic lesions of the hepatic parenchyma have been classified as
centrilobular, midzonal or periportal. The simple acinus concept has been developed to
indicate the three circulatory zones within each acinus. Zone one first receives blood from the
afferent venules and arterides, followed by zone two, and finally zone three. Hence there will
be metabolic differences between the zones, because of the blood flow. The concentration of
oxygen and nutrients will decrease as blood flows from zone one to zone three, which leaves
zone three more sensitive to damage from toxic compounds.
The liver is a target organ for toxic substances for the following main reasons:
•
•
•
•
The large and diverse metabolic capabilities of the liver enable it to metabolise many foreign
compounds, but as metabolism does not always result in detoxification, this may make it a
target.
Because of the extensive role that the liver plays in intermediary metabolism and synthesis,
it consequently interferes with endogenous metabolic pathways, which may lead to toxic
effects.
Bile secretion by the liver may also be a factor. Biliary excretion of foreign compounds may
lead to high concentrations, especially if saturation occurs, as has been experienced with
the hepatotoxic drug “furosemide”. Alternatively, enterophepatic circulation can give rise to
prolonged high concentrations in the liver. Any interference to the bile production or bile
flow may lead to damage to the biliary system and surrounding hepatocytes.
The relatively high blood supply ensures that the liver is exposed to high concentrations of
toxic substances absorbed from the gastrointestinal tract.
3.3.3.4
Gastrointestinal tract
The gastrointestinal tract starts at the mouth and leads to the stomach, which is linked to the
mouth via the oesophagus. The far end of the stomach ends in the pylorus, a thick
circumferential muscular sphincter that separates the stomach from the duodenum. The
duodenum links the stomach to the ileum, also known as the small intestine, and has the
largest surface area of the gastrointestinal tract, 6,5-m long and 35-mm in width. The ileum
mouths into the large intestine or colon, which is 1,8-m long and 65-mm in width. The last part
of the colon is known as the rectum, which passes straight down through the back of the pelvis
to open to the exterior through the anus.
The gastrointestinal tract is the first organ exposed to ingested foreign substances.
Consequently, local concentrations at the contact tissue may often be many times higher than
concentrations elsewhere in the body. However, intoxication normally arises from either
intentional or accidental overexposure. This is rare in comparison with chronic intoxication,
37
which may induce pathologies elsewhere in the body. The most significant elements that affect
the gastrointestinal tract are cadmium, mercury, lead, and arsenic.
3.3.3.5
Respiratory tract
The pulmonary system may be considered as having three major regions, namely the
nasopharyngeal, the tracheobronchial and the pulmonary. The nasopharynx starts at the
anterior nares, extending back and down to the level of the larynx. It is lined with vascular
mucous epithelium, which is characterised by ciliated columnar epithelium and mucous glands.
The function of the nasopharyngeal is to filter out large inhaled particles, to increase the relative
humidity of inhaled air, and to moderate the temperature of inhaled air.
The tracheobronchial region consists of the trachea, bronchi and the bronchioles, and serves
as an airway between the nasopharyngeal and the alveoli in the lung. This airway is lined with
epithelium cells and a thin layer of mucus. The mucus-covered surface serves as a mucociliary
escalator, moving particles from the deep pulmonary area to the oral cavities to be swallowed
and excreated.
In the pulmonary system the bronchioles decrease in diameter, forming the alveoli, which end in
an alveoli sac with a complex blood vessel arrangement around the alveoli. Air pockets and
cells form a large surface area available for oxygen absorption and gas exchange. It is in these
areas of the lung where gas exchange takes place.
The left lung has two lobes divided by a single fissure, while the right lung is split by two deep
fissures, dividing it into three lobes. The two lungs are encapsulated in a pleural cavity formed
by two layers of membranes surrounding the lungs, except at the point where the bronchi enter.
The respiratory tract is a target organ because:
•
•
•
•
Exposure to and absorption of toxic compounds in the lungs are influenced by many
anatomic features, including lung volume and alveolar surface area. The uptake of toxic
gases occurs throughout the respiratory system, starting at the nasopharyngeal cavity.
Diffusion is the dominant driving force in the absorption of toxicants.
2
The lung surface area is approximately 70 m in humans and the cellular barrier between air
and blood is minimal. Consequently, foreign particles may be absorbed rapidly.
Since the lungs receive 100 per cent of the cardiac blood output, they are extensively
exposed to toxins that may be in the blood stream. The function of the lung is to exchange
gases between ambient air and the blood, which means it is efficient in absorbing toxic
substances from the air. The high oxygen concentration in the lung allows it to be sensitive
to reactive oxygen species.
The lung is particularly vulnerable, because of the various cell types that all exhibit different
susceptibilities to toxic damage.
For human exposure through inhalation of airborne particulates, three size-dependent fractions
have been defined:
•
•
•
The inhalable fraction (diameter ≤ 100 µm) is the fraction that enters the body through the
nose and mouth during breathing. It may be linked to health effects anywhere in the
respiratory tract, such as rhinitis, nasal cancer, or systemic effects.
The thoracic fraction (diameter ≤ 20 µm) penetrates into the lung below the larynx, and is
relevant for asthma, bronchitis, and lung cancer.
The respirable fraction (diameter ≤ 10 µm) enters the alveolar region of the lung, and is linked
to such chronic diseases as pneumoconiosis and emphysema. Some agencies also consider
a fraction ≤ 2.5 µm, suspected to have more serious health consequences than the fraction up
to 10 µm.
38
3.3.3.6
Haematopoietic system
The haematopoietic system is the transport system that supplies substances absorbed from the
gastrointestinal tract, as well as oxygen from the lungs, to the tissues. It returns carbon dioxide
to the lungs and other products of metabolism to the kidneys. Blood also functions as a
regulator for the body temperature and distributes hormones and other agents to regulate
tissue cell functions.
Blood consists of cellular components suspended in plasma. In the adult the red blood cells
(erythrocytes), white blood cells (leucocytes), and platelets are formed in the bone marrow
which is one of the largest organs in the body. Approximately 75 per cent of the cells in the
marrow belong to the white blood cells and 25 per cent are mature red blood cells. In the blood
circulation however, there are five hundred times as many red blood cells as there are white
blood cells. This difference is due to the fact that the red blood cell life span is much longer
than that of the white blood cells. Red blood cells are biconcave discs with a diameter of
approximately 7,5 µm. They contain haemoglobin, an iron-containing porphyrin compound,
which takes up oxygen in the lungs and releases it in the tissues. White blood cells are of
various types. They can leave the circulation and move through tissues where they are
involved in combating infection, wound healing, and rejection of foreign bodies. Platelets are
the smallest cellular components in the haematopoietic system and play an important role in
blood coagulation.
As almost all foreign compounds are distributed via the blood stream, the components of the
blood are exposed at least initially to toxic compounds. Damage to and destruction of the red
blood cells results in a reduced ability to carry oxygen from the lungs to the tissues.
Destruction of white blood cells results in an increased susceptibility to bacterial and virus
infections, and may result in death.
As the production of blood cells takes place in the bone marrow, bone marrow suppression is
characterised by a deficiency of all or some cellular elements in the peripheral blood. This
condition results from either a decrease in production of cells, or an inability of bone marrow to
manufacture adequate numbers of these cells. Inorganic arsenic compounds, mercury, cobalt,
zinc and lead have all been shown to have effects on bone marrow function.
Several metals are known to have acute and direct haemolytic effects, e.g. arsenic, copper,
cobalt, lead, mercury and zinc. Metals may directly impair red cell function either by inhibiting
erythropoiesis in bone marrow or by decreasing red cell survival in the circulation, leading to
anaemia. Haemolytic anaemia occurs when the rate of cell destruction in peripheral blood
exceeds the normal rate of production in the bone marrow. Other conditions include
leukopenia, polycythemia, thrombocytopenia, decreased haemoglobin, and decreased
haematocrit.
3.3.3.7
Bone
Bone tissue is a major receptor for storage of certain toxic substances. It serves as a reservoir
for metals such as lead. The mechanism of skeletal uptake of substances is a surfacechemistry phenomenon, in which the exchange takes place between the bone surface and the
extra-cellular fluid in contact with it. The bone surface is the hydroxyapatite crystals of the bone
mineral. Because of the dimensions of the crystals the surface area is large in proportion to the
mass, enhancing the possibility for uptake.
The deposition and storage of toxic elements in bone may or may not be toxic. For example,
the accumulation of lead has not been confirmed unambiguously to be toxic to the bone. Under
certain conditions the process of uptake is reversible, leading to release by ion exchange at the
crystal surface and by dissolution of bone crystals through osteoclastic activity. This will be
reflected by an increased plasma concentration of the toxicant.
39
Exposure of humans to cadmium has been associated with osteodystrophy. Cadmium tends to
replace calcium from bone, leading to demineralisation, and it also inhibits bone formation.
Other effects relate to a disturbance of uptake of essential elements, which may lead to
osteotoxicity.
3.3.3.8
Endocrine system
The endocrine system consists of those organs that secrete hormones into the blood or lymph
systems. These hormones play an important role in the activities of other organs, and general
chemical changes in the human body. The primary endocrine glands are the thyroid, adrenal,
pituitary, parathyroid, pancreas, ovaries, and testicles. Although not much is known about the
effects of heavy metals on the endocrine system, some effects have been indicated tentatively,
such as the effects of arsenic on the thyroid, and development of diabetes mellitus. This was
shown to be consistent with hyperglycemia and glucose intolerance reported in animal studies
(Garcia-Vargas & Cebrian, 1996: 428). Testicular tumours in test animals have been
associated with exposure to cadmium.
3.3.3.9
Muscle
Muscular tissue is divided according to its function into two main groups, i.e. voluntary and
involuntary muscle. Voluntary muscle, being under control of the will, is mainly attached to the
skeleton, and hence often called skeletal muscle. Involuntary muscle functions independently,
and is found in the heart, the inner and middle coats of the stomach and intestines, the ureters
and urinary bladder, the windpipe and bronchial tubes, the ducts of glands, the gall bladder, the
uterus and fallopian tubes, the middle coat of the blood and lymph vessels, the iris and ciliary
muscle of the eye, the dartos muscle of the scrotum, and in association with the various glands
and hairs in the skin. The effects of heavy metals on muscular tissue have not been well
described, but it is known that muscle degeneration has been reported for exposure to indium
2+
(Doull, Klaassen & Amdur, 1980: 445). Heavy metals such as cobalt interferes with Ca in the
muscle tissue, leading to muscle spasma.
3.3.3.10
Eye
The eye is a relatively small, very complex organ, and is the sensory organ of sight. It is an
elaborate photoreceptor that detects information in the form of light from the environment, and
transmits this information by a series of electrochemical processes to the brain.
The cornea and the conjunctiva are the portions of the eye directly exposed to external insults.
The conjunctiva is a transparent mucous membrane that extends from the lumbus over the
anterior sclera. It does not cover the cornea, but passes from the eye onto the inner surface of
the eyelid. A scar or vascularisation that can be tolerated by other body structures with no
adverse effects may, in the case of the cornea, destroy function completely. A very small
amount of a corrosive substance, which would be of no consequence elsewhere in the body,
can therefore be the cause of blindness if it reaches the cornea.
The eye can thus be regarded as a target organ, because of its external position in the
organism and direct exposure, as well as from systemic exposure. Exposure to dust and
corrosive substances such as calcium oxide would lead to severe eye irritation. Heavy metal
ions in high concentrations may combine with protein functional groups, which results in tissue
destruction.
3.3.3.11
Skin
The skin is the largest organ of the body. It consists of two basic elements, i.e. an outer
epidermis of which the main function is a protective one. It covers the underlying muscles,
protecting them and maintaining a constant body temperature. A secondary function is
secreation, the two secreations being sebaceous material and perspiration. The dermis lying
under the epidermis provides inherent strength to the skin, largely through its collagen content.
40
The waterproofing capability of the epidermis is potentially a problem, as the greasy surface
aids absorption of fat-soluble materials and hence a ready route of entry for many organic
chemicals. Chemicals may also pass through the cells of the sweat glands, or the sebaceous
glands or through the hair follicles.
The first phase of absorption is diffusion of the toxicant through the epidermis and it is in this
area that the rate-limiting barrier for absorption of toxicants exists.
The second phase of absorption is diffusion of the toxicant through the dermis, which is inferior
to the epidermis. The dermis contains a porous, non-selective, watery diffusion medium. The
toxicants pass through this area by simple diffusion into the systematic system, entering the
blood stream.
Dermatosis may be readily divided into two groups, i.e. primary irritant contact dermatitis, and
allergic contact dermatitis. Contact dermatitis is normally influenced by immunoregulatory
mechanisms.
3.3.3.12
Cardiovascular system
The heart is known as the pump that circulates blood through the body. It consists of four
cavities, each provided at its outlet with a valve, resulting in a pumping action as blood flows
from one cavity to the other, eventually forcing the blood through the circulation systems. Two
main circulation systems are distinguished, i.e. the pulmonary circulatory system and the
systemic circulatory system, with the heart in-between.
The cardiovascular system is occasionally affected by toxic compounds and becomes a target
organ mainly because of:
•
•
The high concentration of blood flow. Toxic compounds that might be present in the blood
have to pass through the heart and may damage the heart as well as other vascular tissue.
The sensitivity of the heart muscles to electrolyte changes. Heavy metals such as cobalt
2+
interferes with Ca in the muscle tissue, leading to muscle spasma.
Artherosclerosis is the primary cause of myocardial infarction and cerebral infarction in the
industrial world. Chemical elements exert biological effects via enzymes, hormones, and
various messenger molecules. Excess zinc can disrupt the utilisation of copper, an essential
element in the protection of the cardiovascular system. It also disrupts the metabolism of
cholesterol. Both cadmium and lead have been linked to essential hypertension, that is,
hypertension of unknown origin.
3.3.3.13
Immune system
The immune system consists of a network of cells and chemical mediators, having the primary
function of protecting the human body against infections. The major components of the
immune system are the leukocytes, the immunoglobulins and the complement system,
consisting of several plasma proteins. They interact with each other to keep the balance of
immunity. Immunosuppression, autoimmunity, hypersensitivity or allergy, and neoplasia are the
main toxic reactions of the immune system. Heavy metals are known to interfere with the
immune system in several ways. The effects may be associated with membrane alterations,
modifications in signal transduction, displacement of essential metals, and interactions with
cellular proteins or enzymes. In the case of essential elements, both a deficiency and excess
can result in modification of cell-mediated immune responses. In most cases of exposure to
metals, effects on the immune system are observed at exposure levels that also cause other
systemic effects. Allergic contact dermatitis is believed to be influenced by both epidermal
penetration and by immunoregulatory mechanisms.
41
3.3.3.14
Reproductive system
Male reproductive system
The testis is the organ responsible for the male reproductivity. The testis is an ovoid organ and
is located at the end of the spermatic cord. The testes are freely moveable in the scrotal sac.
This sac is composed of skin, a thin layer of dartos muscle and connective tissue. A thick
capsule, the tunica albuginea, surrounds the testes. Inside the testes a number of smaller
compartments are formed by numerous septa. Inside each compartment are two to four highly
tortuous seminiferous tubules. The adult testis has two functions:
•
•
Spermatozoa are produced by the seminiferous tubes.
Androgens are produced by cells outside the seminiferous tubes, the Leydig cells.
These two environments are separated from each other by the blood-testis barrier and maintain
a special microenvironment within the seminiferous tubules. This microenvironment protects
the developing germ cells from external noxious substances.
Spermatogenesis starts at puberty with the mitotic division of spermatogonia, and continues
throughout the life of a human male, although production decreases with age. The
spermatogonia are located next to the basal lamina between the Sertoli cells. However, in the
human at the onset of spermatogenesis, all spermatogonia in the entire cross section of the
seminiferous tubule do not divide, but may become active at a later stage.
Each
spermatogonial cell undergoes a number of mitotic divisions, producing a clone of daughter
cells.
The structure of the sperm cell is important to ensure proper fertilisation and penetration of the
oocyte, as well as the consistence of the androgens. A number of chemicals are known to
have an impact on these processes, thus causing the testis to be a target organ for toxic
substances. The rapidly growing and dividing tissue of the testis leaves it vulnerable to
chemicals such as anti-cancer drugs, which may damage the cells. Because the testes have a
limited blood supply, a chemical like cadmium that causes reduced blood flow may cause
ischaemia in the testes.
Female reproductive system
The female reproductive tract includes the ovary, uterus, cervix and vagina. Each of these
organs is highly specialised to ensure the production of normal offspring for the propagation of
the species. Although these are different organs, their proper functioning depends on the
functioning of the neroendocrine system as well as the functioning of the ovary itself. The
ovaries have a dual function:
•
•
To produce oocytes or eggs, and
To secrete the steroid hormones.
The process of germ cell production in the female is called oogenesis. In the human female
oogenesis starts long before birth, and undergoes a series of mitoses so that by the time of
birth the ovaries of the human female will contain a finite number of oocytes. The female
reproductive tract is considered an important target organ, because if these oocytes are
damaged or lost, for example due to exposure to hazardous chemicals or radiation, they cannot
be replaced by stem cells. The particular woman will then be infertile for the rest of her life. If
exposure to chemicals or radiation injury caused chromosomal damage to the oocytes, there
would be no new oocyte formation. Toxic chemicals causing damage to the female
reproductive system can be divided into two categories:
•
•
Direct-acting toxicants and indirect-acting toxicants. Direct-acting toxicants cause direct
damage to the sub-cellular organelles and the micro molecules within the cells.
Indirect-acting toxicants alter the metabolic activity of a cell or cause hormone imbalance.
42
3.3.4
Toxicology of the elements
This section provides descriptions and summaries of the toxicology of metals in alphabetical
order. For each element and its compounds a general description of the metabolism and toxic
effects is given, followed by a summary table listing short-term and long-term effects in target
organ systems, as well as references to regulatory guidelines.
Short-term effects are those adverse health effects observed after short-term exposures, i.e.
over hours or days. It is likely that these effects would disappear if the source were removed.
Long-term effects occur after short-term or chronic exposures, and the effects may persist if the
source is eliminated.
Several of the elements have not been identified to be of significance in any of the mineral
processes. In accordance with the overall structure of the document, however, the toxicological
assessments in this section include all those elements listed in the hazard assessment.
3.3.4.1
Antimony (Sb)
Absorption:
Inorganic antimony enters the human body through the oral and pulmonary routes (Lauwerys &
Hoet, 1993: 19). No quantitative data are available for absorption of antimony after inhalation.
Animal studies indicate that absorption after ingestion is of the order of 15 to 50 per cent (rat,
hamster) (Elinder & Friberg, 1979a: 285). No similar data for humans have been documented.
Distribution:
After absorption the highest levels of antimony were observed in the liver, thyroid, heart, and
kidneys (Elinder et al. 1979a: 283, 286).
Excretion:
Elimination and excretion depend on the type of antimony compound. Most absorbed antimony
5+
3+
is reportedly excreted rapidly via the urine (mainly Sb ) and faeces (mainly Sb ). A small part
of the absorbed substance may have a long biological half-life (Elinder et al., 1979a: 283, 286;
Van der Voet & de Wolff. 1996a: 458).
Acute effects:
Respiratory irritation has been reported after acute occupational exposure to SbCl3 at relatively
3
high concentrations (73 mg/m ). Acute systemic exposure to antimony compounds causes dry,
scaly skin, weight loss and hair loss. (Van der Voet et al., 1996a: 457). Severe (fatal)
pulmonary oedema was noted after exposure to SbCl5, but the exposure level was not known
(Elinder et al., 1979a: 289).
The compound stibine (SbH3) is an odourless toxic gas, which causes haemolysis (Elinder et
al., 1979a: 289).
Heavy exposure to smelter fumes was reported to lead to stomach cramps, nausea, vomiting
and diarrhoea. (Elinder et al., 1979a: 283).
43
Table 3.3.4.1
Antimony: Toxicological properties and target-organ effects
Carcinogen
Sb2O3 possible human
carcinogen, IARC Group 2B
Species listed
Antimony and compounds
as Sb
OEL-RL and OEL-CL
BEI
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical Substances
(Department of Labour, 1995).
Medical surveillance
Biological effect monitoring
Biological monitoring
See Table 3.4.6.3
Speciation in mineral processing plants: Sb, Sb2O3, SbCl3, Sb2S3, Sb2S5, Sb2(SO4)3
Absorption: Inhalation (rapid), ingestion
Target organs
Deposition: Lung, kidney, liver, thyroid
Excretion: Rapid in urine and faeces, small fraction has long retention
Short-term effects
Long-term effects
Renal system
Damage
Nervous system
Liver
Damage
Gastrointestinal tract
Vomiting, nausea
Ulcer
Respiratory tract
Irritant; rhinitis, pharyngitis,
Soreness, nosebleeds, pneumoconiosis, emphysema, obstructive lung disease,
Haematopoietic system
Haemolysis (SbH3)
Bone
Endocrine system
Muscle
Eye
Skin
Transient skin eruptions (antimony spots), scaly appearance,
air loss
Cardiovascular system
Heart failure
Sb2O3, Sb2S3 : circulatory disease, ECG (T-wave) changes
Immune system
Reproductive system
44
Chronic effects:
3
Soreness and nosebleeds were common amongst workers exposed to 4.7 to 11.8 mg/m of
antimony during smelting operations. Other respiratory irritations were also reported (Elinder et
al., 1979a: 289). The supporting information on chronic studies listed pulmonary toxicity and
chronic interstitial inflammation as the critical effects (IRIS, 1999: database).
Pneumoconiosis-like X-ray pictures were noted by several authors in workers with long-term
exposure, and antimony seems to accumulate in the lungs. After chronic exposure to SbO3,
signs of obstructive lung disease and emphysema were also found (Elinder et al., 1979a: 289;
Van der Voet et al., 1996a: 458).
The cardiovascular system can also be affected. Changes in the electrocardiogram and death
3
from heart failure have been documented after exposure to SbS3 (0.6 to 5.5 mg/m for 8 to 24
months) (Elinder et al., 1979a: 289).
An increased incidence of stomach ulcers was reported for a group of antimony workers in
comparison to a control group (Elinder et al., 1979a: 290).
Transient skin irritation (antimony spots) is common amongst people working with antimony or
its salts (Elinder et al., 1979a: 289; Van der Voet et al., 1996a: 458).
Carcinogenicity:
Evidence for carcinogenic action in laboratory animals was judged by the International Agency
for Research on Cancer as sufficient for antimony trioxide, and limited for antimony trisulfide.
In humans, antimony trioxide is considered a possible carcinogen (Group 2B) (IARC, 1989: Vol.
47). Antimony has not undergone complete review by the USEPA (IRIS, 1999: database).
Reproductive effects:
One study has indicated that female workers exposed to antimony were more prone to
spontaneous abortions than a control group. In another study, a high incidence of premature
deliveries was noted amongst women occupied in antimony smelting and processing (IRIS:
1999: database). These studies were conducted in 1967 and 1955, respectively, and it is
uncertain how the data should be interpreted in terms of dose-response correlation.
3.3.4.2
Arsenic (As)
Absorption:
The extent of deposition, absorption and distribution in the system depends on the solubility and
possibly the oxidation state of arsenic.
For the inhalation route the size of the aerosols is important. Up to 85 to 90 per cent of watersoluble trivalent arsenic deposited in the lungs can be bio-available (Hrudey, Chen, Rousseaux,
1996: 78, 83). Particles larger than 5 microns will be deposited in the upper respiratory tract
where mucociliary clearance will lead to ingestion and absorption from the gastrointestinal tract
(Fowler, Ishinishi, Tsuchiya, Vahter, 1979a: 299). Both organic and soluble inorganic arsenic
are easily and rapidly absorbed (70 – 90 per cent) from the gastrointestinal tract (Fowler et al.,
1979a: 299; Hrudey et al., 1996: 80).
45
Table 3.3.4.2
Arsenic: Toxicological properties and target-organ effects
Carcinogen
Species listed
Human carcinogen
As and compounds (as As)
IARC Group 1
Arsine (AsH3) :
OEL-RL and OEL-CL
BEI
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical Substances
(Department of Labour, 1995).
Medical surveillance
Biological effect monitoring
Biological monitoring
See Table 3.4.6.3
Speciation in mineral processing plants: As2O3, NaAsO2, AsCl3
Absorption: Inhalation (good); ingestion (high); skin (possible)
Target organs
Renal system
Deposition: Skin, hair, bone
Short-term effects
Long-term effects
High initial concentration, rapid excretion
Nervous system
Liver
Excretion: Urine (rapid)
Peripheral neuritis, loss of touch
High initial concentration, rapid excretion
Swelling, cancer
Irritation, cough, dyspnoea, chest pain, bronchitis
Ulcers (mucous membranes), lung cancer
Gastrointestinal Tract
Respiratory tract
Haematopoietic system
Anaemia, leucopenia
Bone
Endocrine system
Muscle
Eye
Skin
Irritation, contact dermatitis (As2O3)
Hyperkeratosis, cancer, pigmentation
Cardiovascular system
Abnormal ECG, vascular disorders, gangrene
Immune system
Reproductive system
Foetal absorption (bone, skin, liver, brain)
46
Distribution:
Once absorbed, arsenic is rapidly cleared from the blood (24 hours) and widely distributed in
the body, mainly to the liver, kidney, spleen, lung and gastrointestinal tract. Over the next 2 - 4
weeks the arsenic is then redistributed to the hair, nail, skin and bone (Hrudey et al. 1996: 77).
Clearance from the skin and bones is much slower and the major portion of the body burden is
situated in the bone, muscle and skin (Fowler et al., 1979a: 300; Hrudey et al., 1996: 80).
Excretion:
The major part of absorbed arsenic is excreted in the urine within 48 hours either unchanged,
or in detoxified form as methyl-arsenic compounds (Fowler et al., 1979a: 293; Lauwerys &
Hoet, 1993 22).
Care must be taken when monitoring arsenic in the urine, as consumption of certain seafood
can give rise to very high (organic) arsenic levels. For occupational monitoring the levels of
inorganic arsenic should rather be measured (Lauwerys et al., 1993: 23).
Acute effects:
Acute or sub-acute exposure to arsenic (especially to arsenic trioxide or arsenic trichloride) can
cause coughing, dyspnoea, chest pain and irritation of the skin, mucous membranes and eyes.
Gastrointestinal effects such as vomiting and diarrhoea have been noted (Fowler et al., 1979a:
304; Garcia-Vargas & Cebrian, 1996: 424).
Chronic effects:
Chronic exposure in the occupational environment can cause melanosis, lesions of the skin and
mucous membranes, (including perforation of the nasal septum), palmar and plantar
hyperkeratosis, nervous and respiratory disorders and lung cancer.
Abnormal ECG,
disturbance of peripheral circulation and gangrene of the extremities (Blackfoot disease) have
also been reported (Fowler et al., 1979a: 305; Garcia-Vargas et al., 1996: 424). The likelihood
for Blackfoot disease has been found to increase with dose and age, especially for persons
older than 40 (IRIS, 1999: database).
Gastrointestinal disturbances such as loss of appetite, cramps, nausea, constipation, or
diarrhoea may occur.
Liver damage with resulting jaundice may occur, as well as disturbances of the blood, kidneys
and nervous system (Lewis, 1995: database; Garcia-Vargas et al., 1996: 424).
Painful peripheral nervous disturbance (neuritis) in the extremities, anaemia, and liver
disturbance have also been reported and are symptomatic of chronic arsenic intoxication.
Abnormal neurological findings can persist for years after a poisoning incident (Fowler et al.,
1979a: 307).
Chronic exposure in the general public can arise from environmental contamination, especially
from drinking water, and consumption of contaminated beverages or food. Studies have shown
in such cases an occurrence of skin lesions, vascular disorders, and “black foot” disease
(Fowler et al., 1979a: 305).
Carcinogenicity:
Arsenic is a Group 1 human carcinogen (IARC 1987: Vol. 1, Suppl. 7), causing tumours of the
lung, liver, bladder, prostate and skin (IRIS, 1999: database; Garcia-Vargas et al., 1996: 433).
Reproductive effects:
Arsenic seems to cross the placental barrier, as levels in foetal bone, liver, skin and brain have
been reported to increase with duration of the pregnancy (Fowler et al., 1979a: 300). There are
47
some studies that suggest involvement of the immune system and possible genotoxic effects
(Garcia-Vargas et al., 1996: 431-432).
Teratogenic effects have been demonstrated in animal studies (Fowler et al., 1979a: 309).
Arsine
Arsine (hydrogen arsenide, AsH3) is a colourless flammable gas with a slight garlicky odour and
is formed whenever nascent hydrogen is evolved in material containing arsenic. Many ores
contain arsenic as impurity and arsine can therefore be generated in the ore processing, nonferrous metal refining and silicon steel industries when ores being processed could accidentally
come into contact with acids. Arsine can also be formed via the hydrogen ion during hydrolysis
reactions, for example between arsenic containing dross and moisture (Fowler et al., 1979a:
313; IRIS, 1999: database)
The mechanism of arsine toxicity differs from that of other arsenic compounds. It is a potent
3
haemolytic poison. The lethal dose is 250 mg/m for 30 min. Symptoms appear within a few
3
hours at exposure levels of 0.5 to ten mg/m and include upset stomach, shortness of breath,
palpitations and backache, followed by red urine and jaundice (Fowler et al., 1979a: 313).
Arsine is a confirmed human carcinogen (Lewis, 1995: database).
3.3.4.3
Barium (Ba)
Absorption:
The toxicity of barium salts depends on their solubility. Soluble barium compounds are readily
absorbed from the respiratory and gastrointestinal tract and act as potassium antagonists in the
muscles, causing initial stimulation followed by paralysis (Reeves, 1979a: 321).
Barium sulphate is highly insoluble in water and is routinely used as X-ray contrast medium,
with negligible absorption during its residence time in the alimentary canal (Reeves, 1979a:
324).
Inhaled barium sulphate seems to be slightly soluble in bodily fluids, possibly in colloidal form.
Clearance from the lung (half-life eight to nine days) depends on the specific surface area and
thermal history of the particles (Reeves, 1979a: 324).
Distribution:
Upon chronic exposure barium is deposited in the bones (three to five times as readily as
calcium or strontium) and pigmented parts of the eye (Reeves, 1979a: 325).
Excretion:
After ingestion, barium is excreted mainly via the faeces (91 per cent), with sweat and urine
being minor routes (Reeves, 1979a: 325).
Acute effects:
2+
The Ba ion in toxic doses (0,2 to 0,5 g in adults) is a muscle poison, causing initial
stimulation, followed by paralysis. Gastrointestinal symptoms are followed by skeletomuscular
and cardiac stimulation. Barium is a potassium antagonist and it appears that the symptoms
may be attributable to severe hypokalemia. (Reeves, 1979a: 326; Lewis, 1995: database).
Barium sulphide, barium carbonate and barium oxide cause respiratory and eye irritation, and
incidences of dermatitis after skin contact have been reported (Lewis, 1995: database).
.
48
Table 3.3.4.3
Barium: Toxicological properties and target-organ effects
Carcinogen
Species listed
OEL-RL and OEL-CL
Soluble compounds as Ba:
Not carcinogenic
BaSO4 respirable dust
BEI
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical Substances
(Department of Labour, 1995).
Medical surveillance
Biological effect monitoring
Biological monitoring
See Table 3.4.6.3
Speciation in mineral processing plants: BaCO3, BaO, BaSO4, BaS, BaCl2
Absorption: Inhalation, ingestion (soluble salts)
Deposition: Bone, eye
Excretion: Faeces, sweat, urine
Short-term effects
Long-term effects
Renal system
Nervous system
Liver
Gastrointestinal tract
Vomiting, colic, diarrhoea (soluble salts)
Respiratory tract
Irritant (BaO, BaCO3, BaS)
Benign pneumoconiosis (baritosis). Radiologically conspicuous. (BaSO4)
Haematopoietic system
Bone
Accumulation
Endocrine system
Muscle
Severe hypokalemia, convulsive tremors
Eye
Irritant (BaO, BaCO3, BaS)
Skin
Irritant (BaO, BaCO3, BaS)
Cardiovascular system
Slow, irregular heartbeat, transient high blood pressure
Accumulation
Immune system
Reproductive system
BaCl2 (male rat)
49
Chronic effects:
Although several studies have been conducted to test a connection between barium exposure
and elevated blood pressure, no conclusive evidence was found for humans (IRIS, 1999:
database).
Inhalation of barium sulphate can lead to a benign, symptomless form of pneumoconiosis
(baritosis) with conspicuous radiographic manifestations. There is no apparent impairment of
pulmonary function. There are indications that accumulation of barium in the lungs will diminish
after cessation of exposure (Reeves, A L. 1979a: 321; IRIS, 1999: database.)
Carcinogenicity:
Barium is not likely to be carcinogenic to humans (IRIS, 1999: database).
Reproductive effects:
Reproductive effects have been observed with BaCl2 and BaCO3 under experimental conditions
(Lewis, 1995: database).
3.3.4.4
Beryllium (Be)
Absorption:
Soluble beryllium compounds are considerably more hazardous by inhalation than by ingestion
or skin contact. At physiological pH, most of these compounds are rendered insoluble, and are
therefore not easily absorbed by the body (Reeves, 1979b: 329).
The largest proportion of ingested beryllium is passed through the gastrointestinal tract
unabsorbed.
Distribution:
Short-term storage of beryllium takes place in the liver, and long-term storage in the skeleton.
Excretion:
During the excretion process kidney damage may result.
Elimination of beryllium from the lung seems to be a two-phase process. The first phase has a
half-life of two to three weeks, leaving a long-term residue.
Acute effects:
Inhalation of soluble beryllium compounds can cause acute respiratory tract effects such as
rhinitis, pharyngitis, tracheobronchitis and occasionally fatal pneumonitis (Reeves, 1979b: 335;
Lewis, 1995: database).
During contact with the skin, beryllium is bound to the epidermis and not easily absorbed into
the system. Contact dermatitis is fairly common when handling soluble beryllium compounds
(Reeves, 1979b: 335).
Chronic effects:
The chemical reactivity and toxicity of beryllium oxide are inversely related to the firing
temperature during which it is prepared in a calcining process (500 – 1750 °C) (Reeves, 1979b:
335). Chronic occupational exposure to so-called “low-fired” beryllium oxide is associated with
berylliosis or chronic beryllium disease (CBD). This is a slow-developing pulmonary disease
which in the past had a relatively high mortality rate, and can appear from 1 to 25 years after
exposure (Reeves, 1979b: 336).
50
Table 3.3.4.4
Beryllium: Toxicological properties and target-organ effects
Carcinogen
Human carcinogen
IARC Group 1
Species listed
Beryllium
OEL-RL and OEL-CL
BEI
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical Substances
(Department of Labour, 1995).
Medical surveillance
Biological effect monitoring
Biological monitoring
Speciation in mineral processing plants: BeO, BeSO4, Be(OH)2, BeCl2, BePO4
Absorption: Mainly lung
Deposition: Lung, liver, kidney, bone
Excretion: Urine
Short-term effects
Long-term effects
Renal system
Kidney damage
Nervous system
Liver
Short term storage
Granulomas
Rhinitis, tracheitis, bronchitis, pneumonitis (BeF2)
Berylliosis, (“low-fired” BeO), pulmonary insufficiency
Gastrointestinal tract
Respiratory tract
Haematopoietic system
Disturbances (animals)
Bone
Rickets (animals)
Endocrine system
Muscle
Eye
Conjunctivitis
Skin
Allergic dermatitis, ulceration
Dermatitis, ulceration
Cardiovascular system
Immune system
Reproductive system
51
See Table 3.4.6.3
CBD is characterised by dyspnoea, cough, reduced pulmonary function and weight loss
(Benson & Zelikoff 1996: 929; Lewis 1995: database; Reeves, 1979b: 336). CBD has also
been reported for people not occupationally exposed, and family members who had been
exposed to workers’ contaminated clothing (IRIS, 1999: database; Lewis, 1995: database).
The extreme sensitivity of some individuals towards CBD is thought to be linked to immune
factors (IRIS, 1999: database).
3
The injurious threshold level (mg Be/m ) for the “high fired” oxide is considered to be about 30,
compared to one to three for “low-fired” oxide and 0,1 to 0,5 for the sulphate (Reeves, 1979b:
335).
Non-healing skin granuloma from beryllium-contaminated wounds and abnormal lymphocyte
tests have been reported for occupational exposure (IRIS: 1999: database; Lewis 1995:
database). Granulomatous and fibrotic changes to the liver and spleen have been reported
(Lewis 1995: database).
Carcinogenicity:
Beryllium inhibits phosphatases and other enzymes and is thought to interfere with DNA
replication (Reeves, 1979b: 338 - 339). It is classified as a Group 1 human carcinogen (IARC
1993: Vol. 58).
Reproductive effects:
No data have been documented to indicate reproductive effects in humans.
3.3.4.5
Bismuth (Bi)
Absorption:
Bismuth compounds taken up via inhalation and ingestion are slightly to moderately absorbed
in the system, depending on their solubility. No quantitative data are available (Fowler et al.,
1979b: 348).
Distribution:
After absorption it is distributed to the soft tissues and bone, with the highest concentration
being found in the kidney and liver (Fowler et al., 1979b: 348).
Excretion:
A large proportion of ingested bismuth passes through the gastrointestinal tract unabsorbed
and is excreted in the faeces. Absorbed bismuth is excreted mainly in the urine, with the rate
dependent on the solubility (Fowler et al., 1979b: 348).
The following biological half-lives have been adopted for humans (Fowler et al., 1979b: 349):
System
Biological half-life (days)
Whole body retention
5
Kidney
6
Liver
15
Spleen
10
Bone
13,3
52
Table 3.3.4.5
Bismuth: Toxicological properties and target-organ effects
Carcinogen
Species listed
Bismuth telluride
Not a human carcinogen
Bismuth telluride (Se-doped)
OEL-RL and OEL-CL
BEI
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical Substances
(Department of Labour, 1995).
Medical surveillance
Biological effect monitoring
Biological monitoring
Speciation in mineral processing plants: Bi, Bi2O3, Bi2S3, Bi2(SO4)3, BiCl3
Absorption: Poor. Ingestion, inhalation
Deposition: Kidney, liver, bone
Excretion: Urine, faeces
Target System
Short-term effects
Long-term effects
Renal system
Acute failure
Storage
Nervous system
Confusion, tremors, clumsiness
Liver
Fatty degeneration, hepatitis
Gastrointestinal tract
Irritant (BiF5)
Respiratory tract
Irritant (BiF5), (trimethyl bismuth)
Gingivitis, lead-like pigmentation of gums
Haematopoietic system
Bone
Endocrine system
Muscle
Eye
Irritant (trimethyl bismuth)
Skin
Irritant (trimethyl bismuth)
Eruptions, pigmentation
Bi(NO3)3
Vaginal pigmentation
Cardiovascular system
Immune system
Reproductive system
53
See Table 3.4.6.3
Acute effects:
In the industrial environment bismuth is considered to be one of the less toxic heavy metals.
Up to 1996 no industrial bismuth poisoning had been reported (Lewis, 1995: database).
Reported cases of intoxication are mainly due to therapeutic and cosmetic uses of bismuth
compounds (Lewis, 1995: database; Fowler & Vouk, 1979b: 345). During therapeutic use,
acute kidney failure and fatty degeneration of the liver have been reported (Fowler et al.,
1979b: 350).
Trimethylbismuth has been reported to irritate the upper airways, eyes and broken skin (Fowler
et al., 1979b: 349).
Chronic effects:
The literature notes the similarity in the pharmacological and toxic behaviour of lead and
bismuth. The dark line in the gums, sometimes noted in cases of lead poisoning, can also be
caused by exposure to bismuth. This can complicate the diagnosis of plumbism (Lewis, 1995:
database).
Some kidney and liver damage and neurological symptoms have been associated with
therapeutic uses (Fowler et al., 1979b: 351). No adverse effects have been reported for
occupational exposure (Lewis, 1995: database).
Carcinogenicity:
IARC has not classified bismuth a human carcinogen.
Reproductive effects:
Absorbed bismuth can be transported across the placenta (animal studies) (Fowler et al.,
1979b: 345).
3.3.4.6
Cadmium (Cd)
Absorption:
Occupational uptake of cadmium is mainly attributable to inhalation of dust and fumes (CdO
particles, predominantly < 10 µm) (Hrudey, Chen, Rousseaux, 1996: 91). Extensive information
is available on the bioavailability of cadmium by various routes in both animals and man
(Hrudey et al., 1996: 96 - 99). The pulmonary absorption rate is dependent on the solubility
and particle size of inhaled material (Hrudey, et al., 1996: 92), and can be up to 50 per cent
(Friberg, Kjellstr!m, Nordberg, Piscator, 1979a: 361). A fraction of the dust particles deposited
in the respiratory tract will be cleared to the digestive system (Lauwerys & Hoet, 1993: 32).
Absorption from the gastrointestinal tract is low, (more than 90 per cent is excreted in the
faeces), but is increased in persons with a low dietary intake of iron, calcium or protein
(Lauwerys, et al., 1993: 32; Hrudey, et al., 1996: 94; Gerhardsson & Skerfving, 1996: 85).
Distribution:
Cadmium accumulates in the liver, bone and kidneys. About 50 per cent of the body burden
can be found in the kidney and liver (Friberg, 1979a: 361). The kidney is the critical target
organ, showing the first signs of damage and urinary analysis will determine when
precautionary measures are to be taken.
Excretion:
Once absorbed, clearance from the body is slow. The literature quotes a biological half-life of
10 to more than 20 years (Friberg et al., 1979a: 355; Lauwerys, et al., 1993: 32; Hrudey, et al.,
1996: 92).
54
Table 3.3.4.6
Cadmium: Toxicological properties and target-organ effects
Carcinogen
Human carcinogen
IARC Group 1
Species listed
OEL-RL and OEL-CL
BEI
Cd and compounds (except CdO
fume and CdS pigments) (as Cd)
Occupational Health And Safety Act, 1993
Cadmium oxide (CdO) fume (as Cd) Regulations for Hazardous Chemical Substances
Cadmium sulphide (CdS) pigments (Department of Labour, 1995).
Medical surveillance
Biological effect monitoring
Biological monitoring
See Table
3.4.6.3
(respirable dust Cd)
Speciation in mineral processing plants: CdO, CdS, CdSO4, CdCO3, Cd stearate, Cd acetate
Absorption: Inhalation, ingestion
Deposition: Kidney, lung, pancreas
Excretion: Very slow. Faeces, urine
Short-term effects
Long-term effects
Storage; chronic disease, proteinuria, kidney stones,
calcuria
Renal system
Nervous system
Headache
Liver
Storage; disturbed function
Gastrointestinal tract
Nausea, vomiting, cramps, diarrhoea
Respiratory tract
Shortness of breath, pulmonary oedema, pneumonitis
Emphysema
Haematopoietic system
Anaemia
Bone
Mineral depletion, osteoporosis, osteomalacia
Endocrine system
Muscle
Eye
Skin
Cardiovascular system
Hypertension
Immune system
Reproductive system
Possible prostate cancer; reproductively active
Experimental
55
Acute effects:
Brief inhalation of high concentrations can cause acute pulmonary oedema and death. Fatal
amounts of fumes and dust can be inhaled without sufficient discomfort to warn workers to
leave the area (Lewis, 1995: database). Symptoms may appear only 24 hours after acute
exposure (Friberg et al., 1979a: 367).
Acute poisoning in the industrial environment is usually caused by inhalation during activities
like welding, brazing or smelting of cadmium-containing metals. An airborne concentration of 1
3
mg/m for 8 hours is considered to be sufficient to cause clinical symptoms, whilst levels of 5
3
mg/m for 8 hours could possibly be lethal. Symptoms include shortness of breath, general
weakness and fever, and in severe cases, pulmonary insufficiency, shock and death (Friberg,
et al., 1979a: 363).
Ingestion can cause acute pulmonary oedema (CdCl2) (Lewis, 1995: database). Cadmium
compounds are irritants with such a violent emetic effect that there is little chance of
absorption.(Lewis, 1995: database).
CdO fumes can lead to metal fume fever, similar to that caused by ZnO. Pulmonary effects are
characterised by coughing, difficult breathing and cyanosis. Inhalation of CdO dust can lead to
changes in pulse rate, sense of smell, elevated blood pressure and proteinuria (Lewis, 1995:
database).
Chronic effects:
The effects of chronic inhalation exposure seem to depend on the intensity of exposure: the
more intense the exposure the more likely lung damage like emphysema is, as opposed to
almost exclusive renal damage seen in chronic low-level exposure (Friberg et al., 1979a: 368).
The primary target organ is the kidney, irrespective of exposure route. Up to 30 per cent of the
total body burden will normally be stored in the kidneys (Friberg et al., 1979a: 361). The first
sign of chronic cadmium poisoning is an increase of proteins in the urine (proteinuria).
Increased levels of amino acids, glucose and phosphates may be seen at a later stage (Friberg
et al., 1979a: 368). Increased excretion of calcium (calcuria) has been noticed following
exposure to cadmium (Fowler & Nordberg, 1996e: 760). Once kidney damage has occurred,
cadmium excretion rises considerably, and in the most severely poisoned people, kidney levels
are almost normal, in contrast to liver levels (Friberg et al., 1979a: 362).
Anaemia and disturbed liver function may also occur. In addition, the lung, bone (Itai-Itai
disease), cardiovascular, and reproductive systems can be affected by chronic ingestion
(Friberg et al., 1979a: 368).
Carcinogenicity:
Cadmium compounds are Group 1 human carcinogens (IARC 1993: Vol. 58). Occupational
exposure has been shown to increase the risk of prostate cancer (Friberg et al., 1979a: 355,
371). Inhalation of cadmium compounds can contribute to the development of lung cancer
(Benson, & Zelikoff, 1996: 934).
Reproductive effects:
Cadmium does not cross the placental barrier (Friberg et al., 1979a: 362). Experimental data
have shown that cadmium compounds exhibit teratogenic, mutagenic and reproductive effects
(Friberg et al., 1979a: 371 - 372).
56
3.3.4.7
Calcium (Ca)
Absorption:
Calcium compounds are common air pollutants and nuisance dusts and should be considered
toxic only when they contain toxic components, such as arsenic or cyanide, or as calcium oxide
or calcium hydroxide. Calcium carbonate, calcium hydroxide and especially calcium oxide are
skin, eye and mucous membrane irritants (Lewis 1995: database). For the purpose of this
investigation assessments were limited to calcium hydroxide and calcium oxide. Cyanides,
although prominent in mineral processing, were not included in the current assessment.
Distribution:
Consider only irritation effects, no systemic distribution.
Excretion:
Consider only irritation effects, no systemic distribution.
Acute effects:
Calcium oxide is an irritant, powerfully caustic to living tissue (Lewis 1995: database).
Calcium hydroxide is a severe eye irritant and a skin, mucous membrane and respiratory irritant
(Lewis 1995: database).
Chronic effects:
Irritation effects are more concentration dependent than time dependent.
Carcinogenicity:
Carcinogenicity of certain calcium compounds is ambiguous and subject to study regarding
both as chemo-preventive agents and co-carcinogens (Poirer & Littlefield., 1996: 290). Calcium
arsenate is a confirmed human carcinogen, but this is due to the anion rather than calcium
(Lewis 1995: database; IARC 1987: Vol. 23, Suppl. 7).
Reproductive effects:
CaF2 has shown experimental reproductive effects (Lewis 1995: database).
57
Table 3.3.4.7
Calcium: Toxicological properties and target-organ effects
Carcinogen
Species listed
OEL-RL and OEL-CL
BEI
Calcium carbonate/ silicate total inhalable
Ca arsenate confirmed,
certain compounds
possible cocarcinogens
Calcium carbonate/silicate total respirable
Calcium hydroxide
Calcium oxide
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical Substances
(Department of Labour, 1995).
Medical surveillance
Biological effect monitoring
Biological monitoring
Calcium cyanamide
Speciation in mineral processing plants: CaO, Ca(OH)2, CaCO3, CaSO4, CaS, Ca phosphates
Absorption: No data available
Target organ
Deposition: No data available
Excretion: No data available
Short-term effects
Renal system
Nervous System
Liver
Gastrointestinal tract
Respiratory tract
Poison (CaS); irritant (CaO, Ca(OH)2, Ca(NO3)2)
Haematopoietic system
Bone
Endocrine system
Muscle
Eye
Irritant (CaO, Ca(OH)2 (severe), CaCO3, Ca phosphates (di, tribasic), Ca(NO3)2)
Skin
Irritant (CaO, Ca(OH)2, CaCO3, Ca phosphates (di, tribasic), Ca(NO3)2); dermatitis (Ca(OH)2)
Cardiovascular system
Immune system
Reproductive system
58
Long-term effects
See Table
3.4.6.3
3.3.4.8
Chromium (Cr)
Absorption:
6+
Cr compounds are more readily absorbed from the lungs, gastrointestinal tract and skin than
3+
Cr compounds (Langard et al., 1979: 383; Hrudey, Chen, Rousseaux, 1996:103, 105, 107).
The bioavailability of chromium is governed by a very complex biochemistry of which the
6+
3+
reduction of Cr to Cr in the cells renders it difficult to transport (Klein, 1996: 209). The rate
of absorption from the respiratory system depends on solubility. Insoluble compounds tend to
remain in the lung (Hrudey et al., 1996: 103).
Cr
3+
compounds are poorly absorbed from the gastrointestinal tract (Hrudey et al., 1996: 105).
Distribution:
Absorbed chromium compounds (except chromates) are rapidly removed from the blood and
distributed in various tissues (lung, lymph nodes, kidney, liver, bladder, bone), or excreted in
the urine (Hrudey et al., 1996:103).
Animal studies have shown chromium retention to be dependent on the route of administration
and speciation. Accumulation can occur in the hair, reticulo-endothelial system, liver, spleen,
bone marrow and kidneys (Langard et al., 1979: 388).
Excretion:
Absorbed chromium is excreted mainly in urine. Studies of the kinetics suggest the existence
of three compartments with excretion half-lives of seven hours, 15 to 30 days, and three to five
years (Lauwerys & Hoet, 1993: 42).
Acute effects:
Bronchial asthma has been reported after inhalation of chromate or chromic acid (Langard et
al., 1979: 392).
6+
Irritative dermatitis has been reported after contact with Cr salts. Sensitivity seems to
diminish with renewed exposure. Allergic eczematous dermatitis is wide-spread and not only
6+
3+
associated with industrial exposure to Cr , but is also caused by Cr (Lewis, 1995: database;
Langard et al., 1979: 390).
Chronic effects:
Chromium accumulates in the lungs with age, while decreasing in all other organs.(Langard et
al., 1979: 389; Lauwerys et al., 1993: 42). Long-term effects include damage to the kidneys.
Respiratory cancer is associated with inhalation of water-soluble chromium (Benson & Zelikoff,
1996: 930).
Deep, slow-healing skin ulcers have been noted in industry, especially after contact of chromic
compounds with broken skin. Ulceration of the nasal mucosa and perforation of the nasal
septum have also been reported (Langard et al., 1979: 390).
Carcinogenicity:
6+
Cr compounds are Group 1 human carcinogens (IARC, 1990: Vol. 49). There is a well6+
established link between inhalation of Cr
compounds and lung cancer (Lewis, 1995:
database; Lauwerys et al., 1993: 42; Hrudey, et al., 1996: 101; Klein, 1996: 208; Benson et al.,
1996: 930). A latency period of 15 to 17 years has been reported (Langard et al., 1979: 393).
Skin cancers have been elicited in animal studies (Langard, 1979: 383).
59
Table 3.3.4.8
Chromium: Toxicological properties and target-organ effects
Carcinogen
Species listed
OEL-RL and OEL-CL
BEI
Chromium
6+
Cr is a human carcinogen
IARC Group 1
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical Substances
(Department of Labour, 1995).
Chromium (II) compounds (as Cr)
Chromium (III) compounds (as Cr)
Medical surveillance
Biological effect monitoring
Biological monitoring
See Table
3.4.6.3
Chromium (VI) compounds (as (Cr)
Speciation in mineral processing plants: Cr, Cr2O3, CrO3, Cr2O6, FeCr, carbides, silicides, flourides, sulphates, nitrates, phosphates
Absorption: Inhalation, ingestion
Deposition: Lung, hair, liver, kidney, bladder, lymph nodes, bone
Target organ
Renal system
Excretion: Urine, multistage
Short-term effects
Long-term effects
Increased levels
Nephrotoxicity
Nervous system
Liver
Increased levels
Gastrointestinal tract
Respiratory tract
Irritant cough, allergic asthma
Accumulation, cancer, allergic asthma, nasal ulceration
Increased levels
Increased levels
Irritative and allergic dermatitis,
Cancer, ulceration,
Haematopoietic system
Bone
Endocrine system
Muscle
Eye
Skin
Cardiovascular system
Immune system
Reproductive system
Crosses placental barrier
60
Reproductive system:
Chromium can cross the placental barrier, (possibly as the glucose tolerance factor) as
evidenced by its presence in the newborn (Langard et al., 1979: 388). Some mutation effects
have been reported (Lewis, 1995: database).
3.3.4.9
Cobalt (Co)
Absorption:
Only limited data are available for the absorption of cobalt from the lung and gastrointestinal
tract. The evidence points to solubility and the presence of other metals as possible
determining factors. Absorption after ingestion varies widely, depending on the amount
ingested and nutritional factors (Elinder & Friberg, 1979b: 402; Gerhardsson & Skerfving, 1996:
99).
Distribution:
Absorbed cobalt is distributed mainly to the liver and kidneys (Elinder et al., 1979b: 403;
Gerhardsson et al., 1996: 99).
Excretion:
After ingestion the major portion of cobalt is excreted, unabsorbed, in the faeces. Absorbed
cobalt will be excreted mainly through the urine, irrespective of route of uptake. Renal
clearance is thought to be in two phases: fast excretion (half-life 0,5 to 2,7 days), followed by
pronounced retention (half-life several years) (Elinder et al., 1979b: 400; Lauwerys & Hoet,
1993: 47).
Acute effects:
Ingestion of soluble cobalt salts can cause irritation evidenced by nausea and vomiting (Lewis,
1995: database).
Cases have been reported of cobalt chloride ingestion causing
cardiomyopathy (Gerhardsson et al., 1996: 99; Elinder et al., 1979b: 406).
Inhalation of cobalt may lead to irritation of the mucous membranes and allergic reactions
(coughing, wheezing, shortness of breath). Skin contact can cause dermatitis. (Elinder et al.,
1979b: 405; Gerhardsson et al., 1996: 99; Lewis, 1995: database).
Chronic effects:
Progressive lung disease (hard metal disease) was reported amongst workers in the hard
metals industry (Elinder et al., 1979b: 405; Gerhardsson et al., 1996: 99).
Carcinogenicity:
Cobalt compounds are classified as possible human carcinogens, Group 2b (IARC 1991: Vol.
52).
Reproductive effects:
No data have been documented to indicate reproductive effects in humans.
61
Table 3.3.4.9
Cobalt: Toxicological properties and target-organ effects
Carcinogen
Possible human carcinogen
IARC Group 2b
Species listed
OEL-RL and OEL-CL
Cobalt and compounds (as Co)
BEI
Medical surveillance
Occupational Health And Safety Act, 1993
Biological effect monitoring
Regulations for Hazardous Chemical Substances Biological monitoring
(Department of Labour, 1995).
Speciation in mineral processing plants: Co, CoO, Co(OH)2, CoCl2, CoS, CoSO4, Co(CN)2
Absorption: Inhalation, ingestion
Deposition: Liver
Target organ
Excretion: Urine (inhalation)( two-phase); faeces (ingestion)
Short-term effects
Renal system
Accumulation
Nervous system
Liver
Accumulation
Gastrointestinal tract
Irritant (soluble compounds); nausea, vomiting
Respiratory tract
Allergy (wheezing, coughing)
Pneumoconiosis ( “hard metal” disease)
Haematopoietic system
Bone
Endocrine system
Muscle
Eye
Skin
Irritation
Cardiovascular system
Cardiomyopathy
Immune system
Reproductive system
62
See Table
3.4.6.3
3.3.4.10
Copper (Cu)
Absorption:
Absorption from the gastrointestinal tract is homeostatically controlled (largely by the liver) and
variable, except in copper-related diseases (Wilson’s, and Menke’s diseases). The presence of
other metal ions (Cd, Fe, Zn), age, gender, pregnancy, diet and ascorbic acid can also
contribute to the variability of copper absorption (Hrudey et al.,1996: 118, 119).
Absorption of copper via dermal exposure has been reported (Hrudey et al., 1996: 120), but
there are no quantitative data available for absorption from copper deposited in the lungs
(Hrudey et al., 1996: 119).
Distribution:
Once absorbed, copper is transported to the liver which then redistributes part of this to other
organs, especially the brain, heart and kidneys (Hrudey et al., 1996: 118).
Excretion:
Excretion is mainly via the bile in the faeces. Urinary excretion is minor. Biological half-life is
about 4 weeks in humans (Piscator, 1979a: 414, 415).
Acute effects:
Copper sulphate is a powerful emetic (Piscator, 1979a: 417). Copper dust and fumes are
respiratory irritants. Copper sulphate and chloride have also been reported to be responsible for
irritation of the skin and conjunctivae, possibly due to allergic reaction. Cuprous oxide is an eye
and upper respiratory tract irritant (Lewis, 1995: database). Exposure to copper and copper
oxide fumes has been responsible for metal fume fever (fever, chills, dyspnoea, muscular
soreness, nausea and fatigue) (Piscator, 1979a: 416; Benson et al., 1996: 935).
Chronic effects:
Industrial exposure has caused congestion of respiratory mucous membranes and perforation
of the nasal septum (Benson et al., 1996: 935).
Carcinogenicity:
Copper compounds as a group are not classified as carcinogenic by IARC, although an excess
of cancer cases has been claimed in the copper smelting industry (Lewis, 1995: database).
Reproductive effects:
There is no information in the literature to indicate reproductive effects in humans by excess
copper.
63
Table 3.3.4.10
Copper: Toxicological properties and target-organ effects
Carcinogen
Species listed
Copper fume
Not a human carcinogen
Dusts & mists as Cu
OEL-RL and OEL-CL
BEI
Medical surveillance
Biological effect monitoring
Biological monitoring
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical Substances
(Department of Labour, 1995).
Speciation in mineral processing plants: Cu, Cu(CN)4, Cu2S, CuSO4, CuO, CuFe sulphides, Cu hydroxides, Cu phosphate
Absorption: Unknown
Deposition: Liver, brain, heart, kidney, muscles
Target organ
Excretion: Unknown
Short-term effects
Long-term effects
Renal System
Storage
Nervous System
Liver
Storage
Gastrointestinal Tract
Emetic (CuSO4)
Respiratory tract
Irritant (fumes)
Storage
None reported
Haematopoietic System
Bone
Endocrine System
Muscle
Storage
Eye
Irritant (CuSO4, CuCl2)(possible allergen)
Skin
Irritant (CuSO4, CuCl2)(possible allergen)
Cardiovascular system
Storage
Immune system
Reproductive system
64
See Table 3.4.6.3
3.3.4.11
Indium (In)
Absorption:
Absorption of inhaled indium oxide (In2O3) has been shown to be low to moderate ion animal
studies (Fowler, 1979c: 431). In2O3 has low toxicity (Lewis, 1995: database).
Distribution:
The chemical form of indium mainly determines distribution in body tissues. Ionic species are
mainly concentrated in the kidneys. Colloidal indium oxide is accumulated in the liver, spleen
and other organs of the reticulo-endothelial system (Fowler, 1979c: 431).
Excretion:
Animal experiments showed a biphasic excretion pattern, with half-lives of about two and 69 to
74 days, respectively. In mice, excretion of indium is primarily dependent on the chemical form
exposed to. Ionic species are mainly excreted via the kidneys, while colloidal material is
excreted mainly in the faeces (Fowler, 1979c: 431).
Acute effects:
Indium affects the liver, heart, kidneys, and the blood. The results of animal studies showed
that the more soluble salts of indium were very toxic (ASOSH, 2000). Inhalation of indium
compounds may cause damage to the respiratory system (Lewis, 1995: database; Fowler,
1979c: 432). No cases have been reported of systemic effects in humans exposed to indium.
Chronic effects:
Indium chloride is nephrotoxic (Fowler, 1996f, 725; Yamauchi & Fowler, 1996: 752)
Carcinogenicity:
No agency in the world has listed indium as carcinogenic.
Reproductive effects:
Teratogenic effects have been observed in animal experiments (Fowler, 1979c: 433), but no
human cases relating to industrial exposure have been documented.
65
Table 3.3.4.11
Indium: Toxicological properties and target-organ effects
Carcinogen
Not a human carcinogen
Species listed
OEL-RL and OEL-CL
Indium & compounds (as In)
BEI
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical
(Department of Labour, 1995).
Medical surveillance
Biological effect monitoring
Substances Biological monitoring
Speciation in mineral processing plants: Not identified
Absorption: Unknown
Deposition: Unknown
Target organ
Renal System
Excretion: Urine (ionic); faeces (colloidal)
Short-term effects
Long-term effects
Histological damage (animals)
Concentration, failure
Nervous System
Liver
Damage (colloidal material)
Gastrointestinal tract
Respiratory tract
Haematopoietic system
Blood
Blood
Bone
Storage
Endocrine system
Muscle
Storage
Eye
Skin
Severe irritant (nitrate)
Storage
Cardiovascular system
Heart
Heart
Immune system
Reproductive system
Teratogenic (animals)
66
See Table 3.4.6.3
3.3.4.12
Iron (Fe)
Absorption
2+
Iron is potentially toxic by all routes of exposure, and in all dosages and forms. Fe is more
3+
toxic than Fe (Lewis, 1995: database).
Elinder et al., (Elinder & Piscator, 1979c: 439) could not find supporting data for the calculation
of the pulmonary absorption of iron. No other reference could be located to more recent
studies.
Absorption of ingested iron is regulated by homeostasis (the level of iron in the body
determines the absorption). In addition factors such as age, health of the gastrointestinal tract,
chemical speciation and dietary factors also play a role. Absorbed iron is detoxified in the
serum by binding to transferrin and transported by this means to storage sites (Elinder et al.,
1979c: 439).
Distribution:
About two-thirds of the iron in the body is bound to haemoglobin in the blood. Most of the
remaining iron is stored as protein complexes in the liver, bone marrow and spleen (Elinder et
al., 1979c: 440, 441).
Excretion:
About 0,01 per cent of the body burden of iron is excreted per day via the urine, faeces and
skin. Large amounts of iron can be lost during haemorrhaging. The normal biological half-life
of iron is estimated to be 10 to 20 years (Elinder et al., 1979c: 440).
Clearance of particles from the lung takes place at about 20 to 40 per cent of the deposited
amount per year (Elinder et al., 1979c: 441).
Acute effects:
Acute iron intoxication happens most often by the accidental ingestion of iron-containing
medicine by young children. It is characterised by vomiting and shock, which, if survived, is
followed by liver damage and kidney failure (Elinder et al., 1979c: 442).
Animal studies have shown irritation of the upper airways, coughing and respiratory difficulties
3
and after inhalation of iron oxide dust (500 mg Fe/m ). Transient histological changes were
also noticed (Elinder et al., 1979c: 442). With prolonged contact iron dust can cause
conjunctivitis, choroiditis, and retinitis (Lewis, 1995: database).
Chronic effects:
Chronic inhalation studies on animals resulted in alveolar fibrosis and other cell damage
(Elinder et al., 1979c: 442). Excessive inhalation of iron-containing dust can lead to siderosis,
which is radiographically similar to silicosis and miliary tuberculosis. Siderosis may be benign,
although some cases of pulmonary fibrosis and impaired function were reported amongst
welders and miners. However, other fumes and dusts are usually also present during welding
and mining. It has been shown that iron tends to accumulate in the lungs as a result of chronic
exposure (Elinder et al., 1979c: 443).
High dietary intake of absorbable iron amongst South African men has been associated with
excessive haemosiderin deposits in the liver and an increased incidence of cirrhosis of the liver.
Excess haemosiderin deposited in the pancreas may be associated with fibrosis and diabetes
mellitus (Elinder et al., 1979c: 444; Nieminen & Lemasters, 1996: 895). For these reasons iron
oxide dust should not be considered in the same category as nuisance dusts.
67
Table 3.3.4.12
Iron: Toxicological properties and target-organ effects
Carcinogen
Species listed
Iron oxide fume (as Fe)
Not a human carcinogen
Iron salts as (Fe)
OEL-RL and OEL-CL
BEI
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical Substances
(Department of Labour, 1995).
Medical surveillance
Biological effect monitoring
Biological monitoring
3-
See Table 3.4.6.3
Speciation in mineral processing plants: Fe, FeS, Fe2S3, FeO, Fe2O3, Fe3O4, Fe(CN)6 , FeCr, FeCr3, FeSi, FeMn, FeTi, FeTiO3,FeB, carbide FeSO4, Fe carbides
Absorption: Ingestion, inhalation Deposition: Liver, spleen, bone marrow
Target organ
Excretion: Slow. Faeces, urine
Short-term effects
Long-term effects
Renal system
Nervous system
Liver
Storage, redistribution
Storage, cirrhosis, haemosiderosis
Respiratory tract
Animals : coughing, nasal irritation
Pulmonary fibrosis, lung cancer
Haematopoietic system
Storage
Storage
Gastrointestinal tract
Bone
Storage(marrow)
Endocrine system
Diabetis(severe intoxication)
Muscle
Eye
Conjunctivitis, choroiditis, retinitis
Skin
Discolouration
Cardiovascular system
Heart (haemosiderosis)(severe intoxication)
Immune system
Reproductive system
68
Carcinogenicity:
Some iron compounds are suspected carcinogens, amongst them iron dust and red iron oxide
(Lewis, 1995: database; Elinder, 1979: 445). IARC has not classified these compounds as
carcinogens (Lewis 1995: database), and epidemiological data are not available to support any
suggestion of carcinogenicity. Based on animal experiments it is suspected that iron oxide dust
might serve as a cocarcinogenic substance, i.e. enhancing the development of cancer at a
simultaneous exposure to a carcinogenic substance (Elinder, 1979: 435).
Reproductive effects:
No conclusive evidence is available to show reproductive effects associated with excess body
burdens of iron (Keen, 1996: 988).
3.3.4.13
Lead (Pb)
Absorption:
Lead is absorbed more readily from the lungs than from the gastrointestinal tract and symptoms
tend to develop sooner (Lewis, 1995: database).
Deposition and absorption of inhaled particles depends on the physicochemical properties
(size, solubility, concentration) (Gerhardsson & Skerfving, 1996: 87; Hrudey, Chen, Rousseaux,
1996: 136). About ten to 60 per cent of inhaled lead particles in the size range 0,01 to 5 µm is
deposited in the lungs. Larger particles are deposited in the upper airways where the major
part is cleared and swallowed (Gerhardsson et al., 1996: 87). No evidence could be found to
show that inhaled lead accumulates in the lungs (Tsuchiya, 1979: 457).
Absorption of ingested lead is dependent on biological factors (age, sex, iron store, nutritional
status) and can consequently vary widely between individuals (Lauwerys, 1993: 56;
Gerhardsson et al., 1996: 87; Hrudey et al., 1996: 137). The major portion of ingested lead is
passed through the gastrointestinal tract unabsorbed. The absorbed portion (about 4 to 13 per
cent) enters the entero-hepatic cycle and some of this material is eventually excreted in the
faeces (Tsuchiya, 1979: 458, 459; Hrudey et al., 1996: 137).
Some compounds and finely powdered metal can be absorbed through the skin (Lauwerys et
al., 1993: 56; Hrudey et al., 1996: 138).
More-detailed information on the bioavailability of lead compounds is available in the cited
literature (Hrudey et al., 1996: 140 - 143).
Distribution:
Absorbed lead is distributed to three biological compartments:
• Blood (mainly bound to red cells), half-life about 1 month. (Hrudey et al., 1996: 135;
Lauwerys, 1993: 56).
• Soft tissues (brain, kidney, lungs, liver, heart, spleen) Half-life about 19 to 40 days
(Tsuchiya, 1979: 460; Lauwerys, 1993: 56)
• Bone which contains about 90 per cent of the total body burden (half-life about 10 to 30
years) (Hrudey et al., 1996: 136; Lauwerys et al., 1993: 56).
Excretion:
Excretion of absorbed lead takes place mainly via the kidneys. Lesser pathways include
gastrointestinal secretions, hair, nails and sweat. Lead concentrations in the bile are high, and
a large proportion is probably reabsorbed in the gut and excreted in the urine (Lauwerys et al.,
1993: 56).
69
Table 3.3.4.13
Lead: Toxicological properties and target-organ effects
Carcinogen
Possible human carcinogen
IARC Group 2b
Species listed
Lead, elemental and
inorganic compounds
(as Pb)
Lead chromate, Lead
arsenate
OEL-RL and OEL-CL
BEI
Medical surveillance
Occupational Health And Safety Act, 1993
Biological effect monitoring
Regulations for Hazardous Chemical Substances Biological monitoring
(Department of Labour, 1995).
See Table 3.4.6.3
Speciation in mineral processing plants: Pb, PbO, PbS, PbSO4, PbCO3, PbCl2, Pb(NO3)2, Pb(CN)2, phosphates
Absorption: Inhalation, ingestion, skin
Deposition: Bone; soft tissue, blood
Target organ
Renal System
Excretion: Mainly urine
Short-term effects
Long-term effects
Reversible damage
Kidney disease
Nervous System
Brain (accumulation, damage), impaired peripheral function
Liver
Interim storage, disturbed function
Gastrointestinal Tract
Dyspepsia, constipation, anorexia, colic
Gastritis, anorexia
Respiratory tract
Absorption
Interim storage
Hematopoietic System
Anaemia,
Bone
Deposition, build-up, sore joints
Endocrine System
Muscle
Pain
Eye
Skin
Absorption
Cardiovascular system
Raised blood pressure
Immune system
Impairment
Reproductive system
Placental transfer, developmental defects, decreased male fertility, stillbirth,
miscarriage
70
Acute effects:
Acute intoxication is usually accompanied initially by anorexia, dyspepsia, constipation followed
by gastrointestinal colic accompanied by paleness and possibly elevated blood pressure.
Neurological symptoms have been noted (Tsuchiya, 1979: 458, 465), and reversible kidney
damage may also occur (Gerhardsson et al., 1996: 88).
Chronic effects:
Chronic lead exposure is manifested by a whole range of possible symptoms and effects, e.g.
anaemia, kidney diseases, brain damage, high systolic blood pressure (middle-aged men),
reproductive abnormalities, developmental defects, anorexia, feelings of unwellness,
sleeplesness, headache, irritability, muscle and joint pains, central and peripheral nervous
disturbances, muscle weakness, gastritis and liver changes, abnormal vitamin D metabolism
and even death in severe cases (Lewis, 1995: database; Gerhardsson et al., 1996: 88 – 89;
Tsuchiya, 1979: 466 - 473). There is also evidence for lead-related cognitive and behavioural
disturbances (Gerhardsson et al., 1996: 89).
Heavy chronic exposure is often accompanied by a dark lead line on the edges of the gums
(Gerhardsson et al., 1996: 88).
Carcinogenicity:
Lead and inorganic lead compounds are classified as possible human carcinogens, Group 2B
(IARC, 1987: Vol. 23, Suppl. 7). There is no conclusive evidence for mutagenic activity
(Cohen, Bowser, Costa, 1996: 261-262).
Reproductive effects:
Severe intoxication can cause sterility (male), abortion and increased mortality and morbidity
amongst the newborn. A good correlation was found between lead levels in the blood of the
mother and newborn.
3.3.4.14
Manganese (Mn)
Absorption:
The solubility of most industrial manganese products is low. Only particles small enough to
reach the alveoli are therefore likely to be absorbed from the lungs. Large particles will be
cleared from the respiratory tract to the digestive system (Inoue & Makita, 1996: 416). After
3+
absorption, most manganese seems to be present in the blood as a Mn -transferrin complex
(Romero, Abbott, Bradbury, 1996: 567).
Absorption of ingested manganese is homeostatically controlled and is normally about 3 per
cent. It is reduced by simultaneous intake of calcium (Piscator, 1979b: 488) and increased by
iron deficiency (Gerhardsson et al., 1996: 101).
Retention half-life for inhaled manganese in the lungs is 2 - 3 months (Gerhardsson et al.,
1996: 101). Fairly high absorption from the lungs has been inferred: 40 to 70 per cent of inhaled
isotopically labelled manganese was excreted in the faeces of two groups of exposed persons
(Piscator, 1979b: 488).
Distribution:
After inhalation or ingestion absorbed manganese is quickly eliminated from the blood. It is
distributed to mainly the liver, and to a lesser extent the kidneys and endocrine glands
(Piscator, 1979b: 489; Inoue et al., 1996: 416).
71
Table 3.3.4.14
Manganese: Toxicological properties and target-organ effects
Carcinogen
Species listed
Fume (as Mn)
Not a human carcinogen
Mn and compounds (as Mn)
OEL-RL and OEL-CL
BEI
Medical surveillance
Occupational Health And Safety Act, 1993
Biological effect monitoring
Regulations for Hazardous Chemical Substances Biological monitoring
(Department of Labour, 1995).
See Table 3.4.6.3
Speciation in mineral processing plants: Mn, MnO, MnO2, Mn3O4, MnS, MnP, MnCO3, Mn(OH)2, MnSO4, carbides, silicides, phosphates
Absorption: Ingestion, inhalation Deposition: Liver, kidneys, intestine; brain, bone, endocrine system
Target organ
Excretion: Bile (faeces)
Short-term effects
Long-term effects
Renal system
Nervous system
Brain critical organ. Storage (brain, long-term); irreversible Parkinson’s- like
degeneration; motor disturbance, speech disturbance, hallucinations, illusions,
delusions
Liver
Storage (20%)
Gastrointestinal tract
Storage (intestine)
Respiratory tract
Increased infections, pneumonia
Haematopoietic system
Bone
Storage (45%)
Endocrine system
Muscle
Storage (35%); weakness
Eye
Irritant
Skin
Irritant
Cardiovascular system
Immune system
Reproductive system
Crosses placental barrier
72
Animal experiments have shown that minor amounts are taken up in the central nervous
system. Rate of manganese uptake into the brain is thought to be determined by speciation
2+
3+
and transport mechanism, Mn
crossing the blood-brain barrier rapidly, and the Mn transferrin complex crossing it slowly. The distribution of manganese species in the blood is
not known (Romero et al., 1996: 567).
Excretion:
Absorbed manganese is excreted almost exclusively in the bile and passed with the faeces
(Inoue et al., 1996: 416).
Acute effects:
Ingestion
Very few poisonings have occurred by ingestion (Lewis, 1995: database).
Respiratory
Manganese pneumonia is associated with acute alveolar inflammation, shortness of breath and
often does not respond to antibiotics. An increase in bronchitis has also been found. No
permanent pulmonary changes have been reported. Increased susceptibility to respiratory
infections was also found in animals (Piscator, 1979b: 493).
The following dose-response relationships have been reported:
3
• 0,39 to 16,35 mg/m : Increased pneumonia, bronchitis (Piscator, 1979b: 493; Lewis, 1995:
database).
3
• 6,7 mg/m (average): Nose and throat symptoms have been observed (Piscator, 1979b:
494).
3
• Less than 0,3 mg/m : No pulmonary symptoms (WHO guideline (1979)) (Piscator, 1979b:
495).
Manganese is a skin and eye irritant (Lewis, 1995: database).
Chronic effects:
Chronic effects have been documented for both ingestion and inhalation exposure (8 to 16
years). Time of onset can vary from a few months to (usually) 1 to 3 years after exposure.
Cases of unusual sensitivity towards manganese have been reported (Piscator, 1979b: 497).
There is a possibility to reverse the course of intoxication if it is diagnosed early enough, and
the patient is removed from exposure (Lewis, 1995: database).
The brain is the critical organ. Chronic intoxication (manganism) is characterised by initial
progressive psychiatric and neurological symptoms with continued exposure (Piscator, 1979b:
497; Inoue et al., 1996: 416). Symptoms are:
•
•
•
Asthenia; languor; sleepiness.
Incoherent, slow monotonous speech; aggression; staggering walk, weakness in the legs
mask-like face; increased clumsiness. Neurological examination reveals nothing specific,
except increased reflexes in lower limbs.
Disease fully developed: difficult walking and writing; tremors in upper limbs; nocturnal
cramps in legs; symptoms resembling Parkinson’s or Wilson’s disease.
The history of exposure is often the only aid to diagnosis.
Carcinogenicity:
IARC has not listed manganese as a human carcinogen.
73
Reproductive effects:
Deficiency can cause malformation. There are no indications that inhalation or ingestion will
cause malformations in man or animals (Piscator, 1979b: 497). Decreased libido or impotence
is a frequent early symptom of manganese intoxication (Inoue et al., 1996: 416). Decreased
male fertility has been reported (Corbella & Domingo, 1996: 1085).
3.3.4.15
Mercury (Hg)
Absorption:
Upon exposure the absorption rate depends on particle size and deposition rate in the
respiratory tract.
Metallic mercury
• Inhalation: Vapour is rapidly and efficiently (about 80 per cent) absorbed from lungs by
diffusion in the alveoli.(Lauwerys & Hoet, 1993: 74; Gerhardsson & Skerfving, 1996: 93).
• Ingestion: Liquid metal is poorly absorbed from the gastrointestinal tract and depends on
the exposed surface area (Berlin, 1979: 510).
• Skin: Absorption is possible but unimportant in the workplace compared to inhalation.
Vapour emanating from contaminated skin or clothing will be inhaled, forming a much more
efficient pathway (Berlin, 1979: 510).
Inorganic salts
• Inhalation: Little quantitative data are available, but in animals the absorption of inorganic
salts of mercury is lower than for the metal vapour (Hrudey, Chen, Rousseaux, 1996:127).
• Ingestion: Mercuric salts are corrosive to mucous membranes, and may cause damage
which can increase absorption from the intestine to more than the 10 per cent which has
been reported (Berlin, 1979: 516).
• Skin: Absorption is low (Berlin, 1979: 516).
Organo-mercurials
• Inhalation: Methyl mercury can be absorbed by inhalation. In animal experiments (rats,
mice) absorption was rapid and almost complete (Berlin, 1979: 519).
• Ingestion: Absorption is almost complete in humans (Berlin, 1979: 519).
• Skin: Animal experiments showed low absorption (Hrudey, 1996:128).
Distribution:
Mercury has a particular affinity for organs with epithelial cells and glands (gastrointestinal tract,
kidney, skin, hair, salivary glands, thyroid, liver, pancreas, sweat glands, testicles, prostate). In
the brain it accumulates in the grey matter, cerebellum and brain stem (Berlin, 1979: 511).
Metallic mercury
Can penetrate the blood-brain barrier and remain in the brain for a long time (half-life about 1
year) causing a wide range of neurological and psychic disorders (Hrudey, 1996:126; Berlin,
1979: 512; Lewis, 1995: database).
Mercury salts
2+
Mercuric mercury (Hg ) is not easily transported over the blood-brain or the placental barriers.
Uptake in and elimination from the various organ systems vary widely (Berlin, 1979: 516). Most
of the body pool, however, is in the kidney (Nieminen & Lemasters, 1996: 890).
Organo-mercurials
Methyl mercury is carried in the blood bound largely to red blood cells and is slowly distributed
to the brain and other organs. Some of the bound mercury in the blood can be transformed to
mercuric species, which are distributed to the kidneys and liver. Mercury in the bile is subject to
entero-hepatic recirculation (Berlin, 1979: 520; Hrudey, 1996: 126).
74
Table 3.3.4.15
Mercury: Toxicological properties and target-organ effects
Carcinogen
Unclassifiable
IARC Group 3
Species listed
OEL-RL and OEL-CL
Mercury alkyls
BEI
Occupational Health And Safety Act, 1993
Mercury and compounds Regulations for Hazardous Chemical Substances
(Department of Labour, 1995).
(as Hg)
Medical surveillance
Biological effect monitoring
Biological monitoring
See Table 3.4.6.3
Speciation in mineral processing plants: Hg, HgS, Hg2S, HgO, Hg2O
Absorption: Inhalation, ingestion, skin
Deposition: Liver, spleen, kidneys, bone
Target organ
Excretion: Urine
Short-term effects
Long-term effects
Renal system
Target organ : necrosis, acute failure (inorganic compounds)
Nervous system
CNS critical organ (vapour).
disturbances, insomnia
Dizziness, tremors, psychic
Liver
Gastrointestinal tract
Respiratory tract
Salivation, stomatitis, gums (black rim)
Lung critical organ: bronchitis, pneumonitis, pulmonary insufficiency
Hematopoietic system
Bone
Endocrine system
Muscle
Eye
Skin
Irritation
Cardiovascular system
Immune system
Palpitations
Allergens (inorganic compounds)
Foetal intoxication: Minamata disease, brain damage.
Accumulation in testicle and prostate
Reproductive system
75
Excretion:
Retention time differs widely amongst different organs. The brain, kidneys and testicles have
the longest retention time. These organs are therefore likely to show accumulation on repeated
exposure. Excretion for all forms of mercury is mainly by way of the faeces and urine. Minor
pathways are saliva, sweat, breast milk, tears and exhalation of vapour (Berlin, 1979: 516).
Acute effects:
The lung is the critical organ in acute accidental exposure to high levels of mercury vapour,
showing erosive bronchitis, bronchiolitis and interstitial pneumonitis, eventually terminating in
death due to respiratory insufficiency. Some central nervous system effects such as tremors
and excitability may accompany these symptoms (Lewis 1995: database; Berlin, 1979: 512).
Soluble salts are violently corrosive to skin and mucous membranes (Lewis 1995: database).
Chronic effects:
The brain is the primary target organ for chronic mercury vapour exposure. With increasing
dose the symptoms of so-called micro-mercurialism appear:
•
•
•
•
Weakness, fatigue, anorexia, loss of weight.
Disturbance of gastrointestinal functions.
At higher exposure levels intentional tremors in the fingers, eyelids and lips are seen, which
may develop into tremors of the whole body with violent spasms of the extremities.
Parallel to these symptoms severe behavioural and personality changes take place,
accompanied by excitability, loss of memory, and insomnia.
Severe intoxication can cause hallucination and delirium, changes to the gums and excessive
salivation (Berlin, 1979: 512; Lewis 1995: database; Gerhardsson, 1996: 93).
Kidney damage may occur in cases of exposure to a combination of mercury vapour and dust.
Necrosis and acute failure are possible (Berlin, 1979: 518; Gerhardsson, 1996: 93; Fowler,
1996f: 723).
Carcinogenicity:
IARC has designated mercury and inorganic mercury compounds to Group 3, unclassifiable as
to carcinogenicity to humans (IARC, 1993: Vol. 58).
Reproductive effects:
Methyl mercury and inhaled metallic mercury can pass the placental barrier, leading to foetal
uptake when the mother is exposed. Brain damage and cerebral palsy (Minamata disease)
may result (Berlin, 1979: 511; Hamada & Osame, 1996: 337- 351).
Mercury accumulates in the testicles and prostate (Berlin, 1979: 511).
3.3.4.16
Molybdenum (Mo)
Absorption:
Soluble compounds are readily absorbed after inhalation and ingestion. Animal experiments
with inhalation of MoS2 and hexavalent molybdenum supported this conclusion. No human
data are available (Friberg, 1979: 533).
6+
Molybdenum compounds are poisonous by ingestion. Gastrointestinal absorption of Mo
high in both animals and humans (about 50 per cent) (Friberg, 1979: 533).
76
is
Table 3.3.4.16
Molybdenum: Toxicological properties and target-organ effects
Carcinogen
Species listed
OEL-RL and OEL-CL
Molybdenum compounds (soluble) (as Mo)
Not a human carcinogen
Molybdenum compounds (insoluble) (as Mo)
BEI
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical
Substances (Department of Labour, 1995).
Medical surveillance
Biological effect monitoring
Biological monitoring
See Table 3.4.6.3
Speciation in mineral processing plants: Mo, MoO, MoO2, MoS2, Mo(SO4)2, carbides, silicides
Absorption: Ingestion, inhalation Deposition: Kidney, liver, bone
Target system
Excretion: Mainly urine
Short-term effects
Long-term effects
Renal system
Nervous system
Liver
Gastrointestinal tract
Respiratory tract
Irritant (MoO3)
Pneumoconiosis, fibrosis, “hard metal disease”
Haematopoietic system
Bone
Arthritis
Endocrine system
Muscle
Eye
Skin
Cardiovascular system
Immune system
Reproductive system
77
Distribution:
Animal studies showed distribution of ingested MoO3 in the liver, pancreas, kidneys and bones
(Friberg, 1979: 534). No data for humans are available.
Excretion:
Limited data are available. Animal studies indicate low retention. Two studies with humans
indicated that urine is the main route for excretion. Molybdenum is rapidly excreted, showing a
biological half-life about 10 days (Friberg, 1979: 534; Lewis, 1995: database).
Acute effects:
Acute oral poisoning caused severe gastrointestinal irritation with diarrhoea, coma and death
through heart failure (animal experiments) (Lewis, 1995: database).
Precautions are advised against inhalation of the more-soluble compounds like MoO3 and
NaMoO4. MoO3 is a powerful irritant causing pulmonary fibrosis and coughing in humans
(Lewis, 1995: database; Friberg, 1979: 535).
Chronic effects:
High dietary exposure to molybdenum has been seen to increase the incidence of arthritis-like
complaints and elevated uric acid levels in the blood (Friberg, 1979: 536).
3
Workers exposed to Mo and MoO3 dust (one to 19 mg Mo/m ) for 3 to 7 years have developed
pneumoconiosis. Inhalation of Mo-containing alloy or carbide dust can lead to ”hard metal
disease” (Lewis, 1995: database; Friberg, 1979: 535).
Carcinogenicity:
IARC does not classify molybdenum or its compounds as human carcinogens
Reproductive effects:
No information is available for humans. Some unspecified effects were noticed (Lewis 1995:
database).
3.3.4.17
Nickel (Ni)
Absorption:
Nickel is not a cumulative toxin (Lauwerys & Hoet, 1993: 82).
Inhalation
About 25 per cent of nickel in particulate matter deposited in the lungs after inhalation is
absorbed (Gerhardsson et al., 1996: 102). Insoluble species are retained in the lung for long
periods, causing associated elevated levels of nickel in the system (Lauwerys, 1993: 84).
Soluble species are absorbed and excreted fairly quickly (Lauwerys, 1993: 82).
Ingestion
Gastrointestinal absorption is low (one per cent) and strongly influenced by dietary constituents.
Unabsorbed material is excreted in the faeces (Lauwerys, 1993: 82; Gerhardsson et al., 1996:
102).
Skin
Soluble compounds can penetrate the skin during contact. (Norseth et al., 1979: 549).
78
Table 3.3.4.17
Nickel: Toxicological properties and target-organ effects
Carcinogen
Species listed
Nickel compounds : Human carcinogens
IARC Group 1.
Nickel & alloys: Possible human
carcinogens
IARC Group 2B
Nickel
Inorganic: Soluble compounds
Inorganic: Insoluble compounds
OEL-RL and OEL-CL
BEI
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical
Substances (Department of Labour, 1995).
Medical surveillance
Biological effect monitoring
Biological monitoring
See Table 3.4.6.3
Speciation in mineral processing plants: Ni, NiO, Ni(CN)2, Ni(CN)4, NiS, Ni3S2 NiSO4, Ni(NO3)2, NiF2, Ni(OH)2
Absorption: Inhalation, skin, ingestion
Deposition: Bone, kidney, liver, lung
Target organ
Excretion: Urine, saliva, sweat; faeces (ingestion)
Short-term effects
Long-term effects
Renal system
Nervous system
Liver
Gastrointestinal tract
Respiratory tract
Asthma
Nasopharingeal cancer, lung cancer, nasal ulceration, asthma, pneumoconiosis
Haematopoietic system
Bone
Storage
Endocrine system
Muscle
Eye
Conjunctivitis
Skin
Irritant, contact dermatitis, eczema
Sensitiser, dermatitis
Cardiovascular system
Immune system
Sensitiser, experimental immune effects
Reproductive system
79
Distribution:
Nickel is bound mainly to albumin and amino acids in the blood stream before being deposited
in the bone (the highest concentration), kidney, liver, and lungs. Biological half-life in blood is
about 20 to 34 hours and in urine about 17 to 39 hours (Gerhardsson et al., 1996: 102;
Lauwerys, 1993: 82).
Excretion:
Urine is the dominant excretion route for absorbed nickel. The predominant fraction of ingested
nickel is excreted, unabsorbed, in the faeces (Gerhardsson et al., 1996: 102).
Acute effects:
Hypersensitivity to nickel is common, and asthma, dermatitis and conjunctivitis have been noted
amongst sensitive workers exposed to mists of soluble Ni compounds in the plating industry
(Benson & Zelikoff, 1996: 932; Norseth et al., 1979: 549; Lewis, 1995: database). It was shown
to have an adverse effect on the immune system of experimental animals (Zelikoff &
Smialowicz, 1996: 816, 821).
Chronic effects:
Little data are available on systemic effects of long-term exposure in humans. The critical
organs for chronic exposure are the upper respiratory tract (nose), skin, and immune system
(Gerhardsson et al.,1996: 102).
Soluble salts like nickel sulphate are strong irritants and in nickel refineries and plating plants
where mists are formed, sinusitis, rhinitis, perforation of the nasal septum and bronchial asthma
have been observed (Lewis, 1995: database; Norseth et al., 1979: 549).
Nickel and its compounds are strong skin sensitisers and are responsible for a significant
number of eczema-like conditions (Kimber & Basketter, 1996: 827).
Carcinogenicity:
Nickel compounds are classified Group 1 carcinogens (IARC, 1990: Vol. 49). Nickel metal and
alloys are classified as Group 2B carcinogens (IARC, 1990: Vol. 49).
Long-term exposure to soluble (NiSO4) and insoluble (Ni3S2, NiO) compounds leads to a high
risk of nasal and pulmonary malignancy and an increased risk for liver cancer (Gerhardsson et
al., 1996: 102; Costa, 1996: 246). Nickel iron sulfide matte contains a high concentration of
crystalline nickel subsulphide. This is a potent carcinogen, which has reportedly caused a high
incidence of nasal and pharyngeal cancers amongst persons employed in crushing operations
where they were exposed to crusher dusts. During comparative experiments amorphous nickel
subsulphide (Ni3S2) did not exhibit carcinogenic properties. Black, low-calcined NiO is also
considered to be a potent carcinogen (Costa, 1996: 247).
Reproductive effects:
Although an increase in birth defects was noted in animal experiments, there are no reports of
similar effects in humans.
3.3.4.18
Osmium (Os)
Absorption:
The effects of osmium tetroxide relate to local irritation, with systemic effects through inhalation
and ingestion.
Distribution:
No data available.
80
Table 3.3.4.18
Osmium: Toxicological properties and target-organ effects
Carcinogen
Not a human carcinogen
Species listed
OEL-RL and OEL-CL
Osmium tetraoxide (OsO4) (as Os)
BEI
Medical surveillance
Occupational Health And Safety Act, 1993
Biological effect monitoring
Regulations
for
Hazardous
Chemical Biological monitoring
Substances (Department of Labour, 1995).
Speciation in mineral processing plants: Os, OsO4, OsF6
Absorption: Inhalation, ingestion, skin
Deposition: No data
Target organ
Excretion: No data
Short-term effects
Long-term effects
Renal system
Nervous system
Liver
Gastrointestinal tract
Respiratory tract
Corrosive, irritant; asthma
Bronchitis
Haematopoietic system
Bone
Endocrine system
Muscle
Eye
Corrosive, irritant; lacrymation
Skin
Corrosive, irritant; dermatitis, ulceration
Dermatitis, ulceration
Cardiovascular system
Immune system
Reproductive system
81
See Table 3.4.6.3
Excretion:
No data available.
Acute effects:
Os metal is not highly toxic, and most data on osmium toxicity relate to osmium tetroxide. It is
an eye and mucous membrane irritant, causing asthmatic symptoms upon inhalation, and
dermatitis and ulceration upon skin contact. Persons with pre-existing skin disorders or
impaired respiratory function may be more susceptible to the effects of osmium tetroxide.
OsO4 has a nauseating odour as warning of possible toxic concentrations in the air. It is
poisonous by ingestion and inhalation. Pulmonary oedema and unspecified systemic effects
have been noted after inhalation. The oxide is an irritant causing lacrimation and other eye
effects, and structural and functional changes in the trachea and bronchi (HHMI, 2000).
OsF6 is highly poisonous and a very corrosive irritant to eyes, skin and mucous membranes.
Chronic effects:
Long term exposure from inhalation to osmium tetroxide can cause chronic coughs, broncho
pneumonia, sterile lung abscess and gangrene. Prolonged exposure can result in damage to
the cornea, blindness, disturbances of the digestive system and inflammatory disorders of the
lungs and kidneys (HHMI, 2000).
Carcinogenicity:
Osmium and its compounds have not been listed for carcinogenic effects.
Reproductive effects:
Experimental reproductive effects have been noted, but no actual cases have been
documented (Lewis, 1995: database).
3.3.4.19
Platinum (Pt)
Absorption:
Respiratory and dermal absorption are the primary occupational concerns. It has been
hypothesised that platinum interferes with the antigen recognition step of the immune response
system (Kusaka, 1993: 75-87).
Distribution:
Distribution data are available only for cisplatin (Van der Voet & de Wolff, 1996: 459). It has
been noted that exposure to platinum leads to a relative lymphocytosis.
Excretion:
No data describing excretion of platinum are available. Removal from platinum salt exposure
results in almost immediate relief of asthma (see below). The dermatitis may be persistent, but
usually clears in a few days (see below).
Acute effects:
Pt metal is relatively non-toxic in its pure form (Van der Voet et al., 1996: 459). Exposure to
complex platinum salts has been shown to cause symptoms of irritation in the eyes, nose and
throat. (Lewis, 1995: database). Toxic effects have however not been indicated for
nonsensitised individuals (see below).
Chronic effects:
Platinum salts (mainly the ionic platinum chloro compounds) are sensitisers upon chronic
exposure causing allergies like rhinitis, conjunctivitis, asthma, urticaria and contact dermatitis
(Lewis, 1995: database). The respiratory reaction starts with sneezing and a runny nose. The
effects may be followed by chest tightness, shortness of breath, blue discolouration of the
82
Table 3.3.4.19
Platinum: Toxicological properties and target-organ effects
Carcinogen
Species listed
Platinum metal (as Pt)
Not a human carcinogen
Platinum salts (soluble) (as Pt)
OEL-RL and OEL-CL
BEI
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical
Substances (Department of Labour, 1995).
Medical surveillance
Biological effect monitoring
Biological monitoring
Speciation in mineral processing plants: Pt, sulphides, sulphates, chlorides, oxide
Absorption: Unknown
Deposition: Unknown
Target organ
Excretion: Unknown
Short-term effects
Long-term effects
Renal system
Nervous system
Liver
Gastrointestinal tract
Poisonous
Respiratory tract
Irritant.; sensitiser
Rhinitis, asthma
Eye
Irritant; sensitiser
Conjunctivitis
Skin
Irritant; sensitiser
Dermatitis, urticaria
Haematopoietic system
Bone
Endocrine system
Muscle
Cardiovascular system
Immune system
Reproductive system
Experimental data
83
See Table 3.4.6.3
skin, and wheezing. The skin shows an itchy red rash. Symptoms become progressively
worse with the length of employment. Some workers may show several allergic manifestations
with the involvement of the nasal mucosa, bronchi and the skin. Persons with a history of
asthma, allergies, or known sensitisation to platinum salts would be expected to be at increased
risk from exposure.
Carcinogenicity:
Cisplatin (cis-Pt(NH3)2Cl2) is a probable human carcinogen (Group 2a) (IARC, 1987: Vol. 26,
Suppl. 7), but platinum and its inorganic salts have not been listed by IARC as carcinogens.
Tetrachloroplatinates are mutagens (Lewis, 1995: database).
Reproductive effects:
Reproductive effects have not been identified.
3.3.4.20
Rhodium (Rh)
Absorption:
Rhodium is one of the rarest elements in the earth’s crust, and is found in small quantities
associated with platinum and some copper-nickel ores. Because of its rarity of occurrence, little
is known about its toxicology.
Distribution:
No data available.
Excretion:
No data available.
Acute effects:
Most rhodium compounds are only moderately toxic by ingestion (Lewis, 1995: database).
Chronic effects:
Rhodium may be a sensitiser, but not necessarily to the same extent as platinum. The ability of
soluble salts of rhodium to lead to allergic reactions in human has not been adequately
demonstrated. Occupational exposure limits have been set for rhodium and its salts, based on
analogy with platinum.
Carcinogenicity:
Rhodium has not been listed as a carcinogen.
Reproductive effects:
Experimental reproductive effects have been noted (Lewis 1995: database), but no actual
occurrence has been documented.
84
Table 3.3.4.20
Rhodium: Toxicological properties and target-organ effects
Carcinogen
Species listed
Rhodium metal (as Rh)
Not a human carcinogen
Rhodium salts (as Rh)
OEL-RL and OEL-CL
BEI
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical
Substances (Department of Labour, 1995).
Medical surveillance
Biological effect monitoring
Biological monitoring
Speciation in mineral processing plants:: Not identified
Absorption: No data available
Deposition: No data available
Target organ
Excretion: No data available
Short-term effects
Long-term effects
Renal system
Nervous system
Liver
Gastrointestinal tract
Poisonous
Respiratory tract
Sensitiser
Haematopoietic system
Bone
Endocrine system
Muscle
Eye
Sensitiser
Skin
Sensitiser
Cardiovascular system
Immune system
Reproductive system
Experimental effects
85
See Table 3.4.6.3
3.3.4.21
Selenium (Se)
Absorption:
There is a lack of quantitative data for absorption due to inhalation. Soluble salts are efficiently
absorbed after ingestion (about 80 per cent). Selenium metabolism may be strongly influenced
by dietary and other factors (Glover, Levander, Parizek, Vouk, 1979a: 555), and there does not
appear to be any homeostatic control (Lauwerys & Hoet, 1993: 86).
Distribution:
Absorbed selenium is distributed mainly to the liver and kidneys (animal studies) (Glover et al.,
1979a: 560), but the major portion of the total body burden is stored in the muscle (Lauwerys et
al., 1993: 86).
Excretion:
Urine excretion is the main route for elimination (Lauwerys et al., 1993: 86). The process can
be described with a three-phasic model, with biological half-times of 24 hours (90 per cent
excretion), 103 days and 234 days (Glover et al., 1979a: 562).
Some selenium is excreted through the lungs as volatile compounds, giving rise to a
characteristic garlic odour, which disappears after a few days (Glover et al., 1979a: 568).
Acute effects:
Inhalation of selenium dust or fumes can cause serious irritation of the respiratory tract (Lewis,
1995: database). On contact, SeO2 can cause pulmonary oedema (sudden large exposure),
irritation or burns of the eyes, and skin rashes. Rhinitis, nosebleeds, headache, anorexia,
irritability and nervous disturbances have also been reported (Glover et al., 1979a: 568).
Chronic effects:
Most of the chronic intoxication cases in humans are described for excessive dietary selenium
intake (Lewis, 1995: database; Glover et al., 1979a: 569). Some of the symptoms are common
to those for occupational exposure (Glover et al., 1979a: 568).
Occupational inhalation exposure can cause a wide range of non-specific symptoms:
Irritation of the eyes, nose and throat, gastro-intestinal disturbances, increased body
temperature, headaches and tiredness, irritability, unstable blood pressure, metallic taste,
yellowish skin coloration (Glover et al., 1979a: 568).
At high levels of exposure breath and sweat can assume a garlicky odour due to the excretion
of volatile dimethyl selenide. The odour disappears after seven to ten days (Glover et al.,
1979a: 568).
Carcinogenicity:
There is conflicting epidemiological evidence regarding the role of selenium in carcinogenesis
(Cohen, Bowser, Costa, 1996:264 – 265; Poirer & Littlefield, 1996: 292). IARC (1987) has
determined that there is inadequate evidence for evaluation and classified selenium and its
compounds as Group 3 substances (IARC, 1987: Vol. 9, Suppl. 7).
Reproductive effects:
Although some old observations about miscarriages and birth defects amongst women exposed
to selenite powder, this could not later be verified (Keen, 1996: 990).
Other effects:
There is experimental evidence that selenium exerts immunological effects (Sharma & Dugyala,
1996: 792).
86
Table 3.3.4.21
Selenium: Toxicological properties and target-organ effects
Carcinogen
Unclassifiable
IARC Group 3
Species listed
Se and compounds
(except H2Se) (as Se)
OEL-RL and OEL-CL
BEI
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical Substances
(Department of Labour, 1995).
Medical surveillance
Biological effect monitoring
Biological monitoring
See Table
3.4.6.3
Speciation in mineral processing plants: Se, sulphides, chlorides, sulphate.
Absorption: Inhalation, ingestion Deposition: Muscle, kidneys, liver, heart
Taregt organ
Renal system
Excretion: Two phase. Urine (rapid), faeces, lungs
Short-term effects
Long-term effects
Storage
Storage
Nervous system
Hyperreflexia, peripheral anaesthesia
Liver
Storage
Storage
Gastrointestinal tract
Nausea, vomiting
Indigestion, intestinal disturbances
Respiratory tract
Irritant (H2Se), pulmonary oedema (SeO2)
Haematopoietic system
Lymphocytosis
Bone
Endocrine system
Muscle
Major storage
Eye
Irritant
Skin
Dermatitis
SeO2 : dermatitis, burns, body rash; yellowish skin colour, brittle hair
Cardiovascular system
Unstable blood pressure; storage (heart)
Immune system
Experimental effects
Reproductive system
Women: irregular menses, menostasis
87
3.3.4.22
Silver (Ag)
Absorption:
No data are available for the deposition rate of inhaled material in humans. Little is known
about absorption rate, either from the lungs or gastrointestinal tract (Fowler & Nordberg, 1979d:
581; Lauwerys & Hoet, 1993: 90). The absorption half-life in the human lung has been
estimated at about 1 day (Fowler et al., 1979d: 582).
In animals, gastrointestinal absorption is low (less than 10 per cent) (Fowler et al., 1979d: 581).
Silver nitrate solution (0,5 per cent) has been extensively used as burn treatment. No evidence
has been found for local or systemic toxicity (Fowler et al., 1979d: 583).
Distribution:
Silver is widely distributed in the body. After accidental inhalation of radioactive silver in one
case, about half the body burden was found in the liver after 16 days. It has also been found in
the walls of blood vessels, testes, pituitary, kidneys, mucous membranes and choroid plexus in
the brain (Lewis, 1995: database). In a single reported case, the liver was the main deposition
site, followed by the skin (Fowler et al., 1979d: 582).
Excretion:
Excretion of absorbed silver is largely in faeces via the bile (animal studies). Based on limited
information, the half-life in human liver has been estimated at 48 to 52 days (Fowler et al.,
1979d: 582).
Acute effects:
Soluble compounds (especially AgNO3) are corrosive and irritating to skin, eyes and mucous
membranes and may cause death if ingested (Lewis, 1995: database).
Exposure to fine metallic particles causes local pigmentation in broken skin (Lewis, 1995:
database).
Chronic effects:
3
Long term inhalation of dusts (two to 25 years) at about one mg Ag/m can cause argyrosis, a
grey pigmentation of the skin and mucous membranes. The conjunctivae of the eyes show the
first signs, followed by the mucous membranes of the mouth and skin. The condition develops
slowly and shows no systemic symptoms or physical disability. The pigmentation is permanent
(Lewis, 1995: database). Argyria may also affect organs such as the cornea and lens of the
eye. Reports of systemic effects such as chronic bronchitis and abdominal discomfort have not
been sufficiently evaluated, and silver is therefore not necessarily the causal factor (Fowler et
al., 1979d: 584). In more recent literature argyria is not considered to cause any systemic
symptoms or physical disability (Lewis, 1995: database).
Carcinogenicity:
IARC has not classified silver or its compounds as carcinogens.
Reproductive effects:
Reproductive effects have not been identified.
88
Table 3.3.4.22
Silver: Toxicological properties and target-organ effects
Carcinogen
Species listed
Silver
Not a human carcinogen
Silver compounds (as Ag)
OEL-RL and OEL-CL
BEI
Medical surveillance
Biological effect monitoring
Biological monitoring
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical Substances
(Department of Labour, 1995).
Speciation in mineral processing plants: Ag, AgCN, AgS
Absorption: Inhalation, ingestion, skin
Deposition: Skin, mucous membranes, internal organs, blood vessels
Target organ
Excretion: Bile (faeces)
Short-term effects
Long-term effects
Renal system
Deposition (argyria)
Nervous system
Liver
Storage, clearance via bile
Gastrointestinal tract
Respiratory tract
Argyria (mouth, gums)
Absorption
Argyria (nose, trachea, bronchi)
Haematopoietic system
Bone
Endocrine system
Argyria (pituitary)
Muscle
Eye
Irritation
Argyria (conjunctivae, cornea, lens)
Skin
Irritation
Deposition (argyria)
Cardiovascular system
Deposition (argyria)
Immune system
Reproductive system
Argyria (testes)
89
See Table
3.4.6.3
3.3.4.23
Tantalum (Ta)
Absorption:
Ingested salts of tantalum are poorly absorbed, but no information is available on absorption
from inhalation or dermal exposure.
Distribution:
After intramuscular injection the liver, bone, and kidney were shown to contain high levels of
tantalum (Doull, Klaassen & Amdur, 1980: 457).
Excretion:
Pathways of excretion are not known.
Acute effects:
Tantalum has a low order of toxicity but has produced transient inflammatory lesions in the
lungs of animals. Intratracheal administration of tantalum oxide to guinea pigs produced
transient bronchitis, interstitial pneumonitis, and hyperemia (ASOSH, 2000). Some industrial
skin injuries from tantalum have been reported. TaCl5 is moderately toxic when ingested
(Lewis, 1995: database).
Chronic effects:
Industrial systemic poisoning is unknown (Lewis, 1995: database). Implantation of tanatlum
has not shown any adverse tissue effects in either humans or animals (Doull, Klaassen &
Amdur, 1980: 445).
Carcinogenicity:
IARC has not classified tantalum or its compounds as carcinogenic.
Reproductive:
Reproductive effects have not been documented in animals or humans.
90
Table 3.3.4.23
Tantalum: Toxicological properties and target-organ effects
Carcinogen
Not a human carcinogen
Species listed
Tantalum
OEL-RL and OEL-CL
Occupational Health And Safety Act, 1993
Regulations
for
Hazardous
Chemical
(Department of Labour, 1995).
BEI
Medical surveillance
Biological effect monitoring
Substances Biological monitoring
Speciation in mineral processing plants: Ta, Ta2O5, TaCl5, TaS2, Ta2S4
Absorption: Unknown
Deposition: Unknown
Excretion: Unknown
Target organ
Short-term effects
Long-term effects
Renal system
Nervous system
Liver
Gastrointestinal tract
Moderately toxic (TaCl5) Corrosive (TaF5)
Respiratory tract
Inhalation hazard (Ta)
Haematopoietic system
Bone
Endocrine system
Muscle
Eye
Skin
Injury (Ta)
Cardiovascular system
Immune system
Reproductive system
91
See Table 3.4.6.3
3.3.4.24
Tellurium (Te)
Absorption:
Tellurium is associated with copper and lead production and is mostly used in metallurgical
applications and exposure to other metals (Pb, Zn, As, Se, Cd, Tl) as co-factors should be
considered. Inhalation is the main occupational exposure route (Glover & Vouk, 1979b: 587).
Absorption in humans has not been quantifiable with the available information. In animal
studies estimates for gastrointestinal absorption vary from ten to 15 per cent to 25 per cent.
Some tellurium compounds can be absorbed through the skin to a great enough extent to
cause garlic breath (Glover et al., 1979b: 590; Lauwerys & Hoet, 1993: 91 - 92).
Distribution:
The highest concentrations of tellurium are found in the blood, liver, kidneys, lungs, thyroid and
spleen, but long-term accumulation takes place in bone (Glover et al., 1979b: 590).
Excretion:
Excretion is partly through urine, the faeces and lungs (as dimethyl telluride) (Lauwerys et al.,
1993: 92) with a whole-body half time estimated at about 3 weeks (Glover et al., 1979b: 591).
Acute effects:
Ingestion
Nausea, vomiting, tremors, convulsions, respiratory arrest, central nervous system depression,
garlic odour to breath (Lewis, 1995: database).
Inhalation
Aerosols of Te, TeO2, H2Te cause respiratory irritation, sometimes leading to bronchitis and
pneumonia. Heavy exposure can lead to headache, drowsiness anorexia, metallic taste,
nausea, tremors, convulsions and respiratory arrest (Lewis, 1995: database; Glover et al.,
1979b: 594).
Dermal
Skin irritation can occur upon direct contact in the form of burns or rashes (Glover et al., 1979b:
590). Evidence for skin effects upon occupational exposure to dusts and vapours of TeO2 is
not considered conclusive (Glover et al., 1979b: 592).
Chronic effects:
Tellurium tends to accumulate in the choroid plexus in the brain (Zheng, 1996: 618). The metal
has relatively low toxicity. It is converted in the body to dimethyl telluride, which gives a garlicky
3
odour to the urine, breath and sweat. Foundry workers exposed to less than 0,1 mg Te/m
developed the typical garlicky odour, anorexia, nausea, depression, sleepiness, itchy skin and
metallic taste (Lewis, 1995: database; Glover et al., 1979b: 594).
Carcinogenicity:
IARC has not listed tellurium or its compounds as carcinogenic.
Reproductive effects:
Tellurium is an experimental teratogen (rats) causing hydrocephalus (Glover et al., 1979b: 594),
but no manifestation of this nature has been observed in humans.
92
Table 3.3.4.24
Tellurium: Toxicological properties and target-organ effects
Carcinogen
Not a human carcinogen
Species listed
Te and compounds (except H2Te) as (Te)
OEL-RL and OEL-CL
BEI
Medical surveillance
Occupational Health And Safety Act, 1993
Biological effect monitoring
Regulations
for
Hazardous
Chemical Biological monitoring
Substances (Department of Labour, 1995).
Speciation in mineral processing plants: Te, TeS, TeSO4, TeCl4
Absorption: Inhalation, ingestion, skin
Deposition: Liver, kidneys, lungs, thyroid, spleen
Target organ
Excretion: Urine, faeces, lungs
Short-term effects
Long-term effects
Renal system
Nervous system
Tremors, convulsions, CNS depression, headache
Accumulation (choroid plexus)
Gastrointestinal tract
Anorexia, nausea, vomiting, metallic taste,
Anorexia, nausea, vomiting, metallic taste
Respiratory tract
Respiratory irritation, bronchitis, pneumonia, respiratory arrest
Garlicky breath
Liver
Haematopoietic system
Bone
Accumulation
Endocrine system
Muscle
Eye
Skin
Irritation, burns, rashes
Pruritis
Cardiovascular system
Immune system
Reproductive system
93
See Table 3.4.6.3
3.3.4.25
Thallium (Tl)
Absorption:
Absorption of soluble salts of thallium from the gastrointestinal tract and respiratory system is
rapid and almost complete (Kazantzis, 1979b: 602).
Distribution:
Absorbed thallium is widely distributed in the human body. The highest concentration after
exposure is usually found in the kidneys (Kazantzis, 1979b: 603). It is also distributed to the
heart, brain, skin, liver, bones and brain (Van der Voet & de Wolff, 1996: 457).
Excretion:
Excretion is mainly via urine and faeces (Kazantzis, 1979b: 603).
Acute effects:
Acute poisoning is manifested in gastrointestinal disturbance (gastro-enteritis, nausea,
vomiting, abdominal pain), muscular pain, collapse, peripheral neuropathy, psychological
changes (confusion, delirium, fear, lethargy) cardiovascular involvement (tachycardia,
hypertension, dysrythmia), respiratory and circulatory collapse, and death.
Survival for more than one week after acute poisoning is characterised by headache, ataxia,
tremor, paresthesia, and muscular atrophy. For survival after two to three weeks, hair loss; and
mental disturbances (psychosis, paranoia, and hallucinations) occur. Recovery may be
complete or partial, with remaining mental abnormality, ataxia, and tremors (Kazantzis, 1979b:
606; Van der Voet et al., 1996: 457).
The lethal dose by ingestion is 0,2 to 1,0 grams of absorbed thallium (Van der Voet et al., 1996:
456). The effects are cumulative and with continuous exposure intoxication appears at much
lower levels (Lewis, 1995: database).
Chronic effects:
Occupational exposure is usually long-term and at lower levels than for acute intoxication.
Effects such as discoloration and loss of hair (alopecia), white bands in nails, skin atrophy,
fatigue, anorexia, pains in the legs, visual disturbances (optic neuritis), albuminuria, blood
disturbances, and polyneuropathy have been reported (Kazantzis, 1979b: 608; Lewis, 1995:
database; Van der Voet et al., 1996: 456).
Carcinogenicity:
IARC does not classify thallium as a carcinogen.
Reproductive effects:
Thallium can cross the placental barrier (Van der Voet et al., 1996: 457), and the reproductive
organs and foetus are highly susceptible to harm (Lewis, 1995: database).
94
Table 3.3.4.25
Thallium: Toxicological properties and target-organ effects
Carcinogen
Not a human carcinogen
Species listed
Thallium (soluble compounds) (as Tl)
OEL-RL and OEL-CL
BEI
Medical surveillance
Occupational Health And Safety Act, 1993
Biological effect monitoring
Regulations
for
Hazardous
Chemical Biological monitoring
Substances (Department of Labour, 1995).
Speciation in mineral processing plants: TlO2
Absorption: Rapid by ingestion and inhalation; skin
Target organ
Deposition: Hair, kidneys
Excretion: Urine (initial); faeces (long term)
Short-term effects
Long-term effects
Renal system
Initial concentration
Albuminuria
Nervous system
Polyneuropathy, headache, ataxia
Polyneuropathy, mental abnormality, ataxia
Gastrointestinal tract
Gastro-enteritis, nausea, vomiting, pain
Anorexia
Respiratory tract
Respiratory collapse
Liver
Hematopoietic system
Eosinophilia, lymphcytosis
Bone
Endocrine system
Muscle
Pain
Pain, atrophy, tremors
Eye
Optic neuritis
Skin
Absorption
Cardiovascular system
Tachycardia, hypertension, dysrythmia
Discoloration and loss of hair; atrophy
Immune system
Reproductive system
Can cross placental barrier
Foetal susceptibility, experimental teratogen
95
See Table 3.4.6.3
3.3.4.26
Tin (Sn)
Absorption:
Absorption of ingested inorganic and metallic tin is low (Lewis, 1995: database). Animal
2+
4+
experiments have shown a tendency of Sn to be absorbed more readily than Sn (Piscator,
1979c: 616).
Organotin compounds are highly toxic (especially triethyltin) and can be absorbed through the
skin and from the gastrointestinal tract (Piscator, 1979c: 616).
Distribution:
Inhaled tin tends to accumulate in the lungs with age (Zelikoff & Smialowicz, 1996: 817).
In animal experiments the highest concentrations were found in the kidneys, liver and bone.
The main deposit was in the bone. Elimination from the soft tissues seemed to be fairly rapid.
The deposition pattern in humans was largely the same, with inclusion of the kidneys (Piscator,
1979c: 617). Experiments have shown that powdered, crystalline or liquid inorganic tin
compounds tend to concentrate in the lymphatic system (Zelikoff et al., 1996: 817).
Excretion:
Absorbed tin is excreted mainly in the urine. Excretion of alkyltin compounds varies quite
widely and the route seems to depend on the specific compound in question (Piscator, 1979c:
618).
Acute effects:
Tin(IV) chloride is a corrosive irritant (skin, eyes, mucous membranes)(Lewis, 1995: database).
Several cases of food poisoning due to tin-contaminated food are on record (Piscator, M.
1979c: 622). Experimental results showed that Sn tends to suppress immune reactions (Zelikoff
2+
et al., 1996: 818) and cause DNA damage (Sn highly active) (Cohen, Bowser, Costa, 1996:
269).
Chronic effects:
Chronic inhalation of tin dusts may cause pneumoconiosis (″stannosis″), which in the past was
considered benign (Piscator, 1979c: 620) (Lewis, 1995: database).
Animal studies have shown species differences. Systemic effects like neurological and renal
damage and anaemia were reported. In the one human study reported, no effects were found
(Piscator, 1979c: 620).
Carcinogenicity:
IARC does not classify tin and its compounds as carcinogenic.
Reproductive effects:
No data are available that indicate reproductive effects.
96
Table 3.3.4.26
Tin: Toxicological properties and target-organ effects
Carcinogen
Species listed
OEL-RL and OEL-CL
BEI
Medical surveillance
Occupational Health And Safety Act, 1993
Biological effect monitoring
for
Hazardous
Chemical Biological monitoring
Tin compounds, organic (except Cyhexatin (ISO)) Regulations
Substances (Department of Labour, 1995).
(as Sn)
Tin, compounds, inorganic (except SnH4) as Sn
Not a human carcinogen
See Table 3.4.6.3
Speciation in mineral processing plants: Sulphides, sulphates, hydroxides.
Absorption: Ingestion (low), inhalation
Deposition: Lungs, bone
Target organ
Excretion: Urine, faeces
Short-term effects
Long-term effects
Renal system
Storage
Nervous system
Liver
Gastrointestinal tract
Storage
Food poisoning
Respiratory tract
Storage, accumulation; benign pneumoconiosis
Hematopoietic system
Bone
Storage
Endocrine system
Muscle
Eye
Irritant
Skin
Irritant
Cardiovascular system
Immune system
Suppression (experimental)
Suppression
Reproductive system
97
3.3.4.27
Titanium (Ti)
Absorption:
Absorption of titanium after ingestion is poor (Berlin & Nordman, 1979b: 631). No data are
available for absorption after inhalation or through the skin.
Distribution:
Titanium is consistently found in the lung, probably due to inhalation of dust particles. Titanium
dioxide has been found in the lymph nodes (Berlin et al., 1979b: 631, 632).
Titanium can cross both the blood-brain and placental barriers (Berlin et al., 1979b: 631).
Excretion:
No explicit data are available.
Acute effects:
Dusts have mainly nuisance value. The dioxide can be a skin irritant in some cases. The
chlorides and sulphate are corrosive irritants to the skin, eyes and mucous membranes (Lewis,
1995: database; Berlin, 1979b: 633).
Chronic effects:
Workers exposed to TiO2 pigment for several years showed only minor fibrosis of the lungs,
which was more probably caused by the presence of silica particles in the dust (Berlin, 1979b:
633).
Carcinogenicity:
IARC does not list titanium and its compounds. No carcinogenisis could be shown for exposed
humans, although some animal studies have indicated carcinogenic activity (Cohen, Bowser,
Costa, 1996: 270).
Reproductive effects:
Reproductive effects have been noted in experimental animals (Berlin, 1979b: 634), but no
effects in humans have been documented.
98
Table 3.3.4.27
Titanium: Toxicological properties and target-organ effects
Carcinogen
Species listed
Titanium dioxide total inhalable dust
Not a human carcinogen
Titanium dioxide total respirable dust
OEL-RL and OEL-CL
BEI
Medical surveillance
Occupational Health And Safety Act, 1993
Biological effect monitoring
Regulations for Hazardous Chemical Biological monitoring
Substances (Department of Labour, 1995).
Speciation in mineral processing plants: Ti, TiO2, TiCl4, Ti(SO4)2
Absorption: Ingestion (poor), inhalation
Target organ
Deposition: Lung, lymph nodes
Excretion: Unknown
Short-term effects
Long-term effects
Renal system
Nervous system
Liver
Gastrointestinal tract
Respiratory tract
Nuisance dust (TiO2); corrosive, irritant (chlorides, sulphate)
Nuisance dust (TiO2)
Haematopoietic system
Bone
Endocrine system
Muscle
Eye
Corrosive, irritant (chlorides, sulphate)
Skin
Corrosive, irritant (chlorides, sulphate)
Cardiovascular system
Immune system
Reproductive system
Experimental effects (animals)
99
See Table 3.4.6.3
3.3.4.28
Tungsten (W)
Absorption:
No data are available for humans. In animal studies about 50 per cent of ingested soluble salt
and about 30 per cent of inhaled tungstic oxide aerosol were rapidly absorbed, followed by
rapid excretion in urine and faeces (Kazantzis, 1979b: 640).
Distribution:
The body burden is very small. Absorbed tungsten is initially distributed to the spleen, kidney
and bone, which is also the site for long-term storage (animal studies). (Kazantzis, 1979b:
637).
Excretion:
Most absorbed tungsten is rapidly excreted via urine (animal studies) (Kazantzis, 1979b: 637).
Acute effects:
Most absorbed tungsten is rapidly excreted via urine (animal studies) (Kazantzis, 1979b: 637).
Chronic effects:
Industrially tungsten does not constitute an important health hazard (Lewis, 1995: database).
Effects and symptoms of exposure are mainly respiratory (cough, expectoration, shortness of
breath, tightness in the chest, pulmonary fibrosis) (Kazantzis, 1979b: 643). No data is available
for long-term systemic effects in humans (Kazantzis, 1979b: 645).
Carcinogenicity:
IARC has classified the tungsten ore Wollastonite as Group 3 (unclassifiable as human
carcinogen) (IARC, 1997: Vol. 68). Tungsten and its compounds have not been listed as
carcinogenic.
Reproductive effects:
No data are available that indicate reproductive effects.
100
Table 3.3.4.28
Tungsten: Toxicological properties and target-organ effects
Carcinogen
Not a human carcinogen
IARC Group 3 (Wollastonite ore)
Species listed
Tungsten and soluble compounds (as W)
Insoluble compounds
OEL-RL and OEL-CL
BEI
Medical surveillance
Occupational Health And Safety Act, 1993
Biological effect monitoring
Regulations
for
Hazardous
Chemical Biological monitoring
Substances (Department of Labour, 1995).
See Table 3.4.6.3
Speciation in mineral processing plants: Unknown
Absorption: Rapid by inhalation, ingestion
Target organ
Deposition: Bone; spleen, kidney
Excretion: Urine (rapid)
Short-term effects
Long-term effects
Renal system
Nervous system
Liver
Gastrointestinal tract
Cough, expectoration, shortness of breath, tightness in chest, pulmonary
fibrosis.
Respiratory tract
Hematopoietic system
Bone
Storage
Endocrine system
Muscle
Eye
Irritation
Skin
Irritation
Cardiovascular system
Immune system
Reproductive system
101
3.3.4.29
Uranium (U)
Absorption:
Inhalation
The high density of uranium and its compounds will cause most of the inhaled material to be
deposited in the upper respiratory tract where mucociliary clearance will cause it to be ingested.
Measurements of occupational exposure have led to estimates that only about one to five per
cent of inhaled material will be carried into the lung. Absorption of inhaled uranium is critically
dependent on its solubility in biological media. Soluble material deposited in the alveoli will be
2+
absorbed completely (Berlin et al., 1979c: 651). The uranyl (UO2 ) species have great affinity
for proteins, nucleotides and bone (Berlin et al., 1979c: 651).
Ingestion
Absorption of uranium from the digestive tract varies with solubility, but even soluble
compounds are poorly absorbed (Berlin et al., 1979c: 652).
Skin contact
Animal experiments have shown some absorption by dermal contact with soluble compounds.
No data are available for humans (Berlin et al., 1979c: 652).
Distribution:
On entering the blood stream the absorbed uranium undergoes bio-transformation to water
soluble complexes or colloids and rapidly (66 per cent in six minutes) distributed throughout the
body. Excluding material deposited in the lungs, about 85 per cent of the steady state body
burden in occupationally exposed persons was found in the bone, about 90 per cent of the rest
in the kidney, with detectable amounts in the liver (Berlin et al., 1979c: 650, 652).
Inhaled less-soluble products are found in the bronchial lymph nodes and the lung itself (Berlin
et al., 1979c: 652)
Excretion:
6+
U is rapidly and primarily excreted by the kidneys as a uranium carbonate complex. The
excretion is a two-phase process with about 70 per cent of the dose after exposure being
excreted in the first 24 hours and the rest over a period of several months. Re-absorption of
the uranium is controlled by urinary pH. Acidic conditions are associated with functional
4+
impairment of the kidneys due to uranium binding to the walls of the tubules. U is bound to
proteins in the serum and cleared very slowly (Berlin et al., 1979c: 653; Fowler, 1996f: 726).
Particle size and solubility determine the rate of clearance of uranium from the lungs.
Published results show a two-phase process with an initial half-life of somewhere between 11
days and three months. The slow phase has a half-life of three months to about five years
(Berlin et al., 1979c: 653).
Acute effects:
Uranyl nitrate and its hexahydrate are corrosive and irritating to the skin, eyes, and mucous
membranes (Lewis, 1995: database).
102
Table 3.3.4.29
Uranium: Toxicological properties and target-organ effects
Carcinogen
Carcinogenic
radioactivity
due
Species listed
to
OEL-RL and OEL-CL
Uranium compounds, natural, soluble (as U)
BEI
Medical surveillance
Occupational Health And Safety Act, 1993
Biological effect monitoring
Regulations
for
Hazardous
Chemical Biological monitoring
Substances (Department of Labour, 1995).
See Table 3.4.6.3
Speciation in mineral processing plants: Oxides, phosphates
Absorption: Inhalation, ingestion
Deposition: Bone, kidney
Target organ
Excretion: Urine
Short-term effects
Long-term effects
Renal System
Functional impairment, kidney failure, storage
Nervous System
Liver
Gastrointestinal Tract
Respiratory tract
Corrosive, irritant (UO2(NO3)2), deposition (insoluble salts)
Haematopoietic System
Bound to serum protein (U ) slow clearance
Radiation damage (insoluble compounds)
4+
Bone
Main storage
Endocrine System
Muscle
Eye
Corrosive, irritant (UO2(NO3)2)
Skin
Corrosive, irritant (UO2(NO3)2)
Cardiovascular system
Immune system
Reproductive system
Foetal abnormalities (animals)
103
Chronic effects:
Chronic effects can arise due to two factors:
• The chemical toxicity of soluble uranium compounds leading to kidney damage and possible
failure. Animal experiments have shown that for non-lethal exposure, a form of resistance
develops through epithelial regeneration in the kidneys. After cessation of exposure, the
epithelium gradually returns to normal (Berlin et al., 1979c: 654).
The radiological damage caused by insoluble uranium compounds not cleared from the lungs
depends on the isotope composition of the material (Berlin et al., 1979c: 654).
Carcinogenicity:
Uranium and its compounds are carcinogenic as a result of radiological activity.
Reproductive:
Some reproductive effects and foetal abnormalities were found in animal experiments. Some
reproductive effects in humans were found in World War Two experiments, but they have not
been repeated (Corbella & Domingo, 1996: 1088 - 1091).
3.3.4.30
Vanadium (V)
Absorption:
An estimated 25 per cent of soluble compounds may be absorbed from the lungs (WHO
(1988)) (Lauwerys & Hoet, 1993: 95). V2O5 is specifically reported to be nearly 100 per cent
absorbed by inhalation (Lewis, 1995: database).
Absorption via the oral route appears to be low (less than one per cent) (Vouk, 1979b: 657).
Distribution:
The major fraction (about 90 per cent) of vanadium circulating in the blood stream is bound to
the plasma and widely distributed in the tissues. Tissue levels of vanadium are generally low
(Lauwerys et al., 1995: 94; Vouk, 1979b: 663), but seem to be highest in the liver, kidney and
lungs.
Excretion:
Excretion is mainly via urine. Biological half-life is about 20 to 40 hours (Lauwerys et al., 1995:
95). Faecal excretion is minor, except in the case of ingested material, where excretion is
mainly through the faeces due to the low absorption in the gastrointestinal tract (Vouk, 1979b:
654). Older estimates of half-life are about 42 days (Vouk, 1979b: 664).
Acute effects:
There is some experimental evidence that respiratory exposure to vanadium can lead to
sensitisation (Vouk, 1979b: 665). Responses to industrial exposure are thought usually to be
acute rather than chronic, involving irritation of the eyes and respiratory system in the form of
conjunctivitis, bronchospasm, bronchitis and asthma-like diseases. There seems to be some
controversy over involvement of other organ systems (Lewis 1995: database).
Respiratory symptoms (persistent cough) have an induction period of 12 to 20 hours and are
reversible, disappearing within two to five days (Vouk, 1979b: 665).
Chronic effects:
The older literature (Vouk, 1979b: 659), mentioned symptoms quoted below that have not been
supported by more recent works (Lewis, 1995: database):
Vague general signs
Weakness, nausea, vomiting, tinnitus, headache, dizziness.
104
Table 3.3.4.30
Vanadium: Toxicological properties and target-organ effects
Carcinogen
Species listed
OEL-RL and OEL-CL
Vanadium pentoxide (total inhalable dust)
Not a human carcinogen
Vanadium pentoxide (fume and respirable dust)
BEI
Medical surveillance
Occupational Health And Safety Act, 1993
Biological effect monitoring
Regulations for Hazardous Chemical Biological monitoring
Substances (Department of Labour, 1995).
See Table 3.4.6.3
Speciation in mineral processing plants: V, oxides, sulphate, sulphide, (Ca, Na, ammonium) vanadates
Absorption: Lungs
Deposition: Liver, lungs, kidney
Target organ
Renal system
Excretion: Urine (rapid)
Short-term effects
Long-term effects
Deposition
Deposition
Deposition
Deposition
Deposition, irritation, sneeze, cough
Deposition
Nervous system
Liver
Gastrointestinal tract
Respiratory tract
Haematopoietic system
Anaemia, leukopenia, leukcocyte granulation
Bone
Endocrine system
Muscle
Eye
Irritation
Skin
Irritation
Palpitations, extrasystoles, bradycardia, coronary
insufficiency
Cardiovascular system
Immune system
Reproductive system
Experimental effects (mouse, rat, hamster)
105
Heart
Palpitations, transient coronary insufficiency, bradycardia, and unexpectedly many extra
systoles.
Blood
Anaemia, leukopenia, leucocyte granulation, lowering of cholesterol levels (unconfirmed).
Evidence for long-term respiratory effects of occupational exposure has been mentioned, but
the ecidence is considered inadequate (Vouk, 1979b: 666). Sensitisation is possible as
manifested by increasingly severe symptoms (respiratory, dermatitis) upon repeated exposure,
even for shorter duration or at lower levels (Vouk, 1979b: 669).
Carcinogenicity:
IARC has not classified vanadium and its compounds as human carcinogens.
Reproductive effects:
Experimental reproductive effects have been found (mice, rats, hamsters) (Corbella &
Domingo, 1996: 1091 – 1093; Keen, 1996: 995), but no effects have been documented for
humans.
3.3.4.31
Yttrium (Y)
Absorption:
The rare earth elements have low toxicity by ingestion. Skin and lung granulomas have been
noted after exposure (Lewis, 1995: database). Animal studies showed no accumulation of
yttrium in bones.
Distribution:
Animal data suggest that the pulmonary system and liver are the primary target organs.
Excretion:
No data are avalable to indicate mechanisms of excretion of yttrium.
Acute effects:
Toxic doses cause systemic effects such as writhing, ataxia, laboured respiration, sedation and
walking on the toes with the back arched (animal studies). Yttrium is a possible anticoagulant
and the nitrate is a skin and eye irritant (Lewis, 1995: database). Based on effects observed in
animals, acute exposure would lead to fibrotic lung disease, manifested as shortness of breath,
cough, chest pain, and cyanosis.
Chronic effects:
No signs or symptoms of chronic exposure to yttrium or its compounds have been reported.
Carcinogenicity:
Yttrium and its compounds are not included in the IARC classification for carcinogens
Reproductive effects:
No data are available to indicate reproductive effects in humans.
106
Table 3.3.4.31
Yttrium (and rare earth elements): Toxicological properties and target-organ effects
Carcinogen
Not a human carcinogen
Species listed
Metal and compounds
OEL-RL and OEL-CL
BEI
Occupational Health And Safety Act, 1993
Regulations
for
Hazardous
Chemical
Substances (Department of Labour, 1995).
Medical surveillance
Biological effect monitoring
Biological monitoring
Speciation in mineral processing plants: Unknown
Absorption: Lung, skin Deposition: Unknown
Excretion: Unknown
Target organ
Short-term effects
Renal system
Nervous system
Ataxia, sedation
Liver
Gastrointestinal tract
Toxic by ingestion
Respiratory tract
Laboured respiration
Hematopoietic system
Possible anticoagulant (Y)
Bone
Endocrine system
Muscle
Eye
Irritant (Y(NO3)2)
Skin
Irritant (Y(NO3)2)
Cardiovascular system
Immune system
Reproductive system
107
Long-term effects
See Table 3.4.6.3
3.3.4.32
Zinc (Zn)
Absorption:
The zinc balance in the body is homeostatically controlled (Elinder & Piscator, 1979d: 675).
There is insufficient information available to calculate the absorption of zinc after inhalation
(Elinder et al., 1979d: 679). Absorption of ingested zinc is highly variable (10 to 90 per cent in
animals) and controlled by the zinc status in the body, dietary, and health factors (Elinder et al.,
1979d: 697).
Distribution:
In humans the major portion of the body burden of zinc is found in the muscles (60 per cent)
and bone (30 per cent). The highest concentration however, is found in the prostate (Elinder et
al., 1979d: 679).
Excretion:
Excretion takes place mainly via faeces (75 per cent) with urine as a secondary route (25 per
cent). Excretion rate and biological half-life are regulated according to the zinc status in the
body. In normal persons the biological half-life is 162 to 500 days (Elinder et al., 1979d: 680).
Urinary excretion is reported to have a circadian rhythm (Lauwerys, 1993: 97).
Acute effects:
Zn metal
Zinc is a human skin irritant. Ingestion causes systemic effects like coughing, shortness of
breath and sweating (Lewis, 1995: database).
ZnO
Inhalation of freshly formed fumes can lead to so-called “metal fume fever” with influenza-like
symptoms (fever, chills, dyspnoea, muscle soreness, nausea, fatigue) (Benson & Zelikoff,
1996: 935) which on cessation of exposure disappear completely in about two days. The
possible presence of contaminants like Pb, As, Cd, Sb complicates the picture (Lewis, 1995:
database). The syndrome may be coupled to a sensitisation mechanism and it is possible to
become temporarily immune to it (Lewis, 1995: database). It is estimated that symptoms will
3
not develop at air concentrations below 15 mg/m (Elinder et al., 1979d: 682).
ZnCl2
Inhalation causes irritation and damage to respiratory mucous membranes and grey cyanosis
(Lewis, 1995: database).
Chronic effects:
Chronic zinc intoxication in humans has not been described in much detail (Elinder et al., 1979:
673).
Long-term excess zinc intake has led to secondary copper deficiency and
immunosuppression in humans (Keen, 1996: 982).
ZnO dust can block sebaceous gland ducts with resultant pustular skin complaints. Allergy to
ZnO is extremely rare (Lewis, 1995: database). ZnCl2 and ZnSO4 are caustic and chronic
exposure can lead to skin ulcers (Lewis, 1995: database).
Carcinogenicity:
Zinc chromates are confirmed carcinogens (Lewis, 1995: database), but this is due to the
chromium. Zinc has not been identified as carcinogenic by IARC.
Reproductive effects:
Excess zinc intake in animals has reportedly led to foetal secondary copper deficiency, which
has caused birth defects (Keen, 1996: 982). Similar data are not available for humans.
108
Table 3.3.4.32
Zinc: Toxicological properties and target-organ effects
Carcinogen
Not a human carcinogen
Species listed
OEL-RL and OEL-CL
BEI
Medical surveillance
Biological effect monitoring
Biological monitoring
Zinc chloride fume (ZnCl2) Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical Substances
Zinc oxide fume (ZnO)
(Department of Labour, 1995).
Speciation in mineral processing plants: Unknown
Absorption: Inhalation, ingestion
Deposition: Muscle, bone
Target organ
Excretion: Faeces, urine
Short-term effects
Long-term effects
Renal system
Nervous system
Liver
Gastrointestinal tract
Respiratory tract
Acute pneumonitis, pulmonary oedema (ZnCl2)(heavy exposure)
Haematopoietic system
Bone
Storage
Endocrine system
Muscle
Storage
Eye
Skin
Irritant (ZnCl2, ZnSO4)
Ulceration (ZnCl2, ZnSO4)
Cardiovascular system
Immune system
Reproductive system
Storage in prostate
109
See Table 3.4.6.3
3.3.4.33
Zirconium (Zr)
Absorption:
Most zirconium compounds in common use are insoluble and considered inert. Metabolic
studies are not available, but tissue concentrations indicate that significant amounts of
zirconium may be adsorbed orally (Doull, Klaassen & Amdur, 1980: 462). Inhalation exposure
to water-soluble ZrOCl2 indicated that the highest concentration of zirconium occurred in the
lungs and pulmonary nodes.
Distribution:
The body burden of zirconium is distributed across the liver, blood (cells and lipids), lung,
kidneys, muscle, brain, pancreas, stomach, spleen, and testes (Doull, Klaassen & Amdur,
1980: 462).
Excretion:
Zirconium is excreted by the intestine, probably in the bile. Milk is a secondary route of
excretion, but levels in the urine are negligible (Doull, Klaassen & Amdur, 1980: 462).
Acute effects:
Soluble zirconium salts are poisonous (Lewis, 1995: database), but the oral toxicity of zirconium
and its compounds is generally considered to be low. No evidence of industrial disease as a
result of zrconium exposure has been documented (Doull, Klaassen & Amdur, 1980: 462).
ZrCl4 is a corrosive skin, eye and mucous membrane irritant (Lewis, 1995: database).
Chronic effects:
3
Pulmonary granuloma has been reported in zirconium workers. Inhalation of ZrCl4 (6 mg Zr/m )
for 60 days produced slightly decreased haemoglobin and red blood cell counts and increased
mortality in animals (Lewis, 1995: database).
Carcinogenicity:
IARC does not classify zirconium or its compounds as carcinogens.
Reproductive effects:
Zr(SO4)2 has been shown to be reproductively active in animal studies (Lewis, 1995: database),
but similar data have not been reported for humans.
110
Table 3.3.4.33
Zirconium: Toxicological properties and target-organ effects
Carcinogen
Not human carcinogen
Species listed
OEL-RL and OEL-CL
Zirconium compounds (as Zr)
BEI
Occupational Health And Safety Act, 1993
Regulations for Hazardous Chemical Substances
(Department of Labour, 1995).
Medical surveillance
Biological effect monitoring
Biological monitoring
Speciation in mineral processing plants: ZrO2, Zr(SO4)2
Absorption: Ingestion
Deposition: Unknown
Excretion: Unknown
Target organ
Short-term effects
Long-term effects
Renal system
Nervous system
Liver
Gastrointestinal tract
Toxic, corrosive (Zr(SO4)2)
Respiratory tract
Corrosive irritant (ZrCl4)
Lung granuloma (NaZr lactate)
Hematopoietic system
Bone
Endocrine system
Muscle
Eye
Corrosive irritant (ZrCl4)
Skin
Corrosive irritant (ZrCl4, ZrOClH)
Granuloma (NaZr lactate)
Cardiovascular system
Immune system
Reproductive system
Experimental effects
111
See Table
3.4.6.3
3.4
Exposure
assessment:
General
guidelines
for
occupational health risk assessment and management.
3.4.1
Context
An exposure assessment estimates the magnitude and frequency of actual or potential
exposures to characterised substances, and identifies the pathways by which exposure occurs.
The complete exposure assessment also identifies the routes through which the hazardous
substances may enter the human body.
Exposure under normal working conditions is determined through physical monitoring of the
workplace, personal monitoring using monitoring equipment carried by the workers, or
biological monitoring where exposure is estimated from the analysis of body fluids. A medical
surveillance programme identifies deterioration of health in employees at an early stage, when
such effects may still be reversible when the source of exposure is removed. Emergency plans
and other health risk management practices should be in place for the handling of incidents.
3.4.2
The relationship between dust and heavy metals in exposure
assessment
As a rule, control of exposure to particulates/dust in the occupational environment would also
protect against exposure to particulate-associated heavy metals. In some cases, however, the
guideline concentration for dust may not be adequately protective for all of the constituents in
the dust. Table 3.4.2 lists the maximum concentrations of heavy metals that can be tolerated at
the highest permissible level of airborne dust in the occupational environment. Values are
given for particulates as total dust and for the respirable fraction. Where concentrations of
heavy metals in dust exceed the listed values, additional measures have to be introduced to
protect employees against particulate-associated exposure to heavy metals. For example, if
dust is controlled within permissible levels but the concentration of beryllium in the dust exceeds
200 parts per million (0.02 per cent), additional protective actions may be required to account
for exposure to beryllium. Dusts containing more than 20 per cent calcium oxide, as another
example, would pose a hazard for irritation effects.
Table 3.4.2
Maximum concentrations of heavy metals that can be tolerated at the maximum
permissible dust loads in the occupational environment
Heavy metal
TLV mg/m
total dust
3
3
TLV mg/m
respirable dust
Mass % of metal in
total dust
Antimony
0.5
5
Arsenic
0.01
0.1
Barium
0.5
5
Beryllium
0.002
0.02
Cadmium
0.01
Calcium oxide
0.002
0.1
2
20
Chromium (water-soluble)
0.05
0.5
Chromium metal and Cr (III)
0.5
5
Chromium (insoluble in water)
0.01
0.1
Cobalt
0.02
0.2
112
Mass % of metal in
respirable dust
0.006
Heavy metal
Copper (dust & mist)
TLV mg/m
total dust
3
3
TLV mg/m
respirable dust
Mass % of metal in
total dust
1
10
Copper (fume)
0.2
2
Indium
0.1
1
Iron oxide dust & fume as Fe
5
50
Iron (water-soluble)
1
10
Lead
0.05
0.5
Manganese
0.05
0.5
Mercury
0.025
0.25
Molybdenum (water-soluble)
5
50
Molybdenum (insoluble in
water)
10
100
Nickel (metal)
1
10
0.1
1
1
10
0.0016
0.016
1
10
0.002
0.02
1
10
0.01
0.1
1
10
Selenium
0.2
2
Silver (metal)
0.1
1
Silver (water-soluble)
0.01
0.1
Tantalum
5
50
Tellurium
0.1
1
Thallium (metal & watersoluble)
0.1
1
Tin
2
20
Titanium
6
Tungsten (water-soluble)
1
10
Tungsten (insoluble in water)
5
50
0.2
2
Nickel (water-soluble)
Nickel (insoluble in water)
Osmium
Platinum (metal)
Platinum (water-soluble)
Rhodium metal
Rhodium (water-soluble)
Rhodium (insoluble in water)
Uranium
Vanadium pentoxide (dust)
3
60
0.05
9
0.15
Yttrium
1
10
Zinc oxide dust
10
100
Zirconium
5
50
113
Mass % of metal in
respirable dust
3.4.3
3.4.3.1
Physical monitoring of the workplace
Direct-reading instruments
Where exposures may be due to releases from component failures or other incidents, and
where it is likely that short term exposure limits (or ceiling levels) will be exceeded, directreading instruments and alarm systems are the preferable approach to manage employee
exposure and health risks. In the case of managing the risk of exposure to heavy metals,
however, exposure is largely in the form of particulate-associated substances, and directreading instruments are not widely applicable. Furthermore, concerns are related more to
exposures during normal operation of the plants rather than under upset conditions.
3.4.3.2
Detector-tube measurements
A detector tube is a vial that contains a chemical preparation that reacts with the measured
substance in a way that produces a colour change (Dräger, 1992: 26). The length of stain
discolouration is an indication of the concentration of the substance. Alternatively, quantitative
indication is based on interpretation of the colour intensity according to a reference standard or
set of standards.
The measurement system consists of a detector tube and a gas detector pump. The pump
must pass the sample through the tube at a prescribed rate until a required volume has been
sampled.
The measured value shows the actual concentration during the period of
measurement. Detector tubes are not intended to be used for quantitative exposure
measurements. Standard deviations of measurements are frequently in the range of 30 per
cent, and cross sensitivities commonly occur where compounds are present in mixtures. These
devices are nevertheless extremely useful to screen work areas where leaks of hazardous
substances may occur from time to time, or to determine concentration ranges for ambient
sampling.
There are not many detector tubes available for screening assessments for exposure to heavy
metals, but Table 3.4.3.2 lists those that are available.
Table 3.4.3.2
Some detector tubes for screening assessment of exposure
Substance
Reference
Arsenic trioxide
Arsine
Mercury vapour
67 28951
CH 25001
Dr≅ger, 1997
CH 23101
Nickel
3.4.3.3
Product code
67 28871
Air sampling and analysis
Ambient monitoring assesses the health risk by measuring external exposure to the chemical.
In industry, ambient monitoring usually means monitoring the airborne concentration of the
chemical. Sampling can be stationary, i.e. at selected positions in the workplace. This is
known as area monitoring. Personal sampling is the technique followed when the sampling
equipment is carried on the person to be monitored, to measure exposure as a time-weighted
average over an entire shift. Sampling is usually conducted in the breathing zone, and covers
all the work areas in which the person has to perform tasks. Sampling for heavy metals covers
vapours, fumes, mists and particulates.
114
Active sampling
Active or dynamic sampling for heavy metals normally uses an air sampling pump and a filter
system, to collect the substances of interest. The collected particulates are then extracted or
dissolved, and the metals quantified with an analytical instrument. The National Institute for
Occupational Safety and Health (NIOSH) and the Occupational Safety and Health
Administration (OSHA) have published a range of standard, validated sampling and analytical
methods. These are listed in Section 3.4.3.6. Where possible, these methods for active
sampling and analysis should be used to quantify exposure levels of hazardous substances in
occupational environments.
Passive sampling
Passive sampling offers an attractive alternative to dynamic sampling, but the nature of the
samplers limits their use to gases and vapours, thereby leaving very limited application to heavy
metals. In contrast to active sampling where forced convection brings the substances of
interest in contact with the sorbent, a passive sampler collects the species by natural diffusion.
Sampling rates are calculated either from predicted diffusion coefficients, or determined
experimentally in the laboratory. Extraction and analysis are the same as for active sampling.
Some of the passive samplers produce colour changes that are proportional to concentration
and exposure time, in which case quantification of exposure can be achieved through calibrated
colour comparisons. The ChromAir passive badge (K&M Environmental, 1996) is available for
quantification of mercury exposure.
Categories of sampling
Sampling can be conducted in three categories, as described below.
Full-period, continuous single sampling
This sampling approach is defined as sampling over the entire sampling period, to collect only
one sample. The sampling may be for a full-shift sample or for a short period ceiling
determination.
Full-period, consecutive sampling
The sampling strategy in this case is to use multiple consecutive samples of equal or unequal
time duration which, if combined, equal the total time duration of the required sample. An
example would be to take four two-hour samples and combine these for assessment of an
eight-hour shift. Advantages of this approach are:
•
•
•
If one of the samples were lost due to pump failure, contamination or other reason, at least
some data would have been acquired to assess the situation.
The use of multiple samples has statistical advantages. If a sufficient number of samples
are taken, this may lead to lower errors of observation.
Collection of several samples may indicate how exposures vary over the workday, and how
this would affect overall exposure.
Grab sampling
Grab sampling is defined as collecting a number of short-term samples at various times during
the sampling period which, when combined, provide an estimate of exposure over the total
period. A typical example would be a number of high-volume air samples collected on filters
over a period of time.
3.4.3.4
Selection of appropriate positions for monitoring
All the areas with a potential to release a toxic substance of interest have to be identified.
Because of many potential release points, it is sometimes not practical to sample at every point
during all the surveys. A decision has to be taken on the overall frequency of monitoring, based
on the level of risk and the cost of monitoring. A selection (subgroup) of the sampling points
115
has to be taken for each survey (NIOSH, 1977: 33). On a statistical basis, this subgroup has to
be of adequate size, so that there would be a high probability that the random sample will
contain at least one area with a high exposure level, assuming that such high level is possible.
The sample size drawn from a group is listed in Table 3.43.4a. The philosophy is to ensure
with 90 per cent confidence that at least one sampling point from the highest ten per cent
potential release areas is included in the sample.
Table 3.4.3.4a
Size of partial sample for the top 10 % potential release points at a confidence
level of 90 %
Size of potential release points (N)
Number of points to measure (n)
7
8
9
10
11
12
13
14
15
16
17
18
8
9
10
11 to 12
13 to 14
15 to 17
18 to 20
21 to 24
25 to 29
30 to 37
38 to 49
50
N = original equal risk group size.
n = sample size or subgroup size.
n = N if N is less than 7.
To limit any bias to certain positions by the sampler, it is recommended that a system of
random sampling be followed. Table 3.4.3.4b lists a selection of random numbers. Of course,
where information about specific positions has to be obtained, these can be done as separate
surveys.
116
Table 3.4.3.4b
Table of random numbers after NIOSH (1977)
The procedure for random sampling is as follows:
•
•
Assign each potential area of toxicant release a number from one to N, where N is the total
number of areas in the facility. During a particular sampling session, a subgroup of n
samples has to be taken.
Arbitrarily choose a column in Table 3.4.3.4b and read down the list. Ignore zero and all
values larger than N. If necessary, proceed to the next column until a partial sample of n
numbers has been selected.
Areas that have been assigned the selected numbers will form the randomly selected subgroup
for monitoring.
117
3.4.3.5
Personal sampling
Selection of the maximum exposed individual
Following a positive indication that an employee or employees may be exposed at
concentrations of a toxic substance at or above the action level, then the employer is required
to determine the exposure level of an employee who would be expected to have the highest
exposure. The approach is known as exposure assessment of the maximum exposed
individual. The assessment is an approximate one, and those employees that are expected to
have lower exposure than those at maximum risk are not sampled initially.
The best information for selection is normally obtained from a preliminary survey of the work
environment, so that a well-informed person can make a valid judgement as to the employee
with the highest exposure. If there are work situations in which the exposures in the
assignments vary, either because of the work patterns of employees or the varying nature of
the production process, the most severe situations are selected for initial sampling.
The employee closest to the source of the hazardous substance would most likely be the
person at maximum risk. Air movement patterns within a workroom should be analysed to
determine the risk potential of employees. The locations of ventilation systems, open doors
and windows, and the size and shape of the work area, would all be factors that could affect air
flow patterns and result in higher contaminant concentrations further away from the source.
Employee work patterns should also be observed to get an idea of time-concentration
exposures. Differences in work habits of individuals with the same work patterns can affect
exposure levels significantly.
If a maximum risk worker cannot be identified for an operation with reasonable certainty, the
approach of random sampling of the group of workers has to be followed.
Random sampling of a homogeneous risk group
The procedure is to sample the group of workers with similar work patterns randomly. The
approach is similar to that outlined in Section 3.4.3.4 for statistical selection of monitoring
positions. A subgroup of adequate size is selected, so that there would be a high probability
that the random sample will contain at least one person with high exposure, assuming that such
high exposure is possible. Initial sampling should begin with at least six (preferably nine)
personal samples collected on at least three different days for each job assignment.
The sample size drawn from a group is listed in Table 3.4.3.5. The philosophy is to ensure with
90 per cent confidence that at least one individual from the highest ten per cent exposure group
is included in the sample.
118
Table 3.4.3.5
Size of partial sample for the top 10 % exposure subgroup at a confidence level
of 90 %
Size of group (N)
Number of individuals (n)
8
9
10
11 to 12
13 to 14
15 to 17
18 to 20
21 to 24
25 to 29
30 to 37
38 to 49
50
7
8
9
10
11
12
13
14
15
16
17
18
N = original equal risk group size
n = sample size or subgroup size
n = N if N is less than 7
Random sampling is conducted with the use of a table of random numbers (see Table 3.4.3.4b
above).
The procedure for random sampling is as follows:
•
•
Assign each employee a number from 1 to N, where N is the total number of employees in
the group.
Arbitrarily choose a column in Table 3.6 and read down the list. The subgroup that has to
be selected has a size n. Ignore zero and all values larger than N. If necessary, proceed to
the next column until a partial sample of n numbers has been selected.
Individuals who have been assigned the selected numbers will form the randomly selected
subgroup for monitoring.
Selection of employees for periodic monitoring
If any of the measurements on the maximum exposed individual or the selected subgroup
shows exposures to a toxicant at or above the occupational exposure limit (OEL), the employer
has to follow the guidelines presented below:
•
•
•
Identify all employees who may be exposed at or above the OEL.
Measure the exposure levels of all the identified employees. The purpose of this approach
is to restrict measurements to those employees with significant exposures. It is not
adequate to sample a subgroup and assign the average value to all the employees in the
exposure scenario.
If the exposure level of the maximum exposed individual or those of the selected subgroup
were below the OEL, it is reasonable to assume that exposure levels of the other
employees would also be lower than the OEL. No further action should be necessary until
some change in the operation or control measures is introduced.
Personal monitoring
Sampling should be conducted for an entire shift, minus not more than two hours for equipment
setup and dismantling, i.e. at least six hours of an eight-hour shift or ten hours of a 12-hour
119
shift. Good occupational hygiene judgement should be used to interpret exposures during the
period not sampled.
Under regulations of the USA Occupational Health and Safety Administration (OSHA), minimum
legal requirements have been proposed, i.e.:
•
•
•
•
The exposure of an employee whose measurement is at or above the action level, but not
above the permissible exposure (or occupational exposure limit), must be measured at least
every two months. The action level of exposure is usually half or one third of the
permissible level, and necessitates the application of specified precautionary measures.
These measures may include biological monitoring and medical examinations. More
frequent measurements may be made on the basis of professional judgement of the
exposure situation.
For an employee whose exposure measurement exceeds the permissible level, the
employee’s exposure must be measured at least every month until the exposure is reduced
to below the standard by appropriate control measures. More frequent measurements may
be made on the basis of professional judgement of the exposure situation.
If two consecutive exposure measurements on an employee taken at least one week apart
reveal that each of the measurements is less than the action level, exposure monitoring on
the particular individual may be terminated.
In situations of infrequent (non-routine) exposure, the question of how often to monitor
infrequent operations is best answered with professional judgement. The physiological risk
from the chemical and its toxicological profile should be important considerations in
determining the need to monitor employees with infrequent exposure.
3.4.3.6
Sampling and analytical methods for exposure assessment
Table 3.4.3.6
List of NIOSH and OSHA sampling and analytical methods for air monitoring
Element
Agency
Reference
Analytical method
Antimony and compounds
NIOSH
2 (S2)
AA
Antimony and compounds
OSHA
ID 121
AA
Antimony and compounds
OSHA
ID 125
ICP-AES
Antimony particulates
NIOSH
4 (261)
AA
Arsenic and compounds
NIOSH
7900
AA, FLARGN
Arsenic (elements)
NIOSH
7300
ICP-AES
Arsenic, inorganic compounds
OSHA
ID 105
AA-GF
Arsenic, organic compounds
OSHA
CIM
IC-AA
Arsenic organo
NIOSH
5022
IC-AA
Arsenic trioxide
NIOSH
7901
AA-GF
Barium chloride, soluble compounds
NIOSH
7056
AA
Barium, insoluble compounds
OSHA
ID 121
AA
Barium, soluble compounds
NIOSH
7056
AA
Barium, soluble compounds
OSHA
ID 121
AA
Barium sulphate, respirable fraction
OSHA
ID 121
GR
Barium sulphate (total dust)
OSHA
ID 121
GR
Beryllium & compounds
OSHA
ID125
ICP
120
Element
Agency
Reference
Analytical method
Beryllium & compounds
NIOSH
7102
AA-GF
Beryllium (elements)
NIOSH
7300
ICP-AES
Bismuth
OSHA
CIM
AA
Bismuth telluride, Se-doped
OSHA
ID 121
GR-AA
Bismuth telluride, undoped, respirable dust
OSHA
ID 121
GR-AA
Bismuth telluride, undoped, total dust
OSHA
CIM
GR
Cadmium
OSHA
ID 189
AA
Cadmium & compounds
NIOSH
7048
AA-F
Cadmium (elements)
NIOSH
7300
ICP-AES
Calcium & compounds
NIOSH
7020
AA-F
Calcium (elements)
NIOSH
7300
ICP-AES
Calcium oxide
OSHA
ID 121
AA
Calcium oxide
NIOSH
7020
AA-F
Calcium oxide (elements)
NIOSH
7300
ICP-AES
Calcium (see specific compounds)
NIOSH
7020
AA-F
Chromium (chromic acid and chromates)
OSHA
ID 103
POL
Chromium (chromic acid and chromates)
NIOSH
7600
VAS
Chromium (chromic acid and chromates)
NIOSH
7604
IC-ECN
Chromium acetate
OSHA
ID 121
AA
Chromium carbonate
OSHA
ID 121
AA
Chromium & compounds
NIOSH
7024
AA-F
Chromium (elements)
NIOSH
7300
ICP-AES
Chromium, hexavalent
NIOSH
7600
VAS
Chromium, hexavalent
NIOSH
7604
IC-ECN
Chromium, hexavalent
OSHA
ID 103
DPP
Chromium, hexavalent
OSHA
ID 215
IC
Chromium, metal and insoluble compounds
OSHA
ID 121
AA
Chromium, metal and insoluble compounds
OSHA
ID 125
ICP
Chromium, soluble salts
OSHA
ID 121
AA
Cobalt acetate
OSHA
ID 125 G
ICP-AES
Cobalt carbonyl
OSHA
ID 121
AA
Cobalt & compounds
NIOSH
7027
AA-F
Cobalt (elements)
NIOSH
7300
ICP-AES
Cobalt hydrocarbonyl
OSHA
ID 121
AA
Cobalt, metal dust and fume
OSHA
ID 121
AA
Cobalt, metal dust and fume
OSHA
ID 125 G
ICP
Copper dust
NIOSH
7029
AA-F
121
Element
Agency
Reference
Analytical method
Copper, dusts and mists
OSHA
ID 125 G
ICP-AES
Copper, dusts and mists
OSHA
ID 121
AA
Copper (elements)
NIOSH
7300
ICP-AES
Copper fume
NIOSH
7029
AA-F
Copper fume
OSHA
ID 121
AA
Copper fume
OSHA
ID 125 G
ICP-AES
Indium
NIOSH
1 (190)
ASV
Iron and compounds
OSHA
ID 121
AA
Iron (elements)
NIOSH
7300
ICP-AES
Iron oxide fume
OSHA
ID 121
AA
Iron oxide fume
OSHA
ID 125
ICP
Lead
NIOSH
7082
AA
Lead
NIOSH
7105
AA-GF
Lead (elements)
NIOSH
7300
ICP-AES
Lead, inorganic fumes and dusts
OSHA
ID 121
AA
Lead, inorganic fumes and dusts
OSHA
ID 125 G
ICP-AES
Lead, inorganic surface dusts
OSHA
ID 121
AA
Lead sulphide
HIOSH
7505
X DIF
Manganese (elements)
NIOSH
7300
ICP-AES
Manganese fume
OSHA
ID 121
AA
Manganese fume
OSHA
ID 125 G
ICP-AES
Manganese tetroxide
OSHA
ID 121
AA
Manganese tetroxide
OSHA
ID 125 G
ICP-AES
Mercury
NIOSH
6009
AA
Mercury, aryl and inorganic
OSHA
ID 145
AA
Mercury, vapour
OSHA
ID 140
AA
Molybdenum (elements)
NIOSH
7300
ICP-AES
Molybdenum, insolubles
OSHA
ID 121
AA
Molybdenum, insolubles
OSHA
ID 125
ICP-AES
Molybdenum, solubles
OSHA
ID 121
AA
Nickel (elements)
NIOSH
7300
ICP-AES
Nickel, metal and insoluble compounds
OSHA
ID 125
ICP-AES
Nickel, metal and insoluble compounds
OSHA
ID 121
AA
Nickel, soluble compounds
OSHA
ID 125
ICP-AES
Nickel, soluble compounds
OSHA
ID 121
AA
Osmium tetroxide
OSHA
CIM
ICP-AES
Platinum (elements)
NIOSH
7300
ICP-AES
122
Element
Agency
Reference
Analytical method
Platinum, soluble salts
OSHA
CIM
AA-GH
Rhodium, metal fume and dust
NIOSH
3(S188)
AA
Rhodium, metal fume and dust
OSHA
CIM
AA-GF
Rhodium, soluble salts
NIOSH
3(S189)
AA-HGA
Rhodium, soluble salts
OSH
CIM
AA-GF
Selenium compounds
OSHA
CIM
AA-GF
Selenium (elements)
NIOSH
7300
ICP-AES
Silver (elements)
NIOSH
7300
ICP-AES
Silver metals and soluble compounds
OSHA
ID 121
AA
Silver metals and soluble compounds
OSHA
ID 206
ICP-AES
Tantalum, metal, oxide dusts
OSHA
CIM
GR
Tellurium
OSHA
ID 121
AA
Tellurium (elements)
NIOSH
7300
ICP-AES
Thallium (elements)
NIOSH
7300
ICP-AES
Thallium, soluble compounds
OSHA
ID 121
AA
Tin (elements)
NIOSH
7300
ICP-AES
Tin, inorganic compounds except oxides
OSHA
ID 121
AA
Tin, inorganic compounds except oxides
OSHA
ID 206
ICP-AES
Tin oxide
OSHA
ID 121
AA
Titanium dioxide
NIOSH
3(S385)
AA
Titanium dioxide (total dust)
OSHA
CIM
GR
Titanium (elements)
NIOSH
7300
ICP-AES
Tungsten and compounds
OSHA
ID 213
ICP-AES
Tungsten, insoluble compounds
NIOSH
7074
AA-F
Tungsten, insoluble (elements)
NIOSH
7300
ICP-AES
Tungsten, soluble compounds
NIOSH
7074
AA-F
Uranium, insoluble compounds
OSHA
CIM
ICP-AES
Uranium, soluble compounds
OSHA
ID 170
POL
Vanadium, fume (pentoxide)
OSHA
ID 125 G
ICP-AES
Vanadium (elements)
NIOSH
7300
ICP-AES
Vanadium oxides
NIOSH
7504
X DIF
Vanadium, respirable dust
OSHA
ID 125 G
ICP-AES
Yttrium
OSHA
CIM
AA
Yttrium (elements)
NIOSH
7300
ICP-AES
Zinc
OSHA
ID 121
AA
Zinc
OSHA
ID 125 G
ICP-AES
Zinc and compounds
NIOSH
7030
AA-F
123
Element
Agency
Reference
Analytical method
Zinc oxide
NIOSH
7502
X DIF
Zinc oxide (elements)
NIOS
7300
ICP-AES
Zinc oxide fume
OSHA
ID 121
GR, AA
Zinc oxide fume
OSHA
ID 125
GR, ICP-AES
Zinc oxide fume
OSHA
ID 143
GR, X DIF
Zirconium compounds
OSHA
ID 121
GR, AA
Zirconium (elements)
NIOSH
7300
ICP-AES
Atomic absorption spectrometry
Atomic absorption spectrometry, flame
Atomic absorption spectrometry, graphite furnace
Atomic emission spectrometry
Gravimetric analysis
Inductively coupled plasma
Polarography
X-ray diffraction
3.4.4
AA
AA-F
AA-GF
AES
GR
ICP
POL
X DIF
Medical evaluation
Medical evaluation refers to a planned programme of periodic examination, which may include
clinical examinations, biological monitoring, or medical tests of employees by an occupational
health practitioner or, in prescribed cases, by an occupational medicine practitioner.
3.4.4.1
Medical surveillance
The purpose of a medical surveillance programme is to detect a disease at the subclinical or
presymptomatic stage, in order to take appropriate action to reverse the effects, or the slow
progression of the disease towards the clinical status. In industry the objective is not only to
detect adverse effects in employees, but also to relate the findings to the effectiveness of
exposure control measures.
The number of validated screening tests associated with exposure to hazardous metals is
smaller than tests available in general preventive medicine. Target-organ toxicity associated
with heavy metals is important to direct medical surveillance. Although interpretation criteria
are available for some of the tests, in many cases occupational health practitioners have to
develop pragmatic approaches in the context of the specific exposure scenario. The
Regulations for Hazardous Chemical Substances under the Occupational Health and Safety Act
provide some guidance for medical surveillance. The programme should include education of
employers and employees about occupational hazards, placement of staff in positions that do
not jeopardise their safety and health, early detection of adverse health effects, and referral of
individuals for diagnostic confirmation and treatment.
Pre-placement medical evaluation
Prior to placing a worker in a job with a potential for exposure, the occupational health
practitioner or occupational medical practitioner should evaluate and document the worker’s
baseline health status with thorough medical, environmental, and occupational histories, a
physical examination and physiological and laboratory tests appropriate for the anticipated
occupational risks. This is important even though the exposure may be within the regulatory
guidelines. A pre-placement medical evaluation is recommended in order to detect and assess
pre-existing or concurrent conditions that may be aggravated or result in increased risk in other
respects that may be associated with the exposure.
124
Periodic medical evaluation
Workers with potential exposures to chemical hazards should be monitored in a systematic
programme of medical surveillance intended to prevent or control occupational injury and
disease. Additional examinations may be necessary should a worker develop symptoms that
may be attributed to exposure. The interviews, examinations and appropriate biological effect
monitoring and/or biological monitoring tests should be directed at identifying an excessive,
decrease or adverse trend in the integrity and physiological function of the target organs. The
baseline health status of the individual, trends in the occupational group, or data on a suitable
reference population, serve as reference for comparison and interpretation. Again, the organs
of the body that are vulnerable to the exposure determine the elements of the medical
screening.
The programme should include education of employers and workers about work-related
hazards, placement of workers in jobs that do not jeopardise their safety and health, earliest
possible detection of adverse health effects, and referral of workers for diagnostic confirmation
and treatment.
Intrinsic to a medical surveillance programme is the dissemination of summary data to those
who need to know, including employers, occupational health professionals, potentially exposed
workers, and regulatory and public health agencies.
The occurrence of disease (a “sentinel health event”, SHE) or other work-related adverse
health effects should prompt immediate evaluation of primary preventive measures, e.g.
engineering controls, and personal protective equipment. A medical surveillance programme is
intended to supplement, not replace such measures. A medical surveillance programme should
include systematic collection and epidemiologic analysis of relevant environmental and
biological monitoring, medical screening, and morbidity and mortality data. This analysis may
provide information about the relatedness of adverse health effects and occupational exposure
that cannot be discerned from results in individual workers. Sensitivity, specificity, and
predictive values of biological monitoring and medical screening tests should be evaluated on
an industry-wide basis prior to application in any given work group.
Job transfer or termination evaluation
The medical, environmental and occupational history interviews, the physical examination, and
selected physiological and laboratory tests which were conducted at the time of placement,
should be repeated at the time of job transfer or termination. Any changes in the worker’s
health status should be compared to those expected for a suitable reference population.
Because occupational exposure may cause diseases of prolonged induction-latency, the need
for medical surveillance may extend well beyond termination of employment.
3.4.4.2
Biological effect monitoring
Biological effect monitoring determines the intensity of biochemical or physiological change due
to exposure, e.g. red cell cholinesterase for exposure to organophosphate pesticides, or zinc
protoporphyrin (ZPP) for exposure to inorganic lead.
3.4.4.3
Biological monitoring
Traditionally, exposure to hazardous substances in industry has been controlled by setting
standards for the concentration of pollutants in ambient air. This monitoring method considers
only exposure by the pulmonary route and, even for chemicals that enter the human body
mainly with the inspired air, it does not always reflect the true uptake of the exposed workers.
Biological monitoring of exposure attempts to estimate the internal dose. It takes into account
absorption by routes other than the lungs. The greatest advantage of biological monitoring is
the fact that the biological parameter of exposure is more directly related to the adverse health
effect which one attempts to prevent than any environmental measurement. Therefore, it may
offer a better estimate of risk than ambient monitoring. Because of its capability to evaluate the
125
overall exposure, whatever the route of entry, biological monitoring presents the advantage that
it can be used to test the efficiency of various protective measures such as gloves, masks, and
barrier creams. Another advantage is the fact that non-occupational background exposures
may also be expressed in the biological level.
Practical considerations and regulatory aspects relating to biological monitoring
Biological monitoring of exposure is of practical value only when relationships between external
exposure, internal dose, and adverse effects are known. Figure 3.4.4.3 provides a useful
illustration of relationships between monitoring approaches and the types of information
obtained (Lauwerys and Hoet, 1993: 9).
Figure 3.4.4.3
Types of monitoring in occupational health protection (after
Lauwerys and Hoet, 1993: 9)
If only the relationship between external exposure and internal dose is known, the biological
parameter can be used as a measure of exposure, but it will not give an indication of the
associated health risks (situation ‘a’ in Figure 3.4.4.3). Most of the published studies on
chemical exposure have focused on the relationship between external exposure and internal
dose, and little is known about the relationship between internal dose and health effects. A lot
more is known about the relationship between external exposure and adverse effects, as
reflected in regulatory standards, i.e. threshold limit values (TLVs) and other parameters. If
internal dose-response relationships are known, biological monitoring allows for a direct health
risk assessment. Unfortunately, for many chemicals this relationship has not been established,
and the biological limit values (BLVs) have been derived indirectly from exposure limits in air,
and the relationship between external exposure and internal dose.
The Regulations for Hazardous Chemical Substances under the Occupational Health and
Safety Act (No 85 of 1993) are quite explicit for biological monitoring of exposure (Department
of Labour, 1995). Biological exposure indices (BEIs) have been listed as reference values
intended as guidelines for the evaluation of potential health hazards in risk management. A BEI
126
in this context represents the level of a hazardous chemical substance or metabolite most likely
to be observed in a biological sample from a healthy individual who has been exposed to the
substance to the same extent as another person with inhalation exposure to an OEL-TWA
(occupational exposure limit - time-weighted average). This is a simplified approach, because
many physicochemical and biological factors preclude the existence of such clear relationships.
Great individual variation exists in the absorption rate of a chemical through the various
exposure routes.
Application of biological monitoring methods
A complete overview has been published by the U.S. National Institute for Occupational Safety
and Health (NIOSH) (1998: 52).
Normally, where meaningful, pre-placement or baseline samples should be taken from all
employees that may be exposed to hazardous substances in their work environments. Total
body burdens of all employees that may be exposed have to be determined annually
NIOSH recommends that biological monitoring be done at regular intervals, for example an
interval not exceeding every three months to at least 25 per cent of all employees that may be
subject to the exposure. Participating workers at the same exposure level, selected in
subgroups for monitoring, should be rotated to provide all workers the opportunity for analysis
every year.
Depending on the particular scenarios, sampling may be done in sets on a totally random basis,
to include all possible events, some of which may be scheduled only on certain days. A set of
samples is understood to be one pre-shift and one post-shift sample of biological fluid from a
particular person. Three sets of samples from unexposed workers (also pre-shift and postshift) have to be collected as controls, and submitted for analysis with each batch of samples
from exposed workers.
List of biological exposure assessment methods
Table 3.4.4.3
Analytical methods for biological monitoring
Element
Blood or tissue
Antimony, cadmium, chromium, cobalt,
copper,
iron,
lead,
manganese,
molybdenum, nickel, platinum, silver, tin,
titanium, zinc
Urine
Barium, cadmium, chromium, copper,
iron, Lead, manganese, molybdenum,
nickel, platinum, silver, tin, titanium, zinc
Blood and urine
Lead
3.4.4.4
Agency
Reference
Analytical method
NIOSH
8005
ICP-AES
NIOSH
8310
ICP-AES
NIOSH
8003
AA-F
Medical evaluation summary: procedures relevant to the various heavy
metals
Table 3.4.4.4 presents a summary of procedures for medical surveillance, biological effects
monitoring, and biological monitoring. The information should be used as a checklist, with the
understanding that each item requires specialist knowledge for application and interpretation.
The abbreviation APMSP (as per medical surveillance programme) refers to programmes that
should be developed to address occupational health risk issues that are pertinent to specific
exposure scenarios. It is not possible to design a generic medical surveillance programme for
all the mineral processing industries.
127
Because medical surveillance and biological effect monitoring rely on a combination of
diagnostic interpretations, it is beyond the scope of this investigation to provide comprehensive
guidelines for assessment in this field. Biological exposure indices are not listed in Table
3.4.4.4, but it is shown for which substances BEI’s have been developed for application in
South Africa. Only cadmium, chromium and mercury are listed in the Regulations for
Hazardous Chemical Substances under the Occupational Health and Safety Act (Department of
Labour, 1995). There are many complexities around the interpretation of biological monitoring
data. More information on biological monitoring for metal exposures and some interpretations
are discussed in the sections that deal with the individual mineral processing plants.
128
Table 3.4.4.4
Summary of medical surveillance, biological effects monitoring, and biological monitoring
Code:
B:
APMSP:
E:
SHE:
P:
Baseline
As per medical surveillance programme
Exit
Sentinal health event
Periodic (A: annual)
Hazardous substance
Medical surveillance
Item SHE
Antimony
Arsenic
Barium
Sulphate
Carbonate
Beryllium
Bismuth inorganic
(Mainly by ingestion)
Bismuth organic
Frequency
Skin
Nose septum
Respiratory
B
E
P
Hair loss
P. neuritis
Eyes
Weight
Nose septum
Skin
B
E
P
Skin
Ear Nose Throat
Skin contact
Nose septum
Respiratory
Skin
Psychiatric
Biological effect monitoring
B
E
P
B
E
P
Item
Biological monitoring
Frequency
Chest X ray
Pulmonary function test
Kidney function test
Liver function test
Full blood count
Liver function test
Pulmonary function test
(Baseline CXR)
B
APMSP
Chest X ray
Pulmonary function test
ECG
Pulmonary function test
Liver function test
Chest x-ray
B
APMSP
B
APMSP
Item\
Urine
Serum
No BEI listed
Urine
B
APMSP
Urine
No BEI listed
Urine
B
APMSP
B
APMSP
B
APMSP
No BEI listed
Urine
129
B
APMSP
BEI for urine
B
E
P
Kidney test
Liver function test If large
quantities consumed
Frequency
B
APMSP
Urine
No BEI listed
B
APMSP
Medical surveillance
Nose septum
Anosmia
Respiratory
Cadmium
Calcium oxide
Chromium
Cobalt
Dust
Fume
Copper
Indium
Iron
Oxide
(VI)
(III)
Nose septum
Respiratory
Liver function test
Skin
CVS
Kidney function
test
Nose septum
Respiratory
Liver
Skin
Eyes
Wilson’s Disease
Kidney function
test
Nose septum
Respiratory
Liver/kidney
Skin
Respiratory
Biological monitoring
B
APMSP
Chest X-ray
Pulmonary function test
Full blood count
Kidney function test
Liver
Chest X-ray
Pulmonary function test
Liver function test
ECG
B
APMSP
No BEI listed
Urine
Red cells
B
APMSP
B
APMSP
BEI
for
urine,
Cr(VI) and total Cr
Urine
Blood
B
APMSP
B
E
P
B
APMSP
No BEI listed
Urine
Serum
B
APMSP
B
E
P
B
APMSP
Dust
Fume
Skin
Lump
Eyes
Nose Septum
Vision
Nose septum
Skin
Respiratory
Biological effect monitoring
Pulmonary function test
Chest X-ray
Liver function test
Kidney function tests
Full Blood Count
(anaemia)
Protein (Low MW)
Pulmonary function test
Baseline chest X-ray
B
E
P
B
E
P
B
E
P
B
E
P
Urine
B
APMSP
Blood
No BEI listed
B
APMSP
B
APMSP
No BEI listed
Urine
B
APMSP
No BEI listed
B
E
P
Pulmonary function test
Chest X-ray
B
APMSP
B
APMSP
No BEI listed
130
Medical surveillance
Lead
Manganese
Mercury (inorganic)
Molybdenum
Nickel
Osmium (tetroxide)
Platinum
Rhodium
Selenium
Compounds
Radial nerve
Neurological
Kidney function
test
Reproductive
Anaemia
Psychological
Neurological
Speech
Neurological
Psychological
Skin
Neurological
Kidney function
test
Eyes
Respiratory
Skin allergies
Respiratory
Eye
Skin
Respiratory
Kidney function
test
Allergy
Skin/URT
Respiratory
Nose Septum
Allergy
Skin/URT
Respiratory
Nose Septum
Skin
Eyes
Nails
Biological effect monitoring
B
E
P
Full Blood Count (HB)
ZPP
B
APMSP
B
E
P
B
E
P
Full blood count
Chest X-ray
Pulmonary function test
Kidney function test
Pulmonary function Test
B
APMSP
B
APMSP
Biological monitoring
Urine
Blood
No BEI listed
Urine
Blood
No BEI listed
Urine
Blood
B
APMSP
B
APMSP
B
APMSP
BEI for blood and
urine
Chest X Ray
Pulmonary function Test
B
APMSP
B
APMSP
B
E
P
Chest X Ray
Pulmonary function Test
Sputum cytology
Skin test
Chest X-ray
Pulmonary function test
Skin
B
E
P
Chest X-ray
Pulmonary function test
Skin
B
APMSP
B
E
P
Chest X-ray
Pulmonary function test
Skin
B
APMSP
B
E
P
Chest X-ray
Pulmonary function test
Urinalysis
ALT/AST/GGT
Full blood count
B
APMSP
B
E
P
B
E
P
131
B
APMSP
Urine
No BEI listed
Urine
No BEI listed
Urine
B
APMSP
B
APMSP
B
APMSP
No BEI listed
Urine
No BEI listed
Urine
B
APMSP
B
APMSP
No BEI listed
Serum
Urine
No BEI listed
B
APMSP
Medical surveillance
Silver
Skin
Eye test
Observe for agyria
Nose septum Respiratory
Tantalum
Tellurium
Thallium
Tin
Smell breath
Skin
Neurological
Skin
Hair Loss
Skin
Respiratory
Compounds/alloys
Titanium
Respiratory
Eyes
Tungsten
Skin
Respiratory
Respiratory
Skin
Uranium
Vanadium
Yttrium
Zinc
Compounds/salts
Respiratory
Skin
Eyes
Green Tongue
Respiratory
Eye
Respiratory
Skin
Dental
Nose septum
Eyes
Vision
Biological effect monitoring
B
E
P
Baseline chest X-ray
Pulmonary function test
B
APMSP
B
E
P
Chest X-ray
Pulmonary function test
B
APMSP
Urinalysis
B
APMSP
urinalysis
B
APMSP
Pulmonary function test
Chest X-ray
B
APMSP
Pulmonary function test
Chest X-ray
B
APMSP
Lung function test
Chest X-ray
B
APMSP
Chest x ray
Pulmonary function test
Full blood count+
ESR+DIFF
Urine: urinalysis +
microscopy
Chest X-ray
Pulmonary function test
B
APMSP
Chest X-ray
Pulmonary function test
B
APMSP
Chest X-ray
Pulmonary function test
B
APMSP
Biological monitoring
Urine
Faeces
B
APMSP
No BEI listed
B
E
P
B
E
P
B
E
P
B
E
P
B
E
P
B
E
P
B
E
P
B
APMSP
No BEI listed
Urine
No BEI listed
Urine
B
APMSP
B
APMSP
No BEI listed
B
APMSP
No BEI listed
B
APMSP
No BEI listed
B
APMSP
B
APMSP
No BEI listed
Urine
Whole body
radiation
No BEI listed
Urine
B
APMSP
B
APMSP
No BEI listed
B
E
P
B
E
P
B
APMSP
No BEI listed
Urine
No BEI listed
132
B
APMSP
Medical surveillance
Zirconium
Compounds
Respiratory
Skin
B
E
P
Biological effect monitoring
Baseline chest X-ray
Pulmonary function test
Biological monitoring
B
APMSP
B
APMSP
No BEI listed
133
3.5
Risk characterisation
Human health risk characterisation is generally divided into the evaluation of carcinogenic and
non-carcinogenic risks.
Carcinogenic risks are interpreted in terms of excess lifetime cancer risks. In the occupational
exposure range the estimated cancer risk is assumed to be linear and proportional to dose.
Risks are assumed to be additive per target organ across chemicals and pathways, unless data
are available that would support synergistic or antagonistic effects. Risks are expressed as
excess cancer risk, i.e. risk not taking into account any existing risk as a result of background
exposure to substances that have the same carcinogenic properties. Unit cancer risk factors
derived for lifetime exposure (70 years) are adjusted for 30 years’ exposure, following the
approach outlined by Hallenbeck (Hallenbeck, 1993: 102). This is based on the assumption
that exposure over an occupational lifetime of 30 years covers the latency period of the
carcinogen. The excess cancer risk is calculated as follows:
Excess risk = C1(URF1) + C2(URF2) + ...........+ Cn(URFn)
where the excess risk refers to a particular target organ, and Ci(URFi) refers to the exposure
concentration of substance i multiplied by the unit risk factor for that compound, URFi. It is
assumed that substances 1 to i all have carcinogenic effects on the same endpoint.
Noncarcinogenic risks are evaluated by comparison with reference concentrations. If the ratio
of the air concentration to the reference concentration (hazard quotient) exceeds one, there is a
potential that adverse health effects may occur. For multiple chemical exposures, hazard
quotients are summed per target organ, unless data are available to demonstrate synergistic or
antagonistic effects. This is based on the assumption that the response of a target organ to
multiple toxic agents is additive in a linear relationship. It is measured in terms of a hazard
index (HI), which is the sum of the hazard quotients (HQ’s) for the individual substances, (i).
Hazard Index (HI) = HQ1 + HQ2 + ......... + HQn
where the hazard quotients
where i = 1, 2, ........ , n.
3.6
HQi = Intake of substance i / reference dose for substance i,
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139
140
4
4.1
Carbon steel process with blast furnace and basic
oxygen furnace
Introduction
This section provides a process description and process diagram of a typical carbon steel
process employing a blast furnace (BF) and basic oxygen furnace (BOF). The process
description and process diagram contain data on the process streams and identify the
hazardous substances as well as potential exposure points.
Trace elements are commonly distributed in processes according to the following classification
(Clarke, 1993: 731):
Group 1 elements are concentrated in coarse residues or may be equally partitioned between
coarse residues and finer particles. The following elements are in this category:
Eu, Hf, La, Mn, Rb, Sc, Sm Th, Zr
Group 2 elements are often volatilised in the process, but may condense downstream. They
are concentrated in finer particles that may escape particulate control systems. Group 2
elements are:
As, Cd, Ga, Ge, Pb, Sb, Sn, Te, Ti, Zn
There is considerable overlap between the groups, as shown by the number of elements that
fall into more than one group. Elements classifiable into groups 1 and 2 are:
Ba, Be, Bi, Co, Cr, Cs, Cu, Mo, Ni, Sr, Ta, U, V, W
Group 3 elements are the most volatile and are depleted in all solid phases and may remain in
the gas phase during passage through the plant. These include:
Hg, Br, Cl, F, Rn
Elements classifiable into groups 2 and 3 are:
B, Se, I
Although very generalised, this classification provides some idea of the overall distribution of
metals in various parts of an industrial process.
4.2
Process description
This section provides a process description and process diagram of a typical production facility
for carbon steel with blast furnace and basic oxygen furnace. The process description and
process diagram contain data on the process streams and identify the hazardous substances
as well as potential exposure points.
4.2.1
Coke preparation
o
Coke is produced by heating coal lumps up to a temperature of 1 500 C which is then
maintained for a period of 24 hours. This is carried out in the controlled atmosphere of
externally heated coke oven batteries. The product is then rapidly cooled in a stream of cold
water, screened, dried, and transferred to storage ready for feeding to the blast furnace. Coal
consumption is in the range of 1,5 t per t of coke produced. Gas from the coke oven is used to
heat the oven, as well as a number of heat-treatment and re-heat furnaces. The flue gas from
the furnaces is dry- and/or wet-scrubbed before venting to the stack.
Waste slurry from the scrubber contains phenols, cyanides, sulphides and ammonia.
141
The slurry/dust from the scrubber is either transferred to the sinter and/or the pelletising plant,
or is dumped.
Table 4.2.1
Coke preparation
Stream
Component
Total
Coal dust
Fly ash (containing
mainly SiO2,
Al2O3 and carbon)
Gas
Dust
Flue gas
(containing
mainly
SiO2
and Al2O3)
SO2
NOx
Waste
(mainly SiO2
Waste water/dust ex
and Al2O3)
scrubber
NH3
CN
S2
Trace elements
Dust from coke oven
4.2.2
Typical flow
1 kg/t
0,6 kg/t
0.4 kg/t
Heavy metals
Exposure
Ash contains 2%
Coke oven area/dust
trace elements as
collection
metals, chlorides and
oxides
3
1 500 m /t
0,4 kg/t
Dust contains 1%
trace
elements, Stack
mainly as oxides
0,1 kg/t
0,23 kg/t
3
0,35 m /t
2,8 kg/t
0,2 kg/t
0,02 kg/t
0,001 kg/t
Solids contain trace
elements mainly as Scrubber waste
oxides
Sintering
Sinter is produced by firing a mixture of coke breeze, iron ore fines, lime and/ or dolomite on a
sinter machine. The sinter is conveyed to storage prior to feeding to the blast furnace.
Gas/fume from the sintering machine is wet-scrubbed before being vented to the stack.
The residue from the scrubber goes back to the sinter machine, or to the pelletiser, or to a
waste site.
Table 4.2.2
Sintering
Stream
Component
Typical flow
Dust from sintering Total dust
machine
Fine ore
Residuals
Coke fines
Returning fines
Fluxes
Dust also contains
SiO2 and
CaO
0,8 kg/t
0,48 kg/t
0,05 kg/t
0,1 kg/t
Iron ore dust
See later
See later
0,12 kg/t
0,05 kg/t
142
Heavy metals
Exposure
Fine ore contains
Sinter machine
mainly Fe2O3
And FeO with 0,1%
trace elements as
oxides.
Residuals contain 1–
2% trace elements
as oxides.
Fluxes contain
CaO and 0,1% trace
elements as oxides
See later
Sinter machine
Stream
Flue gas dust
Component
Total dust
Fine ore
Fly ash
Fluxes
Typical flow
0,24 kg/t
0,08 kg/t
0,14 kg/t
0,02 kg/t
Heavy metals
Fine ore contains
0,1% trace elements
as oxides.
Exposure
Stack
Fly ash contains 2%
trace elements as
oxides.
Lime
Scrubber effluent
4.2.3
Total
CaO
SiO2
MgO
FeO
TE
Total
Sludge
Organics
NH3
S2
CN
Fluxes contain CaO
and 0,1% trace
elements as oxides.
CaO, FeO, trace
elements as oxides
0,1 kg/t
95%
1%
0,4%
0,1%
3
0,1 m /t
0,4 kg/t
0,1 kg/t
0,1 kg/t
0,001 kg/t
0,001 kg/t
Lime make-up
Sludge contains
Scrubber effluent
mainly FeO, Fe2O3,
CaO, and 0,1% trace
elements as oxides
Storage/blending/material handling
The main iron ore feed is delivered into storage bins together with coke and sinter, prepared as
described above. Material handling facilities are provided to feed the required blend of these
constituents to the blast furnace.
Table 4.2.3
Storage, blending and material handling
Stream
Iron ore feed/dust
4.2.4
Component
Total
Fe2O3
SiO2
Al2O3
MgO
Trace elements
Typical flow
0,008 kg/t
94%
4%
1%
1%
0,1%
Heavy metals
Fe2O3
Trace elements as
oxides
Exposure
Storage area
Blast furnace treatment
In the blast furnace, iron units are added as lump ore, pellets and sinter. Coke is added in
layers which alternate with the iron ore layers. Pulverised coal, together with preheated air at
o
1 000 C, which is enriched with two per cent oxygen, is blown into the furnace through tuyeres
which are placed above the furnace hearth. The top gas is used to heat furnace stoves in
which the air blast is preheated. Hot metal and slag are regularly tapped from the hearth at
o
around 1 465 C. The hot metal, which usually contains around 4.5 per cent C, 0.5 per cent Si,
0.05 per cent S and 0.03 per cent P, is further refined as described below to control the level
and shape of S and P contaminants.
Blast furnace slag is granulated and removed from the plant and may be used in the building
industry.
143
Table 4.2.4
Blast furnace treatment
Stream
Blast furnace gas
Blast furnace slag
Waste water
From scrubber
4.2.5
Component
Total gas
Dust
NOx
S2
Total slag
FeO
MgO
SiO2
Al2O3
CaO
Trace elements
Waste water
Total sludge
NH3
S2
CN
Organics
Typical flow
3
1525 m /t
0,005 kg/t
0,15 kg/t
0,001 kg/t
320 kg/t
5%
15%
30%
15%
30%
0,1%
3
2 m /t
0,9 kg/t
0,6 kg/t
Trace
1,5%
1.4 kg/t
Heavy metals
Dust is mainly FeO,
Fe2O3 with 0,1%
trace elements as
oxides
FeO
CaO
Trace elements as
oxides
Exposure
Blast furnace area
Slag storage
Sludge is mainly
FeO, Fe2O3 with
0,1% trace elements
as oxides
Basic oxygen furnace treatment
Refining of hot metal to steel is carried out in the basic oxygen furnace by blowing oxygen
into/onto the melt to lower the levels of C and Si. Steel scrap and direct reduced iron are also
added to the blast furnace, both as iron units as a coolant, with some lime and/or dolomite to
control the physicochemical properties of the slag. The basic oxygen furnace gaseous product
is wet/dry-scrubbed before its utilisation as a fuel gas. The steel product of the basic oxygen
furnace is further refined to control the level of dissolved gases such as O, H, and N.
The basic oxygen furnace slag is first crushed for recovery of entrapped metal particles and
then removed and used for micronutrient purposes.
The basic oxygen furnace dust is collected and may be used as iron units, although it could
often be contaminated with S, P, C, Ca, Zn, Pb, Ni, and Cr. Zinc is accumulated in the basic
oxygen furnace dust up to around 20 per cent by mass.
Sludge from the scrubber is collected and may be used for its iron units.
Table 4.2.5
Basic oxygen furnace treatment
Stream
Component
Basic oxygen furnace Gas
gas
Dust
SO2
NOx
P2O5
Trace elements
ZnO
PbO
NiO
Cr2O3
CrO3
Typical flow
3
60 m /t
0,001 kg/t
0,003 kg/t
0,003 kg/t
0,002 kg/t
144
Heavy metals
Dust is mainly
FeO, Fe2O3, CaO
with O,1% trace
elements as oxides
ZnO
PbO
NiO
Cr2O3
CrO3
Exposure
Basic oxygen furnace
area
Stream
Component
Typical flow
Heavy metals
Exposure
Basic oxygen furnace Total slag
slag
FeO
SiO2
CaO
Al2O3
MgO
Trace elements
Waste water/dust
Total
From scrubber
Sludge
Fe2O3/FeO
CaO
SiO2
Al2O3
MgO
C
S
Trace elements
Trace elements
ZnO, PbO,
NiO, Cr2O3,
CrO3
Lime
As before
150 kg/t
25%
18%
32%
10%
10%
0,1%
3
0,1 m /t
1 kg/t
45%
30%
5%
3%
10%
4%
3%
0,1%
FeO
CaO
Trace elements as
oxides
Slag storage area
Fe2O3
FeO
CaO
ZnO
PbO
NiO
Cr2O3
CrO3
Trace elements as
oxides and chlorides
Scrubber effluent
As before
As before
Flux
0,07 kg/t
47%
48%
3%
2%
0,1%
CaO
FeO
Trace elements as
oxides
Lime storage/
handling
Flux storage area
4.2.6
Total
CaO
MgO
SiO2
FeO
TE
Further refining, casting, rolling, pickling, galvanising
The refining of hot metal and steel for the removal of S and P may be carried out in a torpedo
or transfer ladle. The agents used are usually a mix of Mg powder, calcium carbide, sodium
oxide and lime in an oxidising atmosphere (sodium carbonate is commonly used as a source of
sodium oxide). The use of sodium oxide is limited because the reduction of sodium oxide by
the carbon in the melt produces large amounts of sodium fume.
De-oxidation of the steel is usually performed by inserting aluminium wires in the melt in a ladle
or crucible.
De-gassing of steel to remove dissolved nitrogen and/or hydrogen may be carried out in a reheat furnace or by argon arc stirring under vacuum.
Steel ingots are usually abrasion ground and heated in a re-heat furnace before sending them
to the rolling mills, although continuous casters accept hot molten steel.
Mill scale from the rolling mills is internally used for iron units.
Pickling is carried out using hydrochloric or sulphuric acid, using an amine-based reagent as a
protector, before hot galvanisation of steel products in zinc melt.
145
Table 4.2.6
Further refining, casting, rolling, pickling, galvanising
Stream
Dust/fume from
refining
Pickle liquors
Calcium carbide
Lime
Galvanising fume
4.3
Component
Total
Desulph.:
CO/CO2
SO2
CaO
TE
Dephos.:
CO/CO2
SO2
CaO
Trace elements
0,0001 kg
H2SO4
HCl
Total
C
Ca
Trace elements
Total
CaO
SiO2
MgO
FeO
Trace elements
Zn
Typical flow
0,001 kg/t
20%
40%
40%
0,1%
40%
40%
20%
0,2%
0,0001 kg/t
H2SO4
HCl
1 kg/t
25%
75%
0,2%
0,1 kg/t
95%
1%
0,4%
0,1%
80%
Heavy metals
Exposure
Dust contains mainly Finishing area
FeO and CaO with
TE as metals, MnS
and other sulphides
Dust contains mainly
FeO and CaO with
trace elements as
oxides
Iron sulphates or
chlorides
and trace elements
CaC2
Trace elements as
metals
Finishing area
CaO
FeO
Trace elements as
oxides
Reagent make-up
area
Zn
0,1% trace elements
as
chlorides and
sulphides
Finishing area
Finishing area
Process diagram
The process diagram for the carbon steel process with blast furnace and basic oxygen furnace
is shown in Figure 4.3.
4.4
4.4.1
Process assessment
Hazard identification
Exposure to dust is a primary concern in this industry. Exposure to iron oxide (Fe2O3) present
as a major constituent in the feed material, and consequently the dust, is controlled by
3
regulations at a level of 5-mg Fe/m .
The other substances of interest are calcium oxide and zinc oxide. Following the guidance in
Table 3.4.2, calcium oxide may be present at levels higher than 20 per cent in basic oxygen
furnace slag, and zinc has to be assessed as fumes in the galvanising area.
Other metals present at trace levels would be significant only in quantities that exceed their
individual threshold limits. It appears unlikely that the carbon steel process has the potential to
release heavy metals other than those identified above into air at any significant levels.
146
Figure 4.3
Process diagram for the carbon steel process with blast furnace
and basic oxygen furnace.
147
4.4.2
Toxicological assessment
Iron oxide is not considered to be inert dust (particulates not otherwise classifiable), because
inhalation may lead to effects known as siderosis, iron pneumoconiosis, hematite
pneumoconiosis, and iron pigmentation of the lung. It appears that the pulmonary effects are
somewhat more serious than those caused by inert dust. Systemic effects relating to excessive
haemosiderin deposits have also been documented. It has not been proved that iron oxides
are carcinogenic following chronic pulmonary exposure. The toxicity of iron and its compounds
has been discussed in Section 3.3.4.12.
Calcium in itself is not toxic to humans, but in the form of calcium oxide it acts as an irritant.
The toxicology of calcium oxide has been discussed in Section 3.3.4.7.
The toxicity of zinc has been discussed in Section 3.3.4.32.
4.4.3
Exposure assessment
Exposure to dust containing iron oxide may occur in areas where iron ore is handled, at the
sinter machine, and at the blast furnace. Sampling and analytical methods for airborne iron
have been listed in Table 3.4.2.6. There is no biological monitoring method to assess exposure
to iron, because iron is an essential element present in the human body.
Exposure to calcium may occur at the lime storage and handling area, in slag from the basic
oxygen furnace, and in flux. Sampling and analytical methods have been listed in Table 3.4.2.6
for calcium. Biological monitoring would not give an indication of exposure because of the large
body burden of calcium.
Exposure to zinc may be possible in the final galvanising steps. The most widely known
systemic effect resulting from acute inhalation of freshly formed zinc oxide fumes is a disease
called metal fume fever. Table 3.4.2.6 lists sampling and analytical methods for zinc oxide.
Zinc is an essential element and is present in abundance in various parts of the human body.
Biological monitoring would therefore not provide useful information for exposure assessment.
Section 3.4.4 provides an overview of medical evaluation procedures that are relevant for
exposure assessment and interpretation of health effects.
4.4.4
Risk quantification
3
In controlling exposure to iron oxide, it is not adequate to control dust levels to 10 mg/m ,
3
because the level of iron may be above 5 mg/ m at particulate levels slightly lower than 10 mg
3
total dust/m .
Because of its irritation effects, exposure to calcium oxide should be assessed against
maximum concentration peaks rather than average values.
For exposure to zinc oxide, the concentration at which metal fume fever would develop is not
entirely certain, but it has been estimated that symptoms are unlikely to develop at air
3
concentrations below 15 mg/m (Elinder & Piscator, 1979: 682). The ACGIH guidelines of 5
3
3
mg/m for zinc oxide fume and 10 mg/m for zinc oxide dust therefore provide adequate
margins of safety.
4.5
References
Clarke, L.B. 1993. The fate of trace elements during coal combustion and gasification: an
overview. Fuel, 72 (6):731 - 736.
148
Elinder, C-G. & Piscator, M. 1979d. Zinc. (In: Friberg, L, et al. Handbook on the Toxicology
of Metals. Amsterdam: Elsevier/ North-Holland Biomedical Press, p. 675 - 685).
Peacey, J.G. & Davenport W.G. 1979. The iron blast furnace: theory and practice. Oxford:
Pergamon, 251p.
Von Bogdandy, L. & Engell, H.J. 1971. The reduction of iron ores; scientific basis and
technology. Dusseldorf: Verlag Stahleissen, 592p.
149
150
5
Carbon steel process with direct reduced iron and
electric arc furnace
5.1
Introduction
A process description and flow diagram of a typical carbon steel process involving the direct
reduced iron (DRI) process and electric arc furnace (EAF) are included in this section. The
process description and flow diagram contain data on the process streams and identify the toxic
substances as well as the potential exposure points.
Trace elements are commonly distributed in processes according to the following classification
(Clarke, 1993: 731):
Group 1 elements are concentrated in coarse residues or may be equally partitioned between
coarse residues and finer particles. The following elements are in this category:
Eu, Hf, La, Mn, Rb, Sc, Sm Th, Zr
Group 2 elements are often volatilised in the process, but may condense downstream. They
are concentrated in finer particles that may escape particulate control systems. Group 2
elements are:
As, Cd, Ga, Ge, Pb, Sb, Sn, Te, Ti, Zn
There is considerable overlap between the groups, as shown by the number of elements that
fall into more than one group. Elements classifiable into groups 1 and 2 are:
Ba, Be, Bi, Co, Cr, Cs, Cu, Mo, Ni, Sr, Ta, U, V, W
Group 3 elements are the most volatile and are depleted in all solid phases and may remain in
the gas phase during passage through the plant. These include:
Hg, Br, Cl, F, Rn
Elements classifiable into groups 2 and 3 are:
B, Se, I
Although very generalised, this classification provides some idea of the overall distribution of
metals in various parts of an industrial process.
5.2
Process description
This section provides a process description and process diagram of a typical production facility
for carbon steel with direct reduced iron and electric arc furnace. The process description and
process diagram contain data on the process streams and identify the hazardous substances
as well as potential exposure points.
5.2.1
Grinding
Iron ore fines, together with additives are continuously ground in a ball mill prior to pelletisation.
Table 5.2.1
Grinding
Stream
Component
Ore fines/dust
See “lump ore”
Typical flow
See “lump ore”
Heavy metals
See “lump ore”
151
Exposure
Grinding area
5.2.2
Pelletisation
Ground ore fines are mixed with recycled sludge from the slimes dam and bentonite and are
then mixed with water using a paddle mixer. The mixtures are fed to a pelletiser typically
comprising a rotating disc or drum which pelletises the moist mix into 10 to 25 mm diameter
pellets. Wet pellets may be continuously dried in a drier heated by hot gas or fuel burner to
about 120 to 150 °C.
Table 5.2.2
Pelletisation
Stream
Flue gas
Waste water
5.2.3
Component
Gas
Dust
SO2
NOx
Trace elements
in dust
Sludge
Trace elements
Typical flow
Heavy metals
Exposure
3
2 500 m /t
0,125 kg/t
0,05 kg/t
0,25 kg/t
0,1%
Mainly Fe2O3,
Trace elements
as oxides
Pelletiser area
0,95 kg/t
0,1%
Mainly Fe2O3,
Trace elements
as oxides
Slimes dam
Direct reduction
Pelletised iron ore, lump ore, coal, and dolomite are fed to rotary kilns where reduction takes
place. Carbon monoxide forms during the reaction. Air is blown into the freeboard of the kiln at
eight positions to combust the CO gas and the volatile matter that rise from the bed so that the
o
bed temperature remains at around 1 000 C. The product is a solid-state reduced iron, and is
called sponge iron (SI) or directly reduced iron (DRI).
The product from the rotary kiln is cooled, magnetically separated from the ash and char,
screened, and sent to the melt-shop. The gaseous byproduct of the kiln is further combusted in
a steam boiler, then scrubbed, and finally vented to the stack.
Wastewater is treated in a number of thickeners, using various types of flocculant for removal
of the solids as slimes. The slimes are partially de-watered in the slimes dam and recycled to
the pelletising plant. The slimes-dam water is recycled back to the circuit for re-use. Solids are
recycled from the thickener or, occasionally, from the dam.
Table 5.2.3
Direct reduction
Stream
Lump ore/dust
Dust from kilns
Component
Total
Fe2O3
SiO2
Al2O3
MgO
Trace
elements
Total
FeO
SiO2
Al2O3
MgO
CaO
C
Trace
elements
Typical flow
Heavy metals
Exposure
0,001 kg/t
94%
4%
1%
1%
0,1%
Fe2O3,
Trace elements
as oxides
Ore storage/feed system
0,02 kg/t
54%
10%
15%
12%
5%
5%
0,5%
FeO
CaO
Trace elements
as metals and
oxides
Dust cleaning area
152
Stream
Component
Solids in stream to
slimes dam
Flocculant
Dust from magnetic
separator and
screens
Ash
5.2.4
Total
FeO
SiO2
Al2O3
MgO
CaO
Trace
elements
Ferric chloride
Trace
elements
Total
Fe
FeO
C
SiO2
MgO
Al2O3
CaO
Trace
elements
Total
FeO
SiO2
Al2O3
MgO
CaO
Trace
elements
Typical flow
Heavy metals
Exposure
0,004 kg/t
54%
10%
15%
12%
5%
1%
FeO
CaO
Trace elements
as metals and
oxides
Slimes dam
Approx 100%
FeCl3
Trace elements
as chlorides
Fe
FeO
CaO
Trace elements
as metals
Flocculant storage/make-up
FeO
Trace elements
as oxides
Magnetic separator/
slimes dam
0,1%
kg/t
35%
15%
10%
25%
5%
5%
5%
0,1%
150 kg/t
5%
45%
35%
5%
8%
2%
Magnetic separator
Electric arc furnace
DC-arc furnaces are used and these are usually charged with hot metal from a blast furnace,
scrap, and direct reduced iron together with some lime or dolomite. The electric arc furnace
may however use only scrap steel, or DRI only.
Table 5.2.4
Electric arc furnace
Stream
Electric arc
furnace gas
Electric arc
furnace slag
Component
Total
Dust:
FeO
ZnO
PbO
MnO
SiO2
CaO
MgO
Trace elements
NOx
SO2
Total
FeO
SiO2
Al2O3
MgO
CaO
Trace elements
Typical flow
Heavy metals
3
2 000 m /t
0,02 kg/t
41%
25%
3%
4%
4%
8%
3%
2%
0,25 kg/t
0,1 kg/t
150 kg/t
35
20
2
8
35
0,1%
Exposure
Dust cleaning area
Dust contains
FeO
ZnO
PbO
MnO
CaO
Trace elements
as oxides and
chlorides
FeO
CaO
Trace elements
as oxides
153
Slag dump
Stream
Lime
Component
Total
CaO
SiO2
Al2O3
FeO
MgO
Trace elements
5.2.5
Typical flow
Heavy metals
CaO
FeO
Trace elements
as oxides
100 kg/t
95%
1%
0,5%
0,1%
0,4%
0,1%
Exposure
Reagent storage/make-up
Casting, rolling, pickling, galvanising
Refined, liquid steel is transferred, in molten state, by crucible, from the electric arc furnace or
basic oxygen furnace to the tundish of the continuous casting machine (Concast). In cases
where billets or blooms are cast they will be re-heated then rolled to the required shape. If the
plate sections are to be galvanised, they are cleaned in HCl or H2SO4 and then hot-dip
galvanised.
Table 5.2.5
Casting, rolling, pickling, galvanising
Stream
Component
Dust/fume from De-sulph.:
refining
CO/CO2
SO2
CaO
Trace elements
De-phosph.:
CO/CO2
Na2O
CaO
Trace elements
Typical flow
Exposure
Mainly FeO, CaO Finishing area
and
Trace elements
metals and
sulphides, MnS
etc.
0,001 kg/t
20%
40%
40%
0,1%
40%
40%
20%
0,2%
Pickle liquors
Total
SO4
HCl
0,0001% TE
Galvanising
fume
Total
Zn
0,0001 kg/t
80%
5.3
Heavy metals
Mainly FeO, CaO,
with trace
elements as
oxides
Finishing area
Iron sulphates
and chlorides
with trace
elements
Finishing area
Zn
Trace elements
as metals
Flow diagram
The flow diagram for the carbon steel process with with direct reduced iron and electric arc
furnace is shown in Figure 5.3.
154
Figure 5.3
Process diagram for the carbon steel process with with direct
reduced iron and electric arc furnace.
155
5.4
5.4.1
Process assessment
Hazard identification
Similar to the carbon steel process with blast furnace and basic oxygen furnace, exposure to
dust is a primary concern in steel production using direct reduced iron and electric arc furnace.
Exposure to iron oxide (Fe2O3) present as a major constituent in the feed material, and
3
consequently the dust, is controlled by regulations at a level of 5-mg Fe/m .
The other substances of interest are calcium oxide and zinc oxide. Following the guidance in
Table 3.4.2, calcium oxide may be present at levels higher than 20 per cent in electric arc
furnace slag, and zinc has to be assessed as fumes in the galvanising area.
Other metals present at trace levels would be significant only in quantities that exceed their
individual threshold limits. It appears unlikely that the carbon steel process has the potential to
release heavy metals other than those identified above into air at any significant levels.
5.4.2
Toxicological assessment
Iron oxide is not considered to be inert dust (particulates not otherwise classifiable), because
inhalation may lead to effects known as siderosis, iron pneumoconiosis, hematite
pneumoconiosis, and iron pigmentation of the lung. It appears that the pulmonary effects are
somewhat more serious than those caused by inert dust. Systemic effects relating to excessive
haemosiderin deposits have also been documented. It has not been proved that iron oxides
are carcinogenic following chronic pulmonary exposure. The toxicity of iron and its compounds
has been discussed in Section 3.3.4.12.
Calcium in itself is not toxic to humans, but in the form of calcium oxide it acts as an irritant.
The toxicity of calcium oxide has been discussed in Section 3.3.4.7.
The toxicity of zinc has been discussed in Section 3.3.4.33.
5.4.3
Exposure assessment
Exposure to dust containing iron oxide may occur in areas where iron ore is handled, and at
various positions during the process as indicated in the process flow diagram. Sampling and
analytical methods for airborne iron have been listed in Table 3.4.2.6. There is no biological
monitoring method to assess exposure to iron, because iron is an essential element present in
the human body.
Exposure to calcium oxide may occur in dust at various locations during the direct reduction
steps, and most prominently in slag from the electric arc furnace. Sampling and analytical
methods have been listed in Table 3.4.2.6 for calcium. Biological monitoring would not give an
indication of exposure because of the large body burden of calcium.
Exposure to zinc may be possible in the final galvanising steps. The most widely known
systemic effect resulting from acute inhalation of freshly formed zinc oxide fumes is a disease
called metal fume fever. Table 3.4.2.6 has given sampling and analytical methods for zinc
oxide. Zinc is an essential element and is present in abundance in various parts of the human
body. Biological monitoring would therefore not provide useful information for exposure
assessment.
Section 3.4.4 provides an overview of medical evaluation procedures that are relevant for
exposure assessment and interpretation of health effects.
156
5.4.4
Risk quantification
3
In controlling exposure to iron oxide, it is not adequate to control dust levels to 10 mg/m ,
3
3
because the level of iron may be above 5 mg/ m at or slightly lower than 10 mg total dust/m .
Because of its irritation effects, exposure to calcium oxide should be assessed against
maximum concentration peaks rather than average values.
For exposure to zinc oxide, the concentration at which metal fume fever would develop is not
entirely certain, but it has been estimated that symptoms are unlikely to develop at air
3
concentrations below 15 mg/m (Elinder & Piscator, 1979: 682). The ACGIH guidelines of 5
3
3
mg/m for zinc oxide fume and 10 mg/m for zinc oxide dust therefore provide adequate
margins of safety.
5.5
References
Elinder, C-G. & Piscator, M. 1979d. Zinc. (In: Friberg, L, et al. Handbook on the Toxicology
of Metals. Amsterdam: Elsevier/North-Holland Biomedical Press, p. 675 - 685).
Ross, H. U. 1980. Physical chemistry, DRI technology and economics of production and use.
Warrendale USA Iron and Steel Section of the AIME, Society of Mining Engineers, pre-print: 9–
26.
Kepplinger, W. 1995. Impact on the environment of new and emerging alternative iron making
processes. Proceedings of the SAIMM Conference, University of Pretoria.
157
158
6
Typical copper recovery circuit
6.1
Introduction
This section provides a process description and process diagram of a typical copper production
facility. The process description and process diagram contain data on the process streams and
identify the hazardous substances as well as potential exposure points.
6.2
Process description
6.2.1
Crushing and milling
The run of mine ore is subjected to primary gyratory dry crushing with a setting of 175 mm and
stock piled. Some of the ore is subjected to further dry crushing to provide feed for rod and ball
milling. The other portion of the ore may be taken directly to autogenous wet milling.
The ore does not contain free quartz and thus no toxic SiO2 dust is produced. The ore contains
about 0.7 per cent Cu as copper sulphide minerals. Normal dust control measures are
employed.
The ore is wet milled in closed circuit with hydrocyclone classifiers to produce a feed to flotation
at about 55 per cent solids with about 80 per cent passing 300 microns.
Table 6.2.1
Crushing and milling
Stream
Crushed ore/dust
from ore
6.2.2
Component
Magnetite, Fe3O4
TiO2
Calcite, CaCO3
Dolomite, CaCO3,
MgCO3
Diopside (pyroxenes)
CaMg(SiO3)2
Apatite, Ca5F(PO4)3
Phlogopite,
K2Mg2Al2Si3O10(OH)2
Copper sulphides,
CuFeS2, Cu5FeS4
Cu2Fe4S6, Cu2S
Baddeleyite, ZrO2
Uranothoranite,
UO2.2ThO2
Typical concentrations
(as % of dry solids)
25
0.5
15
20
20
10
5
0,7% total
Cu
~ 0.06% ZrO2
<0.01%
Heavy metals
Fe3O4
TiO2
CaCO3
CaCO3, MgCO3
CaMg(SiO3)2
Ca5F(PO4)3
K2Mg2Al2Si3O10(OH)2
CuFeS2, Cu5FeS4,
Cu2Fe4S6, Cu2S
ZrO2
UO2.2ThO2
Exposure
Crushers
Flotation and magnetic separation
Sulfhydryl (xanthate-type) collectors are added as dilute solutions to the slurry, which is passed
through flotation cells. The flotation froth, containing the copper sulphide minerals, is pumped
to the product-thickening and filtration plant. The flotation tailings are treated for separation of
the magnetite and non-magnetic components prior to further processing and disposal.
Some of the magnetite from the flotation tailings is reground, upgraded and sold for coal
washing and the remainder is deposited on dumps from which it can be recovered in future for
steel-making.
The non-magnetic tailings sands are lightly milled and refloated for further copper recovery and
gravity separated for heavy mineral (zirconia and urano-thorianite) recovery. Tailings with an
159
economically recoverable phosphate content are pumped to Foskor. The main bulk of the nonmagnetic tailings are impounded in a granite-based valley with sand wall construction and
excess supernatant water recycled to the concentrator plant.
Table 6.2.2
Flotation and magnetic separation
Stream
Component
Non-magnetic tailings Calcite, CaCO3
Dolomite, CaCO3,
MgCO3
Diopside
(pyroxenes)CaMg(Si
O3)2
Apatite, Ca5F(PO4)3
Phlogopite,
K2Mg2Al2Si3O10(OH)2
Copper sulphides,
CuFeS2, Cu5FeS4
Cu2Fe4S6, Cu2S
Baddeleyite, ZrO2
Uranothoranite,
UO2.2ThO2
Fe3O4
Magnetite from
magnetic
FeTiO3
separator
CaCO3, MgCO3
Flotation reagents
Xanthate
frothers
(organic)
6.2.3
Typical
concentrations
(as % of dry solids)
23
26
29
14,4
7,3
0,3
Heavy metals
Potential exposure
points
CaCO3
CaCO3, MgCO3
CaMg(SiO3)2
Ca5F(PO4)3
CuFeS2, Cu5FeS4
Cu2Fe4S6, Cu2S
ZrO2
UO2.2ThO2
Tailings dam
Fe3O4
FeTiO3
CaCO3, MgCO3
By product storage
Trace
Trace
88
4
8
25 g/t
20 g/t
Liquid/solid separation/drying
Copper concentrate is thickened and filtered on disk filters. Filtrate is recycled and the filter
cake is dried, at low temperature, and delivered to the smelter feed stockpile.
Table 6.2.3
Liquid/solid separation/drying
Stream
Copper concentrate
Typical
concentrations
Heavy metals
(as % of dry solids)
CuFeS2
Total Cu
34
Copper
containing
Cu5FeS4
species:
Cu2Fe4S6,
Chalcopyrite, CuFeS2 40
Cu2S
40
Bornite, Cu5FeS4
10
Cubanite, Cu2Fe4S6
10
ChalcociteCu2S
Component
Mainly CaCO3=
6.2.4
Balance
Exposure
Drier/
Concentrate storage
CaCO3
Smelting and converting
The flotation concentrate containing the copper-iron-sulphide minerals plus some CaCO3-rich
gangue is blended with SiO2 in the form of river sand and smelted in a coal-fired, reverberatory
furnace to produce a copper-iron-sulphide matte and a calcium-iron-silicate slag. Gas from the
reverberatory furnace, containing 0,5 to 1,0 per cent sulphur dioxide, is passed to a 150 m high
stack.
The cooled reverberatory slag is disposed of on a stockpile, which, like the magnetite, drains
any run-off water into the main tailings dam.
160
The molten matte from the reverberatory furnace is treated in a converter where introduction of
oxygen oxidises the iron and sulphur components. The molten converter slag is recycled to the
reverberatory furnace. The converter metal is cast into anodes. The converter off-gas, which
is rich in SO2, is sent to an acid plant where, using a V2O5 catalyst, it is converted to H2SO4.
Table 6.2.4
Smelting and converting
Stream
Gas from
reverberatory furnace
to ESP/stack
Slag from
reverberatory
furnace
Gas from converter( to
acid plant)
Silica
Impurities removed
from converter off gas
(feed to acid plant)
6.2.5
Typical
concentrations
(as % of dry solids)
Component
1% SO2
Fayalite,CaFeSiO3
90
Heavy metals
Exposure
Copper dust
Stack emissions
CaFeSiO3
Slag dump
12 – 18% SO2
SiO2
100
Analysis not available
(recycled)
Acid plant
Refining and rod casting
All of the copper in the form of cast anodes is electrolytically refined. The anodes are placed in
electrolytic cells, with dilute sulphuric acid as the electrolyte and copper starter sheets, onto
which the refined copper is deposited. More recently, certain plants have changed to the use of
permanent stainless steel cathodes.
Approximately 60 per cent of the production of copper is consumed locally as continuous-cast
rod. The remainder is exported as cathode.
During the electrorefining process anode slimes, rich in precious metals, particularly silver and
gold, is deposited in the cells and is sold as a by-product. Nickel sulphate is recovered during
the process of removing impurities from the electrolyte solution and this is also sold as a byproduct.
Table 6.2.5
Refining and rod casting
Stream
Component
Acid mist from
electrolytic cells
Copper product
Cu
NiSO4 product
NiSO4
Anode slimes
Containing Au, Ag
and PGM’s
6.3
Typical
concentrations
(as % of dry solids)
Cu, Ni, As
Heavy metals
Exposure
Cu, Ni, As
Cell house
100
Cu
100
NiSO4
Product storage/
handling area
Nickel sulphate
byproduct
Cell house/
handling area
Ag, Pt, Rh, Se, Te, As
Flow diagram
The flow diagram for the copper recovery circuit is shown in Figure 6.3.
161
6.4
6.4.1
Process assessment
Hazard identification
Iron oxide levels are high in the magnetite from the magnetic separator. Copper
concentrations are high in dust at the drier and concentrate storage areas. The major potential
for exposure is to copper dust and fumes during smelting and converting, and during refining
and rod casting. The presence of nickel in the electrorefining process may result in exposure,
and during refinery bath maintenance employees may be exposed to lead.
6.4.2
Toxicological assessment
Iron oxide is not considered to be inert dust (particulates not otherwise classifiable), because
inhalation may lead to effects known as siderosis, iron pneumoconiosis, hematite
pneumoconiosis, and iron pigmentation of the lung. It appears that the pulmonary effects are
somewhat more serious than those caused by inert dust. Systemic effects relating to excessive
haemosiderin deposits have also been documented. It has not been proved that iron oxides
are carcinogenic following chronic pulmonary exposure. The toxicity of iron and its compounds
has been discussed in Section 3.3.4.12.
Copper is an essential element in humans, but copper dust and fumes are respiratory irritants.
The toxicity of copper and its compounds is discussed in Section 3.3.4.10.
Certain nickel compounds are classified as human carcinogens, but noncarcinogenic
systemic effects have not been documented. Hypersensitivity to nickel is common, as
discussed in the summary of nickel toxicity (Section 3.3.4.17).
Lead is a cumulative toxin. It is well known for neurotoxic effects, but has been associated with
a whole range of other possible symptoms and effects. Section 3.3.4.13 provides an overview
of lead toxicity.
6.4.3
Exposure assessment
The dust released during dry crushing of the ore does not contain heavy metals at a level that
requires exposure protection other than for inert dust. Magnetite from the magnetic separator
contains a high level of iron oxide, but the material is wet and exposure to particulates would
not occur.
Monitoring for copper dust and fumes is needed primarily at the reverberatory furnace and in
the refining and anode casting steps. Methods for sampling and analysis have been listed in
Table 3.4.3.6. Data concerning the relationship between occupational exposure to copper and
internal dose and effect are inadequate to suggest reliable biological monitoring values.
Soluble nickel sulphate, a by-product at the refining step, has been linked to cancer, as
indicated in the toxicological review for nickel (Section 3.3.4.17). Sampling and analysis
methods for airborne nickel compounds have been listed in Table 3.4.3.6. Several studies have
demonstrated that concentrations of nickel and plasma are indicators of recent exposure. An
3
ambient air exposure level of 0.1 mg Ni/m corresponds approximately to a concentration of
nickel in plasma and in urine collected at the end of the workshift of 0.7 µg Ni/100 ml and 70 µg
Ni/l (corrected for a specific gravity of 1.018), respectively (Lauwerys and Hoet, 1993: 82).
162
Figure 6.3
Process diagram for the copper recovery circuit
163
Several sampling and analytical methods have been listed for airborne lead in Table 3.4.3.6.
Lead in blood does not necessarily correlate with the total body burden of lead. It has been
3
estimated, however, that an increase of 1 µg Pb/ m in air is reflected by an increase of 1 to 2
µg Pb/100 ml in whole blood. The relationship does not hold at higher exposure levels, though.
Lead blood levels between 50 and 70 µg Pb/100 ml has been considered acceptable in male
workers. It has to be noted, however, that subclinical neurotoxic effects can already be detected
at levels exceeding 50 µg Pb/100 ml (Lauwerys and Hoet, 1993: 55).
Lead in urine reflects the amount of lead recently absorbed. A concentration of lead in blood of
50 µg /100 ml usually corresponds with a level of 150 µg /g creatinine, but the correlation
across a wider exposure range is poor. The level of 150 µg Pb/g creatinine corresponds with
3
an air concentration of 50 µg Pb/ m (Lauwerys and Hoet, 1993: 55).
Section 3.4.4 provides an overview of medical evaluation procedures that are relevant for
exposure assessment and interpretation of health effects.
6.4.4
Risk quantification
Exposure to copper can be assessed directly against the occupational exposure guideline.
Exposure to nickel and assessment for irritation effects is assessed on the same basis. It is
however recommended that exposure to nickel be quantified in order to estimate cancer risks.
Biological monitoring would assist in the quantification of dose.
Seeing that it is likely that protective equipment will be used during maintenance activities and
potential exposure to lead at the refinery baths, it should be appropriate to conduct biological
monitoring of the employees in that area.
6.5
References
Beale, C.O. 1985. Copper in South Africa - Part I. Journal of the South African Institute of
Mining and Metallurgy, 85 (3): 73 – 80.
Beale, C.O. 1985. Copper in South Africa - Part II. Journal of the South African Institute of
Mining and Metallurgy, 85 (4): 109 – 124.
Crosson C.C. 1984. Evolutionary development of Palabora. Transactions of the Institute of
Mining and Metallurgy, 93: A58 – A69.
Lauwerys, R. R. & Hoet P. 1993. Industrial Chemical Exposure, Guidelines for Biological
Monitoring. Second Edition. Boca Raton: Lewis Publishers, 318p.
164
7
7.1
Typical ferrochrome production process
Introduction
A typical flowsheet of processing chromite ore to produce ferrochrome is described, showing
heavy metal species where they arise in the process.
The model is generic, using a conventional submerged arc furnace smelting a chromite ore
charge of agglomerated ore and lump ore. Variations on the smelting process, i.e. fine ore
smelting in a DC plasma arc furnace, pelletisation and sintering or pre-reduction of the ore in
shaft furnaces, belt sintering furnaces and/or rotary kilns, are processes prior to smelting and
are mentioned where an alteration to the form of the heavy metals may take place.
7.2
Process description
This section provides a process description and process diagram of a typical ferrochrome
production facility. The process description and process diagram contain data on the process
streams and identify the hazardous substances as well as potential exposure points.
7.2.1
Beneficiation
Chromite ore, as mined, occurs as competent hard lump, friable lump and fine sandy minerals.
South African ores contain at best 25 to 40 percent of hard to friable "lump" (10 mm to 200
mm), the balance being an intermediate fraction (6 mm to 10 mm) and a fine fraction (0,124
mm to 6 mm).
Ore received from the mine (open cast or underground) contains gangue (pyroxenite, quartzite
mainly) which is removed first by crushing the ore to the specified top size (typically 100 mm),
and screening the ore, (grizzly bars or screens) into the lump fractions and fine fractions. Ore
from underground is normally damp giving rise to very little dust. Screening and sizing
thereafter is normally under water sprays. Should dust arise, there will be silica, silicates and
chromite (trivalent chromium) in the air-borne dust. Hand sorting of the gangue material from
the ore is frequently carried out, but this practice is giving way to dense media separation in
rotating drum separators using 15 per cent ferrosilicon as the dense medium. The ferro-silicon
is recovered from both the gangue material and the upgraded lump, and thickened to the
correct density.
Intermediate material is upgraded in a dense medium cyclone, also using 15 per cent FeSi.
The fine ore is screened at 1 mm, the -1 mm containing the gangue fraction. Gravity
concentration using spiral concentrators is carried out. The tailings from this process,
containing 20 to 25 per cent Cr2O3 is deposited in slimes dams and is typically -0,125 mm in
size. As no chemical process has occurred, the chromite is still in the trivalent form.
Lump waste is typically stockpiled for use as road making material, where possible.
165
Table 7.2.1
Beneficiation
Stream
Run-of mine ore
(chromite)/
dust
Waste rock
Slimes
Flocculant e.g.
Magnafloc
7.2.2
Component
Al2O3
CaO
Cr2O3
FeO
MgO
MnO
SiO2
Ni
TiO2
ZnO
As
Bi
Similar to ore
except lower Cr
Similar to waste
rock
Long chain
organic
compound
Typical
concentrations
(as % of dry
solids)
13 – 15
1 – 1,5
35 – 45
22 – 25
10 – 12
0,1 – 0,3
9.7 – 9.8
Traces
< 5% of chromite
in input ore
Similar to waste
rock
10 ppm
Heavy metals
CaO
Cr2O
FeO
MnO
NiO
NiS
TiO2
ZnO
As
Bi
Potential exposure points
Crushers
Stockpiles
Similar to ore
Waste rock pile
Similar to waste
rock
Slimes dam
Material Handling
Chromite is delivered to the smelter by road or rail. Lump ore is generally dry (approximately 2
per cent moisture) and gives off dust when off-loaded, transported to stockpiles, recovered for
conveyance to the furnaces and weighed off with the other materials required for smelting. The
dust will contain some free quartz, silicates (mainly iron-silicates) and chromite (trivalent).
Fluxes, quartzite and limestone are received via the same material handling system, as are the
carbonaceous reductants, coal, coke, anthracite and char. Dusts from this source obviously will
be typically quartzite, limestone and reductant. Until this point chromite will not have undergone
any chemical change and is generally regarded as non-toxic in the trivalent state.
Table 7.2.2
Material handling
Stream
Quarzite
Limestone
Component
Al2O3
CaO
FeO
MgO
MnO
SiO2
Al2O3
CaO
FeO
MgO
MnO
SiO2
Typical
concentrations
(as % of dry
solids)
0,4
0.2
0,3
0,5
0,3
97 - 98
0,5
53,0
0,5
1,5
0,2
1,0
Heavy metals
Exposure
CaO
FeO
MnO
Road boxes/rail
tipplers/conveyor transfer points/
weigh hoppers and bins
CaO
FeO
MnO
Road boxes/rail
tipplers/conveyor transfer points/
weigh hoppers and bins
166
Stream
Dolomite
7.2.3
Component
Al2O3
CaO
FeO
MgO
MnO
SiO2
Typical
concentrations
(as % of dry
solids)
0,3
30,0
1,0
20,0
0,5
2,0
Heavy metals
CaO
FeO
MnO
Exposure
Road boxes/rail
tipplers/conveyor transfer points/
weigh hoppers and bins
Smelting
Fine chromite ore may be agglomerated by briquetting, pelletising, or sintering. Common
binders for briquettes are 3,5 - 4 per cent hydrated lime/3 - 4 per cent molasses; 3 - 5 per cent
bentonite/2 per cent molasses.
Pelletising requires that the ore be milled to 80 per cent passing 360 µm to 530 µm, and
pelletised with coke breeze, ~ 2000 µm and two per cent bentonite binder. As milling is dry,
dust containing chromite (trivalent), coke, quartzite and silicates can occur. The pellets can
either be pre-heated and pre-reduced in a rotary kiln or sintered in a steel-belt sintering plant or
shaft kiln. Pre-heating of these pellets using furnace gas is frequently carried out.
Cold charging requires the weighing off of the ore, flux and carbonaceous reductant by weighcones or continuous weigh-belts. Dust from these materials arises and is collected in filters to
be returned to the weigh-feed hoppers.
Chromite is proportioned at 1,85 to 2,3 t/t FeCr, the ore containing typically 44 to 48 per cent
Cr2O3. Hot charging is via insulated cylinders through a hot charging system. Dust can occur
at this point.
The smelting operation can take place in open; semi-closed or closed top AC submerged arc
furnaces ranging from 10 MVA to 60 MVA capacity and DC plasma arc furnaces (closed-top)
ranging from 40 MVA to 63 MVA capacity. Electrical energy is supplied to heat the raw material
to reaction temperature, and the products, slag and FeCr alloy to tapping temperatures of the
order of 1 650 °C to 1 750 °C.
During smelting the reaction gases, CO/CO2 and in the case of open furnaces excess air, carry
3
3
fine ore and dust from the furnace. The dust loading varies form 50 mg/Nm to 150 mg/Nm at
normal operating conditions. Dust contains carbon, chromium and volatile metals such as Zn,
Ge, which occur as trace elements in the raw materials.
Molten alloy and slag are tapped at predetermined intervals. During the tapping period (20 to
35 minutes normally) dust and fumes will come off the tapping launder, from the tap hole and
off the molten alloy/slag. This fume is normally extracted back into the furnace.
Dust from the furnace is collected by wet-scrubbing systems in the case of the closed-top
furnaces, and bag-filters in the case of open to semi-closed top furnaces.
The scrubber sludges and effluents contain some dissolved heavy metals notably hexavalent
6+
chromium, which can occur in concentrations of one to five ppm Cr .
167
Table 7.2.3
Smelting
Stream
Ferrochrome
product
Slag
Furnace dust
Cr
Fe
Si
C
Mn
S
P
As
Bi
Ca
Co
Cu
Pb
Mo
Ni
Sb
Ag
Ta
Te
Ti
W
V
Zn
Zr
Al2O3
CaO
Cr2O3
FeO
MgO
MnO
SiO2
TiO2
C
Typical
concentrations
(as % of dry
solids)
51 – 54
35 – 37
2–5
6 – 7,5
0,02
0,04
0,02
25 ppm
70 ppm
2000 ppm
500 ppm
40 ppm
70 ppm
30 ppm
2000 ppm
40 ppm
<500 ppm
55 ppm
<1 ppm
4000 ppm
200 ppm
3000 ppm
70 ppm
70 ppm
20
2
12 – 14
6–8
12
0,2
30 - 35
0,5
2,0
Al2O3
CaO
Cr2O3
FeO
MgO
MnO
SiO2
TiO2
ZnO
CrO3
As
Bi
C
S
As2O3
Bi2O3
2,0
0,2
2,0
1,2
1,9 – 10
0,3
30 – 35
0,002
10,0
<5 ppm
18 ppm
630 ppm
1,0
2,0
Trace
Trace
Component
168
Heavy metals
Exposure
Fe
Cr
Cr3C2
Cr7C3
Cr3Si
CrSi
Cr5Si3
Cr23C6
CrFe
Furnace area/
crushers
CaO
Cr2O3
FeO
MnO
TiO2
Fe2SiO4
Ca2SiO4
Ca3SiO7
MgCr2O4
Mg2SiO4
CaO
Cr2O3
FeO
MnO
TiO2
ZnO
CrO3 (hexavalent
chrome)
As2O3
Bi2O3
Slag ex furnace
Furnace tapping
platform
Baghouse dust collector
Stream
Component
Waste
scrubber
from Al2O3
CaO
Cr2O3
FeO
MgO
MnO
SiO2
TiO2
Tar
phenols
hexavalent chrome
(CrO3)
S
P
Treated waste
As for “scrubber
from scrubber
waste”
(FeSO4 added to
reduce CrO3
to Cr2O3)
Ferrous sulphate
7.2.4
Typical
concentrations
(as % of dry
solids)
6,0
0,2
2,0
3,0
1,0
0,05
86,0
0,5
< 5 ppm
0,1%
Trace
As for “scrubber
waste”
FeSO4
Heavy metals
CaO
Cr2O3
FeO
MnO
TiO2
Tar
phenols
hexavalent chrome
(CrO3)
Exposure
Scrubber effluent
As “scrubber waste” Effluent dams
except for hexavalent
chrome
FeSO4
Storage/make-up/dosing
Alloy casting and sizing
The molten ore can be water-granulated. Some steam arises in this operation. Alternatively
the alloy is cast into ingots, allowed to solidify and cool, or further cooled by water sprays and
then sized to customer requirements. Ingots are broken by hydraulic hammers and crushers
(jaw) and sized by screening. In these operations FeCr dust arises generally 0,05 mm - 0.1
mm in size.
Table 7.2.4
Alloy casting and sizing
Stream
Component
Ferrochrome
product
As “smelting”
Typical
concentrations
(as % of dry
solids)
As “smelting”
Heavy metals
As “smelting”
Exposure
Ferrochrome crushers
Sizing screens
Final slag
Sludge
7.2.5
Similar to slag
“smelting”
Similar to slag
“furnace”
Similar to slag
“smelting”
Similar to slag
“furnace”
Similar to slag
“smelting”
Similar to slag
“furnace”
Conveyor transfer points
Slag dump
Slimes dam
Metal recovery from slag
Molten slag is granulated and cooled in water or transported molten in cast steel ladles and
tipped on slag dumps. The chrome has been found to be fixed in the slag (i.e. not leachable),
and in the trivalent state. Entrapped FeCr metal prills are recovered through jigging and gravity
spiral concentration. Wet processes are used, but dust arises at the crushers containing Cr2O3,
FeO and silicates.
169
7.3
Flow diagram
The flow diagram for the ferrochrome recovery circuit is shown in Figure 7.3.
7.4
7.4.1
Process assessment
Hazard identification
Dust generated during off-loading, transport to stockpiles, and other activities involving the
chromite ore, does not contain heavy elements in a form that would be bioavailable, and the
dust should be assessed as inert particulates (not otherwise classifiable).
The elemental distribution in furnace slag dust is such that it can be regarded as inert
particulates. Hexavalent chromium is present in scrubber sludges and effluents. Chromium
throughout the other stages of the process is in the trivalent state.
7.4.2
Toxicological assessment
Chromium is an essential element in humans. Hexavalent chromium is a human carcinogen,
as outlined in the toxicity assessment for chromium (see Section 3.3.4.8). Trivalent chromium
is poorly absorbed, but allergic eczematous dermatitis has been observed following industrial
exposures.
7.4.3
Exposure assessment
Hexavalent chromium levels in scrubber sludges and effluents are low, and should not pose a
cancer risk if dust concentrations are managed according to dust exposure guidelines. At the
smelting and alloy casting areas chromium may be present in air associated to particulates,
possibly in the hexavalent state. Exposure can be quantified using sampling and analytical
methods listed in Table 3.4.3.6. Determination of chromium in urine is the preferred method for
assessing exposure to hexavalent chromium. Exposure to an air concentration of 0.05 mg
3
Cr/m would be reflected in a urine concentration of 30 µg Cr/g creatinine at the end of the
exposure period. Exposure to trivalent chromium compounds does not correlate with levels of
chromium in urine (Lauwerys and Hoet, 1993: 42).
Section 3.4.4 provides an overview of medical evaluation procedures that are relevant for
exposure assessment and interpretation of health effects.
7.4.4
Risk quantification
Exposure to total chromium can be assessed directly against the occupational exposure
guideline. For assessment of exposure to hexavalent chromium, biological monitoring and
quantification of cancer risk should be the preferred approach.
170
Figure 7.3
Process diagram for the ferrochrome recovery circuit
171
7.5
References
Elyutin, V.P., Pavlov, Y. A., Levin B. E. & Alekseev E. M. 1957. Production of ferroalloys
nd
electrometallurgy, 2 Ed. Translated from Russian, National Science Foundation, Washington
DC, Israel Program for Scientific Translators, 450.
Lauwerys, R. R. & Hoet P. 1993. Industrial Chemical Exposure, Guidelines for Biological
Monitoring. Second Edition. Boca Raton: Lewis Publishers, 318p.
Woollacott, L. C. & Eric, R. H. 1994. Mineral and metal extraction, an overview. SAIMM
Monograph Series M8, Johannesburg, 412p.
172
8
8.1
Typical ferromanganese production process
Introduction
Manganese ores are smelted in submerged arc furnaces, which can be totally closed–top or
partly closed. The ores smelted are in lumpy form or sintered fine ore. The furnace chosen will
determine the pollution abatement system employed on the furnace and in turn will influence
the effluent composition of the streams from these systems. Sintering generally takes place at
the mines, but will be dealt with in this section as part of the processing.
8.2
Process description
This section provides a process description and process diagram of a typical ferromanganese
production facility. The process description and process diagram contain data on the process
streams and identify the hazardous substances as well as potential exposure points.
8.2.1
Beneficiation
The South African manganese ore used by the major ferromanganese producers are those of
the Jaspilite type found in and near Kuruman. They are composed chiefly of braunite, with
small amounts of hausmanite and hematite. The gangue material consists mainly of calcium
carbonate and magnesium carbonate.
Manganese ores as mined, occur as competent lump and a fine product, which is the result of
both the mining operation and crushing to size. Mining operations can be both open cast and
underground. In a typical open cast operation in-pit crushing in jaw or gyratory cone crushers is
performed. Crushing and sorting is also carried out underground.
Ore from the mining areas is transported via conveyers to be crushed to –150 mm. Further
crushing and screening processes follow to produce a series of sized material to customer
specifications and to enable further beneficiation. In the beneficiation process dense medium
separation of gangue from a typically –19 mm size ore is carried out. The medium used is a
slurry of fine ferrosilicon 15 per cent Si. This medium is fed together with the sized ore to
dense medium cyclones. The gangue separated from the ore is washed clean and deposited
on waste stockpiles. Slimes arising from the screening and washing processes, typically –0,15
mm, are pumped to slimes dams.
The slimes dams and waste rock dumps will contain the carbonates of manganese, some iron
oxides, and calcium and magnesium carbonates
Potential exposure points to dust arising from the ore mining and beneficiation process are in
the open cast pit and underground workings at the crushers, at screens and at conveyer
transfer points. Material deposited on waste stockpiles and in slimes dams may leach, but as
the ore has not been altered in any way, chemically, there should not be a contamination risk.
173
Table 8.2.1
Beneficiation
Stream
Manganese
ore/dust
Component
Al2O3
CaO
Fe2O3
MgO
MnO
MnO2
SiO2
Na2O
K2O
P2O5
BaO
TiO2
CO2
Combined water
SO3
Typical
concentrations
(as % of dry
solids)
0,1-0,4
2-14
6-15
0,3-2,5
24-37
33-40
3-5
0,2-0,3
0.1-0.4
0,05-0,12
0.15-0.7
0,02-0,025
1-14
Waste rock
Similar to ore
1-3
0,03-0,06
Similar to ore
Slimes
Similar to waste
rock
Similar to waste
rock
8.2.2
Heavy metals
Exposure
CaCO3
MnCO3
Fe2O3
MnO
MnO2
BaO
BaCO3
TiO2
Crushers
Screens
Conveyor transfer points
Similar to ore
Waste rock dump
Similar to waste
rock
Slimes dam
Sintering
Sintering is required to agglomerate the –6 mm ore and dusts collected throughout the
beneficiation process and to upgrade the manganese content of the ore. The ore is – 6 mm in
size. Coke is milled in a rod mill and screened to pass through three-mm mesh. Ore and coke
are proportioned and conveyed to a nodulising drum and agglomerated using water. This
mixture is sintered on a moving grate sintering machine. The sinter product is crushed in a
tooth roll crusher and screened, and the undersize (- 6 mm) is returned to the sintering process.
On-size material is stockpiled for shipment to the users. Dedusting of the waste gas from the
sintering windboxes is through electrostatic precipitators, the dust collected and returned to the
sintering process. The air from the sinter cooling section is cleaned by cycloning, the dust
returned to the sintering process. Screens and belts are usually covered and sealed and dust
collected from these areas returned to the sintering process.
Table 8.2.2
Sintering
Stream
Sinter dust
8.2.3
Component
Similar to ore
Plus carbon
Typical
concentrations
(as % of dry
solids)
Similar to ore
Heavy metals
Similar to ore
Exposure
Sinter machine
Electrostatic precipitators
Crushers
Material handling
Manganese ore and sinter are delivered to the smelter by rail and road. Ores are usually
blended as they are stockpiled in blending and reclaiming systems. Here dust arises which is
of a similar nature to those found at the mines. Fluxes, quartzite and dolomite are received via
a separate handling system, together with coke and coal, transported to stockpiles or storage
silos and recovered for conveyance to the furnace storage bins. Dusts arising from these areas
174
arise from transfer points and would be mixtures of the ore, sinter, fluxes and carbonaceous
reducing agents.
Table 8.2.3
Material handling
Stream
Quartzite
Limestone
Dolomite
8.2.4
Component
Al2O3
CaO
Fe2O3
MgO
MnO
SiO2
Al2O3
CaO
MgO
MnO
SiO2
Al2O3
CaO
Fe2O3
MgO
SiO2
Typical
concentrations
(as % of dry
solids)
0,4
0,2
0,5
0,5
0,3
97-98
0,5
53,0
1,2-1,5
0,2
1,0-1,5
0.3
30
1.5-2.0
20
0.5
2
Heavy metals
Exposure
CaO
Fe2O3
MnO
Conveyor transfer points
Weigh hoppers
Furnace bins
CaCO3
Fe2O3
MnO
Conveyor transfer points
Weigh hoppers
Furnace bins
CaO
Fe2O3
MnO
CaCO3
FeCO3
Conveyor transfer points
Weigh hoppers
Furnace bins
Smelting
The feed materials are batch or continuously weighed and blended and fed to bunkers above
the furnaces. The mix is gravity fed to the furnaces through multiple feed ports in the furnace
roof.
Manganese ores are proportioned at 2.0 to 2.2 tons/ ton ferromanganese.
Smelting takes place in open, semi-closed and closed top furnaces ranging in capacity from 10
to 80 MVA. Electricity is supplied to heat the burden to the reaction temperature, and the
o
o
ferromanganese and slag tapped at temperatures of 1 650 C to 1 750 C. During tapping the
reaction gases, CO and CO2 and volatilised manganese, carry fine ore and other dusts from the
furnace. These dusts are removed by water scrubbing systems, bag house filters or electroprecipitators.
3
Discharge gas could contain 50 to 100 mg/ Nm of dust at normal operating conditions. Dusts
contain carbon, manganese, Zn, Ge, Fe, Ni, Co, and K.
Dust from the furnaces is collected in bag house filters in the case of open-top furnaces and
scrubber systems in the case of closed-top furnaces.
The scrubber effluents and sludges contain dissolved heavy metals, coal tars, phenols and
thiocyanates.
175
Table 8.2.4
Smelting
Stream
Ferromanganese
product
Component
Mn
Fe
Si
C
S
P
As
Bi
Co
Cu
Ni
Zn
Typical
concentrations
(as % of dry
solids)
Al2O3
CaO
FeO
MgO
SiO2
MnO
K2O
Na2O
4,5-5,5
35 - 38
0,1 - 0,3
8 - 10
31 - 33
18 - 22
Furnace dust
Al2O3
CaO
FeO
MgO
SiO2
MnO
K2O
Na2O
C
Al2O3
CaO
FeO
MgO
SiO2
MnO
K2O
Na2O
Long chain
organic
compound
5–6
6–7
11– 12
10 – 12
15 – 17
38 – 40
1,3 – 1,6
0,3 – 0,7
5 – 10
6–7
6–7
8–9
10 – 12
12 – 14
28 – 32
0,5 - ,5
0,2 - 0,4
10 ppm
Scrubber
effluent/slimes dam
Flocculant e.g.
Magnafloc
8.2.5
Exposure
Metallics:
Furnace/
Mn, Si, Co, Fe, Cu, product area
Ni, Zn.
14 - 16
0,5
6,5-7,5
0,05
0,1
Trace
Trace
Trace
Trace
Trace
Trace
Furnace slag
Heavy metals
Intermetallics:
Mn3C, Mn3Si,
MnC3, MnP3,
MnS, MnAs,
MnSi, Fe2As,
Fe3P, Fe3C,
Fe3Si, FeAsS,
FeS, FeSi,
FeSi2
CaO
Fe2O3
Fe2SiO4
FeAl2O4
FeO
FeS
MnS
FeSiO3
MnO
CaO
FeO
MnO
Mn3O4
MnO2
MnS
MnSiO3
C
CaO
FeO
MnO
Mn3O4
MnO2
MnS
MnSiO3
C
Furnace area
Bag house/
electro static precipitator
Scrubber discharge
Slimes dam
Alloy casting, crushing and sizing
The molten alloy can be cast into ingots via a casting machine or into moulds fashioned from
fine ferromanganese alloy. The solidified alloy is sized by crushing and screening to
specifications. In this operation ferromanganese dust will arise. The dust particles are of the
order of 0.05 – 0.1 mm in size.
176
Table 8.2.5
Alloy casting, crushing and sizing
Stream
Ferromanganese
dust
8.2.6
Component
As ferro-manganese
product – see
Section 8.2.4
Typical
concentrations
(as % of dry
solids)
As ferromanganese
product – see
Section 8.2.4
Heavy metals
Exposure
As ferro-manganese Crushers
Screens
product – see
Transfer points
Section 8.2.4
Metal recovery from slag
Molten slag is separated from the alloy during the tapping operation and tapped into cast steel
ladles. The slag is transported to a slag dump where it is tipped and solidifies. Entrapped alloy
is recovered through a crushing jigging and gravity separation operation. Wet processes are
used, but crushing does give rise to dust of the composition of the slag.
Table 8.2.6
Metal recovery from slag
Stream
Component
Ferromanganese
product
As ferro-manganese
product – see
Section 8.2.4
Final slag/slimes to
waste dump
Similar to slag from
furnace – see
Section 8.2.4
Long chain organic
compound
Flocculant
8.3
Typical
concentrations
(as % of dry
solids)
As ferromanganese
product – see
Section 8.2.4
Similar to slag
from furnace –
see Section 8.2.4
Heavy metals
Exposure
As ferro-manganese Product storage
product – see
Section 8.2.4
Similar to slag from
furnace – see
Section 8.2.4
Waste dump
Flow diagram
The flow diagram for the ferromanganese production process is shown in Figure 8.3.
8.4
8.4.1
Process assessment
Hazard identification
Manganese is the primary element of concern in the ferromanganese production process.
Particulates containing more than 0.5 per cent of manganese should not be considered to be
inert, and management according to guidelines for particulates would not be adequate.
8.4.2
Toxicological assessment
Manganese compounds in various forms are considered to be neurotoxic, with subclinical
effects occurring at low exposure levels. Section 3.3.4.14 presents an overview of the toxicity
of manganese.
177
Figure 8.3
Process diagram for the ferromanganese production process
178
8.4.3
Exposure assessment
Dust from manganese ore contains high levels of manganese, but it is unlikely that the
manganese would be in a form that is bioavailable. Various manganese oxides have however
been shown to be neurotoxic, and in the assessment of exposure all forms of manganese are
normally considered. Exposure may occur in the furnace/product area as a result of high
manganese levels in furnace slag and dust. Manganese levels are also high in scrubber
effluents. Sampling and analytical methods to quantify airborne manganese have been listed in
Table 3.4.3.6.
The normal concentration of manganese in urine is usually less than 3 µg/l, and in whole blood
and plasma less than 1 µg/100 ml and 0.1 µg/100 ml, respectively. There is however no
consistent relationship between manganese exposure and blood levels, and it appears that
measurement of urinary levels is the preferred method for assessment. The relationship with
exposure is however not that well-defined and no biological threshold limit value has been
proposed (Lauwerys and Hoet, 1993: 71).
Section 3.4.4 provides an overview of medical evaluation procedures that are relevant for
exposure assessment and interpretation of health effects.
8.4.4
Risk quantification
The potential for development of neurotoxic effects is assessed through determination of a
hazard quotient on the basis of the guideline concentration for manganese in air.
8.5
References
Elyutin, V.P., Pavlov, Y. A., Levin B. E. & Alekseev E. M. 1957. Production of ferroalloys
nd
electrometallurgy, 2 Ed. Translated from Russian, National Science Foundation, Washington
DC, Israel Program for Scientific Translators. 450p.
Lauwerys, R. R. & Hoet P. 1993. Industrial Chemical Exposure, Guidelines for Biological
Monitoring. Second Edition. Boca Raton: Lewis Publishers, 318p.
Potgieter, F. J. 1980. Operation of an 81 MVA high carbon ferromanganese furnace at
Samancor, Meyerton Works. Proceedings of the International Ferro-alloys Conference,
Lausanne Switzerland: IPFED, p. 244 – 252.
179
180
9
Bacterial oxidation circuit for the pre-oxidation of
refractory gold ores
9.1
Introduction
This section provides a process description and process diagram of a typical bacterial oxidation
circuit for the pre-oxidation of refractory gold ores. The process description and flow diagram
contain data on the process streams and identify the toxic substances as well as the potential
exposure points.
9.2
Process description
9.2.1
Crushing, Screening and Milling
Physical size reduction of run-of mine ore is usually carried out in several stages of jaw and/or
cone crushing. The ore is crushed to a P100 (100 per cent passing) size of 20 to 50 mm (P80 of
ten to 30mm). Crusher product is then wet-milled in rod or ball mills to a P100 of 212 to 300 µm
(P80 of 75 to 106 µm), and transferred to the bacterial oxidation section. Flotation and bacterial
oxidation may also be done in the reverse order.
Table 9.2.1
Crushing, screening, wet milling
Stream
Component
Crushed ROM
(run-of mine)
ore/
dust
Silicates, SiO2
Carbonates, CaCO3 etc.
Oxides
Sulphides
Milled ore
slurry
Solids – same as ROM ore
9.2.2
Typical
concentrations
(as % of dry
solids)
80
1 – 10
5
max 2 %
Solids – same
as ROM ore
Heavy metals
Pyrite, FeS2
Arsenopyrite,
FeAsS
CaCO3
Metal sulphides
Solids – same as
ROM ore
Exposure
Crushers
Mill
Gravity concentration
Free, coarse gold is removed from the milled ore using Knelson concentrators, jigs, or shaking
tables.
9.2.3
Flotation
The gold-containing sulphide minerals in the milled ore are separated from the gangue material
by a froth flotation process. Thickener underflow is pumped to the bacterial oxidation section.
Overflow water is recycled. The flotation concentrate is then re-ground to a P100 of 106 to 150
µm (P80 of 45 to 75 µm).
181
Table 9.2.3
Flotation
Stream
Flotation tails
Flotation
concentrate
Flotation
reagents
Flocculant
9.2.4
Component
Silicates
Carbonates
Oxides
Minor sulphides
Pyrite
Arsenopyrite
Base metal sulphides
Silicates
Carbonates
Oxides
Not known – site specific
Typical
concentrations
(as % of dry
solids)
Variable – site
specific
0.04
20 – 40
2 – 25
0 – 10
20 – 50
2 – 15
2 – 15
Not known - site specific
Heavy metals
CaCO3
Trace metal
sulphides as in
conc.
CuFeS2
NiS
ZnS
FeS2
FeAsS
CaCO3
Not known
Not known
Exposure
Concentrator/
tailings dam
Concentrator
Flotation reagent
make-up
Flocculant make-up
Bacterial oxidation and gold recovery
In the bacterial oxidation section a portion of the sulphide minerals (pyrite and arsenopyrite) in
the thickener underflow is oxidised due to the presence of bacteria which are introduced as an
initial inoculum, to form sulphates, thus freeing gold entrapped in the sulphide minerals. This is
o
carried out in mechanically agitated, aerated, open-top tanks at a temperature of 35 to 45 C
and at a pH of 1,0 to 1,6. Minor quantities of nutrients are fed to the reactors in order to feed
the bacteria.
In the bacterial oxidation process, the pyrite and arsenopyrite are solubilised, and large
quantities of iron, arsenic, sulphate, and sulphuric acid appear in solution. Smaller amounts of
metals such as cobalt, nickel, copper, and zinc will also be solubilised if they are present in the
feed concentrate. Table 9.2.4 shows typical concentrations that the dissolved metals will reach
in the bacterial oxidation process, as well as the typical quantities of these metals that will
remain in the solid residue.
As mentioned, the bacterial oxidation process is carried out in large, mechanically agitated,
aerated, open-top tanks. Exposure to the dissolved metals could occur if there is an aerosol
effect at the top of the tank owing to the aeration. Exposure to both dissolved species and the
solids could occur if there is foam on the top of the tank, and the foam is lifted and transported
by the wind action.
In some applications, pH levels in the bacterial oxidation process will be controlled by the
addition of lime. If this is the case, partial precipitation of iron, arsenic, and sulphate will occur
in the bacterial oxidation process. Some gypsum will also be precipitated. These precipitates
will then report to the solids residue, and will pass through the gold recovery process before
reporting to the tailings.
The residue from bacterial oxidation is fed to three or four thickeners where it is washed by a
counter-current flow of water. Thickened slurry, at about 20 to 35 per cent solids, and
containing the freed gold, is transferred to a conventional cyanide-leach/carbon-in-pulp gold
recovery plant, described as a separate process package (see Section 10). The final waste
from the gold recovery plant is transferred to a slimes dam. Thickener overflow is pumped to
the neutralisation section.
182
Table 9.2.4
Bacterial oxidation and gold recovery
Stream
Component
3+
Solution in
slurry after
bacterial
oxidation
Solids in slurry
after bacterial
oxidation
Fe
2+
Fe
5+
As
3+
As
H2SO4
Co
Ni
Cu
Zn
Mg
Ca
+ other metal species in
minor to trace amounts
Pyrite
Arsenopyrite
Base metal sulphides
Silicates
Oxides +
Iron-arsenic-sulphate
precipitates +
Gypsum (CaSO4).2H2O)
Typical
concentrations
(as % of dry solids)
10 - 50 g/l
< 0.5 g/l
3 - 25 g/l
< 20 mg/l
2 - 20 g/l
< 1 g/l
< 1 g/l
1 – 5 g/l
< 1 g/l
< 1 g/l
1 –2 g/l
Heavy metals
Fe2(SO4)3
FeSO4
H3AsO3
CoSO4
NiSO4
CuSO4
ZnSO4
CaSO4
H2SO4
FeS2
FeAsS
Fe(OH)3
FeAsO4
Ca3(AsO4)2
0.04 – 2
0–1
0.04 – 2
20 – 50
50 – 80
Exposure
Bacterial oxidation
tanks; aerosol and
foam from the open
tanks
Slimes dam
FeAsO4.0,8Fe(OH)3.
0,2Fe(OH)SO4
FeAsO4.Fe(OH)3
Approx 20
FeAsO4.2Fe(OH)3.
Fe(OH)SO4
Lime
Nutrients
Flocculant
9.2.5
Al2O3
CaO
MgO
MnO
SiO2
Di-ammonium phosphate
Potassium sulphate
Magnesium sulphate
Not known - site specific
FeAsO4.3Fe(OH)3
CaSO4.2H2O
H3O.Fe3(SO4)2(OH)6
K3Fe3(SO4)2(OH)6
(NH4)3Fe3(SO4)2(OH)6
NiS
CuFeS2
ZnS
CaCO3
Fe2O3
MnO
0,5
53,0
1,2-1,5
0,2
1,0-1,5
Not known
Lime
make-up/transfer
Flocculant make-up
Bioliquor neutralisation/thickening and disposal
The acid in the bioliquor is neutralised, and iron and arsenic are precipitated, by the addition of
limestone and possibly lime. This is carried out in a series of four mechanically agitated,
aerated, open-top tanks. The slurry from the tanks is transferred to a thickener. Thickener
underflow is pumped to a tailings dam and clear liquor overflow is recycled.
183
Table 9.2.5
Bioliquor neutralisation/thickening and disposal
Typical
concentrations
Stream
Heavy metals
Component
Exposure
(as % of dry
solids)
Thickener
underflow/
tailings dam solids
Lime
Flocculant
9.3
Iron-arsenicsulphate
precipitates.
Gypsum
Fe
As
2SO4
Ca
CaO
MgO
Al2O3
FeO
MnO
SiO2
Fe2O3
Not known - site
specific
10 – 20
1 – 10
30 – 40
10 – 20
91,3
1,7
0,3
0,3
0,1
0,8
Iron-arsenicTailings dam
Sulphur precipitates
And gypsum
(CaSO4.2H2O)
Ferric arsenate
CaO
MnO
FeO
Fe2O3
Lime make-up/transfer
Not known
Flocculant make-up
Flow diagram
The flow diagram for the bacterial oxidation circuit for the pre-oxidation of refractory gold ores is
shown in Figure 9.3.
9.4
9.4.1
Process assessment
Hazard identification
Exposure to inert dust and arsenic in certain areas presents the primary focus for health risk
management. Normally, material pumped to the slimes dam does not contain any hazardous
substances that would be leachable, and by implication, bioavailable. The toxicity characteristic
leaching procedure (TCLP) may be used to confirm these properties. Arsenic is the substance
of primary concern in the process.
9.4.2
Toxicological assessment
Dust at the positions of potential exposure is considered inert, and should be assessed
according to guidelines for management of particulates.
Arsenic is a confirmed human carcinogen, and is known to cause contact dermatitis. See
Section 3.3.4.2 for a description of arsenic toxicity.
9.4.3
Exposure assessment
The primary areas of potential exposure are at the bacterial oxidation tanks, where arsenic is
present in the foam and mist. The arsenic is present in the process in forms that are highly
bioavailable.
Area monitoring and personal sampling may be conducted using NIOSH Method 7901, as listed
in Table 3.4.3.6. NIOSH Method 7900 is valid only for particulate-associated inorganic arsenic
compounds.
184
Figure 9.3
Process diagram for the bacterial oxidation circuit for the preoxidation of refractory gold ores
185
Mean serum and blood levels of arsenic vary greatly depending on the level of seafood content
in the diet. Therefore, when employees have not been instructed to refrain from eating fish or
shellfish for two to three days before biological monitoring, high levels of arsenic may be found
that might not be associated with occupational exposure. In the past, biological monitoring for
assessment of occupational exposure was conducted by measuring the total amount of arsenic
in urine at the end of a shift. It is however now well established that inorganic arsenic,
monomethylarsonic acid, and cacodylic acid in urine is the method of choice. Monitoring of
employees exposed to inorganic arsenic using this method is not influenced by
organoarsenicals from marine origin.
Some controversial results may be obtained in the correlation between air-concentration
exposure assessment and biological monitoring. It has been established that background
levels of the sum of the three metabolites of arsenic (inorganic arsenic, monomethylarsonic
acid, and cacodylic acid) in urine vary between 10 µg/l and 50 µg/l. It appears that the best
3
relationship for occupational exposure at air concentrations between 50 and 200 µg As/m
would lead to post-shift concentrations of the total metabolites between 54 and 88 µg/g
creatinine (Lauwerys and Hoet, 1993: 25).
Section 3.4.4 provides an overview of medical evaluation procedures that are relevant for
exposure assessment and interpretation of health effects.
9.4.4
Risk quantification
Occupational exposure levels have to be assessed through interpretation of area and personal
monitoring data, in conjunction with biological monitoring and exposure effects monitoring.
Cancer risks can be quantified through interpretation of exposure data and arsenic doseresponse information.
9.5
References
Claassen, R., et al. 1991. The effect of mineralogy on the bacterial oxidation of refractory goldbearing sulphides from a Barberton deposit. Also 10 other papers. Colloquium, Bacterial
Oxidation. Randburg, Megawatt Park, 18 June. Johannesburg: The South African Institute of
Mining and Metallurgy.
Lauwerys, R. R. & Hoet, P. 1993. Industrial Chemical Exposure, Guidelines for Biological
Monitoring: Second Edition. Boca Raton: Lewis Publishers, 318p.
Nicholson, H. & Oti-atakorah, S.& Lunt, D.J. & Ritchie, I.C. 1993. Selection of a refractory
gold treatment process for the Sansu project. Biomine’93. Glenside, Australia: Australian
Mineral Foundation, p. 20.1 – 20.11
Nicholson, H.M., Lunt, D.J., Ritchie, I.C. & Marais, H.J. 1994 The design of the Sansu
concentrator and BIOX facility. XVth CMMI Congress. Johannesburg: South African Institute
of Mining and Metallurgy, Vol. 2, p. 393 – 402.
Van Aswegen, P.C. 1993. Biooxidation of refractory gold ores – the Genmin experience.
Biomine’93. Glenside, Australia: Australian Mineral Foundation, p. 15.1 – 15.14.
186
10 Carbon-in-pulp circuit for gold recovery
10.1 Introduction
This section provides a process description and process diagram of a typical carbon-in-pulp
circuit for gold recovery. The process description and flow diagram contain data on the process
streams and identify the toxic substances as well as the potential exposure points.
10.2 Process description
10.2.1 Crushing
Run of mine ore from the shaft head is fed by a conveyor system to the primary crushing
station. Tramp waste material is removed either by hand or in the case of metallic constituents,
by means of electro-magnets. The crushed product is delivered to a vibrating grizzly screen.
The oversize material from this primary screening unit is sent to a jaw-crusher. The grizzly
undersize fraction (-150mm) together with the crushed product is conveyed to a stockpile.
From this storage area, the material is transported to mill surge bins.
The analysis of the ore provided in Table 10.2.1 is the best obtainable at this stage. It appears
that operating companies do not analyse for heavy metals and such an analysis was not in the
possession of the plant manager. It is likely that the original geological survey of the deposit
would have to be retrieved in order to obtain more specific data. As the main constituent
removed from the ore by the process is gold, the slimes dam/waste dump should have a similar
heavy metal analysis to that of the ore.
Table 10.2.1
Crushing
Stream
ROM ore
Component
Quartz, SiO2
Typical
concentrations
> 90%
5 – 20%
Pyrite, FeS2
+ Arsenopyrite,
FeAsS + traces of
Pyrophylite, mica,
calcite, dolomite
including majority of
heavy metals in trace
quantities as sulphides,
oxides and sulphates
Heavy metals
FeS2
FeAsS
CaCO3
Exposure
Ore storage/
handling/
crushing
Majority of heavy
metals in trace
quantities as sulphides,
oxides and sulphates
10.2.2 Milling
The crusher product is delivered to the milling circuit and introduced into the mill via a hopper
feeder system, which may be either static or mobile. A variety of different comminution process
options are applied. In instances in which the ore itself is sufficiently competent to act as the
grinding media, autogenous milling may be applied. In other instances, grinding media, in the
form of steel ball (50 to 100mm) are added to the mill together with the ore. Process water and
lime (CaO), either as a dry powder or as a slurry, is added at the inlet feed trunnion (i.e. point of
ore entry) of the mill. The mills are generally operated in closed circuit with hydro-cyclone
classifiers that serve to separate the ground ore particles according to size and solids density.
The coarser or heavier fraction is recycled back into the mill for further size reduction while the
finer overflow fraction is delivered to a tramp removal section utilising linear belt screens to
187
remove grit and wood-chips. This screening step is of critical importance to the efficiency of the
subsequent carbon-in-pulp (CIP) process.
Table 10.2.3
Milling
Stream
Lime, CaO
Component
Typical
concentrations in g/t
91,3
1,7
0,3
0,3
0,1
0,8
CaO
Lime storage/handling
MnO
FeO
Fe2O3
+ traces Zn, Co,
Pb, Ag, Ni
As ore + lime
As ore + lime
CaO
MgO
Al2O3
FeO
MnO
SiO2
Fe2O3
+ traces Zn,
Co, Pb, Ag, Ni 500 - 10000 g/t ore
Lime conc.
Limed ore slurry As ore + lime
Heavy metals
Exposure
Mill house
10.2.3 Thickening
The pre-screened slurry (typically ~30 per cent solids) is pumped to a thickener. Lime (CaO) is
added, either as a dry powder or slurry for final pH adjustment together with flocculant to assist
the settling of the solids. The thickened slurry (thickener underflow stream) is pumped to the
leaching circuit while the thickener overflow water reports to the milling circuit. Make-up water
used in the circuit is supplied from mine water, slimes dam return solution and Rand Water
Board (potable).
Table 10.2.3
Thickening
Flocculant
(Magnafloc 351)
Lime, CaO
Not known
Typical
concentrations
3 – 10 g/t ore
As above
As above
Slurry
As milled slurry + As milled slurry + As milled slurry +
flocculant.
flocculant,
flocculant.
Stream
Component
Heavy metals
Not known
As above
Exposure
Flocculant
up/handling
Lime storage/
handling
Thickener
make-
10.2.4 Leaching
The thickened slurry is pumped to a series of air-agitated leach tanks. Cyanide (NaCN or
Ca(CN)2), either in solid or liquid form, is fed to the leach tanks. The leached slurry is pumped
to the carbon-in-pulp (CIP) adsorption circuit.
Table 10.2.4
Leaching
Stream
Reagents
Component
NaCN/
Ca(CN)2
Typical concentrations
200 – 1000 g/t
200 – 1000 g/t
188
Heavy metals
Ca(CN)2
Exposure
Reagent makeup/handling
Stream
Leach slurry
Component
Elements in
solution:
Au
Ag
Si
Ca
Ni
Fe
Cu
Al
Mg
Zn
Co
Pb
Cyanide
Complexes in
solution:
2-
Zn(CN) 6
3Cu(CN) 4
2Ni(CN) 4
Au(CN) 2
3Fe(CN) 6
2Co(CN) 6
CN
SCN
CNO
Typical concentrations
mg/l
10
1.6
8.5
257
5.5
<1
12
<0.5
<0.5
5
<0,5
<0,5
Heavy metals
Complexed cyanide
solutions and vapours
Exposure
Leach tanks
Elements in solution:
Ag
Ca
Ni
Fe
Cu
Zn
Co
Pb
Cyanide complexes in
solution:
2-
mg/l
Zn(CN) 6
3Cu(CN) 4
2Ni(CN) 4
3Fe(CN) 6
2Co(CN) 6
<0,1
600
2,5 – 15
<0,1
2 – 60
<0,1 – 3
200 – 400
700 – 1000
<0,1 – 3,5
10.2.5 Adsorption
The leached slurry gravitates through a number of CIP stages with a typical pulp residence time
of about one-hour per stage. Reactivated carbon, at a particle size of between 1 and 3 mm, is
added to the final stage of the CIP train and flows upstream, counter current to the pulp flow.
As the carbon inventory makes its way up the cascade train, the solubilised gold adsorbs onto
the carbon. Batches of loaded carbon are periodically removed from the upper-most stage
(stage 1) of the circuit. Carbon is prevented from flowing back downstream by inter-stage
screens, which allow free passage to the slurry, but retain the carbon. The pulp containing the
loaded carbon transferred from the head CIP contactor is delivered to a linear screen where the
carbon is separated from the pulp. The pulp gravitates back to the adsorption circuit. The
residue pulp exiting the final stage of the adsorption train is passed over linear screens to
recover any carbon particles that may have escaped the circuit. This carbon product is
returned back to the adsorption circuit. The undersize from this screen is pumped either to the
backfill preparation plant or to the slimes dam.
189
Table 10.2.5
Adsorption
Stream
Component
Loaded activated
carbon
Au
Ag
Si
Ca
Ni
Fe
Cu
Al
Mg
Zn
Co
Pb
Tailings slurry to Elements in
residue dam
solution:
Au
Ag
Si
Ca
Ni
Fe
Cu
Al
Mg
Zn
Co
Pb
Typical
concentrations
2-
Exposure
Adsorption tanks
Complexed cyanide
solutions or vapours of
Ag
Ca
Ni
Fe
Cu
Zn
Co
Pb
Hg
g/t
11 927
1 201
1 726
7 663
2 002
522
185
640
200
mg/l
Complexed cyanide
solutions and vapours
0,01
0,02
9
2,7
<1,0
11
<0,5
<0,5
4,5
<0,5
<0,5
<0,5
Residue dam
Elements in solution –
Ag
Ca
Pb
As cyanides
Cyanide
Complexes in solution.
Identified species:
2Zn(CN) 6
3Cu(CN) 4
2Ni(CN) 4
Au(CN) 2
3Fe(CN) 6
2Co(CN) 6
But also other
complexes of these
metals
Cyanide
Complexes in
solution:
Zn(CN) 6
3Cu(CN) 4
2Ni(CN) 4
Au(CN) 2
3Fe(CN) 6
2Co(CN) 6
CN
SCN
CNO
Heavy metals
No
analysis
available
10.2.6 Stripping and carbon regeneration
The loaded carbon is transferred to the elution circuit. The adsorbent is stored in holding tanks
prior to batch-wise elution. Prior to stripping, the batch of carbon is elutriated with water to
remove fine slime and wood chips. The carbon is acid washed with dilute hydrochloric acid
o
(HCl) at ambient or elevated temperature (~70 C) to remove calcium carbonate and other
base metal impurities, after which it is water washed to remove excess acid. Stripping of the
o
gold from the carbon is effected using a strong caustic soda (NaOH) solution at 120 C.
The stripped carbon is pumped to holding tanks from where it is sent via a screw-feeder into a
o
rotary kiln operating at 700 C. Within this unit, the carbon is reactivated to its original active
state by heat treatment in a non-oxidising atmosphere. The carbon leaving the kiln is quenched
in water and returned to the adsorption circuit via a fine screen to remove any fine carbon
produced. New carbon is added to the quench tank as and when required to supplement lost
190
adsorbent. The water used for quenching is filtered to remove the carbon fines and is treated
for gold recovery.
Table 10.2.6
Stripping and carbon regeneration
Stream
Typical
concentrations
10 %
Component
HCl solution
HCl
Cyanide solution
NaCN
NaOH
Gases: HCN,
H2, NH3,
Heavy metals
Exposure
1%
0,5%
Au
Ag
Si
Ca
Ni
Fe
Cu
Mg
Zn
Eluate handling
Ag
Ca
Ni
Fe
Cu
Zn
as cyanides
mg/l
347
42
52
3
59
6
5
<1
<1
Eluate
NaCN
solution,
NaCN
vapours,
NaOH
solution,
NaOH vapours
Activated carbon
Steam
activated
carbon
Au
Ag
Si
Ca
Ni
Fe
Cu
Al
Mg
Zn, Co, Pb
and CO, CO2
Decomposition
products
g/t
63
110
1020
463
40
304
74
318
130
Activated carbon handling
CaCO3
Ag, Ni, Fe, Cu,
Zn, Co, Pb,
typically as
cyanide complexes
Carbon regeneration
10.2.7 Electrowinning
The gold bearing eluate is circulated through the electrowinning cells following pH adjustment.
The gold plates out onto steel wool cathodes, which are digested in H2SO4 to dissolve the steel.
Table 10.2.7
Electrowinning
Stream
Spent electrolyte
Gold sludge
Component
NaCN solution,
NaCN vapours,
NaOH solution,
NaOH vapours,
Gases: HCN,
H2, NH3, CO2
Au
Ag
Fe, Cu, Ni
Typical
concentrations
2% (50% dry
basis)
Heavy metals
Exposure
Traces of Ag, Ni,
Fe, Cu, Zn, Co,
Pb, as cyanides
Electrowinning cells
Traces of Ag, Ni,
Fe, Cu, Zn, Co,
Pb, Hg, in
metallic form
Cells
2% (50% dry
basis)
70%
3%
low %
191
10.2.8 Smelting
The gold-rich sludge is filtered, dried, fluxed and smelted to bullion in an induction furnace.
Table 10.2.8
Smelting
Stream
Smelting flux
Gold bullion
Slag
Typical
concentrations
Component
Na2CO3
Borax
SiO2
Au
Ag, Ni, Fe, Cu,
Zn, Co, Pb
Au, Ag
Heavy metals
85%
Ag, Ni, Fe, Cu,
Zn, Co, Pb in
Metallic form
Ag
Exposure
Smelter/
storage
Slag disposal
10.2.9 Residue disposal
The residue from the adsorption circuit is pumped to a storage tank. If designated for back-fill,
the fine fraction of solids is removed using high-pressure cyclones. The cyclone overflow
fraction is thickened in Double-V thickeners and pumped to a slimes dam. The cyclone
underflow fraction is pumped to a shaft storage pachuca. The residual cyanide is destroyed
using ferrous sulphate or Ca(OCl)2 prior to backfilling underground. Portion of the residue
slurry, when deemed necessary is pumped directly to the slimes dam. The slimes dam water is
recycled back to the process circuit for reuse.
Table 10.3.9
Residue disposal
Stream
Component
Typical
concentrations
Heavy metals
Ca(OCl)2
Ca(OCl)2
Ca(OCl)2
Flocculant
(Magnafloc 351)
Not known
Not known
Residue slurry
SiO2
Traces of heavy
metals as
contained in ore
Bulk
FeS2
FeAsS
CaCO3
Exposure
Reagent storage/
handling
Flocculant make-up/handling
Residue dam
Majority of heavy
metals in trace
quantities as
sulphides, oxides
and sulphates
10.3 Flow diagram
The flow diagram for the carbon-in-pulp circuit for gold recovery is shown in Figure 10.3.
192
Figure 10.3
Process diagram for the carbon-in-pulp circuit for gold recovery
193
10.4 Process assessment
10.4.1 Hazard identification
Heavy metals in the ore are present at trace levels. The dust at ore storage, handling, and
crushing, should therefore be assessed as inert particulates (not otherwise classifiable).
Calcium oxide is of concern for its irritation effects. The process is largely wet, with a low risk
of exposure to heavy metals.
10.4.2 Toxicological assessment
Calcium in itself is not toxic to humans, but in the form of calcium oxide it acts as an irritant.
The toxicology of calcium oxide has been discussed in Section 3.3.4.7.
10.4.3 Exposure assessment
Exposure to calcium oxide may occur at the milling section and lime storage areas. Sampling
and analytical methods have been listed in Table 3.4.2.6 for calcium. Biological monitoring
would not give an indication of exposure because of the large body burden of calcium.
Section 3.4.4 provides an overview of medical evaluation procedures that are relevant for
exposure assessment and interpretation of health effects.
10.4.4 Risk quantification
Because of its irritation effects, exposure to calcium oxide should be assessed against
maximum concentration peaks rather than average values.
10.5 References
All authors/chapters. 1972. (In: Adamson, R.J. Gold metallurgy in South Africa. South
Africa: Chamber of Mines of South Africa, Cape and Transvaal Printers, all pages).
All authors/chapters. 1987. (In: Stanley, G.G. The extractive metallurgy of gold in South
Africa. South Africa: South African Institute of Mining and Metallurgy, Monograph Series, all
pages).
194
11 Nickel, copper, cobalt refining processes
11.1 Introduction
The processes described are typical of those used in base metal refineries in the South African
platinum industry. The technology is adapted in each application to meet specific product
requirements, which may in turn be dictated by the composition of the feed material and the
scale of operation, and consequently flowsheets differ significantly in each installation. Two or
three stage pressure leaching may be employed. In some applications, the first stage pressure
leach may be replaced with an atmospheric leach for economic or other reasons.
The process described as Option 1 includes first stage atmospheric leaching with a second
stage pressure leach. Products are nickel sulphate crystals, cathode copper and an upgraded
PGM concentrate. This flowsheet is suited to a smaller operation with a relatively low base
metal output, such as may be produced from a UG2 ore. Comment will be made in the
following text of alternative unit operations to produce upgraded products.
The feed to the refinery is a converter matte with the typical composition shown in the table
below. Solutions containing the salts of the base metals present occur throughout the process.
The process described here as Option 2 varies quite significantly from Option 1. Although
much of the equipment is similar, involving atmospheric and pressure leaching and multiple
solid-liquid separation stages, the chemical and physical principles employed to achieve the
separation of PGMs, copper, nickel etc., differ.
The PGMs are produced as a concentrate and the copper as metal, as before. Nickel is
however produced as a metal and cobalt is produced as a byproduct. Sulphur is removed in a
process that produces a saleable sodium sulphate crystal.
The feed is again a converter matte having a fairly similar composition to that for Option 1.
Copper electrowinning is also a common operation to that described in Option 1. Solutions
containing the salts of the base metals present occur throughout the process.
11.2 Process description: option 1
11.2.1 Matte grinding
Crushed or granulated white matte delivered from the smelter is ground in water in a ball mill.
The fine material is then thickened to typically 80 per cent solids in a settler cone or thickener
and pumped to the first stage leach.
195
Table 11.2.1
Matte grinding
Stream
White matte
Component
Copper
Iron
Nickel
Cobalt
Selenium
Sulphur
PGM’s + Au
Typical
concentrations
(as % of dry solids)
Heavy metals
Cu, Fe, Ni, Co,
Se, Te and other
metal sulphides
e.g. Ni3S2,
Cu2S
Some Ni-Cu-Fe
alloy and many
others
27 – 35
1–2
35 – 45
0,3 – 0,7
0,05
20 – 25
2000–3000 ppm
11.2.2 Atmospheric
Pressure
Crystallisation
Leach
Exposure
Matte handling/mill area
and
Nickel
Sulphate
The atmospheric pressure leach is designed to extract nickel and iron contained in the matte,
while simultaneously precipitating copper and any PGM’s contained in recycled spent
electrolyte leachate.
The matte slurry is mixed with pre-heated spent electrolyte. Oxygen is sparged into the slurry
to promote the reaction between the nickel in the matte and the sulphuric acid. The terminal
leach solution pH is maintained at about 4 to allow copper precipitation, which co-precipitates
o
dissolved PGM’s. Retention time is 6-8 hours at about 80 C.
The slurry and solution contain dissolved base metals, principally nickel and copper from this
point onwards.
The leach discharge is transferred to a thickener.
In the selected flowsheet, the nickel bearing solution is clarified and transferred to a nickel
sulphate evaporator/crystalliser where nickel is recovered as nickel sulphate hexahydrate while
the thickened slurry is pumped to the pressure leach circuit.
Solution feed to the crystalliser is controlled on level. Steam ejectors supply the vacuum
o
required to operate the crystalliser at about 50 C, which ensures the hexavalent product. The
slurry of nickel sulphate crystals and mother liquor is circulated through a steam heated heat
exchanger. Larger crystals are separated from the circulating slurry by means of an elutriation
leg in the crystalliser. These are typically centrifuged, then dried in a rotary dryer. Gases from
the dryer are scrubbed with water.
A number of alternative process options are available. Depending on product requirements and
its economics, cobalt may be precipitated and separated from the nickel sulphate solution
before nickel crystallisation. The precipitate could then be purified for the production of a cobalt
product, for example cobalt sulphate heptahydrate (CoSO4.7H2O). Alternative nickel products
may also be produced, including nickel oxide, nickel cathode or nickel powder.
196
Table 11.2.2
Atmospheric pressure leach and nickel sulphate crystallisation
Stream
Component
Thickener
underflow
Cu
Ni
Co
S
Thickener overflow Cu
Ni
Co
Nickel sulphate
Al, As, Cd, Cr,
Fe, Mg, Mn, Mo,
Pb, Se, Te
Ni/Co sulphate
Typical
concentrations
(as % of dry
solids)
40 – 45
25 – 35
0,5
22 – 26
0,1 – 0,3 g/l
90 - 100 g/l
0,1 – 0,5 g/l
Heavy metals
Cu, Ni, Co,
sulphides and
metallics
Exposure
Thickener/
slurry handling
Se precipitate handling, nickel
Cu, Ni, Co,
Se, Al, As, Cd, Cr, sulphate
crystalliser area
Fe, Mg, Mn, Mo,
Pb, Te sulphates
Total 0,0001 –
0,5 g/l
NiSO4
CoSO4
Storage/
handling
11.2.3 Pressure leach
Leach solution, comprising a blend of spent electrolyte, water and sulphuric acid is added to the
thickened slurry, and the mixture fed to the pressure leach autoclave. The objective is to
quantitatively leach the remaining copper and nickel sulphides to yield a high-grade PGM
concentrate. The charge make-up is adjusted to yield a discharge solution containing about
100g/l of copper plus nickel and 20g/l of sulphuric acid.
Oxygen is sparged into the leach slurry to maintain oxidising conditions. The slurry is heated by
steam injection while cooling coils are provided to control temperature. Leach retention time is
o
4-6 hours at a total pressure of about 1100kPa and a temperature of 140 to 160 C.
The discharge slurry is filtered to recover the PGM concentrate, while the filtrate is transferred
to selenium removal and copper electrowinning unit operations.
Table 11.2.3
Pressure leach
Stream
Solids from filter
Filtrate
Component
PGM + Au
Ni + Cu + Co
Fe
S
SiO2
Other
Ni
Cu
Co
Fe
Pt
Pd
Rh
Ru
Se
Te
Typical
concentrations
(as % of dry
solids)
20 – 30
12 – 15
15 – 20
5 – 10
5 – 10
20 - 30
65 - 70 g/l
40 – 50 g/l
0,5 – 1,0 g/l
0,5 g/l
0,05 mg/l
0,2 mg/l
4 mg/l
10 mg/l
40 mg/l
10 mg/l
197
Heavy metals
Filter cake/
Ni, Cu, Co, Pt,
handling
Pd, Rh, Os, Ru,
Se, Te,
Fe sulphides,
oxides, arsenates
and metallics
Filter
Ni, Cu, Co, Pt,
Pd, Rh, Ru, Se,
Te sulphates
Exposure
11.2.4 Selenium removal
The filtered pressure leach solution is treated with sulphur dioxide in a reactor to precipitate
selenium, tellurium, palladium plus some copper, and some of the other PGM’s which partly
dissolve in the pressure leach.
The copper selenide precipitate is filtered off, roasted and caustic-leached to extract selenium
and tellurium. The PGM containing residue may be recycled to the pressure leach, or treated
for copper removal for direct transfer to the PGM refinery.
Table 11.2.4
Selenium removal
Stream
Filter cake
Component
Se, Te
Cu
PGM’s
Typical
concentrations
(as % of dry
solids)
30 – 35
60 – 70
3-5
Heavy metals
Not known
Exposure
Filter and filter cake handling
11.2.5 Copper electrowinning
Copper is recovered from the purified pressure leach solution by electrowinning. The copper
level in solution is typically reduced from about 50 g/l to about 20 g/l.
Table 11.2.5
Copper electrowinning
Stream
Component
Typical
concentrations
(as % of dry solids)
Heavy metals
Copper product
Cu
99+
Cu
Cell house mist
CuSO4
NiSO4
Not known
CuSO4
NiSO4
Exposure
Cell house/
Product storage
Cell house
11.3 Flow diagram: option 1
The flow diagram for the nickel, copper, and cobalt refining process (Option 1) is shown in
Figure 11.3.
198
Figure 11.3
Process diagram for the Ni, Cu, Co refining process – option 1
199
11.4 Process assessment: option 1
11.4.1 Hazard identification
Because of variations in process conditions at different installations, all the potential hazards
have been identified in this section. The hazards may not be applicable in all cases.
The matte grinding process is wet, and exposure to heavy metals should not be possible. The
atmospheric pressure leach and nickel sulphate crystallisation steps are also done under wet
conditions. If the nickel and cobalt products produced in this area are in a dry powder or
crystalline form, the possibility of exposure should be considered. The filter cake produced
from the pressure leach would contain nickel, copper and cobalt, and also the platinum group
metals, and exposure may occur if dry filter cake is handled. Similarly, the filter cake produced
from the selenium removal step would contain high levels of both selenium and to a lesser
extent tellurium. In the electrowinning cell house, exposure would be largely to copper and
nickel in mists.
11.4.2 Toxicological assessment
Certain nickel compounds are classified as human carcinogens, but noncarcinogenic
systemic effects have not been documented. Hypersensitivity to nickel is common, as
discussed in the summary of nickel toxicity (Section 3.3.4.17).
Copper is an essential element in humans, but copper dust and fumes are respiratory irritants.
The toxicity of copper and its compounds is discussed in Section 3.3.4.10.
The critical effects associated with the inhalation of cobalt as metal, dust, or fume are
pulmonary fibrosis and pulmonary sensitisation. The toxicity of cobalt and its compounds is
discussed in Section 3.3.4.9.
Salts of the platinum group metals are sensitisers upon chronic exposure, causing allergies
like rhinitis, conjunctivitis, asthma, urticaria and contact dermatitis. See Sections 3.3.4.18,
3.3.4.19, and 3.3.4.20 for descriptions of the toxicity of platinum group metals.
Occupational exposure to selenium may cause a wide range of non-specific symptoms, as
described in Section 3.3.4.21.
Tellurium has relatively low toxicity, but can be converted in the body to form dimethyl telluride,
which gives a garlicky odour to the urine, breath and sweat. Section 3.3.4.24 provides an
overview of tellurium toxicity.
11.4.3 Exposure assessment
Soluble nickel sulphate has been linked to cancer, as indicated in the toxicological review for
nickel (Section 3.3.4.17). Sampling and analysis methods for airborne nickel compounds have
been listed in Table 3.4.3.6. Several studies have demonstrated that the concentration of
nickel in plasma is an indicator of recent exposure. An ambient air exposure level of 0.1 mg
3
Ni/m corresponds approximately to a concentration of nickel in plasma and in urine collected at
the end of the workshift of 0.7 µg Ni/100 ml and 70 µg Ni/l (corrected for a specific gravity of
1.018), respectively (Lauwerys and Hoet, 1993: 82).
Methods for sampling and analysis of copper in ambient air have been listed in Table 3.4.3.6.
Data concerning the relationship between occupational exposure to copper and internal dose
and effect are inadequate to suggest reliable biological monitoring values.
200
Methods for sampling and analysis of cobalt in ambient air have been listed in Table 3.4.3.6. It
is believed that normal levels of cobalt are below 2 µg/g creatinine for urine and 0.05 µg/100 ml
for serum and plasma (Lauwerys and Hoet, 1993: 47). The concentration of cobalt in blood
and urine below which the risk of adverse effects is negligible has not yet been clarified. For
3
refinery exposure it has been shown that a time-weighted average of 50 µg Co/m leads to an
average concentration of 33 and 46 µg/g creatinine in the urine collected at the end of shift on
Monday and Friday, respectively. Exposure at this air concentration is expected to lead to a
mean blood level of 2.5 µg/l (Lauwerys and Hoet, 1993: 47).
Area monitoring and personal sampling for the platinum group metals and compounds may
be conducted using NIOSH Method 7300 and OSHA CIM. The most appropriate method has to
be selected for the particular exposure scenario.
Platinum can be determined in blood or tissue using NIOSH Method 8005, but the relationship
between these levels and exposure has not been established.
Area monitoring and personal sampling for selenium and its compounds may be conducted
using NIOSH Method 7300 and OSHA CIM.
The biological significance of selenium in blood and urine is not clear, but it appears that the
concentration in serum (or plasma) and urine reflects short-term exposure, whereas the
selenium content of erythrocytes may be associated with long-term exposure. There is no
indication that selenium in hair may be used to assess the selenium body burden. A biological
threshold limit of 100 µg/l for selenium in urine has been proposed, but this is associated with
great uncertainty (Lauwerys and Hoet, 1993:86). There is no guideline for biological monitoring
in South Africa.
Area monitoring and personal sampling for tellurium and its compounds may be conducted
using NIOSH Method 7300 and OSHA ID 121.
Little is known about the human metabolism of tellurium, and concentrations in urine may be
related to amounts absorbed. Direct correlations are however unknown. It has been
suggested that levels in urine below 1 µg/l would prevent the tellurium-associated garlic odour
of breath. No guideline for biological monitoring has been set in South Africa.
11.4.4 Risk quantification
Depending on the specific nickel compounds, it is appropriate to quantify cancer risks.
Copper, cobalt, the platinum group metals, selenium, and tellurium exposures can be
assessed on the basis of hazard quotients, using the documented occupational exposure limits.
For cobalt, biological monitoring may add some information to the assessment.
11.5 References: option 1
Brugman, C, F. & Kerfoot, D.G. 1986. Treatment of nickel matte at Western Platinum by the
Sherritt acid leach process. Nickel extraction and refining: Proceedings of the 25th Annual
Conference of Metallurgists, 1986, Toronto, Ontario, 17 – 20 August: CIM.
Hofirek, Z. & Kerfoot, D. G. E. 1992. The chemistry of the nickel-copper matte leach and its
application to process control and optimisation. Hydrometallurgy, 29(1): 357 – 381. (Paper
presented at the Ernest Peters International Symposium, Hydrometallurgy. Theory and practice.
Lauwerys, R. R. & Hoet, P. 1993. Industrial Chemical Exposure, Guidelines for Biological
Monitoring. Second Edition. Boca Raton: Lewis Publishers, 318p.
201
Plasket, R.P. and Ramandruk, S. 1978. Recovery of nickel and copper from high-grade matte
at Impala Platinum by the Sherritt process. Hydrometallurgy, 3 (2): 135 – 151.
11.6 Process description: option 2
11.6.1 Slow cool/crush/mill/magnetic concentration
White matte from the smelter/converter is cast into moulds and slow cooled for a period of 3
days. During this process a Ni-Cu-Fe alloy (mainly Ni) separates out as platelets. This alloy
acts as a collector for PGMs of which around 99 per cent migrate into the alloy. After the slow
cooling process the matte is crushed and wet milled and passes to magnetic separation. The
alloy formed in the slow cooling process is magnetic and this fraction amounts to approximately
15 per cent of the total matte. The non-magnetic fraction comprises Cu2S and Ni3S2 and traces
of PGMs. The Se and Te sulphides are also included in the non-magnetics. The magnetic
fraction is subjected to a leaching process from which a solid PGM concentrate, containing
approximately 60 per cent PGMs is produced. This is fed to a precious metals refinery for
separation/refining into the final products. The solution from the leach process, containing
copper and nickel, together with the larger stream of non-magnetics, containing the bulk of the
copper, nickel and cobalt, are transferred to the base metals refinery.
Table 11.6.1
Slow cool/crush/mill/magnetic concentration
Stream
White matte
PGM concentrate
Typical
concentrations
(as % of dry solids)
Component
Heavy metals*
Exposure
Cu, Fe, Ni, Co,
Matte crushing/
Se, Te and other handling
metal sulphides
e.g. Ni3S2,
Cu2S
Some Ni-Cu-Fe
alloy and many
others.
10 to 300 ppm levels
Sb, As, Bi, Cr,
Sb, As, Bi, Cr,
Pb, Mn, Ag, Te,
Pb, Mn, Ag, Te,
Sn, Zn
Sn, Zn
compounds in
small amounts
Pt, Pd, Rh, Ru, Ir, 60% in solids (small Pt, Pd, Rh, Ru, Ir, Filter cake
Os
quantity)
Os
Copper
Iron
Nickel
Cobalt
Selenium
Sulphur
PGM’s + Au
29
2
45
0,6
0,05
21
2000 ppm
11.6.2 Copper cementation
The non-magnetic material is fed to a copper removal (cementation) stage, which is carried out
in reactors operating at atmospheric pressure. Here the matte is contacted with primary leach
discharge solution and solution from the sulphur removal stage. Copper and iron are cemented
out of solution and some of the nickel in the matte is dissolved. The slurry undergoes solidliquid separation in a thickener. The thickener underflow solids, containing 35 per cent Ni and
30 per cent Cu, are fed to the first stage leach and the nickel-rich solution (thickener overflow)
passes to nickel solution purification.
The atmospheric pressure leach is designed to extract nickel and iron contained in the matte,
while simultaneously precipitating copper and any PGM’s contained in recycled spent
electrolyte leachant.
202
11.6.3 Primary pressure leach
o
In the primary leach the copper residue is subjected to a pressure leach at 1000 kPa and 135 C
in autoclaves. Spent electrolyte from copper electrowinning, containing sulphuric acid, is used
to leach further nickel and cobalt. Solution from the magnetic fraction leach process is also
added at this point. Nickel dissolves to the point of a total dissolution of 80 to 85 per cent over
the cementation and first stage leach operations. Copper is retained out of solution by
operating the final stages of the autoclave in a non-oxidsing mode. Slurry from the autoclave
passes to a thickener and overflow from which it is recycled to the cementation stage.
Underflow solids, containing copper and residual nickel and cobalt, is filtered on a belt filter and
washed before being transferred to the second stage leach.
Table 11.6.3
Primary pressure leach
Stream
Component
Lead-containing
waste
Lead hydroxide
Barium hydroxide
Ba(OH)2
Typical
concentrations
Heavy metals
Exposure
(as % of dry solids)
Not known
Lead hydroxide, some Filter cake/handling
Zn, Mn and Fe species
~100
Ba(OH)2
Storage/handling
11.6.4 Secondary pressure leach
o
The second stage leach is carried out at 1000 kPa and 145 C in autoclaves. Oxygen-enriched
air is fed to the autoclaves. Here copper, nickel and cobalt are leached up to the point of
achieving an overall copper dissolution, for all operations, of > 98 per cent and an overall nickel
dissolution of > 99 per cent. Iron is precipitated as hematite (Fe2O3). Exit slurry passes to
solid-liquid separation (plate and frame press). The residue, comprising mainly iron but also
containing many of the impurities in the feed (Se, Te, As, Sb, Bi), together with the traces of
PGMs which were contained in the non-magnetic fraction, is exported. Selenium remaining in
the liquor is removed by the addition of sulphur dioxide, which results in the formation of Cu2Se.
This is filtered off and combined with the waste iron stream for export.
Table 11.6.4
Secondary pressure leach
Stream
Main
iron/selenium
residue
Component
Typical
concentrations
(as % of dry solids)
Cu2Se, Te, Sb,
Mainly Fe
Bi
compounds
with iron, trace
PGMs
Heavy metals
Fe2O3, Cu2Se, Te, Sb,
Bi compounds with
iron, trace PGMs
Exposure
Filter cake
11.6.5 Copper electrowinning
Copper is recovered from the purified pressure leach solution by electrowinning. The feed
solution typically contains 75g/l Cu, 30 g/l Ni, and 60 g/l sulphuric acid . The electrowinning
cells have lead anodes and copper starter sheet cathodes. The starter sheets are formed by
plating copper onto titanium cathodes to form thin copper sheets. These are stripped from the
cathodes, trimmed, and fabricated into starter sheet cathodes. After copper deposition on the
cathode the copper spent electrolyte is reduced to a Cu content of 25 g/l and acid content of 90
g/l.
203
Table 11.6.5
Copper electrowinning
Stream
Component
Typical
concentrations
(as % of dry solids)
Heavy metals
Copper product
Cu
99.9
Cu
Cell house mist
CuSO4
NiSO4
Not known
CuSO4
NiSO4
Exposure
Cell house/
Product storage
Cell house
11.6.6 Cobalt removal
The nickel-containing liquor exiting the thickener downstream of the cementation process
requires the removal of lead, copper and cobalt prior to the recovery of nickel by electrowinning.
Lead (from the lead anodes used in copper electrowinning) is removed by precipitation with
barium hydroxide and the precipitate is recycled back to the smelter. Cobalt is removed by
precipitation as cobalt hydroxide by the addition of nickelic hydroxide. The nickelic hydroxide is
produced by taking a portion of the main nickel sulphate stream, adding sodium hydroxide and
then passing the nickelous hydroxide formed through an electrolytic cell. The cobalt hydroxide
cake is filtered off and leached in nickel spent electrolyte to dissolve nickel hydroxides. The
cake is then washed and leached in sulphuric acid to dissolve the remaining nickel and the
cobalt. The solution is then purified to remove Cu, Fe and Pb. Manganese is also removed by
the addition of sodium persulphate to form manganese dioxide, which is recycled to the
smelter. The cobalt sulphate in the solution is then separated from the nickel sulphate by
solvent extraction. Cobalt sulphate is then crystallised as CoSO4.7H2O and marketed.
Table 11.6.6
Cobalt removal
Stream
Component
Cobalt
sulphate CoSO4.7H2O
product
MnO2 recycle
MnO2
Typical
concentrations
Heavy metals
(as % of dry solids)
~100
CoSO4.7H2O
Product storage
Not known
Filter cake
MnO2
Exposure
11.6.7 Nickel electrowinning
The main solution, after cobalt removal, is clarified and transferred to nickel electrowinning.
This is carried out in electrolytic cells with lead anodes. The cathodes are nickel starter sheets
made by depositing a thin sheet of nickel onto titanium blanks. The cathodes are enclosed in
permeable bags and the feed liquor is introduced into the bags. A positive head of liquor is
kept in the cathode bag which separates the relatively acidic solution at the anode (anolyte)
from the relatively neutral feed solution. This ensures the predominant reaction at the cathode
is the deposition of nickel rather than the evolution of hydrogen which would otherwise
preferentially occur if the solution were acidic. Sulphur from the feed matte is now present at
the anode as sulphuric acid and must be removed from the circuit. Evolution of acid mist which
will contain copper and nickel sulphates is kept very low by covering the liquid surface of the
cells with small polystyrene beads. Operators are required to wear masks to ensure that
exposure levels are brought down below maximum permissible TLV levels.
204
Table 11.6.7
Nickel electrowinning
Stream
Nickel cathode
product
Cell house
mist
Component
Typical
concentrations
(as % of dry solids)
Heavy metals
Ni
99.9
Ni
NiSO4
Not known
NiSO4
Exposure
Cell house/
Product storage
Cell house
11.6.8 Sulphur removal
Approximately half of the nickel spent electrolyte leaving the electrowinning cells is reacted with
sodium hydroxide to neutralise the acid and in so doing sulphur is removed from the circuit in
the form of sodium sulphate solution. This solution is transferred to an evaporator/crystalliser
that produces anhydrous sodium sulphate for sale as a byproduct. Nickel in the spent
electrolyte is precipitated as nickelous hydroxide which is filtered off and re-dissolved in the
other half of the spent electrolyte and the solution produced is then returned to primary leach.
11.7 Flow diagram: option 2
The flow diagram for the nickel, copper, cobalt refining process (Option 2) is shown in Figure
11.7.
11.8 Process assessment: option 2
11.8.1 Hazard identification
The process in option 2 is largely a closed system, with minimal exposure to employees. For
completeness, however, the species that are present in filter cake have been listed in Tables
11.6.1, 11.6.4, and 11.6.6. It appears that the areas of primary interest are the electrowinning
steps for nickel, copper, and cobalt, and the assessment of exposure therefore will focus on
these metals.
11.8.2 Toxicological assessment
Certain nickel compounds are classified as human carcinogens, but noncarcinogenic
systemic effects have not been documented. Hypersensitivity to nickel is common, as
discussed in the summary of nickel toxicity (Section 3.3.4.17).
Copper is an essential element in humans, but copper dust and fumes are respiratory irritants.
The toxicity of copper and its compounds is discussed in Section 3.3.4.10.
The critical effects associated with the inhalation of cobalt as metal, dust, or fume are
pulmonary fibrosis and pulmonary sensitisation. The toxicity of cobalt and its compounds is
discussed in Section 3.3.4.9.
205
Figure 11.7
Process diagram for the Ni, Cu, Co refining process – option 2
206
11.8.3 Exposure assessment
Soluble nickel sulphate has been linked to cancer, as indicated in the toxicological review for
nickel (Section 3.3.4.17). Sampling and analysis methods for airborne nickel compounds have
been listed in Table 3.4.3.6. Several studies have demonstrated that concentrations of nickel
3
and plasma are indicators of recent exposure. An ambient air exposure level of 0.1 mg Ni/m
corresponds approximately to a concentration of nickel in plasma and in urine collected at the
end of the workshift of 0.7 µg Ni/100 ml and 70 µg Ni/l (corrected for a specific gravity of
1.018), respectively (Lauwerys and Hoet, 1993: 82).
Methods for sampling and analysis of copper in ambient air have been listed in Table 3.4.3.6.
Data concerning the relationship between occupational exposure to copper and internal dose
and effect are inadequate to suggest reliable biological monitoring values.
Methods for sampling and analysis of cobalt in ambient air have been listed in Table 3.4.3.6. It
is believed that normal levels of cobalt are below 2 µg/g creatinine for urine and 0.05 µg/100 ml
for serum and plasma (Lauwerys and Hoet, 1993: 47). The concentration of cobalt in blood
and urine below which the risk of adverse effects is negligible has not yet been clarified. For
3
refinery exposure it has been shown that a time-weighted average of 50 µg Co/m leads to an
average concentration of 33 and 46 µg/g creatinine in the urine collected at the end of shift on
Monday and Friday, respectively. Exposure at this air concentration is expected to lead to a
mean blood level of 2.5 µg/l (Lauwerys and Hoet, 1993: 47).
Section 3.4.4 provides an overview of medical evaluation procedures that are relevant for
exposure assessment and interpretation of health effects.
11.8.4
Risk quantification
Depending on the specific nickel compounds, it is appropriate to quantify cancer risks in the
occupational exposure scenario.
Copper and cobalt exposures can be assessed on the basis of hazard quotients, using the
documented occupational exposure limits. For cobalt, biological monitoring may add some
information to the assessment.
11.9 References: option 2
Anonymous. 1981. Matthey Rustenburg Refiners. Journal of the South African Institute for
Mining and Metallurgy, 81:11-14.
Hofirek, Z. and Halton, P. 1990. Production of high quality electrowon nickel at Rustenburg
Base Metals Refiners (Pty) Ltd. Theory and practice. (In: Claessens, P.L. and Harris, G.B.
Electrometallurgical plant practice. New York: Pergamon, p. 233-251).
Lauwerys, R. R. & Hoet P. 1993. Industrial Chemical Exposure, Guidelines for Biological
Monitoring. Second Edition. Boca Raton: Lewis Publishers, 318p.
207
208
12 Typical phosphate rock production process
12.1 Introduction
The following process description is for a typical phosphate rock production plant, as operated
by Foskor at Phalaborwa, and a typical plant producing phosphoric acid from phosphate rock,
as operated by Fedmis at Phalaborwa, Omnia at Rustenburg and Indian Ocean Fertilisers at
Richards Bay.
12.2 Process description
12.2.1 Crushing and Milling
Foskorite and pyroxenite ores are dry crushed separately using primary, secondary, and tertiary
crushing. The ores are then wet milled with rod and ball mills to about 15 per cent plus 300 µm
and 20 per cent minus 74 µm. Dry milling may also be used.
Table 12.2.1
Crushing and milling
Stream
Ore
Component
P2O5
CaO
CO2
Fe3O4
MgO
TiO2
ZrO2
Rare earths
F
SiO2
MnO
K2O
Na2O
Cu
Ni
S
Al2O3
Foskorite
%
8,0
23,6
10,9
28,5
12,7
2,1
0,6
0,1
0,73
10,0
0,54
0,78
0,48
0,23
0,02
0,1
2,5
Pyroxenite
%
7,5
24,9
0,8
2,3
14,5
0,5
0,05
0,2
0,74
35,6
0,05
2,10
0,67
0,004
0,01
trace
6,4
Heavy metals
Ca5(F,OH)(PO4)3
(Ca,Mg)CO3
Fe3O4
FeTiO2
ZrO2
Mn3O4
Cu, Fe, Ni sulphides
Exposure
Crushers/ ore handling
12.2.2 Flotation of copper sulphide
Copper sulphide minerals are recovered from the milled foskorite ore by flotation using
potassium amyl xanthate as the collector and sodium ethyl xanthate as the co-collector, and triethoxy butane as the frother. The copper concentrate is thickened, filtered, dried to about eight
per cent moisture, and stored for sale.
209
Table 12.2.2
Flotation of copper sulphide
Stream
Component
Copper
concentrate
CuS+CuFeS2 +
Cu5FeS4+Cu2S
Typical
concentrations
as % dry solids
35,0
Heavy metals
CuS+CuFeS2
+Cu5FeS4+Cu2S
+ low
concentrations of
heavy metals in
same species as
found in ore
Exposure
Copper concentrate
storage/handling
+ low concentrations of
heavy metals in same
species as found in ore
12.2.3 Magnetic separation of magnetite
After removal of copper by flotation, magnetite (Fe3O4) is removed from the foskorite stream
using low-intensity drum magnets.
Table 12.2.3
Magnetic separation of magnetite
Stream
Component
Magnetite product Fe2O3
FeO
MgO
TiO2
NiO
Low concentrations
of “heavy” metals in
same species as
found in ore
Typical
concentrations
as % dry solids
Heavy metals
Fe3O4
NiO
TiO2
73,0
23,5
2,5
3.0
0,01
Exposure
Magnetite
Product storage/handling
Low concentrations of
heavy metals in same
species as found in ore
12.2.4 Phosphate flotation
A stream of phosphate-containing slurry joins the non-magnetic stream of foskorite from the
magnetic concentrator. This slurry originates from a foskorite ore (10 per cent P2O5) from
which copper and magnetite have been removed.
Flotation reagents, comprising sodium silicate as dispersant, nonyl phenyl tetraglycol ether as a
modifier and depressant, and distilled tall-oil fatty acid as a collector are added to the combined
stream and concentrates, designated 88S and 88SL are produced.
The milled pyroxenite ore is treated with sulphonate and tall-oil as flotation reagents and
concentrate designated 88P is produced.
12.2.5 Phosphate rock concentrate treatment
The flotation concentrates are thickened. A portion is utilised for local phosphoric acid
production. The remainder is filtered, dried, and stored in various stockpiles (according to
market specification) for domestic and overseas sale.
210
Table 12.2.5
Phosphate rock concentrate treatment
Stream
Concentrates
Component
P2O5
CaO
MgO
Al2O3
Fe2O3
F
Cl (ppm)
SiO2
La2O3
CeO2
ThO2 (ppm)
TiO2 (ppm)
SrO
Y2O3
Na2O
K2O
88S
%
by
mass
40,2
53,0
0,54
0,06
0,19
2,48
670
0,37
0,11
0,24
150
130
0,45
214
0,13
0,03
88P
%
by
mass
40,3
53,9
0,44
0,12
0,14
2,8
240
0,82
0,14
0,30
132
128
0,47
240
0,13
0,07
88SL
%
by
mass
40,2
53,9
0,65
0,05
0,21
2,41
670
0,41
0,09
0,21
<100
130
0,55
214
0,13
0,03
Heavy
metals
Exposure
Apatite:
Ca5(F,OH)(PO4)3
Monazite:
(Ce, La, Y, Th)PO4
Magnetite:
Fe3O4
TiO2
Phosphate rock
product handling/
storage
12.2.6 Phosphoric acid production
The phosphate rock concentrate, containing fluorapatite, Ca10(PO4)6F2, is despatched locally via
slurry pipeline. Phosphoric acid is manufactured by acidulation using sulphuric acid. The
reaction results in the formation of mainly phosphoric acid (H3PO4) and gypsum (CaSO4.2H2O),
in this case known as phosphogypsum.
Phosphogypsum comprises mainly CaSO4.2H2O with P2O5. The table below shows the heavy
metals present.
Table 12.2.6
Phosphoric acid production
Stream
Component
Phosphoric acid
P2O5
MgO
Fe2O3
Al2O3
K2O
Na2O
SO4
F
Cl
As
Cd
Cu
Pb
V
Mn
Sr
Th
U
Cr
Similar to phosphogypsum
Waste from scrubber
Typical
concentrations
%
55
2
0,45
0,05
0,04
0,05
3,18
0,28
175 ppm
14 ppm
2 ppm
200 ppm
1 ppm
20 ppm
250 ppm
2 ppm
8 ppm
5 ppm
30 ppm
Similar to phosphogypsum
211
Heavy metals
Exposure
As, Cd, Cu, Fe
Pb,V, Mn,
Sr, Th, U,
Cr - present as
ionic species in
highly acidic
medium , probably
as phosphates
Phosphoric acid
product storage
Similar to phosphogypsum
Waste storage/
handling
Stream
Phosphogypsum
Typical
concentrations
%
Component
Ca
SiO2
P2O5
H2SiF6
F
SO4
V
Cr
Cu
Se
Y
Zr
La
Ce
Pr
Nd
Sm
Eu
Gd
Tb
Dy
Ho
Er
Tm
Yb
Lu
Th
U
26 – 34
0,1 - 2
1,0
0,3
54
55 – 59
10 ppm
50 ppm
30 ppm
75 ppm
200 ppm
700 ppm
1600 ppm
240 – 3000 ppm
1000 ppm
150 ppm
25 ppm
120 ppm
10 ppm
35 ppm
4 ppm
7 ppm
1 ppm
3 ppm
0,4 ppm
< 1 ppm
50 – 150 ppm
5 – 10 ppm
Heavy metals
CaSO4
V, Cr, Cu,
Se, Y, Zr, U
as sulphates
Exposure
Phosphogypsum
handling/waste
dump
12.3 Flow diagram
The flow diagram for the phosphate rock production process is shown in Figure 12.3.
12.4 Process assessment
12.4.1 Hazard identification
`The major concern in the phosphate rock production plant is the possibility of exposure to dust
in some areas. The copper sulphide concentrate from the flotation step is stored at
approximately 8 per cent moisture, thereby minimising the potential for dust dispersion. At the
magnetite storage and handling facilities dust may be generated. This contains approximately
73 per cent Fe2O3, and 23.5 per cent FeO. Because of the high iron content, the dust should
be managed to lower ambient air concentrations than for particulates not classified in terms of
specific toxic elements (see Table 3.4.2). At the phosphogypsum handling and waste dump
areas levels of heavy elements are so low that management of dust would also effectively
control exposure to heavy metals. Most of the process steps are under wet conditions without
any potential for generating dust or airborne heavy metals.
212
Figure 12.3
Process diagram for the phosphate rock production process
213
12.4.2 Toxicological assessment
Iron oxide is not considered to be inert dust (particulates not otherwise classifiable), because
inhalation may lead to effects known as siderosis, iron pneumoconiosis, hematite
pneumoconiosis, and iron pigmentation of the lung. It appears that the pulmonary effects are
somewhat more serious than those caused by inert dust. Systemic effects relating to excessive
haemosiderin deposits have also been documented. It has not been proved that iron oxides
are carcinogenic following chronic pulmonary exposure. The toxicity of iron and its compounds
has been discussed in Section 3.3.4.12.
12.4.3 Exposure assessment
Sampling and analytical methods for airborne iron have been listed in Table 3.4.2.6. NIOSH
Method 7300 and OSHA ID 121 are appropriate for quantification of particulate-associated iron.
There is no biological monitoring method to assess exposure to iron, because iron is an
essential element present in the human body.
Section 3.4.4 provides an overview of medical evaluation procedures that are relevant for
exposure assessment and interpretation of health effects.
12.4.4 Risk quantification
3
In controlling exposure to iron oxide, it is not adequate to control dust levels to 10 mg/m ,
3
because the level of iron may be above 5 mg/ m at particulate levels lower than 10 mg total
3
dust/m .
12.5 References
Roux et al. 1989. Phosphate in South Africa. Journal of the South African Institute of Mining
and Metallurgy, 89 (5):129 -139.
Schorr, M. et al. 1997. Wet process phosphoric acid:production, problems and solutions.
Industrial Minerals, 355: 61-71.
Rutherford, P.M., Dudas, M.J. & Samek R.A. 1994. Science of the Total Environment, 149: 1
– 38.
214
13 Platinum group metal refining
13.1 Introduction
The platinum group metals (PGM), platinum, palladium, rhodium, ruthenium, iridium and
osmium together with gold and silver generally occur in nature associated with base metals
such as iron, copper, nickel and cobalt, as well as a wide range of minor elements such as
selenium, tellurium and arsenic. Initial processing of PGM ores (e.g. flotation, smelting and
base metal leaching) results in a concentrate containing 30 per cent to 60 per cent PGM plus
varying amounts of base metals, minor elements and silica. Where impurity levels are high, the
concentrate may be subjected to an upgrade step such as a sulphate roast/acid leach to
remove remaining heavy metals, followed by a reductive roast of the residue to remove oxygen.
Obviously where such roasting takes place, the roaster gases will contain toxic materials, such
as arsenic and selenium.
Classical refining processes are based on leaching and complex selective precipitation
techniques. These often have poor separation efficiencies, complicated by the presence of
impurities. As a result of the multiple filtration and washing steps which generate recycled
liquids and residues, which also have to be processed, primary yields are low and there is a
significant ‘lock-up’ of PGM’s. Because of the multiple handling, the process is labour intensive
with a high risk of exposure to allergenic platinum salts.
Extensive research by refining companies into newer, more selective separation technologies
such as solvent extraction and ion exchange, has led to the development of more continuous,
‘single-stream’ processing. The advantages of the new processes include a very much smaller
lock-up, reduced operating costs and a lower occupational health risk resulting from the use of
enclosed plant and equipment.
Because of the competitive nature of the business and the high value of the products, very little
detail of the processes used by the individual South African refiners has been published. It is
therefore not possible to identify species and specific health hazards associated with individual
unit operations. Without input from the producers about their specific processes, the
occupational health risk can only be dealt with in general terms.
It is known that all dusts containing PGM salts are hazardous and the industry takes stringent
precautions to prevent emissions.
13.2 Process description
As noted above, details of the South African producers’ refining processes are not published in
the open literature, and the sequence in which the PGM’s are extracted and the processes
used differ from refiner to refiner. The ‘side-stream’ processes for the production of the final
product may also be different.
The health risk in the ‘single-stream’ extraction area is likely to be a function of how well the
processes are enclosed, ventilation efficiency, and process liquor spillage control. Greater
exposure is likely in the ‘side-stream’ processing areas where there is more intensive handling
of the products.
13.2.1 Leaching
The first stage of the newer processes is the total leaching of the PGM’s and gold. A
hydrochloric acid-chlorine medium is used. Leaching is carried at above ambient temperatures.
Silver remains as insoluble silver chloride and is recovered from the residue after filtration.
215
The filtrate containing the dissolved precious metals proceeds through the unit operations
where the individual metals are extracted.
Table 13.2.1
Leaching
Stream
Component
PGM concentrate
PGM + Au
Cu + Ni + Co
Fe
S
SiO2
Other
Typical
concentrations
%
20 - 30
12 - 15
15 – 20
5 – 10
5 – 10
20 - 30
Heavy metals
Exposure
Base metal and PGM
sulphides, oxides and
metallics
-
Leach solution
(AuCl4)
22(PtCl4) , (PtCl6)
22
(PdCl4) , (PdCl6)
3(RhCl6)
23(RuCl6) , (RuCl6)
4(Ru2OCl10) ,
2(RuCl5H2O)
23(IrCl6) , (IrCl6)
2(OsCl6)
Base metal cations
Gold
Platinum
Palladium
Rhodium
Ruthenium
Iridium
Osmium
Base metals
13.2.2 Gold extraction
Gold is extracted on a selective ion exchange resin. When the resin is loaded, solution flow is
switched to a standby resin column and the gold eluted from the loaded column, possibly after
an initial resin wash.
Some refiners use solvent extraction to extract gold.
Gold is recovered from the eluate or scrubbed solvent by reduction.
Table 13.2.2
Gold extraction
Stream
Au extraction
Component
PGM salts
Typical
concentrations
%
No data
Heavy metals
PGM salts
Exposure
Handling areas
13.2.3 Palladium extraction
Following gold extraction, the solution is pumped to the palladium separation circuit where
palladium is extracted using “Molecular Recognition Technology”. This is also an ion exchange
process. Palladium is recovered from an eluate by means of ‘palladium salting’.
Solvent extraction is also an option for palladium extraction. Alternative recovery processes
include the precipitation of palladium as a salt.
216
Table 13.2.3
Palladium extraction
Stream
Component
Pd extraction
PGM salts
Typical
concentrations
%
No data
Heavy metals
PGM salts
Exposure
Handling areas
13.2.4 Base metal separation
The next step in the flowsheet described is a base metal ion exchange to remove residual base
metals, which are eluted as described earlier and precipitated from the eluate.
Table 13.2.4
Base metal separation
Stream
Base metal
separation
Component
Typical
concentrations
%
PGM salts
+
Se, Te, Pb, As, Sb
chlorides
No data
Heavy metals
PGM salts
+
Se, Te, Pb, As, Sb
chlorides
Exposure
Handling areas
13.2.5 Ruthenium separation
Ruthenium is the next PGM removed from solution. This is normally achieved by oxidising the
ruthenium and distilling it off as ruthenium tetroxide with an air sparge. Osmium will distil off
with the ruthenium, and this is removed from the distillate by a second air distillation.
Ruthenium is recovered by palladium salting.
In some refineries, osmium is distilled off, and ruthenium subsequently recovered by solvent
extraction and precipitation.
Table 13.2.5
Ruthenium separation
Stream
Component
Ru extraction
PGM salts
Typical
concentrations
%
No data
Heavy metals
PGM salts
Exposure
Handling areas
13.2.6 Rhodium/iridium/osmium separation
The solution in the example used now contains platinum, rhodium and iridium. Rhodium and
iridium are removed by ion exchange and then separated in a further ion exchange process,
followed by purification and final product.
In an alternative process, where platinum is extracted higher up the chain, rhodium/iridium
separation may be achieved using solvent extraction.
217
Table 13.2.6
Rhodium/iridium/osmium separation
Stream
Component
Rh, Ir, Os
PGM salts
Typical
concentrations
%
No data
Heavy metals
PGM salts
Particularly OsO4
Exposure
Handling areas
13.2.7 Platinum recovery
The barren solution, after rhodium/iridium removal, still contains the platinum values.
solution is purified ahead of final platinum production.
The
Platinum may be recovered higher up the chain by solvent extraction, and as with palladium,
precipitated as a salt.
Table 13.2.7
Platinum recovery
Stream
Component
Typical
concentrations
%
Heavy metals
Exposure
Pt extraction
PGM salts
No data
PGM salts
Handling areas
Barren brine
Se, Te, Pb, As, Sb
chlorides
No data
Se, Te, Pb, As, Sb
chlorides
Handling/
evaporation ponds
13.3 Flow diagram
The flow diagram for the platinum group metal refining process is shown in Figure 13.3.
13.4 Process assessment
13.4.1 Hazard identification
Although the extraction and separation processes are conducted in closed reactor systems,
certain reaction conditions are at elevated temperatures and it is known that leaks may occur at
valves and flange seals. Exposure may also occur during maintenance activities on ventilation
systems. This may lead to exposure not only to the platinum group metals, but also to other
elements, for example arsenic, selenium, and others as indicated in the tables above. It
appears that apart from the platinum group metals, arsenic is the major element of concern. A
better understanding of potential hazards would however require investigation of particular
process steps and materials, relying on confidential information. The following discussions
cover all the elements that may be of interest, leaving it up to the particular plant health risk
manager to select the priorities for monitoring and control.
The elements below have been identified to be of potential concern:
• The platinum group, i.e. Pt, Pd, Rh, Ru, Ir and Os.
• Associated elements Au and Ag.
• Base metals Fe, Co, Cu and Ni.
• Minor elements such as As, Pb, Sb, Se and Te.
It is unlikely that exposure will be relevant in all cases, but the exposure assessment
nevertheless provides information on all the elements of interest. Gold has not been included in
the selection of hazardous heavy metals (see Section 3.2), and silver is unlikely to be present at
218
Figure 13.3
Process diagram for a platinum group metal refining process
219
levels of concern except where refining is specifically for silver. The base metals Fe, Co, Cu
and Ni are normally separated from the platinum group metals and are processed separately,
as described in Section 11.
13.4.2 Toxicological assessment
Salts of the platinum group metals are sensitisers upon chronic exposure, causing allergies
like rhinitis, conjunctivitis, asthma, urticaria and contact dermatitis. See Sections 3.3.4.18,
3.3.4.19, and 3.3.4.20 for a description of the toxicity of platinum group metals.
Arsenic is a confirmed human carcinogen, and is known to cause contact dermatitis. See
Section 3.3.4.2 for a description of arsenic toxicity.
Lead is a cumulative toxin. It is well known for neurotoxic effects, but has been associated with
a whole range of other possible symptoms and effects. Section 3.3.4.13 provides an overview
of lead toxicity.
Occupational exposures to antimony compounds have been associated with the development
of pneumoconiosis as well as impairment of the lung function, and some antimony compounds
are considered to be possible carcinogens. See Section 3.3.4.1 for an overview of antimony
toxicity.
Occupational exposure to selenium may cause a wide range of non-specific symptoms, as
described in Section 3.3.4.21.
Tellurium has relatively low toxicity, but can be converted in the body to form dimethyl telluride,
which gives a garlicky odour to the urine, breath and sweat. Section 3.3.4.24 provides an
overview of tellurium toxicity.
13.4.3 Exposure assessment
Area monitoring and personal sampling for antimony and its compounds may be conducted
using NIOSH Methods 2(S2) and 4(261), and OSHA ID 121 and ID 125.
NIOSH has developed Method 8005 to determine antimony in blood or tissue, and Method 107
for determination in urine. Based on somewhat limited data on exposure to pentavalent
3
antimony, it has been estimated that an airborne concentration of 0.5 mg/m would lead to a
urinary concentration of 35 µg/g creatinine during a shift. Background concentrations in urine
have been determined in the range of 0.2 and 1 µg/g creatinine (Lauwerys and Hoet, 1993:19).
Antimony has not been listed for biological monitoring in South Africa.
Area monitoring and personal sampling for arsenic and its compounds may be conducted
using NIOSH Methods 7300, 7900 and 7901, and OSHA ID 105 and OSHA CIM. NIOSH
Method 7900 is valid only for particulate-associated inorganic arsenic compounds. The most
appropriate method for the exposure scenerio has to be selected.
Mean serum and blood levels of arsenic vary greatly depending on the level of seafood content
in the diet. Therefore, when employees have not been instructed to refrain from eating fish or
shellfish for two to three days before biological monitoring, high levels of arsenic may be found
that might not be associated with occupational exposure.
In the past, biological monitoring for assessment of occupational exposure was conducted by
measuring the total amount of arsenic in urine at the end of a shift. It is however now well
established that inorganic arsenic, monomethylarsonic acid, and cacodylic acid in urine is the
method of choice. Monitoring of employees exposed to inorganic arsenic using this method is
not influenced by organoarsenicals from marine origin.
220
Some controversial results may be obtained in the correlation between air-concentration
exposure assessment and biological monitoring. It has been established that background
levels of the sum of the three metabolites of arsenic (inorganic arsenic, monomethylarsonic
acid, and cacodylic acid) in urine vary between 10 µg/l and 50 µg/l. It appears that the best
3
relationship for occupational exposure at air concentrations between 50 and 200 µg As/m
would lead to post-shift concentrations of the total metabolites between 54 and 88 µg/g
creatinine (Lauwerys and Hoet, 1993: 25).
Medical surveillance for monitoring of effects include full blood count, liver function tests, urine
tests for creatinine and proteinurea, spirometry, and electrocardiography in selected cases
Area monitoring and personal sampling for the lead and its compounds may be conducted
using NIOSH Methods 7082, 7105, 7300, 7505, and OSHA ID 121 and ID 125 G G (see Table
3.4.3.6). The most appropriate method has to be selected for the particular exposure scenario.
Approximately 50 per cent of the lead deposited in the lung is absorbed, whereas less than 10
per cent of ingested lead normally gets into the systemic circulation. Dermal absorption of lead
is also a significant route of exposure. Biological tests for lead exposure can be divided into
two groups, i.e. those directly reflecting the exposure through assessment of the amount stored
in blood, urine, hair, and bone, and those indicating the early biological effects of lead in
relation to exposure. These effects are shown in haemoglobin, haematocrit, stippled cells,
coproporphyrin in urine, etc. In a steady-state situation, lead in blood is considered to be the
best indicator of recent exposure. It has been shown that under low exposure conditions
3
(environmental levels) an increase of 1 µg/m in air leads to an increase of 1 to 2 µg/100 ml of
whole blood. There is however not a clear correlation between air concentrations and blood
lead at higher exposure concentrations, and it is therefore difficult to assess occupational
exposures. The situation is further complicated by the fact that lead is a ubiquitous pollutant,
leading also to nonoccupational exposures. As a rule, it is accepted that blood-lead levels of
non-occupationally exposed individuals lie between 15 and 30 µg/100 ml of whole blood.
Levels up to 70 µg/100 ml in lead-related occupations are normally considered acceptable.
However, subclinical effects may occur at levels exceeding 50 µg/100 ml of whole blood. The
World Health Organisation has proposed 40 µg/100 ml as the maximum tolerable lead value in
blood for adult male workers, and 30 µg/100 ml for women of childbearing age (Lauwerys and
Hoet, 1993:86). No guideline has been proposed for biological monitoring of lead exposure in
South Africa.
Lead in urine is often preferred to blood analysis, and reflects the amount of lead recently
absorbed. There is however a poor association between lead in blood and lead in urine, and
blood-lead is considered the more reliable measure for routine assessment of lead exposure. A
concentration of lead in blood of 50 µg /100 ml usually corresponds with a level of 150 µg /g
creatinine, but the correlation across a wider exposure range is poor. The level of 150 µg Pb/g
3
creatinine corresponds with an air concentration of 50 µg Pb/ m .
Although it has been suggested that hair provide a time-integrated index of lead absorption, it
has drawn limited interest because of potential lead contamination in hair-washing procedures
(Lauwerys and Hoet, 1993:86).
Area monitoring and personal sampling for the platinum group metals and compounds may
be conducted using NIOSH Method 7300 and OSHA CIM. The most appropriate method has to
be selected for the particular exposure scenario.
Platinum can be determined in blood or tissue using NIOSH Method 8005, but the relationship
between these levels and exposure has not been established.
221
Area monitoring and personal sampling for selenium and its compounds may be conducted
using NIOSH Method 7300 and OSHA CIM.
The biological significance of selenium in blood and urine is not clear, but it appears that the
concentration in serum (or plasma) and urine reflects short-term exposure, whereas the
selenium content of erythrocytes may be associated with long-term exposure. There is no
indication that selenium in hair may be used to assess the selenium body burden. A biological
threshold limit of 100 µg/l for selenium in urine has been proposed, but this is associated with
great uncertainty (Lauwerys and Hoet, 1993:86). There is no guideline for biological monitoring
in South Africa.
Area monitoring and personal sampling for tellurium and its compounds may be conducted
using NIOSH Method 7300 and OSHA ID 121.
Little is known about the human metabolism of tellurium, and concentrations in urine may be
related to amounts absorbed. Direct correlations are however unknown. It has been
suggested that levels in urine below 1 µg/l would prevent the tellurium-associated garlic odour
of breath. No guideline for biological monitoring has been set in South Africa.
Section 3.4.4 provides an overview of medical evaluation procedures that are relevant for
exposure assessment and interpretation of health effects.
13.4.4 Risk quantification
Traditionally, the primary concern in refining of the platinum group of metals has been
sensitisation of employees. This is manifested primarily as bronchial dysfunction, which may
require from a few days to several years of exposure to develop. The platinum group metals,
as well as lead, selenium and tellurium, can be assessed against occupational threshold limits
using the hazard-quotient approach. Exposure to lead can also be quantified through biological
monitoring.
Occupational exposure levels for arsenic have to be assessed through interpretation of area
and personal monitoring data, in conjunction with biological monitoring and exposure effects
monitoring. Cancer risks can be quantified through interpretation of exposure data and arsenic
dose-response information.
13.5 References
Anonymous. 1988. The development and implementation of novel refining processes for the
platinum group metals (including the refining of anode slimes). Mintek Application Report No.
14. Randburg: Mintek,
Anonymous. 1998. Impala platinum metals refinery at Springs upgraded. Mining Mirror.
August.
Anonymous. 1999. Impala refinery completes its upgrade. SA Mining, Coal, Gold and Base
Metals, May.
Charlesworth, P. 1981. Separating the platinum group metals by liquid-liquid extraction.
Platinum Metal Review, 25(3): 106 – 112..
Lauwerys, R. R. & Hoet P. 1993. Industrial Chemical Exposure, Guidelines for Biological
Monitoring. Second Edition. Boca Raton: Lewis Publishers, 318p.
Republic of South Africa, Mintek. 1988. The development and implementation of novel
refining processes for the platinum group metals. . Application Report No. 14.
222
Rimmer, B.F. 1987. Refining of platinum group metals. Transactions of the Institution of
Mining and Metallurgy, Section A, 96: A117 – A119.
223
224
14 Typical stainless steel process
14.1 Introduction
Stainless steel is produced in a series of process functions viz. melting, refining, casting of
ingots, ingot conditioning, ingot re-heating prior to rolling, hot rolling, de-scaling, annealing and
pickling, cold rolling, annealing and pickling after cold rolling, skin passing, levelling, cutting to
size and packing. Bright annealing is also done for some steel grades and applications.
14.2 Process description
The process description and flow diagrams of a typical stainless steel process are included in
this section. The process description and diagrams contain data on the process streams and
identify the species containing heavy metals, which occur on the plant, as well as the potential
exposure points.
14.2.1 Raw material receipts and charge preparation
Stainless steel is made by melting steel scrap in an electric arc furnace together with stainless
steel scrap and ferroalloys. Fluxes are added to aid the removal of impurities and to produce a
slag, which will allow clean separation of the slag-forming constituents in the furnace charge
from the crude stainless steel.
Many of the alloys charged are friable and attrition of the surface causes dust formation. The
dusts formed naturally have an analysis typical of the alloy from which they are abraded.
Ferrochrome or charge chrome, and ferrosilicon are fairly friable compared with
ferromanganese, ferroboron, ferrotitanium, low carbon ferrochromium and ferromolybdenum.
Typical fluxes used in the operation are burnt lime and fluorspar. The dusts occur in the
process of off-loading the materials on receipt and in recovering the materials when weighing
them off for charging into the electric arc furnace. The heavy elements are in the alloy form,
often in solid solution with iron. The elements chromium, iron, manganese and silicon will be in
higher concentration than titanium, molybdenum and other minor alloys. Table 14.2.1 shows
the composition of the more usual alloys.
The alloys are weighed off together with steel scrap, stainless steel scrap and flux and can be
charged directly into the electric arc furnace or via feed ports in the furnace roof.
Table 14.2.1
Raw material receipts and charge preparation
Stream
Stainless steel scrap
Component
Fe
C
Mn
P
S
Si
Cr
Ni
Mo
Ti
N
Typical
concentrations
(as % of dry
solids)
Balance
0,03 – 0,15
2
0,045
0,03
1 – 1,5
16 – 26
6 – 22
2–4
0,7
0,1
225
Heavy metals
Fe
Mn
Cr
Ni
Mo
Ti
Exposure
Raw material off-loading/
storage/handling
Stream
Steel scrap
Nickel
Ferrochrome
Ferromanganese
Ferrosilicon
Ferrotitanium
Ferronickel
Ferroboron
Ferromolybdenum
Cr
Fe
C
Mn
S
P
Ni
Cu
Co
Cr
Fe
Si
C
S
P
Al
Fe
Si
C
Mn
S
P
Al
Fe
Si
S
P
Al
Fe
Si
C
Ti
S
P
Al
Typical
concentrations
(as % of dry
solids)
<1
99
0,15
0,2
<0,05
< 0,5
100
Trace
Trace
52
33
2–4
6–8
< 0,03
< 0,02
< 0,03
15
< 1,2
7,5
> 75
< 0,02
< 0,02
<0,02
24
>75
<0,02
< 0.02
< 0,5
60
<5
<0,15
25
<0.02
< 0,02
<8
Fe
Ni
C
S
P
Al
Fe
B
Al
Si
Fe
Mo
C
Si
S
P
Sb
Cu
Sn
Component
Heavy metals
Exposure
Cr
Fe
Mn
FeCr3
Cr7C3
Raw material off-loading/
storage/handling
Ni
Cu
Co
Cr
Fe
Cr3C2,Cr7C3,
Cr3Si, CrSi,
Cr5Si3, Cr23C6,
CrFe (solid solution)
Raw material off-loading/
storage/handling
Fe
Mn
Mn3C, Mn3Si,
Mn5Si3, Mn7C3,
MnC2, MnC12,
MnS. MnP,
MnSi, MnC12
FeSi, FeSi2,
Fe3Si, Fe3Si7,
Raw material off-loading/
storage/handling
Raw material off-loading/
storage/handling
Raw material off-loading/
storage/handling
TiFe, TiFe2,
TiAl, TiAl3,
TiC, TiS2,
TiS3, TiSi2,
Ti5Si3 TiS2,
TiS3
Raw material off-loading/
storage/handling
74
25
< 0,1
<0,02
<0,02
<0.02
Balance
15 – 17
1–3
<1
Fe
Ni
NiS
Fe3C
Raw material off-loading/
storage/handling
Fe
B
Intermetallic
compounds
FeB, Fe2B
Raw material off-loading/
storage/handling
Balance
> 55
0,1 – 0,2
1–2
0,2
0,1 – 0,2
0,05 – 0,1
0,08 – 2,5
0,05 – 0,1
Fe, Sb, Cu.
Mo, Mo2C,
Mo3Si, Mo5Si,
MoC, MoS2,
MoSi2
Raw material off-loading/
storage/handling
226
Stream
Lime
Fluorspar
Dolomite (burnt)
Component
CaO
MgO
Al2O3
FeO
MnO
SiO2
Fe2O3
CaF2
SiO2
Sulphides
Pb
Phosphate
Dolomite
MgO
CaO
Al2O3
Loss on ignition
Typical
concentrations
(as % of dry
solids)
91,3
1,7
0,3
0,3
0,1
0,8
85 min
5 max
0,3 max
0,5 max
0,3 max
0,2 max
38.2
53.3
0,4
6,3
Heavy metals
Exposure
CaO
MnO
FeO
Fe2O3
Raw material off-loading/
storage/handling
CaF2
PbO
Raw material off-loading/
storage/handling
CaO
Storage/
handling
14.2.2 Furnace charging and melting
The charge weighed off for the furnace may be in several charging boxes and some of the
alloys could be charged via a charging port in the furnace roof. Dust will occur in the furnace
when charging, and should under normal circumstances be retained in the furnace or be
sucked of into the furnace dust collection system. Stray dust plumes can arise from the sidecharging door of the furnace.
The initial arc struck in the furnace is unstable as the scrap is melted. This causes more dust
and gas evolution than normal. Once the bath is molten a steady arc is formed and gas and
dust evolutions are low. Some refining of the crude stainless steel can be done in the furnace
by lancing the bath with oxygen. During this operation heavy fumes can be formed, some of
which can escape the furnace. These fumes contain the oxides of the easily oxidized alloys,
manganese, molybdenum, silicon, chromium and iron. When melting has been completed,
O
fluxes are added, the melt heated to the tapping temperature of 1600 to 1700 C and tapped
into a transfer ladle. Ferrosilicon and lime are added to the ladle to reduce oxidized chromium
and manganese, with the evolution of reaction gases containing some volatilised oxides, mainly
silicon and manganese, with some iron and chromium. The reaction is normally carried out
under an extraction hood and the dust and fume captured in the dust collection system.
The slag produced from the melting operations is transported in the molten state, in ladles, to a
slag dump, where it is tipped out and solidifies. The slag is recovered, crushed, and the metal
removed magnetically or by gravity separation techniques. The recovered stainless steel is remelted, whilst the slag is deposited on a slag dump.
227
Table 14.2.2
Furnace charging and melting
Stream
Component
Furnace dust
Fe2O3
MnO
Cr2O3
NiO
ZnO
PbO
CaO
MgO
Al2O3
C
S
K2O
Na2O
Melting furnace slag Cr2O3
FeO
SiO2
CaO
MgO
Al2O3
NiO
Magnesia - carbon MgO
refractories – new C
and spent
Dolomite
– MgO
CaO
magnesite
refractories – new
and spent
Typical
concentrations
(as % of dry
solids)
40 – 42
1,5 – 2,5
11 – 13
0,5 – 1,5
22 – 28
0,5 – 1
4–6
1–2
0,5 – 1,0
0,1 – 0,2
0,2 – 0,5
0,35 – 0,45
0,5 - 1
10 –12
0,7
30 – 32
12 - 15
18 – 20
20 – 24
<1
Heavy metals
FeO
Fe2O
MoO2
Fe2O3
MnO
Cr2O3
CrO3
NiO
ZnO
PbO
CaO
Furnace area/
bag house
Cr2O3
FeO
CaO
NiO
Fe2SiO4
Fe2TiO5
Ca2SiO4
Ca3SiO7
88 – 95
5 - 12
38,0
58,0
Exposure
Storage/
handling
CaO
Storage/
handling
14.2.3 Stainless steel refining
After removing the slag from the molten steel, the metal is transferred to a refining vessel. This
could be an Argon-Oxygen Decarburisation (AOD) converter, a Creusot-Loire Uddeholm (CLU)
converter or a Vacuum Oxygen Decarburisation (VOD) unit. In the case of the CLU, refining is
carried out using oxygen and superheated steam as refining agents, which are introduced
through tuyeres placed in the bottom of the vessel. The reaction is controlled at 1680 to 1780
O
C through the introduction of argon or nitrogen into the gas mixture at various ratios to the
oxygen and steam. After decarburisation has been completed, the steel is purged with argon or
an argon and nitrogen gas mixture and lime and ferrosilicon are added to reduce chromium and
manganese oxides from the slag.
Oxygen is blown into the top of the converter to aid post combustion of the reaction gases.
Specific consumption rates for a typical stainless steel are:
Oxygen
Nitrogen
Nitrogen
Argon
3
35 m /ton
3
25 m /ton
3
15 m /ton
3
4 m /ton
3
(m refers to normal cubic meters, i.e. at 25 °C and atmospheric pressure.) Refining of a 100ton load takes approximately 60 minutes.
228
The oxides of all the heavy metals in the scrap and ferroalloys are present in the off-gases from
this process. The fume is captured and collected in a dust collection system. Slag from this
process is dumped onto a slag dump that may be processed to recover metal.
Slag produced from the converting operation is transported in the molten state, in ladles, to the
same slag dump as used for the furnace slag, and stainless steel is recovered in the same way.
Table 14.2.3
Stainless steel refining
Stream
Component
Dust and fume from Fe2O3
converter
MnO
Cr2O3
NiO
PbO
CaO
MgO
Al2O3
C
S
K2O
Na2O
ZnO
Slag
Similar to
furnace slag
Magnesia - carbon MgO
refractories – new C
and spent
Dolomite
– MgO
CaO
magnesite
refractories – new
and spent
Typical
concentrations
(as % of dry
solids)
35 – 40
5 – 10
12 – 20
0,5 – 0,2
0,4 – 0,6
6 – 12
0,5 – 1
0,4 – 0,6
0,5 – 1,2
0,2
0,2 – 0,4
0,4 – 0,5
Not known
Similar to furnace
slag
88 – 95
5 - 12
38,0
58,0
Heavy metals
Exposure
FeO
Fe2O3
MnO
Cr2O3
NiO
PbO
CaO
ZnO
Refining area/
dust cleaning plant
Similar to furnace
slag
Slag dump
Storage/
handling
CaO
Storage/
handling
14.2.4 Continuous casting
The refined steel is transferred to the continuous casting machine where the molten steel is
tapped into an oscillating mould via a tundish. Controlled solidification of the slab cast occurs in
the mould and caster. The string of slab is cut to length for further processing. The cooled slab
is surface ground to remove casting defects. In the casting process various mould powders are
used. These have a low melting point and coat the mould so as to promote a defect-free
surface. Fumes will be emitted from the casting process and will contain the oxides of the
heavy metals in the stainless steel. In the slab grinding bay the metal removed is in the form of
swarf, a mixture of metal and metal oxides and grinding wheel compound. This material is remelted.
Table 14.2.4
Continuous casting
Stream
Dust/fume
Component
Same as refining
Typical
concentrations
(as % of dry solids)
Same as refining
229
Heavy metals
Same as refining
Exposure
Casting machine
Stream
Grindings from
slab
Component
Ni
Cr
Fe
Mo
Ti
Si
Typical
concentrations
(as % of dry solids)
8 – 20
18 – 25
Balance
0,1 – 3
0,2 – 0,5
0,3 – 0,5
Heavy metals
Ni
Cr
Fe
Mo
Ti
Exposure
Slab grinding station
14.2.5 Hot rolling
Slabs are charged into a walking-beam furnace for re-heating before rolling. The slabs
o
discharge from the furnace at the required temperature, approximately 1300 C for austenitic
o
stainless steel grades, and 1150 C for ferritic grades.
Hot ingots are rolled from 150 to 250 mm to two to ten mm thick steel which is cooled and
coiled. Ingots are also rolled to plate more than ten mm thick.
Fuel gas from Sasol is used to fire the furnaces. The gas is a synthetic gas containing 80
3
percent methane with a calorific value of 31 to 35 MJ/m . The slab is rolled down in a rougher
mill and finished off by rolling to the required thickness in a Steckle tandem mill. This mill has a
coil-heating furnace where coils are kept hot during the rolling process. Water is used to break
the scale formed during the re-heating and rolling process. Millscale is collected from the
sump, supplying the de-scaling water for recycling to the process. This will typically contain
chromium, nickel, manganese and iron oxides.
Table 14.2.5
Hot rolling
Stream
Millscale
Component
FeO
Cr2O3
NiO
MnO2
MoO
SiO
Typical
concentrations
(as % of dry solids)
53 – 70
20 - 27
8 – 19
0,3 – 0,5
0,3 – 0,5
0,5 – 0,7
Heavy metals
FeO
Cr2O3
NiO
MnO2
MoO
Exposure
De-scaling water pit
14.2.6 Annealing and pickling
Coils and plate rolled on the mills require scale removal. Plates could be annealed in an
o
annealing furnace at 1 050 to 1 120 C for austenitic steels, followed by pickling in acids. These
could be a dilute sulphuric acid pickle followed by a mixed acid, 100 to 220 g/l nitric acid and 15
to 60 g/l hydrofluoric acid solution.
The spent acids are neutralised with lime and treated in an acid recovery plant. Hot mill coil
can be annealed and pickled in a continuous process electrolytically using a 150 – 200 g/l
sodium sulphate solution followed by a mixed acid nitric acid and hydrofluoric acid pickling.
o
Ferritic steels are annealed in a batch-anneal furnace at 850- 950 C before pickling.
230
Table 14.2.6
Annealing and pickling
Stream
Waste pickling
acid
Acid recovery
Lime
Component
HNO3
H2SO4
HF
Ni, Fe, Cr,
salts
HNO3
H2SO4
HF
As previous
Typical
concentrations
(as % of dry solids)
Not known
Not known
As previous
Heavy metals
Exposure
Ni, Fe, Cr,
sulphates,
nitrates,
fluorides +
Fe scale
Similar to waste
pickling acid
Pickling/
reagent recovery area
As previous
Lime storage/
handling
Acid recovery
disposal
area/waste
14.2.7 Cold rolling and bright annealing
The annealed and pickled coil is transported to cold-rolling mills, which are normally of the
Sendzimar type or 4-high mills. The cold-rolled band is annealed and pickled or bright
annealed. Bright annealing requires the annealing of the band in an inert atmosphere, which is
provided by a cracked ammonia atmosphere. The gas from this furnace is recovered and
recycled.
For special finishes grinding and polishing is carried out. Emery cloth of varying grit is used. In
this process fine stainless steel and corundum arises, but as the process is carried out under a
hood and the dusts extracted, there is a low probability of the dust becoming a hazard. The
dust is recycled to the melting process.
Table 14.2.7
Cold rolling and bright annealing
Stream
Steel
product/dust
Component
Fe
C
Mn
P
S
Si
Cr
Ni
Mo
Ti
N
Typical
concentrations
(as % of dry
solids)
Balance
0,03 – 0,15
2
0,045
0,03
1 – 1,5
16 – 26
6 – 22
2–4
0,7
0,1
Heavy metals
Fe
Mni
Cr
Ni
Mo
Ti
Exposure
Cold rolling area
Bright annealing area
14.2.8 Cutting to length, slitting, packing and despatching
After annealing and pickling, or bright annealing the cold rolled band goes to the finishing lines,
which consist of skin, pass mills, cut-to-length, slitting and packing lines. The finished product
is dispatched to customers.
231
Table 14.2.8
Cutting to length, slitting, packing and despatching
Stream
Steel
product/dust
Component
As previous
Typical
concentrations
(as % of dry
solids)
As previous
Heavy metals
As previous
Exposure
Cut – to-length,
packing,despatch areas
14.2.9 Effluent treatment plant
The effluents from pickling and annealing are treated by adjusting the liquor pH with caustic
soda. Nickel, chromium and iron are precipitated as metal hydroxides and filtered. The filter
cake is deposited in a registered disposal site. Hexavalent chromium in the pickling effluent is
reduced with ferric chloride before precipitation with caustic soda.
14.2.10 Water treatment/handling
A central water-treatment plant is usually installed, which would contain a pre-treatment plant, a
process water plant and a high quality water plant. The process water is used mainly as a
make-up water for re-circulation to direct cooling systems serving e.g. continuous casting water
sprays, cold-mill roll cooling and rinsing, scrubbing and strip quenching in the annealing and
pickling circuit. High quality water is used as steam–boiler feed, finished product rinsing and
cooling water for critical cold mill parts. The water is firstly softened using lime and a
polyelectrolyte, the sludge going to a sludge disposal area. The softened water will be further
treated by filtration and cation and anion exchange systems to produce the high quality water.
14.3 Flow diagram
The flow diagrams for a typical stainless steel process are shown in Figures 14.3.1 and 14.3.2.
232
Figure 14.3.1 Process diagram for a typical stainless steel process, sheet 1 of 2
233
Figure 14.3.2 Process diagram for a typical stainless steel process, sheet 2 of 2
234
14.4 Process assessment
14.4.1 Hazard identification
It is not certain how much dust can actually form due to the friability of the scrap metals in the
raw materials handling area. The following discussion is based on the assumption that some
dust may form, and that exposure to metals would therefore be of interest for assessment. The
metals in this context are iron, chromium, nickel, manganese and lead. Furnace dust that
forms during charging and melting may also lead to exposure to manganese oxide, chromium
trioxide, nickel oxide, and zinc oxide.
Calcium oxide and calcium fluoride are present in certain areas, and exposure should be
assessed for the potential development of irritation effects.
14.4.2 Toxicological assessment
Iron oxide is not considered to be inert dust (particulates not otherwise classifiable), because
inhalation may lead to effects known as siderosis, iron pneumoconiosis, hematite
pneumoconiosis, and iron pigmentation of the lung. It appears that the pulmonary effects are
somewhat more serious than those caused by inert dust. Systemic effects relating to excessive
haemosiderin deposits have also been documented. It has not been proved that iron oxides
are carcinogenic following chronic pulmonary exposure. The toxicity of iron and its compounds
has been discussed in Section 3.3.4.12.
Chromium is an essential element in humans. Hexavalent chromium is a human carcinogen,
as outlined in the toxicological assessment for chromium (see Section 3.3.4.8). Trivalent
chromium is poorly absorbed, but allergic eczematous dermatitis has been observed following
industrial exposures.
Certain nickel compounds are classified as human carcinogens, but noncarcinogenic
systemic effects have not been documented. Hypersensitivity to nickel is common, as
discussed in the summary of nickel toxicity (Section 3.3.4.17).
Lead is a cumulative toxin. It is well known for neurotoxic effects, but has been associated with
a whole range of other possible symptoms and effects. Section 3.3.4.13 provides an overview
of lead toxicity.
The primary concern of exposure to zinc is the oxide (ZnO), associated with what is known as
metal fume fever. Metal fume fever is generally considered to be transitory, but the possibility
of chronic respiratory effects resulting from ZnO inhalation cannot be dismissed.
Calcium in itself is not toxic to humans, but in the form of calcium oxide it acts as an irritant.
The toxicology of calcium oxide has been discussed in Section 3.3.4.7. Calcium fluoride is
also an irritant.
14.4.3 Exposure assessment
Iron levels in the scrap stainless steel used as a raw material may be around 50 per cent.
Taking exposure to iron oxide as a guideline, it can be shown that control of the dust should be
adequate for control of exposure to iron in this area.
Levels of chromium and nickel in the scrap stainless steel are however high, and exposure
should be controlled not only for dust. For steel scrap the concern is for iron in the metal form.
In nickel and ferrochrome the concern is also for nickel, chromium and iron.
235
Manganese levels are high in ferromanganese. In ferrosilicon and ferrotitanium, iron levels are
high, and nickel and iron are present at high concentrations in ferronickel.
Calcium oxide is present at the raw materials storage and handling areas as lime and in burnt
dolomite, and exposure should be assessed for its irritation effects. Inorganic fluorides such as
calcium fluoride are generally highly irritating, and exposure is normally assessed on the basis
of exposure to the fluoride. Exposure to lead from fluorspar would not exceed guideline
concentrations if dust levels were controlled within the guideline concentrations. Please see
Tables 3.4.2 and 14.2.1 for the concentrations of metals in dust and the relationship with
maximum levels that would be controlled adequately when dust exposure is controlled.
Furnace dust that forms during charging and melting appears to be the highest priority for
control of exposure. Table 14.2.2 indicates that exposure to manganese oxide, chromium
trioxide, nickel oxide, and zinc oxide is of potential concern in this area. Also at the refining
vessel that operates at over 1 600 °C, similar exposure may occur. Although at relatively low
levels, exposure to lead may be possible in this area. Although this appears to be of low
probability, it is neverthesless listed as a precautionary item for discussion and assessment.
Sampling and analytical methods for airborne iron have been listed in Table 3.4.2.6. NIOSH
Method 7300 and OSHA ID 121 are appropriate for quantification of particulate-associated iron.
There is no biological monitoring method to assess exposure to iron, because iron is an
essential element present in the human body.
Exposure to chromium can be quantified using sampling and analytical methods listed in Table
3.4.3.6. Determination of chromium in urine is the preferred method for assessing exposure to
3
hexavalent chromium. Exposure to an air concentration of 0.05 mg Cr/m would be reflected in
a urine concentration of 30 µg Cr/g creatinine at the end of the exposure period. Exposure to
trivalent chromium compounds does not correlate with levels of chromium in urine.
Some nickel compounds have been linked to cancer, as indicated in the toxicological review
for nickel (Section 3.3.4.17). Sampling and analysis methods for airborne nickel compounds
have been listed in Table 3.4.3.6. Several studies have demonstrated that the concentrations
of nickel in plasma and urine are indicators of recent exposure. An ambient air exposure level
3
of 0.1 mg Ni/m corresponds approximately to a concentration of nickel in plasma and in urine
collected at the end of the workshift of 0.7 µg Ni/100 ml and 70 µg Ni/l (corrected for a specific
gravity of 1.018), respectively.
Area monitoring and personal sampling for the lead and its compounds may be conducted
using NIOSH Methods 7082, 7105, 7300, 7505, and OSHA ID 121 and ID 125 G (see Table
3.4.3.6). The most appropriate method has to be selected for the particular exposure scenario.
Approximately 50 per cent of the lead deposited in the lung is absorbed, whereas less than 10
per cent of ingested lead normally gets into the systemic circulation. Dermal absorption of lead
is also a significant route of exposure. Biological tests for lead exposure can be divided into
two groups, i.e. those directly reflecting the exposure through assessment of the amount stored
in blood, urine, hair, and bone, and those indicating the early biological effects of lead in
relation to exposure. These effects are shown in haemoglobin, haematocrit, stippled cells,
coproporphyrin in urine, etc. In a steady-state situation, lead in blood is considered to be the
best indicator of recent exposure. It has been shown that under low exposure conditions
3
(environmental levels) an increase of 1 µg/m in air leads to an increase of 1 to 2 µg/100 ml of
whole blood. There is however not a clear correlation between air concentrations and blood
lead at higher exposure concentrations, and it is therefore difficult to assess occupational
exposures. The situation is further complicated by the fact that lead is a ubiquitous pollutant,
leading also to nonoccupational exposures. As a rule, it is accepted that blood-lead levels of
non-occupationally exposed individuals lie between 15 and 30 µg/100 ml of whole blood.
236
Levels up to 70 µg/100 ml in lead-related occupations are normally considered acceptable.
However, subclinical effects may occur at levels exceeding 50 µg/100 ml of whole blood. The
World Health Organisation has proposed 40 µg/100 ml as the maximum tolerable lead value in
blood for adult male workers, and 30 µg/100 ml for women of childbearing age (Lauwerys and
Hoet, 1993:86). No guideline has been proposed for biological monitoring of lead exposure in
South Africa.
Lead in urine is often preferred to blood analysis, and reflects the amount of lead recently
absorbed. There is however a poor association between lead in blood and lead in urine, and
blood-lead is considered the more reliable measure for routine assessment of lead exposure. A
concentration of lead in blood of 50 µg /100 ml usually corresponds with a level of 150 µg /g
creatinine, but the correlation across a wider exposure range is poor. The level of 150 µg Pb/g
3
creatinine corresponds with an air concentration of 50 µg Pb/ m (Lauwerys and Hoet,
1993:55).
Although it has been suggested that hair provide a time-integrated index of lead absorption, it
has drawn limited interest because of potential lead contamination in hair-washing procedures
(Lauwerys and Hoet, 1993:86).
Various manganese oxides have been shown to be neurotoxic, and in the assessment of
exposure all forms of manganese are normally considered. Exposure may occur in the
furnace/product area as a result of high manganese levels in furnace slag and dust.
Manganese levels are also high in scrubber effluents. Sampling and analytical methods to
quantify airborne manganese have been listed in Table 3.4.3.6. The normal concentration of
manganese in urine is usually less than 3 µg/l, and in whole blood and plasma less than 1
µg/100 ml and 0.1 µg/100 ml, respectively. There is however no consistent relationship
between manganese exposure and blood levels, and it appears that measurement of urinary
levels is the preferred method for assessment. The relationship with exposure is however not
that well-defined and no biological threshold limit value has been proposed (Lauwerys and
Hoet, 1993: 71).
Section 3.4.4 provides an overview of medical evaluation procedures that are relevant for
exposure assessment and interpretation of health effects.
14.4.4 Risk quantification
In controlling exposure to metals and metal oxides in some of the materials, it is not adequate
3
to control dust levels to 10 mg/m , because the levels of the metals may be above their
3
exposure threshold concentrations at particulate levels lower than 10 mg total dust/m .
14.5 References
Johansson, S. E. E. 1994. Columbus Joint Venture.
Congress, Johannesburg, SAIMM, 2: 191 – 202.
Proceedings of the XVth CMMI
Lauwerys, R. R. & Hoet P. 1993. Industrial Chemical Exposure, Guidelines for Biological
Monitoring. Second Edition. Boca Raton: Lewis Publishers, 318p.
237
238
15 Typical titanium dioxide production process
15.1 Introduction
This section provides a process description and process diagram of a typical titanium dioxide
production process. The example is a highly condensed version of a plant producing pigment
from a typical 85 per cent titania slag as produced by Richards Bay Minerals or Namakwa
Sands. The process description and flow diagram contain data on the process streams and
identify the toxic substances as well as the potential exposure points.
15.2 Process description
While sulphate-route pigment plants produce substantial amounts of wastes, with those using
ilmenite being much bigger waste producers than where slag is the feedstock, they are not
regarded as being hazardous to any great extent. For example, in the UK, untreated wastes
from two plants were discharged directly into rivers in 1987. For the plant under consideration,
acidic wastes are neutralised with sodium hydroxide and lime.
To put some perspective on the situation, a plant producing 50 000 t/a of final titanium dioxide
pigment product was considered. Wastes arising from the feed slag will be silica (SiO2) and
gypsum (CaSO4). Other metals will be present in the insoluble hydroxide form after
neutralisation. Totals in all exit streams will amount to around 5 000 t/a of iron, 780 t/a of Mn,
400 t/a of Al, 150 t/a of vanadium and 40 t/a of chromium.
15.2.1 Milling
Titania slag is received in bulk and stored under cover. It is conveyed to the comminution
station where continuous air-swept ball mills yield a product of less than 40 micron, which is
stored in intermediate hoppers.
The approximate analysis of the titania slag is shown in Table 15.2.1 below. Traces of uranium
(1 to 4 ppm) and thorium (10 to 25 ppm) may also be present.
Table 15.2.1
Milling
Stream
Titania slag
Component
TiO2 (total)
Fe (total)
SiO2
Al2O3
CaO
MgO
V2O5
Cr2O5
MnO
Trace U, Th
Typical
concentrations
(as % of dry
solids)
85 - 87
8,3
1,9
1,4
0,2
1,1
0,5
0,1
1,8
Heavy metals
TiO2
Ti2O3
FeO
CaO
V2O5
Cr2O5
MnO
Exposure
Storage/
handling/
milling areas
15.2.2 Digestion/production of digester residue byproduct
Weighed amounts of 98 to 100 per cent H2SO4 and slag are batched to lined digesters in
parallel. Steam or water is added to cause a rise in temperature. At about 100 °C a violent
reaction occurs with the emission of copious quantities of water vapour (with entrained acid mist
etc.), SO2, SO3, and H2S.
239
The gas stream is scrubbed with sodium hydroxide in scrubbing towers to absorb SO2 and H2S
and to neutralise any acid present. The sulphur is subsequently stripped from the solution in
packed columns and passes to the “Sulphacid” process where it is converted into dilute
sulphuric acid (about 20%), for re-use. Neutralised solution from the stripping towers is
pumped out to sea via a pipeline. It has been assumed that there will some carry over of
dissolved metals due to the violent reaction in the digesters and these will be present in this
waste stream as shown in the table below.
After some 8-9 hours the reaction is complete and the porous, sticky mass is leached with
dilute sulphuric acid over a prolonged period to solubilise TiO2 and to dissolve TiOSO4 and the
metal sulphates. The liquor is transferred to the next stage. The residue is separately
submitted to a digester residue-treatment process in which it is reacted with slaked lime
(Ca(OH)2 ) to form a byproduct which is used in brick and clinker manufacture.
Apart from activities during normal operation, it should be noted that safety precautions/health
monitoring procedures have to be applied to maintenance operations, one of these being lead
burning which takes place during the maintenance and repair of lead-lined equipment.
Table 15.2.2
Digestion
Stream
Discharge to sea
Component
TiO2
Fe
Mn
Zn
V
Cr
Typical
concentrations
(as % of dry
solids)
13
70
14
0,4
1,6
0,9
Heavy metals
Ti, Fe, Ca, Mg, V, Pipeline discharge
Cr, Mn, Zn, Cu,
Pb, Ni, Cd, Hg, As
-as hydroxides
Cu, Pb, Ni, Cd
Hg, As
Traces
SiO2
Fe2O3
MgO
CaO
Na2O
K2O
V2O5
TiO2
MnO
42,0
1,4
0,3
2,0
0,3
0,7
0,9
50,5
0,5
CaSO4
CaO
Lime, CaO
added as slaked MgO
Al2O3
lime (Ca(OH)2)
FeO
MnO
SiO2
Fe2O3
91,3
1,7
0,3
0,3
0,1
0,8
CaO
MnO
FeO
Fe2O3
Digester residue
Exposure
Byproduct storage/
handling area
Ti, Fe, Mg, V, Cr,
Mn as hydroxides
Lime storage/
handling area
15.2.3 Hydrolysis/leaching/washing
Liquor from the digesters is transferred to hydrolysis reactors where, by means of the addition
of NaOH and seed (nuclei) material, the titanium present is converted into titanium hydroxide.
240
This pulp is cooled and transferred to a re-pulp vessel where it is washed with washings from
the post-leach wash stage.
The washed pulp is transferred to the leach section where dilute sulphuric acid and a reducing
agent (possibly zinc) are used to dissolve remaining iron.
The pulp is then washed with fresh water to remove dissolved impurities and most of the
excess acid and is then filtered.
Table 15.2.3
Hydrolysis/Leaching/Washing
Stream
Filter cake
hydrolysis/
leach
Component
after Ti(OH)4
TiO(OH)2
TiOSO4
Fe, Al, Mg, Mn,
Ca, Cr, V,
Zn as sulphates
Typical
concentrations
(as % of dry
solids)
0,7
32
15
Some H2SO4
in solution
Heavy metals
Ti(OH)4
TiO(OH)2
TiOSO4
Cr2(SO4)3
FeSO4
MnSO4
ZnSO4
Vanadium
sulphate
Exposure
Filter cake from hydrolysis/
leach
15.2.4 Production of gypsum byproduct
The washings from hydrolysis and leach are reacted with lime to form a byproduct which is
basically gypsum. As much as possible of this is sold for use in cement and brick manufacture,
excess being stored on a dump.
Table 15.2.4
Production of Gypsum Byproduct
Stream
Limestone,
CaCO3
Typical
concentrations
Component
(as % of dry
solids)
94,5
CaCO3
2,0
MgCO3
2,0
SiO2
Other
metal 1,7
oxides (Al, Fe,
Mn)
241
Heavy metals
CaCO3
MnO
FeO
Fe2O3
Exposure
Limestone storage/
handling area
Stream
Gypsum
Byproduct
Component
Ca
Mg
K
Fe
Mn
Zn
Cu
Al
Cd
CN
As
Cr
Na
Hg
V
Sr
Si
Typical
concentrations
(as % of dry
solids)
mg/kg
100 400
1 953
17
29 100
933
20
3.4
2 823
0.2
< 0.33
0.4
457
114
< 0.06
584
76
737
Heavy metals
CaSO4.2H2O
CaSO3
Exposure
Gypsum byproduct storage/
handling area
Ca, Fe, Mn, Zn, Cu,
Cd, As, Cr, Hg, V, as
hydroxides
15.2.5 Calcining
Titanium hydroxide filter cake is calcined in a rotary kiln. There is a small addition of modifiers
to ensure that the desired crystal formation is obtained. Any residual sulphate in the reaction
mass is driven off as SO2 or SO3. The gases pass to the “sulphacid” plant for conversion of
SO2/SO3 to dilute sulphuric acid.
Table 15.2.5
Calcining
Stream
Calcined TiO2
Component
Typical
concentrations
(as % of dry solids)
approx 99%
TiO2
Heavy metals
TiO2
Exposure
Calcining kiln
15.2.6 Pigment finishing
Calcined TiO2 is sent to the so called "white end" for production of the final pigment. During
this process it goes through 3 to 9 comminution steps, e.g. hammer milling, sand milling and
micronising. It is important that the end product is very fine with a closely controlled particle
size range. Depending on the end use, the TiO2 particles may be coated with a range of
oxides, e.g. SiO2, ZrO2, and Al2O3. Finally, dried pigment is bagged for sale.
Table 15.2.6
Pigment Finishing
Stream
TiO2 product
Component
TiO2
Al2O3
Amorphous silicate
ZrO2
Typical
concentrations
(as % of dry solids)
80 to 99,5
0 to 7,0
0 to 11,0
0 to 1,0
242
Heavy metals
TiO2
ZrO2
Exposure
Product storage/
handling area
15.3 Flow diagram
The flow diagram for a typical titanium dioxide production process is shown in Figure 15.3.
15.4 Process assessment
15.4.1 Hazard identification
The primary substance of interest in the milling process is titanium dioxide. The digestion,
hydrolysis, leaching and washing steps are wet processes with insignificant potential for
exposure to heavy metals. Handling of calcium oxide in the lime storage and handling areas
may be a source of exposure.
Potential exposure to lead during maintenance operations is an important factor to consider.
15.4.2 Toxicological assessment
No data on dose-response or dose-effect relationships are available for systemic changes in
humans on exposure to titanium compounds. It has been shown in epidemiological surveys of
workers that titanium dioxide exposure does not increase the risk of developing lung or distal
cancers, or other fateal repiratory diseases (Cohen, Bowser and Costa, 1996: 253).
Toxicological information on titanium and its compounds is summarised in Section 3.3.4.28.
Calcium in itself is not toxic to humans, but in the form of calcium oxide it acts as an irritant.
The toxicology of calcium oxide has been discussed in Section 3.3.4.7.
The toxicity of lead is related to interference with different enzyme systems. For this reason,
almost all organ systems may be considered potential targets for lead toxicity, and a wide range
of biological effects have been documented. Among these are effects on haem biosynthesis,
the kidneys, the immune system, neurotoxic effects, reproductive effects, and also
cardiovascular, hepatic, endocrynal and gastrointestinal effects. The toxic effects of lead have
been summarised in Table 3.3.4.13.
243
Figure 15.3
Process diagram for a typical titanium dioxide production
process
244
15.4.3 Exposure assessment
Area monitoring and personal sampling for titanium dioxide may be conducted using NIOSH
Methods 3(S385) and 7300, and OSHA CIM. Methods for biological monitoring have not been
developed.
Area monitoring and personal sampling for the lead and its compounds may be conducted
using NIOSH Methods 7082, 7105, 7300, 7505, and OSHA ID 121 and ID 125 G (see Table
3.4.3.6). The most appropriate method has to be selected for the particular exposure scenario.
Approximately 50 per cent of the lead deposited in the lung is absorbed, whereas less than 10
per cent of ingested lead normally gets into the systemic circulation. Dermal absorption of lead
is also a significant route of exposure. Biological tests for lead exposure can be divided into
two groups, i.e. those directly reflecting the exposure through assessment of the amount stored
in blood, urine, hair, and bone, and those indicating the early biological effects of lead in
relation to exposure. These effects are shown in haemoglobin, haematocrit, stippled cells,
coproporphyrin in urine, etc. In a steady-state situation, lead in blood is considered to be the
best indicator of recent exposure. It has been shown that under low exposure conditions
3
(environmental levels) an increase of 1 µg/m in air leads to an increase of 1 to 2 µg/100 ml of
whole blood. There is however not a clear correlation between air concentrations and blood
lead at higher exposure concentrations, and it is therefore difficult to assess occupational
exposures. The situation is further complicated by the fact that lead is a ubiquitous pollutant,
leading also to nonoccupational exposures. As a rule, it is accepted that blood-lead levels of
non-occupationally exposed individuals lie between 15 and 30 µg/100 ml of whole blood.
Levels up to 70 µg/100 ml in lead-related occupations are normally considered acceptable.
However, subclinical effects may occur at levels exceeding 50 µg/100 ml of whole blood. The
World Health Organisation has proposed 40 µg/100 ml as the maximum tolerable lead value in
blood for adult male workers, and 30 µg/100 ml for women of childbearing age (Lauwerys and
Hoet, 1993:86). No guideline has been proposed for biological monitoring of lead exposure in
South Africa.
Lead in urine is often preferred to blood analysis, and reflects the amount of lead recently
absorbed. There is however a poor association between lead in blood and lead in urine, and
blood-lead is considered the more reliable measure for routine assessment of lead exposure. A
concentration of lead in blood of 50 µg /100 ml usually corresponds with a level of 150 µg /g
creatinine, but the correlation across a wider exposure range is poor. The level of 150 µg Pb/g
3
creatinine corresponds with an air concentration of 50 µg Pb/ m (Lauwerys and Hoet,
1993:55).
Although it has been suggested that hair provide a time-integrated index of lead absorption, it
has drawn limited interest because of potential lead contamination in hair-washing procedures
(Lauwerys and Hoet, 1993:86).
Calcium oxide can be determined using NIOSH Method 7021, or OSHA ID 121. Because
CaO is of interest for its irritation effects, biological monitoring of exposure is not relevant.
Section 3.4.4 provides an overview of medical evaluation procedures that are relevant for
exposure assessment and interpretation of health effects.
15.4.4 Risk quantification
Because of its irritation effects, exposure to calcium oxide should be assessed against
maximum concentration peaks rather than average values.
245
15.5 References
Adams, R. 1988 Titanium and Titanium Dioxide. Financial Times Business Information,
London, 243p.
Klein, J. & Rechman, H. 1995. 50 Years of the Titanium Dioxide Pigment Industry.
Leverkusen: Kronos Titan GmbH, 16p.
Lauwerys, R. R. & Hoet P. 1993. Industrial Chemical Exposure, Guidelines for Biological
Monitoring. Second Edition. Boca Raton: Lewis Publishers, 318p.
Roskill, 1996. The Economics of Titanium Minerals and Pigments.
Information Services, 338p.
246
London: Roskill
16 The salt-roast process for vanadium pentoxide
production
16.1 Introduction
The process description and flow diagram of a typical salt-roast circuit for production of
vanadium pentoxide are included in this section. The process description and flow diagram
contain data on the process streams and identify the species containing heavy metals, which
occur on the plant, as well as the potential exposure points.
16.2 Process description
16.2.1 Crushing and milling
Crushing is the first of the ore comminution steps and is followed by milling.
From field stockpiles, ore is delivered to the ore treatment plant using trucks. Here the ore is
first crushed and screened, before being sent to an intermediate stockpile. The crushed ore is
delivered to the milling circuit where it is wet-milled in a ball or rod mill and then conveyed to the
magnetic separation plant.
Table 16.2.1
Crushing and milling
Stream
Component
Crushed ore/dust V2O5
Fe (total)
TiO2
Cr2O3
SiO2
Al2O3
Typical concentrations
(as % of dry solids)
0.52 - 0.67
16.5 - 18
3.5 - 4.5
0.1 - 0.3
65 - 75
4.8 - 11.2
Heavy metals
Exposure
Crushers/mill/
Vanadium occurs as
3+
V in solid solution in loading/
Storage
the magnetite –
ulvospinel, Fe2TiO4
3+
where the V replaces
3+
Fe . Since the V is
locked in the spinel it is
not considered as
being toxic.
TiO2
Cr2O3
16.2.2 Magnetic separation and de-watering
The crushed ore is delivered to the milling circuit where it is wet-milled in a ball or rod mill and
then sent to the magnetic separation plant. Here the vanadium-containing magnetite fraction is
separated from the silica- and alumina-rich gangue by high-intensity magnetic separation. The
concentrate is de-watered to yield a filter cake that analyses from 1.6 to 2.4 per cent V2O5. The
non-magnetic fraction, about 70 to 80 per cent of the mill feed, is pumped to the slimes dam,
and the clear water returned to the mills.
247
Table 16.2.2
Magnetic separation and de-watering
Stream
Gangue from
magnetic
separation
Magnetite
concentrate
Component
Typical
concentrations
(as % of dry solids)
Mainly SiO2
and Al2O3
with small amounts of
other species in ore
(see ore analysis)
Mainly SiO2
and Al2O3
with small
amounts of other
species in ore
(see ore analysis)
Similar to ore except
Similar to ore
SiO2,
except SiO2,
Al2O3 removed
Al2O3 removed
Heavy metals
Mainly SiO2
and Al2O3
with small amounts
of other species in
ore (see ore
analysis)
Similar to ore except
SiO2,
Al2O3 removed
Exposure
Slimes dam
Filter cake
16.2.3 Roasting
On the feed tables, sodium carbonate, sodium sulphate, or a mixture of the two is added to the
milled ore before it is charged to the roasting units. The roasting units consist of coal- or gaso
fired rotary kilns, with a maximum temperature of > 1000 C. The sodium salts react with the
vanadium in the magnetite to form a water-soluble sodium metavanadate during the oxidative
roast.
Table 16.2.3
Roasting
Stream
Component
Calcine/dust
Hematite, Fe2O3
Pseudobrookite,
Fe2TiO5
Nepheline,
NaAlSiO4
Typical
concentrations
Heavy metals
(as % of dry solids)
66
Fe2O3
Fe2TiO5
14
CaTiO3
NaVO3
10
Calcium titanate
CaTiO3
NaVO3
Dust may contain
particles of calcine
with composition as
above
5
5
Dust may contain
particles of calcine
with composition as
above
Kiln off-gases
Scrubber liquor
Fe2O3
Fe2TiO5
CaTiO3
NaVO3
3+
4+
V and V
complexes
Exposure
Kiln area
Gas to stack
Scrubber/dam
16.2.4 Leaching
The hot discharge from the kilns (calcine) is mixed with water, and transported to leach dams.
During the filling of these dams, the sodium vanadate, which is soluble in water, is leached from
the ore. The leach liquor or pregnant solution is pumped to storage tanks once a concentration
of 50 to 60 g/l V2O5 is reached. After several displacement washes, the leached calcine is
removed from the leaching dams and discarded onto the tailings dumps.
248
Table 16.2.4
Leaching
Stream
Component
Pregnant leach High concentration of V, Na,
liquor
and SO4 in solution, low
concentration of other metals
as follows:
V
Na
SO4
Spent calcine
Ca, Al, Si, Ti, Cr,
Fe
(Al, Si inert as locked into
glassy phase)
Similar to calcine but lower V
concentration
Typical
concentrations
(as % of dry solids)
Heavy metals
HVO4
2-
Exposure
Leach dams,
storage tanks
Ca, Ti, Cr, Fe
sulphates
20 g/l
40 g/l
60 g/l
Low ppm levels
Similar to calcine but Fe2O3
Waste dump
lower
V Fe2TiO5
concentration
Residual V is
insoluble , existing in
a variety of forms
e.g. CaO.V2O5,
CaTiO3
16.2.5 Precipitation and vanadium pentoxide production
Vanadium is recovered from the leach liquor by precipitation as ammonium metavanadate
(AMV) or ammonium polyvanadate (APV).
In the AMV-precipitation process, an excess of ammonium sulphate is added to a continuous
flow of pregnant solution inside an air-agitated reactor. The overflow from this precipitation
reactor passes to a second reactor and finally into a thickener, where the settled AMV is raked
towards the centre discharge port and pumped into filter boxes. The barren solution is pumped
to evaporators where the solution is evaporated to produce ammonium sulphate and sodium
sulphate that is returned to the precipitation plant for re-use. After filtration and washing, the
AMV is discharged from the box filters and fed to electrically heated rotary dryer deammoniators. During this process, the white AMV powder is converted into vanadium
pentoxide powder with the loss of water and ammonia. The vanadium pentoxide powder is
o
melted in a glowbar-heated furnace at 850 C and tapped onto a cooling wheel, where the melt
solidifies into a flake that is scraped off into a bucket elevator for drumming.
In the APV-precipitation process, pregnant leach liquor is pumped into a cylindrical reactor
where sulphuric acid is added until a pH of 5.5 is reached. The required quantity of ammonium
sulphate is then added, followed by further additions of sulphuric acid to give a final pH of 2.
The solution is steam-heated and maintained at temperature until the vanadium level of the
mother liquor has dropped to about 0.5 g/l V2O5. Once this value has been reached, the
coarse, bright-orange precipitate is pumped into box filters, filtered and washed. The APV is
processed further to vanadium pentoxide flake via deammoniation and fusion furnaces as for
the AMV route.
249
Table 16.2.5
Precipitation and V2O5 production
Stream
Component
Typical
concentrations
(as % of dry solids)
50 – 500 mg/l
Barren solutions
V
Al
Ca
K
Si
SO4
V2O5 powder
V2O5
99 %
V2O5 flake
Al
Fe
Si
SO4
V2O5
Trace
Trace
Trace
Trace
99 %
Al
Fe
Si
SO4
Trace
Trace
Trace
Trace
Heavy metals
2-
Exposure
HVO4
CaSO4
Filters, storage
evaporators
tanks,
V2O5
Fe
Rotary
ammoniator
V2O5
Fe
Fusion furnace, cooling
wheel, drumming plant
dryer-de-
16.3 Flow diagram
The flow diagram for the vanadium pentoxide production circuit is shown in Figure 16.3.
16.4 Process assessment
16.4.1 Hazard identification
The primary occupational hazard relating to the vanadium industry is the irritation effects of
vanadium pentoxide. Exposure of employees would occur mostly in the final product zones of
the vanadium pentoxide production process. Filter cake, which is handled as waste, in the final
production stages, may contain small quantities of V2O5. In other areas the primary concern is
exposure to respirable dust. It has to be noted that where feed materials are imported from
other sources, it may be necessary to monitor for other heavy metals, for example hexavalent
chromium. The ore dust contains high levels of iron, and as such can not be managed as
particulates without particular toxicity.
16.4.2 Toxicological assessment
Chromium is an essential element in humans. Hexavalent chromium is a human carcinogen,
as outlined in the toxicological assessment for chromium (see Section 3.3.4.8). Trivalent
chromium is poorly absorbed, but allergic eczematous dermatitis has been observed following
industrial exposures.
Most of the reported clinical symptoms of vanadium exposure reflect irritation effects on the
respiratory tract. There is insufficient evidence that vanadium causes generalised systemic
effects in humans, except at extremely high concentrations (WHO, 1987: 366). The
toxicological assessment for vanadium has been summarised in Table 3.3.4.30.
250
Figure 16.3
Process diagram for the vanadium pentoxide production circuit
251
16.4.3 Exposure assessment
Lauwerys and Hoet (1993:95) have summarised the available biological exposure information of
vanadium. It has been estimated that 25 per cent of soluble vanadium compounds may be
absorbed through exposure by the pulmonary route. Dermal absorption is very small.
Approximately 90 per cent of circulating vanadium is associated to plasma transferrin. It is
excreted in urine with a biological half-life of 20 to 40 hours. Some excretion may also occur in
feces, and there are data that suggest slow accumulation in the body in the course of chronic
exposure.
Limited data are available on the relationship between vanadium in blood and urine and
airborne concentration levels, and considerable variations have been reported between
vanadium in serum, whole blood and urine. It appears that the background level in whole blood
should lie below 0.1 µg/100 ml, and in urine it is lower than 1 µg/g creatinine. Vanadium levels
in urine are believed to be a better reflection of exposure than blood vanadium. It has been
proposed that exposure assessment is best conducted through pre- and post-shift sampling of
urine, and accumulation may be assessed through monitoring two days after cessation of
exposure. A biological threshold limit of 50 µg/g creatinine has been proposed.
Exposure to chromium can be quantified using sampling and analytical methods listed in Table
3.4.3.6. Determination of chromium in urine is the preferred method for assessing exposure to
3
hexavalent chromium. Exposure to an air concentration of 0.05 mg Cr/m would be reflected in
a urine concentration of 30 µg Cr/g creatinine at the end of the exposure period. Exposure to
trivalent chromium compounds does not correlate with levels of chromium in urine (Lauwerys
and Hoet, 1993: 42).
Section 3.4.4 provides an overview of medical evaluation procedures that are relevant for
exposure assessment and interpretation of health effects.
16.4.4 Risk quantification
The proposed biological threshold limit is tentative, and results of biological monitoring and the
calculated hazard quotients for air monitoring should be considered together to estimate the
significance of exposure.
252
16.5 References
Gupta, C. K. & Krishnamurthy, N. 1992. Extractive Metallurgy of Vanadium, Elsevier, 689p.
Lauwerys, R. R. & Hoet P. 1993. Industrial Chemical Exposure, Guidelines for Biological
Monitoring. Lewis Publishers, 318p.
Rohrmann, B. 1985. Vanadium in South Africa, Journal of the South African Institute for
Mining and Metallurgy, 85 (5): 141–150.
Slotvinskii-Sidak, N. P. 1962. Extraction of vanadium directly from iron-vanadium (titano
magnetite) concentrates. Stal 1: 7-10.
WHO 1987. Air quality standards for Europe. Geneva, World Health Organisation, p. 361-371.
253
254
17 Vanadium slag production process
17.1 Introduction
The following process description is for a typical production plant for pig iron and vanadium slag
from Bushveld titaniferous magnetites.
17.2 Process description
The process description and flow diagram of a typical salt-roast circuit for production of
vanadium pentoxide are included in this section. The process description and flow diagram
contain data on the process streams and identify the species containing heavy metals, which
occur on the plant, as well as the potential exposure points.
17.2.1 Crushing, screening and magnetic separation
The ore treatment plant comprises crushing, screening, and magnetic separation to produce a
”lumpy” ore (typically 6 mm to 32 mm) and an upgraded minus 6 mm product. The ore contains
a fine fraction that is liable to cause dust, and further dust is created in the crushing and
screening operations. Much of this is collected in dust suppression/collection systems. The
composition of the dust is likely to be similar to that of the ore. These operations may be
carried out at the mine site and fines, generated from mining and crushing operations, are
despatched for treatment in a roast-leach operation to produce vanadium pentoxide, or are
stockpiled.
The lumpy ore is transported to the pre-reduction kiln for vanadium slag production.
Table 17.2.1
Crushing, screening and magnetic separation
Stream
Crushed ore
Non-magnetic
fraction
Component
Typical
concentrations
(as % dry solids)
Heavy metals
Exposure
Fe
TiO2
V2O5
Cr2O3
MnO
SiO2
Al2O3
CaO
MgO
Na2SO
Na2O
Ni
54 – 57
12 – 15
1.4 - 1.9
0,15 - 0,6
0,2 - 0,3
0.8
3.4
0.1
1.4
0.4
0.9
0.1
Fe2O3
Crushing, screening,
transfer points
FeO
TiO2
V2O5
Cr2O3
MnO
Others not known
No information
No information
No information
Magnetic separator,
stockpile
17.2.2 Pre-reduction
The magnetite ore is mixed with metallurgical coal, dolomite and silica and fed to a rotary kiln,
fired with pulverised coal. Here the ore is pre-reduced to the point of 50 to 70 per cent of the
oxygen being removed. The metallurgical coal has a high volatile content and serves as the
reductant for the magnetite and as char for the subsequent smelting operation. The dolomite,
which is calcined in the kiln, and silica are used as fluxes to produce a fluid titania slag in the
smelting step.
255
0
The kiln temperature is maintained at about 1 120 C by controlling the air flow to the kiln.
Waste gas from the kiln, which contains dust, is extracted, cooled and cleaned in dust collection
system, e.g. an electrostatic precipitator. The dust that is collected is slurried and pumped to a
tailings dam.
Table 17.2.2
Pre-reduction
Stream
Pre-reduced ore
Dust from kiln
Component
Similar to ore,
but Fe now
mainly reduced
to FeO, also
CaO,MgO, and
SiO2
Typical
concentrations
(as % dry solids)
Similar to ore,
some FeO, also
CaO,MgO, and
SiO2
Similar to pre- Similar to
reduced ore
reduced ore
Heavy metals
Exposure
Similar to ore, but Kiln/pre-reduced ore handling
Fe now mainly as
FeO
pre- Similar to
reduced ore
pre-
Kiln/
Electrostatic precipitator/slimes
dam
17.2.3 Electric arc smelting
The pre-reduced magnetite from the kiln is charged hot to an electric submerged arc smelting
o
furnace operating at about 1 350 C. Here the magnetite is converted to vanadium pig iron and
titania-rich slag. The pig iron is tapped into transfer ladles and taken to the shaking ladle plant.
The slag is tapped into slag pots, transported to cooling beds and then stockpiled.
The furnace off-gas, which is rich in carbon monoxide (50 to 90 per cent CO, 5 to 25 per cent
CO2), is extracted, washed to remove particulates and pumped to a gas tank for distribution for
heating purposes. The collected dust is slurried and pumped to a tailings dam.
The furnace is normally fitted with an extraction system, but stray dust and fume could escape.
Table 17.2.3
Electric arc smelting
Stream
Dust in furnace
off-gas
Titania slag
Component
Mixture of prereduced ore, titania
slag, and
vanadium pig
iron
TiO2
SiO2
CaO
MgO
Al2O3
FeO
V2O5
S
Typical
concentrations
(as % dry solids)
Mixture of prereduced ore,
titania slag, and
vanadium pig
iron
29.6
21
16.7
14.1
13.9
2.6
1.2
0,2
256
Heavy metals
As contained in
pre-reduced ore,
titania slag, and
vanadium pig
Iron
TiO2
CaO
FeO
V2O5
Exposure
Furnace/gas handling system
Furnace/
Titania-rich slag stockpile
Stream
Vanadium pig iron
Component
Fe
V
Ti
Cr
Mn
Si
Ni
Cu
S
P
C
Typical
concentrations
(as % dry solids)
Heavy metals
Fe
V
Ti
Cr
Mn
Ni
Cu
94 to 95
1,1
0,21
0,33
0,14
0,3
0,1
0,03
0.1
0.03
3.0
Exposure
Furnace/pig iron handling
17.2.4 Shaking ladles/vanadium slag upgrading
In this operation, the melt is blown with oxygen while the ladle is agitated in a specially
designed cradle. Scrap and mill scale are added to control the bath temperature at a maximum
o
of 1 400 C, and small amounts of anthracite are added to compensate for carbon losses from
the pig iron. The vanadium transfers to the slag phase, leaving a blown metal (pig iron) product
which can be converted to steel.
The operation is carried out under an extraction hood that extracts fume to a scrubber system.
This ensures that there is virtually no escape of fume during the blowing operation. Some
escape of fume, which will contain oxides of the heavy metals present, occurs during pouring of
hot metal into the shaking ladle and during transfer of the blown metal into the basic oxygen
furnace at the end of the operation. The dust that is collected is slurried and pumped to a
tailings dam.
Table 17.2.4
Shaking ladles
Stream
Component
Typical
concentrations
(as % dry solids)
Dust and fume
from shaking ladle
Mixture of
vanadium pig
iron, pig iron and
vanadium rich
slag
Fe
Mn
V
Ni
Cr
Cu
Al
C
S
P
Mixture of
vanadium pig iron,
pig iron and
vanadium rich
slag
92.5
0.03
0.19
0.11
0.11
0.03
0.20
3.31
0.11
0.02
Pig iron
Heavy metals
Exposure
Shaking ladle area
As contained in
vanadium pig iron,
pig iron and
vanadium rich
slag
Shaking ladle, pig iron handling/
Fe
storage
Mn
V
Ni
Cr
Cu
257
Stream
Component
Vanadium rich slag V2O5
FeO
SiO2
Fe
Cr2O3
TiO2
Al2O3
MnO
MgO
CaO
Typical
concentrations
(as % dry solids)
24,5
26
17
10
5
4,5
4
4
3
2
Heavy metals
V2O5
FeO
Fe
Cr2O3
TiO2
MnO
CaO
(spinel – slagmetal composite)
Exposure
Shaking ladle
Vanadium-rich slag handling/
storage
17.3 Flow diagram
The flow diagram for the vanadium slag production process is shown in Figure 17.3.
258
Figure 17.3
Process diagram for the vanadium slag production process
259
17.4 Process assessment
17.4.1 Hazard identification
The primary occupational hazards relating to vanadium slag production is the generation of
dust and exposure to constituents in the dust. During crushing, screening and magnetic
separation, and in the pre-reduction step, the dust has a composition similar to the ore.
Vanadium and chromium oxides are the primary substances of interest for exposure control.
Table 3.4.2 shows that very low concentrations in dust may exceed threshold limits during
occupational exposure to the dust. Chromium is likely to be in the trivalent state, which is less
hazardous than hexavalent chromium. Although effective ventilation is expected to control
human exposure to dust and fumes in the furnace and ladle areas, some discretion should be
applied in the assessment of potential exposure.
17.4.2 Toxicological assessment
Most of the reported clinical symptoms of vanadium exposure reflect irritation effects on the
respiratory tract. There is insufficient evidence that vanadium causes generalised systemic
effects in humans, except at extremely high concentrations (WHO, 1987: 366). The
toxicological assessment for vanadium has been summarised in Table 3.3.4.30. The toxic
effects of chromium have been listed in Table 3.3.4.8.
Chromium is an essential element in humans. Hexavalent chromium is a human carcinogen,
as outlined in the toxicological assessment for chromium (see Section 3.3.4.8). Trivalent
chromium is poorly absorbed, but allergic eczematous dermatitis has been observed following
industrial exposures.
17.4.3 Exposure assessment
Sampling and analytical methods for vanadium fume and in dust have been listed in Table
3.4.3.6. Lauwerys and Hoet (1993:95) have summarised the available biological exposure
information of vanadium. It has been estimated that 25 per cent of soluble vanadium
compounds may be absorbed through exposure by the pulmonary route. Dermal absorption is
very small. Approximately 90 per cent of circulating vanadium is associated to plasma
transferrin. It is excreted in urine with a biological half-life of 20 to 40 hours. Some excretion
may also occur in feces, and there are data that suggest slow accumulation in the body in the
course of chronic exposure.
Limited data are available on the relationship between vanadium in blood and urine and
airborne concentration levels, and considerable variations have been reported between
vanadium in serum, whole blood and urine. It appears that the background level in whole blood
should lie below 0.1 µg/100 ml, and in urine it is lower than 1 µg/g creatinine. Vanadium levels
in urine are believed to be a better reflection of exposure than blood vanadium. It has been
proposed that exposure assessment is best conducted through pre- and post-shift sampling,
and accumulation may be assessed through monitoring two days after cessation of exposure.
A biological threshold limit of 50 µg/g creatinine has been proposed.
Exposure to chromium can be quantified using sampling and analytical methods listed in Table
3.4.3.6. Determination of chromium in urine is the preferred method for assessing exposure to
3
hexavalent chromium. Exposure to an air concentration of 0.05 mg Cr/m would be reflected in
a urine concentration of 30 µg Cr/g creatinine at the end of the exposure period. Exposure to
trivalent chromium compounds does not correlate with levels of chromium in urine.
Section 3.4.4 provides an overview of medical evaluation procedures that are relevant for
exposure assessment and interpretation of health effects.
260
17.4.4 Risk quantification
The proposed biological threshold limit for vanadium is tentative, and results of biological
monitoring and the calculated hazard quotients for air monitoring should be considered together
to estimate the significance of exposure.
Exposure to total chromium can be assessed directly against the occupational exposure
guideline. For assessment of exposure to hexavalent chromium, biological monitoring and
quantification of cancer risk should be the preferred approach.
17.5 References
Lauwerys, R. R. & Hoet P. 1993. Industrial Chemical Exposure, Guidelines for Biological
Monitoring. Second Edition. Boca Raton: Lewis Publishers, 318p.
Rohrmann, B. 1985. Vanadium in South Africa. Journal of the South African Institute for
Mining and Metallurgy, 85 (5): 141-150.
WHO 1987. Air quality standards for Europe. Geneva: World Health Organisation, p. 361-371.
261
262
18 Typical circuit for zinc recovery from concentrate
18.1 Introduction
This section provides a process description and process diagram of a typical zinc production
facility. The process description and process diagram contain data on the process streams and
identify the hazardous substances as well as potential exposure points.
18.2 Process description
The roast-leach-electrowinning process accounts for at least 80 per cent of annual primary zinc
production. The process consists of five major steps, namely:
•
•
•
•
•
Roasting of sulphide concentrates to produce acid-soluble zinc oxide
Leaching of acid soluble zinc oxide
Precipitation of dissolved iron and other impurities as hydroxides by neutralisation
Purification of solution to remove all impurities by zinc dust cementation
Recovery of zinc from purified electrolyte by electrowinning onto aluminium cathode sheets,
followed by stripping, melting
18.2.1 Roasting
Concentrates containing zinc sulphide and several other impurities are roasted in air at 800 to
o
975 C to form acid-soluble zinc oxide, other less-soluble oxides and sulphur dioxide gas. A
typical analysis of zinc concentrate and calcine (the oxidised roaster product) is given in the
following table.
After cleaning, the SO2 gas is converted to liquid SO2 or sulphuric acid.
Table 18.2.1
Roasting
Stream
Concentrate
Roaster off gas
Component
Zn
S
Pb
SiO2
Al2O3
Ag
Fe
As
Sb
Ge
Sn
Cd
Cu
Co
Ni
Ca
Mn
Mg
Cl
F
Hg
Te
Th
SO2,
F, Cl, Hg, Te, Th
Typical concentrations
(as % dry solids)
46 – 60
30 – 34
1–8
0,1 – 5
0,1 – 2
<0,01
4 – 12
< 0.5
< 0.5
< 0.5
< 0.5
O,1 – 1
0,1 – 1,5
< 0.5
< 0.5
0,1 – 1
0,1 – 0,3
0,05 – 1
< 0,1
<0,1
<0,1
10
263
Heavy metals
Exposure
ZnS, PbS, FeS, Storage/
Fe2O3,
handling/
roasting area
+ Ag, As, Sb, Ge,
Sn, Cd, Cu, Co, Ni,
Ca, Mn, and Hg,
Te, Th - mainly as
sulphides
CaCO3
MnCO3
MnO2
MgCO3
Traces of Hg, Te,
Th - species not
known
Gas
cleaning
–
eventually slimes dam
Stream
Calcine/dust
Typical concentrations
(as % dry solids)
60 – 65
1-2
1 – 10
0,1 – 7
0,1 – 3
< 0,12
4 – 15
< 0.03
< 0.03
< 0,03
< 0.03
< 0.1 – 0,5
0,1 – 2
< 0.05
< 0.05
0,1 – 1,5
< 0,1
0,05 – 1
< 0,1
<0,1
<0,001
Component
Zn
S
Pb
SiO2
Al2O3
Ag
Fe
As
Sb
Ge
Sn
Cd
Cu
Co
Ni
Ca
Mn
Mg
Cl
F
Hg
Heavy metals
ZnO +
Exposure
Roasting area
Pb, Ag, Fe, As
Sb, Sn, Cd, Cu,
Co, Ni, Ca, Mn,
Hg mostly as
oxides with some
sulphides
+ zinc ferrites
(ZnO.Fe2O3)
18.2.2 Leaching and precipitation
The calcine is leached in a 2-stage process using sulphuric acid contained in electrolyte
recycled from the electrowinning step. The first stage leach is a mildly acidic leach, (referred to
as neutral leach) where approximately 80% of the zinc and most of the other trace metals are
dissolved. After filtration the residue from the first stage leach is then re-leached in a second
stage leach under more aggressive conditions (higher acid concentration and higher
temperature) to dissolve the remaining zinc and all the iron. This second stage leach is
referred to as the hot-acid leach (HAL).
The remaining residue from the second stage leach (hot acid leach) is referred to as Pb-Ag
residue. After filtration and washing, this residue is limed and pumped onto a slimes dam.
The filtrate from the hot acid leach contains high levels of iron in the ferric state. This is
precipitated out as ferric hydroxide, which after filtration is limed and pumped onto a slimes
dam. The iron residue will contain trace of other elements such as As, Sb, Ge and Sn. The
iron-free zinc sulphate filtrate is pumped back to neutral leach.
Although both the Pb-Ag and Fe residues are washed thoroughly during filtration, some soluble
losses do occur and as a result traces of the various elements end up on the slimes dams.
Table 18.2.2
Leaching and precipitation
Stream
Neutral leach
liquor
Component
Zn
Mn
Mg
Typical
concentrations
Heavy metals
(as % dry solids)
140 g/l
ZnSO4
5 g/l
Mn, As, Sb, Sn, Cd,
5 g/l
Cu, Co, Ni, as
sulphates
As, Sb, Ge, Sn, Cd,
Cu, Co, Mn, Ni
264
Exposure
Leach area
Stream
Neutral
residue
Hot acid
liquor
Hot acid
residue
Component
leach Zn
Typical
concentrations
Heavy metals
(as % dry solids)
15% of solids
ZnO + ZnO.Fe2O3
Pb, SiO2, Al2O3,
Ag, ZnO.Fe2O3,
As, Sb, Ge, Sn, Cd,
Cu, Co, Mn, Ni
leach Zn
100 g/l
Fe
20 g/l
Thickener solids
Small amounts of
Pb, Ag, As, Sb, Ge,
Sn, Cd, Cu, Co, Mn,
Ni as sulphides
ZnSO4
As, Sb, Ge, Sn, Cd, traces < 10 mg/l
Cu, Co, Mn, Ni
leach Pb/Ag cake:
Major portion
Pb, Ag
ZnO.Fe2O3
SiO2
+
As, Sb, Ge, Sn, Cd, Traces
Cu, Co, Mn, Ni as
sulphides
Iron cake:
Fe2O3.SO3.H2O
+FeO.OH
Exposure
As, Sb, Sn, Cd, Cu,
Co, Mn, Ni as
sulphates
Pb and Ag as
sulphides
ZnO.Fe2O3
Leach area
Filter cake
As, Sb, Ge, Sn, Cd,
Cu, Co, Mn, Ni as
sulphides
Filter cake
Major portion
Traces of soluble Traces
Zn, Ge, As, Sb, Sn,
Cd, Cu, Co, Mn, Ni
as sulphates and
hydroxides
Fe2O3.SO3.H2O
+FeO.OH
Traces of soluble Zn,
Ge, As, Sb, Sn, Cd,
Cu, Co, Mn, Ni as
sulphates and
hydroxides
18.2.3 Purification
The filtrate from the neutral leach is pumped to a purification circuit where dissolved impurities
such as Cd, Cu, Co and Ni are removed from the zinc solution by zinc dust cementation.
Arsenic is usually added in the purification step to catalyse the cementation of Co and Ni. Two
residues are typically produced during purification, namely, a Cd-Zn cake and a Cu-Ni-Co-AsZn cake. Both cakes may be stockpiled, processed, upgraded or sold.
Table 18.2.3
Purification
Stream
1 st stage
purification
residue
Component
Zn
Co, Ni, Cu, As,
Zn
Typical
concentrations
Heavy metals
Exposure
(as % dry solids)
Majority
Zn, Cu, Ni, Co, as Purification area
metals (cemented
out)
+ As species
Co, Cu, As, Zn
etc. as sulphates
2 nd stage
purification
residue
Zinc dust
Cd
Zn
30 – 60
Zn/Cd as metals
(cemented out)
Purification area
Zn
100
Zn
Reagent As2O3
As2O3
Zn storage/
handling area
Reagent storage/
handling
As2O3
265
18.2.3 Electrowinning
The purified solution from the purification step is then pumped to the electrowinning circuit
where the zinc is recovered as metal sheets on aluminium cathodes.
During electrowinning zinc sulphate is reduced to zinc metal and sulphuric acid is generated.
This sulphuric acid is recycled to the leach step. The electrowinning time may vary from 24
hours to 96 hours. After the desired electrowinning time has elapsed the zinc deposits are
stripped as sheets from the cathodes, melted and cast into ingots. Alloying elements may be
added during the melting process to produce numerous alloys.
Table 18.2.4
Electrowinning
Stream
Typical
concentrations
as % dry solids
basis
99,99
Component
Zinc product
Zn
Acid mist
ZnSO4
MnSO4
MgSO4
H2SO4
Not known
Heavy metals
Zn
ZnSO4
MnSO4
Exposure
Cell house/
Melting/
casting area
Cell house
18.2.4 Effluent treatment
A bleed is taken from the spent electrolyte to control the build up of impurities such as Mg and
Mn. The bleed solution is neutralised with lime and pumped onto a slimes dam. Zinc is
selectively precipitated from solution as Zn(OH)2. These solids are returned to the neutral
leach.
Table 18.2.5
Effluent treatment
Stream
Slimes
Component
Gypsum
Typical
concentrations
as % dry solids
basis
Majority
+ trace amounts
of heavy metals
Lime
Calcine
CaSO4.2H2O
Mn(OH)2
CuO
Traces of “toxic
metals”
as hydroxides
Zn(OH)2
CaSO4.2H2O +
Mn as hydroxides
Zn
Zn(OH)2
Heavy metals
Majority
Zn(OH)2
+
Mn, Mg, Ca as Traces
hydroxides
+ CaSO4.2H2O
CaO
91,3
MgO
1,7
Al2O3
0,3
0,3
FeO
0,1
MnO
0,8
SiO2
Fe2O3
See previous
See previous
266
Exposure
Slimes dam
Recycle liquor
CaO
MnO
FeO
Fe2O3
Lime storage/handling
See previous
Calcine handling
18.3 Flow diagram
The flow diagram for a typical circuit for zinc recovery from concentrate is shown in Figure
18.3..
18.4 Process assessment
18.4.1 Hazard identification
Occupational exposure assessment will be determined by the composition of the concentrate
feed. Specifying the feed composition can control the presence of heavy metals, and the
discussion below does not infer that exposure would in fact occur in all zinc production facilities.
In the generic example discussed here, the presence of lead with zinc in nature is reflected by
its presence in the concentrate at a level of up to eight per cent. Other heavy metals are
expected to be present at low concentrations in the concentrate. In the roasting area, zinc
oxide may be present in the occupational environment, as well as lead as an oxide or sulphate.
The purification step is a closed system, but exposure to zinc, copper, nickel and cobalt, as
well as arsenic (possibly as arsine) should be considered. In the electrowinning step zinc
sulphate could be carried in the acid mist, as well as manganese. The concentration of
manganese is however unknown and it is uncertain whether it would be of any significance.
Calcium oxide may be of importance in the lime storage and handling areas. Manganese and
copper may be present in dust at the slimes dams.
267
Figure 18.3
Process diagram for a typical circuit for zinc recovery from
concentrate
268
18.4.2 Toxicological assessment
Arsenic and its compounds have been confirmed as carcinogens.
There are no quantitative data available for absorption from copper deposited in the lungs. At
relatively high occupational exposures, copper dust and fumes are respiratory irritants.
Exposure to copper and copper oxide fumes at high concentrations has been responsible for
metal fume fever. Toxic effects of copper have been documented in Table 3.3.4.10.
The toxicity of lead has a relationship with the interference with different enzyme systems. For
this reason, almost all organ systems may be considered potential targets for lead toxicity, and
a wide range of biological effects have been documented. Among these are effects on haem
biosynthesis, the kidneys, the immune system, neurotoxic effects, reproductive effects, and
also cardiovascular, hepatic, endocrynal and gastrointestinal effects. The toxic effects of lead
have been summarised in Table 3.3.4.13.
Manganese compounds in various forms are considered to be neurotoxic, with subclinical
effects occurring at low exposure levels. Section 3.3.4.14 presents an overview of the
toxicology of manganese.
Calcium in itself is not toxic to humans, but in the form of calcium oxide it acts as an irritant.
The toxicology of calcium oxide has been discussed in Section 3.3.4.7.
Occupational exposure to cobalt metal, dust and fume is associated mainly with pulmonary
fibrosis and sensitisation. The toxicicity of cobalt and its compounds has been discussed in
Section 3.3.4.9.
The most widely known systemic effect resulting from acute inhalation of freshly formed zinc
oxide fumes is a disease called metal fume fever. The toxicity of zinc has been discussed in
Section 3.3.4.32.
18.4.3 Exposure assessment
Area monitoring and personal sampling for arsenic and its compounds may be conducted
using NIOSH Methods 7300, 7900 and 7901, and OSHA ID 105 and OSHA CIM. NIOSH
Method 7900 is valid only for particulate-associated inorganic arsenic compounds. The most
appropriate method for the exposure scenerio has to be selected.
Mean serum and blood levels of arsenic vary greatly depending on the level of seafood content
in the diet. Therefore, when employees have not been instructed to refrain from eating fish or
shellfish for two to three days before biological monitoring, high levels of arsenic may be found
that might not be associated with occupational exposure.
In the past, biological monitoring for assessment of occupational exposure was conducted by
measuring the total amount of arsenic in urine at the end of a shift. It is however now well
established that inorganic arsenic, monomethylarsonic acid, and cacodylic acid in urine is the
method of choice. Monitoring of employees exposed to inorganic arsenic using this method is
not influenced by organoarsenicals from marine origin.
Some controversial results may be obtained in the correlation between air-concentration
exposure assessment and biological monitoring. It has been established that background
levels of the sum of the three metabolites of arsenic (inorganic arsenic, monomethylarsonic
acid, and cacodylic acid) in urine vary between 10 µg/l and 50 µg/l. It appears that the best
3
relationship for occupational exposure at air concentrations between 50 and 200 µg As/m
269
would lead to post-shift concentrations of the total metabolites between 54 and 88 µg/g
creatinine (Lauwerys and Hoet, 1993: 25).
Area monitoring and personal sampling for the lead and its compounds may be conducted
using NIOSH Methods 7082, 7105, 7300, 7505, and OSHA ID 121 and ID 125 G (see Table
3.4.3.6). The most appropriate method has to be selected for the particular exposure scenario.
Approximately 50 per cent of the lead deposited in the lung is absorbed, whereas less than 10
per cent of ingested lead normally gets into the systemic circulation. Dermal absorption of lead
is also a significant route of exposure. Biological tests for lead exposure can be divided into
two groups, i.e. those directly reflecting the exposure through assessment of the amount stored
in blood, urine, hair, and bone, and those indicating the early biological effects of lead in
relation to exposure. These effects are shown in haemoglobin, haematocrit, stippled cells,
coproporphyrin in urine, etc. In a steady-state situation, lead in blood is considered to be the
best indicator of recent exposure. It has been shown that under low exposure conditions
3
(environmental levels) an increase of 1 µg/m in air leads to an increase of 1 to 2 µg/100 ml of
whole blood. There is however not a clear correlation between air concentrations and blood
lead at higher exposure concentrations, and it is therefore difficult to assess occupational
exposures. The situation is further complicated by the fact that lead is a ubiquitous pollutant,
leading also to nonoccupational exposures. As a rule, it is accepted that blood-lead levels of
non-occupationally exposed individuals lie between 15 and 30 µg/100 ml of whole blood.
Levels up to 70 µg/100 ml in lead-related occupations are normally considered acceptable.
However, subclinical effects may occur at levels exceeding 50 µg/100 ml of whole blood. The
World Health Organisation has proposed 40 µg/100 ml as the maximum tolerable lead value in
blood for adult male workers, and 30 µg/100 ml for women of childbearing age (Lauwerys and
Hoet, 1993:86). No guideline has been proposed for biological monitoring of lead exposure in
South Africa.
Lead in urine is often preferred to blood analysis, and reflects the amount of lead recently
absorbed. There is however a poor association between lead in blood and lead in urine, and
blood-lead is considered the more reliable measure for routine assessment of lead exposure. A
concentration of lead in blood of 50 µg /100 ml usually corresponds with a level of 150 µg /g
creatinine, but the correlation across a wider exposure range is poor. The level of 150 µg Pb/g
3
creatinine corresponds with an air concentration of 50 µg Pb/ m .
Although it has been suggested that hair provide a time-integrated index of lead absorption, it
has drawn limited interest because of potential lead contamination in hair-washing procedures
(Lauwerys and Hoet, 1993:86).
The normal concentration of manganese in urine is usually less than 3 µg/l, and in whole blood
and plasma less than 1 µg/100 ml and 0.1 µg/100 ml, respectively. There is however no
consistent relationship between manganese exposure and blood levels, and it appears that
measurement of urinary levels is the preferred method for assessment. The relationship with
exposure is however not that well-defined, and no biological threshold limit value has been
proposed (Lauwerys and Hoet, 1993: 71).
Table 3.4.2.6 lists sampling and analytical methods for zinc oxide. Zinc is an essential element
and is present in abundance in various parts of the human body. Biological monitoring would
therefore not provide useful information for exposure assessment.The levels of zinc in healthy,
nonexposed individuals in serum and plasma are in the order of 0.1 mg/100 ml. Urinary
excretion is in the range of 0.1 to 1.2 mg over a period of 24 hours. Zinc in blood (whole blood,
plasma and serum) and urine have been used as biological indicators of exposure, but no
correlation has been established between these values and the levels of exposure, and no
biological threshold has been set. In general, after exposure the levels in blood and urine are
significantly higher than the controls.
270
Section 3.4.4 provides an overview of medical evaluation procedures that are relevant for
exposure assessment and interpretation of health effects.
18.4.4 Risk quantification
In controlling exposure to lead at the concentrate storage and handling steps it is not adequate
3
to control dust levels to 10 mg/m , because the level of lead may be above its occupational
3
exposure limit at particulate levels lower than the 10 mg total dust/m threshold.
Because of its irritation effects, exposure to calcium oxide should be assessed against
maximum concentration peaks rather than average values.
For exposure to zinc oxide, the concentration at which metal fume fever would develop, is not
entirely certain, but it has been estimated that symptoms are unlikely to develop at air
3
concentrations below 15 mg/m (Elinder & Piscator, 1979: 682). The ACGIH guidelines of 5
3
3
mg/m for zinc oxide fume and 10 mg/m for zinc oxide dust therefore provide adequate
margins of safety. It is recommended that exposure to zinc oxide, as well as for cobalt and
copper, be assessed against maximum concentration peaks rather than average values. This
is because the manifestation of irritation effects is more concentration dependent than time
dependent.
Cancer risks relating to exposure to arsenic and its compounds can be quantified through
interpretation of exposure data and the respective dose-response information.
18.5 References
Kirk-Othmer, Encyclopaedia of Chemical Technology. Zinc and zinc alloys. Fourth Edition
Volume 25 P 789 – 835.
Van Niekerk, C. J. & Begley, C. C. 1991. Zinc in South Africa. Journal of the South African
Institute for Mining and Metallurgy, 91 (7): 233-248.
271

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