Risk Assessment of STX group toxins in Abalone v13

Transcription

Commercial In Confidence
Semi-Quantitative Risk Assessment of
Paralytic Shellfish Toxins in Canned
Australian Abalone
Catherine McLeod, Gustaaf Hallegraeff, Natalie Homan, Andreas
Kiermeier and John Sumner
Project 2008/909
May 2010
South Australian Research & Development Institute
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Executive Summary
European Commission regulation 854/2004 requires abalone to be grown and
harvested from production areas that are classified and have marine biotoxin
monitoring programmes in place. It is generally accepted that Australian abalone are
a low risk shellfish species with respect to marine biotoxins, because unlike bivalve
molluscs abalone do not filter feed and significant levels of biotoxins have not been
detected in Australian species. However, there was a lack of objective scientific
information on the level of risk associated with marine biotoxins and abalone to
substantiate this claim. This risk assessment was undertaken to independently
evaluate the probability of humans living in the EU and China becoming ill from
paralytic shellfish poisoning (PSP) via the consumption of canned Australian wild
caught abalone. The risk was evaluated using both qualitative and semi-quantitative
methods.
Key findings of this risk assessment are:
- 52 routine marine biotoxin analyses of Australian abalone have been
undertaken (2002 – 04) and no marine biotoxins were detected.
- One ‘adverse sample’ of abalone was taken during a significant algal bloom
event and 123 µg 100g-1 paralytic shellfish toxins (PSTs) was detected in the
gut tissue; mussels sampled during the same event contained levels of
>10,000 µg 100g-1. This demonstrates the extremely low propensity of
abalone to uptake marine biotoxins compared with bivalves.
- A laboratory based study on the uptake of PSTs by Australian Greenlip
abalone also confirmed that abalone have limited ability to bioaccumulate
these toxins.
- The pre-canning process (removal of side foot epithelial layers) decreases
levels of PSTs in abalone by ~75% and the thermal canning process likely
reduces the remaining PSTs by 50%, resulting in an overall reduction of
87.5%. This suggests that abalone, potentially containing levels of
~600 µg 100g-1 in the whole animal prior to canning, would be compliant with
the regulatory limit of 80 µg 100g-1 following canning.
- Given the limited ability of Australian abalone to take up significant levels of
PSTs it is extremely unlikely that levels above 600 µg 100g-1 would occur.
The semi-quantitative risk estimate derived in this assessment predicts that 0.01
people may potentially become ill in the EU per annum from the consumption of
canned wild caught Australian abalone. This equates to only one case of illness
every 100 years (‘illness’ includes cases with minor symptoms and is not necessarily
severe). Likewise the estimated burden of illness in China was very low with 0.53
predicted illnesses per annum from a total of 12,180,000 servings of canned wild
caught Australian abalone. A qualitative risk estimate derived in this assessment also
confirms that the probability of EU and Chinese consumers becoming ill from PSP via
the consumption of canned wild caught Australian abalone is Extremely Low. The
extremely low probability of PSP illness resulting from the consumption of canned
wild caught Australian abalone provides guidance for consideration of commensurate
risk management options.
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Contents
Terms of Reference............................................................................................................... 4
Definitions ............................................................................................................................. 7
Introduction ........................................................................................................................... 9
Hazard Identification............................................................................................................ 11
Hazard Characterisation...................................................................................................... 14
Exposure Assessment......................................................................................................... 18
Risk Characterisation .......................................................................................................... 38
Uncertainty.......................................................................................................................... 43
Conclusions and Recommendations ................................................................................... 44
References.......................................................................................................................... 45
Appendix One ..................................................................................................................... 50
Appendix Two ..................................................................................................................... 54
Appendix Three................................................................................................................... 57
Copyright Australian Seafood CRC and the South Australian Research and Development
Institute 2010.
This work is copyright. Except as permitted under the Copyright Act 1968 (Cth), no part of
this publication may be reproduced by any process, electronic or otherwise, without the
specific written permission of the copyright owners. Neither may information be stored
electronically in any form whatsoever without such permission.
The Australian Seafood CRC is established and supported under the Australian
Government’s Cooperative Research Centres Programme. Other investors in the CRC are
the Fisheries Research and Development Corporation, Seafood CRC company members,
and supporting participants.
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1.
Terms of Reference
1.1 Background
In February 2007 the European Commission (EC) undertook a mission to Australia to
evaluate the control systems in place for the production of fishery, aquaculture
products and live bivalve molluscs. A key finding of the mission was that “marine
gastropods (i.e. abalone) should undergo official controls at least equivalent to EC
regulation 854/2004”. EC regulation 854/2004 includes the requirement that
gastropods (including abalone) must be grown and harvested from production areas
that are classified. This means that abalone being exported from Australia to the
European Union (EU) are required to be taken from classified production areas that
have microbiological, chemical and biotoxin monitoring programmes to control the
food safety risks. Following the 2007 EC mission to Australia the Australian
Quarantine and Inspection Service (AQIS) were unable to supply health certificates
for abalone being exported from Australia to the EU because abalone-harvesting
areas in Australia were not classified. Due to the lack of information on the level of
food safety risk associated with wild-caught Australian abalone, it was suggested that
an assessment of the risks should be undertaken. This would inform risk
management considerations for wild-caught abalone and facilitate improved trade
negotiations on this issue between Australia and the EU.
1.2 Scope
The scope of the risk assessment was refined in consultation with the project ‘Expert
Consultation Group’ (comprising scientists, industry representatives and state and
federal regulators) to focus on paralytic shellfish toxins (PSTs) in wild caught canned
abalone products. The rationale for the refinement of the scope is described below:
- Monitoring of bivalve shellfish growing areas in Australia provides gatherers and
growers with warnings that bivalve shellfish may be in danger of containing
microbiological or chemical hazards. The warnings for bivalve shellfish also
potentially provide an indication of risk for abalone caught within these areas.
- Most areas where abalone are commercially fished are outside currently
monitored bivalve shellfish growing areas and, therefore, warnings of potential
microbiological and chemical hazards would not be provided through current
bivalve shellfish monitoring programmes.
- Many zones within the wild-capture abalone fishery in Australia are remote from
human habitation and are not impacted by any actual or potential microbiological
pollution sources. If these areas were to be classified many would likely achieve
the classification status of ‘Approved Remote’.
- Current Australian requirements for ‘Approved Remote’ areas are for a minimal
microbiological monitoring programme (e.g. two samples/annum) – this approach
is currently accepted by the EC. However ‘Approved Remote’ areas are still
required to have marine biotoxin management plans, including routine biotoxin
analysis (e.g. minimum of fortnightly sampling for the EU) (Anon 2009b).
- Due to the intensity of the marine biotoxin requirements compared with
microbiological requirements the focus of this risk assessment is biotoxin
contamination of abalone (as opposed to microbiological contamination).
- Researchers based in Europe are currently assessing microbiological risks in
abalone via an EU Framework 7 project entitled ‘Sustainable Development of
European SMEs Engaged in Abalone Aquaculture’ (SUDEVAB). Future data
exchange may result in a more holistic assessment of risk in the longer term.
- To date, of the eight different marine biotoxin groups, only the PSTs have been
reported in the literature as being detected in abalone. Out of the characterised
marine biotoxins identified PSTs produce the most severe adverse symptoms in
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humans with extreme cases resulting in fatal respiratory paralysis. Therefore, this
risk-based assessment focuses on PSTs as opposed to other marine biotoxins
which produce less severe symptoms in humans.
The majority (~80%) of Australian abalone exported to ‘other countries’ (including
the EU) is canned (section 6.2). For this reason the hazard-commodity
combination of PSTs and canned abalone are covered in this assessment. As a
significant amount of frozen and live product is also exported to Asia,
supplementary risk characterisation data for PSTs in ‘fresh, chilled and frozen’
abalone are provided in Appendix One. Relatively small quantities of modified
atmosphere packaged (MAP) abalone are exported to Asia and, therefore, are
not covered in this assessment.
Aquaculture abalone production in Australia is still relatively low, comprising
<10% of total Australian production. It is likely that the majority of aquaculture
abalone is sold in the frozen format in Asia and Australia (section 6.2).
Due to the relatively low level of aquaculture abalone production in Australia and
the predominantly frozen format the risk has not been characterised in this
assessment for abalone produced using aquaculture techniques.
Future work may focus on broadening the scope to include other marine biotoxins
and potential microbiological hazards, and covering additional abalone product
types.
1.3 Statement of Purpose
This project was jointly commissioned by the Australian Seafood CRC (and
associated participants) and the Abalone Association of Australasia to primarily
provide an assessment of the risks of PSTs to consumers of canned wild caught
abalone. The specific project objectives were to:
- Assess the probability of humans living in the EU and China becoming ill from
paralytic shellfish poisoning (PSP) via the consumption of canned Australian wild
caught abalone.
- Identify key information gaps that may influence the quality of the risk
assessment.
This risk assessment provides both qualitative and semi-quantitative risk estimates.
The qualitative estimate ranks the potential risk of PSP from consumption of canned
abalone as low, moderate or high. The semi-quantitative risk estimates comprise a
‘Risk Ranking’ score of between 0 and 100 and an approximation of the total
predicted illnesses/annum in Europe and China from the consumption of canned
Australian abalone. Supplementary information contained in Appendix One provides
a Risk Ranking and predicted illnesses/annum for the consumption of ‘fresh, chilled
and frozen’ abalone in China.
1.4 Method
This risk-based assessment follows the concepts described in the “Draft Working
principles for Risk Analysis for Application in the Framework of the Codex
Alimentarius” (Codex Alimentarius Commission 2003) using existing data and
literature.
1.5 Outcomes
The information generated in this risk assessment will provide the Australian
regulatory authorities and industry with necessary data to support:
- Technical market access discussions on abalone with the Health and
Consumer Protection Directorate General (DG SANCO) of the EC;
- Input into the development of the Codex abalone standard;
- Technical discussions with other key markets such as China on an ‘as
needed’ basis; and
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The development of potential risk management strategies.
Two other related pieces of work have also been commissioned:
- Experimental work to determine the anatomical distribution and depuration of
PSTs in abalone (Homan et al. 2010); and
- A briefing of risk management options for PSTs in Australia. This also includes
evaluation of the current Australian and EU regulations for marine biotoxins.
1.6 Project Expert Consultation Group
An Expert Consultation Group was engaged to guide the methodology used, provide
advice on technical aspects, and review and give insights on the interpretation of
data. The Expert Consultation Group comprised:
Dr Fay Stenhouse/Lynda Feazey (AQIS)
Ray Brown (TSQAP)
Ken Lee/Clinton Wilkinson (SASQAP)
Anthony Zammit (NSWFA)
Professor Gustaaf Hallegraeff (UTAS)
Dr Susan Blackburn (CSIRO)
Dr Wayne O’Connor (NSW DPI)
Tony Johnston (Chair, AAA)
Dean Lisson (Chair, ACA)
Alex Ziolkowski (AAA)
Brenda Hay (AquaBio Consultants, NZ)
Jayne Gallagher (Seafood CRC)
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2.
Definitions
The definitions used are primarily based on the Codex Alimentarius Commission
Principles and Guidelines for the Conduct of Microbiological Risk Assessment (Anon
1999) and supplemented with definitions found in other key texts.
Acute reference dose (ARfD) - An estimate of the amount of substance in food,
normally expressed on a body-weight basis (mg/kg or mg/kg of body weight), that
can be ingested in a period of 24 hours or less without appreciable health risk to the
consumer on the basis of all known facts at the time of evaluation.
Allowable Daily Intake – See tolerable daily intake (TDI)
Exposure Assessment - The qualitative and/or quantitative evaluation of the likely
intake of biological, chemical, and physical agents via food as well as exposures from
other sources if relevant.
Hazard - A biological, chemical or physical agent in, or condition of, food with the
potential to cause an adverse health effect.
Hazard Characterization - The qualitative and/or quantitative evaluation of the
nature of the adverse health effects associated with the hazard.
Hazard Identification - The identification of biological, chemical, and physical agents
capable of causing adverse health effects and which may be present in a particular
food or group of foods.
LD50 - The dose of a substance required to cause death in half the members of a
tested population after a specified test duration.
Lowest Observed Adverse Effect Level (LOAEL) - The lowest concentration or
amount of a substance found by experiment or observation which causes an adverse
alteration of morphology, function, capacity, growth, development or life span of a
target organism distinguished from normal organisms of the same species under
defined conditions of exposure.
No Observable Adverse Effect Level (NOAEL) - The level of exposure of an
organism found by experiment or observation, at which there is no biologically or
statistically significant increase in the frequency or severity of any adverse effects in
the exposed population when compared to its appropriate control.
Paralytic Shellfish Toxins (PSTs) – A group of ~30 hydrophilic toxins produced
primarily by dinoflagellates.
Paralytic Shellfish Poisoning (PSP) – Human illness induced by the consumption
of significant levels of PSTs.
Quantitative Risk Assessment - A Risk Assessment that provides numerical
expressions of risk and indication of the attendant uncertainties (stated in the 1995
Expert Consultation definition on Risk Analysis).
Qualitative Risk Assessment - A Risk Assessment based on data which, while
forming an inadequate basis for numerical risk estimations, nonetheless, when
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conditioned by prior expert knowledge and identification of attendant uncertainties,
permits risk ranking or separation into descriptive categories of risk.
Risk - A function of the probability of an adverse health effect and the severity of that
effect, consequential to a hazard(s) in food.
Risk Analysis - A process consisting of three components: risk assessment, risk
management and risk communication.
Risk Assessment - A scientifically based process consisting of the following steps:
(i) hazard identification;
(ii) hazard characterization;
(iii) exposure assessment; and
(iv) risk characterization.
Risk Characterization - The process of determining the qualitative and/or
quantitative estimation, including attendant uncertainties, of the probability of
occurrence and severity of known or potential adverse health effects in a given
population based on hazard identification, hazard characterization and exposure
assessment.
Risk Communication - The interactive exchange of information and opinions
concerning risk and risk management among risk assessors, risk managers,
consumers and other interested parties.
Risk Estimate - Output of Risk Characterization.
Risk Management - The process of weighing policy alternatives in the light of the
results of risk assessment and, if required, selecting and implementing appropriate
control options, including regulatory measures.
Sensitivity analysis - A method used to examine the behaviour of a model by
measuring the variation in its outputs resulting from changes to its inputs.
Tolerable daily intake (TDI) - an estimated maximum amount of an agent,
expressed on a body mass basis, to which an individual in a (sub)population may be
exposed daily over the individuals lifetime without appreciable health risk (Anon
2009c). Sometimes referred to as Allowable Daily Intake.
Transparent - Characteristics of a process where the rationale, the logic of
development, constraints, assumptions, value judgements, decisions, limitations and
uncertainties of the expressed determination are fully and systematically stated,
documented, and accessible for review.
Uncertainty analysis - A method used to estimate the uncertainty associated with
model inputs, assumptions and structure/form.
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3.
Introduction
Paralytic Shellfish Toxins (PSTs) are naturally occurring toxins produced primarily by
a group of eukaryotic microalgae known as dinoflagellates. They are also produced
by certain types of cyanobacteria (commonly called ‘blue-green algae’) and
macroalgae (Etheridge et al. 2004; Kotaki et al. 1983; Llewellyn and Negri 2006).
The key dinoflagellates that produce PSTs include: Alexandrium minutum,
A. tamarense, A. catenella, A. fraterculus, A. fundyense, Gymnodinium catenatum
and Pyrodinium bahamense (Llewellyn and Negri 2006; Negri et al. 2003).
Dinoflagellates that produce PSTs occur throughout the world (Figure 1) and PSTs
have been detected in various marine organisms in the coastal waters of many
countries within Europe, Africa, North America, Central and South America, Asia and
Oceania (van Egmond et al. 2004). It has been suggested that PST-producing
dinoflagellate blooms have increased in frequency, intensity and geographic
distribution since the 1970’s (Bolch and de Salas 2007; Hallegraeff 1993).
Figure 1.
Global distribution of PST-producing dinoflagellates (Gymnodinum
catenatum, Alexandrium spp. and Pyrodinium bahamense). Kindly
provided by Professor Gustaaf Hallegraeff.
Changes in environmental factors such as light intensity, nutrient availability,
seawater temperature and salinity can promote the growth of PST-producing
dinoflagellates and result in significant blooms of these species. Bivalve molluscan
shellfish are filter feeding animals that selectively feed on microorganisms in the
seawater, including dinoflagellates. When toxic dinoflagellate blooms occur
significant levels of the PSTs can accumulate in the flesh of bivalve molluscan
shellfish, due to their ability to filter large quantities of seawater e.g. pacific oysters
have been shown to have a filtration rate of between 2 and 4 L h-1 for particles above
7 µM in size (Ropert and Goulletquer 2000). Due to their ability to retain the toxins
produced by the algae in their flesh there has been a multitude of human illness
outbreaks of PSP related to the consumption of bivalve molluscan shellfish
throughout the world (van Dolah, 2000). PSP produces mild to severe symptoms in
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humans ranging from tingling and numbness of lips to fatal respiratory paralysis (van
Egmond et al. 2004;Gessner and Middaugh, 1995).
Abalone are members of the Haliotidae family, class Gastropoda and their feeding
habits are significantly different from bivalve shellfish (i.e. they do not filter large
quantities of seawater). They are grazing animals that utilise a structure known as a
radula which is a toothed ‘tongue’ to scrape and cut food prior to ingestion of their
preferred food source of red or brown macroalgae (seaweed). Abalone have not
been documented to be associated with PSP poisoning of humans worldwide.
However PSTs have been detected in the tissues of abalone from Spain and South
Africa (Bravo et al. 2001; Bravo et al. 1999; Llewellyn and Negri 2006; Martinez et al.
1993; Pitcher et al. 2001).
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4.
Hazard Identification
“The identification of biological, chemical and physical agents capable
of causing adverse health effects and that may be present in a particular
food or group of foods (Anon 1999)”
4.1 Paralytic Shellfish Toxins
The PSTs are a group of hydrophilic toxins comprised ~30 related saxitoxin (STX)
analogues that have been identified in toxic algae and shellfish (Dell'Aversano et al.
2005; Dell'Aversano et al. 2008; van Egmond et al. 2004; Alexander et al. 2009).
There are four main groups of STX analogues:
(i)
The carbamate toxins (e.g. STX, GTX 1-4 and neoSTX);
(ii)
The decarbamoyl toxins (e.g. dcSTX, dcGTX1-4);
(iii)
The N-sulfocarbamoyl toxins (e.g. B1 [GTX5], B2 [GTX6] and C1–4); and
(iv)
The deoxydecarbamoyl toxins.
The potencies of the various analogues vary by more than 10 fold with the carbamate
toxins being the most potent group (Alexander et al. 2009; Deeds et al. 2008;
Etheridge 2010; Oshima 1995).
4.2 Toxin Profiles in Algae and Shellfish
The toxicity of dinoflagellates varies between and within species (Anderson et al.
1994; Anderson et al. 1990; Chang et al. 1997; Wang et al. 2006). The variation in
toxicity is related to differences in the toxin profiles (e.g. composition) and in the
quantity of each toxin analogue (concentration) present (Deeds et al. 2008). Many
factors appear to influence the toxin composition and concentration within
dinoflagellates including: geographical location, nutrient availability, temperature and
other environmental factors (Anderson et al. 1994). The PSTs are reported to be
generally heat stable at acidic pH but unstable under alkaline conditions (Alexander
et al. 2009; van Egmond et al. 2004).
Studies on PST profiles have demonstrated differences in the quantities and types of
analogues present in the causative algal species when compared with contaminated
shellfish. This is likely due to physico-chemical driven reactions that are catalysed by
enzymes and bacteria contained within shellfish (Dell'Aversano et al. 2008; Jaime et
al. 2007; Llewellyn and Negri 2006). Consistent with this, various researchers have
identified significant differences between the toxin profile in gastropods (including
abalone) and the PST-producing dinoflagellate or macroalgae thought to be
responsible for toxicity. In several instances STX has been found to be the
predominant analogue detected in the gastropod muscle tissue compared with GTX
and C toxins detected in the potentially causative toxic algae (Homan et al. 2010;
Jaime et al. 2007; Kotaki et al. 1983; Martinez et al. 1993; Pitcher et al. 2001). This
indicates a high degree of toxin transformation in abalone.
4.3 Symptoms of Paralytic Shellfish Poisoning
The symptoms of Paralytic Shellfish Poisoning (PSP) intoxification in humans range
from mild to severe and are categorised in Table 1 (Alexander et al. 2009; Gessner
and Middaugh, 1995; van Dolah, 2000). In fatal cases in which artificial respiration is
not able to be administered, death is caused by respiratory paralysis.
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Table 1.
Symptoms of Paralytic Shellfish Poisoning in Humans
Mild
Prickly sensation in
fingers and toes
Tingling sensation or
numbness around lips
Headache
Dizziness
Nausea
Moderate
Extremity numbness and tingling
Incoherent speech
Stiffness and non coordination
of limbs
General weakness and feeling
of lightness (floating sensation)
Slight respiratory difficulty/
shortness of breath and rapid
pulse plus backache
Severe
Muscular/limb
paralysis
Pronounced
respiratory difficulty
Choking sensation
Vomiting
Dry mouth
Diarrhoea
4.4 PSP Related to Bivalve Shellfish Consumption
There have been many written accounts of PSP in humans dating from 1793 through
to current times. The vast majority of PSP cases have involved the consumption of
bivalve shellfish (e.g. mussels, oysters, clams, scallops etc) (Chung et al. 2006;
Gessner and Middaugh 1995; White et al. 1993). PSP cases have been documented
throughout the world including in North America & Canada, Europe, Japan, China,
South America, South Africa, Australia & New Zealand, Southeast Asia and India.
These illness outbreaks have been reviewed thoroughly in a number of historical and
recent publications, and the majority of cases resulted in mild and moderate
symptoms (Alexander et al. 2009; van Dolah, 2000; van Egmond et al. 2004).
Overall, one estimate suggests that there are ~2000 human cases of PSP worldwide
through fish or shellfish consumption reported each year with a 15% mortality rate
(Hallegraeff 1993).
However, there have been very few reported cases of PSP intoxication resulting from
consumption of bivalve shellfish in Australia. Five mild human poisoning cases
associated with the consumption of wild bivalve shellfish from Tasmania were
reported in the literature – the causative dinoflagellate was purported to be
G. catenatum which predominantly produces the N-sulfocarbamoyl toxins (which are
less potent than other STX group toxins), accounting for the relatively mild symptoms
in humans (Hallegraeff 1992). Other anecdotal cases occurred when levels
exceeding 30,000 µg 100g-1 flesh were detected in shellfish grown in Tasmania. The
victims were farmers who consumed a shellfish broth nightly. Commercial production
areas were all closed at the time (Personal Communication, Alison Turnbull,
Tasmanian Shellfish Quality Assurance Programme, Feb 2010). Despite these
reports, none of the cases have been confirmed by public health authorities.
4.5 PSP Related to Gastropod Consumption
While most PSP cases reported worldwide involve the consumption of bivalves, a
few cases have resulted from the consumption of non-traditional vectors such as
crustaceans, fish and gastropods. Several reviews have been undertaken on non
traditional vectors of PSP. These reviews highlight cases of human illness caused by
the consumption of gastropods, which occurred in Malaysia, China and the USA. The
species of gastropod reportedly eaten by victims of these outbreaks were; sitka
periwinkles (Littorina sitkana), northern moon snail (Lunatia heros), waved whelk
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(Buccinum undatum), spider conch (Lambis lambis), olive (Oliva vidua fulminans),
tekuyong (Natica sp.) and nassa (Nassarium sp.) (Deeds et al. 2008; Shumway
1995). In contrast to these gastropods, there have been no PSP cases recorded that
were related to the consumption of abalone (Haliotis sp.). It is thought that
transmission of PSTs to carnivorous gastropods (e.g. whelks) occurs through the
food chain from toxic dinoflagellates to bivalve shellfish to gastropod (Llewellyn and
Negri 2006). Herbivorous gastropods, such as abalone, probably become intoxicated
by grazing on toxic macroalgae or via the consumption of toxic dinoflagellates that
have settled onto the surface of macroalgal food. It is probable that carnivorous
gastropods pose a higher food safety risk than herbivorous gastropods.
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5.
Hazard Characterisation
“The qualitative and/or quantitative evaluation of the nature of the adverse
health effects associated with the hazard (Anon 1999)”
5.1 Severity and Duration of Adverse Effects in Humans
The time to onset of PSP symptoms can be as short as several minutes
(paraesthesia and numbness around the lips, tongue and mouth), but may start up to
12 hours (latent period) after consumption of toxic shellfish (Sumner, 2000; van
Dolah, 2000; Alexander et al. 2009; Gessner and Middaugh, 1995; Chung et al.
2006).
In a retrospective analysis of 54 outbreaks of PSP in Alaska over the period 1973 to
1992 the time from ingestion of shellfish to recovery from illness ranged from 30
minutes to 24 hours (Gessner and Middaugh 1995). However, in a study of a large
outbreak (58 cases) of PSP caused by the consumption of scallops in Hong Kong in
2005, the duration of symptoms in some cases was found to be much longer, with a
reported range of 1 to 228 hours (Chung et al. 2006).
In the review of PSP outbreaks in Alaska (1973 – 1992) 1 % of affected people were
reported to die (Gessner and Middaugh 1995). However in some outbreaks the
fatality rate has been higher, for example in Guatemala in 1987, 187 cases of PSP
resulted from the consumption of clams (meat and soup) causing 26 people to die.
The fatality rate for victims under the age of 6 was 50 % and for those older than 18
the fatality rate was 7 %, overall the fatality rate was 14% (Rodrigue et al. 1990).
Several reviews note that patients surviving beyond 24 hours have a high probability
of full recovery (Alexander et al. 2009; Sumner 2000).
5.2 Uptake, Distribution and Elimination of PSTs by Humans
In 2002 two fishermen working in the Patagonia Chilean fjords consumed the bivalve
shellfish species Aulacomya ater (ribbed mussel). Within 3 - 4 h of shellfish
consumption the fishermen died. A forensic examination of the fishermen was
undertaken and HPLC analysis for PSTs was carried out on various body fluids and
tissue samples (liver, kidney, lung, stomach, spleen, heart, brain, adrenal glands,
pancreas and thyroid glands). A wide variety of PSTs were detected in all tissue
types tested as well as the bile and urine. Due to the rapid time to onset of symptoms
reported (within 30 minutes of consumption the fishermen displayed symptoms) and
time to death (3 - 4 hours) it is clear that PSTs are rapidly absorbed in the blood and
transported efficiently throughout the body (Garcia et al. 2004).
The HPLC analysis of body tissue and fluid samples from the fishermen showed that
the stomach samples contained mainly STX and GTX's 1-5, however the toxins
found in urine and bile samples mainly comprised neo-STX and GTX-1,4. The
authors suggested that the differences in toxin composition indicated significant
interconversion/metabolism of toxins in the human body. (Garcia et al. 2004).
Glucuronidation is one of the most important detoxification pathways in humans and
it involves a conjugation reaction which results in the conversion of toxic compounds
in the body into substances that have increased water solubility. The increased
hydrophilic nature of these metabolites facilitates their removal from the body via
urine or bile. Recent research has confirmed the sequential oxidation and
glucuronidation of several major PSTs (STX and GTX-2,3). The bioconversion of
STX to neo-STX, and GTX-2,3 to GTX-1,4 followed by glucuronidation and excretion
via bile and urine is likely to represent the major detoxification route in humans
(Garcia et al. 2010; Garcia et al. 2005). This is consistent with information provided in
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a review of victims medical records undertaken following four PSP outbreaks on
Kodiak Island, Alaska. The review revealed that PSTs were cleared from serum in
< 24 hours and urine was identified as the major route of toxin excretion in humans
(Gessner et al. 1997).
5.3 Mode of Action
PSTs bind with high affinity to the voltage dependent sodium channels within cellular
membranes at site one of the α subunit (Cestele and Catterall 2000). This binding
activity plugs the sodium channels thereby inhibiting the flow of sodium through the
channel. This inhibits action potential and prevents nerve transmission impulses (or
‘signals’ being passed from cell to cell). This is what leads to the reported paralytic
effects of PSTs in humans e.g. muscular paralysis, respiratory distress etc. (Anon
2001).
Different forms of the α subunits of the sodium channel exist and it has been
suggested that differences in sensitivity of the various channels to the PSTs may
occur (Alexander et al. 2009). Related to this, in a retrospective review of 54 PSP
outbreaks in Alaska no association was found between human illness and the
shellfish toxin level or dose ingested. The authors postulated that ‘single amino acid
substitutions in the sodium channel pore region may greatly alter the binding capacity
of STX, suggesting a possible genetic basis for illness susceptibility’ (Gessner and
Middaugh 1995). Supporting this another review of illness outbreaks suggested that
there is no clear correlation between occurrence and severity of illness, and the
shellfish toxin level or dose ingested (Prakash et al. 1971). This may indicate that
some groups of people have immunity to PSTs; however further research is required
to fully evaluate this possibility.
PSTs were thought to be highly specific in their cellular target and only effect sodium
channels, however recent research has suggested that PSTs may also impair the
function of both potassium and calcium channels (Su et al. 2004; Wang et al. 2003).
The STX dose required to affect the function of potassium and calcium channels is
much higher than that required to block sodium channels and therefore the biological
relevance of this interaction is currently unknown.
5.4 Acute Toxicity in Laboratory Animals
In the 1990’s Oshima (Oshima 1995) and Hall (Hall et al. 1990) separately evaluated
the intra-peritoneal toxicity of the major PSTs in mice. The specific toxicities of PSTs
reported by Oshima (1995) are detailed in Table 2. These specific toxicity values are
widely used as the basis for Toxicity Equivalence Factors (TEFs) which are applied
by laboratories that use chemical based methods of analysis e.g. High Performance
Liquid Chromatography (HPLC) to account for differences in toxicity between
analogues. Recently the European Food Safety Authority (EFSA) evaluated the
relative potency of the PSTs reported in nine separate studies. From this evaluation
the EFSA Panel proposed a revised series of TEFs to be applied when using
chemical methods of analysis (Table 2).
15
Table 2.
Specific toxicities (established via intra-peritoneal route in mice) of the
Paralytic Shellfish Toxins and the ‘Toxicity Equivalence Factors’
proposed by the European Food Safety Authority (EFSA).
Specific Toxicity EFSA Proposed
TEFs
(MU µmol-1)
STX
2483
1.0
GTX1
2468
1.0
NeoSTX
2295
1.0
GTX4
1803
0.7
GTX3
1584
0.6
dcSTX
1274
1.0
dcGTX3
935*
0.4
GTX2
892
0.4
dcGTX2
382*
0.2
C2
239
0.1
B1 (GTX5)
160
0.1
C4
143
0.1
C3
33
C1
15
*dcGTX2 and dcGTX3 were originally reported as 1617 and 1872 MU µmol-1
respectively (Oshima 1995). These values were corrected in a later publication.
Toxin
The oral toxicity of PSTs to mice was evaluated by Health Canada in the late 1950s.
The toxicity study was undertaken using a purified extract of STX that was prepared
from toxic clams and mussels. The LD50 of STX was found to be 263 µg/kg (95%
confidence limit = 251 – 267 µg/kg) by oral administration, compared with 10 µg/kg
(95% confidence limit = 9.7 – 10.5 µg/kg) by intra-peritoneal inoculation (Wiberg and
Stephenson 1960). Unfortunately the mode of oral uptake (e.g. gavage or voluntary
consumption) is not noted in the manuscript. Further oral dosing studies (preferably
via the voluntary consumption route) are required for the other major analogues of
STX found in shellfish. This would enable TEFs that are more relevant to the mode of
human intoxification, which occurs via the oral route, to be determined. These studies
may be hampered by the lack of sufficient quantities of purified toxin standards for
this type of analysis.
5.5 Evaluation of Toxicity in Humans
Several expert working groups have evaluated the toxicity of PSTs in humans and in
animals over the past five years. Both the EFSA Panel on Contaminants in the Food
Chain (2009) and the WHO/IOC/FAO Expert Consultation (2004) found that there
was insufficient data on the chronic effects of PSTs on humans and animals and so
were unable to establish a Tolerable Daily Intake (TDI) (Alexander et al. 2009; Anon
2004).
Based on data from around 20 outbreaks of human poisoning (related to bivalve
shellfish consumption) in Canada between 1970 and 1990 the WHO/IOC/FAO Expert
Consultation recommended a lowest-observed-effect level (LOAEL) of 2.0 µg kg-1
body weight (bw) (Anon 2004). The EFSA Panel similarly assessed reports of human
poisoning involving around 500 cases and derived a LOAEL of 1.5 µg kg-1 bw
(Alexander et al. 2009). Both the EFSA Panel and the WHO/IOC/FAO Expert
Consultation utilised a safety factor (to determine a criterion that is considered safe
or without appreciable risk) of 3.0 to arrive at a no-observed-effect level (NOAEL)
and derive an acute reference dose (ARfD). Table 3 shows the LOAEL’s and ARfD’s
16
estimated by the EFSA Panel and the WHO/IOC/FAO Expert Consultation. No
rationale for the discrepancy in the ARfDs derived by these two separate expert
groups was provided in the 2009 EFSA evaluation.
Table 3.
Lowest-Observed-Effect Level and Acute Reference Dose for PSTs
EFSA
Panel
Lowest-Observed-Effect Level (µg/kg bw)
Acute Reference Dose (µg STX
equivalents/kg b.w.)
1.5
0.5
WHO/IOC/FAO
Expert
Consultation
2.0
0.7
17
6.
Exposure Assessment
“The qualitative and/or quantitative evaluation of the likely intake of biological,
chemical, and physical agents via food as well as exposures from other
sources if relevant (Anon 1999).”
6.1 Prevalence of PST Producers in Australia
To support the assessment of the likelihood of uptake of PSTs by Australian abalone
a summary of the prevalence of PST-producing marine organisms in Australia has
been reviewed in this section.
6.1.1 Macroalgae
The macroalgae species Jania sp. and Ecklonia maxima have been suggested to
produce PSTs in Japan and South Africa respectively (Etheridge et al. 2004; Kotaki
et al. 1983). In the research undertaken by Kotaki et al (1983) to determine the
potential production of PSTs by Jania, the surface of Jania was cleaned to remove
trapped microalgal cells, however it is still possible that organisms that produce PST
may have been adhered to the macroalgae and are the ultimate source of the toxin.
Both Jania spp. and Ecklonia spp. are reported to be abundant in Australian waters,
however PST production by Australian species is not well studied and has not yet
been confirmed.
6.1.2 Microalgae
A diverse array of Australian microalgae sourced from collections housed at CSIRO
and the Australian Institute of Marine Science were screened for PST production
using sodium channel and saxiphilin binding assays. In the study 234 diverse isolates
of Australian freshwater and marine microalgae were screened for PST production
and five toxic species were confirmed, including one freshwater cyanobacterium
(Anabaena circinalis Rabenhorst) and four species of marine dinoflagellates
(A. minutum Halim, A. catenella Balech, A. tamarense Balech, and G. catenatum
Graham). A Liquid Chromatography-Fluorescence method was used to confirm the
toxin profiles of microalgae shown to produce PSTs (Negri et al. 2003). Despite this
finding, multiple cultures of A. tamarense tested from South Australia and Tasmania
have repeatedly been shown to be non-toxic. A recent review summarised the
Australian distribution of G. catenatum , A. tamarense and A. catenella (Figure 2).
PST-producing dinoflagellate species have been confirmed to be present in each of
the five abalone producing states of Australia (NSW, Victoria, Tasmania, South
Australia and Western Australia). The following sections summarise the current
knowledge on the prevalence of PST-producing dinoflagellates along the coastline of
these abalone producing states. The information has been obtained from routine
monitoring data gathered as part of the bivalve shellfish quality assurance
programmes and from research articles.
18
Figure 2.
Known distribution of A. catenella (blue dots), A. tamarense (green
dots) and G. catenatum (red dots) in Australian waters. Figure based
on information provided in Bolch and de Salas, 2007.
New South Wales
A. catenella and A. minutum have been detected at several locations along the mid
to southern NSW coastline, between Port Stephens and Port Phillip Bay in Victoria.
A. tamarense has also been detected in seawater samples taken from several sites
around Coffs Harbour in the northern region of NSW, but unlike A. catenella and A.
minutum has not been recorded in the mid or southern NSW coastline. G. catenatum
has been detected in routine phytoplankton monitoring samples taken as part of the
shellfish quality assurance programme at several sites between Laurieton (north of
Port Stephens) and Eden (south of Batemans Bay). On rare occasions shellfish
samples tested as part of the quality assurance programme have contained low
levels of PSTs, however levels above the regulatory threshold have not been
detected (Personal Communication, Anthony Zammit, New South Wales Food
Authority, January 2010). The Australian medical literature contains a single account
of wild mussels collected in 1935 near Batemans Bay producing typical PSP
symptoms in mice (Hallegraeff et al. 1991). While PST-producing dinoflagellates
have infrequently been isolated along the NSW coastline at low levels, there have
been no confirmed cases of human PSP illness related to the consumption of
shellfish from NSW.
Victoria
A. catenella was first identified in Port Phillip Bay, Victoria from net tow plankton
samples taken in 1986 (Hallegraeff et al. 1988). Due to the occurrence of this species
phytoplankton monitoring was implemented as part of the bivalve shellfish quality
assurance programme in Port Phillip Bay in 1987. The production of PSTs by this
species was confirmed by mouse bioassay and HPLC and in 1988 wild mussels from
Willamstown in Port Phillip Bay were found to contain up to 480 µg 100g-1 PST (Anon
2001; Hallegraeff et al. 1991). Various other PST-producing species have
subsequently been identified, including A. tamarense, A. minutum and G. catenatum.
19
Significant blooms of A. catenella occurred in 1988, 1992, 1994 and 1995 (Walker
2009). The highest levels of PSTs were recorded in 1992 in Hobsons Bay mussels
(10,000 µg 100g-1 PST) (Hallegraeff 1992), fortunately the bay was closed for bivalve
harvesting at the time and illnesses were not reported to occur (Arnott 1998; Lehane
2000).
Tasmania
The dinoflagellates A. catenella, A. ostenfeldii and G. catenatum have been detected
and confirmed to produce PSTs in Tasmanian waters. A. tamarense from Tasmania
and South Australia have consistently been shown to be non-toxic. G. catenatum
was first noticed in southern Tasmanian waters in 1980 (Derwent estuary) and dense
blooms of this species were then observed in the summer and autumn of 1986, 1987,
1991 and 1993 in the Huon Estuary and D’Entrecasteaux Channel of south eastern
Tasmania (Figure 3) (Hallegraeff et al. 1988). In response routine monitoring of
bivalve shellfish was instituted in 1986 and shellfish were found to contain up to
18000 µg 100g-1 PST causing closure of farms for extended periods (Hallegraeff
1992; Hallegraeff et al. 1995; Lehane 2000). G. catenatum has now been detected
as far south as Recherche Bay, up the majority of the eastern coast of Tasmania and
across the north coast to Smithton (Figure 3); however it is usually confined to the
southern region of the east coast. G. catenatum has been found to bloom in most
years in autumn through to spring, although blooms are known to persist into
summer in some years (Alison Turnbull, Tasmanian Shellfish Quality Assurance
Programme, January 2010). Analysis of historic plankton samples and cysts in
sediment depth cores have led scientists to postulate that G. catenatum is not
indigenous to Tasmania but was introduced into the region after 1973 (Hallegraeff et
al. 1995). A. catenella was detected on the east coast of Tasmania in 2005 and
resulted in low levels of PSTs in mussels and oysters (Alison Turnbull, Tasmanian
Shellfish Quality Assurance Programme, January 2010). A recent review confirms
the presence of A. catenella and A. tamarense from multiple locations on both the
north and east coasts of Tasmania (Bolch and de Salas 2007).
PSP Algae/toxins above closure values
PSP Algae/toxins below closure values
Figure 3.
Distribution of G. catenatum in Tasmania in 2009. Red dots show
PSTs and algal counts above closure levels, blue dots show PSTs
and algal counts below closure levels. Figure provided by Alison
Turnbull, Tasmanian Shellfish Quality Assurance Programme.
20
South Australia
A. minutum, A. catenella, A. tamarense and G. catenatum have been detected in
South Australia. A. minutum blooms were first identified in the Port River in Adelaide
in 1986, wild mussels taken from the Port River at the same time were found to
contain up to 2700 µg 100g-1 PST (Hallegraeff et al. 1991; Hallegraeff et al. 1988).
Subsequently A. minutum has been detected along much of the South Australian
coastline from Denial Bay in the west to the Coorong in the south east. Similarly
A. tamarense has been detected at many sites along the coastline between Smokey
Bay and the Coorong. A. minutum and A. tamarense are mainly detected in the
routine phytoplankton monitoring programme (as part of the bivalve shellfish quality
assurance programme) from October through to May. G. catenatum has not been
detected at as many sites as A. minutum and A. tamarense, with detections at Denial
Bay, Smokey Bay, Streaky Bay, Port Lincoln and American River. As previously
noted, A. tamarense from South Australia has consistently been shown to be nontoxic (Bolch and de Salas 2007). A. catenella appears to be restricted to the south
eastern coastline of South Australia between the Port River and the Coorong.
Approximately 670 bivalve shellfish samples from farms in South Australia have been
tested for PSTs since 2000. Of samples tested to date only 1 sample from
Coobowie, Yorke Peninsula gave a positive result (0.46 mg kg-1), albeit below the
regulatory limit for PSTs (Clinton Wilkinson, Personal Communication, January
2010).
Western Australia
Routine testing of bivalve shellfish for PSTs in Western Australia occurred for five
years from 1994 to 1999 during which time PSTs were not detected, subsequently
PST testing of shellfish was discontinued. Routine plankton samples are taken and
A. minutum has been infrequently detected in Perth and Bunbury. A recent review
also suggests the presence of A. tamarense in Fremantle (Bolch and de Salas 2007).
Summary
PST-producing dinoflagellates have been detected at many sites along the Australian
coastline. However significant levels of PSPs have only been detected in bivalve
shellfish from Victoria and Tasmania. The lack of significant levels of PSTs in
shellfish sourced from New South Wales, Western Australia and South Australia
could be the result of several factors e.g. low concentrations of dinoflagellate cells in
the water column, environmental conditions that do not support significant blooms
and low concentrations of PST produced per cell etc.
6.2 Production and Export of Wild Caught Australian Abalone
Production
The Australian abalone fishery is the largest wild caught fishery in the world. There
was a total Australian catch of approximately 4800 tonnes in 2008 and the catch has
remained relatively stable over the past decade (Figure 4) (Anon 2009a). In Australia,
Haliotis roei (roe’s), Haliotis laevigata (greenlip) and Haliotis rubra (black-lip) are the
three main species harvested commercially.
21
Australian Wild Caught Abalone Production
7 000
6 000
Tonnes
5 000
4 000
3 000
2 000
1 000
0
2007-2008
2006-2007
2005-2006
2004-2005
2003-2004
2002-2003
2001-2002
2000-2001
1999-2000
1998-1999
Year
Figure 4.
Total Wild Caught Abalone Capture (Landed Weight) in Australia
(1998 – 2008)(Anon 2009a).
The majority of the abalone is caught from fishing zones off the coasts of Tasmania
(48% of total capture), Victoria (25%) and South Australia (18%). A small amount of
abalone is also caught on the coasts of Western Australia (6%) and New South
Wales (2%) (Table 4) (Figures 5 and 6). Abalone are not reported as being
commercially caught in Queensland or Northern Territory (Anon 2009a).
Table 4.
Wild Caught Abalone Production (quantity of abalone landed) in
Tasmania, Victoria, South Australia, Western Australia and New South
Wales (2008).
State
Tasmania
Victoria
South Australia
Western Australia
New South Wales
TOTAL
1
Tonnes
2552
1194
886
291
109
5032
2
Tonnes
2317
1219
890
281
109
4816
1
Sources: Data was obtained directly from Fisheries Victoria, Department of Primary Industries; New
South Wales Department of Primary Industries; South Australian Research and Development Institute;
Tasmanian Aquaculture and Fisheries Institute, Government of Western Australia Department of
Fisheries.
2
Source: Australian fisheries statistics 2008. Canberra, Australian Bureau of Agricultural and Resource
Economics: 1-87.
22
Figure 5.
Quantity (Tonnes) of Abalone Landed (Wild Capture) in Western
Australia in 2008. Top Panel shows Greenlip and Brownlip Abalone
Capture. Bottom Panel shows Roe Abalone Capture.
23
Figure 6.
Quantity (Tonnes) of Abalone Landed (Wild Capture) in New South
Wales in 2008.
In Tasmania most of the abalone is caught in the Eastern (33% of Tasmanian ‘catch’)
and Western Zones (49%) (Figure 7). In South Australia the majority of abalone are
caught in the Western A Zone (59% of SA ‘catch’) (Figure 8), and in Victoria the
Central (49%) and Eastern (41%) Zones are the most prolific (Figure 9). The catch
from these more prolific zones was approximately 4057 tonnes in 2008, representing
84% of total Australian wild caught production.
24
Figure 7.
Quantity (Tonnes) of Abalone Landed (Wild Capture) in Tasmania in
2008.
Figure 8.
Quantity (Tonnes) of Abalone Landed (Wild Capture) in South
Australia in 2008.
25
Figure 9.
Quantity (Tonnes) of Abalone Landed (Wild Capture) in Victoria in
2008.
Aquaculture production of abalone in Australia is still relatively small compared with
wild caught volumes with <10 % of the total Australian production per annum
comprising aquaculture product (Table 5). The Australian fisheries statistics do not
specify the product form (e.g. canned, frozen etc) of aquaculture abalone. However
anecdotal information supplied by a major producer, suggests that the majority of
aquaculture product is sold in frozen form in Asia, with some live product consumed
in the domestic food service sector.
Table 5.
Australian Wild Caught Abalone Landed and Aquaculture Production
(tonnes landed and produced) 2004 – 2008.
Wild caught
Aquaculture3
Total
2004
5,588
249
5,837
2005
5,594
390
5,984
2006
5,011
506
5,517
2007
5,002
468
5,470
2008
4,816
503
5,319
Export
A large proportion of Australian abalone is exported to overseas destinations, with
approximately 74 % of total production exported in 2008. Most Australian abalone is
exported to Asian destinations and small amounts are also exported to the United
3
Calculated as difference between Total and Wild Caught data
26
States and Canada. Exports of Australian abalone to other countries are so small
that they are not specifically attributed to a particular country in the Australian
fisheries statistics, but are pooled together in a general category described as ‘other’.
The ‘other’ category includes minor volumes of exports to Asia Pacific Economic
Cooperation (APEC) countries and EU countries. Table 6 shows the total volume of
abalone (wild caught and aquaculture) exported to various countries between 2006
and 2008.
The Australian fisheries statistics records the product form of abalone in two
categories: (a) ‘fresh, chilled or frozen’; and (b) ‘canned’. The ‘fresh, chilled and
frozen’ category contains various forms of product including live abalone, modified
atmosphere packaged (MAP) abalone, and frozen abalone. A significant amount
(~2000 tonnes) of live abalone is purported to be exported (Personal
Communication, Tony Johnston, Chair, Abalone Association Australasia). MAP
abalone represents a very minor component of total exports. It is noteworthy that the
majority of abalone exported to ‘other’ countries (this includes EU countries) is
canned. Of the total abalone exported to ‘other’ countries in 2006 87% was canned,
compared with 79% and 63% in 2007 and 2008 respectively. The decreased
percentage of canned abalone in the ‘other’ category in 2008 (compared with 2006)
probably reflects the cessation of Australian abalone exported to the EU (exports
ceased in mid 2007). It is highly likely that the vast majority (probably all) of abalone
exported to the EU was canned due to the extended transportation times involved
and the difficulties associated with maintaining shelf life for fresh or chilled abalone
products over prolonged periods.
The Australian fisheries statistics show that of the total exports of 3,665 tonnes (all
product forms, data not corrected for shell weight loss in canned product), 3,644
tonnes was exported to APEC countries in 2005/2006. Therefore, by deduction, 21
tonnes of Australian abalone was exported to the rest of the world in 2005/2006. A
conservative approach in this risk assessment is to assume that all 21 tonnes was
exported to Europe. As previously noted, it is highly likely that all 21 tonnes was
canned product. Of note, ‘other’ exports to non APEC countries (e.g. Europe) in
2006/2007 and 2007/2008 decreased markedly from 21 tonnes to 6 tonnes,
demonstrating the effect of the ‘closure’ of the European market to Australian
abalone.
27
Table 6.
Total Abalone (Wild Caught and Aquaculture) Exported from Australia to Overseas Destinations 2006-2008 (Net Tonnes
Exported)4
2006
Export Destination
Hong Kong, China
Japan
Singapore
Chinese Taipei
United States
Canada
Total ‘Other’5
Total exported6
Total live-weight
equivalent exported7
Total Exported
Total Abalone Landed
and Produced
Fresh, chilled
or frozen
1 628
404
16
63
0
10
12
2133
2133
2007
609
404
249
153
37
0
80
1532
Fresh, chilled
or frozen
1 762
391
15
44
0
12
16
2240
3064
2240
Canned
2008
883
229
324
134
39
0
61
1670
Fresh, chilled
or frozen
1 656
381
23
34
0
14
41
2149
3340
2149
Canned
Canned
732
183
339
66
41
0
70
1431
2862
5197
5580
5011
5517
54708
5319
4
Source: Australian fisheries statistics 2008. Canberra, Australian Bureau of Agricultural and Resource Economics: 1-87.
Total ‘other’ includes APEC and non APEC countries. The Australian fisheries statistics shows that export of abalone to non-APEC ‘other’ countries were 21, 16 and 6 tonnes
in 2006, 2007 and 2008 respectively.
6
Canned volumes reported do not account for the loss of weight due to removal of the shell and viscera.
7
To compensate for loss of weight due to removal of the shell and viscera in the canning process a factor of 2 has been applied to adjust the canned weight to a ‘live-weight’
equivalent.
8
These figures do not account for small volumes of abalone potentially imported into Australia, this may explain the discrepancy in the total volume of abalone exported in
2007 compared with the total landed/produced in Australia. The discrepancy may also reflect the time lapse between production and subsequent export.
5
28
6.3 Occurrence of PSTs in Abalone
PSTs have been detected in abalone sourced from a fishery in Spain and also from
wild caught and farmed abalone from South Africa. The following comprises a review
of the literature with respect to PST contamination of abalone from Spain, South
Africa and Australia.
6.3.1 Spain
In 1991 research was undertaken to determine if abalone (H. tuberculata) sourced
from an area in Galicia, Spain, contained PSTs. The fishery was known to be
affected by blooms of the PST-producing dinoflagellate G. catenatum and mussels in
the area had previously been found to contain PSTs. The study confirmed (by mouse
bioassay and HPLC) that PSTs were present in the foot, viscera and whole tissues of
the abalone. The results demonstrated that larger quantities of PSTs were present in
the foot compared with samples comprising viscera only and the whole animal
(Martinez et al. 1993).
Following this the abalone fishery in Galicia was closed due to the discovery of
significant levels of PSTs in abalone that were exported to Japan (Huchette and
Clavier 2004; Nagashima et al. 1995c). Initial work was undertaken by Japanese
scientists to identify the type of PSTs contained within the abalone tissues and to
assess the safety of the abalone from a food hygiene perspective. The work
demonstrated that the abalone contained levels of PSTs well over the regulatory limit
(the regulatory limit was 4 MU/g compared with levels > 3,000 MU/g detected in
Galician abalone)9. The predominant analogues found in the abalone were the highly
toxic carbamate toxins e.g. STX, neo-STX and dcSTX. The Japanese data also
confirmed the unusual distribution of PSTs throughout the abalone tissues with the
muscular tissues (foot, epipodial fringe and mouth) containing significantly higher
levels of PSTs than the visceral components (Nagashima et al. 1995c). It was
identified through depuration studies, that H. tuberculata retained PSTs in the foot
tissue for extended periods and this resulted in the Spanish fishery closing until 2002
(Huchette and Clavier 2004).
6.3.2 South Africa
In 1999 abalone (H. midae) from a farm in South Africa were reported to be
paralysed (not able to attach to substrate) and some abalone mortalities were
recorded. Several tests of the farmed abalone using the PSP mouse bioassay
indicated that the animals contained PSTs. Subsequently 300 individual abalone
obtained from farms and wild fisheries in the immediate area were tested (by mouse
bioassay) and toxicity was found to be widespread. The highest value was found to
be 1609 µg 100 g-1 – well in excess of the regulatory threshold (80 µg 100 g-1)
(Pitcher et al. 2001).
Coincident with the toxicity found in the abalone there was a bloom of A. catenella in
the region. The authors used HPLC methods to determine the toxin composition in
A. catenella and H. midae. A. catenella was found to contain a high proportion of C1
and C2 toxins and a moderate level of STX, GTX-4 and dcGTX-3 toxins. In contrast,
the H. midae were found to contain only STX. This profile was somewhat similar to
that detected in abalone from Spain, with the carbamate toxins (e.g. STX) dominating
in the abalone tissues. This may indicate a high degree of biotransformation of PSTs
9
Definition of mouse unit (MU): A mouse unit (MU) is defined as the minimum amount needed to cause
the death of an 18 to 22 g white mouse in 15 minutes. One MU has been determined to have a value of
0.18 µg STX.2HCl , and this value has frequently been applied in converting concentrations of STX
reported in MU into STX equivalents (Alexander et al, 2009).
29
by abalone or alternatively that A. catenella was not the causative organism (Pitcher
et al. 2001).
6.3.3 Australia
Testing of wild caught Australian abalone for marine biotoxins has been undertaken
through the National Residue Survey (NRS) in 2002, 2003 and 2004. During this
period ~ 52 samples of greenlip (H. laevigata), blacklip (H. rubra) and roe (H. roei)
abalone were taken from each of the different abalone fishery areas in Australia (e.g.
Western Australia, South Australia, Tasmania, Victoria and New South Wales). The
samples were tested for PSTs (by mouse bioassay), neurotoxic shellfish poisons (by
mouse bioassay), amnesic shellfish poisons (by HPLC) and diarrhetic shellfish
poisons (by mouse bioassay). Sample types included whole abalone (gut on), meat
only, canned product and whole frozen product. No marine biotoxins were detected
in any samples tested (Appendix Two, data kindly provided by the Australian
Quarantine and Inspection Service).
Unfortunately the data collected by the NRS do not comprehensively detail the
location from which samples were taken, the abalone species sampled, or the
sample type (e.g. whole tissue, gut or meat, canned etc). Additionally, the limit of
detection of the mouse bioassay for PSTs is reported to be ~ 37 µg STX eq 100 g-1
tissue (Alexander et al. 2009), therefore it is possible that levels of PSTs below this
value were present in the samples tested by the NRS and not detected by the mouse
bioassay. Further data is required to more robustly establish background levels of
marine biotoxins in the various product forms of Australian abalone species;
nonetheless, this information is indicative of low marine biotoxin risk.
In July 1992 potential PST-producing dinoflagellates (G. catenatum and
A. tamarense) were detected in water samples along the Victorian coastline
(between Lorne and Portland). In response the Victoria Shellfish Quality Assurance
Programme undertook testing of a single abalone sample for PSTs. A level of 123 µg
STX eq 100 g-1 was reported to be detected in the gut tissue of the abalone (Arnott
1998). The sample was tested using the PSP mouse bioassay (Personal
Communication, Graham Arnott, May 2010). Around the same time significant levels
of PSTs (10,000 µg 100g-1) were recorded in mussels from Hobsons Bay, Victoria.
This suggests a much lower level of uptake of PSTs by abalone compared to bivalve
shellfish.
Experimental studies undertaken with H. laevigata (greenlip abalone) by Homan et al
(2010) demonstrated a low propensity for this species of Australian abalone to take
up PSTs produced by A. minutum. A. minutum is a prolific species in nature,
commonly reaching 102 – 103 cells mL-1, but reported to reach as high as
105 cells mL-1 in dense blooms (Hallegraeff et al. 1991). To approximate a dense
bloom situation, the abalone were fed food pellets containing ~4 x 105 A. minutum
cells every second day for 50 days. The levels of PSTs detected were ~50 times
lower than the maximum permissible limit of 80 µg 100g-1 (Australia and Europe) for
PSTs in shellfish. The low level of uptake in this study, when abalone were exposed
to relatively high numbers of A. minutum cells over a prolonged period, may indicate
decreased risk of PSP poisoning to humans from the consumption of H. laevigata
that have been exposed to blooms of potentially toxic A. minutum in Australia
(Homan et al. 2010).
6.3.4 Summary
In total approximately 63 Australian abalone samples have been tested for PST
toxins (as reported in the literature and through the National Residue Survey). In
contrast to Australian species of abalone (H. laevigata, H. rubra and H. roei),
30
H. midae from South Africa and H. tuberculata from Spain have been reported to
contain PSTs well in excess of the regulatory limit (Table 7)(Bravo et al. 1996; Bravo
et al. 1999; Martinez et al. 1993; Nagashima et al. 1995a; Pitcher et al. 2001).
Table 7.
Reported PST Results in Australian, Spanish and South African
Abalone.
Region
Australia (routine monitoring)
11
Australia (ad hoc reports)
Spain
South Africa
10
Number of Abalone
Samples Tested for PST
52
11
> 54
304
Maximum Level of PST
-1
Detected (µg 100 g )
0
123
1300
1609
The mode by which the South African and Spanish species of abalone accumulate
such high levels of PSTs is unclear, and should be the subject of further study. As
previously discussed, macroalgae may be a potential vector for the transfer of PSTs
to abalone (Etheridge et al. 2004; Kotaki et al. 1983). PST-producing macroalgae
species have not as yet been identified in Australian waters and recent research on
the greenlip abalone indicates very low level PST content of abalone via ingestion of
PST-producing dinoflagellates (Homan et al. 2010); together this data may explain
the absence of PST toxins in Australian abalone tested as part of the National
Residue Survey between 2002 and 2004 (Appendix Two).
6.4 Consumption of Australian Abalone in Europe and China
The United Nations Food and Agricultural Organisation (FAO) gather various
statistics on production, imports, exports and consumption of seafood worldwide.
Unfortunately actual statistics on the amount of abalone consumed are not gathered
by the FAO, with ‘apparent consumption estimates for broad groups of species
calculated on the basis of ‘production + imports – exports’ (Personal Communication
Stefania Vannuccini, FAO, January 2010). European Union consumption data
available for individual shellfish species are also limited.
6.4.1 Servings of Australian Canned Abalone Available
Due to the lack of actual data, an estimate of the number of servings of Australian
abalone available for consumption in Europe and China has been made based on
the volume of Australian abalone exported (Table 8). While the Australian fisheries
statistics do not specifically note the product form of the 21 tonnes exported to ‘other
non APEC’ countries the data suggest that all of this product is canned (section 6.2).
10
Details of the samples tested are available in Appendix Two.
10 samples of Australian abalone sourced from a farm in South Australia were tested for PSTs as part
of a research project undertaken in 2010 (Homan et al, 2010). One sample was recorded as being
-1
tested in western Victoria in 1992, 123 µg 100 g PST was reported in the gut of the abalone (Arnott,
-1
1998). Mussels tested during the same bloom contained ~10,000 µg 100 g PST. This suggests
significantly lower levels of uptake by abalone compared with bivalves.
11
31
Table 8.
Volume of abalone exported to Hong Kong and China, and ‘Other
Non-APEC Countries’12 in 2005/200613 and the associated number of
servings.
Fresh, Chilled, Frozen
Canned
Total
Export to Hong Kong +
China
Tonnes
Servings (50 g)
1628
32560000
609
12180000
2237
44,740,000
Export to ‘Other NonAPEC’ Countries’
Tonnes
Servings (50 g)
21
420,000
21
420,000
A serving size of 50 g has been selected based on the following:
a. Anecdotal industry knowledge of the amount of abalone consumed by individuals
suggests 50 g is a conservative estimate;
b. A previous risk analysis on marine toxins in abalone utilised a 50 g portion size
(Sumner 2000);
c. Prior to 2007 (when exports ceased) Australian abalone was predominantly sold
into high class eating establishments in Europe where it is considered a delicacy
and significantly smaller serving sizes were utilised compared with bivalve
molluscs;
d. The mean portion size for bivalve mollusc consumption in five European
countries was estimated as ranging between 10 g and 136 g (Alexander et al.
2009). It is highly likely that abalone consumption would be significantly lower
than that of bivalves;
e. The high prices and scarcity of abalone in the market place compared with
bivalve molluscs mean that smaller portion sizes are likely to be consumed;
f. A survey of four Chinese restaurants in Adelaide (Australia) resulted in an
estimate of a serving size of 100 g of abalone per person (Appendix Three); and
g. Selection of a 50 g serving size is conservative as it results in a higher number of
servings being consumed in a given population and less elapsed time between
servings.
6.4.2 Frequency of Consumption
There is no market research available with which to accurately determine the
proportion of the population that consume abalone or the frequency of consumption
by individuals. Therefore several scenarios have been devised to consider differing
proportions of the European and Chinese population consuming abalone and the
influence this has on the frequency of consumption of Australian abalone (Table 9).
12
The Australian fisheries statistics do not directly specify the volume of abalone exported to Europe.
The category ‘other non APEC’ includes European countries and other countries that are of minor
significance in terms of total export volumes. Therefore the data in this Table overestimates the volume
of abalone exported to Europe.
13
This Table was based on 2005/2006 data because exports of Australian abalone to Europe ceased in
2007.
32
Table 9.
Days between servings of Australian abalone (‘canned’ and ‘fresh,
chilled or frozen’) for each member of the consuming population.
Proportion of the
Population Consuming
Australian Abalone
100 %
75 %
50 %
25 %
10 %
5%
1%
0.1 %
Days between servings
Europe
Canned
China
Canned
China
Fresh, Chilled, Frozen
636143
477107
318071
159036
63614
31807
6361
636
40054
30040
20027
10014
4005
2003
401
40
14983
11238
7492
3746
1498
749
150
15
The population of Europe and China was estimated to be 732,000,000 and
1,336,610,000 respectively in 200914. Based on the serving numbers estimated in
Table 8, if all the population consumed Australian canned abalone this would equate
to approximately one serving for each person every 1743 years in Europe and every
110 years in China. However it is extremely unlikely that each member of the
European and Chinese population would consume Australian abalone.
European Population Consuming Abalone
In order to estimate the proportion of the European population that consume abalone
the following rationale and assumptions have been applied:
a.
b.
c.
d.
e.
f.
The Chinese population residing in Europe is ~1,000,000;
Of these 1,000,000 it could be assumed that most children (~15 % of the
population14) would not eat abalone as it is highly regarded and would only be
served on special occasions. Based on this, 85% of the Chinese population in
Europe (~ 850,000) would potentially consume abalone;
Abalone was traditionally fished in France, Spain and the Channel Islands and
is considered a delicacy among these populations (Huchette and Clavier 2004).
Small abalone industries still exist in these countries (~ 25 tonnes/annum),
however various environmental problems have hampered the development of
larger scale production;
Market research in Europe undertaken in the past year has suggested that
abalone would retail in traditional European restaurants for ~€50 per serving. It
was estimated that approximately 1000 ‘high class’ restaurants in France,
Spain, Germany, Italy, UK and Switzerland would potentially serve abalone (EU
Framework 7 project entitled ‘Sustainable Development of European SMEs
Engaged in Abalone Aquaculture’);
Assuming an average of 5 servings per week for each of these restaurants, this
would equate to 260,000 servings per annum;
Assuming that people rarely eat at top class restaurants due to the expense,
this would suggest an additional 260,000 European consumers in addition to
the European-Chinese abalone consumers; and
14
Source: Department of Economic and Social Affairs Population Division of the United Nations
Secretariat (2009). World Population Prospects, Table A.1.
33
g.
h.
Based on traditional and European-Chinese consumption an estimate of the
proportion of the European population that consume abalone is around
1,110,000 people.
Based on the proportion of the European population consuming abalone and
the number of servings of Australian canned abalone available this would result
in 965 days between servings for each consuming individual.
Population in China Consuming Abalone
In order to estimate the proportion of the Chinese population that consume abalone
the following rationale and assumptions have been applied:
a.
b.
c.
d.
e.
f.
g.
Due to the large land mass of China, it is likely that the majority of abalone
would be consumed by those who live in the eastern coastal areas.
Significant cities along the eastern plane include: Hong Kong, Guangzhou (15
million), Shenzen (8 million), Fuzhou (6 million), Shanghai (20 million), Qingdao
(8 million), Beijing (17 million), Tianjin (10 million) and Dalian (7 million).
An estimate of the total population of the eastern Chinese provinces is
450,000,000. Approximately 20% of the population is under 15 years of age.
Dining out at premium restaurants is considered prestigious and there is no
more highly regarded foodstuff than abalone in China. It has been estimated
that there are over 10,000 restaurants in Shanghai alone serving abalone. One
estimate suggests Australian abalone can retail in Chinese markets for up to
$100 AUD/kg (Lisson 2005).
The distribution of disposable income and consumption among urban
households in China reveals that 60% of the population earned less than
11,051 yuan (< $2000 AUD) in 2004 and ~10 % lived below the national
poverty line (Ramstetter et al. 2006). Given the high price it is likely that the
costs of abalone would be prohibitive for this proportion of the population.
Assuming that 60 % of the total population of the eastern provinces would not
consume abalone due to prohibitive costs, and that a further 20 % of those
remaining would be under the age of 15, it can be deduced that approximately
144,000,000 Chinese people potentially consume abalone.
Based on the proportion of the population potentially consuming abalone, and
the number of servings of Australian ‘canned’ and ‘fresh, chilled and frozen’
abalone available in China, there is an estimated 4,315 days between servings
of canned Australian abalone and 1,614 days between servings of ‘fresh,
chilled and frozen’ abalone for each consuming individual.
6.5 Influence of Processing on PST Levels in Abalone
6.5.1
Overview of Canning Process
A brief description of a commercial canning process is provided below. The process
described is used by one of the large Australian abalone processing companies and
other companies may have slightly different processing parameters.
The abalone are sacrificed by severing the mantle from their shell. The animal is then
removed from the shell without the viscera. The edible portion of the animal is placed
into a tap water ice slurry for 30 mins to cool the meat down and allow the animals to
bleed out. The animals are then placed in a heated saturated saltwater brine solution
(approximately 45 - 50ºC) and rumbled (mixed) to begin removing the black pigment.
The mouths of the animals are removed and then they are cooled to 5ºC by again
placing them in a freshwater ice slurry. A nylon brush is used to scrub the edible
portions of the animal to remove the remaining black pigment without damaging the
34
fringe. Once scrubbed, the animals are graded and the abalone meat is chilled and
packed into cans. The cans are then filled with brine at ambient temperature and a
vacuum is created by filling the headspace with steam, the cans are hermetically
sealed and cooked in retorts at ~113ºC for 55 minutes (Figure 10).
Shuck fresh chilled abalone, remove
mouth & visceral portions
Fresh water ice slurry
30 minutes
30 minutes
Rumble in a 45-50ºC
saturated salt-water
brine solution
Gently scrub ‘side foot’ with a nylon nail
brush or abrasive pads to remove black
pigmentation, making sure not to damage
the delicate fringe.
Abalone graded and chilled
Canning
113 ºC 55 minutes
Figure 10.
Overview of the Commercial Canning Processing of Abalone
6.5.2 Effect of Pre-Canning Process on PST Levels in Edible Portion
Investigations were undertaken to elucidate the anatomical distribution of PSTs in the
South African abalone (H. midae), Spanish abalone (H. tuberculata), and the
Australian Greenlip abalone (H. laevigata). It was established that much higher levels
of PSTs were present in the epipodial fringe (~ 900 µg STX eq 100g-1) of H. midae
compared with the muscular tissue of the foot and the visceral portions (~100 µg STX
ex 100g-1 each). The removal of the epithelial tissue via scrubbing both the surface of
the foot and the epipodial fringe was found to ‘dramatically’ lower the toxin levels in
these tissues suggesting that the PSTs were predominantly located in the epithelium.
35
The authors concluded that scrubbing could provide a management tool to reduce
levels of PSTs prior to marketing the product for consumption (Pitcher et al. 2001).
A similar distribution of PSTs in H. tuberculata (Galician abalone) was demonstrated
in a study by Bravo et al (1996), which showed significantly higher levels of PSTs in
the foot (220 µg STX eq 100g-1) when compared with the viscera (104 µg STX eq
100g-1). A more detailed study on the anatomical distribution of PSTs in
H. tuberculata was then undertaken. This revealed that the epithelium of the abalone
foot contained significantly higher levels of toxins in comparison with the gut and the
muscular foot tissue. It was estimated that the foot epithelium alone contributed to
~ 64% of the total toxicity of the abalone, and that removal of the viscera and
epithelial layers on the foot would decrease toxicity by around 75%. These findings
raised the possibility of reducing the risk from PSTs in Galician abalone via a
processing step to remove the epithelium of the foot and the gut (NB: this is a
standard part of the current commercial process for canned abalone in Australia). In
the context of the contamination found throughout the Galician fishery in the 1990’s
this would have reduced the toxin levels present in abalone to below the legal
maximum of 80 µg 100g-1 (Bravo et al. 1999).
Subsequently, immunohistochemical analysis of H. tuberculata foot samples was
undertaken by Bravo et al (2001). The research showed that the epithelial cells on
the ‘side foot’ (where the dark pigmentation can be seen) comprised some cells that
contained STX. In contrast epithelial cells on the ‘foot sole’ did not include epithelial
cells that contained STX. These results were corroborated by HPLC analysis which
showed 3200 µg 100g-1 dcSTX and 2400 µg 100g-1 STX in the ‘side foot’ epithelial
tissue and undetectable levels of STX/dcSTX in the ‘foot sole’ epithelial tissue (Bravo
et al. 2001).
Similar to the South African and Spanish studies, recent research on the Australian
Greenlip abalone demonstrated that the pre-canning processing steps, which
involves removal of the epithelial layers on the side-foot (black pigment) via
scrubbing, reduced the PST levels in the foot tissue by ~ 72% (Homan et al. 2010).
The authors concluded that these separate studies on three different abalone
species indicate that there is probably no major species variation effect with respect
to localisation of toxin within the tissues of abalone. Removal of the black pigment is
already a common undertaking in Australia for commercial product destined for
canning due to the market preference for this type of presentation and as such
provides an effective risk reduction step.
6.5.3 Canning
The industrial canning process for abalone involves cooking the abalone within cans
in retorts at ~113ºC for 55 minutes, plus the come-up and come-down thermal
process. The effect of regular commercial and modified canning on the concentration
of PSTs in clams and scallops was reviewed in 1971 by Prakash. A key finding was
that the commercial canning process reduced the total toxicity (determined by mouse
bioassay) of clams by more than 90%. The reduction of canning on initial levels in
scallop livers and ‘rims’ was also shown to be greater than 90% (Prakash et al.
1971).
Similar research on the effect of the industrial canning process on PST levels in
cockles and mussels has also been undertaken. These results indicate that the
canning process reduces the concentration of total PSTs in cockles (Acanthocardia
tuberculata L.) by 75 % (Berenguer et al. 1993). In response to this finding, the
European Commission has allowed the harvesting and importation of cockles
(Acanthocardia tuberculata L.) that contain an ‘initial level of contamination’ not
36
exceeding 300 µg STX eq 100g-1 provided that they undergo processing (‘suitable
heat treatment’) and end product testing. PST levels in mussels were also shown to
be reduced by at least 50% in samples containing a wide range of initial PST
concentrations (Vieites et al. 1999). It is suggested that some reduction may be due
to a combination of transfer of PSTs into the liquor within the can and thermal
destruction of the toxins (Vieites et al. 1999).
There are a wide range of different analogues within the PST group and they are
likely to behave slightly differently upon canning. Studies on the presence of PSTs in
abalone have shown that abalone mainly contain the carbamate group of PSTs. This
is likely due to biotransformation of other PSTs into carbamate toxins (Homan et al.
2010; Jaime et al. 2007; Nagashima et al. 1995b; Pitcher et al. 2001). Therefore, the
carbamate group (e.g. STX) of PSTs is the main concern with respect to the thermal
resistance of PSTs during the abalone canning process.
Recent studies have been undertaken on the effects of heating (60 minutes at
120ºC) followed by various storage temperatures (5, 25 and -35ºC) on the
concentration of individual PSTs. A study undertaken on scallop homogenates
revealed that samples heated for 60 minutes at 120ºC (roughly equivalent to the
thermal process involved in canning abalone) and then stored for 12 months at 5ºC
showed a 61% decrease in the level of STX present and a 41% decrease after 1
month storage at 25ºC (Indrasena and Gill 2000).
In summary, the reductions of PSTs reported in the literature for cockles, scallops,
mussels and clams ranged between 41 and 90%, with only one study showing a
reduction less than 50%. As discussed, the pre-canning processing of abalone to
remove the black pigmentation reduces levels of PSTs in abalone by ~ 75%.
Unfortunately no direct data are available on the further reduction in concentration of
PSTs through the actual canning process. However, based on the above data it
seems highly probable that the canning of abalone will result in further substantial
decreases in PST concentration, probably in the order of at least a 50% reduction.
Overall this would result in a reduction of toxin levels of 87.5%, this indicates that
initial levels of ~600 µg 100g-1 in the whole animal prior to canning would be
compliant with the regulatory limit of 80 µg 100g-1 following canning.
6.5.4 Depuration
Research into the depuration of PSTs from H. midae (South African abalone)
suggested that the toxins can be significantly reduced by placing abalone in clean
seawater and feeding them uncontaminated artificial feed pellets. This treatment
resulted in a reduction of PSTs from 160 to 72 µg STX eq 100 g-1 tissue over two
weeks. Contaminated abalone that were fed a diet of the macroalgae Ecklonia
maxima during the cleansing period, or were starved, did not show a significant
reduction in the level of PST detected however mean levels were 40 % lower than
the initial toxic animals (Etheridge et al. 2004).
A recent study on Australian greenlip abalone (H. laevigata) showed a 76% decrease
in PST levels in the foot tissue compared with the initial contaminated animals when
they were depurated for 65 days in fresh seawater and fed commercial feed pellets
(Homan et al. 2010). These results highlight the possibility of reducing the PST
concentrations through extended depuration should a harmful algal bloom event
arise. However, the practicality of applying such a management step will depend on
how rapidly PSTs depurate following the event and if the toxins depurate to the same
level when the abalone feed on macroalgae rather than commercially manufactured
diets, as this is not yet known.
37
7.
Risk Characterisation
“The process of determining the qualitative and/or quantitative estimation of
the probability of occurrence and severity of known or potential adverse health
effects in a given population based on hazard identification, hazard
characterisation and exposure assessment (Anon 1999).”
The probability of humans living in the EU and China becoming ill with PSP via the
consumption of Australian wild caught canned abalone has been determined both
qualitatively and semi-quantitatively in this section. The two separate approaches
(qualitative and semi-quantitative) were undertaken to provide an additional level of
confidence in the outcomes, as both methods have shortcomings e.g. inadequacy of
data currently available, assumptions in the mathematical model, variability of data
inputs. Appendix One details a semi-quantitative risk assessment on the probability
of humans living in China becoming ill with PSP via the consumption of Australian
wild caught ‘fresh, chilled, frozen’ abalone. An assessment of the risk of PSP to EU
consumers via the consumption of ‘fresh, chilled, frozen’ Australian abalone has not
been made as it is not likely that Australian abalone of this product type would be
exported to the EU.
7.1 Qualitative Risk Characterisation
Several different qualitative risk characterisation schemes have been devised (Huss
et al. 2000; Sumner et al. 2004). A simple risk ranking scheme outlined in the FAO
Fisheries technical paper 442 has been utilised here to derive a risk ranking estimate
of high, medium or low (Sumner et al. 2004). Data identified in the hazard
identification, hazard characterisation and exposure assessment sections of this risk
assessment have been used to answer six questions and assign a qualitative risk
ranking (Table 10). The outcome of the qualitative risk ranking indicates that the
likelihood of occurrence of PSTs in Australian wild caught canned abalone and
exposure of humans to significant levels is ‘Extremely Low’.
7.2 Semi Quantitative Risk Characterisation
Ross and Sumner (2002) developed a simple spreadsheet tool called Risk Ranger to
characterise risk and derive semi-quantitative risk estimates, including:
- The total predicted illnesses per annum in selected population; and
- A risk ranking (Ross and Sumner 2002).
The tool requires the selection of qualitative statements and also the input of
quantitative data on factors that will affect the food safety risk to a specific population
from harvest to consumption. The spreadsheet tool then applies a series of
mathematical and logical steps to derive the estimates of public health risk. Steps for
calculating the mathematical estimates used in this semi-quantitative risk
assessment are available in Ross and Sumner (2002). The data required to complete
this semi-quantitative risk assessment were obtained from the hazard identification,
hazard characterisation and exposure assessment sections of this report, or were
based on the expert opinion of the risk assessors. Full details of the semiquantitative assessment are presented in Table 11.
The major outcome of the semi-quantitative risk assessment is a predicted illness
rate of 0.01 (EU) and 0.53 (China) per annum in the selected population associated
with the consumption of Australian wild caught canned abalone. Risk Ranking (RR)
scores between 0 and 100 were also derived, with RRs of 28 and 26 elucidated for
the EU and China respectively. To ‘reality check’ these results a comparison of these
RR values against those obtained in a semi-quantitative seafood safety risk
38
assessment of 10 product/hazard combinations has been made (Sumner and Ross
2002).
The authors found that based on their RR values Australian seafood products fell into
three distinct categories:
- Risk Ranking of < 32 (Low Risk)
- Risk Ranking of 32 – 48 (Medium Risk)
- Risk Ranking of >48 (High Risk)
The product/hazard combinations that were ranked as <32 included mercury
poisoning (RR = 24), Clostridium botulinum in canned fish (RR = 25), C. botulinum in
vacuum-packed cold-smoked fish (RR = 28), parasites in sushi/sashimi (RR = 31),
viruses in shellfish from uncontaminated waters (RR = 31), enteric bacteria in
imported cooked shrimp (RR = 31) and algal biotoxins from controlled waters (RR =
31). The authors reported that there have been no documented cases of food-borne
illness from any of the above hazard/product pairings in Australia. In contrast,
product/hazard combinations that fell in the other higher ‘RR’ categories were known
to cause food borne illness periodically (Sumner and Ross 2002). Consistent with
this there have been no documented cases of food borne illness resulting from PSTs
in canned wild caught Australian abalone, therefore the RR values of 28 (EU) and 26
(China) seem appropriate in scale. The RR values also agree with the outcome of the
qualitative assessment which suggests an ‘Extremely Low’ risk status for PSTs in
Australian wild caught canned abalone (section 7.1).
39
Table 10.
Qualitative risk ranking of PSTs in canned wild caught Australian abalone
Product
Severity of hazard
Likelihood of occurrence
Growth required to cause disease
Effect of production/processing on hazard
Canned Australian Abalone
Moderate
Low
Not Applicable
Reduction
Consumer terminal inactivation step
None
Linkage with illness
None
Note
The majority of cases result in minor or moderate
symptoms (Table 1) and most people fully recover.
Therefore the severity has been classified as
moderate in line with the recommendations of
Sumner et al. (2004).
0/52 samples tested as part of the National Residue
Survey in Australia were positive for PSTs. 1 sample
taken during a significant algal bloom in Victoria
showed low levels of PST in abalone gut (123 µg
100 g-1), compared with extremely high levels in
bivalves (>10,000 µg 100 g-1).
The concentration of PST does not increase post
harvest.
The pre-canning process to remove the black
pigmentation has been found to reduce levels of
PSTs by ~75 %. Canning is likely to reduce levels by
a further 50 %. An overall reduction of 87.5% is
expected.
Home cooking may further reduce levels of PSTs.
However the literature is limited on the effect of
cooking on PST composition and concentration in
abalone. Therefore a conservative approach of ‘no
change’ has been taken.
There have been no documented or anecdotal
cases of PSP from the consumption of abalone.
Risk Ranking
Extremely Low
Note: A simple risk ranking scheme outlined in the FAO Fisheries technical paper 442 has been utilised here to derive the risk ranking (Sumner
et al. 2004).
40
Table 11.
Semi-quantitative risk characterisation of consumption of canned wild caught Australian abalone containing PSTs
Risk Criteria
Dose and Severity
1.
Hazard Severity
2.
Susceptibility
Probability of Exposure
3.
Frequency of Consumption
4.
Proportion Consuming
5.
Size of Consuming Population
Probability of Contamination
6.
Probability of raw product
contaminated
European Union
China
Moderate Hazard
Moderate Hazard
General – all
population
General – all
population
Every 965 days
Every 4315 days
0.15 %
11 %
1,110,000
144,000,000
Rare: 1 in a 1000
Rare: 1 in a 1000
Note
The definition of moderate hazard is: ‘requires
medical intervention in most cases’ (Sumner et al.
2004). This is likely a conservative classification as
the majority of PSP cases would result in minor or
moderate symptoms (Table 1) and would not
require medical intervention.
While some data suggests certain groups of people
may be more susceptible than others, this is not
well understood. Therefore a conservative
assumption that all members of the population are
equally susceptible was taken.
The frequency is based on Australian abalone
export data and a 50 g serving size.
This is based on the consumption of abalone in the
EU by Chinese residents and a small number of
traditional consumers in prestigious restaurants;
and on the proportion of high income earners in the
eastern coastal zones of China (section 6.4.2).
Total populations of Europe and China were
732,000,000 and 1,336,610,000 respectively in
2009. Section 6.4.2 details assumptions made to
deduce size of consuming population.
0/52 samples tested as part of the National
Residue Survey in Australia were positive for PSTs.
41
7.
Effect of Processing
Entire process
results in reduction
of 87.5%
Entire process
results in reduction
of 87.5%
8.
9.
10.
Possibility of recontamination
Post-process control
Increase in infective dose
Not Applicable
Not relevant
Not Applicable
Not relevant
2710
2710
11.
Further cooking before eating
No effect
No effect
0.010
0.53
28
26
Total predicted illnesses per
annum in selected population
Risk Ranking
One sample taken during a significant algal bloom
in Victoria showed low levels of PSTs in abalone
gut (123 µg 100 g-1), compared with extremely high
levels in bivalves (>10,000 µg 100 g-1), indicating
low propensity of abalone to uptake toxins.
The pre-canning process to remove the black
pigmentation has been found to reduce levels of
PSTs by ~75 %. Canning is estimated to further
reduce PSTs by at least 50 %
Level of PST does not change post processing.
The LOAEL estimated by the WHO/FAO Expert
Consultation group was 2.0 µg kg-1 bw. For a 60 kg
person this equates to a single dose of 120 µg.
Background PST levels obtained from HPLC
testing of control Australian abalone were
~0.07 µg g-1 (Homan et al. 2010). Based on a 50 g
portion size, and a decrease in the background
level of 87.5% through processing, the factor of
increase needed to cause PSP would therefore be
a minimum of 2710. The LOAEL was used in the
model as opposed to the LD50, this is a
conservative approach, as 50 % of the population
would not die if this dose was consumed.
Home cooking may result in additional reduction of
PST levels in abalone, however there is a lack of
scientific data on abalone to support this so a
conservative classification of ‘no effect’ is applied
42
8.
Uncertainty
Several sources of uncertainty have been identified in this risk based assessment. A
summary of the uncertainties is provided below; these data gaps impact the reliability
of the final risk estimates detailed in Section 7.
• No actual data are available on the proportion of the EU and Chinese
populations that consume abalone.
• No actual data are available on serving sizes of abalone in the EU or China.
• No actual data are available on the frequency of abalone consumption by EU
or Chinese consumers.
Probability of Contamination (Pre-Processing)
• Various modes of PST uptake by abalone have been postulated, including
uptake of PSTs via consumption of macroalgae, dinoflagellates and bacteria.
However, the mode(s) of uptake of PSTs by abalone require confirmation.
This makes it difficult to identify factors (e.g. certain environmental conditions)
that may increase risk.
• A relatively small number of samples (n=70) of Australian abalone have been
sampled and tested for PSTs. The data do not comprehensively detail the
location from which samples were taken, the abalone species sampled, or the
sample type (e.g. whole tissue, gut or meat, canned etc). Unfortunately this
may mean that the data are not representative of PST occurrence in high
productivity Australian abalone fishing zones.
• Most Australian data on the occurrence of PSTs in abalone have been
generated using the mouse bioassay which has a relatively high limit of
detection. This means that lower levels of PSTs may have been present in
abalone but not detected.
• The semi-quantitative risk estimates were derived using a small sample size
of abalone (n=10) that were analysed by HPLC methods and as such is not
representative of PST levels across all high production abalone fishing zones.
Influence of Processing
• The pre-canning process has been investigated in three different abalone
species and is suggested to reduce PST levels by ~ 75 %. It is uncertain if
this PST reduction is similar in other species of abalone.
• It is suggested that canning significantly reduces levels of PSTs in the flesh of
cockles, mussels and clams (by at least 50 %), however no data are available
on the effect of canning on PST levels in the edible portion of abalone. This is
likely to further decrease risk of PSP in humans from consumption of
Australian abalone.
• No information is available on the influence of home cooking on the
concentrations and composition of PSTs in Australian abalone.
• Information is scant on the dynamics of depuration (cleansing) of PSTs from
Australian abalone in the wild.
43
9.
Conclusions and Recommendations
The pre-canning process (removal of side foot epithelial layers) decreases levels of
PSTs in abalone by ~75% and the thermal canning process likely reduces the
remaining PSTs by 50%, resulting in an overall reduction of 87.5%. This suggests
that abalone that potentially contained levels of ~600 µg 100g-1 in the whole animal
prior to canning would be compliant with the regulatory limit of 80 µg 100g-1 following
canning. Given the limited ability of Australian abalone to take up significant levels of
PSTs it is extremely unlikely that levels above 600 µg 100g-1 would occur.
The semi-quantitative risk estimate derived in this assessment predicts that 0.01
people may become ill in the EU per annum from the consumption of canned wild
caught Australian abalone (based on the consumption of ~420,000 servings of
Australian canned abalone per annum). This equates to only one case of illness
every 100 years (‘illness’ includes cases with minor symptoms and is not necessarily
severe). Likewise the estimated burden of illness in China was very low with 0.53
predicted illnesses per annum from a total of 12,180,000 servings of canned wild
caught Australian abalone.
A qualitative risk estimate derived in this assessment also confirms that the
probability of EU and Chinese consumers becoming ill from PSP via the consumption
of canned wild caught Australian abalone is Extremely Low.
These risk estimates are corroborated by the lack of documented and anecdotal
cases of PSP associated with the consumption of abalone worldwide. The extremely
low probability of PSP illness resulting from the consumption of canned wild caught
Australian abalone provides guidance for consideration of commensurate risk
management options.
Several sources of uncertainty were identified through the course of this risk
assessment (Section 8). To improve the reliability of the risk estimates generated in
this risk assessment it is specifically recommended that further research be
undertaken to address the following key data gaps:
• More accurately determine the serving size and frequency of Australian
abalone consumption by EU and Chinese consumers and the proportion of
the EU and Chinese population that consume Australian abalone.
• Ascertain PST levels in a representative number of abalone from key fishing
zones in Australia.
• Investigate the effect of the canning process on PST levels in the edible
portion of abalone and potential further decreases in toxin concentration.
• Determine the rate of PST depuration from the foot tissue of abalone in their
natural marine habitat.
44
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49
Appendix One
Semi-quantitative risk characterisation of consumption of ‘fresh, chilled and frozen’ wild caught Australian
abalone containing PSTs in China and ‘production flow’ diagrams for ‘fresh, chilled and frozen’ abalone.
Risk Criteria
Dose and Severity
1.
Hazard Severity
2.
Susceptibility
3.
Frequency of Consumption
4.
Proportion Consuming
5.
Size of Consuming Population
Probability of Contamination
6.
Probability of raw product
contaminated
7.
Effect of Processing
8.
Possibility of recontamination
China
Moderate Hazard
General – all
population
Every 1614 days
11 %
144,000,000
Rare: 1 in a 1000
None
Note
Definition of moderate hazard is: ‘requires medical intervention in most cases’
(Sumner et al. 2004). This is likely a conservative classification as the majority of
PSP cases would result in minor or moderate symptoms (Table 1) and would not
require medical intervention.
While some data suggests certain groups of people may be more susceptible than
others, this is not well understood. Therefore a conservative assumption that all
members of the population are equally susceptible was taken.
The frequency is based on Australian abalone export data and a 50 g serving size.
This is based on the number of high income earners in the eastern coastal zones
of China (section 6.4.2).
Total population was 1,336,610,000 in 2009. Section 6.4.2 details assumptions
made to deduce size of consuming population.
0/52 samples tested as part of the National Residue Survey in Australia were
positive for PSTs. One sample taken during a significant algal bloom in Victoria
showed low levels of PSTs in abalone gut (123 µg 100 g-1), compared with
extremely high levels in bivalves (>10,000 µg 100 g-1), indicating low propensity to
uptake toxins.
Some product types within the broad category of ‘fresh, chilled and frozen’ may
have had the black pigment scrubbed off (e.g. cleaned frozen meat) and the toxin
levels reduced by ~75 %. However, not all product types within this category would
have been subjected to this processing step e.g. live abalone. Therefore a
conservative approach is to assume no reduction. See ‘Production Flow’ diagrams
below for details on how product types within this category are processed.
Not Applicable
50
9.
10.
Post-process control
Increase in infective dose
11.
Further cooking before eating
Total predicted illnesses per
annum in selected population
Risk Ranking
Not relevant
339
No effect
Level of PST does not change post processing.
The LOAEL estimated by the WHO/FAO Expert Consultation group was
2.0 µg kg-1 bw. For a 60 kg person this equates to a single dose of 120 µg.
Background PST levels obtained from HPLC testing of control Australian abalone
were ~0.07 µg g-1 (Homan et al. 2010). Based on a 50 g portion size the increase
needed to cause PSP would therefore be a minimum factor of 339. The LOAEL
was used in the model as opposed to the LD50, this is a conservative approach,
as 50 % of the population would not die if this dose was consumed.
Home cooking may result in additional reduction of PST levels in abalone,
however there is a lack of scientific data on abalone to support this so a
conservative classification of ‘no effect’ is applied
0.97
39
51
Live Abalone Production Flow Diagram
Live abalone landed at wharf by
commercial diver is weighed
Animals are packed foot to foot in a
plastic mesh bag and transported to
processing factory in a covered vehicle
Daily
Animals are re-weighed on arrival & packed
into holding crates, then placed into
saltwater holding tanks (10ºC to 13ºC) for a
minimum of 3 days or up to 2-3 weeks.
Quality checks are
undertaken on the animals,
and tank water is analysed
for ammonia, nitrates,
nitrites, pH and salinity.
Animals are removed from tanks, graded for size
and quality, then packed into polystyrene boxes
and consigned to the market.
52
Frozen Abalone Production Flow Diagram
Live abalone landed at wharf by
commercial diver is weighed
Animals are packed foot to foot in a
plastic mesh bag and transported to
processing factory in a covered vehicle
Animals are re-weighed on arrival
Frozen on Shell
Frozen Un-bled 10kg Block or
Individually Quick Frozen (IQF) meat
Graded
Cleaned Frozen Meat
Shucked from shell
Graded
Blast Frozen to
-18ºC
Stored frozen at
-23 to -25 ºC until
dispatched for sale
Shucked from shell and
quickly blast frozen (-18ºC)
to minimise blood loss
Undergoes commercial
scrubbing procedure to
remove pigment on fringe
Graded
Stored frozen at
dispatched for sale
Blast Frozen to
-18ºC
Stored frozen at
dispatched for sale
53
Appendix Two:
Test results of wild caught Australian abalone for marine biotoxins undertaken through the National Residue Survey
(NRS) in 2002, 2003 and 2004 (data kindly provided by the Australian Quarantine and Inspection Service).
nd = not detected
Year
2002
2002
2002
2002
2002
2002
2002
2002
2002
2002
2002
2002
2002
2002
2002
2002
2003
2003
2003
2003
2003
2003
2003
2003
Abalone
Description
Abalone - Blacklip
Abalone - Blacklip
Abalone - Blacklip
Abalone - Blacklip
Abalone - Blacklip
Abalone - Blacklip
Abalone - Blacklip + gut
Abalone - canned
Abalone - canned
Abalone - Greenlip
Abalone - Greenlip
Abalone - Greenlip + gut
Abalone
Abalone
Abalone
Abalone
Abalone - Greenlip
Abalone - Greenlip
Abalone - Greenlip
Abalone - Greenlip, meat
and guts
Location
Name
Pyramid Rock
Sealers Cove
Pyramid Rock
Sealers Cove
Tipara Reef
Tipara Reef
Tipara Reef
Victoria
Victoria
Victoria
Victoria
South Australia
South Australia
South Australia
145.22
146.28
145.22
146.10
137.23.579E
137.23.579E
137.23.579E
38.45
39.03
38.45
38.49
34.03.807S
34.03.807S
34.03.807S
PSP
(µg/100g)
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
not tested
nd
Tipara Reef
South Australia
137.23.579E
34.03.807S
nd
State
Longitude
Latitude
Tasmania
Tasmania
NSP
(MU/100g)
not tested
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
DSP
(µg/100g)
not tested
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
ASP
(mg/kg)
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
54
2003
Abalone - Greenlip, meat
and guts
Tipara Reef
2003
Abalone - whole
Bruny Island
2003
Abalone meat
Bruny Island
2003
Abalone meat
Bruny Island
2003
Abalone meat
Bruny Island
2003
Abalone meat - Greenlip
Cape Arid
2003
Cape Arid
2003
Cape Arid
2003
Canned roe abalone
Hopetoun
2003
Canned roe abalone
2004
Abalone
2004
2004
2004
2004
Abalone
Abalone - Blacklip, whole
Windy Harbour
Apollo Bay - Reef
7.1 Cape Otway
Apollo Bay - Reef
7.1 Cape Otway
South West Cape
South West Cape
SouthPort
2004
Abalone - Brownlip
Israelite Bay
2004
2004
Abalone - Brownlip
Abalone - canned
Israelite Bay
Bass Straight
2004
Abalone - frozen, whole
Eden
South Australia
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
34.01.896S
nd
nd
nd
nd
123.09.082E
34.00.582S
nd
nd
nd
nd
120.01.280E
33.57.700S
nd
nd
nd
nd
120.07E
33.57S
nd
nd
nd
nd
116.01E
34.50S
nd
nd
nd
nd
Victoria
143.30
38.80
nd
nd
nd
nd
Victoria
Tasmania
Tasmania
Tasmania
Western
Australia
Western
Australia
Victoria
New South
Wales
143.30
Block 12B
Block 12B
Block 14D
38.80
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
123.52
33.37
nd
nd
nd
nd
123.52E
33.37S
nd
nd
nd
nd
nd
nd
nd
nd
149.56.30E
37.04.30S
nd
nd
nd
nd
Tasmania
Tasmania
Tasmania
Tasmania
Western
Australia
Western
Australia
Western
Australia
Western
Australia
Western
Australia
137.23.579E
East block
16B
East block
16B
East block
16B
East block
22B
34.03.807S
123.14.662E
55
2004
Eden
2004
2004
Abalone + gut
2004
2004
2004
2004
2004
Abalone + gut
Abalone meat
Abalone meat
Abalone meat
Abalone meat - blacklip
Eden
Sealers Cove
Stony point
(ramp)
Flinders (ramp)
Tipara Reef
Tipara Reef
Nubeena
2004
Abalone roe
Doubtful Bay
New South
Wales
New South
Wales
Victoria
Victoria
Victoria
South Australia
South Australia
Tasmania
Western
Australia
149.56.30E
37.04.30S
nd
nd
nd
nd
149.56.30E
146.26
37.04.30S
39.01
nd
nd
nd
nd
nd
nd
nd
nd
145.13
145.02
137.22.393
137.22.393
Block 20A
38.22.30
38.27
34.02.969
34.02.969
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
nd
124.29E
16.07S
nd
nd
nd
nd
56
Appendix Three
Portion Size of Abalone Servings in Adelaide Chinese
Restaurants
The portion size for individual consumers of abalone in dishes prepared and served
in a typical (Adelaide) Chinese restaurant is difficult to identify with precision for a
number of reasons, including:
- Portion size will vary according to market price - for fixed price dishes
(typically ‘Braised abalone with Chinese mushrooms and vegetables’) as the
market price rises, the portion size will decline; for ‘Whole Abalone’ single
animal offerings, the portion size and the price are both fully flexible,
dependant on market availability;
- Abalone, like many Chinese dishes, are frequently consumed ‘in common’
between all (or some) of the participants at the table, and the proportion of
sharing is clearly an unknown – this applies particularly to ‘Whole abalone’;
- Personal preference will play a major role in the consumption of ‘Whole
Abalone’ purchases.
However, interviews with the limited number of restaurants offering abalone in the
Gouger Street restaurant precinct (only 4/25 Chinese restaurants served abalone clearly an expensive, ‘high end’ product) allows the likely portion size per consumer
to be quantified.
• For the ‘Braised abalone’, with accompanying vegetables (and Sea
Cucumber, on occasion) the variables will be:
- Size of meats and market price (see above);
- Number of slices per presentation;
- Possibly the number of participants at the meal.
• Current availability of meats (average) is for 4-5 animals per Kilogram, with
individuals therefore ranging from 200 – 250 grams; these would be sliced
(pers. Comm.) into 4 – 5 pieces, indicating a weight per slice of around 50
grams. A typical portion for a ‘Braised abalone’ dish (priced at around $50,
including vegetables) would thus be 2 slices or 100 grams.
• This estimate is confirmed by reports concerning ‘Whole abalone’ portions.
These portions would clearly depend upon the size of the product available at
any given time, hence the prices generally being ‘POA’ (‘Price On
Application’); however, one restaurant surveyed quoted a fixed price of
$108.80 (with Sea Cucumber), which is broadly consistent with the above (4
slices per abalone @ average $25/slice).
• Another restaurant indicated that the ‘Whole abalone’ dish was usually
ordered for multiple customers, who would request an appropriate number of
slices (2 abalone for 4 people (equivalent to 1 abalone between 2 or 2 slices
per consumer), 4 abalone for 10 guests, etc.).
D McLeod
19/04/2010
Restaurants surveyed (19 April 2010):
- Ding Hao
- T-Chow
- Dragon Dynasty
- Mongkok
57

Risk Assessment of STX group toxins in Abalone v13

Transcription

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