HeaLTH, HUMan BeingS, and THe enVironMenT

Transcription

SAN FRANCISCO MEDICINE
VOL.81 NO.1 January/February 2008 $5.00
JOURNAL OF THE SAN FRANCISCO MEDICAL SOCIETY
Linked for Life
Health, Human Beings, and the Environment
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CONTENTS
January/February 2008 Volume 81, Number 1
Linked for Life: Health, Human Beings, and the Environment
FEATURE ARTICLES
9
MONTHLY COLUMNS
A New Era for Environmental Health Philip R. Lee, MD; Steve Heilig, MPH;
and Michael Lerner, PhD
4 On Your Behalf
5 Classified Ads
10 Toxic Dilemmas Donald Kennedy, PhD
5 Upcoming SFMS Events
11 Toys, Tots, and Toxic Chemicals David Wallinga, MD, MPA
13 Reproductive Health and the Environment Tracey J. Woodruff, MPH, PhD;
Jackie M. Schwartz, MPH; Alison Carlson; and Linda C. Giudice, MD, PhD
6 Executive Memo
Mary Lou Licwinko, JD, MHSA
17 Early Vulnerability, Lifelong Impacts Philippe A. Grandjean, MD, PhD
7 President’s Message
Steven Fugaro, MD
19 Climate Change and Children’s Health Katherine M. Shea, MD, MPH, and
Sophie J. Balk, MD
8 Editorial
Mike Denney, MD, PhD
22 The Falling Age of Puberty in U.S. Girls Sandra Steingraber, PhD, Jeanne Rizzo, RN
40 Hospital News
24 Cancer and Environmental Chemicals Devra Lee Davis, PhD
41 In Memoriam
Nancy Thomson, MD
26 Mercury Tales Jane Hightower, MD
30 Time to Update Environmental Regulations John Peterson Myers, PhD, and Fred
S. vom Saal, PhD
42 Guest Column: Small-Town Medicine
Alan G. Greenwald, MD
Editorial and Advertising Offices
32 Nanoparticles and Health John M. Balbus, MD, MPH
1003 A O’Reilly
San Francisco, CA 94129
33 Neurodevelopmental Disorders and Environmental Agents Elise Miller, MEd,
and Steve Gilbert, PhD, DABT
Phone: 415.561.0850 ext.261
Fax: 415.561.0833
Email: [email protected]
Web: www.sfms.org
34 Biomonitoring Update Davis Baltz, MA
Subscriptions:
35 Electromagnetic Fields David Carpenter, MD, and Cindy Sage, MA
$45 per year; $5 per issue
35 Chemical Exposures on the Job May Be Linked to Diseases in Nurses Charlotte
Brody, RN
website, www.sfms.org, or can be sent upon
Advertising information is available on our
request.
Printing:
36 The War Goes On: Tobacco Control in California Mi-Kyung Hong, MPH;
Richard L. Barnes, JD; Stanton Glantz, PhD; and Steve Heilig, MPH
Sundance Press
P.O. Box 26605
Tuscon, AZ 85726-6605
37 Agent Orange and Birth Defects Betty Mekdeci
39 Book Review: Exposed Steve Heilig, MPH
www.sfms.org
January/February 2008 San Francisco Medicine January/February 2008
Volume 81, Number 1
ON YOUR BEHALF
A sampling of activities and actions of interest to SFMS members
Editor Mike Denney
Managing Editor Amanda Denz
Copy Editor Mary VanClay
Notes from the
Membership Department
Cover Artist Amanda Denz
Upcoming Events
Editorial Board
Chairman Mike Denney
Obituarist Nancy Thomson
Stephen Askin
Shieva Khayam-Bashi
Toni Brayer
Arthur Lyons
Linda Hawes-Clever
Terri Pickering
Gordon Fung
Ricki Pollycove
Erica Goode
Kathleen Unger
Gretchen Gooding Stephen Walsh
2008 membership activities will include a new event at the de Young Museum, the popular Summer Gallery Mixer,
the return of the SFMS Night at the San
Francisco Symphony, a Holiday Night at
the Nutcracker, and much more! Remember—nonmembers are welcome at SFMS
membership social/cultural events. This is
a great way for them to get to know SFMS
and its membership better.
SFMS Officers
President Steven H. Fugaro
Attention, Young Physicians!
President-Elect Charles J. Wibbelsman
The San Francisco Medical Society has
formed an active and vibrant Young Physicians section to better address the needs and
concerns of members aged forty-five and
younger. A variety of social and educational
gatherings are a featured part of this newest
component to SFMS membership. If you
are interested in participating, contact Tom
Lee, MD, at [email protected].
Secretary Gary L. Chan
Treasurer Michael Rokeach
Editor Mike Denney
Immediate Past President Stephen E. Follansbee
SFMS Executive Staff
Executive Director Mary Lou Licwinko
Director of Public Health & Education Steve Heilig
Director of Administration Posi Lyon
Director of Membership Therese Porter
You Can Make SFMS Even Better!
Director of Communications Amanda Denz
Promoting membership just got easier!
Did you know that your physician peers can
now join the San Francisco Medical Society
online? Joining SFMS/CMA is simple—go
to www.sfms.org and click “Join SFMS” on
the top of the home page. It’s quick and easy,
and new members get a 50 percent discount
on their first year’s dues!
Thank you to our members who have
already referred their fellow physicians—
physicians talking to physicians remains
the strongest and best way for the Medical
Society to grow its ranks and help shape the
future of medicine.
SFMS is always looking for feedback
from its members, as well as suggestions as
to how to make membership more interesting, valuable, and fun. Contact Therese
Porter in the Membership Department at
(415) 561-0850 extension 269 or tporter@
sfms.org.
Board of Directors
Term:
Jan 2008-Dec 2010
Jordan Shlain
George A. Fouras
Lily M. Tan
Keith E. Loring
Shannon Udovic-
William A. Miller
Constant
Jeffrey Newman
Term:
Thomas J. Peitz
Jan 2006-Dec 2008
Daniel M. Raybin
Mei-Ling E. Fong
Michael H. Siu
Thomas H. Lee
Term:
Carolyn D. Mar
Jan 2007-Dec 2009
Rodman S. Rogers
Brian T. Andrews
John B. Sikorski
Lucy S. Crain
Peter W. Sullivan
Jane M. Hightower
John I. Umekubo
Donald C. Kitt
CMA Trustee Robert J. Margolin
AMA Representatives
H. Hugh Vincent, Delegate
Robert J. Margolin, Alternate Delegate
San Francisco Medicine January/February 2008
Revised ’08 Medicare Physician
Fee Schedule Now Available
The revised 2008 Medicare physician
fee schedule is now available at the NHIC
website, www.medicarenhic.com. In the
waning hours of the 2007 legislative session,
Congress passed a Medicare bill that postpones the 10 percent physician payment cut
and instead provides a 0.5 percent increase
for six months. The new fee schedule reflects
this small increase.
Physicians are encouraged to assess
the impact the Medicare payment changes
will have on their practices. It is important
that physicians understand how the new fee
schedule will affect their bottom line so that
they can make informed decisions about
Medicare participation for 2008.
Because Congress acted very late in the
session to stop the physician pay cut, the
Centers for Medicare and Medicaid Services
(CMS) have reopened the participation
decision period for an additional 45 days.
Physicians have until February 15 to make
any changes to their participation status.
However, all status changes will be effective
January 1, 2008.
Physicians are still faced with a 10
percent payment reduction on July 1, 2008,
unless Congress revamps the hopelessly
broken formula used to calculate physician
pay (or acts again with another last-minute
fix). With this cut looming, participation
decisions become more complicated. While
it is possible that CMS will again reopen the
participation decision period, there is no
guarantee that CMS will allow physicians
to change their participation status in July,
should the cut go into effect.
For more information, contact CMA’s
Reimbursement Help Line, (888) 401-5911
or [email protected].
Volunteer with a Young Apprentice
Would you like to share your career
with a young person who dreams of working
in your field? Spark is looking for volunteers
in the Redwood City area this spring.
Spark is a nonprofit program that matches
www.sfms.org
seventh- and eighth-grade students with
hands-on apprenticeships in their dream
job, where they spend a few hours per week
with a local professional. Apprentices and
mentors meet for one-and-a-half to twohour sessions over eight weeks (February
through May) at the volunteer’s workplace
or another public space between San Mateo
and Palo Alto. For more information, watch
the Spark video at www.youtube.com
SparkProgram, visit www.sparkprogram.
org, or contact Elena Sevastopoulos at
[email protected] or (415) 626-5470
extension 103.
staff; $189 for nonmembers.
The CMA House of Delegates
April 18, 2008
Customer Service/Front Office Telephone
Techniques
9:00 a.m. to 12 p.m. (8:40 AM registration/
continental breakfast)
This half-day practice management seminar
will provide valuable staff training to handle
phone calls and scheduling professionally
and efficiently. $99 for SFMS/CMA members and their staff ($89 each for additional
attendees from the same office); $149 each
for nonmembers.
Hugh Vincent, MD, and George Susens, MD
(in background), SFMS delegates
2008 SFMS Seminar Schedule
May 16, 2008
Managing the Team (for office managers
and administrators)
9:00 a.m. to 12:00 p.m. (8:40 a.m. registration and continental breakfast)
Motivating and Managing Your Office
Manager (for physicians)
12:15 to 1:45 p.m. (12:00 p.m. registration
and lunch)
These two seminars are designed to help
physicians and their office managers set
expectations, manage change, and design
a practice culture that helps the practice
thrive. $99 for Managing the Team for
SFMS/CMA members and their staff ($85
each for additional attendees from same office); $149 each for nonmembers.
$69 for Motivating and Managing Your
Office Manager for SFMS/CMA members
($59 each for additional attendees from
same office); $109 for nonmembers.
$150 for both sessions for members; $225
for nonmembers.
Advanced registration is required for all
SFMS seminars. Please contact Posi Lyon,
[email protected] or (415) 561-0850 extension 260, for more information. All seminars
take place at the SFMS offices located in the
Presidio of San Francisco.
February 15, 2008
Repair Leaks and Boost Practice Profits
in 2008: Billing, Coding, and Collection
Strategies
9:00 a.m. to 4:00 p.m. (8:40 a.m., registration and continental breakfast)
Devise strategies for repairing operational
leaks that cause profit losses in your practice.
A full day packed with the latest updates
on new diagnosis and CPT codes; new
Medicare requirements, the Office Inspector General (OIG) work plan for 2008, and
successful Denial and Appeal Management
Strategies. $199 per session for SFMS/CMA
members and their staff ($185 each for additional attendees from same office); $250
each for nonmembers.
March 24, 2008
Transitioning Your Practice: Retiring,
Selling, or Buying a Practice
6:00 to 9:00 p.m. (5:45 p.m. dinner/registration)
This is a not-to-be-missed seminar designed
for all physicians who are contemplating
retirement, bringing in an associate, joining
a practice as an associate, relocating, buying
or selling a practice, or changing careers.
$139 for SFMS/CMA members and their
www.sfms.org
Dexter Louie, MD, SFMS Delegate
Stephen Follansbee, MD, SFMS ImmediatePast President, at the reference committee
Classified Ads
BC FP, CA MD is looking for a job in
the Bay Area—[email protected]
Stonestown Medical Building offers
various sized medical suits for lease in
upper floors and on ground floor. Contact Trask Leonard at (650) 282-4620
or [email protected].
Brian Lewis, MD, Chair of SFMS Delegation
January/February 2008 San Francisco Medicine Executive memo
Mary Lou Licwinko, JD, MHSA
Looking Backward and Forward
I
t is has been two years since the San Francisco Medical Society
(SMFS) sold its Sutter Street mansion headquarters and moved
its operation to the Presidio. At the time of the move from a
building SFMS owned to a property it would rent, there was speculation about what this would mean for SFMS and its members. The
past two years have proved to be particularly successful for SFMS
in terms of membership growth, financial stability, and momentum
building. SFMS has realized an increase in membership of a magnitude that it has not seen in many years, and this year’s membership
numbers are looking even better. SFMS’s financial position is strong,
and the organization is poised for another successful year.
The year 2006 was an extraordinary one for SFMS. Led by then
President Dr. Gordon Fung, SFMS moved to its new headquarters
in the Presidio, restructured its financing, and stabilized staffing.
Dr. Fung’s efforts were followed by those of 2007 SFMS President
Dr. Steve Follansbee. Under Dr. Follansbee’s leadership, SFMS
refocused its mission, made membership a priority, and seized the
opportunity to reenergize. During Dr. Follansbee’s tenure, after
being challenged by the California Medical Association (CMA)
Executive Vice President Joe Dunne to get involved in the health
care reform process, SFMS developed its own health care reform
proposal, submitted it to the CMA, and published it in the July/
August 2007 issue of San Francisco Medicine. SFMS also held a successful event with Mayor Gavin Newsom, advocating for health
care reform in San Francisco and stressing the need to attract more
young physicians to the City. Also in 2007, SFMS experienced a
30 percent increase in new members and a feeling of new energy
for the Society. SFMS 2008 President Dr. Steve Fugaro has already
prioritized increasing both the membership and member activism,
not only on behalf of all San Francisco physicians but on behalf of
the community as well.
In recognition of changes in the practice of medicine and
the decreasing supply of primary care physicians in the Bay Area,
last year Dr. Robert Margolin led efforts that resulted in a forum
on the foundation and other models for delivering health care.
Twenty-five physicians from around the Bay Area attended the
event and discussed various models for delivering primary health
care and changes in the practice of medicine, fueled in part by a
new generation of physicians. The forum was so successful that this
year SFMS plans to expand it to a larger audience.
San Francisco Medicine, the SFMS journal published ten times a
year, also reached new heights in 2007. Under the leadership of the
editor, Dr. Mike Denney, the journal tackled disaster preparedness
and produced a comprehensive guide for physicians in the community. It also covered such weighty topics as money and medicine, the
healing power of love, medicine in the time of war, innovations in
food and health, and what it means to be a “compleat” physician.
SFM once again showed why it is considered one of the premier
county medical journals in the country.
In terms of public health and educational programs, in 2007
SFMS cosponsored an international conference that examined
the effects of the environment on fertility. More than 400 individuals from around world attended the conference. SFMS also
cosponsored, with the Sutter Health Institute, a palliative care
workshop on the state of the art of end-of-life care. In preparation
for a 2008 program for San Francisco high school students, SFMS
also spearheaded an effort to show the HBO series of short films
entitled Addiction and to conduct an educational forum on the
topic of addiction with the National Institute on Drug Abuse, the
California Society of Addiction Medicine, and UCSF.
The success of SFMS over the past two years has been due to
the tremendous work of our leaders, including the SFMS Board of
Directors and our community liaisons, all of whom I cannot thank
enough for the time they volunteer. In addition, SFMS has been
fortunate to have a topflight staff to handle all the day-to-day activities of the Society and make the operation look effortless. My
thanks to my own great staff as well. I have just begun my tenth
year as Executive Director of SFMS, and it is shaping up to be the
best year yet.
The editors of San Francisco Medicine would like to
extend a special thanks to Steve Heilig for his help
assembling this issue!
www.sfms.org
president’s Message
Steven Fugaro, MD
The Year of Membership
T
his is my first message as your SFMS President, but it
is—remarkably—the fifth issue that San Francisco Medicine
has devoted to the theme of environmental health. Steve
Heilig and the Collaborative on Health and the Environment
(CHE), along with the editorial staff of San Francisco Medicine,
have drawn together an extraordinary collection of contributors
and a comprehensive set of articles describing the current status of
environmental scientific knowledge and human health.
The authors include several nationally known scientists and
clinicians, such as Donald Kennedy, PhD, who is the outgoing
editor of Science. This issue also highlights a number of clinicians
and scientists who have a very significant national and international impact on issues of environmental health. Among these
San Francisco authors are local internist Dr. Jane Hightower, who
provides an update on her pioneering work on mercury in our diet;
Dr. Stanton Glantz, a UCSF professor, who reports on his latest
efforts in the ongoing battle against the tobacco epidemic; and Dr.
Philip Lee, emeritus professor at UCSF and former U.S. Secretary
of Health, who editorializes about developing a chemicals policy
for California and the United States. In fact, the CMA has recently
adopted an SFMS-sponsored resolution calling for a comprehensive
state and national chemicals policy incorporating current scientific
knowledge to evaluate the health impact of new and existing industrial chemicals.
SFMS is extremely proud to be involved in this effort to further our knowledge and awareness of environmental health. It is
of course completely consistent with our mission—to advance the
health of our patients and community while serving the needs of
all San Francisco physicians. This focus on environmental health
policy is but one example of the many ways that SFMS works to
advance the health of our community. Other instances include
the involvement of Steve Heilig and former SFMS President
Dr. Gordon Fung with projects including the Mayor’s Universal
Health Care Council and the proposed citywide Health Access
Plan; a recent SFMS Board discussion on supporting a City of San
Francisco plan to require cleaner-burning biodiesel in all construction equipment (to reduce air pollution and thus aid our asthmatic
population); a planned citywide Town Hall Forum on addiction
education for San Francisco youth; and the involvement of SFMS
www.sfms.org
and CMA in the ongoing efforts to reform health care in California
and create statewide universal coverage.
There are numerous other examples of SFMS involvement,
but all illustrate a critical point: SFMS is committed to its goals of
improving access to health care for our community, of serving as
a leader in resolving health care issues, and of being an effective
advocate in influencing decisions concerning health care policy.
These goals can only be achieved by making yet another goal a priority: that SFMS membership will include the entire San Francisco medical
community. We will only be effective if we are seen to represent the
majority of San Francisco physicians, whether in private practice, at
Kaiser Permanente, at UCSF, or in other types of practice. I have
been impressed in my years on the Board that we truly have a “big
tent,” in that physicians of all political persuasions, in all practice
situations, and with varied opinions on many health care issues can
all work together toward yet another SFMS goal—to be an effective
advocate for all of our members.
In order to further our goals as stated above, we must increase
our membership and the overall proportion of San Francisco
physicians who are members. Currently we have approximately
900 members, who represent about 30 percent of the physicians
practicing in San Francisco. Clearly we can do better.
To accomplish this, I am proposing that 2008 be a Year of
Membership, during which we work to actively create a “culture
of membership” and increased physician participation in SFMS. If
each SFMS member could simply recruit one additional physician,
we would have a membership of more than 1,800 doctors, representing the majority of physicians practicing in San Francisco.
Joining the SFMS is remarkably easy. Prospective members
can go to www.sfms.org and click “Join SFMS” on the top of the
home page. New members get a 50 percent discount on their first
year’s dues. Even better, some medical groups, including Kaiser
Permanente, have a policy of paying the entire annual dues for any
of their physicians who elect to join SFMS.
By increasing physician participation in the Medical Society, we
can clearly enhance the effectiveness of our numerous initiatives and
further our overall mission. The end result will be a better environment
for all of us at the Medical Society, and certainly a greater opportunity
to move toward a new era for environmental health.
January/February 2008 San Francisco Medicine Editorial
Mike Denney, MD, PhD
At the Edge of Chaos
C
haos theory refers to the unpredictable behavior of energy
and matter within highly complex systems, such as the
weather, the formation of waves at seashores, and traffic
patterns on freeways. It is of interest to scientists in physical phenomena as mundane as the formation of the whirlpool that forms
when water is released down the bathtub drain, as important as the
electrochemical synaptic connections of the human brain, and as
vast as the earth’s entire ecosystem.
Perhaps the most fascinating aspect of complexity theory is
a phenomenon called emergence. In her book Living at the Edge of
Chaos (Daimon Verlag 1997), Helene Shulman clarifies that in any
complex system at the edge of chaos, factors can interact in multifarious ways so that there spontaneously emerge novel, unforeseeable
phenomena that are beyond the predictability of ordinary science.
The concept can be grasped by visualizing a small round table over
which is an apparatus that can emit one grain of sand at a time.
Slowly, over time, as some grains of sand bounce away but others pile
up on the table, a cone will begin to form. Then the system enters
an unpredictable critical state in which one tiny grain of sand falls
and results in a massive avalanche, thus destroying the cone.
This concept of complexity has direct bearing upon biological
systems. One example of this is the emergence of the first organic
molecule that could replicate itself, which emerged about four billion years ago out of the inorganic chemical debris of the Big Bang.
Other examples might be the sudden extinction of life forms such as
the dinosaurs, species that become unsustainable at a critical state
when one tiny detrimental change occurred in a highly complex
ecosystem.
Recently the New York Times columnist Thomas L. Friedman, reporting from Bali, Indonesia, where representatives from
200 countries attended the United Nations climate conference,
reported that some of the delegates were talking as though it is “too
late for later.” He quoted Barnabas Suebu, the governor of Papua,
as saying, “Think big, start small, act now—before everything
becomes too late.”
At the conference, some delegates, using ordinary cause-andeffect statistical science, predicted that the ice within the Arctic
Circle could disappear by the year 2040. But if we add complexity
theory and its concept of critical states to that thinking, we notice
that our ecological crisis may be even more urgent. Indeed, it may
seem that any minute one additional detrimental change in the
environment, like the one grain of sand producing the avalanche
on the sand cone, could trigger an ecological disaster.
The world may already have reached a critical state at which
there could occur a catastrophic and unpredictable emergence of
properties that could not have been foreseen. We may be living
at the edge of chaos.
Welcome New Members!
The San Francisco Medical Society would like to welcome the following new members:
ACTIVE REGULAR MEMBERS
Beverly Bolinger, MD, The Permanente Medical Group
Jing Dai, MD, The Permanente Medical Group
Kirk Murphy, MD
Brigitte Prinzivalli-Rolfe, MD, The Permanente Medical Group
Lisa Tang, MD, The Permanente Medical Group Referred by Chuck Wibblesman, MD
Chunbo C. Cai, MD, The Permanente Medical Group
Lisa Griffin, MD, The Permanente Medical Group Referred by Suketu Sanghvi, MD
Timothy R. Hamill, MD, UCSF Medical Center Referred by Tom Addison, MD
Linnea Hur, MD, The Permanente Medical Group Referred by Suketu Sanghvi, MD
Shala Rahbar, MD
Andrea H. Yeung, MD, Referred by Brian Schindler, MD
HOUSE OFFICER/RESIDENT
Jessica Evert, MD, UCSF/SFGH—Family Practice
www.sfms.org
Guest Introduction
Philip R. Lee, MD; Steve Heilig, MPH; and Michael Lerner, PhD
A New Era for Environmental Health
T
his issue of San Francisco Medicine is the fifth in the past
decade to have an environmental health theme. Over
that decade, the field has been transformed both by rapidly
expanding scientific knowledge and fast-growing recognition that
many of our educational, clinical, and other approaches to environmental health problems need improvement.
Look at the headlines: known or suspected toxins in products
both foreign and domestic, contaminated foods and water, climate
change, and much more are ever more prominent and worrisome.
There is no doubt that these problems have at least some impact
on human health. We are proud that some of the world’s leading
authors on a wide array of topics are featured in this issue of San
Francisco Medicine.
At a 2002 conference hosted by the San Francisco Medical
Society, an international network known as the Collaborative on
Health and the Environment was founded to bring different disciplines together with patients and others to address environmental
health issues, with a particular focus on chemical contaminants.
The science in that arena has exploded with data about the previously unsuspected ways that industrial chemicals in our bodies can
impact our health. Policy makers are finally taking notice that our
current approaches are archaic—and that we lag behind many other
advanced nations in this regard.
Recently, the California Medical Association’s House of
Delegates adopted the following policy on this topic—initiated
by the SFMS delegation. Our state may well lead the nation on a
scientifically sound chemicals policy.
A Modern Chemicals Policy for California and Beyond:
California Medical Association, 2007
By Lucy Crain, MD, and Robert Gould, MD
Whereas, the state, national, and global scale of industrial chemical production is immense and is expected to grow fourfold by 2050, and the chemical
industry is an important industry with wide contributions to health and human
development; and
Whereas, ever-expanding research confirms that many chemicals that are
useful to society are also known to be hazardous to human biology and health,
particularly in utero and in developing children; and
Whereas, for new and existing medications, the Food and Drug Administrawww.sfms.org
tion has long required preapproval evaluation of safety as well as efficacy, and
many industrial chemicals with known impacts on human biology are present in
human bodies at levels similar to active doses of medications; and
Whereas, numerous nations including Canada and the European Union are
adopting more proactive health-oriented chemicals policies, based upon scientific
knowledge, assessment, and accepted public health principles; and
Whereas, there are long-standing deficiencies in the federal regulation of
industrial chemicals, most notably in the Toxic Substances Control Act (TSCA),
as confirmed by the National Academy of Sciences and others; and the University
of California documented in a 2006 report to the California Legislature that
TSCA’s deficiencies are important and can be remedied; and
Whereas, these problems include the projected appearance of 600 new
hazardous waste sites each month in the U.S. over the next twenty-five years; the
appearance of hundreds of industrial chemicals in human tissues and fluids, including those of infants; and the development of chronic diseases caused by chemical
exposures on the job among 23,000 California workers each year; and
Whereas, the American Public Health Association’s leadership has recently
endorsed a policy entitled Calling on the U.S. Congress to Restructure the
Toxic Substances Control Act and Implement a Modern, Comprehensive
Chemicals Policy; therefore, be it
RESOLVED that the CMA call upon the State of California and United
States to implement a state and national modern, comprehensive chemicals policy
in line with current scientific knowledge on human health, and that requires a full
evaluation of the health impacts of both newly developed and existing industrial
chemicals now in use.
This policy will be taken by the CMA delegation to the
AMA’s policy-making body in 2008. We hope the AMA will see
the wisdom of adopting the SFMS/CMA stance and in advocating
that our new political leaders make up for lost time. The ultimate
aim is, and the result could be, a healthier nation and world, with
the decrease in human suffering that entails. That seems to us a
very worthy goal.
For more information, see www.healthandenvironment.org.
Philip R. Lee is Professor of Medicine Emeritus at both Stanford
and UCSF, where he is also a Chancellor Emeritusformer United States
Secretary of Health; Steve Heilig is with the SFMS; Michael Lerner is
President of Commonweal. All are founding partners of the Collaborative
on Health and the Environment, which Dr. Lee chairs.
January/February 2008 San Francisco Medicine Health, Human Beings,
and The Environment
Toxic Dilemmas
Donald Kennedy, PhD
A
fter all these years of environmental regulation, the laws and rules
regarding the introduction of toxic
chemicals into consumer products and the
environment are still ineffectual. After an
earlier lifetime in which I worried about
lead, polybrominated biphenyls in plastics,
and the like, I got reacquainted with toxic
dilemmas. It happened because of a reunion
with an old friend who has a long familiarity with the use of such toxic substances as
fire retardants in consumer products. Here’s
the story.
In the early 1970s, when I first got to
know Arlene Blum, she was working with
Bruce Ames at the University of California,
Berkeley. They were applying the Ames test
for mutagenicity to various lipid-soluble
chlorinated and brominated compounds
that are double trouble because they concentrate in food chains and wind up in
people, and they aren’t biodegradable. They
discovered widespread use of a compound
called tris (2,3-ibromopropyl) phosphate
as a fire retardant in children’s sleepwear. A
mutagen and putative human carcinogen,
it leeched into children’s bodies. After a
1977 paper by Blum and Ames in Science,
its use was banned. Well, the alert chemical
industry quickly substituted a dichlorinated
tris, which Ames and Blum also found to
be mutagenic and which was subsequently
removed from sleepwear.
The history of residential fire risk is
an interesting one, because it involves the
tobacco industry. Remember them? They
designed cigarettes that, when dropped or
put down, would smolder long enough to
start a fire. For years, cigarette-lit fires were
the greatest cause of fire-related deaths in
the United States. After three decades of
opposition from tobacco lobbyists, twenty-
two states and Canada finally passed laws
requiring that cigarettes be made selfextinguishing. With fewer people smoking
and better enforcement of building codes,
“The real problem is
that the U.S. regulatory
system for toxic
industrial chemicals is
not effective and is a
threat to public health.”
fire-related deaths are decreasing.
I had missed this important development, having lost track of the topic. Arlene,
a high-profile international mountaineer,
was off leading expeditions in the Himalayas
and elsewhere and was writing a memoir
about it. Meanwhile, I had left the U.S.
Food and Drug Administration and was
back at Stanford. I hadn’t seen Arlene for
twenty-five years or so, but a few months
ago, she turned up with an extraordinary
sequel to the tris story, which she tells of
in a recent letter in Science. Fire retardants
are now widely used in furniture foam, and
the second most-used compound is none
other than chlorinated tris! In less than
three decades, this highly toxic mutagen
has moved from your child’s nightgown to
your sofa.
Arlene is scientific adviser for a bill in
the California legislature called AB 706,
which would ban the use of the most toxic
fire retardants from furniture and bedding
unless the manufacturers can show safety. It
has a good chance of passage next year; even
the firefighters support it. Not surprisingly,
chemical manufacturers have launched a
10 San Francisco Medicine January/February 2008
fear campaign in opposition, claiming that
their products have dramatically reduced fire
deaths in California, although the rate of decrease is about the same as that of states that
do not regulate furniture flammability.
But the problem is a national one. The
Consumer Product Safety Commission
(CPSC) Reform Act (S 2045) toyed with a
provision that would rush us into a national
furniture flammability standard. That’s premature, because it leaves no time to develop
a safe way to reduce furniture flammability
and puts potentially persistent toxic chemicals into U.S. homes. Congress should forget
that approach. The real problem is that the
U.S. regulatory system for toxic industrial
chemicals is not effective and is a threat to
public health.
In Europe, the chemical industry is
required to establish safety before a product
can continue to be marketed. The U.S.
Toxic Substances Control Act (TSCA)
originally grandfathered existing chemicals, but none have been reexamined since
the 1980s. Congress should abandon its
attempt to attach a flammability standard
to the CPSC and instead turn to the real
task of reforming TSCA by introducing a
true proof-of-safety provision. That would
stop the chemical industry from making
consumer protection look like a game of
whack-a-mole.
Donald Kennedy is the outgoing Editorin-Chief of Science and former President of
Stanford University and Commissioner of the
Food and Drug Administration. This editorial
is reprinted from Science 318:1217 (2007)
with permission of the author and the American
Academy for the Advancement of Science.
www.sfms.org
Health, Human Beings,
and The Environment
Toys, Tots, and Toxic Chemicals
It’s Time to Act
David Wallinga, MD, MPA
T
oy recalls due to lead have exploded
to more than one hundred in 2007.
Lead on toys is the tip of a bigger
chemical iceberg, however. The real problem? “[T]he U.S. regulatory system for toxic
industrial chemicals,” says Donald Kennedy,
the former Commissioner of the Food and
Drug Administration (FDA) and Science
editor, “is not effective and is a threat to
public health.”1 It is, in other words, a poorly
regulated chemicals problem, not just a
Chinese toy problem.
If you think this is not a medical issue,
think again. Industrial chemicals include
not only lead and other metals but also
solvents, phthalate plasticizers, and perfluorocarbons made into toys, lunch boxes, baby
bottles, nonstick pans, and fabrics. Patients
are exposed to them from birth.
Early chemical exposures contribute
to an array of chronic diseases and disabilities found in children and, the science
strongly suggests, in adults. Among children,
chemical exposures cause 100 percent of
lead poisoning cases and contribute to an
estimated 10 to 35 percent of asthma cases,
2 to 10 percent of certain cancers, and 5 to
20 percent of neurobehavioral disorders and
disabilities. Yet weak laws require no toxicity testing of these chemicals before making
them and entering them into commerce.
Gaps in Knowledge
Dr. Kennedy’s dour assessment of
TSCA, the Toxic Substances Control Act,
is not unique. Its failures also have been
enumerated by the National Academy of
Sciences (1984),2 the General Accounting
Office (1994, 2005),3, 4 the Congressional
Office of Technology Assessment (1995),5
the U.S. Environmental Protection Agency
(1998), 6 the University of California
www.sfms.org
(2006),7 and others.8, 9
TSCA is the 1976 law under which the
EPA registers the 42 billion pounds of industrial chemicals produced or imported into
“Our collective failure to
effectively regulate lead,
plasticizers, and other
industrial chemicals of
concern in everyday
products puts children
in harm’s way. Again,
physician support is
critical if we are to have
a chemicals policy that is
effective.”
the U.S. each day.10 One of TSCA’s chief
failures: it perpetuates long-standing scientific ignorance about the hazards of these
chemicals—what University of California,
Berkeley, public health scientist Michael
Wilson deems the “knowledge gap.”11
The ignorance is partly historical.
Society’s longtime presumption was that
industrial chemical use was medically
harmless, especially for nonworkers. After
World War II, the newly emergent chemical industry excelled at innovating new
chemicals (90 percent of them derived
from petroleum) and products, answering
the pent-up appetites of a war-weary public.
Because of presumed harmlessness, there
was no health or safety testing of these new
substances.
Congress passed TSCA only after rising numbers of industrial chemicals were
detected in polluted air and water. With
the law’s design, however, the Congress ensured our chemical ignorance would persist.
On implementation, TSCA grandfathered in the 62,000 chemicals then in
use, meaning no new toxicological testing
was required for them. TSCA-registered
chemicals produced or imported at “high
volume,” meaning 1 million pounds or
more per year, total 2,943 in number today.
Largely untested grandfathered chemicals
make up 92 percent of these high-volume
chemicals.
TSCA also fails to require makers of
new chemicals—there are about 2,000 such
chemicals per year—to generate or disclose
to EPA or end users any toxicological data
before these chemicals are marketed or
used in products. Total TSCA-registered
chemicals now number 81,600. Of those
in actual use, fewer than half have been
subjected to even token laboratory testing
for toxicity.
By never granting EPA the authority
to make sure chemical toxicity information
would be generated and distributed, TSCA
ensures continued ignorance for every new
generation of chemicals.
Safety Gaps
TSCA’s knowledge gap also creates a
safety gap.
Congress mandates that regulatory
agencies use a “risk-based” approach. To
assess chemical risk requires information
on toxicity or hazard, yet TSCA ensures
that EPA lacks the authority to collect such
data in the first place. Regulatory paralysis
ensues.
By 1994, the General Accounting Office (GAO) found that EPA had managed
to review the risks of only about 1,200 (2
percent) of the 62,000 pre-TSCA chemi-
January/February 2008 San Francisco Medicine 11
cals. EPA told GAO it considered about
16,000 (26 percent) to be of potential concern to human health. How can one make
“evidence-based” public health decisions
when fundamental hazard information is
lacking for tens of thousands of chemicals?
Another way TSCA constrains EPA
is in limiting its authority to take steps to
actually control chemical hazards. Thus,
since 1979, EPA has been able to use its
existing authority to regulate only five of
the 62,000 grandfathered TSCA chemicals:
polychlorinated biphenyls (PCBs), chlorofluorocarbons (CFCs), dioxins, asbestos, and
hexavalent chromium.12
Even for new chemicals, TSCA limits
EPA’s authority. After a manufacturer
registers a new product and EPA reviews
it, TSCA prohibits the agency from requiring any additional toxicity testing. Every
incentive is for manufacturers to do as little
toxicity testing as possible prior to registration. Eighty-five percent of new chemicals
registered under TSCA, the EPA reports,
lack any data on chemical health effects.
TSCA’s costs
TSCA’s costs are multiple. Workers
pay because they typically face the highest
exposures to often untested, ineffectively
regulated chemicals. In California alone,
preventable chronic disease attributable to
workplace exposures to chemicals affects an
estimated 23,000 persons each year.13
What are the costs to children? A landmark 1993 National Academy of Sciences
study reported that children during development are uniquely vulnerable to harm from
environmental chemicals.14 For example,
the young brain’s inherent vulnerability
stems from its rapid early development,
much of it in utero, combined with the fact
that, for optimal brain function, billions
of neurons must successfully differentiate,
migrate, and form synapses with other cells
in an incredibly intricate and well-choreographed process. The precision required is
why the young brain is vulnerable to toxic
injuries that have no parallel in the mature
adult brain.
Like adults, children are exposed to a
complex mixture of dozens or hundreds of
industrial chemicals, including many neurotoxicants.15 Exposure starts before birth; one
analysis of just ten samples of newborn cord
blood, supplied by the American Red Cross,
detected a total of 287 industrial chemicals,
including 217 that are neurotoxic in humans or animals.16
How many are causing developmental
harm in children? There are data that 201
industrial chemicals are clinically neurotoxic in humans. The Congressional Office of
Technology Assessment estimated in 1990
that 3 to 5 percent of the tens of thousands
of industrial chemicals in commerce could
be neurotoxic. For about 80 percent of the
nearly 3,000 high-volume TSCA chemicals, no information is available regarding
developmental or pediatric toxicity. The
lack of required testing means the actual
number of adult or pediatric neurotoxicants
remains unknown.
Only a handful of industrial chemicals
(e.g., lead, methylmercury, polychlorinated
biphenyls [PCBs], arsenic, and toluene)
have been confirmed as causing neurodevelopmental disability or disease in children.
The evolution of science around these five
followed a similar pattern. Widespread use
and human exposure came first. Second,
there was recognition of occupational or
adult neurotoxicity. Only much later was
there human or epidemiologic evidence
to determine harm to children. With that
came the realization that neurodevelopmental impacts occur at low prenatal exposure
levels that would not be toxic to an adult.
Neurodevelopmental harm, we now
know, is often subclinical, i.e., not clinically
apparent. Subclinical toxicity can manifest
not on standard examination but as a finding of special IQ or neurobehavioral testing. Thus, the neurodevelopmental harm
suffered by children exposed early in life to
airborne lead from gasoline, PCBs, and/or
methylmercury have been largely “silent,”
unnoticed pandemics.17
The human and economic costs are
real, however. From 1960 to 1980, about
100 million American children were
exposed to airborne lead. Societal costs
stem largely from diminished economic
productivity, because these children are
less intelligent on the whole due to their
lead exposure; such costs are estimated at
$110 billion to $319 billion per each year’s
birth cohort.18 Today the costs of prenatal
methylmercury exposure are estimated at
$8.7 billion yearly (the range running from
$2.2 to $43.8 billion).19
Ineffective regulation and control of
industrial chemicals carries other costs as
well, imposed on government, on ecosystems, and on business. For example, the
EPA expects 600 new hazardous waste sites
to appear in the U.S. each month over the
next twenty-five years, adding to the 77,000
already in existence.20 Total mitigation costs
are expected to total around $250 billion.
Costs like these will only deepen with
global chemical production, projected to
increase fourfold by 2050.21
A Healthier Way Forward
Regulatory failure once allowed tobacco companies to market Joe Camel and
nicotine addiction to children. Medicine
played an important and appropriate role
in changing that picture. After all, the
American Medical Association’s mission
statement includes the “betterment of
public health.”22
Now, our collective failure to effectively regulate lead, plasticizers, and other
industrial chemicals of concern in everyday
products puts children in harm’s way. Again,
physician support is critical if we are to have
a chemicals policy that is effective.
A better chemicals policy is feasible.
Public health concern has erupted around
chemical plasticizers, such as bisphenol A
and phthalates, which disrupt hormone
function in animals. Limited human studies appear confirmatory. These plasticizers
are widely used in children’s products and
are ubiquitous in human sera. Europe has
phased out phthalates in children’s products. In October, California effectively
phased out the manufacture or sale of young
children’s products containing phthalates by
2009. Alternatives are readily available, as
for most toxic chemicals.
State legislation can help reduce
exposure to certain hazardous chemicals.
However, state initiatives are necessarily
limited. Even after California’s phaseout,
phthalate-containing products will remain
for sale elsewhere in the U.S. Likewise, baby
bottles of polycarbonate plastic, which leach
bisphenol A, are no longer sold in Japan, yet
Continued on Page 18...
www.sfms.org
and The Environment
Reproductive Health and the Environment
What We Need to Know to Face the Challenges
Tracey J. Woodruff, MPH, PhD; Jackie M. Schwartz, MPH; Alison Carlson; and Linda C. Giudice, MD, PhD
S
uccessful reproduction—from conception through pregnancy, child
development, and adulthood—is
an integral part of the continuing life cycle,
and there are increasing indicators of declines
in many aspects of reproductive health.
Among men in the United States, these
include about a 60 percent increase in the
incidence of testicular cancer (1), declining
sperm counts in certain areas (2), and reports
of declining testosterone levels (3), suggesting
a decline in male reproductive function over
approximately the past thirty years. For U.S.
women during the same time period, there
has been a reported decline in age of onset of
breast development and menarche, and more
women, particularly women under the age of
twenty-five, are reporting difficulty conceiving and maintaining their pregnancies (4).
A woman’s lifetime risk of developing breast
cancer has nearly tripled in this country in
the past forty years (5). Thirty percent more
babies are born prematurely, and the median
gestational age at birth has decreased from
forty to thirty-nine weeks (6). These rapid
changes in health endpoints suggest that
environmental—and thus modifiable and
preventable—actors, rather than Mendelian
inheritance, are involved in recent declines
in reproductive health.
Since World War II, chemical production in the United States has increased
more than twenty-fold, and the number of
chemicals registered for commercial use has
grown by more than 30 percent since 1979
(7, 8). As of 2006, there are approximately
87,000 chemical substances registered for use
in commerce in the United States (9).
The scientific evidence linking environmental chemicals to all aspects of reproductive health continues to expand, and concern
over the implications of these findings spurred
www.sfms.org
the 2007 Summit on Environmental Challenges to Reproductive Health and Fertility
(9a). This unique gathering coalesced the
field of environmental reproductive health
by bringing together more than 400 scientists, researchers, health care professionals,
trainees, health-affected groups, community
and political representatives, and members
of the media to discuss what is currently
known about the impacts of environmental
contaminants on reproductive health and
fertility and to identify steps to reduce the
impacts of environmental contaminants on
reproductive health through research, education, communication, and changes in public
health policy.
Critical New Science: Exposures
to Environmental Contaminants
Humans are exposed daily to a mixture
of environmental contaminants in air, water,
food, and consumer products. In a recent
biomonitoring study of more than 150
contaminants, the U.S. Centers for Disease
Control and Prevention reported that all 150
chemicals were detected in some portion of
the U.S. population and that several of the
chemicals, such as environmental tobacco
smoke, lead, mercury, and phthalates, are
detected in nearly all members of the population (10).
While many environmental contaminants can affect reproductive health (see
online appendix at www.sfms.org for a list),
there is an important class of chemicals,
called endocrine-disrupting chemicals, that
interfere with the production, release, transport, metabolism, binding, action, or elimination of natural hormones in the body. Two
examples of endocrine-disrupting chemicals
that have received much media attention
recently, and that will be discussed in this
Key Definitions for Environmental
Reproductive Health
Environmental Reproductive Health:
Interdisciplinary study of exposures to environmental contaminants, particularly during
critical periods in development (such as prior
to conception and during pregnancy), and their
potential effects on all aspects of future reproductive health throughout the life course, including
conception, fertility, pregnancy, child and adolescent development, and adult health.
Environmental Contaminants: Synthetic
chemicals and metals in our environment, including air, water, soil, food, consumer products,
and the workplace.
Reproductive Health: Ability to conceive
and to carry a pregnancy, pregnancy quality and
outcomes, pubertal effects, and adult reproductive health disorders.
article, are bisphenol A (also called BPA)
and phthalates. BPA is found in hard plastic
water and baby bottles and food containers,
the lining of metal food and drink cans,
pacifiers and baby toys, and dental sealants.
Phthalates are a family of chemicals that
are used to soften plastics used in medical
devices, food wrap, flooring, wall coverings,
personal care products (perfumes, lotions,
cosmetics, hair spray), lacquers, varnishes,
and wood finishes and coatings.
Implications of Exposures during
Key Developmental Windows over
the Life Course
While exposures to environmental contaminants during any life stage can increase
risk of adverse health effects, there are times
during development when rapid and often
unique changes occur, and these represent
more susceptible windows. Exposures during
these times can result in irreversible effects
that can have either immediate, lifelong, or
even intergenerational impacts on health.
Windows of susceptibility can occur periconceptually (prior to, during, and shortly
after the fertilization of the egg) and during
pregnancy, infancy, childhood, and puberty.
One example of the influence of the environment during a developmental window
of susceptibility is the Barker hypothesis (or
fetal origins of disease hypothesis): alterations
in the fetal environment that impair fetal
growth result in an increased risk, later in life,
of adult onset of chronic conditions such as
coronary heart disease and diabetes (11).
Researchers during the past decade have
explored the mechanisms whereby exposure
to environmental contaminants during developmental windows of susceptibility results
in compromised function or disease later in
life. They have shown that such exposures
can modify the epigenome (the collection
of biochemical reactions that determine
gene expression), permanently altering gene
expression and leading to metabolic and hormonal disorders, reduced fertility and fecundity, and illnesses such as prostate, uterine,
and cervical cancers later in life (9).
The DES Example
We have learned much about the effects
of exposure to endocrine-disrupting chemicals during susceptible developmental periods
through an unfortunate experience with
diethylstilbestrol (DES). DES is a synthetic
estrogen (and thus an endocrine-disrupting chemical) that was given to pregnant
women in the United States between 1938
and 1971 under the erroneous assumption
it would prevent pregnancy complications.
In fact, in utero exposure to DES can alter
the epigenome and normal programming of
gene families, such as Hox and Wnt, which
play important roles in reproductive tract
differentiation (9, 12-14). Thus, women
exposed to DES in utero are at increased risk
of clear cell adenocarcinoma of the vagina
and cervix, fibroids, structural reproductive tract anomalies, infertility, and poor
pregnancy outcomes, while men have an
increased incidence of genital abnormalities
and a possibly increased risk of prostate and
testicular cancer (15, 16). In addition, effects
can be passed down to a second generation,
including increased menstrual irregularities
(17) and ovarian cancer (18) in the granddaughters and increased hypospadias in the
grandsons (19, 20) of women who took DES
during pregnancy.
Reproductive Effects of Early
Life Exposures
Through a combination of laboratory
animal, human, and wildlife studies, much
as been learned about how exposure to
environmental contaminants can disrupt
reproductive health, particularly during
susceptible windows of development. These
are illustrated briefly below, with a more
thorough review in Woodruff et al. (9).
Prostate Development and the
Environment
Early-life exposures to environmental
contaminants can also affect the developing prostate, which is particularly sensitive
to estrogens. Rats exposed neonatally to
bisphenol A (BPA), then exposed later in life
to hormones that mimic the hormonal profile
of the aging male, showed a significantly
higher incidence of prostatic intraepithelial
neoplasia (a preneoplastic lesion) compared
to controls (23). This heightened predisposition results from permanent alterations to
the prostate epigenome that continue the
expression of the phosphodiesterase type 4
variant 4 gene (an enzyme responsible for
Cyclic adenosine monophosphate (cAMP)
breakdown) at a time when it is normally
silenced with aging.
Males
Testicular Disgenesis Syndrome
Research over the past ten years has
drawn a connection between various malformations and diseases of the male reproductive
system that manifest at birth (cryptorchidism,
hypospadias) or in early and later adulthood
(testicular germ cell cancer and infertility).
These conditions, which are risk factors for
each other, are now considered part of a
testicular dysgenesis syndrome (TDS). The
TDS hypothesis proposes that disruption
of testosterone function during early pregnancy can disrupt testis development, and
lead to these and other disorders of the male
reproductive tract (21). This hypothesis has
been supported by both animal and limited
human studies (21). Exposure of rats in utero
to dibutyl phthalate (a type of phthalate that
is known to disrupt testosterone) induces
cryptorchidism, hypospadias, reduced anogenital distance (a measure of testosteronedependent male reproductive development),
impaired spermatogenesis, and infertility in
a dose-dependent manner (21). Prenatal
exposure to dibutyl phthlate can also alter
development and function of cells and
pathways critical for the development and
functioning of the male reproductive system
(21). A study of pregnant women exposed to
phthalates during pregnancy has also found
a relationship between increasing levels of
phthalates and decreases in the anogenital
distance of their male babies (22).
Females
Uterus Development and the Environment
As described above, prenatal exposures
to DES can modify the epigenome and cause
reproductive tract abnormalities in women.
Studies have now been extended beyond
DES to demonstrate that other environmental estrogens can similarly reprogram
gene expression in the uterus (9): exposure
to genistein and BPA during the period
of maximum sensitivity to developmental
programming induces the expression of the
estrogen-responsive genes calbindin and progesterone receptor, which results in greater
incidence of fibroid tumors.
Oocyte Development and the Environment
Studies find that prenatal exposures to
low doses of BPA perturb oocyte development in unborn female mice, essentially
affecting the second generation (24). These
perturbations result in an increase in chromosomally abnormal eggs and embryos, a
marker for aneuploidy, which is a risk factor
for miscarriages and other fetal abnormalities
(24). The study also indicated that BPA acts
by interfering with the function of one of
the known estrogen receptors, ER-, which
also suggests that other endocrine-disrupting
chemicals that act in a similar manner may
affect early oocyte development (24).
Reproductive Effects of Adult
Exposures
www.sfms.org
While we have focused our discussion
on exposures that occur during developmental windows, exposures to environmental
contaminants during other life stages, such
as adulthood, can also increase the risk of
adverse reproductive health effects (9).
These include impacts on male reproductive function, such as decreased or abnormal
sperm count, and increased rates of infertility.
Similarly, in women, chemical exposures
can increase risk of early onset of puberty,
menstrual and ovarian dysfunction, and
infertility.
Moving Forward
At the summit, participants collaborated to identify critical needs and directions
for advancing reproductive environmental
health through health care, research, policy,
community action, and occupational health.
Recommendations are briefly reviewed
below.
Health Care Professionals
The following actions will help integrate
environmental reproductive health into
health care:
• Reproductive environmental health
topics should be included in medical and
nursing education, and continuing education
should be provided at medical and nursing
society meetings. This training should include information on the sources and effects
of environmental and workplace exposures,
particularly in relationship to windows of
susceptibility.
• Current standards of practice should
be changed so that health care providers
take a work history and inquire about patients’ exposures to chemicals, ideally before
pregnancy.
• Clear, simple health information tools
should be developed to support conversations
between health care providers and patients.
These materials should discuss contaminants
and sources of exposure, along with steps
to reduce exposures. These tools can be
modeled on the Pediatric Environmental
Health Toolkit (http://psr.igc.org/ped-envhlth-toolkit-project.htm) and the Hazard
Evaluation System and Information Service
for workplace hazards (www.dhs.ca.gov/
ohb/hesis).
www.sfms.org
Research
Specific steps can be taken to expand
the research base and support interdisciplinary collaboration:
• Conduct longitudinal human and
animal studies that observe the full life
cycle (e.g., the National Children’s Health
Study).
• Increase funding for emerging areas
of research, including effects from chemical
mixtures, effects on the epigenome, fetal
programming and transgenerational effects,
low-dose effects, and cross talk among endocrine systems.
• Develop and improve biomarkers of
exposure, fertility, and early disease.
• Develop methods to identify emerging
contaminants of concern.
• Establish technologies to promote
collaboration, such as an Internet-based
discussion forum and a Web-based database
of tissue banks.
• Increase government and university
recognition of and support for collaborative,
interdisciplinary research.
Policy
Participants from all sectors represented
at the summit identified four key policy
needs:
• Advance models for comprehensive
chemicals evaluation at local, state, and
national levels for more effective chemical
regulation.
• Increase resources and improve methods to enhance research on reproductive
environmental health.
• Improve the use of science and precaution in decision making by: acknowledging
uncertainty in the science and allowing
for action in the face of this uncertainty;
increasing steps to limit undue influence or
bias in the review and synthesis process; and
incorporating low-dose effects and exposure
to multiple chemicals into decision making
and risk assessment.
• Improve right-to-know information
given to consumers and workers about environmental contaminants in products.
Community Action
Summit participants gathered to talk
about the science in the context of environmental justice, occupational health, and
reproductive justice. Participants recommended that community members, scientists,
epidemiologists, clinicians, activists, communications strategists, and spokespeople work
together toward a reformed and improved
public health policy that adequately regulates
chemicals and reduces exposures.
Safe Work
Participants in the Safe Work group at
the Summit identified the following unique
needs of workers:
• Reduce permissible exposure levels to
harmful chemicals to be more consistent with
environmental exposure limits and take into
account toxicity of exposure to mixtures of
chemicals used in the workplace.
• Expand exposure assessment and
monitoring in occupational settings.
• Expand occupational health researchers’ access to workers so that health consequences can be identified and corrected.
• Develop alliances that can improve
health across different sectors. For example,
make the connections between worker
safety and hospital patient safety concerning
phthalates.
Conclusion
The summit provided a view of critical
scientific information that underscored the
need for further efforts in areas to improve
reproductive health. One common theme
throughout the summit was communication
and collaboration. Communication and
collaboration across scientific disciplines
and among scientists, health care providers, health-affected groups, and the public
(as well as efforts in research, education,
and policy) are key to reducing the adverse
impacts of environmental contaminants and
enhancing the reproductive health of this
and future generations.
Tracey J. Woodruff, PhD, MPH, and Jackie
M. Schwartz, MPH, are with the Program on Reproductive Health and the Environment, National Center
of Excellence in Women’s Health, Department of
Obstetrics, Gynecology and Reproductive Sciences,
U.C. San Francisco. Alison Carlson is with the
Collaborative on Health and the Environment. Linda
C. Giudice, PhD, MD, chairs the Department of
Obstetrics, Gynecology, and Reproductive Sciences,
U.C. San Francisco. References, appendices, and
acknowledgements appear online at www.sfms.org.
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www.sfms.org
and The Environment
Early Vulnerability, Lifelong Impacts
Developmental Exposure to Environmental Chemicals in Disease Etiology
Philippe A. Grandjean, MD, PhD
T
he timing of exposure to a toxic
chemical is a major factor that
determines the biological effects.
This new insight has profound importance
in biomedical research and public health.
Fetal and early postnatal development likely
constitute the most vulnerable time periods
of human life, and toxic exposures during
these susceptible life stages can therefore
lead to much more serious adverse effects
than exposures to the mature organism. Past
research has primarily focused on spontaneous abortion, congenital malformations,
and lowered birth weight as evident effects
of toxic exposures during development.
However, new research is pointing to a new
paradigm, where seemingly subtle changes
incurred during early development lead to
functional deficits and increased risks of
disease later in life.
Programming Effects on Human
Health
The developing embryo and fetus are
extraordinarily susceptible to functional
alterations of the intrauterine environment. Low birth weight has been used as
a marker of fetal nutrient deprivation and
has been linked to subsequent development
of cardiovascular and metabolic disease in
adults. This notion of fetal or developmental programming is now being expanded
by studies that assess the effects in the
offspring of maternal smoking and other
toxic exposures.
An important discovery was made as
early as 1968, when fetal alcohol syndrome
was first described. However, progress in
the field of research has been slow, in part
because of logistic difficulties when dealing
with considerable time intervals between
causative exposure and appearance of adwww.sfms.org
verse effects. Recent studies are now further
supporting the new paradigm of early developmental origins of organ dysfunctions and
disease risks. Some environmental chemicals can alter gene expression by inducing
changes to the DNA configuration. These
epigenetic changes can cause lasting functional changes in specific organs and tissues,
and they may even be heritable, thereby
affecting successive generations.
The Faroes Conference
Because of the substantial implications
both for biomedical research and for public
health, an international conference was
organized to review the current research
and stimulate cross-disciplinary research and
collaboration in regard to developmental
programming caused by environmental
toxicant exposures. This meeting was held
in May 2007 in Torshavn, Faroe Islands, a
North Atlantic archipelago that occupies
an important place in the history of medicine: in 1846, the pathologist Peter Ludvig
Panum described that a measles epidemic
there affected only those residents who were
below the age of sixty-five and who had not
been affected by the previous epidemic.
This time, in 2007, the meeting examined the implications in later life caused
by exposures to environmental chemicals
during early development. The discussion
addressed these issues from three different
angles:
a) The developmental perspective
considered changing risks during different
developmental stages, from preconception
to adolescence;
b) The environmental perspective
considered the types of risks that children
and the fetus may face in different exposure
situations; and
c) The disease perspective considered
the pathogenesis from its initiation and the
etiological role played by environmental
hazards.
The three perspectives illustrate the
multidisciplinary character of the research.
The developmental origin of disease and
dysfunction deserves consideration in
toxicology, developmental biology, nutrition, epidemiology, clinical medicine, and
related fields. The effects of developmental
programming will depend on the particular
organ system’s vulnerability in regard to
the timing of exposure. Past studies have
emphasized disease incidence and mortality
as key outcomes. Thus, certain cancer forms
may be initiated before birth or during early
postnatal life. However, less serious deficits
may be of great importance if they affect
large segments of an exposed population.
This concern is of importance in regard to
adverse effects on the development of the
central nervous system, the cardiovascular
system, the endocrine system, and the immune system.
Illustrative Research Findings
Changes in uterine environment can
affect the developing male reproductive system, which can lead to the so-called testicular dysgenesis syndrome (testicular cancer,
poor semen quality, and cryptorchidism). In
animals, exposure to some phthalate esters
has evoked similar outcomes.
Unfortunate experience with an estrogenic pharmaceutical, diethylstilbestrol,
has shown that maternal exposure to this
compound may lead to vaginal, uterine, and
breast cancer. New evidence on bisphenol
A, a plastics component that also has
estrogenic effects, shows increased susceptibility to breast cancer or prostate cancer
from low-level exposure in animal studies.
Obesity is another effect seen in rodents
exposed prenatally.
Inorganic lead is the paramount example of an environmental chemical that
can cause lifelong deficits in brain function
as a result of developmental exposures. New
evidence suggests that certain pesticides,
methylmercury, and many other substances
can cause similar adverse effects.
Environmental chemicals may also
impact the development of the immune
system. Early exposure to polychlorinated
biphenyls has been linked to deficient
responses to routine childhood immunizations, an adverse effect that could have
serious public health implications. Possible
associations have also been demonstrated
between asthma and allergy development in
regard to prenatal or early postnatal chemical exposures.
Conclusions
The conference demonstrated that
developmental programming is a crucial issue to consider in research and prevention,
for five reasons:
1. There are critical periods of fetal
Toys, Tots, and Toxic Chemicals
Continued from Page 12...
they are widely available in the U.S.
Despite years of warnings about TSCA’s
ineffectiveness, there is little momentum in
this country to reform TSCA at the federal
level. Europe’s overhaul of its own industrial
chemicals policy, called REACH (for Registration, Evaluation, and Authorization of
Chemicals), went into force in June 2007. It
requires that tens of thousands of chemicals
made or imported into the European Union
be registered. For registration, REACH puts
the onus on manufacturers to first provide
specified health and safety information.
Certain chemicals determined to be of
“very high concern” will be targeted for the
substitution of safer alternatives; the law also
will require companies to proactively tell
consumers which products contain these
chemicals.
REACH directly addresses the kind of
knowledge gap found in both TSCA and
development. Effects of physical, chemical,
and biological influences will differ, often
dramatically, depending on the timing of
exposure. Thus, “the dose and the timing
make the poison.”
2. Fetal programming produces longterm and typically permanent changes.
3. While maternal, fetal, and placental
mechanisms compensate for disturbances in
the fetal environment, compensation may
also produce secondary (typically negative)
effects.
4. Continued postnatal exposure and
compensation may have further deleterious effects.
5. Effects of the environment on the
fetus are often different from those on adults
or even infants, and the effects may differ
between males and females.
The evidence that supports the notion of developmental origin of disease
and dysfunction is not yet comprehensive.
However, given the substantial difficulties and delays in documenting later-life
consequences of developmental exposures
to environmental chemicals, the research
results available offer strong support for
this new paradigm. This thriving research
area of developmental programming is
likely to expand further in the future, with
substantial implications for public health.
More research and communication among
researchers is essential in order to ascertain
the factors that affect development and the
associated long-term risks.
We hope our conference helped set
the stage for future accomplishments in
this field. The conference conclusions are
available at www.blackwell-synergy.com,
and the proceedings will be published in
Basic & Clinical Pharmacology & Toxicology
in February 2008.
Dr. Philippe A. Grandjean is a Professor in the Environmental and Occupational
Medicine and Epidemiology Program in the
Department of Environmental Health, Harvard
School of Public Health.
the prior E.U. chemicals law. By requiring
the generation and distribution of toxicity
information, REACH fills an important
“technology gap” that Wilson also identifies in TSCA. That is, if neither consumers
nor industry leaders know which chemicals
are more toxic, the market fails to provide
the incentive for innovation or investment
in cleaner production that uses less toxic
materials.
National policy change is critical for
public health. To make it happen may require American health professionals to play
an active role, as they have around tobacco
use and control.
In part, what’s needed is a change in
perspective. We can easily make toys and
household products that are useful and safe.
We should expect nothing less.
David Wallinga, MD, MPA, is Director
of the Food and Health Program, Institute
for Agriculture and Trade Policy (www.
HealthObservatory.org).
References available at www.sfms.org.
Air Pollution and
Postneonatal Infant Mortality
in the United States 1999–2002
Environmental Health Perspectives
Volume 116, Number 1, January 2008
Tracey J. Woodruff, Lyndsey A.
Darrow, and Jennifer D. Parker
Abstract
Objective: Our goal was to evaluate the relationship between cause-specific postneonatal infant mortality and
chronic early-life exposure to particulate matter and gaseous air pollutants
across the United States.
Conclusions: This study supports
particulate matter air pollution being a
risk factor for respiratory-related postneonatal mortality and suggests that
ozone may be associated with SIDS in
the United States.
www.sfms.org
and The Environment
Climate Change and Children’s Health
What Health Professionals Need to Know and How They Can Act
Katherine M. Shea, MD, MPH; and Sophie J. Balk, MD
C
limate change is occurring at a pace
that greatly concerns scientists and
the public. In this article, we summarize conclusions about climate change
and discuss health effects with a focus on
children. We end with action steps for
health professionals.
Climate Change Is Real and
Indisputable
Climate change refers to any significant
change in measures of climate (such as
temperature, precipitation, wind) lasting
for an extended period (decades or longer).
In February 2007, the Intergovernmental
Panel on Climate Change (IPCC), an independent, international group of scientists
considered the world’s authority on climate
change, began releasing its Fourth Assessment Reports (www.ipcc.ch). Its message is
strong: warming of the earth’s climate is “unequivocal,” and human activity, particularly
the burning of fossil fuels, is a major cause.
Computer models can reliably reproduce
past and present global climate conditions.
Direct observations from around the world,
combined with paleoclimatologic data from
nearly a thousand millennia, paint a picture
of normal climate variation. These data also
indicate that warming over the past decades
is well outside the norm in rate and scale.
That part of the scientific debate is settled;
the uncertainty centers on other questions:
how hot will it get, how fast, how widely
will climate variables fluctuate, what will
be the consequences, and what can we do
about it?1
Climatologists can approach answers to
some questions, but incomplete understanding of major influences (such as melting
of glaciers or response of ocean currents)
remains, possibly leading to overly conserwww.sfms.org
vative predictions. At the least, warming
will continue throughout the twenty-first
century due to the long residence time of
already emitted atmospheric greenhouse
gases (GHG) and the slow response time of
oceans. Climate effects will vary by region
and be most dramatic in higher latitudes
and coastal areas. Rainfall and freshwater
availability, temperatures, agricultural
growth zones, and sea level will change.
Ecological and human health consequences
are anticipated, and some are already being
measured.2, 3 Children are likely to suffer
disproportionately from the consequences
of a rapidly warming world.4
Health Effects of Climate Change
The World Health Organization
recently estimated that 34 percent of childhood illness in the world (compared to 24
percent of all-age illness) and 36 percent of
deaths in children under the age of fourteen
are due to modifiable environmental factors.5 Because of physical, physiologic, and
cognitive immaturity, children are more
sensitive than adults to harm from environmental hazards. Climate change increases
these hazards.
Air quality is threatened for several
reasons. Ground-level ozone production is
favored at high temperatures even without
additional precursor pollutants. For the 6.5
million U.S. children with asthma, ozone
exposure increases the rate and severity of
asthma attacks. Ozone may play a causal role
in asthma onset when exposures are high
and prolonged.6, 7 Population growth and
a warmer climate create increased energy
demands. If society meets this demand by
burning more fossil fuels to create electricity to power air conditioners, all major air
pollutants—including ozone—will increase.
Childhood exposure to specific air pollutants is related to decreased lung growth
and permanent decrements in pulmonary
function; increases in respiratory infection,
asthma, infant mortality, and all-age mortality; and miscarriages, preterm delivery,
and low birth weight.6 Mercury from burning coal ends up in the food chain, thus
threatening the neurologic development of
fetuses and young children. Climate change
is expected to result in changes in the quantity, quality, and distribution of pollens and
other aeroallergens.8 For example, ragweed
pollen production increases with increased
CO2 concentrations; a rise in ambient
ragweed pollen as temperature increases
is already being measured.8 Asthma and
allergies are likely to worsen regionally in
a warmer world.
The IPCC report states that climate
change will result in more frequent and
stronger hurricanes, typhoons, tornadoes,
and floods. In western parts of the country,
we expect longer and more severe droughts
with subsequent wildfires. Children, particularly very small ones, are at increased
risk for death and injury from these events
in part because they depend totally on adults
for protection. Hurricanes Katrina and Rita
taught us how completely a natural disaster
can displace a population and destroy infrastructure. Psychological sequelae, such
as posttraumatic stress disorder and behavior and sleep problems, are documented;
children may be more susceptible than
adults.9, 10
More extreme precipitation events are
likely. Heavy rain correlates with waterborne illness as surface water and groundwater become contaminated.11 Infants and
small children are at higher risk for diarrheal
dehydration and hospitalizations from wa-
Phenomenon
Human Health Impact
Additional Child-Specific Risks
Fewer cold days
and nights
Fewer cold-related deaths
Children will benefit
Increased frequency of warm
spells and heat
waves
Increased heat-related deaths
and illness
Very young at higher risk of
death; older children will have
more heat stress due to time
spent in exercise outside
Increased heavy
precipitation
events
Increased risk of injury, death, Very young vulnerable to hosinfectious, respiratory, GI, and pitalization and complications
skin diseases
from infection
Increased areas of
drought, wildfires
Increased risk of food and
water shortages, malnutrition
and infection, concentration
of toxic water pollutants,
injury, and death
Growth retardation, developmental delay
Increased tropical storms and
cyclones
Increased risk of injury, death,
water-, food-, and vectorborne illness
Children may be more susceptible to injury, posttraumatic
stress, certain infections
Increased air pollution
Exacerbation of respiratory
illness, premature mortality
Children’s small airways more
susceptible to asthma, infection
Changes in disMore severe and more prevatribution and po- lent allergies
tency of allergens,
mycotoxins
Allergies, cancer, birth defects
Increased sea
level, saltwater
intrusion into
fresh water
Disruption of family and school
infrastructure, other social
disruption
Abrupt coastline change,
forced migration, injury,
drowning
terborne infections. Food-borne infections
are likely to increase due to changes in
eating behavior (more outdoor food preparation and dining), and because food-borne
pathogens grow faster in warmer weather.
Researchers in Peru found an 8 percent
increase in hospitalizations for diarrhea with
every degree centigrade increase above normal average temperature.12 In a Canadian
Study, peak temperatures correlated with
peaks in cases of campylobacter, E. coli, and
salmonella infections.13
Patterns of vector-borne illness are
expected to change. Insects and rodents
respond quickly to changes in temperature
and moisture by migrating and, during
favorable conditions, by reproducing
more rapidly, often resulting in localized
“plagues.” Temperature increases accelerate the vector’s life cycle and shorten the
incubation time of parasites living in the
vector. Warmer weather and failure of winter kills will prolong the transmission season
and change the range of vectors, resulting
in more illness. Some of these illnesses are
particularly devastating to children. Malaria, for example, causes 350 to 500 million
illnesses yearly and more than one million
deaths, mostly in young children. Recent
“homegrown” malaria clusters remind us
that vector-borne illness is a reality for the
highly industrialized world.14
Although we can expect that cold-related deaths will decline, heat-related deaths
are likely to increase. While this is a concern
primarily for the elderly, excessive heat is
also a risk for infants and small children.
Unlike adults, very small children do not
have fully developed temperature regulation mechanisms and cannot change their
environments without adult help. Older
children spend more time in outdoor activity and have higher exposures. Some analyses suggest that heat-related mortality may
be declining in the U.S., despite increasing
temperatures, most likely because of the
widespread availability of air-conditioning.15
Unfortunately, this adaptive technology
requires higher energy use, which may add
to further warming.
What the Future Holds
Our children and grandchildren will
inherit a warmer world with more extreme
weather events. Even if we abruptly reduced
GHG emissions to zero, enough energy is
stored in the climate system to guarantee at
least another 0.6o C temperature increase in
this century.16 Depending on how rapidly we
react, the future may be radically different
from what we know. Initially, poor children
in developing countries (and in this country) will suffer disproportionately because of
their limited capacity to adapt, but ultimately climate change will affect everyone. If
business continues as usual—with countries
using traditional fossil fuels—we are likely
to witness crises in food and water supplies,
large-scale species extinctions, forced migrations of populations because of sea-level rise,
drought, loss of natural resources, and major
global economic impacts.17
This doomsday scenario is not inevitable if we act quickly. James Hansen
of NASA’s Goddard Space Institute estimates that if we can limit warming in the
twenty-first century to 1o C, we can expect
an eventual (in a few centuries) sea-level
rise of less than six meters and climate-related extinction of ~10 percent of species.
If emissions continue to increase at current
rates, temperatures will rise by at least 3o C
by 2100 with a sea-level rise of twenty-five
meters and loss of 50 percent of species.18
There may be a “tipping point” temperature
that, if exceeded, could trigger catastrophic
change relatively quickly (in perhaps a few
decades).19
Anthropogenic GHG emissions are
the major cause of climate change. Carbon
dioxide (CO2) is the GHG responsible
for more than 60 percent of cumulative
anthropogenic warming globally, and more
than 90 percent of the warming over the
last ten years.20 The U.S. produces more
GHGs than any other country.18 (Figure
1) In 2005, almost 39 percent of U.S. CO2
emissions came from residential and commercial buildings, and transportation generated 33 percent (60 percent of these from
www.sfms.org
personal vehicle use).21 (Figure 2) Industry
was responsible for the balance of~28 percent. Since 1990, U.S. CO2 emissions from
transportation, residential, and commercial
sources increased by 25 percent, 31.5 percent,
and 34.6 percent respectively, but decreased
by 3.1 percent from industrial sources. Thus
our daily choices—what and how much we
drive, how we heat and light homes and
offices, how we build houses—are major
components of the U.S. emissions story.
There is reason for hope. Using technologies that can be deployed rapidly, scientists and policy analysts have developed
approaches to stabilizing and reducing GHG
emissions. Princeton University’s Carbon
Mitigation Initiative proposed a plan based
on the “stabilization triangle,” the difference
between zero GHG emissions growth and
projected “business as usual” growth over
the next fifty years.22 The initial goal is to
prevent doubling of CO2 from preindustrial
levels—the doubling is a level above which
it is believed that dangerous climate change
is highly likely—buying time to develop
new technologies for future reductions.
Other approaches and technologies are
proposed23 and more will be developed—but
to avoid accelerating toward the “tipping
point,” action must begin now on known
strategies.
Figure 2 (Right) The U.S., the leading
GHG emitter in the world, was responsible
for 27.8 percent of the cumulative emissions
from 1750 to 2005. Per capita emissions in the
U.S. in 2004 were 20.18 metric tonnes/person
compared to 3.62 in China, 1.04 in India, and
4.24 averaged globally (http://www.eia.doe.
gov/environment.html).
www.sfms.org
What the Health Care Community
Can Do
Many needed changes must come from
governmental action, but we have individual opportunities to mitigate human influences on climate change. In anticipation
of more extreme weather events, we can
work with local authorities to strengthen the
public health infrastructure, including early
warning systems and disaster preparedness
and response plans. In areas where vectorborne illness is likely to increase, we can
work to implement preventive strategies,
such as eliminating breeding grounds for
rodents or mosquitoes. In cities subject to
heat waves and concentrated air pollution,
we can develop educational programs on
using the heat and air-quality indices. Each
region faces different challenges;24 professionals who understand the vulnerabilities
of children are needed everywhere.
The voice of health care professionals
is powerful. We can work to become role
models and champions of GHG reduction.
Table 2 lists actions to help create a culture
of conservation and energy efficiency. Educating the families in our care is part of the
process (see “Steps Families Can Take”), as
is educating the next generation of health
professionals.
Responding to climate change often
requires changing long-established personal
practices—this may be difficult, but actions
that mitigate GHG may have additional
benefits. Energy efficiency saves money.
Reducing auto dependence promotes physical activity. GHG reductions will improve
air quality and save lives, hospital visits, and
money. We hope that this article persuades
readers to join the campaign to reduce GHG
pollution—and that we can prevent climate
change from permanently degrading our
children’s future. The responsibilities and
opportunities are ours.
Katherine M. Shea, MD, MPH, is Adjunct Professor of Maternal and Child Health at
the Dennis and Joan Gillings School of Global
Public Health and Project Director, Environmental Resources Program, Institute for the
Environment at UNC, Chapel Hill in Chapel
Hill, North Carolina. She can be reached at
[email protected].
Sophie J. Balk, MD, is Attending Pediatrician at the Children’s Hospital at Montefiore
and Professor of Clinical Pediatrics at Albert
Einstein College of Medicine, Bronx, New
York.
A full list of references, additional tables,
and an informational patient handout are
available on our website, www.sfms.org.
Figure 1 (Upper Left) Sources of CO2 emissions can
be presented by “end-use sector”—residential, commercial,
industrial, transportation—or by fuel source. Electricity, which
is used for lighting, heating, air conditioning, and running
appliances, is separated out because it represents a very large
portion of emissions. Emissions related to electrical generation
vary by fuel type from very low emission (hydroelectric) to very
high emission (coal). More than one-half of the electricity
generated in the U.S. comes from burning coal. Direct fossil
fuel combustion refers to natural gas and heating oil used in
buildings and by industry, and from petroleum (gasoline and diesel) used mostly in transportation.
Taken together, residential and commercial buildings are responsible for 39 percent of
CO2 emissions, three quarters of which are from
electricity use. Industry produces 28 percent of
annual emissions, split evenly between direct
combustion and electricity use. Transportation
is responsible for 33 percent of CO2 emissions,
the majority (60 percent) of which result from
personal vehicle use.
and The Environment
The Falling Age of Puberty in U.S. Girls
What We Need to Know
Sandra Steingraber, PhD, and Jeanne Rizzo, RN
G
irls today get their first periods, on
average, a few months earlier than
did girls forty years ago, but they
get their breasts one to two years earlier.
Menarche and thelarche are occurring earlier and earlier in the lives of U.S. girls, but
the age of thelarche is falling more rapidly
than the age of menarche. Over the course
of just a few decades, the childhoods of
U.S. girls have been significantly shortened.
What does this mean for girls today and for
their health in the future?
Among U.S. white girls, the average
menarchal age has declined slightly over
the past four decades and now stands at
12.6 years. Among U.S. black girls, average
menarchal age is 12.1 years, and the ongoing
rate of decline is swifter. This is also true
among Mexican American girls. Similarly,
the average age of thelarche and pubarche,
the first clinical signs of pubertal onset, have
continued to fall among all groups and with
significant ethnic/racial differences. About
half of all U.S. girls show signs of breast
development by their tenth birthdays, with
14 percent attaining breast buds between
their eighth and ninth birthdays.
Although studies differ somewhat in
their findings, the mean age of thelarche is
about 10 for white girls and 9 for black girls.
Pubertal onset and menarche are apparently
not as tightly coupled to each other as in
years past. However, the data quality on
onset of thelarche and pubarche, and their
changes over time, is not as reliable as that
for menarche.
Possible Causes of Early Puberty
The brain is the driving force that
controls thelarche and menarche through
the secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus. The
GnRH-secreting neurons (of which there
are about 1,000) are themselves regulated by
a plethora of chemical cues. Some of these
are hormones, some are enzymes, and some
“Interventions that
reverse the trend
toward ever-earlier
puberty in girls
are a public health
imperative ... Many
actions can be taken
on the basis of what is
already known.”
are neurotransmitters.
With its multitude of signaling pathways, the neuroendocrine apparatus by
which pubertal onset is controlled is inherently susceptible to disruption. Several
upstream factors can potentially alter the
regulation of the GnRH, secreting neurons
and thereby hastening the onset of puberty
in girls. These include:
• Obesity: Obesity disrupts the
endocrine system; chubbier girls tend to
reach puberty earlier. But obesity is a consequence of early puberty as well as a possible
contributor, adding to the complexity of
studying this phenomenon.
• Endocrine-disrupting chemicals:
Exposures to endocrine-disrupting chemicals we come into contact with regularly are
also playing a role in accelerating puberty
in girls. These include chemicals we are
commonly exposed to in cosmetics, shampoos, cleaning products, baby bottles, and
children’s teething toys.
• Premature birth and low birth
weight: Both premature birth and low birth
weight alter endocrine function and therefore raise the risk of early pubarche. In addition to other factors, a pregnant woman’s
chemical exposures can directly affect her
developing child, in some cases leading to
premature birth and low birth weight.
• Psychosocial stressors: These
stressors, including family dysfunction and
the absence of a father in the home, also
disrupt the endocrine system and are possible contributing factors to early puberty.
The mechanisms behind these psychosocial
stressors are not yet clear.
• Formula feeding: Breastfeeding appears to protect against early puberty in two
ways: by contributing fewer calories than
formula and by offering hormones and other
growth factors that may protect against
early puberty. Further study is needed to
clarify the role of breast milk in pubertal
development.
• Physical inactivity: Leanness and
exercise together appear to protect against
early puberty. While it is difficult to sort
these two factors out in studies, there is
enough evidence for us take preventive
action now.
• Television viewing and media use:
Little is known about the effects of sexualized media content on pubertal timing in
girls. But increased time in front of the
television or a computer can lead to obesity
and physical inactivity, both factors that
contribute directly to early puberty. Additional research is needed to explore the
mechanisms by which chemical signals in
the brain may disrupt pubertal processes.
Negative Consequences of Early
Puberty
Early puberty poses several risks for girls.
www.sfms.org
It is caused by a combination of factors, and
the interactions among these factors can be
complex. Most notably, early puberty raises
the risk factor for breast cancer. When puberty arrives earlier, the window of exposure
to estrogen opens wider and increases a girl’s
chances of developing breast cancer in later
life. Indeed, first menstruation (menarche)
before age 12 increases the risk of breast
cancer by 50 when compared to menarche
at age 16 or beyond.
Early puberty is also associated with
many high-risk behaviors in later adolescence—such as smoking, drinking, drugs,
crime, and unprotected sex—that have
potential lifelong consequences. Girls who
mature early are also more likely to suffer
violent victimization and psychopathologies such as depression and anxiety. It is
not clear whether the social or physiological
experience of pubertal change is responsible
for these negative outcomes. In either case,
interventions that reverse the trend toward
ever-earlier puberty in girls are a public
health imperative.
What We Need To Know
There are areas of research that need to
be supported to fill the holes in the science
of early puberty. These include:
• Basic science: We need to explore
the mechanism behind the initiation of
puberty, the role of signaling devices such
as hormones and enzymes, the impact of
chemical exposure during pregnancy, and
the effect of breastfeeding on endocrine
system development.
• Epidemiology: We need large studies that follow girls from conception to
adulthood, such as the National Children’s
Study, mandated by Congress in 2000 but
not yet fully funded. Studies like those in the
National Institute of Environmental Health
Sciences and National Cancer Institutefunded Breast Cancer and Environment
Research Centers will contribute to our understanding of obesity, endocrine-disrupting
chemicals like bisphenol-A and phthalates,
and pubertal onset.
• Chemical testing: Chemicals are
not tested for their ability to disrupt the
endocrine system before they are allowed
into the marketplace. The Environmental
Protection Agency’s Endocrine-Disruptor
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Screening Program, mandated by Congress,
is eight years behind schedule, and not one
chemical has been screened to date. We
need this screening information in order
to reduce the public’s exposure to these
chemicals.
• Chemical tracking: We also need
to know more about the sources, emissions,
and fate of endocrine-disrupting chemicals
in commercial use in order to reduce exposures. We need full disclosure of ingredients
in consumer products, especially children’s
products. We need more complete inventories of emissions and better monitoring
of air, food, and drinking water. The Toxic
Release Inventory was one good example
of chemical tracking, but it has been significantly weakened.
• Biomonitoring: Biomonitoring, or
measuring the pollution in people, helps
prioritize research on emerging chemicals
of concern by identifying which chemicals
are in our bodies. While the U.S. Centers
for Disease Control and Prevention (CDC)
biomonitors a national sample of the
population for chemical contaminants, it
collects very little information on infants
and children, and what it gathers cannot be
disaggregated in a way that would give us a
snapshot of chemical exposures at the state
or local level. The California Environmental Contaminants Biomonitoring Program
will address some of these gaps and build a
replicable model for other states interested
in creating their own statewide biomonitoring programs.
What We Can Do Now
Many actions can be taken on the
basis of what is already known. Strategies
to tackle childhood obesity and inactivity
include changes to the built environment to
encourage exercise; the resurrection of daily
physical education in school; the elimination of high-calorie, low-nutrient foods
from school lunch programs and school
activities; the development of school and
community gardens; the establishment of
urban farmers’ markets; and partnerships
between local farmers and neighborhood
supermarkets to provide fresh, local produce
in low-income communities. One obesityprevention program in Boston-area schools
already has demonstrated that coordinated
efforts to promote healthy eating, increase
physical activity, and decrease television
viewing have the power to delay menarche
in sixth- and seventh-grade girls.
In addition to both good nutrition
and access to prenatal care, strategies to
lower rates of preterm and low-weight births
include eliminating exposure to tobacco
smoke, chemical solvents, and sources of
air pollution and mercury contamination.
Strategies to lower the burden of endocrinedisrupting chemicals to which girls have
documented exposures include phaseouts
of phthalates and bisphenol A; investments
in organic agriculture; watershed protection;
and nonchemical pest control in homes,
schools, and day care centers.
Early puberty is a problem that does
not arise from a single toxicant, lifestyle,
or dietary shortcoming. Rather, many
different environmental stressors—some
psychosocial, some nutritional, some chemical—interact in the bodies of young girls in
ways that result in accelerated sexual maturation, with its attendant risks for health
and well-being.
The Falling Age of Puberty in U.S. Girls
is a report researched and written by Dr.
Sandra Steingraber. It was commissioned
and published by the Breast Cancer Fund
to explore the state of the evidence on early
puberty in the U.S. Below is a synopsis. The
full report and accompanying Advocate’s
Guide is available online at www.breastcancerfund.org/pubertyreport.
Sandra Steingraber, PhD, is a biologist and
distinguished visiting scholar at Ithaca College
in Ithaca, New York. She is the author of the
books Living Downstream, Having Faith, and
Post-Diagnosis.
Jeanne Rizzo, RN, is the Executive Director of the Breast Cancer Fund in San Francisco,
a breast cancer organization focused solely on
identifying and eliminating the environmental
and other preventable causes of the disease.
With coalition partners, BCF advocates for
the elimination of carcinogenic and endocrinedisrupting chemicals through state and federal
legislative efforts and corporate accountability
campaigns, such as the Campaign for Safe
Cosmetics.
and The Environment
Cancer and Environmental Chemicals
Past Time for Politeness
Devra Lee Davis, PhD
If you want to go fast, go alone. If
you want to go far, go together. —African
proverb
M
y very good friend Andrea Ravinette Martin—the charismatic
founder of the Breast Cancer
Fund—used to say, “The only way I will
know I have really survived breast cancer
is when I die of something else.” She did:
when she was fifty-six, a new and unrelated
malignancy of the brain turned her into a
breast cancer survivor.
Three years before a tangled web of
glioblastoma multiforme invaded her brain,
Andrea was in excellent health. As part of
a pilot research study of the Environmental
Working Group, she was tested for chemical
contaminants. She had never worked in a
factory. She had no chemically intensive
hobbies, like boatbuilding or oil painting.
Yet it turned out that Andrea was a walking
toxic waste site. Her body contained nearly
one hundred different chemical residues,
half of which caused cancer when tested
in experimental animals. Many of these
toxins didn’t exist when she was born in the
middle of the past century. Had they played
any role in causing either her breast or brain
tumors? Did her frequent use of those clunky
first-generation cell phones have anything
to do with it? It is sad that we don’t know.
It is appalling that we can’t find out.
Look around and it seems that cancer
has become the price of modern life. In
America and England, one out of every two
men and one out of every three women will
develop cancer in their lifetime. In America
alone, there are currently more than 10 million cancer survivors. Cancer is the leading
killer of middle-aged persons and, after accidents, is also the leading killer of children.
Yes, deaths have dropped, chiefly because
fewer are smoking and more are surviving
colorectal, prostate, and breast cancer. But
more new cases of the disease are arising that
have nothing to do with smoking, aging, or
screening.
How did this happen? How did a disease that was once so atypical become so
ordinary? Are we simply talking more about
an illness that has always been around?
Some 2,500 years ago, the Greek physician
Hippocrates depicted a tumor as a muddled
irritable cavity with spindly legs, flaring out
of control in all directions. Fascinated with
its evil, animal-like appearance, he termed
it cancer, karkinoma, from the Greek word
for crab. Like Hippocrates, we are drawn to
things of menacing beauty.
To an epidemiologist like myself, explanations of run-amok cancer processes that
routinely capture Nobel Prizes and promising headlines address the how but not the
why of cancer. They can tell us about how
cells and organs behave when they spin out
of control but say nothing about what makes
these things happen to specific groups of
people located in a certain area at a certain
time. Why have so many types of cancer not
known to be tied with smoking increased
from decade to decade in industrial countries and in those areas of the developing
world that are becoming industrialized?
Why do one fifth of all colorectal cancers
in Egypt occur in persons under age thirty,
a rate that is ten times higher than in the
U.S.? Why are so many people in their thirties and forties in many industrial countries
coming down with often fatal cancers of the
bone marrow and pancreas—diseases that
used to occur only in those in their sixties or
older? What can we do to reverse the trend?
How can we get better at keeping cancers
from happening in the first place? Despite
impressive progress in finding and treating
some forms of the disease, more than half of
all those diagnosed with cancer will not last
a decade with their illness.
We have all been told what we are
supposed to do to reduce the risk of cancer
on our own. We are supposed to eat right
and exercise. Even prayer and meditation
are touted as good things to do. Smoking,
of course, is forbidden. And we are certainly
not to drink much alcohol or engage in
dangerous sex.
But we all know people who lead
perfectly clean, even exemplary lives, like
my dear friend Andrea, and still get cancer. They take good care of themselves,
yet somehow cancer hits. The first thing
most cancer patients, and their sometimes
unthinking friends, ask is, what did I do to
make this happen? The answer, often, is not
a bloody thing. Sometimes cancer is due to
a genetic susceptibility that we get from our
fathers or mothers, but mostly it isn’t. We
know that no matter how careful anyone is
about their good and bad habits, where and
when we are born and what we work and
play with has a lot more to do with whether
we get cancer than who our parents happen
to be. For instance, inherited defects do not
account for most breast cancers. Nine out of
ten women who develop breast cancer are
www.sfms.org
born with perfectly healthy genes. When I
was a girl, one in twenty women got breast
cancer in her lifetime; by the time Andrea
and I reached middle age, one in seven did.
Nobody can explain why. We do know that
we live in a sea of synthetic estrogens and
other hormones and routinely are exposed
to myriad materials that never previously
existed. The producers of these agents take
comfort in the fact that any one of them,
tested by itself, looks fairly benign when
gauged by various scientific measures of
carcinogenic potency.
Still, it defies common sense and basic
biology to assume that just because a single
agent looks all right when tested on its
own, we can safely endure encounters with
hundreds of such materials all at once. You
would never take all the different pills in
your medicine chest in one swallow, even
though ingesting one or a few is fine. Why,
then, should we accept that there is no danger in being subjected to combinations of
agents without precedent in human history?
Biologist Tyrone Hayes of the University of
California at Berkeley thinks the tadpoles
of the seed-corn fields of York County, Nebraska, are trying to tell us something: one in
every three dies when exposed to mixtures
of ordinary chemicals in those fields.
The start of my own scientific career
coincided with a short-lived period during
the late 1970s during the presidency of
Jimmy Carter, when the federal government appeared serious about uncovering
the causes of cancer. The National Cancer
Institute and other federal agencies began a
series of programs to assess the true effects of
tobacco and certain widely used industrial
chemicals. In 1978, these programs became
more than rhetoric.
Until that time, the government pretty
much took industry reports on the safety of
chemicals at face value, without requiring
any documentation. This changed when it
was learned that the company doing much
of the testing for industry, Industrial BioTest, could not even find or account for all
the animals it had supposedly studied. Industrial Bio-Test had tested one out of every
three chemicals on which the government
had any data at all. But without adequate
records to show that the testing had been
done properly (or at all), the reports of safety
www.sfms.org
based on this work were worthless.
In 1979 the government set up its own
experimental laboratory to test the cancercausing capacity of chemicals in specially
bred homogenous rodents, under the U.S.
National Toxicology Program. Animals
were reared with well-established body
sizes, types, and inclinations, so that their
responses to potential cancer-causing agents
could be studied carefully in order to predict
and prevent cancer and other chronic ailments in humans.
Even before the Industrial Bio-Test
scandal, Congress had begun passing rules
that appeared to require the government to
act to keep cancer-causing hazards out of the
market. With more than 80,000 chemicals
in widespread use and complete toxicity test
results available on fewer than 1,000, these
laws, like the Toxic Substances Control Act
of 1976, forced the government to come up
with some rational way to review chemicals
and separate the good from the bad, the
ugly, and the ones we don’t even know what
to do about. This was supposed to lead to
efforts to come up with standard methods
for evaluating risks, for making sense of experimental information, and for estimating
ways to protect public health. Instead, the
law has generated so much talk and so little
action that insiders refer to it as the “Toxic
Substances Conversation Act.”
After the 1980 presidential election,
even these meager efforts began to unravel.
The early Reagan administration followed
the lead of the Carter administration in
its tobacco-friendly positions and also jettisoned programs that sought to rein in
cancer-causing industrial sources. The new
administration curtailed funding for testing
chemicals under the National Toxicology
Program, while federal support for scientific
research aimed at designing “safe cigarettes”
grew. The problem with “safe cigarettes” was
that, well before the 1980s, it was widely
known that there is no such thing. Inhaling
thick clouds of smoke into your lungs and
raising levels of carbon monoxide in your
blood and that of your children, spouses,
and office mates, whether from burning tobacco, wood, or coal, is simply an unhealthy
thing to do.
The best wars, to take a line from
President McKinley’s Secretary of State,
are short, splendid little affairs, all pageantry
and little fighting. The protracted war on
cancer has been none of the above. How
did we get to this point?
From the start, this national campaign
was blocked from dealing with some known
causes of the disease, such as tobacco, solar
and X-radiation, and synthetic hormones in
the workplace and the general environment.
Proof that the world in which we live and
work has a lot to do with whether or not we
get the disease was either overlooked or kept
out of sight altogether, often by folks who
had major economic interests in seeing this
happen. Instead, the entire project focused
on devising ways to find, treat, and cure
the disease. We are spending more money
than ever to find and treat cancer—some
$100 billion in direct treatment costs alone.
Today, one subsidiary of the global chemical firm Industrial Chemicals, Inc., makes a
number of cancer-causing pesticides, such as
atrazine—a compound banned in much of
the industrial world—while another division
of ICI, AstraZeneca, produces tamoxifen,
one of the most widely prescribed cancer
drugs in the world. Could this paradoxical
strategy have anything to do with the fact
that both the incidence of cancer not tied
to smoking and its treatment options keep
steadily increasing, while efforts to restrain
environmental causes of the disease remain
stymied?
Of course not. Remember that we live
in a highly technological, interconnected
world. It is safer, and better for your reputation in polite society, to keep reminding
yourself that the disease is just so damned
complex.
Dr. Devra Lee Davis is Director of the
Center for Environmental Oncology at the
University of Pittsburgh Cancer Institute.
This article is adapted from her book The
Secret History of the War on Cancer,
Basic Books, 2007, with permission of Basic Books and Devra Davis. For further
information, visit www.devradavis.com.
and The Environment
Mercury Tales
Jane Hightower, MD
I
n this issue of San Francisco Medicine,
we learn about the many chemicals and
toxicants that face us today. Physicians
now must sort through the toxicants that we
eat, breathe, and absorb through our skin,
as some can cause adverse health effects.
When looking at the toxicant mercury, I
realized the history of its use in medicine was
vast, as practitioners have been poisoning
patients with it for centuries.
Liquid mercury (quicksilver) was experimented with by the alchemists beginning centuries ago. They are the ones who
discovered how to turn poor-grade gold
ore (essentially a rock) into pure gold by
combining mercury and various other earth
salts. Making gold from a rock had mystical value, and the “elixir” that resulted in
the process was thought to have medicinal
qualities. Creating gold from a rock was
called the Magnum Opus, and those who
could achieve it were thought to gain eternal youth. They also were thought to pose
a threat to some governments, since one’s
ability to fabricate gold—currency—could
compete with the ruling powers. As a result,
alchemists were revered in some societies
and executed in others (Goldwater 1972).
Multiple forms of mercury have been
used for medicinal purposes over the centuries. In one report comparing Kentucky
and New Jersey physicians between 1854
to 1887, mercury ranked second only to
opium and morphine in the total number
of prescriptions written. The mercurials,
including corrosive sublimate or mercuric
chloride and calomel or mercurous chloride,
were used for many conditions, from “promoting the flow of the liver” to antisepsis,
and even liver spots.
Before 1938, all one had to do was believe that a remedy worked to avoid being
accused of fraud. But calomel met its match
in 1863, when Dr. William A. Hammond,
the Surgeon General, removed calomel
from the Union Army surgeons’ supply
table, as directed in his infamous Circular
Number 6. His reasoning was that it was
being overused to the point of causing the
side effects of melancholy, hypersalivation,
and gangrene of the mouth.
The army doctors, who, Hammond
thought, were in many cases unqualified,
were furious. The “regulars” (also referred
to as allopaths) thought Hammond had
“done great and inexcusable injustice to a
noble, humane, scientific, and self-sacrificing profession.” They also thought he was
caving in to the homeopaths, who thought
mercury was toxic in all forms. The Transactions of the American Medical Association
in 1864 describe the process whereby the
AMA formed a committee just to address
this circular. They gathered up some of the
army surgeons and asked their opinion.
The army surgeons said they never saw any
cases of mercurialism and that Hammond’s
circular was an “unwarranted assumption of
authority, and a reckless attempt to cut the
Gordian knot of intricate pathology by the
exercise of official power.”
Hammond was court-martialed shortly
thereafter, and many historians have stated
that his removal of calomel from army use
that was the last straw that led to his disgrace. In 1878, a Senate hearing concluded
that his court-martial was a political one
and that there was no dereliction of duty
or improper misconduct. He was fully
exonerated and restored to the U.S. Army
with the rank of Brigadier General, retired
(American Medical Association 1864,
Flannery 2004).
It is curious that, while today mercury
is being removed from our allopathic medicines, a patient brought to me a homeopathic remedy that contained mercurious
solubilis.
Another common mercurial was bichloride of mercury, or corrosive, or sweet
sublimate. Many physicians thought that it
had antiseptic capabilities. It was not until
the 1930s that experiments revealed that
it only had some bacteriostatic properties
and was not adequately bacteriocidal. Regardless, I found in our local San Francisco
history that Dr. Levi Cooper Lane, who
founded and built the Levi Cooper Lane
Hospital in 1875, believed in the virtues of
bichloride so much that he had it added to
the plaster mixture that went onto the walls
of the entire hospital. That hospital is now
in some unfortunate landfill, and in its place
is my office building at 2100 Webster Street.
Even in the “new” Stanford hospital, built
in 1917, surgeons would wash their hands
in bichloride. Some would pour it on the
floor, thinking it would ward off the post-op
infections that were a terrifying complication of the time. I could not find whether the
surgeons had symptoms of mercurialism, but
this practice faded as better rubber gloves
became available and bichloride’s lack of
effectiveness became evident (Brewer 1939,
Deforest 1944, Morton 1948, Deforest 1949,
Stanford University 1959).
As for the surgical practice of yesteryear, an 1895 JAMA printed a story of how a
doctor in training was asked to give a patient
a shot of whiskey after a minor procedure.
Unfortunately, the whiskey was stored next
to the bottle of bichloride. Even the patient
agreed that it did not taste like whiskey. Fast
action was called for, and in four minutes,
the patient was asked to swallow the albumen of half a dozen eggs to coat the stomwww.sfms.org
ach, then in another minute a stomach tube
was introduced to “thoroughly wash out” his
stomach. No mercurialsm was noted in the
patient, the author boasted, and the patient
“suffered no inconvenience from the energetic treatment” (no author, 1895).
Merthiolate, otherwise known as
thimerosal, contains ethylmercury and
has posed a different conundrum. Eli Lilly
patented it in 1928 as an antiseptic and for
treatment of nose and throat infections.
The Lilly scientists later declared many uses
for their wonder remedy, including that it
was a cure for the common cold. This was
quickly refuted by another study. Because
of the antisepsis claims very early in its
use, it wound up in our vaccines from their
beginning. The antisepsis claim continues
to be made even though there is evidence
to the contrary. Mercury has been shown
to stimulate antibody formation; one could
ask, then, whether thimerosal remained in
the vaccines as an adjuvant, and not necessarily as an antiseptic. The only metal that
is currently FDA approved as an adjuvant
is aluminum, which was introduced to
replace thimerosal. To call mercury an
adjuvant would require testing to establish
safety and efficacy. Its antiseptic claim was
grandfathered in. Fortunately, the vaccine
manufacturers have found an alternative,
and we have more requirements for the assessment of safety and efficacy (Bassler 1935,
LeBlanc 1936, Pichichero 2005).
As for the over-the-counter mercurials, they had also been grandfathered in
before the FDA rules of proving safety and
efficacy. They continued to be in use despite
having been linked to the occurrence of
the neurologically disabling and sometimes
fatal acrodynia (pink) disease in children.
In the 1980s, the FDA advisory committee
said that the mercurials should go through
an assessment of safety and efficacy, and
the manufacturers were notified of this. It
was not until 1998, when the remaining
twenty over-the-counter mercurials, made
by eight different companies and including
the popular tincture mercurochrome, met
their demise. When the FDA gave final
rule to have these agents removed from
over-the-counter use, no challenges were
brought forth by the manufacturers to prove
safety or efficacy. These agents just quietly
www.sfms.org
disappeared (Federal Register 1998).
As for the treatment of syphilis, many
mercurial agents, including the blue pill,
were used until penicillin was discovered
to be a cure. Hence the common saying,
“a night with Venus means a life with
Mercury.” But the mercurials were never
proven to cure syphilis; many who had
the condition would go on to have tertiary
syphilis, or the disease would seem to remit
spontaneously. Meanwhile the treatment
with these agents was often thought to be
worse than the disease itself.
The tale of mercurial diuretics will
certainly be of interest to many physicians,
as some still remember using these agents
early in their careers. It was in 1919, when
a child was given the mercurial Novosurol
for his syphilis, that an astute nurse noted
a marked diuresis. The doctors tried it on
other patients in the hospital and it was
noted to have the same effect. A new
diuretic was born. The mercurial diuretics
lasted for decades, despite some fatalities
and adverse effects. For many of these
moribund patients, it was either mercury or
death—sometimes both (Vogl 1950).
As for the prescription mercurial agents
in general, the World Health Organization asked for the phase-out of mercurial
medications in 1972. The prescription-only
mercurial agents disappeared as more effec-
tive agents replaced them (World Health
Organization 1972).
Perhaps you may wonder how much
mercury was contained in one dose of
diuretic or a syphilis pill. It was 40,000 to
66,000 mcg. Although the absorption or
bioavailability is unknown, it was thought
to be near lethal doses.
So here we are today, arguing over
the amount of methylmercury contained
in a serving of fish. This can be anywhere
from undetectable to greater than 170 mcg
per six-ounce serving. The varying toxicities of the many types of mercury makes it
difficult for researchers and policy makers
to sort out how much mercury can lead to
adverse health effects, especially for those
chronically exposed. To date, there is no
known level of methylmercury that has
been determined to be without harm. This
article will serve to give an understanding
of why the medical community has been
puzzled by it all.
Dr. Jane Hightower, a San Francisco
internist, is currently serving on the Board of
Directors of SFMS. In Spring 2008 her latest book will be released, entitled Diagnosis
Mercury: Money, Politics and Poison (Island
Press).
References to this article are available
online at www.sfms.org.
Johnson KC and Glantz SA. Evidence secondhand smoke causes
breast cancer in 2005 stronger than for lung cancer in 1986. Abstract.
Objectives: To compare the strength of evidence from epidemiologic studies of secondhand smoke for the U.S. Surgeon General’s 1986 conclusion that secondhand smoke
caused lung cancer with the California Environmental Protection Agency’s (CalEPA)
similar 2005 conclusion on breast cancer in younger, primarily premenopausal women.
Methods: We reviewed each report for criteria used to assess causality; numbers of
studies, statistically significant increases in risk, and pooled summary risk estimates.
Results: Both the Surgeon General and CalEPA used updated Bradford Hill criteria for assessing causality and found that the evidence met those criteria. Six of 13 lung cancer studies (46
percent) had statistically significant increases (one of three cohort studies). Pooled risk estimates
for lung cancer for spousal exposure were 1.53 for 10 combined case control studies and 1.88
for 7 studies with dose-response results. The CalEPA reported 10 of 14 studies (71 percent) had
statistically significant increases in breast cancer risk (two of four cohort studies). Pooled relative
risk estimates for younger, primarily premenopausal women were 1.68 (95 percent CI: 1.33, 2.12)
for all exposed women and 2.19 (1.68, 2.84) for five studies with better exposure assessment.
Conclusions: The evidence from epidemiologic studies of secondhand smoke in 2005 for breast
cancer in younger, primarily premenopausal women was stronger than for lung cancer in 1986.
This paper, in press at Preventive Medicine, is now available online at http://dx.doi.
org/10.1016/j.ypmed.2007.11.016.
Get Paid
What You’re Worth
All around California, physicians are being pressured by giant PPOs to
accept lower reimbursement rates in exchange for patient volume. It’s a
tough choice, but one fact stands clear: Every time you lower your rates,
you have to work longer hours for less pay.
The Pacific Foundation for Medical Care offers you a better choice.
Since 1957, we have reimbursed physicians at generous rates that maximize your income—not ours. We’re nonprofit, and we’re governed by
physicians. Our Mission is simple: To pay you what you’re worth.
Pacific Foundation for Medical Care
To learn more about PFMC, or for a membership application, visit www.pfmc.org
or call Kathy Pass at 800-548-7677, Ext. 115
Looking for
Long Term
Care Insurance?
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Marsh is part of the family of MMC companies, including Kroll, Guy Carpenter, Mercer, and the Oliver Wyman Group (including Lippincott and NERA Economic Consulting).
and The Environment
Time to Update Environmental Regulations
Should public health standards for endocrine-disrupting compounds be based upon sixteenth-century dogma
or modern endocrinology?
John Peterson Myers, PhD, and Fred S. vom Saal, PhD
H
ealth standards established in the
United States for exposure to toxic
chemicals rest upon a core assumption: high-dose testing procedures used in
regulatory toxicology adequately predict
potential low-dose effects. Scientific discoveries over the past decade have profoundly
challenged that assumption as information
has grown about the commonness of contaminants that behave like hormones.
Endocrinologists long ago discovered
that hormones have effects at low serum
concentrations that can differ dramatically, and unpredictably, from those caused
at high levels (1). Indeed, sometimes they
can be diametrically opposed. This endocrinological reality stands in direct conflict
with any assumption that high-dose studies
predict low-dose impacts. If contaminants
with hormonal characteristics, known as
endocrine disruptors, behave similarly,
then the regulatory tests used to establish
safety standards may be blind to important
impacts.
A growing body of research now confirms that endocrine disruptors, like hormones, can also contradict the expectations
of traditional regulatory testing. This creates
the strong likelihood that some health standards currently used to set exposure limits for
the American public are too weak.
To the nonendocrinologist, it seems
logical that higher doses would lead to
greater effects. This assumption has been at
the core of toxicology for centuries, beginning with Paracelsus’s sixteenth-century
observation that “All things are poison and
nothing is without poison; only the dose
permits something not to be poisonous.”
His quote has been paraphrased to “the
dose makes the poison” and is generally
interpreted to mean that the higher the
exposure, the greater the impact.
For many contaminants, toxins, poisons, and pharmaceuticals, this assumption
has helped protect public health. But sub-
“It is time that the FDA
and EPA move beyond
sixteenth-century dogma
and begin using twentyfirst-century scientific
knowledge.”
stantial evidence is now in hand showing
that people are exposed to hundreds (if
not more) chemicals that can behave like
hormones.
Some endocrine-disrupting chemicals
are produced in very high volumes. The
compounds of greatest concern include plastic monomers and plasticizers used widely
in common consumer goods, leading to
virtual ubiquitous exposure in the U.S. and
other developed countries. For example, the
plastic monomer bisphenol A (BPA) was
discovered to be an estrogen in the 1930s,
but now it is used as the basic chemical
building block for polycarbonate plastic and
an epoxy resin used to line most food cans
sold in U.S. supermarkets today.
The chemical characteristics of polycarbonate and the epoxy resin guarantee
that normal use will contaminate food
and water that comes into contact with
BPA-based materials, especially if heated.
Most plastic baby bottles are made with
polycarbonate, and baby formula cans are
lined with the resin. This will result in substantial, unavoidable exposures for infants
fed warmed formula.
Many studies have shown that BPA is
capable of causing a wide range of adverse
effects in laboratory studies at serum concentrations beneath the median level found
in people throughout the developed world
(2). The adverse effects caused by fetal exposure and infant exposure to BPA in animal
experiments include breast cancer, prostate
cancer, impaired fertility, cystic ovaries,
uterine fibroids, hyperactivity, and obesity.
The current EPA and FDA health standards
for BPA, however, are based upon traditional toxicological testing conducted in the
1980s. Modernizing the BPA standard based
on current science would require lowering
acceptable exposures by a factor of at least
5,000-fold and would require elimination of
BPA from many common products.
Driven by a need to be cost effective,
regulatory toxicology has applied the “dose
makes the poison” concept in practice by
testing first at high doses and then testing at successively lower doses until no
response, or little response, is seen. Often
only three or four doses are used, and for the
vast majority of chemicals these are rarely,
if ever, low enough to be comparable to
levels experienced by the general public.
The assumption is that this high-dose testing protocol predicts the types of effects
that might take place at much lower levels.
And because “the dose makes the poison,”
the expectation is that by working down
the dose-response curve from a level that
clearly causes an effect to one that does not,
this process can identify exposures beneath
which there will be no harm.
Endocrinology, however, is replete with
cases in which hormone action at low levels
differs dramatically from hormone action
at high levels. For example, administering
newborn mice a high dose (1,000 µg/kg/day)
www.sfms.org
of the estrogenic drug diethylstilbestrol
(DES) causes weight loss in adult mice. In
contrast, a dose of 1 µg/kg/day causes grotesque obesity in adulthood (3).
Another example with clinical implications comes from the well-known “tamoxifen flare.” Tamoxifen is useful clinically
because at high doses (administered daily at
20 to 40 mg) it is an antiestrogen, suppressing proliferation of breast cancer cells and
producing tumor regression (4). Early during
treatment, however, when tissue levels are
still rising, tamoxifen administration can
cause several estrogenic effects, including
a slight increase in tumor size. Research
by Wade Welshons at the University of
Missouri has explored the molecular mechanisms of the tamoxifen flare and finds that at
serum concentrations 10,000 times beneath
the level used to suppress breast cancer cell
proliferation, tamoxifen acts as an estrogen,
actually promoting proliferation (Welshons,
pers. comm.). Ironically, his calculations
show that if one were to use standard riskassessment procedures with the tamoxifen
dose-response curve—identifying the highest exposure with no discernable effect and
then applying a series of safety factors that
take into account various sources of uncertainty— the concentration with maximum
proliferative effect would be identified as a
safe level of exposure.
In the tamoxifen flare, the doseresponse curve showed inhibition at high
levels and proliferation at low—that is,
completely opposite effects. This is a special
case of what are called nonmonotonic doseresponse curves: dose-response relationships
in which the slope of the line plotting
response as a function of dose changes its
sign (positive to negative or the reverse)
somewhere over the range of doses used.
Clinicians who treat women and men
for hormone-stimulated diseases (uterine
fibroids, prostate cancer) advise their patients who take a hormone (Lupron) that
some adverse effects occur during the initial
phase of treatment. This is due to the fact
that as the amount of the drug increases
after injection, the low doses of Lupron
result in the ovaries producing estrogen or
the testes producing testosterone; only after
reaching a high dose is the drug’s desired effect, inhibition of estrogen or testosterone
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production, achieved—opposite effects
occur at low and high doses. This is not
just true for hormonally active drugs but
for all hormones and hormone-mimicking
chemicals used in products.
As research has progressed in the toxicology of endocrine-disrupting compounds,
nonmonotonic curves have been reported
regularly (5). One of the earliest examples
involved the response of the mouse prostate
to exposure to several different estrogenic
compounds during fetal development (6).
These experiments examined the adult
prostate weight following fetal exposure,
separately, to estradiol or diethylstilbestrol
(DES); analogous nonmonotonic findings now exist for BPA in human prostate
cancer cells (7). Each experimental series,
conducted over an extremely wide range of
doses, showed that the highest exposures
did not differ from the controls, but that intermediate doses led to significant increases
in prostate weight and also to sensitivity to
androgen stimulation. The dose-response
curve took the shape of an inverted U, a
descriptor now used in the literature to
describe this type of nonmonotonic doseresponse curve. If the dose range had been
extended even higher, the response would
have fallen significantly beneath the controls as exposure moved into a concentration at which the compounds were overtly
toxic. This was demonstrated at the level
of individual genes involved in regulating
prostate growth (8).
Other endocrine-disrupting compounds demonstrating nonmonotonic
patterns include the phthalate DEHP; the
pesticides DDE, dieldrin, endosulfan, and
hexachlorobenzene; and arochlor 1242,
a PCB (5). Some of the reported effects
include strong exacerbation of allergic
reactions following exposures well beneath
current safety standards.
Extensive evidence is now available
on the molecular and physiological mechanisms that are responsible for these findings.
At very low doses, hormones can stimulate
the receptors in cells that allow the hormone
to cause effects in the cells (called “receptor up regulation”), while at higher doses,
receptor “down regulation” occurs and the
number of receptors available to mediate
the action of the hormone is reduced (1, 9).
Also, there are myriad hormonal feedback
mechanisms between the brain, pituitary
gland, and hormone-producing organs
(thyroid gland, adrenal glands, ovaries,
testes) that contribute to the presence of
nonmonotonic dose-response curves.
The chemical risk assessment establishment has been unresponsive to the fact
that one of its core assumptions has been
invalidated. Hence, no standard for any
contaminant has incorporated these wellestablished findings from endocrinology.
Instead, standards continue to be based
upon testing procedures that assume highdose testing can adequately predict low-dose
results.
The American public depends upon
regulatory agencies to set public health standards that will avoid harmful exposures. It is
time that the FDA and EPA move beyond
sixteenth-century dogma and begin using
twenty-first-century scientific knowledge
to accurately determine the safety of the
chemicals being used in plastic, toys, food
containers, pesticides, cosmetics, building
materials, clothes—in other words, countless products and materials we incorrectly
assume are safe. Given the wide range of
health effects now shown to be caused in
animals by exposure to these contaminants,
modernizing the standards may reap large
benefits for public health.
Dr. John Peterson Myers is Founder, CEO,
and Chief Scientist of Environmental Health Sciences and the publisher of EnvironmenalHealthNews.org. His research on endocrine disruption
began in 1989. Along with Theo Colborn and
Dianne Dumanoski, he published Our Stolen
Future in 1996. Dr. Fred vom Saal is Professor
in the Division of Biological Sciences, University of
Missouri, Columbia.
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and The Environment
Nanoparticles and Health
Thoughts on Some Early Findings
John M. Balbus, MD, MPH
T
he promise of nanomedicine relies
in great measure on the tiny size of a
range of different types of nanoparticles and the unique properties that emerge
at this scale. These properties influence the
ways that nanoparticles move through the
body, which differ from the behavior of both
individual chemical molecules in solution
and larger particles. These properties also
lead to unique interactions with receptors
and biomolecules (such as DNA) and physicochemical attributes (such as fluorescence)
that make these materials useful for medical
purposes.
While these properties in nanoparticles may bring medical benefits, they also
may result in unusual toxicity or pathways
for exposure. The good news is that the
regulatory requirements for testing novel
therapeutic and diagnostic tools are likely
to uncover most significant toxicity for
nanoparticles used in medicine, at least
for the routes of administration tested; the
bad news is that nanoparticles with similar
properties are being used for a host of nonmedical applications, and the requirements
for testing before commercialization are
extremely limited (with pesticides being
an exception). To the extent that medical
and nonmedical nanoparticles are similar,
however, the knowledge about potential
risks gained from testing medically-oriented
materials can be combined with the limited
data on nonmedical nanoparticles to try to
design safer, less toxic nonmedical materials. Testing on medical nanoparticles will
provide limited information about target
organ toxicity arising from inhalational or
dermal exposure, and essentially none on
environmental transport and ecological toxicity, which are critical issues for nanoparticle safety. Nonetheless, with hundreds of
nanoparticle products on the market, the
sooner any toxicity information is gathered, the better. This article reviews some
of what has emerged from initial studies of
“A handful of early
studies suggest that some
nanoparticles have the
potential for novel and
serious long-term types
of toxicity, but what we
mostly have are still huge
gaps in our knowledge.”
nanoparticles.
Two points are worth noting at the outset. First, it is impossible to generalize about
nanoparticles. Not only are there many
different types made from different materials—ranging from pure carbon nanotubes
to cadmium-based quantum dots to aminebased dendrimers—but it is also clear that
subtle changes to nanoparticles’ coatings
and structures can result in huge changes in
their behavior and toxicity. Second, practically nothing is known about the long-term
health impacts of any type of nanoparticle.
A handful of early studies suggest that some
nanoparticles have the potential for novel
and serious long-term types of toxicity, but
what we mostly have are still huge gaps in
our knowledge.
Some early surprises have come from
studies of nanoparticle behavior in the
environment. For example, carbon-based
nanoparticles like carbon nanotubes and
buckyballs (also known as fullerenes) are
very poorly water soluble as individual particles and might be expected to adhere to
soil and be relatively immobile in an aqueous environment. Two studies, however,
showed that buckyballs are capable of forming toxic nanocrystals that are stable when
suspended in water (Fortner et al., 2005),
while individual carbon nanotubes can be
stabilized by high organic content in natural river water (Hyung et al., 2007). Many
nanoparticles agglomerate readily and, if
suspended in air, tend to be larger than the
nano-size range (i.e., over 100 nanometers).
If nanoparticles do stay suspended in the
nano-size range, especially if they are smaller
than roughly 30 nanometers, they can deposit in the nasopharynx, from which they
can migrate through the olfactory nerves
into the brain (Oberdorster et al., 2004;
Elder et al., 2006; Ji et al., 2007).
Initial studies have demonstrated the
critical importance of subtle surface changes
to the toxicity and behavior of nanoparticles. One study showed that the coatings
on fullerenes can change the cytotoxic dose
by seven orders of magnitude (Sayes et al.,
2004). Other studies have shown that surface coatings can influence skin penetration
of quantum dots (Ryman-Rasmussen et al.,
2006) and distribution and retention of
carbon nanotubes injected into the bloodstream (Liu et al., 2007). One of the ways
surface coatings moderate the behavior and
toxicity of nanoparticles is by influencing
protein binding. Many studies have demonstrated that nanoparticles immediately
become coated with proteins as soon as they
encounter biological fluids. Some of these,
like apo-lipoproteins, may facilitate uptake
into vascular endothelial cells or across the
blood brain barrier (Kim et al.; 2007, Liu et
al., 2006). The small size of nanoparticles
results in highly curved surfaces that could
distort native protein architecture as prowww.sfms.org
teins bind to them, raising the potential risk
of generating novel epitopes and consequent
autoimmunity (Lynch et al., 2006).
Carbon nanotubes, which are in many
ways the poster children of nanotechnology,
have demonstrated some unusual properties
in toxicity assays. Shvedova et al. (2005)
found that carbon nanotubes caused deposition of collagen in the interstitial areas
of alveoli without inducing inflammation.
This unusual direct stimulatory effect is seen
in a variety of different settings (e.g., WorleKnirsch et al., 2006) and may well have beneficial biomedical applications (Meng et al.,
2006), such as stimulating nerve regrowth
in patients with spinal cord trauma. But the
potential for causing pulmonary fibrosis or
other types of granulomatous lesions must be
thoroughly assessed in the development of
any carbon nanotube application, especially
one that might result in worker or consumer
exposure.
Nanoparticles hold great promise
for enormous advances in treatment and
diagnosis of human illness. But their
unique properties also carry the potential
for unusual toxicity or exposure. As the
makers of nanomedicines test and tinker
with their technologies to create the most
effective and least toxic products, the rest
of the nanotechnology world must take
notice and apply all available information
to the safe development of nonmedical
nanoparticles.
A physician and public health professional,
Dr. John Balbus works and consults on a broad
range of environmental health issues, including
air pollution, built environment and health, climate change, nanotechnology, toxicology, and
antibiotic resistance. Prior to joining Environmental Defense, Dr. Balbus was on the faculty
at the George Washington University Schools
of Medicine and Public Health and Health
Services, where he was founding Director of
the Center for Risk Science and Public Health
and founding Codirector of the Mid-Atlantic
Center for Children’s Health and the Environment. Board-certified in both Internal and Occupational and Environmental Medicine, Dr.
Balbus combines experience as a clinician with
expertise in environmental health sciences. He
is currently a member of the National Academy
of Science Board on Environmental Studies and
Toxicology; the Institute of Medicine Roundtable on Environmental Health Sciences, Research and Medicine; and the EPA Children’s
Health Protection Advisory Committee. He
holds adjunct faculty appointments at the Johns
Hopkins Bloomberg School of Public Health and
at George Washington University.
Neurodevelopmental Disorders and Environmental Agents
A New Consensus Statement
Elise Miller, MEd, and Steve Gilbert, PhD, DABT
T
he Scientific Consensus Statement
on Environmental Agents Associated
with Neurodevelopmental Disorders,
developed by the Collaborative on Health
and the Environment’s Learning and
Developmental Disabilities Initiative, was
finalized in November 2007 and presented
at the XVI International Neurotoxicology
Conference in San Antonio, Texas. The
statement, which has a glossary and more
than 200 references, was drafted and reviewed by a committee of highly respected
scientists and health professionals in the
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neurodevelopmental environmental health
field. Based on detailed documentation, they
agreed to the following:
Given the established knowledge,
protecting children from neurotoxic environmental exposures from the earliest
stages of fetal development clearly is an
essential public health measure if we are to
help prevent learning and developmental
disorders and create an environment in
which children can reach and maintain
their full potential.
Once the document was finalized, other
national and international scientists and
health professionals were asked to sign on as
well. For the full statement and signatories,
please see www.iceh.org/LDDI.html.
This document, along with other
scientific consensus statements generated
through the Collaborative on Health and
Environment initiatives, serve to provide
the best available scientific evidence on
environmental contributors to various diseases and disabilities for researchers, health
professionals, policy makers, advocates, and
other concerned citizens.
and The Environment
Biomonitoring Update
Measuring What is Inside Us
Davis Baltz, MA
T
he field of biomonitoring continues
to develop rapidly. Since San Francisco Medicine last reported on biomonitoring in the January/February 20061
issue (www.sfms.org/archives and select the
January/February 2006 issue from the list),
there have been significant advances in the
use of this scientific data-gathering tool.
Biomonitoring is the measurement of
chemicals and their breakdown products or
metabolites in human tissues such as blood
and urine. Chemicals can also be detected
in meconium, umbilical cord blood, and
breastmilk, providing important information on prenatal and early life exposures to
chemicals in the environment that may be
harmful. For example, researchers recently
showed toxic flame retardants (PBDEs) and
long-banned industrial chemicals (PCBs)
were nearly universally found in umbilical
cord blood (1).
With its real-world exposure data, biomonitoring is important because it provides
baseline data on chemical exposure and allows us to track exposure trends over time.
This is particularly important as evidence
mounts that chemicals can contribute to
disease (2).
One of the most important developments in the field is the approval of the
nation’s first state biomonitoring initiative,
the California Environmental Contaminant Biomonitoring Program (3). The bill
creating the program, authored by Senators
Don Perata and Deborah Ortiz, was signed
by Governor Arnold Schwarzenegger on
September 29, 2006. Despite a tight budget
process, adequate funding has been secured
to launch the program, and a Scientific
Guidance Panel has been named by the
governor and legislature.
The program’s first priority will be to
generate a statistically significant statewide
“snapshot” of environmental chemical
exposure among Californians. In addition,
the program will begin to plan for and then
conduct smaller, localized, communitybased studies. Thus, California will be able
to track statewide exposure trends over
time, as well as investigate highly exposed
communities.
Significantly, the program contains
an important right-to-know provision
whereby individual study contributors will
receive their own results if they choose.
Another important aspect is that there
are no restrictions on the chemicals that
can be considered for testing. For example,
there is no requirement for a risk assessment
to be performed before chemicals can be
scrutinized.
Canada has also committed to begin
to conduct biomonitoring on a national
scale by adding a biomonitoring component
to its Canadian Health Measures Survey
(CHMS) (4). Beginning this winter, the
CHMS is being conducted across Canada
over a two-year period, involving a sample
of 5,000 Canadians of both sexes ranging in
age from six to seventy-nine.
Another significant development was
the July 2006 report by National Research
Council of the National Academy of Sciences, Human Biomonitoring for Environmental Chemicals (5). While recognizing
that biomonitoring by no means answers
all questions about chemicals and human
exposure to them, the NRC notes the immense value of biomonitoring and further
concludes that strategies for communication should be developed at the individual,
community, and population levels; and that
states that fail to share results raise ethical
concerns. The report recommends that biomonitoring studies should also include the
collection of demographic, socioeconomic
status, and lifestyle factors.
Meanwhile, the CDC (Centers for
Disease Control and Prevention) continues
its national monitoring program (6). There
have been three biennial reports since 2001.
At the time of writing, it appears that the
timeline for the next CDC National Exposure Report will slip from 2007 to June of
2008 and provide data on 275 chemicals.
Public health advocates and communities have increasingly used biomonitoring to
point out the widespread nature of exposure
as well as the regulatory failures that have
allowed exposure to continue. For example,
a November 2007 national report entitled
Is It in Us? (7) generated extensive media
attention by reporting on the levels of toxic
flame retardants (polybrominated diphenyl
ethers), bisphenol-A, and phthalates in a
cross section of Americans. Among other
findings, the study showed that average
levels of bisphenol-A found in study participants were higher than those that cause
damage in laboratory animal studies.
Davis Baltz is Special Projects Advisor for
the Collaborative on Health and the Environment.
www.sfms.org
and The Environment
Electromagnetic Fields
A Biologically-based Public Exposure Standard
David Carpenter, MD, and Cindy Sage, MA
A
n international working group of
scientists, researchers, and public
health policy professionals, the BioInitiative Working Group, has released its
report on electromagnetic fields (EMF) and
health. It raises serious concern about the
safety of existing public limits that regulate
how much EMF is allowable from power
lines, cell phones, and many other sources
of EMF exposure in daily life.
The authors reviewed more than 2,000
scientific studies, reviews, and meta-analyses and concluded that the existing public
safety limits are inadequate to protect public
health. From a public health policy standpoint, new public safety limits and limits on
further deployment of risky technologies are
warranted based on the overall evidence.
The report documents scientific evidence
that power line EMF exposure is responsible
for hundreds of new cases of childhood
leukemia every year in the United States
and around the world. Risks for brain tumors and acoustic neuromas (from cell and
cordless phones) and Alzheimer’s disease
are documented and there is evidence that
EMF is a risk factor for both childhood and
adult cancers other than leukemia.
This report stands as a wake-up call that
long-term exposure to some kinds of EMF may
cause serious health effects. We need to educate
people and our decision makers that “business
as usual” is unacceptable.
Coeditor Cindy Sage presented the
evidence from the BioInitiative report at the
Royal Society of London’s November 2007
meeting that discussed the inadequacy of existing international public safety standards.
Brain tumor specialist Dr. Lennart Hardell,
MD, PhD, Professor at University Hospital
in Orebro, Sweden, spoke on his chapter
on brain tumors and acoustic neuromas.
His work on cell phones, cordless phones,
and brain tumors is widely recognized to
be pivotal in the debate about the safety
of wireless radiofrequency and microwave
radiation. Olle Johansson, PhD, of the Karolinska Institute presented his BioInitiative
chapter on EMF effects on immune function
and electrical hypersensitivity.
The full report may be accessed at
www.bioinitiative.org.
Dr. David Carpenter is Director of the
Institute for Health and the Environment at
the University of Albany, New York. Cindy
Sage is with Sage Associates in Santa Barbara,
California.
Chemical Exposures on the Job May Be Linked to Diseases in Nurses
First-ever national survey finds widespread exposure to chemicals and radiation and almost no mandatory
workplace health protections
Charlotte Brody, RN
A
first-ever national survey of nurses’
exposures to chemicals, pharmaceuticals, and radiation on the job
suggests there are links between serious
health problems such as cancer, asthma,
miscarriages, and children’s birth defects
and the duration and intensity of these
exposures. The survey included 1,500 nurses
from all fifty states.
The results were released online at
www.ewg.org/reports/nursesurvey.
Every day, nurses confront low-level
but repeated exposures to mixtures of haz-
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ardous materials that include residues from
medications, anesthetic gases, sterilizing
and disinfecting chemicals, radiation, latex,
cleaning chemicals, hand and skin disinfection products, and even mercury escaping
from broken medical equipment. There
are no workplace safety standards to protect
nurses from the combined effects of these
exposures on their health.
The Centers for Disease Control proposed a National Occupational Exposure
Survey for the health care industry in 2002.
To date, no such survey has been initiated
to better understand the range of potentially
hazardous chemical exposure in the health
care industry and related illnesses.
The project was conducted by the
Environmental Working Group, American
Nurses Association, Health Care without
Harm, and the Environmental Health Education Center at the University of Maryland
School of Nursing.
Charlotte Brody, RN, is Executive Director of Commonweal and co-director of Health
Care Without Harm, www.noharm.org.
and The Environment
The War Goes On
Tobacco Control in California
Mi-Kyung Hong, MPH; Richard L. Barnes, JD; Stanton Glantz, PhD; and Steve Heilig, MPH
Smoking seems insane now—we have
to adapt. —Lisa Zane, Parisian singer and
ex-smoker, on the new Franch ban on smoking in bars and cafes.
T
he human casualties of the ongoing
“tobacco wars” far outstrip those of
any other battle. This war is fought
on many fronts against not only the innate
addictive and health-destroying effects of
tobacco itself, but against the profit-seeking
and well-funded efforts of those who sell it.
What follows is a brief update on the war on
one state front.
Tobacco control, to be truly effective,
relies on decreasing two primary exposures—
that of smokers themselves and that of “environmental” tobacco smoke, now inarguably
shown to be a serious hazard.
While smoking prevalence in California
continued its decline, to an historic low of 13.3
percent in 2006, the decline was slower than
in earlier years, reflecting the fact that tobacco
control efforts in California were drifting, with
no clear indication that the state would regain
leadership in tobacco control. Political leaders
continue to emphasize approaches that are not
proven to be effective, such as school-based
education programs, while moving slowly
with those that are effective, particularly a
strong media campaign. There have also been
marked reductions in funding for important
and innovative tobacco control research.
However, on the brighter side, the Attorney General’s office has vigorously enforced
tobacco industry compliance with the Master
Settlement Agreement. Campaigns to end
tobacco industry violations with regard to
youth marketing tactics and youth access to
tobacco products were successful. Former Attorney General Bill Lockyer was active in the
campaign of a multistate group of Attorneys
General to get smoking out of movies targeted
at children; but current Attorney General Jerry
Brown has not participated in this effort.
The tobacco industry intensified its
efforts to influence California politics with
its campaign contributions to legislators,
legislative candidates, political parties, and
constitutional officers. The industry steadily
increased these contributions from $4,086,553
in 2003–2004 ($1,083,448 to candidates)
to $4,359,205 in 2005–2006 ($1,895,584 to
candidates).
Campaign contributions from the tobacco industry continue to heavily favor
Republicans. In 2005–2006, $1,797,484 was
contributed to the Republican candidates and
officeholders and to the California Republican
Party compared to $98,100 to the Democrats.
Of the fifty-six legislators who took no tobacco
industry contributions in 2005-2006, fifty-two
were Democrats. Perhaps there is a link here
to Governor Schwarzenegger’s veto of two
important tobacco control bills in 2006, a ban
on Internet sales of cigarettes, and a mandate
for health insurance coverage of smoking cessation services. Still, six tobacco control measures were passed in the 2007 session. Among
these is a prohibition on smoking in any motor
vehicle with any minors present.
A most significant event was the 2006
defeat of Proposition 86, which would have increased cigarette taxes by $2.60 a pack. What
began as a well-planned initiative by health
groups for a $1.50 tobacco tax increase became
an excessive, badly structured initiative that
the tobacco industry attacked in its $66 million campaign. Voters rejected Proposition 86,
with 51.3% voting “no.”
Innovations in local tobacco control
policy making have focused on preventing
exposure to environmental smoke, especially
where people live. Momentum for nonsmok-
ing multiunit housing has been building, with
surveys showing that 80 percent of nonsmoking tenants in California wish to live in smokefree buildings. In 2004, the Thousand Oaks
City Council became the first in the nation to
pass a mandate requiring that one-third of new
multiunit affordable housing units funded by
the city be nonsmoking. Another important
first came in 2006 when the City of Calabasas
mandated an all-inclusive smoke-free policy
in the entire city except in small designated
smoking areas in shopping malls. Then, in
October 2007, Belmont became the first city
in California to ban smoking in the residential
units of all multiunit housing. Adding to this
expansion, smoke-free ordinances for public
beaches have also been passed by many local
communities in California.
The history of tobacco control in California has been local activism and voter initiatives, with statewide legislation following.
Local activism is still the key source of innovation. Here perhaps more than anywhere,
prevention is crucial to decreasing suffering
in the future, both in terms of avoiding the
cultivation of new smokers and decreasing
exposure to environmental tobacco smoke.
The current effort to regulate tobacco via
the FDA is very complex, but the fact that
major tobacco companies support this proposal
should give us pause, at minimum. Finally,
for those who might see smokers in clinical
settings, experience and research continues to
confirm that asking about smoking and urging
and helping smokers to quit is one of the best
interventions known to help patients.
For a recent report on many of these issues,
see: Hong MK, Barnes RL, and Glantz S. Tobacco control in California 2003–2007: Missed
opportunities. Center for Tobacco Control Research and Education. 2007. http://repositories.
cdlib.org/ctcre/tcpmus/CA2007.
www.sfms.org
and The Environment
Agent Orange and Birth Defects
The Legacy Continues
Betty Mekdeci
T
he soldiers are dying. As if that
weren’t tragic enough, the children
they have left behind are suffering.
Sometimes at Birth Defect Research for
Children we hear from veterans, but usually it is wives and children who send us
poignant messages:
“I lost my husband from a cancerous
brain tumor thirteen months ago. My son
has many disabilities, including Tourette’s
syndrome, mental retardation, mild cerebral palsy, and hydrocephalus, and he is
profoundly deaf. He will never be able to
live on his own.”
“My father passed away in 1998. He
had many health problems, including type II
diabetes. He was only fifty years old. Agent
Orange has been a part of my life from the
moment I was born. I was born without my
right leg, several of my fingers, and the big
toe on my left foot. My mother had three
miscarriages. My younger brother (age
twenty-nine) has to wear bifocals and suffers
from chronic joint pain.”
“I served four tours in Vietnam. We
have three children: one daughter with
a heart defect, another with scoliosis and
digestive problems, and a son born with a
defective optic nerve that has left him blind
in the right eye. There is no history of birth
defects on either side of our family.”
Since 1991, we have recorded thousands of such cases in our National Birth
Defect Registry.
Some 2.8 million Americans served in
the Vietnam theater of operations. Three to
6 percent of Vietnam veterans’ children are
born with some kind of birth defect (Emory
University School of Medicine reports a 3
to 4 percent birth defect rate among the
general population). An impressive body
of scientific evidence points to increases in
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birth defects and developmental problems in
the children of Vietnam veterans and others
exposed to dioxin-like chemicals.
Agent Orange was a combination of
two defoliants, 2,4,5-T and 2,4-D, contaminated by dioxin (TCDD), a toxic byproduct
of the chemical production process. More
than 19 million gallons of herbicides were
sprayed in Vietnam between 1962 and 1971.
More than 11.2 million gallons sprayed after
1965 were dioxin-contaminated Agent
Orange. Agents Purple, Pink, and Green
used before 1965 were even more highly
contaminated with dioxin.
According to Barry Commoner and
Thomas Webster in their 2003 book Dioxins and Health, “The current scientific
evidence argues not only that dioxin is a
potent carcinogen but that the noncancer
health and environmental hazards of dioxin
may be more serious than believed previously.” They report that dioxin appears to
act like a persistent synthetic hormone that
interferes with important physiological signaling systems that can lead to altered cell
development, differentiation, and regulation. The most troubling consequence is the
possibility of reproductive, developmental,
and immunological effects at the levels of
dioxin-like compounds present in the bodies
of the average person.
Since studies of Vietnam veterans exposed to herbicides in Vietnam have found
much higher levels of dioxin in their bodies
than are found in the average person, these
effects also should be detectable in their
children.
In 1996, the National Academy
of Sciences found “limited/suggestive”
evidence of an association between Agent
Orange exposure and spina bifida, a neural
tube defect, in the children of Vietnam
veterans. In 2000, Dr. H. K. Kang of the
Environmental Epidemiology Service of the
Veterans Health Administration published
a study that found that the risk of moderate
to severe birth defects was significantly associated with the mother’s military service
in Vietnam. As a result of these findings,
the V.A. now funds assistance programs
for spina bifida in the children of male or
female Vietnam veterans and for all birth
defects without other known causes in the
children of female veterans.
The Australian Department of Veterans Affairs (without acknowledging a link to
Agent Orange exposure) provides treatment
to the children of Vietnam veterans with
spina bifida, cleft lip or palate, acute myeloid
leukemia, and adrenal gland cancer.
Other studies offer evidence that many
more birth defects may be associated with
dioxin-contaminated herbicide exposure in
Vietnam. In 1990, an independent scientific review of the literature concluded that
elevated incidences of birth defects in the
children of Vietnam veterans were found
in several studies. These included spina
bifida, oral clefts, cardiovascular defects,
hip dislocations, and malformations of the
urinary tract. In addition, defects of the
digestive tract and other neoplasms, such as
neuroblastoma, also were higher in Vietnam
veterans’ children.
More recent studies have found additional evidence of increases in birth defects
in the children of both male and female veterans. Researchers collaborated on a metaanalysis of Agent Orange and birth defects
in the International Journal of Epidemiology.
They identified all studies from 1966 to 2002
that had examined an association between
Agent Orange or dioxin and birth defects.
The study authors identified twenty-two
studies, including thirteen Vietnamese and
nine non-Vietnamese studies.
Their review indicated that parental
exposure to Agent Orange was associated
with an increased risk in birth defects. The
association increased with greater degrees of
exposure, rated on intensity and duration of
exposure. Although other researchers have
pointed out weaknesses in the studies of
birth defects from Vietnam, the birth defect
association with Agent Orange exposure
was statistically significant even when the
Vietnamese studies were excluded.
Important new research on birth
defects in the children of Vietnam veterans was recently presented at the 2006
meeting of the Society for Epidemiological
Research in Boston, Massachusetts. Drs.
Del Junco, Sweeney, and Papke conducted
a case control study of neural tube defects
(anencephaly, encephalocele, spina bifida)
in the offspring of Vietnam veterans. They
found that paternal blood levels of TCDD
were significantly associated with neural
tube defects in their children and, although
the small sample size limited statistical
power, that a particular paternal genotype
(genetic predisposition) could enhance this
association. A manuscript describing these
findings is currently under preparation for
submission.
Litany of Birth Defects
Since 1990, Birth Defect Research
for Children has collected data on birth
defects and developmental disabilities in
the children of Vietnam veterans. When
compared to children of civilians in the
registry, the children of Vietnam veterans
have shown consistent increases in learning, attention, and behavioral disorders;
all types of skin disorders; problems with
tooth development; allergic conditions and
asthma; immune system disorders, including
chronic infections; some childhood cancers;
and endocrine problems, including thyroid
disorders and childhood diabetes. More and
more studies of prenatal exposures to dioxins
and similar chemicals are adding support for
these associations.
According to Linda Birnbaum of the
U.S. Environmental Protection Agency,
dioxin can modulate growth and development. In the embryo and fetus,
dioxin-altered programming can result in
malformations, anomalies, fetal toxicity,
and functional and structural deficits that
often are not detectable until later in life.
In a paper published in Environmental Health
Perspectives, Birnbaum discusses research
that demonstrates that prenatal exposures
to endocrine disruptors such as TCDD can
alter hormones and reproductive tissue
development and can increase susceptibility to potential carcinogen exposure in the
adult.
Increased susceptibility to chronic
childhood infections and cancers later in
life may be a result of dioxin’s effects on the
developing immune system. Researchers in
2000 investigated the immunological effects
of everyday exposures to PCBs and dioxins
in preschool-age Dutch children. The researchers found that prenatal exposure to
these chemicals was associated with changes
in the T-cell population. They concluded
that the effects of prenatal background
exposure to PCBs and dioxins persist into
childhood and could be associated with a
greater susceptibility to infectious disease.
Another 2003 study by a team of researchers from Quebec reported findings of a
chemical imbalance that could be a marker
for prenatal immune damage caused by
organochlorines (which include dioxin-like
compounds). The researchers found that
the lymphocyte cells of newborns exposed
to higher concentrations of these chemicals
during prenatal development secreted fewer
cytokines than those of a control group of
newborns. These alterations of the immune
system could lead to increased susceptibility
to infection.
A growing body of evidence is linking
prenatal exposures to dioxin-like chemicals to learning and behavioral deficits.
At a Children’s Health Meeting in 2000
sponsored by the National Institute of Environmental Health Sciences, Jerry Heindel
reported on several studies of pregnant
women who had consumed several meals of
PCB-contaminated fish per month during
pregnancy and who gave birth to infants
with small but detectable learning and
behavioral deficits. The children with the
highest exposure averaged six points lower
in IQ compared to children with lower
levels of exposure.
Thomas Zoeller, an endocrinologist
at the University of Massachusetts, has
found that dioxin-like PCBs activate cellular machinery that can alter the structure
of other, nondioxin-like PCBs. Some of
these dioxin-induced metabolites can act
directly on the thyroid hormone receptor.
In the fetal brain, this could alter the course
of development, leading to learning and
developmental disabilities.
The new research on dioxin and dioxin-like chemicals holds the promise of
unraveling the intricate ways in which these
chemicals can alter embryonic development. The research should continue, but it
is now thirty-five years since Agent Orange
was first sprayed in Vietnam. And the calls
keep coming.
In Dioxins and Health, Thomas Webster
and Barry Commoner comment, “Much of
the media coverage of the dioxin debate has
consisted of trying to convince the public
that their common sense is wrong and that
experts know best. In this case, the public’s
view has been largely correct. Dioxin is a
dangerous and unwanted chemical pollutant.”
Vietnam veterans who would like to
add information about their children’s birth
defects or disabilities to the National Birth
Defect Registry sponsored by Birth Defect
Research for Children can register online at
www.birthdefects.org.
Betty Mekdeci is the executive director of
Birth Defect Research for Children.
This article originally appeared in
longer form on the website for The Vietnam
Veterans of America. To see the full length
version, please visit www.vva.org/veteran/1207/agent_orange_feature.html
www.sfms.org
Book Review
Exposed
EXPOSED: The Toxic Chemistry of Everyday Products and
What’s at Stake for American Power, by Mark Schapiro
I
n 2007, many Californians received dramatic mailings from
a group named Californians for Fire Safety warning that if
legislation banning some fire-retardant chemicals is passed,
we would all be at much greater risk of burning to death. But these
“Californians” are actually chemical industry lobbyists; firefighters
themselves support the proposed legislation, and the chemicals
in question have already been banned elsewhere due to concerns
about health impacts such as increased cancer, birth defects, and
reproductive problems.
This latter point—that we in the U.S. allow use of substances deemed too toxic in other nations, especially European
countries—is the primary focus of San Francisco journalist Mark
Schapiro’s Exposed (Chelsea Green, 219 pages, $22.95). And while
environmental science underlies the book’s argument, it is notable
that Schapiro’s perspective is more a “business” one than otherwise.
His startling message is that by lagging behind on environmental
innovation, American industries are jeopardizing their financial
futures. And since money talks, he may have produced a book
with more eventual impact than a crate of dire environmental
warnings.
Public health researchers at U.C. Berkeley “estimate that
forty-two billion pounds of chemicals enter American commerce
daily—enough chemicals to fill up 623,000 tanker trucks, a string
of trucks that could straddle the globe three times, every day” notes
Schapiro. Further, “fewer than five hundred of those substances
… have undergone any substantive risk assessments.” At the same
time as this massive post-World War II production has taken place,
research has demonstrated health hazards even—especially, in
some cases—at very low doses. And children, fetuses, and pregnant
women are especially vulnerable.
Schapiro writes that, ironically, although we like to think of
our nation as more advanced in such arenas, “It is now fair to ask:
Is America itself becoming a new dumping ground for products
forbidden in other countries because of their toxic effects?”
Consider cosmetics. A survey of common products “found
hundreds of varieties of skin and tanning lotions, nail polish and
mascara and other personal-care products that contain known or
possible carcinogens, mutagens, and reproductive toxins.” Contrary to common assumption, most cosmetics are not effectively
tested or regulated for their health effects. European authorities,
however, started to demand toxicity information before multinational companies could continue to market their products there,
www.sfms.org
Steve Heilig, MPH
and this development did garner corporate attention and action.
Chemicals put on the European Union “negative list” were removed
from products—without seeming to hurt the bottom line. Back at
home, however, such as when a Safe Cosmetic Act was proposed
for California, chemical lobbyists convened en masse in Sacramento
to argue that there were no risks from the chemicals used.
The example of cosmetics can be seen as one of voluntary exposure, although consumers would seem to have a right to know exactly what they put onto or into their bodies. But Schapiro provides
similar case studies of other chemicals or categories of substances,
such as phthalates used in plastics, persistent organic pollutants
including pesticides, and genetically modified foods, where much
of our exposures occur even if we do not actively use the product.
Meanwhile, federal agencies we might expect to protect us, such
as the Environmental Protection Agency, have been “eviscerated
from within” by the current Federal administration.
The advent of the European Union has tilted balances of
power in many ways, including how “chemical politics” now take
place. When the E.U. developed far-reaching new regulations to
reduce exposure to harmful substances, American chemical lobbyists
swarmed across the Atlantic to fight them. But E.U. markets are
now bigger than those in America, and as one diplomat there states,
“We are not going to ask the United States for permission.”
“U.S. environmental policies are not sparking innovation;
they are fighting it,” Schapiro holds. European experts calculate
that their new safer chemical policy will “be repaid many times
over by its benefits.” “Europe is looking at the future,” Schapiro
concludes. “This is not utopian; it’s more like a realpolitik for the
twenty-first century.”
How ironic then, that short-sighted, self-serving perspectives
in what was once the “New World” have become outmoded, and
that they are putting Americans at risk not only in terms of our
health but of our economic future.
A previous version of this review appeared in the San Francisco
Chronicle.
Brominated flame retardants—safety at what cost?
Albert L. Juhasz, et al. The Lancet. December 1, 2007.
“The bioaccumulative nature of PBDEs and the increasing concentrations of these compounds in human samples
mirror previous reports for polychlorinated biphenyls (PCBs)
and DDT before their bans ... exposure of fetuses in utero or
infants via breast milk and dust to PBDEs might lead to neurological deficits, which have been observed after exposure to
the structurally similar PCBs.”
hospital news
Saint Francis
Wade Aubrey, MD
At Saint Francis Memorial Hospital, we
recently celebrated the fortieth anniversary of the
Bothin Burn Center and its tradition of excellent
care. Established in December 1967, the Bothin
Burn Center is the largest tertiary service, acute
burn facility in the Bay Area. The Center is the
first burn center in Northern California to be
verified by the American Burn Association and
the American College of Trauma Surgeons. It is
the only verified burn center in San Francisco.
The anniversary was celebrated with a
party on December 15 attended by staff, former
patients and their families, and local community
leaders who included San Francisco Fire Chief
Joanne Hayes-White, Police Chief Heather
Fong, and Supervisors Aaron Peskin and Tom
Ammiano. We also toasted the installation of the
center’s new Medical Director, Clyde Ikeda, MD,
and unveiled plans for the center’s upcoming
expansion. The renovation will expand the unit
from ten beds to fourteen and will add an outpatient burn clinic. It will also offer a day room for
patients and their families, generously donated by
Lisa Nash, survivor of the 2005 PG&E explosion,
and her family.
As the sign above the burn center nursing station says, “Those who treat burns will
reap their reward in heaven.” We’re extremely
grateful to our Burn Center staff and physicians
for the care they have provided over these past
forty years.
In closing, I’d like to wish all our San Francisco colleagues a happy, healthy, and prosperous
New Year.
Kaiser
Robert Mithun, MD
We hear about it every day—health care
costs are on the rise and many employers are
no longer offering insurance to their employees.
Because the burden of health insurance has
been placed directly on the employee, many
workers are unable or unwilling to provide the
coverage they and their families need. The
emotional, physical, and financial impact of
this reality affects not only performance but also
total health.
One of the ways that Kaiser Permanente is
helping employers cope with their rising health
care expenditures is by analyzing their total
health care costs. This includes their direct and
indirect health care costs. Direct costs, which
include medical and pharmacy, account for only
a portion of a company’s outlay. The indirect
costs, which include absenteeism and presenteeism (when an employee is present at work but
not fully productive because of poor health), can
cost two to three times more than direct costs.
Once employers look at their total cost picture,
they are able to implement health promotion
and wellness programs to address these costly
health conditions.
There are three general categories that we
as an organization have identified as targets for
intervention and change: presenteeism, absence
and disability management, and chronic disease
management.
We now have extensive health promotion
and wellness programs, which we coordinate with
our Department of Health Education, to offer
our employer groups. With the addition of these
health promotion and wellness programs, companies are finding that their employees are much
healthier and more productive in their work
environments. The companies also benefit from
lower total health care costs, which contribute to
healthier, more competitive companies.
UCSF
Ronald Miller, MD
The UCSF Cancer Center has been renamed the Helen Diller Family Comprehensive
Cancer Center as a tribute to the Bay Area
philanthropist. A resident of San Mateo County,
Mrs. Diller has a history of giving to programs
in education, science, and the arts throughout
the world. She is recognized for her creativity
in looking for opportunities to contribute and
for her deep involvement in the areas she supports. At a ceremony announcing the name
change, UCSF Chancellor J. Michael Bishop,
MD, said the new name will be synonymous
with a new era of cancer discovery. UCSF was
designated as a Comprehensive Cancer Center
by the National Cancer Institute in 1999. It ranks
first in California and sixth nationwide in NCI
research grants.
Michael Callaham, MD, has been named
the first chair of the new Department of Emergency Medicine. The formation of this new academic department—expected January 1, pending
Academic Senate approval—will unify UCSF’s
research and training programs at UCSF Medical Center on the Parnassus campus and at San
Francisco General Hospital. A new emergency
medicine residency program will welcome its first
trainees in summer 2008. Emergency medicine
is one of the top residency choices for UCSF
medical school graduates, but until now, these
trainees have had to go elsewhere.
UCSF has a new partnership with California Cancer Care and Marin General Hospital to
provide surgical services for breast cancer patients
in Marin County. Under the agreement, UCSF
breast surgeon Cheryl Ewing, MD, now has a
practice at the CCC Greenbrae office. She will
perform surgical procedures at Marin General
Hospital, where she also will serve as medical
director of the Breast Health Program, working
with BHP medical oncologist Bobbie Head, MD,
PhD, and radiation oncologist Francine Halberg,
MD. The agreement is effective through 2012.
www.sfms.org
In Memoriam
Nancy Thomson, MD
Veterans
Diana Nicoll, MD,
PhD, MPA
The Honorable Nancy Pelosi, Speaker of
the U.S. House of Representatives, visited the
San Francisco V.A. Medical Center (SFVAMC)
during the Veteran’s Day holiday.
The Speaker stopped at the Center for the
Imaging of Neurodegenerative Diseases (CIND)
for a briefing on some of the latest medical and
neurological research being conducted at the
Medical Center.
SFVAMC Associate Chief of Staff for
Research Lynn Pulliam, MS, PhD, gave an overview of the research program. In a confidential
briefing, CIND Director Michael Weiner, MD,
presented preliminary results from a study of
veterans of the first Gulf War. SFVAMC Medical
Service Chief Paul A. Volberding, MD, said that
SFVAMC’s research leadership is a direct result
of the medical center’s institutional partnership
with U.C. San Francisco.
“We presented to Speaker Pelosi recent
results concerning our studies of veterans of the
first Gulf War. These include effects of stress and
exposure,” said Weiner. “We are very grateful
to Speaker Pelosi for all her support in allowing
us to perform research on the effects of military
service on our veterans.”
“Strong investments in science help us in
every way,” said Speaker Pelosi during the briefing. “Science for the defense of our country, to
grow the economy, for a healthier America, and
to preserve the planet. We have a moral responsibility to support scientific research.”
Following the research briefing, Speaker Pelosi toured and met with patients at the facility’s
Nursing Home Care Unit.
SFVAMC has the largest medical research
program in the national V.A. system, with more
than 200 research scientists, all of whom are
faculty members at UCSF.
www.sfms.org
Leland David Duffield, MD
Leland “Lee” David Duffield, MD,
passed away October 29, 2007, in Sonoma,
at the age of 87. A third-generation San
Franciscan, he was born at Mt. Zion Hospital on April 2, 1920, to George William
Duffield and May Agnes Ganxert.
Lee graduated from St. Monica’s
School in 1933 and St. Ignatius High
School in 1937. He went on to USF,
graduating in 1941, and received his medical degree from Stanford University School
of Medicine in 1945. Following medical
school, he interned at St. Mary’s Hospital.
He also taught anatomy at the University
of the Pacific Dental School on a part-time
basis for approximately ten years.
He was a veteran of World War II with
the Navy Medical Corps, where he worked
at various dispensaries. He entered as an
ensign in 1942 and was promoted to lieutenant in 1944. He also served as a surgeon
assigned to various naval ships during the
Korean War.
Lee served as a general practitioner
for more than sixty years with the Golden
Gate Medical Group at St. Luke’s, serving
on various committees and advisory boards.
In recognition of his many years of service,
he received an award in 2005 as the
longest-practicing physician at the hospital.
Unfortunately, he was forced to retire on
September 30, 2007, after being diagnosed
with a terminal disease.
Lee met his late wife, Mary Lou, on
a blind date while he was an intern. They
were married in 1947, after his return from
World War II. The couple enjoyed playing
golf, combining vacation trips with golf venues such as St. Andrews in Scotland, Costa
del Sol in Spain, and multiple golf courses
throughout Hawaii and Florida. Lee had a
golf marker from every course and proudly
displayed them in his Sonoma home. He
also made trips with his family to places such
as New York, Costa Rica, and Alaska. He
was a true fan of the San Francisco Giants
and even made several trips to spring training with other males of his family. He was
an avid reader of biographies and historical
books and loved Sudoku puzzles, feeling that
doing one a day kept the mind alert.
He is survived by his children, Carol,
Sandy, Joan, and Bob; their spouses, five
grandchildren, and two great-grandchildren.
His youngest daughter, Mardi, predeceased
him. He will be remembered by his family and the loving friends, golfing buddies,
medical professionals, and patients who
were touched by his personal, unassuming,
gentle demeanor.
Aileen L. Webb, MD
Aileen L. Webb, MD, passed away
November 21, 2007, at Sonoma Hills Retirement Center, surrounded by her loving
family. She was 89. She had lived in Oakmont from 1989 to 2004 but prior to that
had lived in San Francisco for thirty years.
Aileen was born in Oakland to the
late Dr. Walker and Hazel Layne, on November 14, 1918. She graduated from U.C.
Berkeley, where she met her eventual husband, Eugene McDaniel Webb. They both
graduated from McGill University Medical
School in Montreal, Canada.
Dr. Webb completed her residency
at Franklin Hospital and became a boardcertified pathologist in 1945. After taking
an eighteen-year hiatus to raise their three
children, she opened a private practice, Bay
Area Cytopathology, in Oakland in 1972.
She retired in 1992.
She was a member of the University of
California Alumni Association, Alpha Chi
Omega Sorority, McGill University Alumni
Association, the San Francisco Medical
Society (1967), the CMA, the AMA, the
American Pathologists, and the College
of American Pathologists; and she was a
Fellow of the American Society of Clinical
Pathologists. She had also been an active
volunteer in the Meals on Wheels program
for many years.
Small-Town Medicine
I
moved to Port Townsend, Washington, a year and a half ago, after
practicing in San Francisco for more than a quarter century. My reasons
for a change in venue were both practical and personal. I weathered
the transition of San Francisco hospitals operating from an autonomous,
independent style to what I believed to be a more corporate one driven by
practice guideline reimbursement schemes and bottom lines. It definitely
had a more demanding effect on the way I worked. I was tired of driving around to all the campuses of my aggregated hospital and covering
emergency departments on two sides of town. My practice economics
were a constant challenge as insurance reimbursement decreased and the
worker’s compensation industry continually revised itself. In short, it just
wasn’t as much fun to practice medicine. I was frustrated and probably
grumbled about it as much as most did. Since I wasn’t anywhere close to
retirement, I thought that it could be better practicing somewhere else. A
small community could be a good choice: I could simplify life and practice
by having one hospital and working closer to home. I wasn’t trying to go
back in time, but I was trying to change a few of the difficult variables in
the equation.
Well, my move here provided a five-minute commute from home,
without freeways or bridges. In the summer I cycle or walk across the wetlands and check on the herons. My office is smack in the middle of the
hospital, just steps from the ED, OR, and cafeteria. I am in a rural practice
at Jefferson Healthcare, a critical access hospital. Those of you who have
been to Port Townsend know that it is a historical Victorian seaport on
the Olympic peninsula and a popular tourist destination. It is a beautiful
small town of 8,000, rich with arts and cultural events throughout the year.
We have one of the few wooden boatbuilding schools in the world and, as
a result, many talented artisans. It is a sailor’s paradise situated along the
entrance to the Puget Sound. Seattle is southeast, one and a half hours
away by car and ferry. Vancouver Island and Victoria are northwest and
two hours away by car and ferry.
Jefferson Healthcare is a critical access county hospital and has a
catchment of 80,000 people. Jefferson County extends across the Olympic
peninsula, through the national park to the Pacific Ocean. The residents of
our town are generally well educated and fairly well off. A few neighboring
towns are popular retirement areas for the financially affluent who enjoy the
mild weather and life on the water. Many of the county residents, however,
are determined to live in a relatively isolated and rough way. It is common
for me to care for patients who live in “sheds” without running water. The
payer mix is top-heavy with Medicaid, Medicare, and many uninsured
patients. The hospital has twenty-four beds, including a handful of ICU
beds, and a clean, modern physical plant. The medical staff is relatively
young and mainly consists of family practice MDs who run the gamut of
general medical care, including OB. Our staff has two orthopedists, two
general surgeons, a urologist, and a gynecologist who takes some C-section
call. There are no dermatologists, cardiologists, or any internal medicine
Alan G. Greenwald, MD
specialists of any kind in town. The nearest hospitals are an hour away in
opposite directions. Every day, complex cases are transferred by helicopter
to Harborview and Virginia Mason in Seattle.
Jefferson Healthcare is a vertically integrated county hospital system,
which is run by an elected health care board of commissioners. A critical
access hospital is exempt from DRG reimbursement for CMS and private
payers. It is also exempt from the new medical severity DRG system as well.
This means that the hospital can bill fee for service.
What makes this a special and an exciting place for me to practice
is that the mandate of the commissioners is to provide access for all the
residents of Jefferson County. Simply put, the hospital makes it possible for
any patient to be seen by doctors and get care in the hospital. As a critical
access hospital, the reimbursement from CMS and other insurers is at a
higher rate. The increased revenues from this system allow the hospital to
“fuel” the physician practices. The hospital surplus is driven into physician
salary guarantees and stipends. At this time, the majority of physicians
on staff are either salaried or on guarantees. According to the CEO of
the hospital, it is simply a matter of buying county residents access for
medical care. The bottom line for the physicians who are integrated with
the hospital is that we are able to care for outpatients without concern for
their insurance status.
This is as close as it gets to a universal health coverage system. Anyone involved in medical politics in San Francisco, who has testified at the
Health Commission for preservation of the health care “safety net,” or who
has helped their hospital preserve/establish a nonprofit clinic will appreciate
the beauty of this reality. When my salary guarantee expires, I anticipate
receiving a monthly stipend based on my overall practice RVUs in order
to cover the expense of the low and underinsured patients. This works in
Jefferson County, since there is really only one player in the health care
delivery system. Most of the physicians in the county are salaried or on
guarantees from the hospital. Many physicians here believe that the payor
mix would not sustain their practices without the additional support. I am
currently hospital based, using clinic space within the hospital. I operate my
own business independently of the hospital and at present am economically
self-sufficient (covering my guarantee).
Excess hospital capacity and lower revenues in urban areas drove
the trend to aggregation and corporate alignment of hospital in the 1980s
and 1990s. In the single-hospital towns of the Olympic Peninsula, the
corporate entities have come and gone without the same success. Maybe
there was a clash of philosophies with the communities, or they were too
remote to manage. Rural hospitals also must be run efficiently and must
strive to comply with national standards of excellence in patient care. Jefferson Healthcare has aligned with a purchasing cooperative in order to
have increased buying power. We also participate in a consortium of rural
hospitals to establish best practice standards and to share in peer review.
Scaling down to my smaller perspective, I have been able to bring the best
www.sfms.org
technology and orthopedic implants into my
work with little difficulty.
I have made several other observations
about small-town practice over the past
year. It is very evident that my effect on
this community is proportionately greater
than any I had in San Francisco. I am one
of only two orthopedists here. If I don’t fix
Grandma’s broken hip or replace her worn
joints, she would have to travel a long way to
be cared for by someone else. Townspeople
know that it would be a great inconvenience for them to go out of town
for their care and really appreciate having good doctors here. The idea of
competition with doctors fifty miles away doesn’t give me much stress at
all. I know that I do a good job for this town and get acknowledgement
from my patients every day in the office.
I enjoy seeing my patients and their families regularly when I am out
in the community. For some doctors the lack of anonymity might be an
inconvenience. I suppose that one could live out of town for more privacy.
However, I find value in living and working in the same community. It
is gratifying and good for business. On the other hand, it is important to
understand that because there is little privacy in a small town, anything
that is said out loud is likely to travel. Bad news and, especially, bad results
are quickly talked about.
Probably the most challenging aspect of practice in this particular
small town is dealing with the diversity. I thought that San Francisco had
the most diverse population, with its many different races, religions, ethnicities, and gender groups. Well, just about everyone in Port Townsend
is white, European, and appears to be the same. However, they each have
a unique way of looking at life and they celebrate their differences. Maybe
the force that attracts people to this town is its tolerance of emotional and
intellectual diversity. I have come to learn that it is a challenge to treat
people differently in order to get the same good results.
Overall, there have been great rewards for embracing this small town
and its quirkiness. The bonuses are the convenience of a simpler lifestyle,
giving me more time to be at home. The community values the work that
I perform, and I really enjoy being appreciated. I am in a close partnership
with my hospital. The health care system here allows me to achieve my
philosophical goals of providing good medical care for everyone in my
community. The hospital has been extremely generous to me. I have an
autonomy and greater control over the style and operation of my practice
that I was not able to appreciate in the city.
Alan Greenwald practiced orthopedic surgery in San Francisco from 1980
to 2006. He served as SFMS president in 2005. He was elected President of
Jefferson County Medical Society in 2007. He enjoys being a single father, caring
for his two-year-old daughter Jacqueline.
High Resolution PET/CT scans
Fusion Diagnostic Group’s advanced technology
and software bring evaluation and measurement
tools to the Physician to use in the clinical setting.
we also have a full time physician on staff.
Mon - Saturday 8-5 +
(flexible hours with advance request)
Positron Emission Tomography (PET)
Computed Tomography (CT)
Molecular / Functional Imaging
Accurate & Precise Imaging
1700 California St. #260
California at Van Ness in San Francisco, CA
(415) 921-7226 • 1 (800) 334-0336 • (415) 921-7225 FAX
www.fdg-inc.net
California Medical Association Policy, 2007:
The
width
is 3.5 by 4” high
CANCER
AND
ENVIRONMENTAL
CHEMICALS
CALL
KaeLewis,
with any
questions or concerns 415-567-5888
AUTHOR:
Brian
MD*
ENDORSED BY: San Francisco Medical Society
Whereas, a large and growing body of peer-reviewed research increasingly
indicates that some of the many industrial chemicals now in use and present in
human bodies can contribute to the initiation and growth of various cancers,
as recognized by many prominent scientists; and
Whereas, various scientific organizations and cancer advocacy groups
have adopted proactive policies urging better research and preventive strategies
regarding chemicals and cancer; and
Whereas, one prestigious national group, the Canadian Cancer Society,
has adopted a formal policy stating “ Wherever possible, exposure to substances
that are known, or believed, to cause cancer should be identified and eliminated
by substituting safer alternatives. When elimination is not possible, exposure
should be reduced to the lowest possible levels” and “Current scientific
evidence is the cornerstone of our information and positions about cancer.
However, we believe it is important in some circumstances not to wait for
perfect scientific clarity to take action to protect Canadians. As a result, we
also strongly support the precautionary principle that states, ³ when an activity raises threats of harm to human health or the environment, precautionary
measures should be taken even if some cause-and-effect relationships are not
fully established scientifically.²; now be it
RESOLVED: That CMA recognizes the important and growing body of
scientific evidence linking some common environmental chemicals to human
cancers, and encourages educational and advocacy efforts; and be it further
RESOLVED: that this matter be referred for national action
(AMA).
*Clinical oncologist, Clinical Professor of Medicine, University of California, San
Francisco; Chairman, San Francisco Medical Society delegation to the CMA.
www.sfms.org
What Do You Do With Your Patient Who...
...has persistent atrial fibrillation?
...is rapidly deteriorating and has
end-stage heart disease?
...has extensive vascular disease with
cardiovascular involvement?
Refer To The Experts!
We are pleased to welcome world-class talent new to CPMC’s Heart and Vascular Center.
G. James Avery, II, M.D., Preben Brandenhoff, M.D., J. Donald Hill, M.D.
Cardiothoracic surgeons, specializing in end-stage
disease management, heart transplant/LVADs
Andrea Natale, M.D.
Cardiologist and electrophysiologist specializing in atrial
fibrillation and arrhythmias
Daniel Nathanson, M.D.
Vascular surgeon specializing in endovascular surgery
Tomomi Oka, M.D.
Cardiovascular throracic surgeon
John Rhee, M.D.
Interventional radiologist specializing in endovascular procedures
California Pacific’s Heart and Vascular Center offers quality, comprehensive, patient-centered
cardiovascular care by a team of pioneering physicians intergrating leading-edge technology.
Please Join Us in Welcoming
these renowned physicians
January 31, 2008
Hors d’ ouevres and Cocktails
5-7 PM
CPMC – Enright Room
2333 Buchanan Street
San Francisco
RSVP by January 23
to 415 600-5876 or
[email protected]
www.cpmc.org

HeaLTH, HUMan BeingS, and THe enVironMenT

Transcription

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