Content uploaded by Janet M Gray
Author content
All content in this area was uploaded by Janet M Gray
Content may be subject to copyright.
A substantial body of evidence links environmental
exposures to increases in breast cancer incidence over
the past decades. State and federal legislative initiatives
that could help prevent breast cancer include: federal
standards to achieve consistency in radiation-emitting
medical and dental equipment; improved state quality
assurance standards for radiation-emitting equipment;
federal and state exposure limits for electromagnetic
radiation; an overhaul of the federal Toxic Substances
Control Act to reduce unsafe chemical exposures;
strengthened premarket health and safety testing and
regulation of pesticides; a federal ban on the manufac-
ture, distribution and sale of consumer products con-
taining bisphenol A and phthalates; and strengthened
oversight and regulation of the cosmetics industry. We
recommend public and private investment in research
on low dose exposures, mixtures, and the timing of
chemical exposures, as well as the development of
health tracking and biomonitoring programs designed
to link data from pollution surveillance systems with
disease registries. Key words: breast cancer, chemical
regulation, radiation policy, cosmetics, biomonitoring.
INT J OCCUP ENVIRON HEALTH 2009;15:79–101
Worldwide, breast cancer affects more women
than any other type of cancer except skin
cancer. In the United States, a woman’s life-
time risk of breast cancer has increased steadily and
dramatically over the decades of the 20th century.1,2
Between 1973 and 1998, breast cancer incidence rates
in the United States increased by more than 40 per-
cent.3Recent data (2003-2004)4,5 suggest that the
decreased use of hormone replacement therapy (HRT)
has been associated with a decrease in the incidence of
the estrogen-receptor-positive (ER+) form of breast
cancer in white, postmenopausal women.6–8 Neverthe-
less, today, a woman’s lifetime risk of breast cancer in
the United States is one in eight.9
The increasing incidence of breast cancer over
decades following World War II paralleled the prolifera-
tion of synthetic chemicals. An estimated 80,000 synthetic
chemicals are used in commerce today in the United
States; another 1,000 or more are added each year.10
Complete toxicological screening data are available for
just 7% of these chemicals.11 Many of these chemicals
persist in the environment,12,13 accumulate in body fat
and may remain in breast tissue for decades.14 Many have
never been tested for their effects on human health.
Among the 216 compounds identified as mammary
carcinogens in animals in a recent study on the environ-
ment-breast cancer connection, 73 are found in food or
consumer products, 35 are air pollutants, and 29 are pro-
duced in the U.S. in large amounts.15 Many other chem-
icals, especially those classified as endocrine-disrupting
compounds (EDCs) are not listed by the regulatory
agencies, yet the scientific evidence linking EDCs to
breast cancer risk is substantial and growing.16,17
In a companion piece to this article, we examine the
increasingly sophisticated and compelling data linking
radiation and many chemicals in our environment to
the current high rates of breast cancer incidence.
While we acknowledge the importance of commonly
discussed risk factors for breast cancer—primary
genetic mutations,18 reproductive history19 and lifestyle
factors such as weight gain,20 alcohol consumption21,22
and lack of physical exercise23—we assert that these
commonly discussed factors alone do not address a
large portion of the risk for the disease.24
An important body of scientific evidence demon-
strates that exposure to common chemicals and radia-
tion contributes to the incidence of breast cancer. In
our daily lives, we are rarely exposed to these sub-
stances in isolation. The pervasiveness of many of these
substances means we likely have multiple, low-level
79
Commentaries
Policy and Research Recommendations
Emerging from the Scientific Evidence Connecting
Environmental Factors and Breast Cancer
JANET NUDELMAN, MA, BRYNN TAYLOR, MPH, MEM, NANCY EVANS, JEANNE RIZZO, RN,
JANET GRAY, PHD, CONNIE ENGEL, MA, MARISA WALKER
Received from the Breast Cancer Fund, San Francisco, California
(JN, BT, NE, JR, CE, MW) and the Program in Science, Technology,
and Society, Vassar College, Poughkeepsie, New York (JG). This arti-
cle is based on a Breast Cancer Fund report entitled “State of the Evi-
dence: The Connection Between Breast Cancer and the Environ-
ment.” Address correspondence and reprint requests to Connie
Engel, Breast Cancer Fund, 1388 Sutter St., Suite 400, San Francisco,
CA 94109; telephone: +1 415-346-8223; e-mail: cengel@breastcancer-
fund.org.
Disclosures: The authors report no conflict of interest.
exposures over the course of weeks, months, even
years. There are several examples in recent scientific lit-
erature demonstrating that mixtures of environmental
chemicals, chemicals and radiation, or complex combi-
nations of chemicals and particular genetic or hor-
monal profiles may alter biological processes and pos-
sibly lead to increases in breast cancer risk.18
When examining the effects of lifestyle factors, envi-
ronmental chemicals and radiation on future breast
cancer induction, scientists now know that the timing,
duration, and pattern of exposure are at least as important
as the dose. A growing body of evidence from both
human and animal models indicates that exposures of
fetuses, young children, and adolescents to radiation
and environmental chemicals put them at higher risk
for breast cancer in later life.16,17 This evidence reflects
the fact that mammary cells are more susceptible to the
carcinogenic effects of hormones, chemicals, and radi-
ation during early stages of development, from the pre-
natal period through puberty, adolescence and on until
the first full-term pregnancy.25
Together, these new data show that we need to begin
to think of breast cancer causation as a complex web of
often interconnected factors, each exerting direct and
interactive effects on cellular processes in mammary
tissue.
The current paper builds on the data suggesting
that recent declines in cancer incidence rates are asso-
ciated with decreases in HRT use. At the same time, it
recognizes that over the past 30 years there have been
significant improvements in reducing some environ-
mental contaminants associated with breast cancer risk.
By decreasing exposures to carcinogens, such as exoge-
nous estrogens, estrogen mimics, and endocrine dis-
ruptors, we may continue to lower breast cancer
levels—and actually prevent the disease—in the future.
Toward that end, this paper was written for breast
cancer prevention, women’s health and environmental
health and justice advocates as well as others interested
in developing policy and research agendas at the state
and federal levels that call for the identification and
elimination of the environmental links to breast cancer.
It is not meant to provide an exhaustive list of public
policy and research initiatives but rather to present a
variety of policy options for breast cancer prevention.
REDUCE EXPOSURE TO RADIATION
Ionizing Radiation
Exposure to ionizing radiation is the longest-established
environmental cause of human breast cancer in both
women and men. In 2005, the National Toxicology Pro-
gram (NTP) classified X-radiation and gamma radiation
as known human carcinogens, because “exposure to
these kinds of radiation causes many types of cancer
including leukemia and cancers of the thyroid, breast
and lung.”27 Also in 2005, a report from the National
Research Council established that there is no safe dose
of radiation, that “the smallest dose has the potential to
cause a small increase in risk [of cancer] to humans.”28
Multiple exposures to low-dose radiation may cause the
same harm as a single high-dose exposure. Radiation
exposure in combination with exposure to certain syn-
thetic chemicals, including estrogens, can magnify the
effect of radiation and/or result in greater susceptibility
to chemical insults in the future.29
Exposure to ionizing radiation occurs during med-
ical and dental X-rays, computed tomography (CT)
scans, fluoroscopy and other imaging procedures. Diag-
nostic and therapeutic radiation are invaluable in the
practice of medicine and dentistry today. Yet, not all
equipment or procedures are subject to the same stan-
dards, even though legislation to establish federal stan-
dards has been introduced in every Congress since
1999. Mammography equipment has a higher quality
assurance standard than other radiological equipment
as a result of the Mammography Quality Standards Act.
Currently, seven states do not license radiation technol-
ogists and four more only partially license.30 Because
most states only have recommended quality assurance
(QA) standards—if they have standards at all—many
medical and dental offices do not perform the required
tests that ensure the standards are maintained.
Federal Policy Recommendations. The highest possible
standards should be established at the federal level to
achieve consistency among the states. Advocates should
support the 2007 Consistency, Accuracy, Responsibility
and Excellence in Medical Imaging and Radiation
Therapy bill (CARE bill), which requires:
1. People performing medical imaging and radiation
therapy meet federal education and credential stan-
dards in order to participate in federal health pro-
grams such as Medicare, Medicaid and other pro-
grams administered by the Department of Health
and Human Services; and
2. Medical imaging examinations and procedures, as
well as radiation therapy treatments for patients cov-
ered under these programs, would need to be per-
formed by personnel meeting the federal standards
to be eligible for reimbursement.
State Policy Recommendations. States should adopt quality
assurance standards for all radiation-emitting equip-
ment that meet or exceed standards currently in place
for mammography equipment. State QA standards
should require physicians and technologists to use the
smallest dose of radiation possible to capture the high-
est quality image. All states should require licensing of
radiation technologists.
Standards should be established by appropriate state
agencies so health care providers can more effectively
80 • Nudelman et al. www.ijoeh.com • INT J OCCUP ENVIRON HEALTH
measure and track their patients’ lifetime cumulative
exposure to ionizing radiation. Ideally, electronic med-
ical records should include patients’ exposure to diag-
nostic and therapeutic radiation.
States should mandate the use of educational mate-
rials in health care facilities to improve patient and
physician awareness of the benefits and risks of radio-
logical procedures. Radiation tracking cards should be
provided to patients so they can track their cumulative
exposure to ionizing radiation and make better-
informed decisions about optional procedures.
Research Required. Research is needed to develop safer,
noninvasive technologies for breast cancer screening,
diagnosis and treatment. In addition, research is needed
to better understand the possible cumulative, additive,
and synergistic effects that could result from combined
exposure to toxic chemicals and ionizing radiation.
Non-Ionizing Radiation (Electromagnetic Fields)
Continuous daily exposure to electromagnetic fields
(EMF) is a fact of life for everyone living in the indus-
trialized world. EMF is a type of low-intensity, non-ion-
izing radiation that has insufficient energy to break off
electrons from their orbits around atoms and ionize
(charge) the atoms. EMF includes extremely low-fre-
quency radiation (ELF-EMF) from electrical appliances
and power lines, and radiofrequency (RF) radiation
from wireless technologies such as cell phones, cordless
phones, personal data assistants, laptops, the towers
and antennas that support these technologies, and
broadcast transmission towers.
Decades of research indicate that exposure to EMF
is associated with many adverse health effects including
breast cancer (in both men and women) and other can-
cers, neurodegenerative diseases, and impaired
immune function.31,32 Existing public exposure stan-
dards for EMF are inadequate to protect public health
because they are based on the assumption that unless
heating of tissue occurs within 30 minutes (short-term
thermal effect), no harm can result.
There are no federal guidelines for nonthermal
effects or long-term chronic exposure. A growing body
of international research challenges that assumption,
and experts around the globe are debating the need to
strengthen the standards based on newer science show-
ing health risks of chronic, widespread low-level expo-
sure. In September 2007, Germany’s Federal Office for
Radiation Protection advised citizens to avoid WiFi wher-
ever possible because of the risks it may pose to health.33
In the same month, the European Environmental
Agency (EEA) called for immediate action to reduce
exposure to radiation from WiFi and mobile phones and
their masts34 based on an international scientific review
which concluded that safety limits set for these types of
radiation are “thousands of times too lenient.”35 In the
U.S., there has been little federally funded research on
EMF despite the expansion of wireless technologies, par-
ticularly cell phones. Rapid deployment of wireless tech-
nologies is outpacing the policy decisions necessary to
protect public health.
Breast Cancer Fund supports The BioInitiative Report
statement that the scientific evidence is sufficient to
warrant regulatory action for extremely low-frequency
electromagnetic fields (ELF-EMF) and preventive
actions for radiofrequency (RF) radiation.35
Existing government limits do not protect the public
from the adverse health effects of electromagnetic radi-
ation emanating from devices such as power lines, cell
phones, wireless internet, radar, and TV and FM broad-
cast towers.35,36 Most of the existing limits on this form
of radiation are 1,000–4,000 times too lenient to pru-
dently protect against cancers in children and adults,
Alzheimer’s and other neurodegenerative diseases,
reproductive problems, immune function disruption,
electrohypersensitivity and symptoms such as insomnia,
headaches, memory loss, concentration and attention
difficulties.31,35
Federal Policy Recommendations. The federal government
should set exposure limits for electromagnetic radia-
tion based on the scientific evidence set forth in The
BioInitiative Report 35 and a growing body of additional
research. Limits should be set for:
1. Extremely low-frequency electromagnetic fields (ELF-
EMF) including those created by power lines, appli-
ances, interior electric wiring and other devices, and
2. Long-term and cumulative radiofrequency (RF)
radiation from outdoor pulsed sources including
cell phone antennas, radar, TV and FM broadcast
antennas and wireless internet antennas; and from
indoor sources including cell phones, wireless inter-
net equipment and radiation that permeates build-
ings from outdoor sources.37
With the setting of federal limits for non-ionizing radi-
ation, special protections should be required for
homes, schools and places where children spend large
amounts of time.
Research Required. Research is needed to quantify and
monitor the levels and characteristics of ELF-EMF and
RF radiation present in schools, workplaces, and resi-
dential neighborhoods now and into the future. In
addition, research is needed to determine the effects of
chronic exposure to ELF-EMF on women recovering
from breast cancer and other cancers.
REDUCE EXPOSURE TO TOXIC CHEMICALS
There is consensus around the globe that our failure
to adequately assess and regulate chemicals is taking a
VOL 15/NO 1, JAN/MAR 2009 • www.ijoeh.com Policy Recommendations: Environment and Breast Cancer • 81
toll on the health of humans and the environment.
Evidence of public and environmental health prob-
lems related to chemical exposures continues to grow.
With the passage of its new law on chemicals manage-
ment, REACH (Registration, Evaluation, Authoriza-
tion and Restriction of Chemicals), the European
Union is leading the way on the international stage to
protect human health and the environment through
the better and earlier identification of the toxicologi-
cal properties of chemical substances.
Although there are 80,000 chemicals commercially
used in the U.S. and 1,000 new chemicals entering the
market each year, little is known about the toxicity of
the majority of these chemicals.38,39 The federal statute
intended to regulate chemicals before and after they
enter commerce is the Toxic Substances Control Act of
1976 (TSCA).40
Studies by the National Academy of Sciences, U.S.
Government Accountability Office and U.S. Environ-
mental Protection Agency, among others, have con-
cluded that TSCA does not adequately help the public,
industry or government assess the hazards of chemicals
in commerce or control those of greatest concern.41–44
Attempts to reform this inadequate chemicals policy are
underway in Congress. The most recent and promising
is the Kids’ Safe Chemical Act of 2008,45 which would
amend TSCA. Also important are smaller, chemical- or
product-specific bills such as the recently passed Con-
sumer Product Safety Improvement Act, which included
legislation introduced by U.S. Senator Dianne Feinstein
and U.S. Representative Darlene Hooley to ban six toxic
phthalates from children’s toys and childcare articles.46
Along with activity in Congress and efforts at the
federal level by nongovernmental research and advo-
cacy organizations, there have been important state-
level efforts to better understand and regulate unsafe
chemical exposures, such as Proposition 65 in Califor-
nia. Passed in 1986, Proposition 65 requires the gover-
nor to publish, at least annually, a list of chemicals
known to the state to cause cancer or birth defects.47
Businesses are required to provide a “clear and reason-
able” warning before knowingly and intentionally
exposing anyone to a listed chemical, unless exposure
is low enough to pose no significant risk of cancer,
birth defects, or other reproductive harm.
While these efforts are a step in the right direction,
they are not comprehensive enough to fix the broken
chemical regulatory system. More promising are efforts
at the state level on chemical policy reform through the
State Alliance for Federal Reform of Chemicals Policy
(SAFER). SAFER is a strategic campaign whose long-
term vision is to establish a new precautionary federal
chemicals policy as the basis of a clean, green economy
by 2020.48 SAFER is composed of environmental health
and justice coalitions in eight states including Califor-
nia, Connecticut, Maine, Massachusetts, Michigan,
Minnesota, New York, and Washington.
Federal Policy Recommendations. TSCA should be
amended to adhere to the recommendations of the
Louisville Charter for Safer Chemicals, a set of princi-
ples agreed upon in Louisville, Kentucky in May 2004
by a network of environmental health and justice
organizations working to reform the way chemicals are
regulated in the U.S.49 According to the Louisville
Charter, a full-scale overhaul of TSCA is needed that
(1) requires safer substitutes and solutions, (2) phases
out persistent, bio-accumulative or highly toxic chemi-
cals, (3) gives the public and workers the full right to
know and participate, (4) acts on early warnings, (5)
requires comprehensive safety data for all chemicals,
and (6) takes immediate action to protect communities
and workers.
Federal legislation should require manufacturers to
provide health and safety information to government
agencies before releasing a chemical into commerce,
instead of presuming a substance is safe until proven
dangerous.50 Comprehensive federal chemical policy
reform should protect the most vulnerable (children,
women of childbearing age, people with weakened
immune systems, and the elderly) and those who bear
an unequal burden of chemical exposures (workers,
fence-line communities, etc.). Legislation should also
require chemical manufacturers to pay a fee to register
their chemicals to offset the financial burden, similar to
the model of the Federal Insecticide, Fungicide, Roden-
ticide Act/Food Quality Protection Act (FIFRA/FQPA),
in which pesticide manufacturers pay a fee to register
pesticides.51 Proceeds could offset the costs of monitor-
ing and data collection to evaluate the direct impacts of
chemicals in commerce on human health.
Finally, federal tax incentives are needed to stimulate
investments in green chemistry and safe alternatives.
State Policy Recommendations. In the absence of compre-
hensive federal reform, states should assume the regu-
latory authority the federal government has been
unwilling to accept to protect the public from chemical
exposures including, as listed above, the core compo-
nents of the Louisville Charter. States should prioritize
protection of the most vulnerable populations by
requiring the phase-out of chemicals that can cross the
placenta and harm developing fetuses. State policies
should require that manufacturers provide comprehen-
sive health and safety data for chemicals, information
about where and how chemicals are used in consumer
products and industrial processes, and the availability of
safer alternatives. This information should be made
readily available to the public and should also be made
available for data-sharing among states. States should
require the labeling of chemicals linked to adverse
health effects in consumer products. If health data is
not available for a chemical ingredient, labeling should
state that the health and safety of that chemical ingre-
dient is unknown and/or cannot be substantiated.
82 • Nudelman et al. www.ijoeh.com • INT J OCCUP ENVIRON HEALTH
In addition, states should institute producer-take-back
rules requiring manufacturers of computers and other
products made with toxic materials to take back and
reuse or recycle their products to reduce the quantity of
waste that goes to landfills, where it can leach into soil
and water. They should encourage market innovation
and reform by mandating the purchase of nontoxic
products by all state agencies through procurement poli-
cies. Finally, states should augment undergraduate and
graduate chemistry curricula with green chemistry
classes such as coursework in toxicology, exposure
assessment, ecology and environmental science.
Research Required. Premarket testing of new chemicals
and postmarket testing of legacy chemicals (such as
PCBs, DDT, etc.) are needed to assess the impacts of all
chemicals on human health, worker health, and envi-
ronmental health. Green chemistry research is required
to identify or create safer alternatives to toxic chemicals
used in manufacturing and industrial processes.
Air Contaminants
According to a comprehensive scientific review of envi-
ronmental links to breast cancer, 216 chemicals have
been associated with increases in mammary gland
tumors in animals.15 Of those, 35 are air pollutants.
There is widespread public exposure to many of these
chemicals in outdoor air, as well as offices, homes,
restaurants and schools. Another review of studies of
human populations found that the evidence generally
supports an association between breast cancer and ubiq-
uitous air pollutants called polycyclic aromatic hydro-
carbons (PAHs).52 And, while human studies are limited
in number, evidence also points to an association
between breast cancer and two other chemical families
of air pollutants: dioxins and organic solvents.53,54
Most of the air pollutants can be found in primary
and secondhand tobacco smoke, diesel exhaust and/or
in specific occupational settings (see Table 1). Accord-
ing to the California Air Resources Board, there are 20
mammary carcinogens in tobacco smoke alone.55 In
2006, the California EPA determined that “overall, the
weight of evidence . . . is consistent with a causal asso-
ciation between [environmental tobacco smoke] expo-
sure and breast cancer in younger, primarily pre-
menopausal women.”56
Federal and State Policy Recommendations.States should
adopt environmental (second-hand) tobacco smoke
bans in all public locations, including restaurants and
bars. There are 26 states/commonwealths plus the Dis-
trict of Columbia with laws in effect that require 100%
smoke-free workplaces and/or restaurants/bars.57
States should follow California’s lead and adopt
tough emission standards for off-highway diesel vehi-
cles like bulldozers, airport baggage trucks and ski
resort snowcats.58 Diesel engine exhaust contains,
among other toxic substances, PAHs. Evidence in both
animal15 and human52 studies links PAH exposures to
increased risk for breast cancer.
A number of U.S. organizations are working on
reducing air pollution. They have developed a number
of recommendations—both personal and political—
for reducing air contaminants like PAHs, tobacco
smoke and diesel exhaust.59–61
Research Required.State and federal agencies should
increase the number of chemicals that are monitored
in ambient air. Currently, the Clean Air Act requires
tracking of six “criteria pollutants.”62 Air toxicants (188
hazardous air pollutants as defined by the EPA) should
also be tracked. This data should be supplemented with
personal monitoring (for example, devices used on
children to monitor their exposure to diesel exhaust
from school buses) and biomonitoring studies in dis-
proportionately impacted communities, occupational
settings, and communities with disease clusters. Occu-
pational studies that look at workers regularly exposed
to air pollutants like PAHs, tobacco smoke, diesel
exhaust, and organic solvents should be prioritized.
Pesticides
Some pesticides and herbicides have been labeled as
human or animal carcinogens and many are found in
water supplies as well as in air and dust in homes. Though
banned in the U.S. in 1972, dichloro-diphenyl-trichloro-
ethane (DDT) and its metabolite, dichloro-ethylene
(DDE), are still found in the body fat of humans and ani-
mals, as well as in human breast milk and placenta. The
triazine herbicides—atrazine, simazine and cyanazine—
have all been shown to cause mammary cancer in rats.
Atrazine, the most studied of the three, is of particular
concern for breast cancer because it disrupts—in fact
increases—the activity of aromatase, which can lead to
increased estrogen levels. Through different mecha-
nisms, three other pesticides—heptachlor, dieldrin and
aldrin—have also been shown to increase estrogen levels
and/or stimulate growth of breast cancer cells.
Of particular concern is the health of agricultural
workers and their families, and communities affected
by pesticide drift. Biomonitoring studies of children of
agricultural workers revealed that high levels of pesti-
cides can be found in the children’s urine soon after
application in the fields near their homes.63 Many pes-
ticides are endocrine disruptors; children’s exposures
pose a special concern as chidren are at a susceptible
point in their development.64–66
Federal Policy Recommendations. Advocates should pres-
sure the EPA to follow the lead of the EU and ban the
use of atrazine in the U.S. In addition, advocates
should pressure the EPA to ensure that the Endocrine
VOL 15/NO 1, JAN/MAR 2009 • www.ijoeh.com Policy Recommendations: Environment and Breast Cancer • 83
84 • Nudelman et al. www.ijoeh.com • INT J OCCUP ENVIRON HEALTH
TABLE 1 Air Contaminants Associated with Breast Carcinogenesis
Air Pollutant(s) Description Sources of Exposure
Polycyclic Aromatic Class of chemicals produced in • Outdoor and indoor air pollution
Hydrocarbons (PAHs) combustion • Tobacco smoke
Example: benzo(a)pyrene • Coal and coke-burners
•Auto exhaust (diesel)
•Diet
—Smoked and grilled foods
—Foods contaminated by outdoor air pollution
•Occupational exposures
Dioxins Class of chemicals produced in • Outdoor air pollution
combustion of PVC, PCBs and • Waste incineration
other chlorinated compounds • Pulp and paper manufacturing and other
Example: tetra chlorodibenzo- industrial processes
p-dioxin (TCDD) • Diet (indirect, primary exposure)
—Dietary fat, especially in milk, eggs, fish, meat
—Foods contaminated by outdoor air pollution
•Occupational exposures
Organic Solvents Class of chemicals that include • Outdoor and indoor air pollution
chlorinated and other solvents • Waste incineration
Examples: toluene, methylene • Used in manufacture of computer parts
chloride, trichloroethylene, • Used in manufacture of cleaning products and
formaldehyde some cosmetics
•Occupational exposures
Alkylphenols Industrial chemicals used in • Indoor air and dust
manufacturing of consumer • Personal care products
products —Hair products
Example: 4-nonylphenol —Spermicides
•Used in manufacture of cleaning products and
detergents
•Occupational exposures
Vinyl Chloride Released when PVC is produced. PVC • Outdoor and indoor air pollution
is used extensively in food packag- • Tobacco smoke
ing, cars, toys, credit cards, rain- • Air near hazardous waste sites and landfills
wear and other products • Occupational exposures during PVC manufacture
Benzene High production volume • Outdoor and indoor air pollution
petrochemical • Tobacco smoke
•Gasoline fumes
•Auto exhaust (diesel)
•Industrial burning/combustion
•Occupational exposures
Ethylene Oxide Chemical used to sterilize medical • Primarily indoor air pollution
equipment and in some • Possibly from cosmetics
cosmetics • Occupational exposures in sterilization facilities or
cosmetics manufacturing
Aromatic Amines Class of chemicals found in the • Outdoor or indoor air pollution
chemical and plastic industries. • Tobacco smoke
Combustion byproducts of • Combustion of wood chips or rubber
manufacturing. • Formed in production of polyurethane foams,
Types: monocyclic, polycyclic, dyes, pesticides, and pharmaceuticals
heterocyclic • Auto exhaust (diesel)
•Diet—grilled meats and fish
•Occupational exposures
Pesticides Class of chemicals used residentially • Outdoor or indoor air pollution
or in agriculture to kill plant and • Dust in households
animal pests • Diet—non-organic food
Examples: atrazine, heptachlor, • Occupational exposures
dieldrin, DDT
1,3-Butadiene Product of internal combustion • Outdoor or indoor air pollution
engines and petroleum refineries • Tobacco smoke
•In manufacture of rubber products and some
fungicides
•Occupational exposures
Sources: Brody JG, Moysich KB, Humblet O, Attfield KR, Beehler GP, Rudel RA. Environmental pollutants and breast cancer: epidemiologic
studies. Cancer 2007;109(S12):2667-711; Rudel RA, Attfield KA, Schifano JN, Brody JG. Chemicals causing mammary gland tumors in animals
signal new directions for epidemiology, chemicals testing, and risk assessment for breast cancer prevention. Cancer. 2007;109(S12):2635-66.
Disruptor Screening Program gets underway as man-
dated by Congress,67 and that the EPA screens these
chemicals and makes the results readily available to the
public without delay.
Strengthened premarket health and safety testing
and regulation of pesticides should be included in com-
prehensive chemical policy reform, as discussed above.
State Policy Recommendations. In the absence of federal
legislation, states should either ban the use of or require
adequate labeling of home-use pesticides containing
chemicals linked to endocrine disruption, carcinogene-
sis, central nervous system disruption, and reproductive
disorders, and encourage the use of safer substitutes.
States should ban the use of pesticides on or near
school grounds, including day care centers and nurs-
eries. In addition, states and municipalities should ban
the use of “cosmetic” pesticides and the use of pesti-
cides in parks. In Canada, support is growing (mostly at
the municipal level) for bans on cosmetic—purely aes-
thetic—use of pesticides, where the weed or pest poses
no danger to human health, the environment, or prop-
erty.68,69 The cities of San Francisco and Oakland, Cali-
fornia have banned the use of pesticides in their parks
for years.70–72 Such efforts to end the nonessential uses
of pesticides should be supported and ultimately writ-
ten into state legislation.
Research Required. More research is needed on the
cumulative exposures of agricultural workers and their
families to first, protect their health, and second, gain
a greater understanding of the role of pesticides in the
development of breast cancer and other diseases.
Moving away from toxic, endocrine-disrupting pesti-
cides will require a just transition strategy and viable alter-
natives. A significant national investment in integrated
pest management research is essential and long overdue.
Consumer Exposures
Each day, consumers use products that contain chemi-
cals untested for impacts on human health and the
environment. Reducing human exposure will also help
keep these chemicals out of air, waterways, soil, ice
caps, and wildlife.
Plastics
Plastics are widely used in consumer products and
packaging of all kinds. There are, however, serious risks
to human health and the environment from the wide-
spread use of plastics. Most plastics are made from
petroleum, a nonrenewable resource. Not all plastic is
recycled and millions of bottles go to landfills every
year.83 In addition, many plastic products end up in the
ocean where they have formed enormous flotillas,
harming plankton and the entire food chain of fish,
turtles, and birds that depend on these tiny creatures.84
The three plastics that have been shown to leach
toxic chemicals when heated, worn or put under pres-
sure are polycarbonate (leaches bisphenol A), poly-
styrene (leaches styrene) and PVC (leaches phtha-
VOL 15/NO 1, JAN/MAR 2009 • www.ijoeh.com Policy Recommendations: Environment and Breast Cancer • 85
ATRAZINE, FROGS AND BREAST CANCER
Atrazine, a triazine herbicide, has been banned in the European Union since 2005.73 The U.S. EPA concluded it was
an endocrine disruptor in 2000. However, farmers used 77 million pounds of it in the U.S. in 2003.74
Atrazine has been shown to cause mammary cancer in lab rats.75,76 Recent data suggest that the major mechanism
by which atrazine exerts its endocrine-disrupting effects is by increasing the activity of the enzyme aromatase.77,78 Aro-
matase facilitates the conversion of testosterone and other androgens to estrogens, including estradiol.
This pathway of estrogen production is of great enough importance to the development of breast cancer that a
current class of breast cancer drugs aims to block this activity of aromatase. Femara (Letrozole) is one of these drugs.
It targets aromatase, which in turn reduces estrogen and keeps breast cancer cells from growing initially.79,80
Dr. Tyrone Hayes at the University of California at Berkeley has spent his career examining atrazine and its effect
on the growth and development of frogs. He has shown that atrazine chemically castrates and feminizes male
amphibians in the wild and in the lab. He suggests that atrazine-induced deformities result from the depletion of
androgens and production of estrogens, perhaps after atrazine increases the activity of aromatase.81
When Dr. Hayes presents his research, he often tells this story: The maker of atrazine is Syngenta, a multinational
agrichemical corporation. Syngenta was formed in 2000, when another multinational called Novartis merged their
Crop Protection and Seeds businesses with Astra Zeneca’s Agrochemicals.82 What is interesting and very disturbing,
he argues, is that Novartis is also the producer of Femara, the breast cancer drug discussed above. And so, Dr. Hayes
points out, the very company that produces atrazine (that “turns on” aromatase, thereby increasing estrogen which
can lead to breast cancer cell growth) is also producing—and selling at great profit—a medication that has the oppo-
site effect (to “turn off” aromatase).
Sixty percent of Americans are regularly exposed to atrazine, an herbicide that may be negating the positive
effects of breast cancer medications. The company that stands to profit from sales on both sides of the equation is
headquartered in Switzerland, where atrazine is banned.
86 • Nudelman et al. www.ijoeh.com • INT J OCCUP ENVIRON HEALTH
TABLE 2 Pesticides Associated with Breast Cancer
Carcinogenic Hormone Disrupting
_________________________________ ___________________
Animal Disrupts
Mammary Human Endocrine
Gland Carcinogenic System/ Source of Exposure/
Pesticide CarcinogenaRisk ClassificationbEstrogeniccScope of Use
1,2-Dibromo-3- X IARC Possible; NTP Pesticide: banned as soil fumigant in
chloropropane Reasonably Anticipated 1985, air pollutant, exposure through ingestion of
previously contaminated food and water
2,4-Dichloro- X Pesticide: herbicide
phenoxyacetic acid
Atrazine (a X IARC Not Classifiable X Pesticide: herbicide, air pollutant, found
triazine herbicide) widely in water bodies, exposure through ingestion
of food or water, banned in European Union in
2005, 75 million pounds used annually in U.S.,
mainly on corn and sorghum
Captafol X IARC Probable Pesticide: fungicide, not currently
registered for use in U.S.
Chlordane X X Pesticide: insecticide (ticks and mites), veterinary
pharmaceutical, air pollutant, use as insecticide has
been banned, persists in meat and fish, found in
household dust
Chlorpyrifos X Pesticide: insecticide (ticks and mites)
Clonitralid X Pesticide: exposure through dermal contact or
ingestion of water treated with clonitralid (for
water snail and sea lamprey control) or contami-
nated fish
Cypermethrin X Pesticide: insecticide
DDT (Dichloro- NTP Reasonably X Pesticide: contact insecticide, banned
diphenyl- Anticipated in many countries, used for malaria
trichloroethane) control in others, DDT and metabolite DDE still found
in body fat of humans and animals though banned
in U.S. in 1973
Dichlorvos X IARC Possible Pesticide: air pollutant, inhalation of air and dermal
contact with no-pest strips, sprays or flea collars,
ingestion of food prepared where dichlorvos has
been used
Dieldrin, Aldrin, X Pesticide: insecticide, 1950s to 1970s dieldrin and
Endrin (-drin aldrin used on corn and cotton, 1987 both were
pesticides) banned, still persist in environment
Fenvalerate X IARC Not Classifiable Pesticide: landscaping/yard products, pet care
products
Heptachlor IARC Possible X Pesticide: insecticide, used for termite control
through 1980s in U.S., agricultural use continued
until 1993 (especially on pineapple)
Lindane NTP Reasonably Anticipated X Pesticide: insecticide
Malathion X Pesticide: insecticide
Methoxychlor X Pesticide: insecticide, veterinary pharmaceutical
Nifurthiazole X IARC Possible Pesticide
Pentachlorophenol X Pesticide: insecticide (termites), wood preservative
Permethrin, Sumithrin X Pesticide: insecticide
Simazine (a triazine X IARC Not Classifiable Pesticide: air pollutant, widely used to
herbicide) control weeds in food crops and in ponds, algae
control in pools and fountains, detected at low
levels in air, rainwater and surface water
Sulfallate X IARC Possible; NTP Pesticide: herbicide, used until early
Reasonably Anticipated 1990s in U.S., exposure through ingestion of
residues in food crops
Toxaphene NTP Reasonably Anticipated X Pesticide: insecticide
Tributyl Tin (chloride) X Pesticide: biocide, rodent, repellent
Vinclozolin X Pesticide: agricultural fungicide, used in vineyards
aRudel RA, Attfield KA, Schifano JN, Brody JG. Chemicals causing mammary gland tumors in animals signal new directions for epi-
demiology, chemicals testing, and risk assessment for breast cancer prevention. Cancer. 2007;109(S12):2635-66.
bInternational Agency for Research on Cancer (IARC) carcinogenic risk classification is based on evaluation of potential tumor
development at all sites, not only breast/mammary tissue. Categories include: known, probable, possible and others. The National
Toxicology Program (NTP), within the National Institute of Environmental Health Sciences of the National Institutes of Health, pro-
vides carcinogenicity ratings based on scientific evidence in both animals and humans. Categories include: known, reasonably
anticipated, and others (Report on Carcinogens, 11th edition; US Department of Health and Human Services, Public Health Ser-
vice, National Toxicology Program.) Not all chemicals have been rated by IARC or NTP.
cTo date, neither the NTP nor IARC have classified most endocrine disruptors as carcinogens in humans. List of endocrine disruptors
from: Brody JG, Rudel RA. Environmental pollutants and breast cancer. Environ Health Perspect. 2003;111:1007-19.
lates).85 Bisphenol A (BPA) is the building block of
polycarbonate plastic and is used to manufacture baby
bottles, sports water bottles, and dental sealants. BPA is
also a component of the epoxy resins used to line
infant formula and food cans. The evidence on BPA
and its many effects on human health is convincing
and growing. Studies funded by the chemical industry
say it is harmless; nonindustry studies show it is a pow-
erful hormone disruptor linked to breast cancer.86–88
Phthalates, another chemical family of concern, are
used to soften plastics, especially PVC. They are found
in many consumer products including children’s bath
toys and teething toys. Phthalates are endocrine dis-
ruptors that increase the risk of early puberty (and
therefore, breast cancer) in girls, and have been linked
to reduced testosterone levels, lowered sperm counts,
and genital defects in baby boys, and testicular cancer
in young men.89–92
Federal Policy Recommendations. U.S. EPA should fully
implement the Endocrine Disruptor Screening Pro-
gram, as mandated by Congress, to effectively and effi-
ciently screen chemicals for hormonal activity and to
make the results readily available to the public without
delay. Congress should also ban the manufacture, dis-
tribution and sale of consumer products containing
BPA and phthalates.
State Policy Recommendations. In the absence of federal
regulation, states should either ban endocrine-disrupt-
ing chemicals like BPA and phthalates in all consumer
products, or require that consumer products contain-
ing these plastics be adequately labeled. In the mean-
time, advocates should support legislation (as in Cali-
fornia, other states, and at the federal level93–95) that
bans endocrine disruptors like phthalates and BPA in
children’s toys and childcare articles such as baby bot-
tles and “sippy cups.”
Research Required. Funding is needed to support green
chemistry research on bio-based plastics that can be
composted after they have been used in consumer
products. Another need is for human studies of expo-
sure to endocrine-disrupting chemicals—like BPA and
phthalates—and breast cancer outcomes. This may
require an investment in new methodologies because
exposure to these chemicals is widespread in the popu-
lation, challenging currently available testing methods.
Limited (and expensive) human studies should both
inform and be informed by targeted animal studies.
Coordination of these two research models is critical to
moving the research forward.
Household Cleaning Products
Although there are thousands of household cleaning
products on the market, the products’ labels provide
little information about risks to the environment and
human health. The government provides very little
oversight of these products and yet consumers and
their children are exposed to them every day.
Certain occupations are especially vulnerable to the
effects of toxic cleaning products. Housekeepers and
custodians are heavily exposed to cleaning chemicals
and are often not given any information about health
effects or safety precautions. Little exposure assessment
has been done in these occupations. Critical informa-
tion needed to inform public health interventions has
not been collected.
Federal and State Policy Recommendations. The federal gov-
ernment should either ban the use of chemicals linked to
cancer and other long-term health effects in cleaning
products (e.g., phthalates in synthetic fragrance formula-
tions), or require labeling adequate to allow consumers
to make informed and safer purchases. In the absence of
federal regulation, state governments should ban these
substances or adopt strong labeling guidelines.
Research Required. Research is needed on safe alterna-
tives to toxic chemicals in cleaning products. Occupa-
tional research should look at workers regularly
exposed to cleaning products and the possible linkage
to breast cancer later in life. Use of biomarkers of expo-
sure and early disease should be explored as soon as
possible to shorten the length of the study and allow for
occupational health interventions.
Hormones in Meat and Milk
Modern food production methods have introduced
new environmental exposures to carcinogens and
endocrine-disrupting compounds. Pesticides on crops,
antibiotics in poultry, and hormones in cattle, sheep
and hogs expose consumers to unsafe contaminants
every day. Consumption of animal products may hold
inherent risks because animal fat can retain pesticides
and other environmental toxicants consumed by the
animal, and research suggests that some of these expo-
sures increase breast cancer risk.133,134
Since its introduction in 1993, bovine growth hor-
mone (rBGH/rBST) has proven controversial because
of its potential carcinogenic effects. Several studies
have shown an association between dairy consumption
and breast cancer in premenopausal women. rBGH has
been shown to raise insulin-like growth factor 1(IGF-1)
levels in the body, which have, in turn, been associated
with an increased risk of breast cancer.135–140 Another
food additive of concern is zeranol, a growth promoter
used in the beef industry that mimics the effects of nat-
ural estradiol in the body.
Federal and State Policy Recommendations. The federal gov-
ernment should ban the use of hormones in meat and
VOL 15/NO 1, JAN/MAR 2009 • www.ijoeh.com Policy Recommendations: Environment and Breast Cancer • 87
88 • Nudelman et al. www.ijoeh.com • INT J OCCUP ENVIRON HEALTH
BPA AND DES: A TALE OF TWO ESTROGENS
Bisphenol A (BPA) is one of the most widely used chemicals today. It is found in baby bottles, other food and bev-
erage containers, linings of metal food cans, dental sealants and countless other products. It is also found in air,
dust, rivers and estuaries—and in Americans of all ages, including newborns.96 More than 2 billion pounds of BPA
are produced in the United States each year; more than 6 billion pounds are produced worldwide. BPA generates
enormous annual revenues for corporations such as Bayer, Dow, GE Plastics and Sunoco.97
BPA is a result of the search for cheap synthetic estrogens, compounds designed to keep postmenopausal
women “feminine forever” and to promote the rapid growth of cattle and poultry industry profits. Synthesized in
1936,98 BPA was shunted aside two years later by a more potent synthetic estrogen: diethylstilbestrol (DES), now
known to cause cancer and reproductive abnormalities in both males and females.99
Though they differ in potency, DES and BPA share striking similarities in their structures, functions and histo-
ries. Both chemicals:
•were developed when the health effects of estrogen were poorly understood. Early animal studies linked both
chemicals with increased risk of mammary and other cancers and reproductive abnormalities.
•entered the food chain: DES as a livestock drug and BPA through food containers and packaging. DES was pre-
scribed to pregnant women to prevent miscarriage (which it failed to do100), and BPA is associated with recur-
rent miscarriage as seen in a recent study from Japan.101
•were aggressively marketed, despite scientific evidence suggesting the need for caution. BPA is still marketed
globally. The Food and Drug Administration (FDA) ignored animal evidence of DES reproductive toxicity and
approved the drug for medical use in humans in 1941, then for use during pregnancy and for use in livestock
and chickens in 1947.102,103 When male agricultural workers exposed to DES suffered sterility and breast cancer,
FDA banned the use of DES in poultry, but not in cattle or in women.104 Between 1938 and 1971, an estimated
5–10 million women in the U.S. were prescribed DES.105 Use of DES in cattle continued into the 1980s.
In 1970, doctors noted an unprecedented number of rare vaginal cancers in young women whose mothers had
taken DES during their pregnancy. Ultimately, DES proved to be a transgenerational carcinogen and a reproduc-
tive toxicant, resulting in an FDA alert on the drug. Subsequent research showed an indisputable cause-effect rela-
tionship between maternal use of DES and clear cell vaginal carcinoma in daughters.105–107 DES also increased the
risk of breast cancer in the mothers, and studies now show that increased breast cancer risk extends to DES daugh-
ters.108–112 Decades of research on DES daughters and sons have shown that animal studies can be useful in pre-
dicting effects in people.
Discarded as an estrogen replacement therapy pharmaceutical, BPA was rediscovered by polymer scientists in
the late 1940s and quickly became a mainstay of the plastics industry.97,113 It is the building block of polycarbonate
plastic and is also used in the manufacture of epoxy resins and other plastics, such as polyester and styrene.
Although never prescribed as a drug or deliberately added to foods, BPA enters the food chain by leaching from
plastic packaging or containers as the plastic ages or is heated. Once in food, BPA moves quickly into people,
including placental tissue and umbilical cord blood, where it can disrupt normal prenatal development, even at
low levels—parts per billion or parts per trillion.114
BPA exposure during critical windows of development has been linked with increased risk of breast, prostate
and testicular cancer. It is also linked to birth defects, including neurobehavioral disorders, increased risk of mis-
carriage, decreased sperm production, early puberty in females, obesity and insulin-resistant diabetes.115–118
One recent study showed that neonatal exposure to low levels of BPA causes uterine fibroids, cystic ovaries and
precancerous lesions in female middle-aged mice. These results closely parallel the effects of comparable DES expo-
sure.119 In women, such effects are major contributors to infertility and the most common reasons for hysterectomy.
Many scientists and the public are increasingly concerned about BPA because of (1) high production volume,
(2) widespread human exposure, and (3) evidence of reproductive toxicity in laboratory animals.120 Much of the
research indicating health risks of early life exposure to BPA has occurred since 1995, and the accumulated evi-
dence is compelling. However, the chemical is regulated based on research findings prior to 1984. The U.S. EPA
standard for BPA safety, called a reference dose, is 50 micrograms per kilogram of body weight, per day. 121
Although considerable variability in body burdens of BPA have been found, studies consistently indicate significant
levels of the chemical in most people in the U.S., with levels at or above those shown to induce damaging effects
in animal models.122,123
Manufacturing Doubt
Manufacturers of BPA responded to concern about health risks by criticizing the evidence as controversial, limited
and overblown. They called for more research. This all-too-familiar tactic has enabled many industries to continue
VOL 15/NO 1, JAN/MAR 2009 • www.ijoeh.com Policy Recommendations: Environment and Breast Cancer • 89
profiting from tobacco, lead, asbestos, DES and other toxic products while damaging public health.124 When media
reported early studies of BPA’s estrogenic effects on the male reproductive system,125 the chemical industry
attacked, saying their scientists could not replicate the studies.115,126 Laboratories hired by chemical companies
quickly produced studies that found no harmful effects.115,126
A 2005 analysis of the BPA literature revealed a clear pattern of bias in reporting results: the funding source
often determined the findings. Of 115 studies on health effects of BPA, 94 government-funded studies conducted
in academic laboratories in Japan, Europe and the United States found adverse effects at low dose exposure. None
of the studies funded by industry reported adverse effects.115
Leading scientists called for a new assessment of BPA based on mounting evidence of its DES-like effects.
The NTP responded by appointing an advisory committee to assess the evidence and prepare a report. In
March 2007, it was revealed that the advisory committee’s report had been drafted by a private consulting firm
with ties to the chemical industry. NTP fired the firm but accepted the report as unbiased.127
When the advisory committee reconvened in August 2007 to review the report, leading BPA researchers testi-
fied about errors in the report, failure to consider the full range of evidence and reliance on flawed data from
industry.128 The committee remained largely unconvinced, noting in their summary statement “some concern”
only for pregnant women, fetuses, infants and children “that exposure to BPA causes neural and behavioral effects.”
Neural and behavioral effects are a significant concern—particularly for women of childbearing age who are
the first environment for infants. Four million children are born each year in the United States; most may be
exposed to BPA in their mother’s wombs.129 One in every six children in the U.S. suffers from some type of learn-
ing or neurobehavioral disorder, ranging from attention-deficit hyperactivity disorder to autism.130 This amounts
to as many as 640,000 children who are harmed each year—an enormous public health issue and a lifelong prob-
lem for children and families.
In a parallel process, a collaboration of 38 internationally recognized scientific experts on BPA and other
endocrine disruptors published an analysis of the research on BPA which included a consensus statement plus
five peer-reviewed articles.128 Unlike the NTP committee, the international collaboration concluded: “The wide
range of adverse effects of low doses of BPA in laboratory animals exposed both during development and in
adulthood is a great cause for concern with regard to the potential for similar adverse effects in humans.
Recent trends in human diseases relate to adverse effects observed in experimental animals exposed to low
doses of BPA.”
Among the examples of trends they cited:
•Increase in breast and prostate cancer
•Uro-genital abnormalities in male babies
•Decline in semen quality in men
•Early onset of puberty in girls
•Metabolic disorders including insulin-resistant (type 2) diabetes
•Obesity in children and adults
•Neurobehavioral problems such as ADHD
The next step for NTP is to compile the data from the two reports, draft its own report and solicit public comment.
Meanwhile, California may seek a Proposition 65 listing of BPA as a reproductive toxicant.131
One other country has taken action on BPA. Norway has advised the World Trade Organization of its intention
to prohibit BPA and 17 other substances from consumer goods in that country. This prohibition will include cloth-
ing, bags, and toys but will not apply to food products or food packaging.132 While this legislation applies only to
Norway, it could become the new de facto standard for companies exporting to Europe since few companies will
vary a product for one small market.
Regulation of the manufacture and use of BPA in the United States may be years away. Meanwhile, consumers
can limit exposure to this chemical through the following measures recommended by the Environmental Working
Group:
•Minimize the use of plastics, especially plastic wraps and containers, with the recycling label No. 7, which may
contain BPA.
•Use glass baby bottles and dishes.
•Discard old, scratched plastic dishes and containers. Do not wash plastic dishes in the dishwasher using strong
detergents, which can speed up wear and tear.
•Avoid canned foods and drinks.
milk or, at minimum, require labeling of these additives
so consumers can make informed purchases. In the
absence of federal regulation, state governments should
ban these substances or adopt strong labeling guidelines.
Research Required. Exposure studies are needed to meas-
ure the presence and levels of synthetic hormones in
meat and dairy sold and consumed in the U.S. so the
potential for negative health effects can be assessed.
90 • Nudelman et al. www.ijoeh.com • INT J OCCUP ENVIRON HEALTH
TABLE 3 Plastics and Breast Cancer*
Link to Breast Cancer
_______________________________
Breast Hormone
Cancer Carcinogen Disruptors
Fund Byproduct of Can Source of Exposure in
Plastic Rating Manufacturinga,b Leach OutcExplanation Consumer Products
#1 PET PETE OK Soft drink, juice, water,
Polyethylene detergent and cleaning
terephthalate product bottles
ethylene
#2 HDPE OK Opaque plastic milk and
High density water jugs; bleach, deter-
polyethylene gent and shampoo bottles;
some plastic bags
#3 PVC Avoid X X Vinyl chloride and Cling wrap; some plastic
Polyvinyl chloride dioxin, both known squeeze bottles; cooking oil,
human carcinogens detergent and window
(NTP and IARC), are cleaner bottles; toys; vinyl
formed in manufac- shower curtains; wall and
turing; dioxin is also a floor coverings
hormone disruptor;
hormone disrupting
phthalates can
leach out of PVC.
#4 LDPE OK Grocery store bags, most
Low density plastic wraps, some bottles
polyethylene
#5 PP OK Most reusable food-storage
Polypropylene containers; straws; syrup,
yogurt and other clouded
plastic containers; some
baby bottles
#6 PS Avoid X Styrene can leach Styrofoam food trays, egg
Polystyrene from polystyrene, is cartons, disposable cups
an animal mammary and bowls and carryout
carcinogen, and is containers; opaque plastic
possibly carcinogenic cutlery
to humans (IARC).
#7 Other Avoid X Hormone-disrupting Many plastic baby bottles,
Usually bisphenol A can 5-gallon water bottles,
Polycarbonate leach from polycar- “sport” water bottles, metal
bonate under heat food can liners, clear plastic
and pressure or as “sippy” cups, dental
plastic ages. sealants, some clear plastic
cutlery
Portions of this table based on “Smart Plastics Guide: Healthier Food Uses of Plastics,” Institute for Agriculture and Trade Policy, avail-
able at www.iatp.org/foodandhealth.
aRudel RA, Attfield KA, Schifano JN, Brody JG. Chemicals causing mammary gland tumors in animals signal new directions for epi-
demiology, chemicals testing, and risk assessment for breast cancer prevention. Cancer. 2007;109(S12):2635-66.
bInternational Agency for Research on Cancer (IARC) carcinogenic risk classification is based on evaluation of potential tumor
development at all sites, not only breast/mammary tissue. Categories include: known, probable, possible and others. The National
Toxicology Program (NTP), within the National Institute of Environmental Health Sciences of the National Institute of Health, provides
carcinogenicity ratings based on scientific evidence in both animals and humans. Categories include: known, reasonably antici-
pated, and others (Report on Carcinogens, 11th edition; US Department of Health and Human Services, Public Health Service,
National Toxicology Program.) Not all chemicals have been rated by IARC or NTP.
c To date, neither the NTP nor IARC have classified most endocrine disruptors as carcinogens in humans. List of endocrine disruptors
from: Brody JG, Rudel RA. Environmental pollutants and breast cancer. Environ Health Perspect. 2003;111:1007-19.
Research that looks at red meat and dairy consump-
tions and their possible association with breast cancer
should consider—and include in the methodology—the
presence of synthetic hormones within these products.
Without addressing these additives, it is not clear whether
the research findings reflect the dietary nutritional com-
position of the food—e.g., vitamins, fat content and pro-
tein—or the presence of synthetic hormones.
Cosmetics and Personal Care Products
Because the U.S. lacks a premarket screening program,
shampoo, deodorant, make-up, lotions and other prod-
ucts that consumers use every day contain chemicals
linked to cancer, birth defects and other serious health
problems. Words like “natural,” “safe,” and “pure” on
labels have no definition in law and no relationship to the
hazard inside the packaging. Major loopholes in federal
law allow the $50 billion cosmetics industry to put unlim-
ited amounts of chemicals into personal care products
with no required testing, no monitoring of health effects
and woefully inadequate labeling requirements.
The EU’s 27-country, precedent-setting Cosmetics
Directive (76/768/EEC) prohibits the sale of personal
care products that contain any of the 1,100 carcino-
gens, mutagens or reproductive toxins (CMRs) classi-
fied as toxicants by the directive.141 The United States
restricts only 10 substances and there is no enforce-
ment of those restrictions.142,143 Taken alone, the chem-
icals in a single cosmetic product are unlikely to cause
harm. But the average American woman uses 12 per-
sonal care products a day, resulting in exposure to 126
unique chemicals.144 The combined exposure from
personal care products adds to the personal chemical
contamination from other consumer products, food,
water, air and soil. As a result, more than 200 chemicals
have been detected in people’s body fluids and breast
milk and in the cord blood of newborns.145–148 The
unregulated use of chemicals in personal care products
is one aspect of the larger problem of chemicals in
commerce without any functioning government frame-
work to protect public health from harm.
A considerable amount of what consumers put on
their skin ends up inside their bodies149–151—a huge
concern for women of childbearing age. Finally, cos-
metics are only one of many sources of daily toxic expo-
sures. For example, the public is exposed to phthalates
from many different personal care products, as well as
from vinyl shower curtains, vinyl car seats, toys, medical
devices and pharmaceuticals.
Federal Policy Recommendations. Federal legislation is
needed that requires premarket health and safety test-
ing of all cosmetics and personal care products, pro-
vides guidance to the cosmetic and personal care prod-
uct industry on how to test their products for safety,
restricts the use of ingredients that contain any toxic
impurities or that may combine with other ingredients
to form harmful impurities, and institutes mandatory
recalls of cosmetics and personal care products con-
taining ingredients that have not been proven safe
through scientific testing and/or do not bear appro-
priate labels warning consumers that the product
ingredients have not been tested for safety.
In addition, such legislation should require labeling
of the constituent ingredients of fragrance and any
nanomaterials in cosmetics and personal care prod-
ucts. Internet vendors should be required to display a
conspicuous list of ingredients in cosmetic products
sold on their web sites.
Cosmetic and personal care product manufacturers
should be required to test products—especially those
used by and on children—for their estrogenic activity.
They should also be required to make all existing safety
data available to government agencies and consumers.
Finally, manufacturers should be required to invest in
green chemistry solutions to replace toxic chemicals
used in cosmetics and personal care products with safe
alternatives.
Information on health hazards associated with spe-
cific chemicals used to formulate over 27,000 cosmetics
and personal care products can be found by visiting the
Environmental Working Group’s “Skin Deep” database
at www.cosmeticdatabase.org. Information on the Cam-
paign for Safe Cosmetics, a market-based campaign
developed to move the cosmetic industry toward safer
production and secure stronger government oversight
and regulation of the $50 billion cosmetic industry, can
be found at www.safecosmetics.org.
State Policy Recommendations. States should require all
companies selling cosmetic and personal care products
in the state to
•provide certification that their formulations meet
the standards of the EU Cosmetics Directive
76/768/EEC and are free of chemicals that are
known or strongly suspected of causing cancer,
mutation or birth defects.
•submit to their department of health a list of chem-
icals used in the manufacture of personal care prod-
ucts distributed in the state that authoritative scien-
tific bodies have determined are associated with
cancer, endocrine disruption, birth defects, or other
health hazards, as well as persistence in the environ-
ment or bioaccumulation.
•file with the state department of health a timeline
and plan for substituting chemicals of concern with
safe alternatives.
•list fully all ingredients on the label, including com-
ponents of fragrance and other mixtures and nano-
materials; and list fully all ingredients on the com-
pany’s web site if internet sales of their products to
that state are taking place.
VOL 15/NO 1, JAN/MAR 2009 • www.ijoeh.com Policy Recommendations: Environment and Breast Cancer • 91
Research Required. Currently only 11% of the ingredients
used in cosmetic products have been tested for safety.
Research is needed to increase this number to 100%.
Green chemistry solutions are needed to replace toxic
chemicals used in cosmetics with safe alternatives. Finally,
personal care products—especially those used by and on
children—should be tested for their estrogenic activity.
Occupational Exposures
Although women make up nearly half the paid work-
force in the United States, relatively few studies have
been conducted to identify occupational exposures asso-
ciated with breast cancer. Most occupational research on
women reports risk by job type or title, rather than by
specific exposures, making the findings difficult to inter-
pret. Many women in the U.S. have two places of work:
the home and the paid workplace. Each place has its
unique set of exposures to chemicals and non-ionizing
radiation, further complicating exposure assessment.
The evidence that does exist shows increased risk of
breast cancer among two broad categories:
1. Those who work with toxic chemicals, such as
chemists, dental hygienists, paper mill workers and
microelectronics workers.152–155
2. Professionals in higher socioeconomic groups such
as school teachers, social workers, physicians and
journalists.152–155
There are other occupational groups with increased
risk of breast cancer whose work involves chronic expo-
sure to specific chemicals, higher than average levels of
non-ionizing radiation, and in some cases, ionizing
radiation as well.152,156
The U.S. Occupational Health and Safety Adminis-
tration (OSHA) regulatory framework has reduced—
but not eliminated—workers’ exposures to industrial
carcinogens. OSHA requires all chemical manufactur-
ers and importers to develop material safety data sheets
(MSDS) on each product they identify as hazardous.
MSDS list acute and chronic health effects that might
occur as a result of exposure. However, some studies of
workers confirm that exposure to certain industrial
agents, including ionizing radiation, asbestos, and ben-
zene, can increase cancer risk even when the exposure
level is at or below current regulatory limits.156–159
Federal Policy Recommendations.Federal occupational
health policy should require that:
•workers be fully informed of the risks involved in
performing their jobs, including chronic exposures
92 • Nudelman et al. www.ijoeh.com • INT J OCCUP ENVIRON HEALTH
TABLE 4 Household Cleaning Products and Human Health Concerns
Human Health Concern
_________________________________________________
Central
Chemicals Found in Nervous Reproductive Endocrine
Cleaning Products Carcinogen System Toxicant Disruptor Source of Exposure
Diethanolamine X Cleaners, degreasers
Diethylene Glycol X Floor finish, cleaner and polish
Monomethyl Ether
Diethylene Glycol
Monoethyl Ether X X Floor finish, tile and grout cleaner,
microwave oven cleaner
Dibutyl Phthalate X X Floor finish, floor shine and hardener
Nonylphenol Ethoxylate X Cleaners, degreasers, foaming cleaner,
air freshener; spot and stain pretreater;
metal polish
Octylphenol Ethoxylate X Cleaners, degreasers, surface
deodorizer
n-Methyl Pyrolidinone X Floor finish, stripper, floor cleaner
Nitrilotriacetic Acid XaCarpet care products
Coconut Oil Diethanola-
mide (Cocamide DEA) X Cleaners, degreasers, floor cleaner;
metal cleaner and polish
Coconut Oil X Cleaners, degreasers
Diethanolamine
Triethanolamine X Cleaners, degreasers, bleach, floor
bleach, floor cleaner, wood cleaner
Tetrachloroethylene Xa,b XSpray polish, spot remover
Adapted from “Carcinogens and Reproductive Toxins found in Cleaning Products.” [Internet]. Western Sustainability and Pollution
Prevention Network. Available from: http://wsppn.org/Janitorial/factsheets.cfm.
aClassified as a “reasonably anticipated” carcinogen by NTP.
bClassified as a “probable carcinogen” by IARC.
to chemicals and radiation linked to breast cancer
and other adverse health effects; and
•workers receive maximum protection (personal pro-
tective equipment and culturally appropriate train-
ing in its use as well as environmental controls) to
reduce or eliminate occupational exposures that can
contribute to breast cancer.
State Policy Recommendations. States should fund commu-
nity-based biomonitoring studies that include occupa-
tional groups as one of the early communities of focus.
Understanding—and more accurately measuring—the
exposures and resulting health outcomes of workers in
occupations with increased risk of breast cancer is essen-
tial to protecting workers’ health and could contribute
significantly to our broader understanding of environ-
mental exposures and breast cancer.
Research Required. Methodologies need to reflect real-
world exposures. For example, chronic low-dose expo-
sures to mixtures of chemicals must be considered as
well as high-dose acute exposures. For women who
have two workplaces, exposures at home and in the
paid workplace to chemicals and non-ionizing radia-
tion, for example, must be considered as well as their
potential interaction with other risk factors.
Occupational exposure assessment needs to con-
sider nontraditional occupations and work hours.
Occupational health scientists need new methodolo-
gies to account for the fact that women may move in
and out of jobs throughout their lives and work long
hours one day and short shifts another.
Nanotechnology
Nanotechnology has been called the “next industrial
revolution.” It involves the manipulation of materials
and the creation of tiny structures and systems that
exist at the scale of atoms and molecules. (To put
things in perspective, a nanometer is one-billionth of a
meter—to cover the width of a human hair you would
have to line up 80,000 nanometers.) This manipulation
changes the physical properties of materials. Opaque
materials can become transparent, for example, and
chemically stable materials can be made reactive.
These physical changes may lead to medical
advances, more durable products, new ways to clean up
pollution, increased fuel cell efficiency and, market
research suggests, perhaps billions of dollars in profits.
Hundreds of consumer products, including cosmet-
ics and personal care products, stain-resistant clothing,
food storage containers and computers, now include
nanomaterials, according to one academic report. A
2006 report by Friends of the Earth found that at least
116 personal care products containing nanoingredi-
ents—defined as smaller than 100 nanometers—are on
the market.160
Scientists at Rice University’s Center for Biological
and Environmental Nanotechnology are using nanopar-
ticles in new cancer detection and treatment, allowing
them to target and destroy only cancerous cells. As news
of nanotechnology’s promise emerges, however, there
are also concerns about health and environmental risks.
Nanomaterials can be extremely toxic. Due to their
size and structure, they can be inhaled, ingested and
absorbed into the body, enter the blood stream, pene-
trate cells and even interfere with critical DNA
processes. According to the Natural Resources Defense
Council, nanoparticles have caused inflammation and
precancerous lesions, and have damaged brain cells in
animal studies.171
Government is struggling to catch up with this new sci-
ence. At the same time, consumers have a right to know
if the cosmetics and personal care products they use con-
tain untested nanomaterial ingredients. Manufacturers
and retailers should take a precautionary approach to the
use or sale of products with nanosized particles until
these materials have been fully tested for their impact on
the public, workers and environmental health.
Federal Policy Recommendations. To protect workers, con-
sumers and the environment from the known and
unknown consequences of nanomaterials, the FDA
should require manufacturers to conduct comprehen-
sive premarket testing of products formulated with
VOL 15/NO 1, JAN/MAR 2009 • www.ijoeh.com Policy Recommendations: Environment and Breast Cancer • 93
Occupations Associated with Increased Risk of
Breast Cancer
Aircraft and automotive workers161,162
Barbers and hairdressers162,163
Chemists and chemical industry workers162,163
Clinical laboratory technologists162,164
Computer and peripheral equipment operators154,162,165
Crop farmers and fruit and vegetable packers162
Dental hygienists163
Dentists163
Dry cleaning workers 162,163
Flight attendants153
Food, clothing and transportation workers162,163
Furniture and woodworking industry workers166
Homemakers167
Journalists167
Librarians154,164,165
Nurses, particularly chemotherapy nurses162,163,168
Paper mill workers162
Physicians153,162,163
Publishing and printing industry workers162
Meat wrappers and cutters163
Microelectronics workers169
Radiologic technologists170
Rubber and plastics industry workers163
Social workers165
Telephone workers163
94 • Nudelman et al. www.ijoeh.com • INT J OCCUP ENVIRON HEALTH
TABLE 5 Cosmetics and Breast Cancer
Carcinogenic Disrupt Hormones
_________________________________ ___________________
Animal Disrupts
Mammary Human Endocrine
Gland Carcinogenic System/
Chemical CarcinogenaRisk ClassificationbEstrogeniccSource of Exposure in Cosmetics
Benzene X IARC Known; Nail polish and nail polish remover
NTP Known
Bisphenol A X Cosmetic containers/packaging
1,3-Butadiene X IARC Probable; Rubber sponges for applying cosmetics
NTP Known
1,4-Dioxane* X IARC Possible; NTP Petroleum-derived contaminant formed in
Reasonably Anticipated manufacture of shampoos, body wash, children’s
bath products and other sudsing cosmetics
Ethylene Oxide X IARC Known; NTP Known Fragrance
Musks, synthetic X Fragrance
(xylene, ketone,
ambrette, moskene,
tibetene)
N-Nitrosamines* like IARC Possible; NTP Chemical reactions occur over time in the
n-nitrosodi-n-butylamine Reasonably Anticipated product to produce nitrosamines, usually found
in creams, lotions, shampoos and conditioners.
Nonylphenol X Lotions and a wide range of other products
Parabens (butyl-, ethyl-, X Antifungal agent, preservative and
methyl-, propyl-) antimicrobial used in creams, lotions, ointments
and other cosmetics
Petrolatum (polycyclic X IARC Possible; NTP PAHs are petrolatum contaminants; found in
aromatic hydro- Reasonably Anticipated X pretoleum jelly, lipsticks, baby lotions and oils;
carbons [PAHs]* are found in 1 of every 14 personal care products.
common contaminants)
Phthalates (bi-n-butyl- X Nail polish, fragrance
(DBP), di (2-ethylhexyl)-
(DEHP))
Placental extract X NTP Reasonably X Hair conditioners, shampoos and other
(progesterone main Anticipated grooming aids, particularly marketed to
constituent) women of color
1,2-Propylene Oxide X IARC Possible; NTP Fragrance
Reasonably Anticipated
Titanium Dioxide IARC Known; NTP Known X Sunscreens and mineral make-up; use of
(dioxin is a by-product titanium dioxide nanoparticles a possible
of manufacturing threat to human health
and a contaminant)
Triclosan (dioxin is a X IARC Known; NTP Known X Antibacterial used in soaps, toothpate,
by-product of manu- mouthwash and other personal care
facturing and a products
contaminant)
Urethane (ethyl IARC Possible; NTP Hair care products (mousses, gels, sprays),
carbamate) Reasonably Anticipated sunscreens, nail polish, mascara, foundation
*These chemicals do not appear on product labels because they are contaminants and formed in manufacturing through chem-
ical reactions in the product.
aRudel RA, Attfield KA, Schifano JN, Brody JG. Chemicals causing mammary gland tumors in animals signal new directions for epi-
demiology, chemicals testing, and risk assessment for breast cancer prevention. Cancer. 2007;109(S12):2635-66.
bInternational Agency for Research on Cancer (IARC) carcinogenic risk classification is based on evaluation of potential tumor
development at all sites, not only breast/mammary tissue. Categories include: known, probable, possible and others. The National
Toxicology Program (NTP), within the National Institute of Environmental Health Sciences of the National Institutes of Health, pro-
vides carcinogenicity ratings based on scientific evidence in both animals and humans. Categories include: known, reasonably
anticipated, and others (Report on Carcinogens, 11th edition; US Department of Health and Human Services, Public Health Ser-
vice, National Toxicology Program.) Not all chemicals have been rated by IARC or NTP.
cTo date, neither the NTP nor IARC have classified most endocrine disruptors as carcinogens in humans. List of endocrine disruptors
from: Brody JG, Rudel RA. Environmental pollutants and breast cancer. Environ Health Perspect. 2003;111:1007-19.
nanomaterial ingredients for their impact on public
health, worker health and environmental health and
prohibit the unsafe or untested use or sale of nanoma-
terial ingredients in consumer products. In addition,
the FDA should create a publicly accessible database on
the environmental, human health, and worker safety
impacts of nanomaterial ingredients and require man-
ufacturers to label all products they manufacture or sell
that contain nanomaterial ingredients.
Research Required. Research on the health effects of
nanomaterials should be conducted in unison with the
research underway exploring its possible applications.
TOOLS AND RESEARCH NEEDED TO
STRENGTHEN THE EVIDENCE AND
REDUCE EXPOSURES
Statistics on Breast Cancer in All Populations
We need better statistics to help identify trends in breast
cancer incidence and mortality, evaluate current pro-
grams, design new prevention and treatment plans, and
measure our progress in eradicating the disease. There
is general agreement that the incidence of breast cancer
in the United States has risen in past decades; however,
precise statistics on the actual incidence of breast
cancer and the rate of change in various populations is
difficult to establish due to our slow, fragmented and
under-funded state cancer registries system and the
absence of a single national cancer tracking system.
Both the National Cancer Institute (NCI) and the
Centers for Disease Control and Prevention (CDC)
separately fund cancer registries.172,173 National esti-
mates of incidence and mortality are projected from
NCI’s Surveillance, Epidemiology and End Results Pro-
gram (SEER) data. According to the SEER web site, this
population is “comparable to the general U.S. popula-
tion with regard to measures of poverty and education”
but “somewhat more urban and has a higher propor-
tion of foreign-born persons.”174 SEER sites are con-
centrated on coastal cities, omitting much of the South
and Midwest regions.
Cancer tracking has not kept pace with the increas-
ing diversity of the U.S. population. In Asian Pacific
Islanders (API), for example, collecting and reporting
aggregate breast cancer rates tend to obscure those API
groups with high incidence and/or mortality rates,
perpetuating the myth that breast cancer incidence
and mortality are low among all API women.175,176 Dis-
aggregating the data on California API women showed
substantial increases in breast cancer incidence among
Japanese, South Asian, Chinese and Korean women.177
Most research studies only look at women with inva-
sive breast cancer. However, between 1980 and 2001,
with increased use of mammography, diagnoses of
ductal carcinoma in situ (DCIS) have increased seven-
fold. Mainstream cancer organizations such as the
American Cancer Society do not always include in situ
breast cancer incidence rates in their breast cancer
models and statistics. This presents a skewed picture of
breast cancer in the U.S., especially as DCIS is usually
treated the same as invasive breast cancer, with surgery
and possibly radiation and/or chemotherapy.
Finally, under our current system, cancer reporting is
a slow process subject to error due to delays. The 2003
cancer incidence and mortality statistics were reported
in 2007.178 According to the NCI, it takes “four to 16
years for 99 percent of the cancer cases to be
reported.”179 There is much that needs to be done to
mend our fragmented national and state breast cancer
registries. Reliable statistics are essential to measuring
progress toward our goal of eradicating breast cancer.
Federal and State Policy Recommendations.National stan-
dards should be created to strengthen states’ public
accountability and enforce their performance stan-
dards in cancer tracking. If the North American Asso-
ciation of Central Cancer Registries (NAACCR) and
the CDC’s National Program of Cancer Registries
(NPCR) fail to provide leadership on these issues, Con-
gress should mandate that NPCR set these standards
for all registries receiving federal support.
Congress should direct the Institute of Medicine to
conduct a study on the federal management of
cancer registries and make recommendations that
will guide development of a single cancer tracking
system in the U.S.
Finally, state and federal registries should be ade-
quately funded to achieve steady improvement in data
quality and timeliness.
Biomonitoring
Biomonitoring, short for “biological monitoring,”
involves testing biological samples—such as urine or
blood—for the presence of industrial compounds, pol-
lutants and other chemicals in a person’s body. Biomon-
itoring can generate data crucial to better understand-
ing chemical exposures and their relationship to
increasing rates of breast cancer, asthma, birth defects,
autism and other diseases. Biomonitoring can also help
identify communities disproportionately affected by
chemical exposures, support efforts to improve environ-
mental and health regulations, and help set priorities for
legislative and regulatory action to protect public health.
Nationally, the Centers for Disease Control and Pre-
vention (CDC) supports state and local public health
information campaigns about blood lead levels in chil-
dren.180 The National Health and Nutrition Examina-
tion Survey (NHANES), an ongoing population-based
survey carried out by the National Center for Health
Statistics, also monitors chemical levels in blood and
urine, which are published every two years in the
VOL 15/NO 1, JAN/MAR 2009 • www.ijoeh.com Policy Recommendations: Environment and Breast Cancer • 95
CDC’s National Report on Human Exposure to Envi-
ronmental Chemicals.181 The most recent report,
released in 2005, measured and analyzed 148 chemicals
in the blood and urine of almost 8,000 individuals
throughout the United States.182 Aggregated nationally,
the data does not tell states and local communities
about their specific chemical body burdens. A third
NHANES report is expected to be released in 2008.
Federal Policy Recommendations. The CDC should expand
its biomonitoring grants program to support states that
have existing programs with the goal of augmenting
these programs in Fiscal Year 2009. For Fiscal Year 2010
and beyond, federal funds should be appropriated to
support the creation of new state biomonitoring pro-
grams. Federal funds could be used to help states
develop methods for identifying sources and routes of
exposure for biomonitored chemicals; expand labora-
tory capacity; conduct subpopulation studies; conduct
representative analyses of routinely collected blood,
cord blood and other biospecimens; develop protocols
for conducting biomonitoring of sensitive subpopula-
tions such as children; and support biomonitoring field
operations such as participant enrollment, sample col-
lection, data analysis, report generation and results
communications. This work should be coordinated with
EPA’s efforts to identify and monitor ambient air and
other sources of toxic chemical releases.
Federal funding should support the creation of
regional biomonitoring labs to share costs, resources
and the development of analytical testing methods.
State Policy Recommendations. States should fund com-
munity-based studies that couple chemical monitoring
data and biomonitoring of individuals within a geo-
graphic area, occupation, or disproportionately affected
community (e.g., high disease rates and fenceline com-
munities). Biomonitoring can then help assess effec-
tiveness of chemical exposure reduction efforts within
disproportionately affected communities.
Biomonitoring studies at the state level should
include occupational groups. Understanding—and
more accurately and directly measuring—the expo-
sures and resulting health outcomes of workers in occu-
pations with increased risk of breast cancer is essential
to protecting workers’ health and could contribute sig-
nificantly to our broader understanding of environ-
mental exposures and breast cancer.
To better understand early-life exposures and how
they contribute to later-life disease, states should fund
biomonitoring studies that examine cord blood, pla-
centa, meconium, and other appropriate biospecimens.
Health Tracking
With funding from Congress in 2002, the CDC created
the National Environmental Public Health Tracking
Program.183 The program defines health tracking as
“the ongoing collection, integration, analysis, and
interpretation of data about . . . environmental hazards,
exposure to environmental hazards, and health effects
potentially related to exposure to environmental haz-
ards.” Once analyzed, this information can be used by
local, state and federal agencies to better prevent dis-
ease and protect health. Health tracking programs inte-
grate multiple databases such as biomonitoring data,
chemical release data, geographic distribution patterns
of exposure and health outcome data.
The National Environmental Public Health Track-
ing Program has given grants to states to build their
health tracking programs.184 The CDC awarded plan-
ning grants to 27 states and implementation grants to
16 states.184 Prior to these investments, however, most
states had no tracking system to assess many of the
exposures and health conditions that may be related to
environmental hazards. Because health databases, reg-
istries and monitoring systems are not linked, and
because some hazards and chronic diseases are not
tracked at all, their utility is currently limited.185 For
example, for breast cancer, it is difficult to determine if
there is an unusually high rate of the disease in a cer-
tain community or population. It is also difficult to
determine which environmental hazards communities
are exposed to and how they compare to other com-
munities. Making the connections between environ-
mental exposures and disease is an enormous chal-
lenge without comprehensive health tracking systems.
Federal Policy Recommendations. Congress should appro-
priate funds to build state infrastructure, which could
include state laboratories capable of performing bio-
monitoring of human samples for an array of contami-
nants; initiating state Health and Nutrition Examina-
tion Surveys to provide data on a range of health
indicators and environmental exposures; and State
Human Exposure Assessment Surveys (HEXAS) to
identify exposures in the indoor environment, where
many pollutants concentrate.
The CDC should be directed to make funding avail-
able to state environmental health tracking programs
to develop replicable models for disease, hazard and
exposure data-sharing at the local, state and national
levels that incorporate data confidentiality protections.
Advocates should continue to push for enactment of
the Coordinated Environmental Public Health Net-
work Act of 2007 (S 2082/HR 3643), introduced by
House Speaker Nancy Pelosi and Senator Hillary Clin-
ton, which expands and strengthens the nationwide
health tracking network.186
The CDC should be further directed by Congress or
through an executive order to include nongovernmen-
tal organizations representing health-affected con-
stituencies and environmental health and environmen-
tal justice advocates in their advisory groups.
96 • Nudelman et al. www.ijoeh.com • INT J OCCUP ENVIRON HEALTH
State Policy Recommendations. With CDC support, states
should strengthen the coordination between health and
environment agencies of health tracking programs.
Invest in New Science
Research is needed to address key emergent themes on
environmental causes of breast cancer, including low
dose exposures, multiple exposures, timing of exposures
and later-life breast cancer, and early puberty and later-
life breast cancer (see companion piece in this issue18).
Federal and state policy makers can help advance
needed research by providing funding and support.
Federal Policy Recommendations. The federal government
should support large studies that follow girls from con-
ception to adulthood, such as the National Children’s
Study (NCS) mandated by Congress in 2000, which will
follow 100,000 children from conception to adult-
hood.187 Securing congressional funding over the next
five years of the NCS will be critical because during this
time recruitment will be in full swing and prenatal and
early life baseline measurements will take place.
In 2007–08 there were two active federal-level efforts
to investigate the relationship between the environment
and breast cancer: the NIEHS-funded Breast Cancer
and Environment Research Centers (BCERC) explor-
ing early puberty and connections to later-life breast
cancer,188 and the Breast Cancer and Environmental
Research Act (BCERA), federal legislation which Presi-
dent Bush signed into law in October 2008. BCERA, as
originally introduced, would have set up Centers of
Excellence focused on researching environmental links
to breast cancer. However, the bill was significantly
amended prior to its adoption, and no longer mandates
specific research on environmental causes of breast
cancer. Instead, it sets up an Interagency Environmental
Research Coordinating Committee to make recommen-
dations and solicit proposals for breast cancer research
more broadly.189 Even when combined, both of these
efforts represent a small portion of the federal funding
needed to strengthen our understanding of the envi-
ronmental links to breast cancer.
The EPA’s Endocrine Disruptor Screening Program,
mandated by Congress, is eight years behind schedule
and not one chemical has been screened to date.190,191
Advocates should keep the pressure on Congress and
the EPA to ensure this important work is completed in
a timely and fully transparent manner.
State Policy Recommendations. States should use the Cali-
fornia Breast Cancer Research Program as a model of
innovative state research programs. The CBCRP is a
research program created by a ballot initiative and
funded by a cigarette tax that created a special $18 mil-
lion statewide initiative focused on the effects of the
environment on breast cancer.192 The program also
stresses the applicability of research to policy solutions
and emphasizes stakeholder involvement so that advo-
cates, clinicians, researchers, policy makers and the
general public can help direct research funding.
CONCLUSIONS
A substantial body of scientific evidence indicates that
exposures to common chemicals and radiation, alone
and in combination, are contributing to the increases
in breast cancer incidence observed over the past sev-
eral decades. In the first article in this two-part series,
we document this evidence. Based on the evidence, we
conclude that at this time the United States has neither
the public health regulations in place nor the requisite
research underway to eradicate the environmental
causes of breast cancer. It is therefore imperative that
we use this evidence to inform regulatory change and
investment in key areas of research. This article is writ-
ten with the goal of building bridges between scientists
and the many important advocacy communities,
including breast cancer advocates as well as members
of the women’s health, environmental justice and envi-
ronmental health movements. By working together for
these changes in research and legislation, we will
decrease human exposures to toxic substances impli-
cated in high rates of breast cancer, thereby decreasing
the incidence of this disease.
References
1. Cutler SJ, Connelly, RR. Mammary cancer trends. Cancer
1969;23:767-71.
2. Jatoi I, Anderson WF, Rao SR, et al. Breast cancer trends among
black and white women in the United States. J Clin Oncol.
2005;23:7836-41.
3. Howe HL, Wingo PA, Thun MJ, et al. Annual report to the nation
on the status of cancer (1973-1998), featuring cancers with recent
increasing trends. J Natl Cancer Inst. 2001;93:824-842.
4. Ries LAG, Melbert D, Krapcho M, et al. (eds). SEER Cancer sta-
tistics review, 1975-2004. [Internet]. Bethesda, MD: National
Cancer Institute; 2007. Available from: http://seer.cancer.gov/
csr/1975_2004/, based on November 2006 SEER data submis-
sion, posted to the SEER web site, 2007.
5. Hayat MJ, Howlader N, Reichman ME, et al.. Cancer statistics,
trends and multiple primary cancer analyses from the Surveil-
lance, Epidemiology, and End Result (SEER) Program. Oncol-
ogist. 2007;12:20-37.
6. Ravdin PM, Cronin KA, Howlader N, et al. The decrease in
incidence in breast cancer incidence in 2003 in the United
States. N Engl J Med. 2007;356:1670-4.
7. Glass AG, Lacey JV, Carreon JD, et al. Breast cancer incidence,
1980–2006: Combined roles of menopausal hormone therapy,
screening mammography, and estrogen receptor status. J Natl
Cancer Inst. 2007;99:1152-61.
8. Centers for Disease Control and Prevention. Decline in breast
cancer incidence: United States, 1999–2003. Morbidity and
Mortality Weekly Report. 2007;56:549-53.
9. Jemal A, Siegel E, Ward E, et al. Cancer statistics: 2006. CA:
Cancer J Clin. 2006;56:106-30.
10. U.S. Environmental Protection Agency, Office of Pollution Pre-
vention and Toxics. Overview: Office of Pollution Prevention
and Toxics Programs [Internet]. 2007 Oct 8. Available from:
http://www.epa.gov/oppt/pubs/oppt101c2.pdf
11. U.S. Environmental Protection Agency Office of Pollution Pre-
vention and Toxics. Chemical hazard data availability study:
VOL 15/NO 1, JAN/MAR 2009 • www.ijoeh.com Policy Recommendations: Environment and Breast Cancer • 97
What do we really know about the safety of high production
volume chemicals? [Internet]. 2008. Available from:
http://www.epa.gov/HPV/pubs/general/hazchem.pdf
12. Rudel RA, Camann DE, Spengler JD, et al. Phthalates,
alkylphenols, pesticides, polybrominated diphenyl ethers, and
other endocrine-disrupting compounds in air and dust. Envi-
ron Sci Technol. 2003;37:4543-53.
13. Siddiqui MK, Anand M, Mehrotra PK, et al. Biomonitoring of
organochlorines in women with benign and malignant breast
disease. Environ Res. 2004;98:250-7.
14. Nickerson K. Environmental contaminants in breast milk. J
Midwifery Womens Health. 2006;51:26-34.
15. Rudel RA, Attfield KA, Schifano JN, et al. Chemicals causing
mammary gland tumors in animals signal new directions for
epidemiology, chemicals testing, and risk assessment for breast
cancer prevention. Cancer. 2007;109(S12):2635-66.
16. Birnbaum LS, Fenton SE. Cancer and developmental exposure
to endocrine disruptors. Environ Health Persp. 2003;111:389-
94.
17. Fenton SE. Endocrine-disrupting compounds and mammary
gland development: early exposure and later life conse-
quences. Endocrinology. 2006;147:S18-S24.
18. Gray J, Evans N, Taylor B, et al. State of the evidence: The con-
nection between breast cancer and the environment. 2008;Int
J Occup Environ Health. 15:
19. Lux MP, Fasching PA, Beckmann MW. Hereditary breast and
ovarian cancer: review and future perspectives. J Mol Med.
2006;84:16-28.
20. Hankinson SE, Colditz GA, Willett WC. Towards an integrated
model for breast cancer etiology: the lifelong interplay of genes,
lifestyle, and hormones. Breast Cancer Res. 2004;6:213-18.
21. Michels KB, Mohllajee AP, Roset-Bahmanyar ER, et al. Diet and
breast cancer. Cancer. 2007;109(S12):2712-2749.
22. Zheng SM, Lee I-M, Manson JE, et al. Alcohol consumption
and breast cancer risk in the Women’s Health Study. Am J Epi-
demiol. 2007;165:667-76.
23. Visvanathan K, Crum RM, Strickland PT, et al. Alcohol dehy-
drogenase genetic polymorphisms, low-to-moderate alcohol
consumption, and risk of breast cancer. Alcohol Clin Exp Res.
2007;31:467-76.
24. Monninkhof EM, Elias SG, Vlems FA, et al. Physical activity and
breast cancer: a systematic review. Epidemiology. 2007;18:137-57.
25. Kruk J, Aboul-Enein HY. Environmental exposure, and other
behavioral risk factors in breast cancer. Curr Cancer Ther Rev.
2006;2:3-21.
26. Russo J, Hu YF, Silva IDCG, et al. Cancer risk related to mam-
mary gland structure and development. Microsc Res Tech.
2001;52:204-23.
27. National Toxicology Program (2005). Eleventh Report on Car-
cinogens. National Institute of Environmental Health Sciences.
National Institutes of Health.
28. National Research Council (2005). Biologic effects of ionizing
radiation VII: Health risks from exposure to low levels of ioniz-
ing radiation. National Academy of Science, Washington DC
29. Calaf GM, Hei TK. Establishment of a radiation- and estrogen-
induced breast cancer model. Carcinogenesis 2000;21:769-776.
30. American Society of Radiologic Technologists. Does your state
regulate medical imaging and therapy technologists? [Inter-
net]. 2007 Nov 15. Available from https://www.asrt.org/
media/pdf/govrel/doesyourstateregulate.pdf
31. NIEHS Working Group Report. Assessment of health effects
from exposure to power-line frequency electric and magnetic
fields. Research Park Triangle:National Institute of Environmen-
tal Health Sciences of the National Institutes of Health. 1998.
32. Ahlbom A, Cardis E, Green A, et al. Review of the epidemio-
logical literature on EMF and health. Environ Health Persp.
2001;109 (Suppl 6):911-33.
33. German Federal Office for Radiation Protection. [Internet].
Berlin, Germany. 2007 Sept. Available from: http://www.bfs.
de/en/bfs.
34. European Environmental Agency. Radiation risks from every-
day devices assessed [Internet]. 2007 Nov 15. Available from:
www.eea.europa.eu/highlights/radiation-risk-from-everyday-
devices-assessed
35. Carpenter D, Sage C, Davanipour Z, et al. The BioInitiative
Report: A Rationale for a Biologically-based Public Exposure
Standard for Electromagnetic Fields (ELF and RF). [Internet].
2007 August. Available from: http://www.bioinitiative.org/
report/index.htm.
36. Federal Communications Commission. Code of Federal Regu-
lations. [Internet]. 2007 October. Available from: http://wire-
less.fcc.gov/index.htm?job=rules_and_regulations.
37. Electromagnetic Radiation Policy Institute. Frequently asked
questions [Internet]. 2007 Nov 15. Available from: www.emr
policy.org/faq/index.htm
38. U.S. Environmental Protection Agency, Office of Pollution Pre-
vention and Toxics. Overview: Office of Pollution Prevention
and Toxics Programs [Internet]. 2007 Oct 8. Available from:
www.epa.gov/oppt/pubs/oppt101c2.pdf , October 8, 2007.
39. Bennett M, Davis BJ. The identification of mammar y carcino-
gens in rodent bioassays. Environ Mol Mut. 2002;39(2-3):150-7.
40. U.S. Environmental Protection Agency. Summary of the Toxic
Substances Control Act. [Internet] Available from: http://
www.epa.gov/lawsregs/laws/tsca.html
41. Wilson MP, Chia DA, Ehlers BC. Green chemistry in California:
a framework for leadership in chemicals policy and innovation.
2006.Berkeley: California Policy Research Center, University of
California.
42. National Academy of Sciences. Commission on Life Sciences.
Toxicology Testing: Strategies to Determine Needs and Priorities.
1984. Washington, D.C.: National Academy of Sciences Press.
43. U.S. General Accounting Office. Toxic Substances Control Act:
Legislative Changes Could Make the Act More Effective
(GAO/RCED-94-103) [Internet]. Washington, D.C.: U.S. Gov-
ernment Printing Office (1994). Available from: http://
archive.gao.gov/t2pbat2/152799.pdf)
44. U.S. Environmental Protection Agency, Office of Pollution Pre-
vention and Toxics. Chemical Hazard Data Availability Study:
What Do We Really Know About the Safety of High Production
Volume Chemicals? [Internet]]Washington, D.C.: Environ-
mental Protection Agency (1998). Available at: http://www.
epa.gov/hpv/pubs/general/hazchem.pdf
45. 110th Congress of the United States of America. S3040: Kids’
Safe Chemicals Act of 2008. [Internet]. Available from:
http://www.govtrack.us/congress/bill.xpd?bill=s110-3040
46. 110th Congress of the United States of America. HR.4040: Con-
sumer Product Safety Improvement Act. [Internet] Available
from: http://thomas.loc.gov/cgi-bin/query/z?c110:H.R.4040
47. California Environmental ProtectionAgency Office of Environ-
mental Health Hazard Assessment (OEHHA). The Safe Drink-
ing Water and Toxic Enforcement Act of 1986. [Internet].
Available from: http://www.oehha.ca.gov/prop65/law/P65
law72003.html.
48. Safer States. [Internet]. Available from: http://saferstates.com/
49. Thorpe B, Rossi M, Easthope T, et al. . Louisville Charter for
Safer Chemicals: A platform for creating a safe and healthy
environment through innovation. [Internet]. Available from:
http://www.louisvillecharter.org/home.shtml
50. Wingspread Statement on the Precautionary Principle. [Inter-
net]. Available from: http://www.who.int/ifcs/documents/
forums/forum5/precaution/wingspread/en/index.html
51. U.S. Environmental Protection Agency. 1996 Food Quality Pro-
tection Act: Implementation Plan. [Internet]. March 1997,
Washington DC. Available from: http://www.epa.gov/pesti-
cides/regulating/laws/fqpa/fqpa_implementation.htm.
52. Brody JG, Moysich KB, Humblet O, Attfield KR, Beehler GP,
Rudel RA. Environmental pollutants and breast cancer: epi-
demiologic studies. Cancer 2007;109(S12):2667-711.
53. Labreche, FP, Goldberg, MS. Exposure to organic solvents and
breast cancer in women: a hypothesis. Am J Ind Med. 1997;
32(1):1-14.
54. Warner MB, Eskenazi B, Mocarelli P, et al. Serum dioxin con-
centrations and breast cancer risk in the Seveso Women’s
Health Study. Environ Health Persp. 2002;110:625-8.
55. Betts KS. Secondhand Suspicions: Breast Cancer and Passive
Smoking. Environ Health Persp. 2007;115(3):A136-143
56. State of California Air Resources Board. Appendix III: Pro-
posed identification of Environmental Tobacco Smoke as a
Toxic Air Contaminant. [Internet]. 2005 June. p. 7-119. Cali-
fornia Environmental Protection Agency. Office of Environ-
mental Health Hazard Assessment. Available from: ftp://
ftp.arb.ca.gov/carbis/regact/ets2006/app3part%20b.pdf
98 • Nudelman et al. www.ijoeh.com • INT J OCCUP ENVIRON HEALTH
57. American Non-smokers Rights Foundation. Over view list—how
many smokefree laws? [Internet]. 2007 Nov 15. Available from:
www.no-smoke.org/pdf/mediaordlist.pdf
58. State of California. Air Resources Board. Risk Reduction Plan
to Reduce Particulate Matter Emissions from Diesel-Fueled
Engines and Vehicles. [Internet]. California Environmental
Protection Agency. Stationary Source Division. Mobile Source
Control Division. Available from: http://www.arb.ca.gov/
diesel/documents/rrpFinal.pdf
59. American Lung Association. [Internet]. Available from:
http://www.lungusa.org/site/c.dvLUK9O0E/b.33691/
60. Environmental Defense Fund. [Internet]. Available from:
http://www.edf.org/page.cfm?tagID=97
61. Natural Resources Defense Council. [Internet]. Available
from: http://www.nrdc.org/air/default.asp
62. US Environmental Protection Agency. Six Common Air Pollu-
tants. [Internet]. Available from: http://www.epa.gov/air/
urbanair/
63. Alexander BH, Mandel JS, Baker BA, et al. Biomonitoring of
2,4-dichlorophenoxyaceetic acid exposure and dose in farm
families. Environ Health Persp. 2007;115:370-6.
64. Cohn BA, Wolff MA, Cirillo PM, et al. DDT and breast cancer
in young women: new data on the significance of age at expo-
sure. Environ Health Persp. 2007;115:1406-14.
65. Fenton SE. Endocrine-disrupting compounds and mammary
gland development: early exposure and later life conse-
quences. Endocrinology.2006;147(Suppl):S18-S24.
66. Raynor JL, Enoch RR, Fenton SE. Adverse effects of prenatal
exposure to atrazine during a critical period of mammary
gland growth. Toxicol Sci. 2005;87:255-66.
67. US Environmental Protection Agency. Endocrine Disruptor
Screening Program (EDSP). [Internet]. Available from:
http://www.epa.gov/endo/.
68. Canada News Wire. Canadian Cancer Society Applauds Pesti-
cide Ban. [Internet]. 2008 November. Available from: http://
www.newswire.ca/en/releases/archive/November2008/13/
c8287.html.
69. Éditeur officiel du Québec. Pesticides Management Code.
[Internet]. Available from: http://www2.publicationsduque
bec.gouv.qc.ca/dynamicSearch/telecharge.php?type=3&file=/
P_9_3/P9_3R0_01_A.htm
70. San Francisco Administrative Code, Chapter 39 San Francisco
Integrated Pest Management Program. [Internet]. Available
from: http://www.sfgov.org/site/uploadedfiles/bdsupvrs/
ordinances00/o0002-00.pdf
71. Integrated Pest Management Program Report Reduced Risk
Pesticide List 2000, San Francisco Integrated Pest Management
Program. [Internet]. Available from: http://www.ci.sf.ca.us/
ipm/list2000/coverhtm#list2000.
72. Oakland City Council. Resolution adopting integrated pest
management policies for the City of Oakland. [Internet]. 1997
December. Available from: http://www.oaklandpw.com/Asset
Factory.aspx?did=2001
73. European Commission. Commission Decision of 10 March
2004 concerning the non-inclusion of atrazine in Annex I to
Council Directive 91/414/EEC and the withdrawal of authori-
sations for plant protection products containing this active sub-
stance, 2004/248/EC. Off J Eur Union 2004;L78:53-5.
74. US Environmental Protection Agency. Decision Documents for
Atrazine. [Internet]. 2006 April. Available from: http://www.
epa.gov/oppsrrd1/reregistration/REDs/atrazine_combined
_docs.pdf.
75. Cooper RL, Stoker TE, Tyrey L et al. Atrazine disrupts the
hypothalamic control of pituitary-ovarian function. Toxicol Sci.
2000;53:297-307.
76. O’Connor JC, Plowchalk DR, Van Pelt CS, et al. Role of pro-
lactin in chloro-S-triazine rat mammary tumorigenesis. Drug
Chem Toxicol. 2000;23:575-601.
77. Sanderson JT, Letcher RJ, Heneweer M, et al.. Effects of chloro-
S-triazine herbicides and metabolites on aromatase activity in
various human cell lines and on vitellogenin production in
male carp hepatocytes. Environ Health Persp. 2001;109:1027-31
78. Fan WQ, Yanase T, Morinaga H, et al. Atrazine-induced aro-
matase expression in SF-1 dependent: implications for
endocrine disruption in wildlife and reproductive cancers in
humans. Environ Health Rep. 2007;115:720-7.
79. Nabholtz JM. Aromatase inhibitors in the management of
early breast cancer. EurJournal of Surg Oncol. 2008;34(11):
1199-207.
80. Cepa M, Correia-da-Silva G, da Silva EJ, et al. New steroidal aro-
matase inhibitors: suppression of estrogen-dependent breast
cancer cell proliferation and induction of cell death. BMC Cell
Biology. 2008;9:41.
81. Hayes TB, Stuart AA, Mendoza M, et al. Characterization of
atrazine-induced gonadal malformations in African clawed frogs
(Xenopus laevis) and comparisons with effects of an androgen
antagonist (cyproterone acetate) and exogenous estrogen (17b-
estradiol): Support for the demasculinaza-tion/feminization
hypothesis. Environ Health Persp. 2006:114(S1):134-141.
82. U.S. Securities & Exchange Commission. Form 20-F 2000:
Novartis, innovative medicines—improved lives. As filed with
the Securities and Exchange Commission on April 11, 2001
[Internet]. 2007 Aug 10. Available from: www.novartis.
com/downloads/investors/Novartis-20F-2000.pdf
83. Gitlitz J, Franklin P. Water, Water Everywhere: The Growth of
Non-Carbonated Beverages in the United States. 2007: Con-
tainer Recycling Institute. Available at: http://www.container-
recycling.org/assets/pdfs/reports/2007-waterwater.pdf.
84. Moore CJ. Synthetic polymers in the marine environment: A
rapidly increasing long-term threat. Environ Res 2008:108(2):
131-139.
85. Institute for Agriculture and Trade Policy. Smart plastics guide
[Internet]. 2007 Oct 15. Available from: http://www.healthob-
servatory.org/library.cfm?refID=77083
86. Maffini MV, Rubin BS, Sonnenschein C, et al. Endocrine dis-
ruptors and reproductive health: the case of bisphenol-A. Mol
Cell Endocrinol. 2006;254-255:179-86.
87. Markey CM, Luque EH, Munoz-de-Toro MM, et al. In utero
exposure to bisphenol A alters the development and tissue
organization of the mouse mammary gland. Biol Reprod.
2001;65:1215-23.
88. Wadia PR, Vandenberg LN, Schaeberle CM, et al. Perinatal
bisphenol A exposure increases estrogen sensitivity of the
mammary gland in diverse mouse species. Environ Health
Persp. 2007;115:80-6.
89. Swann SH, Main KM, Liu F, et al.(2005). Decrease in anogeni-
tal distance among male infants with prenatal phthalate expo-
sure. Environ Health Persp.2005;113:1056-1061.
90. Jobling S, Reynolds T, White R, et al. A variety of environmentally
persistent chemicals, including some phthalate plasticizers, are
weakly estrogenic. Environ Health Persp 1995;113: 1056-1061.
91. Ohlson CG. Hardell L. Testicular cancer and occupational
exposures with a focus on xenoestrogens in polyvinyl chloride
plastics. Chemosphere. 2000:40(9-11):1277-82.
92. Den Hond E. Schoeters G. Endocrine disrupters and human
puberty. Int J Androl. 2006;29(1):264-71.
93. 110th Congress of the United States of America. HR 6228: Ban
Poisonous Additives Act of 2008. [Internet]. Available from:
http://thomas.loc.gov/cgi-bin/query/D?c110:1:./temp/
~c110fR0Sst
94. State of California. Assembly Bill 1879. [Internet]. Available
from: http://www.leginfo.ca.gov/pub/07-08/bill/asm/ab_
1851-1900/ab_1879_bill_20080929_chaptered.pdf
95. State of California. Senate Bill 1713. [Internet]. Available at:
http://www.leginfo.ca.gov/pub/07-08/bill/sen/sb_1701-
1750/sb_1713_bill_20080822_amended_asm_v94.pdf
96. Schonfelder G, Wittfoht W, Hopp H, et al. Parent bisphenol A
accumulation in the human maternal-fetal-placental unit. Env-
iron Health Persp. 2002;110:A703-7.
97. Burridge E. Bisphenol A: surging polycarbonate in Asia has
boosted bisphenol A’s fortunes. Eur Chem News. 2004;81:17.
98. Dodds EC, Lawson W. Nature. 1936;137:996.
99. Dodds EC, Goldberg L, Lawson W, Robinson R. Oestrogenic
activity of certain synthetic compounds. Nature. 1938;141:247-8.
100. Dieckmann WJ, Davis ME, Rynkiewicz LM, Pottinger RE. Does
the administration of diethylstilbestrol during pregnancy have
therapeutic value? Am J Obstet Gynecol. 1953;66:1062-75.
101. Sugiura-Ogasawara M, Ozaki Y, Sonta S, Makino T, Suzumori K.
Exposure to bisphenol A is associated with recurrent miscar-
riage. Hum Reprod. 2006;20:2325-9.
102. National Toxicology Program. Diethylstilbesterol, CAS No. 56-
53-1. [Internet]. Report on Carcinogens, 11th Edition. Avail-
VOL 15/NO 1, JAN/MAR 2009 • www.ijoeh.com Policy Recommendations: Environment and Breast Cancer • 99
able from: http://ntp.niehs.nih.gov/ntp/roc/eleventh/pro
files/s071diet.pdf.
103. Raun AP, Preston RL. History of dietheylstilbesterol use in
cattle. [Internet]. American Society of Animal Science. Avail-
able from: http://www.asas.org/Bios/Raunhist.pdf
104. Hammes B, Laiman CJ. Diethylstilbestrol for the identification
and management of DES-exposed individuals. J Midwifery
Womens Health 2003:48(1):19-29.
105. Guisti RM, Iwamoto K, Hatch EE. Diethystilbestrol revisited: a
review of the long-term health effects. Ann Intern Med. 1995;
122:778-88.
106. Herbst AL, Scully RE. Adenocarcinoma of the vagina in ado-
lescence: a report of seven cases including six clear cell carci-
nomas (so-called mesonephromas). Cancer. 1970;25:745-57.
107. Herbst AL, Ulfelder H, Poskanzer DC. Adenocarcinoma of the
vagina: Association of maternal stilbestrol therapy with tumor
appearance in young women. N Engl J Med. 1971;284:878-81.
108. Bibbo M, Gill WB, Azizi F, et al. Follow-up study of male and
female offspring of DES-exposed mothers. Obstet Gynecol J.
1977;49:1-8.
109. Colton T, Greenberg ER, Noller K, et al. Breast cancer in moth-
ers prescribed diethylstilbestrol in pregnancy: further follow-
up. J Am Med Assoc. 1993;269:2096-2100.
110. Titus-Ernstoff L, Hatch EE, Hoover RN, et al. Long-term
cancer risk in women given diethylstilbestrol (DES) during
pregnancy. Brit J Cancer 2001; 84: 126-133.
111. Palmer JR, Wise LA, Hatch EE, et al. Prenatal diethylstilbestrol
exposure and risk of breast cancer. Cancer Epidemiol Bio-
markers Prev. 2006;15:1509-14.
112. Troisi R, Hatch EE, Titus-Ernstoff L, et al. Cancer risk in
women prenatally exposed to diethylstilbestrol. Int J Cancer.
2007;121:356-60.
113. Houlihan J, Lunder S, Jacob A. Timeline: BPA: from invention
to phase out. Environmental Working Group Research Report.
2008. [Internet] Available at: http://www.ewg.org/reports/
bpatimeline
114. Grandjean P, Bellinger D, Bergman A, et al. The Faroes state-
ment: human health effects of developmental exposure to
chemicals in our environment. Basic Clin Pharmacol Toxicol.
2007;102:73-75.
115. vom Saal FS, Hughes C. An extensive new literature concern-
ing low-dose effects of bisphenol A shows the need for a new
risk assessment. Environ Health Persp. 2005;113:926-33.
116. Lang IA, Galloway TS, Scarlett A, et al. Association of urinar y
bisphenol A concentration with medical disorders and labora-
tory abnormalities in adults. J Am Med Assoc. 2008;300(11):
1303-10.
117. vom Saal FS, Myers JP. Bisphenol A and risk of metabolic dis-
orders.[comment]. J Am Med Assoc.2008;300(11):1353-5.
118. Ropero AB, Alonso-Magdalena P, Garcia-Garcia E, et al. Bisphe-
nol-A disruption of the endocrine pancreas and blood glucose
homeostasis. Int J Androl.2008;31(2):194-200.
119. Newbold RR, Jefferson WN, Banks EP (2007). Long-term
adverse effects of neonatal exposure to bisphenol A on the
murine female reproductive tract. Reprod Toxicol. 2007;
24:253-258.
120. Richter CA, Birnbaum LS, Farabollini F, et al. In vivo effects of
bisphenol A in laboratory rodent studies. Reprod Toxicol
2007;24:199-224.
121. US Environmental Protection Agency. Integrated Risk Infor-
mation System. Bisphenol A (CASRN 80-05-7). [Internet].
1988. Available from: http://www.epa.gov/iris/subst/0356.
htm.
122. Calafat, AM,Ye X,Wong L-Y, et al.. Exposure of the US popula-
tion to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Env-
iron Health Persp. 2008; 116:39-44.
123. Vandenberg LN, Hauser R, Marcus M, et al. Human exposure
to bisphenol A (BPA). Reprod Toxicol. 2007;24:139-177.
124. Michaels D, Monforton C. Manufacturing Uncertainty: Con-
tested science and the protection of the public’s health and
environment. Am J Pub Health 2005:95(S1):S39-S47.
125. Gross L. The toxic origins of disease. PLoS Biol. 2007;5:1392-
1398.
126. vom Saal, F and W Welshons. Large effects from small expo-
sures. II. The importance of positive controls in low-dose
research on bisphenol A. Environ Res. 2006;100:50-76.
127. Environmental Working Group. Letter to Center for the Eval-
uation of Risks to Human Reproduction: Interim Draft Report
on Bisphenol A. [Internet]. June 2007. Available from: http://
www.ewg.org/node/21835.
128. vom Saal FS, Akingbemi BT, Belcher SM, et al. Chapel Hill
bisphenol A expert panel consensus statement: Integration of
mechanisms, effects in animals and potential to impact human
health at current levels of exposure. Reprod Toxico. 2007;
24:131-138.
129. Schonfelder G, Wittfoht W, Hopp H, et al.. Parent bisphenol A
accumulation in the human maternal-fetal-placental unit. Env-
iron Health Persp.2002;110(11):A703-707.
130.. Boyle CA, Decoufle P, Yeargin-Allsopp M. Prevalence and
health impact of developmental disabilities in U.S. children.
Pediatrics. 1994;93:399-403.
131. California Office of Environmental Health Hazard Assessment.
Announcement of Chemicals Selected by OEHHA for Consid-
eration for Listing by the Developmental and Reproductive
Toxicant Identification Committee and Request for Relevant
Information on the Developmental and Reproductive Toxicity
of These Chemicals EXTENSION OF PUBLIC COMMENT
PERIOD: Bisphenol A. [Internet]. [03/21/08] posted
03/11/08. Available at: http://www.oehha.ca.gov/prop65/
CRNR_notices/state_listing/data_callin/extend031108.html.
132. Norwegian RoHS, 18 substances banned. Reported July 23,
2007. [Inernet] 2007 Pct 15. Available from www.evertig.com/
news/read_news.do?news=8237–&cat=7
133. Horrigan L, Lawrence RS, Walker P. How sustainable sgricul-
ture can address the environmental and human health harms
of industrial agriculture. Environ Health Persp 2002;110(5):
445-456.
134. Schecter A, Papke O, Harris TR,t al. Polybrominated Diphenyl
Ether (PBDE) Levels in an Expanded Market Basket Survey of
U.S. Food and Estimated PBDE Dietary Intake by Age and Sex.
Environ Health Persp 2006;114(10):1515-1520.
135. Hankinson S, Willett WC, Colditz GA, et al. Circulating con-
centrations of insulin-like growth factor 1 and risk of breast
cancer. Lancet. 1998;351:1393-6.
136. Daxenberger, A, Bernhard BH, Sauerwein H. Increased milk
levels of insulin-like growth factor 1 (IGF-1) for the identifica-
tion of bovine somatotropin (bST) treated cows. Analyst.
1998;123:2429-35.
137. Allen NE, Roddam AW, Allen DS, et al. A prospective study of
serum insulin-like growth factor-I (IGF-1), IGF-II, IGF-binding
protein-3 and breast cancer risk. Brit J Cancer. 2005;92: 1283-7.
138. Schernhammer ES, Holly JM, Pollak MN et al.. Circulating
levels of insulin-like growth factors, their binding proteins, and
breast cancer risk. Cancer Epidemiol Biomarkers Prev.
2005;14:699-704.
139. Ciftci K, Su J, Trovitch PB. Growth factors and chemothera-
peutic modulation of breast cancer cells. J Pharm Pharmacol.
2003;55:1135-41.
140. Furstenberger G, Morant R, Senn HJ. Insulin-like growth fac-
tors and breast cancer. Onkologie. 2003;26:290-4.
141. European Commission. Enterprise and Industry Directorate
General. Consumer goods—Cosmetics. Consolidated Version
of Cosmetics Directive 76/768/EEC. [Internet]. Updated
3/10/2008. Available from: http://ec.europa.eu/enterprise/
cosmetics/html/consolidated_dir.htm
142. US Food and Drug Administration. Cosmetic Ingredients:
Understanding the Puffery. [Internet]. FDA Consumer Maga-
zine 1992 May. Available from: http://www.fda.gov/fdac/
reprints/puffery.html
143. CIR (Cosmetics Ingredient Review). Cosmetic ingredients
banned by FDA (11 total, through June, 2008). [Internet].
2008 June. Available from: http://www.cir-safety.org/staff_
files/banned.pdf
144. Environmental Working Group (2004). Exposures Add Up—
Survey Results. [Internet]. Available from: http://www.cosmet
icsdatabase.com/research/exposures/php.
145. Commonweal Biomonitoring Resource Center (2005). Taking
It All In: Documenting Chemical Pollution in Californians
through Biomonitoring. [Internet]. Available from: http://
www.commonweal.org/programs/download/TIAI_1205.pdf
146. Environmental Working Group (2006). Across Generations:
Industrial Chemicals in Mothers and Daughters: The pollution
100 • Nudelman et al. www.ijoeh.com • INT J OCCUP ENVIRON HEALTH
we share and inherit. [Internet]. Available from: http://www.
ewg.org/reports/generations/
147. Environmental Working Group (2005). Body Burden: The Pol-
lution in Newborns. [Internet]. Available from: http://www.
ewg.org/node/17686.
148. Environmental Working Group.). Body Burden: The Pollution
in People. [Internet]. 2003. Available from: http://archive.
ewg.org/reports/bodyburden1/.
149. Bronaugh RL, Collier SW, Macpherson SE, et al. Influence of
metabolism in skin on dosimetry after topical exposure. Envi-
ron Health Persp 1994:102(S11): 71-74.
150. Schettler T. Human exposure to phthalates via consumer prod-
ucts. Int J Androl 2006; 29:134-139.
151. Janjua NR, Frederiksen H, Skakkebæk NE, et al.. Urinary
excretion of phthalates and paraben after repeated whole-body
topical application in humans. Int J Androl.2008; 30:1–11.
152. Cantor KP, Stewart, PA, Brinton LA, et al. Occupational expo-
sures and female breast cancer mortality in the United States. J
Occup Environ Med. 1995;37(3):336-48.
153. Weiderpass E, Pukkala E, Kauppinen T, et al. Breast cancer and
occupational exposures in women in Finland. Am J Ind Med.
1999;36:48-53.
154. Petralia SA, Vena JE, Freudenheim JL, et al. Breast cancer risk
and lifetime occupational history: Employment in professional
and managerial occupations. Occup Environ Med 1998;55:43-48.
155. Habel LA, Standford JL, Vaughan TL et al. Occupation and
Breast Cancer Risk in Middle-Aged Women. J Occup Environ
Med 1995;37(3): 349-356.
156. Cardis E, Vrijheid M, Blettner M, et al. Risk of cancer after low
doses of ionising radiation: retrospective cohort study in 15
countries. Brit Med J 2005;331:77-80.
157. Jacobs M, Clapp R. Industrial Carcinogens: A Need for
Action.[Internet] 2008. Available from: http://www.healthand
environment.org
158. Stayner L, Smith R, Bailer J, et al. Exposure-Response analysis
of risk of respiratory disease associated with occupational expo-
sure to asbestos. Occup Environ Med.1997; 54:646–652.
159. Hayes RB, Songnian Y, Dosmeci M, et al. Benzene and lym-
phohematopoietic malignancies in humans. Am J Indust Med.
2001; 40:117–126.
160. Friends of the Earth. Nanomaterials, sunscreens and cosmetics:
Small ingredients, big risks [Internet]. 2007 Nov 15. Available
from: www.foe.org/camps/comm/nanotech/nanocosmetics.
pdf.
161. Thompson D, Kriebel D, Quinn MM, et al. Occupational expo-
sure to metalworking fluids and risk of breast cancer among
female autoworkers. Am J Ind Med. 2005;47:153-60.
162. Band PR, Le ND, Fang R, et al. Identification of occupational
cancer risks in British Columbia: a population-based case-con-
trol study of 995 incident breast cancer cases by menopausal
status, controlling for confounding factors. J Occup Environ
Med. 2000;42:284-310.
163. Goldberg MS, Labreche F. Occupational risk factors for female
breast cancer: A review. Occup Environ Med. 1996;53(3):145-56.
164. Zheng T, Holford TR, Taylor Mayne S, et al. A case-control
study of occupation and breast-cancer risk in Connecticut. J
Cancer Epidemiol Prev. 2002;7:3-11.
165. Teitelbaum SL, Britton JA, Gammon MD, et al. Occupation
and breast cancer in women 20–44 years of age. Cancer Causes
Control. 2003;14:627-37.
166. Hansen J. Breast cancer risk among relatively young women
employed in solvent-using industries. Am J Indust Med. 1999;
36:43-47.
167. Morton WE. Major differences in breast cancer risks among
occupations. J Occup Environ Med. 1995;37:328-335.
168. Coyle B, Polovich M. Handling hazardous drugs: how safe are
you? Am J Nurs. 2004;104(2):104.
169. Watterson A, LaDou J. Health and safety executive inspection
of UK semiconductor manufacturers. Health and Safety Exec-
utive Inspection; 2003;9:392-395.
170. Sigurdson AJ, Morin Doody M, Rao RS, et al. Cancer incidence
in the U.S. Radiologic Technologists Health Study, 1983–1998.
Cancer. 2003;97:3080-3089.
171. Natural Resources Defense Council. Nanotechnology’s invisi-
ble threat: Small science, big consequences [Internet]. 2007
Nov 15. Available from: www.nrdc.org/health/science/nano/
fnano.pdf
172. National Cancer Institute. Surveillance Epidemiology and End
Results. Available at: http://seer.cancer.gov/
173. Centers for Disease Control and Prevention. National Program
of Cancer Registries (NPCR). [Internet]. Available from:
http://www.cdc.gov/CANCER/npcr/
174. National Cancer Institute. Surveillance Epidemiology and End
Results: Population Characteristics. [Internet]. Available from:
http://seer.cancer.gov/registries/characteristics.html
175. National Cancer Institute. Surveillance Epidemiology and End
Results: Number of Persons by Race and Hispanic Ethnicity for
SEER participants (2000 Census Data). [Internet]. Available
from: http://seer.cancer.gov/registries/data.html#a3
176. Miller BA, Chu KC, Hankey BF, et al. Cancer incidence and
mortality patterns among specific Asian and Pacific Islander
populations in the U.S. Cancer Causes Control. 2008;
19:227–256.
177. Miller BA, Kolonel LN, Bernstein L, et al. Racial/ethnic pat-
terns of cancer in the United States 1988–1992. Bethesda, MD:
National Cancer Institute, 199658.
178. Centers for Disease Control and Prevention. National Program
of Cancer Registries (NPCR). United States Cancer Statistics:
2004 Incidence and Mortality. 2007. [Internet]. Available from:
http://www.cdc.gov/cancer/npcr/npcrpdfs/US_Cancer_Sta-
tistics_2004_Incidence_and_Mortality.pdf
179. Clegg LX, Feuer EJ, Midthune DN, Fay MP, Hankey BF. Impact
of reporting delay and reporting error on cancer incidence
rates and trends. J Natl Cancer Inst. 2002;94:1537-45.
180. Centers for Disease Control and Prevention. Managing Ele-
vated Blood Lead Levels Among Young Children: Recommen-
dations from the Advisory Committee on Childhood Lead Poi-
soning Prevention. [Internet]. March 2002. Available from:
http://www.cdc.gov/nceh/lead/CaseManagement/case
Manage_main.htm .
181. Centers for Disease Control and Prevention. National Report
on Human Exposure to Environmental Chemicals. [Internet].
Available from: http://www.cdc.gov/exposurereport/.
182. Centers for Disease Control and Prevention. Press Release: CDC
Releases Extensive Survey of Americans’ Exposure to Environ-
mental Chemicals. [Internet]. July 21, 2005. Available from:
http://www.cdc.gov/od/oc/media/pressrel/r050721.htm.
183. Centers for Disease Control and Prevention. National Environ-
mental Public Health Tracking Program. [Internet]. Available
from: http://www.cdc.gov/nceh/tracking/default.htm.
184. Centers for Disease Control and Prevention. National Environ-
mental Public Health Tracking Funded Programs. [Internet].
Available from: http://www.cdc.gov/nceh/tracking/projects/
home.htm
185. California Environmental Health Tracking Program. Overview
of environmental health tracking [Internet]. 2007 Nov 15.
Available from: www.catracking.com/sub/eht.htm
186. 110th Congress of the United States of America. S. 2082: Coor-
dinated Environmental Public Health Network Act of 2007.
[Internet]. Available from: http://www.thomas.gov/cgi-bin/
query/D?c110:2:./temp/~mdbsIUt6LC::
187. The National Children’s Study. Funding and Legislation.
[Internet]. Available from: http://www.nationalchildrens
study.gov/about/Pages/funding.aspx
188. National Institute of Environmental Health Sciences and
National Cancer Institute. Breast Cancer and the Environment
Research Centers (BCERC). [Internet]. Available from:
http://www.bcerc.org/home.htm
189. 110th Congress of the United States of America. HR 1157:
Breast Cancer and Environmental Research Act of 2008
(Enrolled as Agreed to or Passed by Both House and Senate)
[Internet]. Available from: http://www.govtrack.us/congress/
bill.xpd?bill=h110-1157
190. U.S. Environmental Protection Agency. Endocrine Disruptor
Screening Program. [Internet]. Available from: http://www.
epa.gov/endo/
191. Erickson BE. Tests of endocrine disruptors delayed. Chem
Engr News.2008;86:60-62.
192. California Breast Cancer Research Program. [Internet]. Avail-
able from: http://www.cbcrp.org/.
VOL 15/NO 1, JAN/MAR 2009 • www.ijoeh.com Policy Recommendations: Environment and Breast Cancer • 101