To start your own free subscription to Rachel's,
send a blank Email to: firstname.lastname@example.org
RACHEL'S ENVIRONMENT & HEALTH NEWS #811
Feb. 17, 2005
Published March 31, 2005
Human Exposure and Health Hazards - Pt. 2
by Anne Steinemann*
Body Burden of Chemicals and Burden of Proof
What are the health effects of all the pollutants in our bodies that
we discussed in Rachel's #810? The magnitudes and multiplicity of
health risks may be impossible to assess fully, because we are dealing
with mixtures of chemicals, non- monotonic dose-response
relationships, cumulative effects, individual susceptibilities, lag
time between exposures and effects, and hundreds of documented and
potential morbidity and mortality effects (NIH, 2003; PSR, 2003). The
complexity of analysis has led to regulatory paralysis, where
chemicals are often assumed safe until proven hazardous, placing a
perhaps insurmountable burden of proof on the public. Nonetheless, we
have another body of evidence:
Rates of diseases with potential links to chemical exposures have been
increasing nationwide. Asthma in children under age five has increased
by 160% (1980-1994)(CDC, 1998). Autism has increased by 1,000% since
the mid-1980s (Chakrabati and Fombonne, 2001; Byrd, 2002).
Hypospadias, a congenital misplacement of the urinary opening in the
penis, has increased by 100% (1968-1993) and now affects one of 125
male babies born (Paulozzi, et al., 1997; Baskin et al., 2001). Cancer
in children has increased by 26% (1975-1999), with sharp increases in
acute lymphocytic leukemia (62%), and brain and nervous system cancers
(50%) (NCI, 2002a). Testicular cancer in young men has increased by
85% (1973-1999), and is now the most common cancer in men ages 15 to
35 (NCI, 2002b). If trends continue, breast cancer would affect 25% of
the granddaughters of today's young women (NCI, 1997). Further,
according to the American Cancer Society, only 5% to 10% of all
cancers can be attributed to inherited factors (ACS, 2001); the rest
occur from environmental exposures and other damage throughout our own
Multiple and complex links between pollutant exposures and health
effects may have obscured perceptions of risk. Exposures do not always
manifest immediate and dramatic health effects; rather, they can cause
subtle, gradual, and often irreversible health damage. And even when
they do cause immediate effects, there is the troubling tendency to
misdiagnose or misattribute common symptoms caused by exposures. For
instance, exposure to pesticides can cause acute symptoms that mimic
the flu, such as fevers, headaches, nausea, joint pain, and
simultaneously cause chronic damage to the endocrine, neurological,
and immune systems (USEPA, 2003; NIH, 2003; Colborn et al., 1993).
Exposures also defy traditional dose-response relationships. Low-level
chemical exposures can produce adverse health effects, even below
regulatory thresholds and "no effects" levels (ASTDR 2003; NAS 2000;
Ashford and Miller, 1998). For instance, chlorinated tap water
byproducts, trihalomethanes, were linked to increased miscarriages at
75 parts per billion (ppb), even though the maximum contaminant level
(MCL) was set at the time at 100 ppb (Waller et al. 1998). The
herbicide atrazine is linked to demasculinization of frogs at levels
as low as 0.1 ppb, even though the MCL is set at 3 ppb (Hayes et al.,
Further, low-level exposures can be more harmful than high-level
exposures of the same pollutant (Schmidt, 2001). Many chemicals, such
as endocrine disruptors, exhibit non-monotonic dose-response
relationships, meaning that the response (such as an adverse health
effect from a chemical exposure) can increase as dose is reduced. One
such chemical is bisphenol A, used in products such as plastic water
bottles and baby bottles. In a series of studies, low-dose exposure to
bisphenol-A caused significant enlargement of the adult prostate
weight of mice exposed in the womb, but high-dose exposure produced
less or no enlargement (vom Saal, et al., 1997; Gupta, 2000).
Thus, we are regularly exposed to hundreds of industrial pollutants,
from everyday products and places, that persist in our bodies and in
the environment, and that are linked to numerous diseases and health
effects. Yet the major sources of these pollutant exposures are not
widely recognized, nor covered by environmental laws.
The Missing Coverage in the Quilt of Laws
Currently, no federal law or agency specifically protects indoor air
environments, which is where we spend more than 90% of our time
(Klepeis, et al. 2001), and which accounts for most of our pollutant
exposures. Instead, federal laws concentrate on outdoor pollution,
usually media-specific or pollutant-specific. Although the laws
address some pieces of indoor air, the responsibilities for those
pieces are scattered among more than 20 federal agencies.
A content analysis of 22 major U.S. environmental laws revealed that
none mentioned "indoor air" (Steinemann, 2004). Further, no regulation
or policy has provided the umbrella coverage needed to address indoor
air or, more generally, human exposures to pollutants, which are
currently greatest in indoor air environments. Nonetheless, several
federal laws have some nexus with indoor air, and could provide the
authority, if exercised.
The Clean Air Act of 1970 (CAA) could provide the U.S. EPA the
authority to address indoor air quality through the regulation of
"ambient air." Yet the original CAA does not define ambient air, and
the EPA has limited its interpretation of ambient air to the
regulation of "outdoor air." Because of this limited interpretation,
the EPA does not currently exercise authority over indoor air
pollution under the CAA. The EPA does, however, indirectly address
indoor air by the regulation of outdoor air, because outdoor air
infiltrates indoors. And the EPA has used its authority under the
National Emission Standards for Hazardous Air Pollutants (NESHAPS) to
ban indoor activities that affect emissions into the atmosphere (such
as the spraying of asbestos insulation).
In 1998, standards were passed (pursuant to the CAA) to regulate
consumer products if they contribute to at least 80% of the VOC
emissions outdoors in areas that violate the National Ambient Air
Quality Standards (NAAQS) for ozone. But these standards exempt some
of the most significant sources of VOC exposures indoors, such as air
fresheners, insecticides, adhesives, and moth-proofing products.
Curiously, air fresheners are exempt if they contain more (rather than
less) toxic constituents -- if they contain at least 98%
paradichlorobenzene or at least 98% naphthalene, or if their VOC
constituents are 100% fragrance materials.
The Toxic Substances Control Act (TSCA) provides the EPA broad
authority to regulate chemicals that present an "unreasonable risk of
injury to health or the environment." Yet "unreasonable risk" is not
defined in TSCA, and it has been difficult for the EPA to develop the
administrative record to meet such a standard, which is a prerequisite
to regulation. The EPA can request data from industry only when it can
provide evidence that their substance may present an unreasonable risk
of injury, or can lead to significant or substantial human exposure,
which the EPA generally cannot prove without such additional data from
industry. Further, the EPA must treat as confidential much of the
industry data submitted under TSCA, further hindering efforts to
protect the public. Thus, until scientists have accumulated a body of
evidence demonstrating potential harm, which often takes decades, a
potentially hazardous chemical can remain on the market (GAO, 1994;
The Consumer Product Safety Commission, through the Consumer Product
Safety Act (CPSA), is directed to protect the public from
"unreasonable risks of injury associated with consumer products," and
thus could regulate consumer products that contribute to indoor air
pollution and exposures. Yet regulation under the Act is constrained
because it relies on voluntary safety standards rather than the
promulgation of standards for protection. Regulation is also
constrained by a cost-benefit analysis for each attempt at standard-
setting by the Commission, and the restrictive definition of a
"consumer product" that excludes several primary sources of exposure,
such as pesticides and cosmetics.
Moreover, Federal laws do not require manufacturers to disclose all of
the ingredients in their products, such as "inert" ingredients in
pesticides, and chemicals in mixtures classified as "trade secrets."
This exclusion is surprising, considering that undisclosed ingredients
often account for more than 95% of the product, and can be even more
toxic than the active ingredients (EPA, 2003). For example, a study of
85 consumer pesticide products found that 72% contained over 95% inert
ingredients, and more than 200 of these inerts were classified as
hazardous pollutants in other federal environmental statutes (NY,
1996). As another example, air "fresheners" containing para-
dichlorobenzene are not required to list the ingredient, even though
it is a registered pesticide and a known rat and mouse carcinogen.
Also surprising, a manufacturer of a fragranced product need only list
"fragrance" on the label, not the actual chemicals, even though more
than 95% of chemicals used in fragrances are known toxics,
sensitizers, and carcinogens (USHR, 1986; Fisher, 1998).
Perhaps the most sweeping federal environmental law, the National
Environmental Policy Act (NEPA), requires an environmental impact
statement (EIS) for federal actions "significantly affecting the
quality of the human environment." Yet in the implementation of NEPA,
impact assessments have focused on impacts to the environment, rather
than impacts on humans. A nationwide and multi-agency study of EISs
(Steinemann, 2000) found that the analysis of human health effects has
been sparse, relegated to another environmental statute, or omitted
entirely. And these EISs were for proposed actions with potentially
significant human health effects, such as pesticide spraying and
The Occupational Safety and Health Act (OSH Act), administered by the
Occupational Safety and Health Administration (OSHA), regulates
occupational environments, but does not protect all employees. For
instance, the OSH Act does not cover federal agency employees, nor
state and municipal government employees unless a state has a plan
approved by the OSHA. Even approved state plans are permitted to
exclude private sector employees. Efforts to establish exposure limits
to toxic substances have generally failed because it is difficult for
OSHA to develop the administrative record to demonstrate a
"significant risk of material health impairment." Also, under the OSH
Act, violations must result in an employee's death in order for the
employer to be subject to criminal sanctions. OSHA has tended to focus
on single hazards within industrial workplaces (such as large
machinery), rather than multiple and often invisible hazards within
typical office buildings (such as formaldehyde off-gassing from
furnishings). And perhaps the largest regulatory gap, the OSH Act
provides no coverage for homes and other non-industrial environments,
where many people work.
More generally, environmental laws tend to focus on emissions, rather
than human exposures -- even though exposures are how pollutants
actually contact the human body and affect health. Our laws have
successfully reduced outdoor emissions, and those efforts should be
continued. But our regulatory lens needs to refocus on total human
exposure, from all media. In this approach, units of human exposure
could replace source emissions as the regulatory "currency" (Wallace,
1991; Smith, 1988).
Thus, our approach to environmental regulation neglects how pollutants
actually reach and affect humans: through exposures (not emissions),
through mixtures of pollutants (rather than isolated pollutants),
through several media (water, air, land, dust, consumer products,
rather than one medium), through several routes (epidermal, ingestion,
inhalation, intergenerational, rather than one route), causing
multiple health effects (such as damage to the immune, neurological,
endocrine, and reproductive systems, in addition to cancer, often the
sole regulatory criterion).
What is a solution? The answer is not just regulatory, but also
scientific, institutional, and educational. The next section discusses
some principles of such an approach.
Reducing Human Exposure: What's Needed
The science of exposure assessment can help us to determine what,
where, and when pollutants come in contact with humans. The handful of
exposure studies, from the EPA TEAM studies through the recent CDC and
EWG studies, have shown that our regulations are missing the major
sources of pollutant exposures and potential health risks. That is,
risks from indoor air pollution, and the consumer products that we
choose, are currently far greater than risks from outdoor air and
sources traditionally regulated.
Paradoxically, the places that we normally consider "safe" (homes,
schools, workplaces, vehicles, public buildings, medical facilities)
and the products that we consider "safe" (because they are widely sold
and used) are precisely the major sources of pollutant exposures. Yet
these sources are virtually unregulated by existing environmental
Fortunately, because many of these exposures are within our control,
we can reduce significant health risks through relatively simple and
cost-effective actions, such using less toxic consumer products and
building materials. Unfortunately, the general public and the medical
community are largely unaware of the major sources of pollutant
exposures, their health effects, and ways to reduce those risks. Thus,
a perilous gap exists between regulation and risk, and between science
and public awareness.
What can be done to bridge these gaps? For one, we should have access
to accurate and complete information about the chemical ingredients in
products, the possible health effects from those chemicals, and the
ways to reduce exposures. This would allow consumers to make more
informed choices about the products they purchase and use, and if they
do use those products, to know how to reduce exposures. This would
also provide the data necessary for more effective regulation and
Another important step would be to require more extensive testing,
labeling, and evaluation of products before being put on the market,
just as currently required for many foods and drugs. As exposure
studies have shown, humans are affected by a wide range of non-food
and non-pharmaceutical chemicals -- chemicals that can cause adverse
health effects and that are contained in common products that
currently receive little or no pre-market testing in the U.S.
We should promote the use and production of safer alternatives to
common products and practices that pose exposure risks. Such
alternatives could provide the same function but with less toxicity,
such as personal care products and laundry supplies without synthetic
fragrances, paints and varnishes that are low-VOC, and pest control
based on integrated pest management rather than synthetic chemical
pesticides. Further, using less toxic products and practices can bring
additional benefits such as improved performance and productivity,
reduced health care costs and liability, and increased profitability.
For instance, estimated savings from reducing indoor exposures exceed
$100 billion annually, with benefits exceeding costs by ten-fold
We should also take advantage of advances in the science and
measurement of exposure; advance that can tell us, with great
accuracy, which pollutants are reaching humans and from where.
Nationwide exposure monitoring programs, much like ambient air and
water monitoring networks currently in place, could provide vital
information on how humans are exposed to environmental pollutants. We
have vast amounts of epidemiological data, suggesting links between
pollutant exposures and illness. To understand and confirm these
links, epidemiology can be supplemented with direct measurements of
physical, chemical, and biological pollutant exposure.
Yet monitoring exposures is only part of the solution. Given that we
have found pollutants in the "wrong places" (e.g., pesticides in human
breast milk), we need to ask ourselves not only how that exposure
occurred, but also why that pollutant is being produced in the first
place. Here, a precautionary approach can be usefully applied
(Wingspread, 1998). We have evidence that humans can be harmed by
substances that are any of the following: persistent, bioaccumulative,
carcinogenic, endocrine disrupting, mutagenic, heavy metals, or toxic
to immune, endocrine, and neurological systems, among other
characteristics. A goal then should be to phase out and significantly
reduce the reliance on these types of substances. And rather than
waiting until a pollutant is emitted and found in the body, and then
trying to assess the resulting harm, we can try to prevent harm in the
first place, using what we already know about human exposures.
I thank Wayne Ott, Lance Wallace, John Roberts, Peter Montague, and
Ann McCampbell for their very helpful reviews of this manuscript. --
* Anne Steinemann holds the title of Professor in the Department of
Civil & Environmental Engineering, and in the School of Public
Affairs, at the University of Washington in Seattle, where she is also
director of the Center for Water and Watershed Studies. This article
is a slightly modified version of "Human exposure, health hazards, and
environmental regulations," Environmental Impact Assessment Review
Vol. 24 (2004), pgs. 695-710.
References for Part 2
(ATSDR) Agency for Toxic Substances and Disease Registry.
Toxicological Profile for Polychlorinated Biphenyls (PCBs).
http://www.atsdr.cdc.gov/toxprofiles/tp17.html accessed September 12,
(ACS) American Cancer Society. Cancer Facts and Figures.
accessed September 12, 2003
Ashford NA, Miller CS. Chemical Exposures: Low Levels and High Stakes.
Van Nostrand Reinhold, New York, 1998.
Baskin LS, Himes L, Colborn T. Hypospadias and Endocrine Disruption:
Is There a Connection? Environmental Health Perspectives,
Byrd RS. The Epidemiology of Autism in California: A Comprehensive
Pilot Study 2002 mindinstitute.ucdmc,ucdavis,edu/news/study_final.pdf
accessed September 12, 2003
(CDC) Centers for Disease Control and Prevention. Forecasted state-
specific estimates of self-reported asthma prevalence -- United
States, MMWR Morb Mortal Wkly Rep. 47:1022-1025. 1998.
Chakrabati S, Fombonne E. Pervasive developmental disorders in
preschool children. JAMA, 285: 3093-9. 2001.
Colborn T, vom Saal FS, Soto, AM, Developmental Effects of Endocrine-
Disrupting Chemicals in Wildlife and Humans, Environmental Health
Perspectives, Vol. 101 No. 5 pgs. 378-384, 1993.
(EPA) U.S. Environmental Protection Agency. Lists of Other (Inert)
Pesticide Ingredients http://www.epa.gov/opprd001/inerts/lists.html
(EPA) U.S. Environmental Protection Agency. Recognition and Management
of Pesticide Poisonings
(EWG) Environmental Working Group. Body Burden: The Pollution in
People. Washington, D.C. http://www.ewg.org/reports/bodyburden 2003
Fisher, BE. Scents and Sensitivities. Environmental Health
Perspectives, 106, A594-A599, November 1998.
Fisk, WJ, Estimates of Potential Nationwide Productivity and Health
Benefits from Better Indoor Environments: An Update, in Spengler, JD,
McCarthy, JF, and Samet, J (eds.), Indoor Air Quality Handbook, New
York: McGraw-Hill, Chapter 4. 2001.
(GAO). Government Accounting Office. Toxic Substances Control Act:
Preliminary Observations on Legislative Changes to Make TSCA More
Effective (GAO/T-RCED-94-263). 1994.
Gupta C. Reproductive malformation of the male offspring following
maternal exposure to estrogenic chemicals. Proceedings of the Society
for Experimental Biology and Medicine 224:61-68. 2000.
Hayes TB, Collins A, Lee M, Mendoza M, Noriega N, Stuart AA, Vonk A.
Hermaphroditic, demasculinized frogs after exposure to the herbicide
atrazine at low ecologically relevant doses. Proc. National Academy of
Science 99: 5476-80. 2002
Klepeis NE, Nelson WC, Ott WR, Robinson JP, Tsang AM, Switzer P,
Behar, JV, Hern, SC, and Engelmann WH. The National Human Activity
Pattern Survey (NHAPS): A Resource for Assessing Exposure to
Environmental Pollutants, Journal of Exposure Analysis and
Environmental Epidemiology, Vol. 11, pp. 231-252. 2001.
(NAS) National Academy of Sciences. Toxicological Effects of
Methylmercury. Washington, DC. National Academy Press. 2000.
(NCI) National Cancer Institute. Female Breast Cancer, SEER Cancer
Statistics Review, 1973-1997.
(NCI) National Cancer Institute. National Cancer Institute Research on
Childhood Cancers. http://cis.nci.nih.gov/fact/6_40.htm 2002a.
(NCI) National Cancer Institute. Surveillance, Epidemiology, End-
Results (SEER) Data Base; cancer of the testis, men ages 15-34.
(NIH) National Institutes of Health. Household Products Database,
Material Safety Data Sheets,
(NY) New York State. The Secret Hazards of Pesticides: Inert
Ingredients, Office of the Attorney General, Environmental Protection
Bureau, February 1996.
Paulozzi, LJ, Erickson JD Jackson RJ. Hypospadias trends in two US
surveillance systems. Pediatrics 100:831-4. 1997.
(PSR) Physicians for Social Responsibility. Bearing the Burden: Health
Implications of Environmental Pollutants in Our Bodies, 2003
Schmidt CW. The Lowdown on Low-Dose Endocrine Disruptors.
Environmental Health Perspectives Volume 109, Number 9, September 2001
Smith, KR. (1988) Air Pollution: Assessing Total Exposure in the
United States, Environment 30:(8)10-38.
Steinemann A. Rethinking Human Health Impact Assessment, Environmental
Impact Assessment Review, 20:627-645, 2000.
Steinemann A. Environmental Laws and Human Exposure, in Ott W. and
Steinemann A. (eds.) Human Exposure Analysis, CRC Press, Boca Raton,
FL, 2004 (draft manuscript available from author).
(USHR) U.S. House of Representatives. Neurotoxins: At Home and the
Workplace, Report by the Committee on Science and Technology, Report
99-827, Sept. 16, 1986.
vom Saal FS, Timms BG, Montano MM, Palanza P, Thayer KA, Nagel SC,
Char MD, Ganjam VK, Parmigiani S, Welshons WV. Prostate enlargement in
mice due to fetal exposure to low doses of estradiol or
diethylstilbestrol and opposite effects at high doses. Proc. Natl Acad
Sci 94: 2056-61. 1997
Wallace LA. Comparison of risks from outdoor and indoor exposure to
toxic chemicals. Environmental Health Perspectives 95:7-13. 1991.
Waller K, Swan SH, DeLorenze G, Hopkins B. Trihalomethanes in drinking
water and spontaneous abortion. Epidemiology 9:134-140, 1998.
(Wingspread) Wingspread Statement on the Precautionary Principle.
Wingspread Conference Center, Racine, Wisconsin, 23-25 January, 1998.
RACHEL'S ENVIRONMENT & HEALTH NEWS
Environmental Research Foundation
P.O. Box 160
New Brunswick, N.J. 08903
Fax (732) 791-4603;
Subscriptions are free. To subscribe, send a blank Email to
The Rachel newsletter is also available free in Spanish; to subscribe,
send a blank Email to email@example.com.
BACK ISSUES IN ENGLISH AND SPANISH
Past issues are on the web at http://www.rachel.org in plain-text and
Permission to reprint Rachel's is hereby granted to everyone, though
we ask that you not change the contents and we ask that you give
In accordance with Title 17 U.S.C. Section 107 this material is
distributed without profit to those who have expressed a prior
interest in receiving it for research and educational purposes.
Some of this material may be copyrighted by others. We believe we are
making "fair use" of the material under Title 17, but if you choose to
use it for your own purposes, you will need to consider "fair use" in
your own case. --Peter Montague, editor