Pesticide Exposure Reduce
Why reducing pesticide exposure is smart
The more that scientists learn about the toxicity of pesticides, the more questions are raised about the potential toxic effects on people. Pesticide manufacturers often portray these unresolved scientific issues, and the uncertainty that comes with them, as safety. Statements like, "there is no conclusive evidence of harm to humans" from exposure to pesticide X are intended to mislead the public into believing that exposures to pesticides and toxic chemicals are without appreciable risks. This is not true. Absence of knowledge is not proof of safety.
There are two chief reasons why it is so difficult to link human harm conclusively to toxic chemicals.
First, most safety tests done for regulatory agencies are not designed to discover whether the low dose exposures to pesticide and chemical mixtures that we all experience are safe, particularly during critical periods of development. In general, the government demands, and companies conduct, high dose studies designed to find gross, obvious toxic effects. In the absence of the appropriate tests at lower doses, pesticide and chemical manufacturers claim safety because no harm at low doses has been conclusively demonstrated (or even studied). Second, because people are contaminated with trace levels of literally hundreds of chemicals, it is generally impossible to attribute a specific health effect to any one of them. There are several worrisome exceptions, however, including chemicals like PCBs and lead, where low doses at critical periods of development have been shown to have significant permanent adverse effects on learning and behavior (CDC 2001, CDC 2003, EWG 2003, ATSDR 1999, ATSDR 2000).
Beyond the narrow confines of regulatory agencies, independent research scientists are beginning to understand the subtle ways in which small doses of pesticides during critical periods of fetal development and childhood can have long lasting adverse effects on people. It is well established that the fetus, infant and small child are typically most vulnerable to the toxic effects of pesticides and toxic chemicals (NRC 1993, EPA 2003, FSA 2003). The metabolism, physiology and biochemistry of a fetus, infant or child is fundamentally different than an adult. A host of vital organ systems continue to grow and mature from conception throughout childhood. At critical periods of developmental change, these systems are susceptible to the toxic effects of pesticides and toxic chemicals, both individually, and in mixtures. Many organ systems, for example the nervous system and brain, can be permanently, if subtly damaged by exposure to toxic substances in-utero or throughout early childhood that, at the same level, cause no measurable harm to adults (Jacobson 1996, CDC 1997, NRC 2000)
The endocrine (hormone) system is perhaps even more sensitive to toxic exposure than the nervous system, and over the past decade, enormous effort has been put into the study of how pesticides and toxic chemicals interfere with normal endocrine signaling and function. A significant body of research in animals now shows that ultra-low doses of pesticides and toxic chemicals on critical days of development can cause changes in hormone function and effects on organ development and function that often only appear later in life. A growing number of these studies show that low doses at a susceptible moment of development can cause more of an effect than high doses (vom Saal 1997, Alworth 2002, Hayes 2003). This is particularly relevant to childhood and fetal exposures via food and water where the timing of the exposure is at least as important as the dose.
Many pesticides are now considered "endocrine disrupters", in part because the term is something of a catch phrase for chemicals that cause a variety of changes in normal hormone signaling. Some better known examples of highly toxic endocrine disrupting pesticides are DDT (and its metabolite DDE) which are now known to exhibit much of their toxicity through anti-androgenic (de-masculinizing) properties (ATSDR 2002), vinclozolin, a heavily used fungicide that is also anti-androgenic (EPA 2000), endosulfan, a DDT relative with estrogenic properties that is found more often in food than any other pesticide (EPA 2002, USDA 1994-2001), and atrazine, a weed killer with broad hormonal activity, that contaminates the drinking water of about 20 million people in the United States (EWG 1999, EWG 1995).
Today scientists know much more about how pesticides can change critical hormone signals in the human body in ways that can have potential life changing effects. Yet in spite of these advances, there is little agreement on how much endocrine disruption is too much, and how much is without harm. The same is true of immune system effects and to a lesser degree effects on the developing nervous system.
As science advances, public health and environmental officials are faced with growing knowledge about the hazards of pesticides, but uncertainty about precise mechanisms and nature of the adverse effects. This conundrum is straining a regulatory system that has become overly dependent on scientific certainty when certainty is increasingly difficult, and even impossible to achieve.
Rather than preventing exposures and putting the burden of proving safety where it belongs, on pesticide and toxic chemical producers, most pesticides remain on the market with no threat of regulatory action. EPA is increasingly mired in complex and arcane scientific arguments, mostly generated by chemical companies, that serve primarily as delaying tactics to keep pesticides and toxic chemicals in the marketplace. With no end in sight to this stalemate, the consumer is wise to minimize exposure to pesticides whenever possible.
Doesn't the government regulate these chemicals?
Yes, but far too slowly. Further, it's important to remember that the government said that highly toxic pesticides like DDT, chlordane, dursban and others were safe right up to the day the EPA banned them.
The EPA is in the process of upgrading pesticide safety standards to comply with a 1996 law (The Food Quality Protection Act) that requires protection of infants and children from pesticides. Several highly toxic pesticides have been banned or restricted under the law, but many have either escaped controls, or have not yet been subjected to them. Pesticide makers, food companies and agribusiness groups are fighting strict application of the statute, and so far have succeeded in weakening several key provisions.
Even the best application of the 1996 law will not protect the public from the combined effect of multiple pesticides. Although a handful of the most dangerous pesticides have been removed from the food supply in recent years, overall, the use of pesticides has remained steady. Once you see the results of the FoodNews Computer, you'll see that multiple exposures are daily events. If you eat in this country, you eat pesticides.
Are these chemicals bad for me?
Pesticides are toxic by design. They kill bugs, weeds, fungi, rodents and other "pests." That's why the government regulates them--though not stringently enough. The risks you encounter when you eat them depend on a number of factors including the toxicity of the pesticide, degree and form of exposure, your age, genetic susceptibility, and exposure to other toxics, including other pesticides. We believe that:
1. You have a right to know what's in your food.
2. The risks from many of these contaminants are unacceptably high, especially for infants and children
3. The government can and should take steps to eliminate toxic chemicals, including pesticides, from the food supply.
Alworth, LC., Howdeshell, KL., Ruhlen, RL., Day, JK., Lubahn, DB., Huang, TH., Besch-Williford, CL and vom Saal, FS. 2002. Uterine responsiveness to estradiol and DNA methylation are altered by fetal exposure to diethylstilbestrol and methoxychlor in CD-1 mice: effects of low versus high doses. Toxicol Appl Pharmacol 183 (1): 10-22.
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ATSDR (Agency for Toxic Substances and Disease Registry). 2003. Toxicological profile for DDT, DDE, and DDD (CASRN DDT 50-29-3, DDE 72-55-9, DDD 72-54-8). Available online at
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EPA (Environmental Protection Agency). 2000. Reregistration eligibility decision for vinclozalin. Office of Prevention, Pesticides and Toxic Substances (OPPTS) EPA 738-R-00-023. Available online at
EPA (Environmental Protection Agency). 2002. Reregistration eligibility decision for endosulfan. Office of Prevention, Pesticides and Toxic Substances (OPPTS) EPA 738-R-02-013. Available online at
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EWG (Environmental Working Group). 1999. Into the Mouth of Babes.
EWG (Environmental Working Group). 2003. BodyBurden: The Pollution in People. Available online at
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Hayes, T., Haston, K., Tsui, M., Hoang, A., Haeffele, C and Vonk, A. 2003. Atrazine-induced hermaphroditism at 0.1 ppb in American Leopard Frogs (Rana pipiens): laboratory and field evidence. Environ Health Perspect 111 (4): 568-75.
Jacobson, JL and Jacobson, SW. 1996. Intellectual impairment in children exposed to polychlorinated biphenyls in utero. N Engl J Med 335 (11): 783-9.
NRC (National Research Council). 2000. Toxicological Effects of Methylmercury. Washington DC, National Academy Press. Available online at
NRC (National Research Council). 1993. Pesticides in the Diets of Infants and Children. National Academy Press, Washington DC. Available online at
USDA (U.S. Department of Agriculture). 1994-2001. Pesticide Data Program.
vom Saal, FS., Timms, BG., Montano, MM., Palanza, P., Thayer, KA., Nagel, SC., Dhar, MD., Ganjam, VK., Parmigiani, S and Welshons, WV. 1997. 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 U S A 94 (5): 2056-61.