Pesticide exposures and children's risk tradeoffs.
Curl et al. (2003) stated that consumption of organic produce shifts children's OP exposures "from a range of uncertain risk to a range of negligible risk." Actually, consumption of organic produce shifts children from a range of almost certainly negligible risk due to potential OP exposures to a range of uncertain risk due to fungal toxins and plant stress-mediated increases in allergens (Midoro-Horiuti et al. 2001) and naturally occurring plant toxins (Beier and Nigg 1994; Wood 1979). Plants use complex chemistry to defend themselves from insects, fungi, viruses, bacteria, and larger herbivores. The need for natural chemical defenses is particularly critical for organically grown produce, which is not otherwise defended by synthetic chemicals. In fact, when plants have to devote more energy to self-defense, they have less energy to devote to nutrient content (e.g., Ojimelukwe et al. 1999).
There are admittedly few reports that directly contrast the levels of natural plant pesticides in organic and nonorganic produce. One example is organically grown parsnips, which have more than twice the levels of genotoxic furocoumarins (also present in carrots, celery, and oranges) than conventional parsnips (Mongeau et al. 1994).
The concentrations of furocoumarins in both conventional and organic parsnips are three orders of magnitude higher than the concentrations of synthetic pesticides (U.S. Department of Agriculture 2000). Another example is the use of fungicides on wheat, which reduces the level of mycotoxins to about one-third that found in untreated wheat (Hicks et al. 1999). Although the relationship between crop protection and decreased natural toxicant levels is largely inferential, there is a large literature documenting the relationship between crop stress and increased levels of plant toxicants (Mattsson 2000 and references cited therein). A particularly well-documented example is the response of potatoes to stress and infection by elevating glycoalkaloid concentrations (Kuc 1973). The toxic properties of glycoalkaloids include anticholinesterase activity, nausea, diarrhea, abdominal pain, and death in humans (Friedman and McDonald 1997) and birth defects and increased fetal mortality in laboratory animals (Friedman et al. 2003; Garfield and Keeler 1996). When produce is grown organically, it is subject to greater stress from pests than when it is grown with synthetic pesticides.
OP and other anthropogenic pesticides have been subjected to extensive toxicologic testing to meet the U.S. Environmental Protection Agency's requirements for registration. Naturally occurring chemical pesticides are not systematically tested for toxic effects. Those natural pesticides that have been tested are just as capable of producing toxicity in laboratory animals under experimental conditions as are anthropogenic pesticides. To be registered, the risks from anthropogenic pesticide products are well characterized and limited to negligible levels by law. The risks from naturally occurring chemical pesticides are seldom characterized or limited by law. A 1996 National Academy of Sciences report concluded that "... natural components of the diet may prove to be of greater concern than synthetic components ..." (National Academy of Sciences/National Research Council 1996).
Most risk decisions involve tradeoffs. It is often the case that reducing one risk increases another. In Curl et al.'s example (Curl et al. 2003), reducing one fairly well-characterized risk most likely increases another fairly well-uncharacterized risk, pointing out an important problem that is receiving inadequate attention. There is a clear need to investigate and characterize the risk tradeoffs associated with the use or omission of synthetic pesticides.
The author declares she has no conflict of interest.
Beier RC, Nigg HN. 1994. Toxicology of naturally occurring chemicals in food. In: Foodborne Disease Handbook, Vol 3 (Hui YH, Gotham JR, Murrell KD, Cliver DO, eds). New York:Marcel Dekker Inc., 1-186.
Curl CL, Fenske RA, Elgethun K. 2003. Organophosphorus pesticide exposure of urban and suburban preschool children with organic and conventional diets. Environ Health Perspect 111:377-382.
Friedman M, Henika PR, Mackey BE. 2003. Effect of feeding solanidine, solasodine and tomatidine to non-pregnant and pregnant mice. Food Chem Toxico141:61-71.
Friedman M, McDonald GM. 1997. Potato glycoalkaloids chemistry analysis, safety and plant physiology. Crit Rev Plant Sci 16(1):55-132.
Gaffield W, Keeler RF. 1996. Induction of terata in hamsters by Solanidane alkaloids derived from Solanum tuberosum. Chem Res Toxicol 9:426-433.
Hicks LR, Brown DR, Storch RH, Bushway RJ. 1999. Relative developmental risks of Fusarium mycotoxin, deoxynivalenol (DON) and benomyl (BEN)in wheat. Toxicologist 48:339.
Kuc JA. 1973. Metabolites accumulating in potato tubers following infection and stress. Teratology 8:333-338.
Mattsson JL. 2000. Do pesticides reduce our total exposure to food borne toxicants? Neurotoxicology 21(1-2):195-202.
Midoro-Horiuti T, Brooks EG, Goldblum RM. 2001. Pathogenesis-related proteins of plants as allergens. Ann Allergy Asthma Immuno187:261-271.
Mongeau R, Brassard R, Cerkauskas R, Chiba M, Lok E, Nera EA, et al. 1994. Effect of addition of dried healthy or diseased parsnip root tissue to a modified AIN-76A diet on cell proliferation and histopathology in the liver, oesophagus and forestomach of male Swiss Webster mice. Food Chem Toxicol 32(3):265-271.
National Academy of Sciences/National Research Council. 1996. Carcinogens and Anticarcinogens in the Human Diet. Washington, DC:National Academy Press.
0jimelukwe PC, Onweluzo JC, Okechukwa E. 1999. Effects of infestation on the nutrient content and physiochemical properties of two cowpea (Vigna unguiculata) varieties. Plant Foods Hum Nutr 53(4):321-332,
U.S. Department of Agriculture. 2000. Pesticide Data Program. Available: http://wwvv.ams.usda.gov/science/ pdp/download.htm [accessed 16 June 2003].
Wood GE. 1979. Stress metabolites of plants--a growing concern. J Food Protect 42(6):496-501.
Society for Risk Analysis Washington, DC E-mail: firstname.lastname@example.org
|Printer friendly Cite/link Email Feedback|
|Publication:||Environmental Health Perspectives|
|Date:||Oct 1, 2003|
|Previous Article:||Preformed biomarkers in produce inflate human organophosphate exposure assessments.|
|Next Article:||Organophosphate exposure: "response to Krieger et al. and Charnley.|