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      OP Pesticides, Organic Diets, and Children’s Health

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          Abstract

          The importance of “judicious use of language in regard to public communication of pesticide health risks” (Lu et al. 2006b) is clearly recognized and acknowledged in recent letters from Avery (2006) and Lu et al. (2006b). Their correspondence concerned perceptions of risk conveyed by the article “Organic Diets Significantly Lower Children’s Dietary Exposure to Organophosphorous Pesticides,” published by Lu et al. (2006a). My concern is more fundamental than the need for effective communication and the stated “public misunderstanding of this important issue” (Lu et al. 2006b). I believe the primary issue concerns science and how we accumulate knowledge. There is no guarantee that judicious use of language can prevent misunderstanding of even the most rigorous and carefully performed studies. It is important, however, to put the results into the existing scientific and regulatory contexts. Lu et al. (2006a) noted that “the paucity of exposure data renders the debate over pesticide-related health risks in children controversial.” Curl et al. (2003) stated that “reduction of children’s risk from pesticides requires an understanding of the pathways by which exposure occurs.” The primary objective of the longitudinal study by Lu et al. (2006a) was determination of “overall pesticide exposure in a group of elementary school-age children.” The authors reported that children who consumed organic diets eliminated (via urine) nondetectable amounts of organophosphorous (OP) insecticide metabolites. The finding supports the consensus that the diet is the predominant source of OP compounds and OP metabolites excreted in urine (Barr et al. 2004; Duggan et al. 2003; Krieger et al. 2003). Lu et al. (2006a) claimed “a convincing demonstration of the ability of organic diets to reduce children’s OP pesticide exposure and the health risks that may be associated with these exposures.” When the study was developed and throughout the period of data collection, analysis, and publication by the University of Washington investigators, there could be no doubt that dietary exposures were very low or miniscule relative to acute toxicity (Curl et al. 2003). Indeed, it is intuitive that the change in diet reduced OP metabolite elimination in urine. If this were not the case, one might expect parked cars to get speeding tickets. Specific health risks have never been associated with such miniscule insecticide exposures. If risk is defined as the likelihood of an adverse effect in an exposed population, the risk of neurotoxicity caused by these dietary OP exposure(s) is zero; that is, disease has not been observed in the population who consumes food that sometimes contains OP pesticides or OP metabolite residues (Krieger et al. 2003). Back-calculated OP exposures are well below the experimental lowest observed adverse effect level (LOAEL), the estimated no observed adverse effect level (NOAEL), and the regulatory reference dose (RfD) for neurotoxicity of any OP insecticide used in crop protection (Barr et al. 2004; Duggan et al. 2003; Fenske et al. 2000). The research is misrepresented with respect to its relevance to risk reduction (that is the point of the fundamental “observed” in the LOAEL and the NOAEL upon which RfDs are based). With zero cases of disease in the population exposed to dietary OP pesticide, the numerator of measurements of risk such as odds ratios or relative risk is also zero. As a result, measured risk of acute neurotoxicity is zero. The axiomatic truth that “dose determines a poison” and its corollary that “there is a safe level of everything” must both be considered in responsible risk communication. Careful choice of words may sometimes prevent misunderstanding of health research reports, but more importantly our common understanding and well-being require that we clearly distinguish chemical exposure and health risk. Lu et al. (2006a) wrote, We were able to demonstrate that an organic diet provides a dramatic and immediate protective effect against exposure to organophosphorus pesticides that are commonly used in agricultural production. Their findings are expected rather than dramatic, and the term “protective” in reference to a no observed effect exposure is misleading at best. Effective communication requires awareness that potential impacts of conjecture about matters of health and pesticides likely include heightened anxiety and fear, and may prompt misallocation of resources as some persons pursue something less than zero risk—a point where scientific evidence and mystical, supernatural beliefs must be distinguished.

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          Most cited references 8

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          Organic Diets Significantly Lower Children’s Dietary Exposure to Organophosphorus Pesticides

          We used a novel study design to measure dietary organophosphorus pesticide exposure in a group of 23 elementary school-age children through urinary biomonitoring. We substituted most of children’s conventional diets with organic food items for 5 consecutive days and collected two spot daily urine samples, first-morning and before-bedtime voids, throughout the 15-day study period. We found that the median urinary concentrations of the specific metabolites for malathion and chlorpyrifos decreased to the nondetect levels immediately after the introduction of organic diets and remained nondetectable until the conventional diets were reintroduced. The median concentrations for other organophosphorus pesticide metabolites were also lower in the organic diet consumption days; however, the detection of those metabolites was not frequent enough to show any statistical significance. In conclusion, we were able to demonstrate that an organic diet provides a dramatic and immediate protective effect against exposures to organophosphorus pesticides that are commonly used in agricultural production. We also concluded that these children were most likely exposed to these organophosphorus pesticides exclusively through their diet. To our knowledge, this is the first study to employ a longitudinal design with a dietary intervention to assess children’s exposure to pesticides. It provides new and persuasive evidence of the effectiveness of this intervention.
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            Concentrations of dialkyl phosphate metabolites of organophosphorus pesticides in the U.S. population.

            We report population-based concentrations, stratified by age, sex, and racial/ethnic groups, of dialkyl phosphate (DAP) metabolites of multiple organophosphorus pesticides. We measured dimethylphosphate (DMP), dimethylthiophosphate (DMTP), dimethyldithiophosphate (DMDTP), diethylphosphate (DEP), diethylthiophosphate (DETP), and diethyldithiophosphate (DEDTP) concentrations in 1,949 urine samples collected in U.S. residents 6-59 years of age during 1999 and 2000 as a part of the ongoing National Health and Nutrition Examination Survey (NHANES). We detected each DAP metabolite in more than 50% of the samples, with DEP being detected most frequently (71%) at a limit of detection of 0.2 microg/L. The geometric means for the metabolites detected in more than 60% of the samples were 1.85 microg/L for DMTP and 1.04 microg/L for DEP. The 95th percentiles for each metabolite were DMP, 13 microg/L; DMTP, 46 microg/L; DMDTP, 19 micro g/L; DEP, 13 microg/L; DETP, 2.2 microg/L; and DEDTP, 0.87 microg/L. We determined the molar sums of the dimethyl-containing and diethyl-containing metabolites; their geometric mean concentrations were 49.4 and 10.5 nmol/L, respectively, and their 95th percentiles were 583 and 108 nmol/L, respectively. These data are also presented as creatinine-adjusted concentrations. Multivariate analyses showed concentrations of DAPs in children 6-11 years of age that were consistently significantly higher than in adults and often higher than in adolescents. Although the concentrations between sexes and among racial/ethnic groups varied, no significant differences were observed. These data will be important in evaluating the impact of organophosphorus pesticide exposure in the U.S. population and the effectiveness of regulatory actions.
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              Organophosphorus pesticide exposure of urban and suburban preschool children with organic and conventional diets.

              We assessed organophosphorus (OP) pesticide exposure from diet by biological monitoring among Seattle, Washington, preschool children. Parents kept food diaries for 3 days before urine collection, and they distinguished organic and conventional foods based on label information. Children were then classified as having consumed either organic or conventional diets based on analysis of the diary data. Residential pesticide use was also recorded for each home. We collected 24-hr urine samples from 18 children with organic diets and 21 children with conventional diets and analyzed them for five OP pesticide metabolites. We found significantly higher median concentrations of total dimethyl alkylphosphate metabolites than total diethyl alkylphosphate metabolites (0.06 and 0.02 micro mol/L, respectively; p = 0.0001). The median total dimethyl metabolite concentration was approximately six times higher for children with conventional diets than for children with organic diets (0.17 and 0.03 micro mol/L; p = 0.0003); mean concentrations differed by a factor of nine (0.34 and 0.04 micro mol/L). We calculated dose estimates from urinary dimethyl metabolites and from agricultural pesticide use data, assuming that all exposure came from a single pesticide. The dose estimates suggest that consumption of organic fruits, vegetables, and juice can reduce children's exposure levels from above to below the U.S. Environmental Protection Agency's current guidelines, thereby shifting exposures from a range of uncertain risk to a range of negligible risk. Consumption of organic produce appears to provide a relatively simple way for parents to reduce their children's exposure to OP pesticides.
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                Author and article information

                Journal
                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                October 2006
                : 114
                : 10
                : A572
                Affiliations
                Personal Chemical Exposure Program, Department of Entomology, University of California, Riverside, Riverside, California, E-mail: bob.krieger@ 123456ucr.edu
                Author notes

                The authors declare they have no competing financial interests.

                ehp0114-a0572a
                1626419
                17035114
                This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose
                Categories
                Perspectives
                Correspondence

                Public health

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