Organic Diets and Children's Health

Referencing: Organic Diets Significantly Lower Children's Dietary Exposure to Organophosphorus Pesticides

In their article "Organic Diets Significantly Lower Children's Dietary Exposure to Organophosphorus Pesticides," Lu et al. (2006) used language that is likely to be misused by organic food marketers to promote high-priced foods and could discourage lower-income parents from providing their children with a diet rich in fruits and vegetables.

Regarding their findings that children's median urinary concentrations of two organophosphorus (OP) pesticides dropped to nondetectable levels within 24-48 hr after switching to an organic diet, Lu et al. (2006) state in the "Abstract" that "an organic diet provides a dramatic and immediate protective effect against exposures" and that these results provide "evidence of the effectiveness of this intervention." Later in their article, they admit that they "did not collect health outcome data in this study," but they claim that

It is intuitive to assume that children whose diets consist of organic food items would have a lower probability of neurologic health risks, a common toxicologic mechanism of the OP pesticide class.

This statement, in particular, seems tailor-made to mislead consumers into believing that organic foods will protect against actual neurologic health risks. A previous article by one of the coauthors presenting similar findings also contains potentially misleading wording (Curl et al. 2003). In the "Abstract," Curl et al. (2003) stated 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 [EPA] current guidelines, thereby shifting exposures from a range of uncertain risk to a range of negligible risk.

Collectively, the wording of both papers strongly implies to consumers and nonspecialists that consuming organic foods reduces likely or actual harm caused by residues of OP pesticides. However, evidence of harm from exposure to the low levels of OP pesticide residues in food is completely lacking in children or adults. Although there is some evidence from animal experiments that in utero exposures to OP pesticides at high enough doses can cause neurodevelopmental effects (Eskenazi et al. 1999), the doses at which such effects were seen were at least three orders of magnitude higher than those consumed as food residues by the children in these two studies (Curl et al. 2003; Lu et al. 2006).

Recent measurements of OP metabolites in the U.S. population by two of the authors of the Lu et al. study (Barr et al. 2005) allowed estimations of doses at the 95th and 50th percentiles of the population for chlorpyrifos (the OP exposure closest to the U.S. EPA reference dose). Barr et al. (2005) estimated that at the 95th percentile, children still consumed less than one-half of the U.S. EPA's chronic population adjusted dose (cPAD), confirming the exposure estimates used in the risk assessment of the Health Effects Division at the U.S. EPA in 2000 (Barr et al. 2005). The cPAD for chlorpyrifos is 1/1,000th of the no observable adverse effect level (NOAEL) in dogs and rats. Thus, children in the 95th percentile consumed < 1/2,000 of the NOAEL, and the median exposure in children was 1/5,000 of the NOAEL.

If it is appropriate to intuitively assume that organic foods pose a lower probability of risk to children, is it not also appropriate to clearly state that all of the risks discussed in these articles are negligible, given that they are tiny fractions of the NOAEL in the most sensitive animal species? It seems that the language chosen by these authors was not appropriate. Already, organic food marketing interests are using these articles as "proof" that organic food is better for you (Organic Consumers Association 2003); Lu et al.'s article is even posted on the Organic Consumers Association website (Organic Consumers Association 2005).

In the future, those of us who communicate with the public on food safety issues should choose our words carefully, not make claims that go beyond the scope of the research, and take the time to accurately place the level of risks being discussed within the context of what is known from animal studies.

The author is employed by the Hudson Institute, a nonprofit organization that has accepted donations from several chemical and pesticide manufacturers over the years, including makers of OP pesticides.

Alex Avery
Center for Global Food Issues
Hudson Institute
Churchville, Virginia
E-mail: aavery@cgfi.org

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Organic Diets: Lu et al. Respond

Avery is concerned that the language used in our recent article (Lu et al. 2005), as well as in an earlier article (Curl et al. 2003), may be used to mislead the public regarding the relative safety of organic foods compared with foods derived from crops treated with pesticides.

We agree that communication of scientific information in general, and health risk information in particular, requires a careful choice of words. However, Avery's analysis misconstrues the current scientific debate regarding children's exposure to pesticides and misrepresents our work, thereby contributing to the public misunderstanding of this important issue.

In fact, we did choose our words carefully, and they reflect the essential findings of our studies. In regard to our earlier publication (Curl et al. 2003), we provided a detailed dose estimation to support our conclusion that consumption of organic fruits, vegetables, and juices in the study population would shift exposure from a range of uncertain risk to a range of negligible risk. In regard to the more recent study (Lu et al. 2005), our data clearly support the conclusion that organophosphorus (OP) pesticide exposures are dramatically reduced when organic foods are substituted for conventional foods. Our statement that children who consume organic foods would likely have a lower probability of neurologic health risks is consistent with current understandings of dose-response relationships. In other words, how could we argue that children with OP pesticide exposures have the same neurologic health risks as children whose urine contain no OP pesticide metabolites?

The assessment of health risks associated with neurotoxic chemicals such as OP pesticides is a complex analysis that includes substantial uncertainty. A child may be exposed to dozens of OP pesticides simultaneously through the diet, as well as through use of these pesticides around the home or in schools. The Food Quality Protection Act (1996) requires the U.S. Environmental Protection Agency to evaluate both children's aggregate exposure (multiple exposure pathways for a single pesticide) and cumulative risk (potential health effects from exposure to multiple compounds that have a common mechanism of toxicity). Thus, current scientific investigations have focused on the relative contributions of specific exposure pathways and have attempted to examine exposure to multiple compounds. Our recent articles provide new information regarding the dietary exposure pathway for several OP pesticides.

Avery's criticism of our work by focusing on a single OP pesticide ignores the central thrust of the Food Quality Protection Act (1996), as well as the scientific advances that have taken place over the past 10 years. We share Avery's concern with the judicious use of language in regard to public communication of pesticide health risks; all of us--including Avery--should follow this advice.

The authors declare they have no competing financial interests.

Chensheng Lu
Rollins School of Public Health
Emory University
Atlanta, Georgia
E-mail: clu2@sph.emory.edu

Kathryn Toepel
Rene Irish
Richard A. Fenske
Department of Environmental and Occupational Health Sciences
University of Washington
Seattle, Washington

Dana B. Barr
Roberto Bravo
National Center for Environmental Health
Centers for Disease Control and Prevention
Atlanta, Georgia

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