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

The National Research Council (NRC) report Pesticides in the Diets of Infants and Children concluded that dietary intake represents the major source of pesticide exposure for infants and children, and this exposure may account for the increased pesticide-related health risks in children compared with adults. However, direct quantitative assessment of dietary pesticide exposure in children to support this conclusion is no simple task: Several studies have analyzed pesticides in representative samples of children’s food, and only two have used biologic monitoring to specifically examine dietary exposures. The paucity of exposure data renders the debate over pesticide-related health risks in children controversial. Nevertheless, those studies have provided valuable information on dietary pesticide exposure among children and have prompted the needs to improve research methods in order to better assess children’s exposure to pesticides through dietary intake.

Discussion

Concerns were raised by the NRC regarding the quantitative and qualitative differences in the toxicity of, and the exposure to, pesticides in children, compared with adults. The NRC report recognized that dietary intake of pesticides represents the major source of exposure for infants and children and concluded that the differences in dietary exposure to pesticide residues account for most of the differences in pesticide-related health risks that were found to exist between children and adults.

Dietary pesticide exposure was commonly assessed by collecting duplicate food samples from the study subjects. This method assumes that the pesticide residues measured in the food samples represent the best surrogate measurements for the dietary intake of pesticide residues; however, the correspondence of pesticide residues in the duplicate food samples and the absorbed pesticide dose measured in biologic samples has rarely been determined. The objective of this study was to assess dietary pesticide exposures in individual children by substituting their conventional diets with organic food items. The results from this study should provide the most direct and relevant data for assessing children’s pesticide exposure through dietary intake.

An important aspect of this study was to assure that the study protocol did not alter children’s diets, qualitatively speaking, from their normal consumption patterns. Children may reject organic food items because of taste or appearance and therefore restrict themselves to a rather simple and less diverse diet during the organic diet phase. Consequently, this may confound the results because one cannot determine whether potentially observed differences in dietary pesticide exposures truly result from consuming organic food items and not from changes in children’s diets.

We performed a few trial runs with different children in the same age range before the study to evaluate children’s acceptance of organic versions of the food items they regularly ate. Parents commented about their child’s response and found that most items were acceptable to their children, especially children considered not very selective in food choices. We then determined that it would be vital to recruit children who are considered not very selective about food taste and appearance. According to the food diaries, children consumed approximately two more items of fresh produce (including juices) and wheat/rice/soybean-based food items in the organic diet phase, comparing with the conventional diet phase. This finding indicates that the study protocol did not change children’s regular diet consumption pattern and therefore should not bias the study results.

We conclude that organic diets provide a protective mechanism against OP pesticide exposure in young children whose diets regularly consist of fresh fruits and vegetables, fruit juices, and wheat-containing items. Such protection is dramatic and immediate. This is particularly true for certain OP pesticides, such as chlorpyrifos and malathion, as measured in this study, and is probably true for other OP pesticides such as azinphosmethyl, dimethoate, and acephate, which are registered only for agricultural production. These results are consistent with our previous finding that none of the dialkylphosphate compounds, a group of nonspecific urinary OP pesticide metabolites, were found in one child from a pool of 110 children. The parents of this child reportedly provided exclusively organic produce and did not use any pesticides at home.

Although we did not collect health outcome data in this study, 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. The persistent existence of OP pesticide metabolites in urine during the conventional diet periods raises a concern of the possible chronic exposures to OP pesticides in children. However, caution should be exercised when inferring exposures and health risks solely based on OP urinary metabolite levels. Recent studies have suggested that the OP metabolites can occur as degradates either in food commodities or in the environment, although the amount of metabolites measured represents only a fraction of OP pesticides. The presence of OP pesticide metabolites in foods and in the environment definitely complicates the estimation of absorbed pesticide doses but should not be used to defend a lower likelihood of direct dietary exposure to OP pesticides. If these degradates are absorbed efficiently and excreted unchanged in urine, they could contribute to the total OP metabolite levels. Future researches should be conducted to determine the magnitude of OP pesticide degradation in the environment and in foods, and the pharmacokinetics of those metabolites in humans.

The lack of residential pesticide use as reported by the parents suggests that children in this study were exposed to OP pesticides exclusively from dietary intakes. Recent regulatory changes aiming to reduce exposures in children have banned or restricted the use of many OP pesticides in the residential environment. This policy change no doubt greatly minimizes the OP pesticide exposures from residential use; however, fewer restrictions have been imposed in agriculture. Chlorpyrifos and malathion residues in selected food commodities were regularly detected in selected food commodities as surveyed by annual USDA PDP from 2000 to 2003. These food items were also commonly consumed by the children in this study. Unfortunately, the trend in agricultural use of these OP pesticides was not assessable after 2002 because completely different commodities were monitored in 2003. The trade-off of the heath risks caused by OP pesticide in children by such regulatory change, therefore, is difficult to quantify.

Last, the magnitude of variability associated with urinary OP pesticide metabolite levels measured in this study is rather large, suggesting that the scenario of dietary exposure is sporadic with significant temporal variations. Such variability reflects the combination of the variation of OP pesticide residues found in food items, the probability of consuming those food items, and the relatively short biologic half-lives of the OP pesticides in humans. The pitfall of such large variability is that it may compromise the true association between exposure and the outcome of interest. Despite this inherent variability, statistically significant trends were evident in this study. A study design that incorporates daily repeatable specimen collection over a period of time in consideration of the pharmacokinetics of the nonpersistent pesticides, such as OP pesticides, is preferable. Spot first morning void urine sample has been suggested as the best representative measurement for the daily OP pesticide exposure.

However, such an approach is deemed not sufficient for assessing dietary exposure to OP pesticides or other exposure scenarios in which subjects’ activities, such as dietary consumption patterns, are dynamic in nature. Many first morning void urine samples collected in this study had no detectable OP metabolite levels, whereas the before bedtime urine samples collected the previous day contained detectable metabolite levels. Depending upon the timing of pesticide residue intake with certain meals, first morning void urine samples may not represent true exposures. Considering the burden of study subjects and the cost of sample analysis, collecting before bedtime and first morning void samples for assessing dietary exposure to OP pesticides seems to be the best choice.

Children and their families participating in this study do not reflect the general U.S. population, and therefore no attempt should be made to extend this conclusion to other children. It will be of interest, from the regulatory and public health points of view, to conduct additional studies that include children living in homes where residential pesticide use is common. If not applied according to label instructions, pesticide use in or around households may contribute more exposure to residents, particularly children, than does dietary intake.

Conclusion

We used a novel study design to provide 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. This reduction in exposure was dramatic and immediate for the OP pesticides malathion and chlorpyrifos, which are commonly and predominantly used in agricultural production and have no or minimal residential uses. The findings for the OP pesticide exposure in children from this study therefore support the conclusion made by the NRC that dietary intake of pesticides could represent the major source of exposure in infants and young children.