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.

This study was designed to determine whether dialkylphosphates (DAPs) are present in fresh fruit juices, as a result of organophosphorus (OP) pesticides degradation. Fresh conventional and organic fruit (apple and orange) juices were purchased from local grocery stores. DAPs were found in both conventional and organic juices, and the original levels were higher, for both apple and orange juices, in conventional than in organic juices. Additional DAPs were found in OP pesticide fortified juices after 72 h of storage at 4 degrees C, suggesting a degradation of OP pesticides in juices. Overall, 12% and 36.2% of fortified azinphosmethyl, a dimethyl OP pesticide, and the combination of fortified diazinon and chlorpyrifos, both diethyl OP pesticides, were degraded to dimethyl and diethyl DAPs, respectively. Although the exact mechanism of the degradation is unknown, hydrolysis is likely the cause of OP pesticide degradation in juice. The presence of DAPs in fresh fruit juices clouds the validity of using urinary DAP measurements for estimating OP pesticide exposures in humans, particularly in children. The overestimated OP pesticide exposures based on urinary DAPs reported in other studies is likely due to the coexistence of preformed DAPs and DAPs resulting from OP pesticide exposures. Thus, before urinary DAP concentrations can be reliably used in exposure and risk assessment, the proportion of the concentration attributable to environmental DAP exposure, particularly through the diet, must be ascertained. In conclusion, urinary DAPs have many limitations when being used as biomarkers for OP pesticides in exposure and risk assessment, and caution should be exercised when interpreting DAPs results.

Alternative biological monitoring methods are currently being pursued to better quantify pesticide exposures. In this study, the feasibility of using saliva as a tool for measuring diazinon exposure was determined in an animal model. Male Spraque-Dawley rats were dosed with 1 or 10 mg/kg diazinon by bolus intravenous injection. Time-matched saliva and arterial blood samples were collected from 10 to 250 min post administration. Diazinon was distributed and eliminated rapidly in rats following intravenous (iv) bolus injection, according to a two-compartmental pharmacokinetic analysis. Salivary concentration of diazinon showed a strong correlation with plasma concentration of diazinon. The saliva/plasma (S/P) concentration ratio of diazinon was not affected by administered dose, sampling time, or salivary flow rate, suggesting that salivary excretion of diazinon in rats is fairly constant. Diazinon concentrations in saliva were consistently lower than those in arterial plasma. The mean S/P concentration ratios of diazinon were 0.16 and 0.13 for 1 and 10 mg/kg iv bolus doses, respectively. It is most likely that the incomplete transfer of diazinon from plasma to saliva is due to protein binding of diazinon in plasma. If the protein-unbound fraction of diazinon in plasma is used to calculate the S/P ratio, the S/P concentration ratio of diazinon is close to unity. The results from this study support the conclusion that diazinon salivary concentrations not only can be used to predict the plasma levels of diazinon in rats, but also reflect the unbound fraction of diazinon in plasma.

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