Assessing early-life human exposure to selected pesticides using urinary biomarkers

Abstract

Pesticides are an important and high use group of chemicals as they increase crop yield in agricultural activities and help control disease spread in public areas. Globally, over 3 billion kilograms of active pesticide ingredients are used per year. The general population may be exposed to these pesticides through dietary ingestion, inhalation, ingestion of dust and soil, and dermal absorption. Pesticide exposure has been linked to numerous adverse health effects, particularly in children who may have additional exposure pathways and metabolise toxicants more slowly and thus are more sensitive to chemical toxicity. Assessing their pesticide exposure and relevant health impact is therefore particularly important. Human biomonitoring using human body fluids is seen as the “gold standard” approach to assess such exposure and risk. Urine is an ideal matrix to investigate recent exposures for currently used pesticides as the majority of them have short half-lives ( 60%) detected in urine samples from Australian and New Zealand children: dialkylphosphate metabolites (DAPs, except for diethyl dithiophosphate (DEDTP)), 3,5,6-trichloro-2-pyridinol (TCPY), para-nitrophenol (PNP), 3-phenoxybenzoic acid, and trans-3-(2,2-dichlorovinyl)-2,2-dimethylcyclopropane-1-carboxylic acid. Urine samples from Australian children also saw a high detection frequency of atrazine mercapturate (ATZ), metabolite of a chlorotriazine herbicide, atrazine. In contrast, detection of ATZ in urine samples from New Zealand children was rare (≤ 2%) but a phenoxyacetic herbicide, 2,4-dichlorophenoxyacetic acid (2,4-D), had a detection frequency of 86%, compared to the Australian study (< 45%). Although comparison between results based on pooled (the Australian study in Chapter 3) and individual (the New Zealand study in Chapter 5) samples should proceed with caution, the above results showed that Australian and New Zealand children share a common exposure of OPs and PYRs but may differ in certain herbicide exposure.Concentrations of DAPs were generally comparable between Australian (0-5 y) and New Zealand children (5-14 y), and were at the lower end compared to other countries. The exception was diethyl thiophosphate (DETP) for Australian pre-schoolers, who had 3 times higher concentration (geometric mean (GM) of 1.8 ng/mL) in urine compared to Japanese peers (~0.6 ng/mL). The other exception was dimethyl phosphate (DMP), for which New Zealand children had a median value of 11 μg/g creatinine, comparable with an existing Australian study on children of the same age but higher than results from other countries such as the US. The profile of DAPs, namely the concentration of ∑DMAP (sum of DMP, dimethyl thiophosphate (DMTP) and dimethyl dithiophosphate (DMDTP)) compared to the one for ∑DEAP (sum of diethyl phosphate (DEP), DETP and DEDTP), were similar between Australia and New Zealand and several other countries such as Canada and Israel. It was however different from some other countries such as Chile and Malaysia, which may reflect the difference in OP use patterns in different countries. The highest level was measured for TCPY, a metabolite for chlorpyrifos, chlorpyrifos-methyl and triclopyr, in both Australian (GM of 9.7 ng/mL urine) and New Zealand (GM of 13 μg/g creatinine) studies. They were generally higher than results from other countries, indicating a prevalent use of and exposure to pesticide products containing the above pesticides in Australia and New Zealand. Although overall exposure risk is low for these pesticides as assessed by calculated daily intake or against Biomonitoring Equivalents, compared to peers in the US, Australian and New Zealand children may have higher exposures to chlorpyrifos/triclopyr and pyrethroids. Biomarker association analysis suggested an important role of permethrin and cypermethrin as sources for pyrethroid exposure for both populations.Age is identified as an important predictor for pesticide exposure but from different directions for children in different ages. Exposure seems to increase following weaning or as a result of increased dietary intake and mobility/activity (0-5 y), and since then, starts decreasing when children are getting older (5-14 y). Girls appear to have elevated concentrations of PNP in urine compared to boys in the 5-14 y group, which may be related to the use of nitrobenzene or PNP itself associated with production of dyes and flavouring agents in cosmetics such as nail polish that girls generally tend to access more than boys.For lifestyle predictors, fruit and vegetable consumptions were found associated with pesticide exposure for children under 3 years but not in the school-age (5-14) group. However, for the school-aged children in New Zealand, urine samples from low spray season had significantly higher concentrations of several biomarkers, which might be associated with consumption of imported fruits and vegetables during this season. Washing fruits and vegetables and hands appear to decrease the exposure to certain pesticides (but not all). Living in rural areas is associated with increased exposure to pyrethroids via pest control practices, whereas children living in urban areas tend to have higher exposure to nitrobenzene or PNP. Having a dog in the home was associated with higher exposure risk to pyrethroids. The exposure risk is further increased for children with a low socioeconomic status.