OBJECTIVES: This study aims to assess workers' lifetime occupational pesticide exposure and examine the relationship with neurobehavioral health.
METHODS: A cross-sectional study was conducted on 158 pesticide-exposed and 176 non-exposed workers. To collect historical exposure and job tasks, a questionnaire and an occupational history interview were used. Pesticide exposure was measured in a subgroup of workers via inhalation and skin contact. The total pesticide intake of each worker was assessed using inhalation and dermal exposure models. CANTAB® computerised neurobehavioral performance assessments were used.
RESULTS: The participants' mean age was 31 (8) years. Pirimiphos-methyl (median = 0.569 mg/m3, Interquartile range [IQR] = 0.151, 0.574) and permethrin (median = 0.136 mg/m3, IQR = 0.116, 0.157) had the highest measured personal inhalation concentrations during thermal spraying. The estimated total lifetime pesticide intake for exposed workers ranged from 0.006 g to 12800 g (median = 379 g and IQR = 131, 794 g). Dermal exposure was the predominant route of pesticide intake for all workers. Compared to controls, workers with high lifetime pesticide intake had lower Match to Sample Visual (adjusted B = -1.4, 95% Confidence Interval (CI) = -2.6, 0.1), Spatial Recognition Memory (adjusted B = -3.3, 95% CI = -5.8, 0.8), Spatial Span (SSP) (adjusted B = -0.6, 95% CI = -0.9, 0.3) scores. Workers with low pesticide intake performed worse than controls (adjusted B = -0.5, 95% CI = -0.8, -0.2) in the SSP test, but scored higher in the Motor Screening test (adjusted B = 0.9, 95% CI = 0.1, 1.6). Higher Paired Associates Learning test scores were observed among higher (adjusted B = 7.4, 95% CI = 2.3, 12.4) and lower (adjusted B = 8.1, 95% CI = 3, 13.2) pesticide intake groups. There was no significant difference between the Reaction Time and Pattern Recognition Memory tests with lifetime pesticide intake after adjusting for confounders.
CONCLUSION: Pesticide exposure has been linked to poorer neurobehavioral performance. As dermal exposure accounts for a major fraction of total intake, pesticide prevention should focus on limiting dermal exposure.
OBJECTIVE: To evaluate the genotoxic risk among children who exposed to pesticides and measure DNA damage due to pesticides exposure.
METHODS: In a cross-sectional study 180 Orang Asli Mah Meri children aged between 7 and 12 years were studied. They were all living in an agricultural island in Kuala Langat, Selangor, Malaysia. The data for this study were collected via modified validated questionnaire and food frequency questionnaire, which consisted of 131 food items. 6 urinary organophosphate metabolites were used as biomarkers for pesticides exposure. For genotoxic risk or genetic damage assessment, the level of DNA damage from exfoliated buccal mucosa cells was measured using the comet assay electrophoresis method.
RESULTS: Out of 180 respondents, 84 (46.7%) showed positive traces of organophosphate metabolites in their urine. Children with detectable urinary pesticide had a longer tail length (median 43.5; IQR 30.9 to 68.1 μm) than those with undetectable urinary pesticides (median 24.7; IQR 9.5 to 48.1 μm). There was a significant association between the extent of DNA damage and the children's age, length of residence in the area, pesticides detection, and frequency of apple consumption.
CONCLUSION: The organophosphate genotoxicity among children is associated with the amount of exposure (detectability of urinary pesticide) and length of residence in (exposure) the study area.