Association of Organophosphate Pesticide Exposure and a Marker of Asthma Morbidity in an Agricultural Community

ABSTRACT

Objectives: We explored the short-term impact of pesticide exposure on asthma exacerbation among children with asthma in an agricultural community.

Methods: We obtained repeated urine samples from a subset of 16 school-age children with asthma (n = 139 samples) as part of the Aggravating Factors of Asthma in a Rural Environment (AFARE) study cohort. Biomarkers of organophosphate (OP) pesticide exposure (dialkylphosphates (DAPs)), and asthma exacerbation (leukotriene E4 (uLTE4)) were assessed in urine samples. We used generalized estimating equations to examine the association of summed measures of creatinine-adjusted DAPs (total dimethyl alkylphosphate (EDM), total diethyl alkylphosphate (EDE), and total dialkylphosphate pesticides (EDAP)) and uLTE4 concentration, adjusting for multiple confounders, yielding beta-coefficients with 95% CIs.

Results: A total of 139 observations were obtained from the 16 children over the study period, the total number of samples per subject ranged from 1 to 12 (median: 10.5). The geometric mean (GM) of creatinine-adjusted EDE, EDM, and EDAP in this population were 81.0, 71.8 and 168.0 nmol/g, respectively. Increase in uLTE4 levels was consistently associated with increased exposures to DAPs (interquartile range in μg/g): β_EDE: 8.7 (95%CI: 2.8, 14.6); β_EDM: 1.1 (0.5, 1.7); β_EDAP: 4.1 (0.7, 7.5).

Conclusion: This study suggests that short-term OP exposure is associated with a higher risk of asthma morbidity, as indicated by increased uLTE4 levels in this cohort of children with asthma in an agricultural community. Additional studies are required to confirm these adverse effects, and explore the mechanisms underlying this relationship.

KEYWORDS:

• Organophosphate pesticides
• pediatric asthma
• biomarkers

Disclosure statement

No potential conflict of interest was reported by the authors.

Supplementary material

Supplementary material can be accessed here.

Additional information

Funding

This work was supported by grants from the National Institute of Environmental Health Sciences (NIEHS) K22-ES023815 (PI: Magzamen) and R21-ES17906 (PI: Karr), and from the University of Washington, Center for Exposures, Diseases, Genomics and Environment (National Institutes of Health award number: P30ES007033) .