Abstract

Chlorpyrifos (CPF) is a commonly used organophosphate insecticide (OP). In adults, exposure to OPs has been inconsistently associated with reduced lung function. OP exposure and lung function has not been assessed in adolescents. The objective of this study was to assess CPF exposure and lung function among Egyptian adolescents. We conducted a 10-month study of male adolescent pesticide applicators (n = 38) and non-applicators of similar age (n = 24). Urinary 3,5,6-trichloro-2-pyridinol (TPCy), a CPF-specific metabolite, was analyzed in specimens collected throughout the study. Spirometry was performed twice after pesticide application: day 146, when TCPy levels were elevated and day 269, when TCPy levels were near baseline. Applicators had higher levels of TCPy (mean cumulative TCPy day 146 = 33,217.6; standard deviation (SD) = 49,179.3) than non-applicators (mean cumulative TCPy day 146 = 3290.8; SD = 3994.9). Compared with non-applicators, applicators had higher odds of reporting wheeze, odds ratio = 3.41 (95% CI: 0.70; 17.41). Cumulative urinary TCPy was inversely associated with spirometric measurements at day 146, but not at day 269. Although generally non-significant, results were consistent with an inverse association between exposure to CPF and lung function.

Highlights

  • Chlorpyrifos (CPF), an organophosphate insecticide (OP), is one of the most widely used insecticides in the United States and worldwide [1]

  • Percent predicted forced expiratory volume in the first second (FEV1) and percent predicted forced vital capacity (FVC) are the primary lung function parameters we report on

  • While several studies have examined the effects of organophosphates on wheeze [14,15,16] and lung function in adults [3,14,20,21,22,23,25], there is a paucity of information on the respiratory effects of pesticides in children [10] and adolescents [26]

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Summary

Introduction

Chlorpyrifos (CPF), an organophosphate insecticide (OP), is one of the most widely used insecticides in the United States and worldwide [1]. In 2007, CPF was the most commonly used OP in the United States with an estimated 8 to 11 million pounds applied [2]. The classic mode of action for CPF is to inhibit acetylcholinesterase (AChE), resulting in acetylcholine accumulation in the nervous system [3]. The respiratory system is a target for acute OP poisoning [4] via this mode of action. At levels lower than those known to inhibit AChE and through mechanisms other than. AChE inhibition, respiratory effects have been observed in animal studies [5,6,7]. Animal studies have suggested that younger animals are less able to detoxify

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