O-186 Interaction of Biomarkers of Exposure, Effect, and Susceptibility on Thyroid Disruption in Pesticide Applicators With Primary Exposure to Chlorpyrifos

Introduction Chlorpyrifos, one of the most frequently used agricultural insecticides, has the potential to alter thyroid function. This study aims to analyze the interaction of several biomarkers on thyroid disruption in pesticide applicators with primary exposure to chlorpyrifos. Methods We analyzed data from a total of 151 pesticide applicators aged 18-65 years who were actively using chlorpyrifos for at least 1 year. We performed pathway analysis to examine possible causal models of the determinants of thyroid disruption. Exogenous variables were CYP2B6 and cumulative exposure levels (CEL), while 3,5,6-Trichloro-2-pyridinol (TCPy), acetylcholinesterase (AChE), CEL, Thyroglobulin/FT4 ratio, and thyroid stimulating hormone (TSH) were endogenous variables. CEL and Thyroglobulin/FT4 ratio was tested as the IV for TSH. Results Our path model was fit. CYP2B6*6 has a negative effect on TCPy and CEL has a negative effect on AChE. Thyroglobulin/FT4 ratio (β=0,490; p<0,001) and CEL (β= 0,175; p=0,018) have a positive direct effect on TSH, while the indirect effect of CEL on TSH was 0.279. All of the coefficients were significant at p<0.05 and the path analysis explained the 30.7% variance in participants’ TSH. Discussion CPF exposure affects TSH levels through direct and indirect effects. This situation described in our model raises the opinion that CPF exposure has the potential to disrupt the thyroid through thyroid follicular damage which causes alteration of the process of thyroglobulin and thyroid hormone synthesis. Conclusion TSH concentrations were affected by the interaction of CYP2B6*6 gene polymorphism, TCPy levels, AChE activity, CEL, and thyroglobulin/FT4 ratio, indicating a dose-response relationship in the development of thyroid disruption.