OP V – 1 Prenatal exposure to organochlorine compounds and lung function until early adulthood

Background/aim Prenatal exposure to organochlorine compounds (OCs) can increase the risk of adverse respiratory symptoms in children and adolescents, but evidence is mainly based on reported symptoms and it is still unknown whether these compounds can impact on lung function. We assessed the longitudinal association between prenatal exposure to OCs and lung function until early adulthood. Methods We included 2750 participants belonging to the INMA (Infancia y Medio Ambiente) prospective birth cohort in Spain in Menorca, Valencia, Gipuzkoa, and Sabadell regions. Prenatal concentrations of OCs (hexachlorobenzene [HCB], dichlorodiphenyltrichloroethane [DDT], dichlorodiphenyldichloroethylene [DDE], and four polychlorinated biphenyls [PCB-118, PCB-138, PCB-153, and PCB-180]) from each participant were measured in maternal or cord serum. Lung function was measured by spirometry at 4, 7, 9, 11, 14, and 18 years of age. Multivariate linear regression models were used to assess the association between prenatal OCs concentrations and lung function. Results High percentage of samples presented quantifiable levels of all the analysed OCs. DDE, HCB, and PCB-153 were the compounds with higher median concentrations (e.g. median for DDE=1.03 ng/mL; Inter quartile range=1.37 ng/mL). Preliminary results in the Menorca cohort (n=327) revealed that prenatal exposure to the second tertile of PCB-153 concentrations was associated with reduced forced vital capacity (FVC) and reduced forced expiratory volume in 1 s (FEV1) when compared to the lowest tertile at 11 and 14 years (e.g. β for FVC at 14 years=-0.17 L; 95% CI: −0.31 to −0.03). Exposure to the second tertile of DDE and PCB-118 was associated with reduced FVC at 11 years, compared to the lowest tertile. No other associations were found. Final results including all cohorts will be presented. Conclusion Preliminary results showed that prenatal exposure to OCs was associated with reduced lung function until adolescence. Such exposure might alter the structural development of the lung and predispose for chronic respiratory diseases later in life.