Prenatal ambient air exposure to polycyclic aromatic hydrocarbons and the occurrence of respiratory symptoms over the first year of life.

The purpose of the study was to test the hypothesis that infants with higher levels of prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) from fossil fuel combustion may be at greater risk of developing respiratory symptoms. The study was carried out in a cohort of 333 newborns in Krakow, Poland, followed over the first year of life, for whom data from prenatal personal air monitoring of mothers in the second trimester of pregnancy were available. The relative risks of respiratory symptoms due to prenatal PAHs exposure were adjusted for potential confounders (gender of child, birth weight, maternal atopy, maternal education as a proxy for the socio-economic status, exposure to postnatal environmental tobacco smoke, and moulds in households) in the Poisson regression models. Increased risk related to prenatal PAH exposure was observed for various respiratory symptoms such as barking cough (RR = 4.80; 95% CI: 2.73–8.44), wheezing without cold (RR = 3.83; 95% CI: 1.18–12.43), sore throat (RR = 1.96; 95% CI: 1.38–2.78), ear infection (RR = 1.82; 95% CI: 1.03–3.23), cough irrespective of respiratory infections (RR=1.27; 95% CI: 1.07–1.52), and cough without cold (RR = 1.72; 95% CI: 1.02–2.92). The exposure to PAHs also had impact on the duration of respiratory symptoms. The effect of PAHs exposure on the occurrence of such symptoms as runny nose or cough was partly modified by the simultaneous exposure to postnatal passive smoking. The analysis performed for the duration of respiratory symptoms confirmed significant interaction between PAHs exposure and postnatal ETS for runny or stuffy nose (RR = 1.82; 95% CI: 1.57–2.10), cough (RR = 1.18; 95% CI: 0.99–1.40), difficulty in breathing (RR = 1.39; 95% CI: 1.01–1.92) and sore throat (RR = 1.74; 1.26–2.39). Obtained results support the hypothesis that prenatal exposure to immunotoxic PAHs may impair the immune function of the fetus and subsequently may be responsible for an increased susceptibility of newborns and young infants to respiratory infections.

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