BACKGROUND: Previously, we reported that prenatal exposures to polycyclic aromatic hydrocarbons (PAH) and postnatal environmental tobacco smoke (ETS) in combination were associated with respiratory symptoms at ages 1 and 2 years. Here, we hypothesized that children exposed to both prenatal PAH and ETS may be at greater risk of asthma and seroatopy at ages 5-6 years, after controlling for current pollution exposure. METHODS: Prenatal PAH exposure was measured by personal air monitoring over 48 h. ETS exposure, respiratory symptoms and asthma at ages 5-6 years were assessed through questionnaire. Immunoglobulin (Ig) E was measured by Immunocap. RESULTS: A significant interaction between prenatal PAH and prenatal (but not postnatal) ETS exposure on asthma (p < 0.05), but not IgE, was detected. Among children exposed to prenatal ETS, a positive nonsignificant association was found between prenatal PAH exposure and asthma (OR 1.96, 95% CI [0.95-4.05]). Among children without exposure to prenatal ETS, a negative nonsignificant association was found between prenatal PAH exposure and asthma (OR 0.65, 95% CI [0.41-1.01]). Prenatal PAH exposure was not associated with asthma or IgE at age 5-6 years. CONCLUSIONS: Combined prenatal exposure to PAH and ETS appears to be associated with asthma but not seroatopy at age 5-6. Exposure to PAH alone does not appear associated with either asthma or seroatopy at age 5-6 years. Discerning the differential effects between ETS exposed and ETS nonexposed children requires further study.
BACKGROUND: Previously, we reported that prenatal exposures to polycyclic aromatic hydrocarbons (PAH) and postnatal environmental tobacco smoke (ETS) in combination were associated with respiratory symptoms at ages 1 and 2 years. Here, we hypothesized that children exposed to both prenatal PAH and ETS may be at greater risk of asthma and seroatopy at ages 5-6 years, after controlling for current pollution exposure. METHODS: Prenatal PAH exposure was measured by personal air monitoring over 48 h. ETS exposure, respiratory symptoms and asthma at ages 5-6 years were assessed through questionnaire. Immunoglobulin (Ig) E was measured by Immunocap. RESULTS: A significant interaction between prenatal PAH and prenatal (but not postnatal) ETS exposure on asthma (p < 0.05), but not IgE, was detected. Among children exposed to prenatal ETS, a positive nonsignificant association was found between prenatal PAH exposure and asthma (OR 1.96, 95% CI [0.95-4.05]). Among children without exposure to prenatal ETS, a negative nonsignificant association was found between prenatal PAH exposure and asthma (OR 0.65, 95% CI [0.41-1.01]). Prenatal PAH exposure was not associated with asthma or IgE at age 5-6 years. CONCLUSIONS: Combined prenatal exposure to PAH and ETS appears to be associated with asthma but not seroatopy at age 5-6. Exposure to PAH alone does not appear associated with either asthma or seroatopy at age 5-6 years. Discerning the differential effects between ETS exposed and ETS nonexposed children requires further study.
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