Prenatal particulate air pollution and newborn telomere length: Effect modification by maternal antioxidant intakes and infant sex

摘要

Background: Evidence links gestational exposure to particulate matter with an aerodynamic diameter of less than 2.5 μm (PM_(2.5)) with changes in leukocyte telomere length in cord blood with some studies showing sex-specific effects. PM_(2.5) exposure in utero increases oxidative stress, which can impact telomere biology. Thus, maternal antioxidant intakes may also modify the particulate air pollution effects. Methods: We examined associations among prenatal PM_(2.5) exposure and newborn relative leukocyte telomere length (rLTL), and the modifying effects of maternal antioxidant intake and infant sex. We estimated daily PM_(2.5) exposures over gestation using a validated spatiotemporally resolved satellite-based model. Maternal dietary and supplemental antioxidant intakes over the prior three months were ascertained during the second trimester using the modified Block98 food frequency questionnaire; high and low antioxidant intakes were categorized based on a median split. We employed Bayesian distributed lag interaction models (BDLIMs) to identify both sensitive windows of exposure and cumulative effect estimates for prenatal PM_(2.5) exposure on newborn rLTL, and to examine effect modification by maternal antioxidant intakes. A 3-way interaction between PM_(2.5) maternal antioxidant intake and infant sex was also explored. Results: For the main effect of PM_(2.5), BDLIMs identified a sensitive window at 12-20 weeks gestation for the association between increased prenatal PM_(2.5) exposure and shorter newborn rLTL and a cumulative effect of PM_(2.5) over gestation on newborn telomere length [cumulative effect estimate (CEE) = -0.29 (95% CI -0.49 to -0.10) per 1μg/m~3 increase in PM_(2.5)]. In models examining maternal antioxidant intake effects, BDLIMs found that children born to mothers reporting low antioxidant intakes were most vulnerable [CEE of low maternal antioxidant intake = -0.31 (95% CI -0.55 to -0.06) vs high maternal antioxidant intake = -0.07 (95% CI -0.34 to 0.17) per 1μg/m~3 increase in PM_(2.5)]. In exploratory models examining effect modification by both maternal antioxidant intakes and infant sex, the cumulative effect remained significant only in boys whose mothers reported low antioxidant intakes [CEE = - 0.38 (95% CI -0.80 to - 0.004)]; no sensitive windows were identified in any group. Conclusions: Prenatal PM_(2.5) exposure in mid-gestation was associated with reduced infant telomere length. Higher maternal antioxidant intakes mitigated these effects.