Maternal exposure to PM2.5 during pregnancy and asthma risk in early childhood: consideration of phases of fetal lung development

Abstract

Background: Increasingly studies suggest prenatal exposure to air pollution may increase risk of childhood asthma. Few studies have investigated exposure during specific fetal pulmonary developmental windows.

Objective: To assess associations between prenatal fine particulate matter exposure and asthma at age 4.

Methods: This study included mother-child dyads from two pregnancy cohorts-CANDLE and TIDES-within the ECHO-PATHWAYS consortium (births in 2007-2013). Three child asthma outcomes were parent-reported: ever asthma, current asthma, and current wheeze. Fine particulate matter (PM_2.5) exposures during the pseudoglandular (5-16 weeks gestation), canalicular (16-24 weeks gestation), saccular (24-36 weeks gestation), and alveolar (36+ weeks gestation) phases of fetal lung development were estimated using a national spatiotemporal model. We estimated associations with Poisson regression with robust standard errors, and adjusted for child, maternal, and neighborhood factors.

Results: Children (n=1469) were on average 4.3 (standard deviation 0.5) years old, 49% were male, and 11.7% had ever asthma; 46% of women identified as black and 53% had at least a college/technical school degree. A 2 μg/m³ higher PM_2.5 exposure during the saccular phase was associated with 1.29 times higher risk of ever asthma (95% CI: 1.06-1.58). A similar association was observed with current asthma (RR 1.27, 95% CI: 1.04-1.54), but not current wheeze (RR 1.11, 95% CI: 0.92-1.33). Effect estimates for associations during other developmental windows had confidence intervals that included the null.

Conclusions: Later phases of prenatal lung development may be particularly sensitive to the developmental toxicity of PM_2.5.

Keywords: Air pollution; Developmental Origins of Health and Disease (DOHaD); PM2.5; child asthma; particulate matter; prenatal.

Figure 1.

Associations between prenatal PM_2.5 exposure during phases of fetal lung development and child asthma at age 4. Risk ratios (95% confidence intervals) per 2 μg/m³ higher PM_2.5 exposure during each window. Fully adjusted models included child age, sex, birth in warm versus cold season, cubic splines for date of birth (1 degree of freedom/year), study site, maternal age, maternal race, maternal education, prepregnancy BMI, prenatal smoking, parity, postnatal secondhand smoke, pets in the home, and Childhood Opportunity Index.

Figure 2.

Sex-specific associations between prenatal PM_2.5 exposure during phases of fetal lung development and child asthma at age 4. Risk ratios (95% confidence intervals) shown for a 2 μg/m³ higher PM_2.5 exposure during each phase of fetal lung development. Models include child age, birth in warm versus cold season, cubic splines for date of birth (1 degree of freedom/year), study site, maternal age, maternal race, maternal education, prepregnancy BMI, prenatal smoking, parity, postnatal secondhand smoke, pets in the home, Childhood Opportunity Index, sex, and a multiplicative interaction term for PM_2.5 by sex. P values are shown for the multiplicative interaction term. No statistically significant effect modification by child sex was observed.

Figure 3.

Effect modification of associations (risk ratios and 95% confidence intervals) between prenatal PM_2.5 exposure during fetal lung developmental windows and child airway outcomes at age 4, by maternal history of asthma. Risk ratios (95% confidence intervals) shown for a 2 μg/m³ higher PM_2.5 exposure during each phase of fetal lung development. Models are adjusted for child age, sex, birth in warm versus cold season, cubic splines for date of birth (1 degree of freedom/year), study site, maternal age, maternal race, maternal education, prepregnancy BMI, prenatal smoking, parity, postnatal secondhand smoke, pets in the home, and Childhood Opportunity Index. P values are shown for the multiplicative interaction term between PM_2.5 and maternal history of asthma.