Prenatal fine particulate exposure and early childhood asthma: Effect of maternal stress and fetal sex

Abstract

Background: The impact of prenatal ambient air pollution on child asthma may be modified by maternal stress, child sex, and exposure dose and timing.

Objective: We prospectively examined associations between coexposure to prenatal particulate matter with an aerodynamic diameter of less than 2.5 microns (PM_2.5) and maternal stress and childhood asthma (n = 736).

Methods: Daily PM_2.5 exposure during pregnancy was estimated using a validated satellite-based spatiotemporally resolved prediction model. Prenatal maternal negative life events (NLEs) were dichotomized around the median (high: NLE ≥ 3; low: NLE < 3). We used Bayesian distributed lag interaction models to identify sensitive windows for prenatal PM_2.5 exposure on children's asthma by age 6 years, and determine effect modification by maternal stress and child sex.

Results: Bayesian distributed lag interaction models identified a critical window of exposure (19-23 weeks' gestation, cumulative odds ratio, 1.15; 95% CI, 1.03-1.26; per interquartile range [1.7 μg/m³] increase in prenatal PM_2.5 level) during which children concomitantly exposed to prenatal PM_2.5 and maternal stress had increased risk of asthma. No significant association was seen in children born to women reporting low prenatal stress. When examining modifying effects of prenatal stress and fetal sex, we found that boys born to mothers with higher prenatal stress were most vulnerable (19-21 weeks' gestation; cumulative odds ratio, 1.28; 95% CI, 1.15-1.41; per interquartile range increase in PM_2.5).

Conclusions: Prenatal PM_2.5 exposure during sensitive windows is associated with increased risk of child asthma, especially in boys concurrently exposed to elevated maternal stress.

Keywords: Particulate matter; ambient air pollution; childhood asthma; negative life events; prenatal stress; sex- and temporal-specific effects.

Figure 1. Associations between prenatal PM_2·5 exposure and children’s asthma: interaction by stress

Odds ratios (95% CIs) per IQR (1.7 μg/m³) increase in PM_2·5 estimated by BDLIM demonstrating the relationship of prenatal stress with children’s asthma diagnosed by age 6 years. Models were adjusted for maternal age, race/ethnicity, education, pre-pregnancy obesity, and prenatal/postnatal smoking and child sex. The x-axis demarcates the gestational age in weeks. The y-axis represents the odds ratio (OR) of developing asthma by age 6 years of age in relation to an IQR (1.7 μg/m³) increase in PM_2.5 exposure, assuming week-specific effects. The solid line represents the predicted OR, and the gray area indicates the 95% confidence interval (CI). A sensitive window is identified when the estimated pointwise 95% CI does not include one.

Figure 2. Associations between prenatal PM_2.5 exposure and children’s asthma: interaction by stress and child sex

Odds ratios (95% CIs) per IQR (1.7 μg/m³) increase in PM_2.5 estimated by BDLIM demonstrating the relationship of prenatal PM_2·5, stress and sex with children’s asthma diagnosed by age 6 years. Models were adjusted for maternal age at enrollment, race/ethnicity, education, pre-pregnancy obesity, and prenatal/postnatal smoking and child sex. The x-axis demarcates the gestational age in weeks. The y-axis represents the odds ratio (OR) of developing asthma by age 6 years of age in relation to an IQR (1.7 μg/m³) increase in PM_2.5 exposure, assuming week-specific effects. The solid line represents the predicted OR, and the gray area indicates the 95% confidence interval (CI). A sensitive window is identified when the estimated pointwise 95% CI does not include one.

Figure 3. Cumulative effect (OR of asthma) of PM_2·5 across pregnancy on childhood asthma

Cumulative effect of PM_2.5 across pregnancy on childhood asthma onset estimated by Bayesian distributed lag interaction models, accounting for both sensitive windows and within-window effects. The model was adjusted for maternal age, race/ethnicity, education, pre-pregnancy obesity and prenatal/postnatal smoking and child sex. Maternal stress assessed using Crisis in Family Systems-Revised (CRISYS-R) survey; multi-item survey summarized into a continuous score, which was dichotomized around median to create High (NLE ≥3) versus Low (NLE <3) categories.