Prenatal fine particulate exposure associated with reduced childhood lung function and nasal epithelia GSTP1 hypermethylation: Sex-specific effects

Abstract

BackgroundIn utero exposure to particulate matter with an aerodynamic diameter of less than 2.5 μm (PM2.5) has been linked to child lung function. Overlapping evidence suggests that child sex and exposure timing may modify effects and associations may be mediated through glutathione S-transferase P1 (GSTP1) methylation.MethodsWe prospectively examined associations among prenatal PM2.5 exposure and child lung function and GSTP1 methylation in an urban pregnancy cohort study. We employed a validated satellite-based spatiotemporally resolved prediction model to estimate daily prenatal PM2.5 exposure over gestation. We used Baysian distributed lag interaction models (BDLIMs) to identify sensitive windows for prenatal PM2.5 exposure on child lung function and nasal epithelia GSTP1 methylation at age 7 years, and to examine effect modification by child sex.ResultsBDLIMs identified a sensitive window for prenatal PM2.5 exposure at 35–40 weeks gestation [cumulative effect estimate (CEE) = − 0.10, 95%CI = − 0.19 to − 0.01, per μg/m3 increase in PM2.5] and at 36–40 weeks (CEE = − 0.12, 95%CI = − 0.20 to − 0.01) on FEV1 and FVC, respectively, in boys. BDLIMs also identified a sensitive window of exposure at 37–40 weeks gestation between higher prenatal PM2.5 exposure and increased GSTP1 percent methylation. The association between higher GSTP1 percent methylation and decreased FEV1 was borderline significant in the sample as a whole (β = − 0.37, SE = 0.20, p = 0.06) and in boys in stratified analyses (β = − 0.56, SE = 0.29, p = 0.05).ConclusionsPrenatal PM2.5 exposure in late pregnancy was associated with impaired early childhood lung function and hypermethylation of GSTPI in DNA isolated from nasal epithelial cells. There was a trend towards higher GSTP1 percent methylation being associated with reduced FEV1. All findings were most evident among boys.

Why Do Intrauterine Exposure to Air Pollution and Cigarette Smoke Increase the Risk of Asthma?

“…Oxidative stress induces adverse effects in tissues. The developing fetus is highly vulnerable to oxidative stress injury, as the immune system remains immature during the prenatal period (Lee A. G. et al, 2018). Free radicals and chemicals inhaled during MSE and maternal PM exposure can pass the blood-placental barrier to directly increase the level of oxidative stress in the offspring.…”

Impact on lung function among children exposed to home new surface materials: The seven Northeastern Cities Study in China

“…For example, in the present study, the time spent for outdoor exercise was significantly higher in males (7.9 ± 7.6 hours) than that in females (7.3 ± 7.9 hours), which, due to time‐activity patterns, may affect the lung function development. However, some other studies found that males were more vulnerable to environmental factors . Therefore, the effects of genders as a modifier on the association between home renovation exposure and lung function are still unclear, and further studies are required to determine the cause of such differences.…”

“…However, some other studies found that males were more vulnerable to environmental factors. [34][35][36] Therefore, the effects of genders as a modifier on the association between home renovation exposure and lung function are still unclear, and further studies are required to determine the cause of such differences.…”

Environmentally Induced Epigenetic Plasticity in Development: Epigenetic Toxicity and Epigenetic Adaptation

“…For example, Kaushal et al reported that prenatal arsenic exposure leads to the changes of five CpGs methylation in cord blood which were in the pathways related to cardiovascular diseases; also, the changed DNA methylation was associated with low-density lipoprotein of the children at the age of 2 to 14 years [30]. Additionally, prenatal particulate matter (PM) 2.5 exposure was associated with hypermethylation of children’s nasal epithelia glutathione S-transferase P1 ( GSTP1 ) gene that is also inversely associated with reduced children’s lung function in early childhood [56]. Although these evidence may suggest potential epigenetic toxicity of environmental exposures on the health later in life, they are powerless to illustrate if the environmentally induced epigenetic changes early in life are stable and functional until the occurrence of health events later in life, and vice versa.…”