Dataset Information

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

ABSTRACT: 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. To assess associations between prenatal fine particulate matter exposure and asthma at age 4. 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 (PM2.5) 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. 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 PM2.5 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. Later phases of prenatal lung development may be particularly sensitive to the developmental toxicity of PM2.5.

SUBMITTER: Hazlehurst MF

PROVIDER: S-EPMC7943175 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Maternal exposure to PM<sub>2.5</sub> during pregnancy and asthma risk in early childhood: consideration of phases of fetal lung development.

Hazlehurst Marnie F MF Carroll Kecia N KN Loftus Christine T CT Szpiro Adam A AA Moore Paul E PE Kaufman Joel D JD Kirwa Kipruto K LeWinn Kaja Z KZ Bush Nicole R NR Sathyanarayana Sheela S Tylavsky Frances A FA Barrett Emily S ES Nguyen Ruby H N RHN Karr Catherine J CJ

Environmental epidemiology (Philadelphia, Pa.) 20210401 2

<h4>Background</h4>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.<h4>Objective</h4>To assess associations between prenatal fine particulate matter exposure and asthma at age 4.<h4>Methods</h4>This study included mother-child dyads from two pregnancy cohorts-CANDLE and TIDES-within the ECHO-PATHWAYS consortium (births in 2007-2013). Three child asth ...[more]

PMID: 33709049

Similar Datasets

Project description:BackgroundElevated homocysteine (Hcy) is a pathogenic mechanism of adverse pregnancy outcomes and PM2.5-induced cardiovascular diseases. We investigated the associations of fine particulate matter (PM2.5) and chemical constituent exposures with maternal circulatory Hcy in early pregnancy.MethodsSerum Hcy and 5-methyltetrahydrofolate in 324 women with pregnancy (162 normal early pregnancy [NEP] and 162 early pregnancy loss [EPL]) were measured by ultra-performance liquid chromatography-tandem triple quadrupole mass spectrometry. Daily exposures to PM2.5 and constituents (black carbon [BC], organic matter, nitrate, ammonium, and sulfate) were accessed using data of Tracking Air Pollution in China platform. Nonlinear and linear associations of average pollutant exposures during the post-conception period with serum Hcy were estimated using generalized additive models and multivariable linear regression models, respectively. Weekly cumulative and distributed lag associations between pollutant exposures within three months before serum collection and Hcy were analyzed by distributed lag nonlinear models combined with multivariable linear regression models. Sensitivity analyses were conducted using constituent residuals instead of constituent concentrations.ResultsThree-month PM2.5 and the five constituent exposures were associated with elevated serum Hcy in all participants, EPL group, and NEP group, with 3-12 weeks before serum collection being the susceptible exposure time windows. Pollutants-related Hcy were generally higher in EPL group than in NEP group. Higher post-conception PM2.5, BC, and sulfate exposures increased serum Hcy in lower but not in higher 5-methyltetrahydrofolate subgroup. Sulfate was the highest risk constituent with residual-related increased Hcy. BC residuals of both post-conception and three-month periods increased Hcy in EPL group but not in NEP group.ConclusionsMaternal circulatory Hcy in early pregnancy increased with PM2.5 and constituent exposures, with sulfate being the highest risk constituent. BC-related increased Hcy may induce EPL.Trial registrationThe study protocol was registered for clinical trials (ChiCTR1900028619) on December 29, 2019.

Project description:BackgroundExposure to particulate matter, particularly with aerodynamic diameter < 2.5 µm (PM2.5), may increase inflammation and oxidative stress in pregnant women and affect fetal growth. We examined trimester specific PM2.5 exposure levels and small for gestational age (SGA) using the statewide birth registry of Ohio from 2007 to 2010.MethodsExposure to PM2.5 in each trimester and for each gestational week was determined using data from 57 Environmental Protection Agency network monitoring stations across the state of Ohio. We restricted the data to 224,921 singleton live births, with a gestational age of 20-42 weeks, no genetic disorders or congenital abnormalities, and who had home addresses within a 10 km radius of any PM2.5 monitoring station. We estimated odds ratios of SGA using Generalized Linear Models (GLMs) and Distributed Lag Models (DLMs), and adjustment for maternal age, race, education, parity, body mass index, insurance type, tobacco use, prenatal care initiation, birth year, season of birth, and sex of the baby.ResultsMean PM2.5 levels during the entire pregnancy were 13.03 µg/m3 with a standard deviation of 1.57 µg/m3. Covariates adjusted odds ratios and 95% confidence intervals of a 10 µg/m3 increase in PM2.5 levels with a 10 km buffer radius for SGA and trimesters modeled separately were 0.94 (0.88, 1.00) for the first trimester, 0.93 (0.86, 1.00) for the second trimester, 1.07 (1.00, 1.15) for the third trimester, and 0.92 (0.81, 1.06) for the entire pregnancy. When a 5 km buffer radius was used, adjusted odds ratios and 95% confidence intervals for SGA were 0.97 (0.89, 1.05) for the first trimester, 0.96 (0.88, 1.05) for the second trimester, 1.09 (1.02, 1.17) for the third trimester, and 0.99 (0.85, 1.14) for the overall pregnancy, indicating sensitivity to buffer choice. DLMs showed gestational weeks 30-35 to be a particular window of vulnerability.ConclusionIncreasing exposure to PM2.5 during the third trimester of pregnancy was associated with a small increase in risk of SGA in this population-based study. Selection of a buffer radius significantly impacted our results in the first trimester, but not in the third trimester.

Dataset Information

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

Publications

Maternal exposure to PM<sub>2.5</sub> during pregnancy and asthma risk in early childhood: consideration of phases of fetal lung development.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets