Dataset Information

Association between ambient particulate matter concentration and fetal growth restriction stratified by maternal employment.

ABSTRACT:

Background

Fetal growth has been known to be associated with particulate matter (PM) air pollution during gestation. Given that regular working may deviate outdoor air pollution exposure, the association between air pollution and fetal growth restriction can be different across maternal working status. This study was to assess possible effect modification by maternal employment in the association between exposure to PM during pregnancy and fetal growth restriction.

Methods

Using hourly PM less than or equal to 10 and 2.5??m in diameter (PM₁₀ and PM_2.5) regulatory monitoring data for 2001-2012 and 2008-2012, respectively, and birth certificate data for 2002-2012, we computed maternal exposures with district-level averages of PM₁₀ and PM_2.5 during one year before birth, entire pregnancy, and the 1st, 2nd and 3rd trimesters. The outcomes of fetal growth restriction were assessed by small for gestational age (SGA, weighted <10th percentile in the same gestational age) as well as low birth weight (LBW, 10 or PM_2.5 stratified by employed and non-employed mothers. We also computed relative excess risk due to interaction (RERI) to investigate additive interaction.

Results

Among 824,011 singleton term births, 34.0% (279,856) were employed and 66.0% (544,155) were non-employed mothers. Proportions of LBW were 1.5% in employed and 1.6% in non-employed (P 10 for one year before birth (OR?=?1.02, 95% confidence intervals (CI): 1.00-1.04, P =?0.028). ORs of SGA for full pregnancy period and the 3rd trimester were also positive but did not reach statistical significance. We did not observe positive association for PM_2.5. RERI was not significant both for PM₁₀ and PM_2.5.

Conclusions

We did not observe evidence of effect modification by maternal employment in the association between ambient PM and fetal growth restriction. Future studies using more refined exposure measures should confirm this finding.

SUBMITTER: Choe SA

PROVIDER: S-EPMC6632189 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature

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Publications

Association between ambient particulate matter concentration and fetal growth restriction stratified by maternal employment.

Choe Seung-Ah SA Jang Jiyeong J Kim Min Jung MJ Jun Yoon-Bae YB Kim Sun-Young SY

BMC pregnancy and childbirth 20190715 1

<h4>Background</h4>Fetal growth has been known to be associated with particulate matter (PM) air pollution during gestation. Given that regular working may deviate outdoor air pollution exposure, the association between air pollution and fetal growth restriction can be different across maternal working status. This study was to assess possible effect modification by maternal employment in the association between exposure to PM during pregnancy and fetal growth restriction.<h4>Methods</h4>Using h ...[more]

PMID: 31307418

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Project description:BackgroundFetal growth restriction (FGR) is not only a major determinant of perinatal morbidity and mortality but also leads to adverse health effects in later life. Over the past decade, numerous studies have indicated that maternal exposure to ambient air pollution has been a risk factor for abnormal fetal growth in developed countries where PM2.5 levels are relatively low. However, studies in highly polluted regions, such as China, and studies that rely on assessments in utero are scarce.MethodsA total of 7965 women were selected from 11,441 women from the Shanghai Maternity and Infant Living Environment (SMILE) cohort who were pregnant between January 1, 2014, and April 30, 2015. From January 1, 2014, to April 30, 2015, weekly average PM2.5 values from 53 monitors were calculated and the inverse distance weighted (IDW) method was used to create a Shanghai pollution surface map according to the participants residential addresses. Individual exposure was the average PM2.5 value of every gestational week between the first gestational week and one week before the ultrasound measurement date (the range of measurements per participant was 1 to 10). Repeated fetal ultrasound measurements during gestational weeks 14~40 were selected. The estimated fetal weight (EFW) was calculated by biparietal diameter (BPD), abdominal circumference (AC), and femur length (FL) formulas. In total, 29,926 ultrasound measurements were analysed. Demographic variables, other pollutants (SO2, NO2, PM10 and O3) and relative humidity and temperature were controlled for potential confounding through generalized estimating equations (GEE).ResultsThe full model showed that with each 10 μg/m3 increase in PM2.5 exposure, the means (mm) of AC, BPD, FL decreased by 5.48 (- 9.06, - 1.91), 5.57 (- 6.66, - 4.47), and 5.47 (- 6.39, - 4.55), respectively; the mean EFW decreased by 14.49 (- 16.05, - 13.49) grams by Hadlock's third formula and 13.56 (- 14.71, - 12.50) grams by Shepard's formula with each 10 μg/m3 increase in PM2.5 exposure.ConclusionsA negative correlation existed between maternal PM2.5 exposure during pregnancy and fetal growth indicators, which may increase the risk of fetal growth restriction.

Project description:Murine Pulmonary Responses to Ambient Baltimore Particulate Matter: Genomic Analysis and Contribution to Airway Hyperresponsiveness Asthma is a complex disease characterized by airway hyperresponsiveness (AHR) and chronic airway inflammation. Environmental factors such as ambient particulate matter (PM), a major air pollutant, has been demonstrated in epidemiological studies to contribute to asthma exacerbation and increased asthma prevalence. OBJECTIVE: We investigated the genomic and pathophysiological effects of Baltimore PM (median diameter 1.78 µm) in a murine model of asthma to identify potential biomarkers. METHODS: A/J mice with ovalbumin (OVA) –induced AHR were exposed to PM (20 mg/kg, intratracheal), and both AHR and bronchoalveolar lavage (BAL) were assayed on days 1, 4, and 7 post exposure. Lung gene expression profiling (Affymetrix Mouse430_ 2.0) by PM (20 mg/kg, intratracheal) were assayed on OVA- and / or PM--challenged mice. RESULTS: Significant increases of airway responsiveness in OVA-treated mice were observed, indicating an asthmatic phenotype. Ambient PM exposure induced significant changes in AHR in both naive mice and OVA-induced asthmatic mice. In both naive and OVA challenged asthmatic mice, PM induced eosinophil and neutrophil infiltration into airways, elevated BAL protein content, and stimulated secretion of TH1 cytokines (IFN-g, IL-6, and TNF-a) and TH2 cytokines (IL-4, IL-5, and eotaxin) into BAL. Consistent with these results, PM induced expression of genes of innate immune response, chemotaxis and complementary system. CONCLUSION: These studies, consistent with epidemiological data, indicate that PM increases AHR and lung inflammation in naïve mice and exacerbates the asthma phenotype of increased AHR and gene expression pattern changes correlated with acute lung inflammation and airway damage. We used microarrays to detail the global programme of gene expression induced by rhPBEF treatment and VALI. Keywords: gene expression

Dataset Information

Association between ambient particulate matter concentration and fetal growth restriction stratified by maternal employment.

Background

Methods

Results

Conclusions

Publications

Association between ambient particulate matter concentration and fetal growth restriction stratified by maternal employment.

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