Dataset Information

Ambient air pollution and hypertensive disorder of pregnancy.

ABSTRACT: Ambient air pollution has been implicated in the development of hypertensive disorders of pregnancy (HDP). However, evidence of the association between air pollution and HDP is still limited, and the effects of gaseous air pollutants on HDP and their time windows of exposure have not been well studied.We used the Florida birth registry data to investigate the associations between air pollutants (NO2, SO2, PM(2.5), O3 and CO) and the risks of HDP in 22,041 pregnant women in Jacksonville, Florida, USA from 2004 to 2005. Further, we examined whether air pollution exposure during different time windows defined by trimesters and the entire pregnancy had different effects on HDP.The single-pollutant logistic regression model showed that exposure to four pollutants during the full pregnancy period was significantly associated with prevalence of HDP after adjusting for covariates: NO2 (OR=1.21, 95% CI 1.09 to 1.35), PM2.5 (OR=1.24, 95% CI 1.08 to 1.43), SO2 (OR=1.13, 95% CI 1.01 to 1.25) and CO (OR=1.12, 95% CI 1.03 to 1.22) per IQR increase. Similar effects were observed when first trimester exposure to NO2, SO2 and CO, and second trimester exposures to PM2.5 were examined. Consistent results were confirmed in multiple-pollutant models.This study suggests that exposure to high levels of air pollution during early pregnancy and the full gestational period was associated with increased prevalence of HDP in Florida, USA.

SUBMITTER: Xu X

PROVIDER: S-EPMC3878158 | biostudies-literature | 2014 Jan

REPOSITORIES: biostudies-literature

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Ambient air pollution and hypertensive disorder of pregnancy.

Xu Xiaohui X Hu Hui H Ha Sandie S Roth Jeffrey J

Journal of epidemiology and community health 20130910 1

<h4>Background</h4>Ambient air pollution has been implicated in the development of hypertensive disorders of pregnancy (HDP). However, evidence of the association between air pollution and HDP is still limited, and the effects of gaseous air pollutants on HDP and their time windows of exposure have not been well studied.<h4>Methods</h4>We used the Florida birth registry data to investigate the associations between air pollutants (NO2, SO2, PM(2.5), O3 and CO) and the risks of HDP in 22,041 pregn ...[more]

PMID: 24022815

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Project description:BackgroundPrevious studies have reported associations between ambient fine particle (PM2.5) concentrations and hypertensive disorders of pregnancy (HDP). However, none have examined whether ultrafine particles (UFP; < 100 nm), accumulation mode particles (AMP; 100-500 nm), markers of traffic pollution (black carbon; BC), or wood burning (Delta-C; (30% of ambient wintertime PM2.5 in Monroe County, NY is from wood burning)) are associated with an increased odds of HDP. We estimated the odds of HDP associated with increased concentrations of PM2.5, UFP, AMP, BC, and Delta-C in each gestational month during winter months.MethodsElectronic medical records and birth certificate data were linked with land-use regression models in Monroe County, New York in 2009-2013 to predict monthly pollutant concentrations during winter (November-April) based on maternal residential address for 16,637 births. Using multivariable logistic regression, we estimated the odds of HDP associated with each interquartile range (IQR) increase in PM2.5, UFP, AMP, BC, and Delta-C concentrations during each gestational month, adjusting for maternal characteristics, birth hospital, temperature, and relative humidity.ResultsEach 0.52 µg/m3 increase in Delta-C concentration during the 7th gestational month was associated with an increased odds of HDP (odds ratio (OR) = 1.21; 95% confidence interval (CI) = 1.01, 1.45), with a similar sized estimate in month 8 (OR = 1.18; 95%CI = 0.98, 1.43). Non-statistically significant increased odds of HDP associated with IQR increases in BC concentrations during months 3 (OR = 1.12; 95%CI = 0.98, 1.28) and 7 (OR = 1.12; 95%CI = 0.96, 1.29) were observed. Increased odds of HDP were not observed for PM2.5, UFP, or AMP.ConclusionsOur findings suggest that maternal exposure to wood smoke in Monroe County during winter is associated with an increased odds of HDP during late gestation. Additional studies are needed to evaluate the effect of wood smoke on HDP and to explore effects on other pregnancy outcomes.

Project description:Importance:Air pollutants interact with estrogen nuclear receptors, but their effect on thyroid signaling is less clear. Thyroid function is of particular importance for pregnant women because of the thyroid's role in fetal brain development. Objective:To determine the short-term association of exposure to air pollution in the first trimester with thyroid function throughout pregnancy. Design, Setting, and Participants:In this cohort study, 9931 pregnant women from 4 European cohorts (the Amsterdam Born Children and Their Development Study, the Generation R Study, Infancia y Medio Ambiente, and Rhea) and 1 US cohort (Project Viva) with data on air pollution exposure and thyroid function during pregnancy were included. The recruitment period for the Amsterdam Born Children and Their Development Study was January 2003 to March 2004; for Generation R, April 2002 to January 2006; for Infancia y Medio Ambiente, November 2003 to January 2008; for Rhea, February 2007 to February 2008; and for Project Viva, April 1999 to November 2002. Statistical analyses were conducted from January 2018 to April 2019. Main Outcomes and Measures:Residential air pollution concentrations (ie, nitrogen oxide and particulate matter [PM]) during the first trimester of pregnancy were estimated using land-use regression and satellite-derived aerosol optical depth models. Free thyroxine, thyrotropin, and thyroid peroxidase antibody levels were measured across gestation. Hypothyroxinemia was defined as free thyroxine below the fifth percentile of the cohort distribution with normal thyrotropin levels, following the American Thyroid Association guidelines. Results:Among 9931 participants, the mean (SD) age was 31.2 (4.8) years, 4853 (48.9%) had more than secondary educational levels, 5616 (56.6%) were nulliparous, 404 (4.2%) had hypothyroxinemia, and 506 (6.7%) tested positive for thyroid peroxidase antibodies. Concentrations of nitrogen dioxide and PM with an aerodynamic diameter of 2.5 ?m or less (PM2.5) were lower and had less variation in women in the US cohort than those in European cohorts. No associations of nitrogen oxide with thyroid function were found. Higher exposures to PM2.5 were associated with higher odds of hypothyroxinemia in pregnant women (odds ratio per 5-?g/m3 change, 1.21; 95% CI, 1.00-1.47). Although exposure to PM with an aerodynamic diameter of 10 ?m or less was not significantly associated with hypothyroxinemia, the coefficient was similar to that for the association of PM2.5 with hypothyroxinemia (odds ratio per 10-?g/m3 change, 1.18; 95% CI, 0.93-1.48). Absorbances of PM2.5 and PM with aerodynamic diameter from 2.5 to 10 ?g and were not associated with hypothyroxinemia. There was substantial heterogeneity among cohorts with respect to thyroid peroxidase antibodies (P for heterogeneity, <.001), showing associations of nitrogen oxide and PM with thyroid autoimmunity only in the women in the Generation R Study. Conclusions and Relevance:The findings of this study suggest that first-trimester exposures to PM2.5 were associated with mild thyroid dysfunction throughout pregnancy. The association of PM2.5 exposure with thyroid function during pregnancy is of global health importance because air pollution exposure is widespread and hypothyroxinemia may adversely influence the brain development of offspring.

Project description:Accumulating evidence suggests that air pollution increases pregnancy loss; however, most previous studies have focused on case identification from medical records, which may underrepresent early pregnancy losses. Our objective was to investigate the association between acute and chronic exposure to ambient air pollution and time to pregnancy loss among women undergoing assisted reproductive technologies (ART) who are closely followed throughout early pregnancy. We included 275 women (345 human chorionic gonadotropin (hCG)-confirmed pregnancies) undergoing ART at a New England academic fertility center. We estimated daily nitrogen dioxide (NO2), ozone (O3), fine particulate matter <2.5 μm (PM2.5), and black carbon (BC) exposures using validated spatiotemporal models estimated from first positive hCG test until day of failure or live birth. Air pollution exposures were averaged over the past week and the whole pregnancy. Multivariable Cox proportional hazards models were used to estimate the hazards ratio (HR) for pregnancy loss for an interquartile range (IQR) increase in pollutant exposure. We tested for violation of proportional hazards by considering an interaction between time (in days) since positive hCG (<30 days vs. ≥30 days) and air pollution. The incidence of pregnancy loss was 29 per 100 confirmed pregnancies (n = 99). Among pregnancies not resulting in live birth, the median (IQR) time to loss was 21 (11, 30) days following positive hCG. Average past week exposures to NO2, O3, PM2.5, and BC were not associated with time to pregnancy loss. Exposure throughout pregnancy to NO2 was not associated with pregnancy loss; however, there was a statistically significant interaction with time (p-for-interaction<0.001). Specifically, an IQR increase in exposure to NO2 was positively associated with pregnancy loss after 30 days (HR = 1.34, 95% CI: 1.13, 1.58), but not in the first 30 days after positive hCG (HR = 0.83, 95% CI: 0.57, 1.20). Overall pregnancy exposure to O3, PM2.5, and BC were not associated with pregnancy loss regardless of timing. Models evaluating joint effects of all pollutants yielded similar findings. In conclusion, acute and chronic exposure to NO2, O3, PM2.5, and BC were not associated with risk of pregnancy loss; however, higher exposure to NO2 throughout pregnancy was associated with increased risk of loss 30 days after positive hCG. In this cohort, later pregnancy losses appeared more susceptible to the detrimental effects of air pollution exposure.

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Ambient air pollution and hypertensive disorder of pregnancy.

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Ambient air pollution and hypertensive disorder of pregnancy.

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