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Differential Effect of Ambient Air Pollution Exposure on Risk of Gestational Hypertension and Preeclampsia.

ABSTRACT: Although ambient air pollution may increase hypertension risk through endothelial damage and oxidative stress, evidence is inconsistent regarding its effect on hypertension in pregnancy. Prior research has evaluated a limited scope of pollution species and often not differentiated preeclampsia, which may have a placental origin, from gestational hypertension. Among 49?607 women with at least 2 singleton deliveries in the Eunice Kennedy Shriver National Institute of Child Health and Human Development Consecutive Pregnancies Study (2002-2010), we estimated criteria pollutant and volatile organic compound levels during pregnancy using Community Multiscale Air Quality models and abstracted gestational hypertension and preeclampsia diagnoses from medical records. Generalized estimating equations accounted for repeat pregnancies and adjusted for ambient temperature and maternal age, race/ethnicity, body mass index, smoking, alcohol, parity, insurance, marital status, and asthma. Air pollution levels were low to moderate (eg, median 41.6 ppb [interquartile range, 38.9-43.7 ppb] for ozone and 35.1 ppb [28.9-40.3 ppb] for nitrogen oxides). Higher levels of most criteria pollutants during preconception and the first trimester were associated with lower preeclampsia risk, while higher second-trimester levels were associated with greater gestational hypertension risk. For example, an interquartile increase in first-trimester carbon monoxide was associated with a relative risk of 0.88 (95% CI, 0.81-0.95) for preeclampsia and second-trimester carbon monoxide a relative risk of 1.14 (95% CI, 1.07-1.22) for gestational hypertension. Volatile organic compounds, conversely, were not associated with gestational hypertension but consistently associated with higher preeclampsia risk. These findings further suggest air pollution may affect the development of hypertension in pregnancy, although differing causes of preeclampsia and gestational hypertension may alter these relationships.

SUBMITTER: Nobles CJ

PROVIDER: S-EPMC6620155 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature

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Differential Effect of Ambient Air Pollution Exposure on Risk of Gestational Hypertension and Preeclampsia.

Nobles Carrie J CJ Williams Andrew A Ouidir Marion M Sherman Seth S Mendola Pauline P

Hypertension (Dallas, Tex. : 1979) 20190624 2

Although ambient air pollution may increase hypertension risk through endothelial damage and oxidative stress, evidence is inconsistent regarding its effect on hypertension in pregnancy. Prior research has evaluated a limited scope of pollution species and often not differentiated preeclampsia, which may have a placental origin, from gestational hypertension. Among 49 607 women with at least 2 singleton deliveries in the Eunice Kennedy Shriver National Institute of Child Health and Human Develop ...[more]

PMID: 31230552

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Project description:BackgroundEmerging evidence suggests a potential association between ambient air pollution and risk of gestational diabetes mellitus (GDM), but results have been inconsistent. Accordingly, we assessed the associations between ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2) levels with risk of GDM.MethodsUsing linked data from birth certificates, hospital discharge diagnoses, and air pollution estimates informed by the New York City Community Air Survey, we fit conditional logistic regression models to evaluate the association between residential levels of PM2.5 and NO2 with risk of GDM among 256,372 singleton live births of non-smoking mothers in New York City born 2008-2010, adjusting for sociodemographic factors and stratified on zip code of maternal address.ResultsGDM was identified in 17,065 women, yielding a risk of GDM in the study sample of 67 per 1000 deliveries. In single pollutant models, 1st and 2nd trimester PM2.5 was associated with a lower and higher risk of GDM, respectively. In models mutually adjusting for PM2.5 levels in both trimesters, GDM was associated with PM2.5 levels in the 2nd trimester (OR: 1.06, 95% CI: 1.02, 1.10 per interquartile range increase in PM2.5), but not the 1st trimester (OR: 0.99, 95% CI: 0.96, 1.02). Conversely, GDM was associated with NO2 during the 1st trimester (OR: 1.05, 95% CI: 1.01, 1.09), but not the 2nd trimester (OR: 1.02, 95% CI: 0.98, 1.06). The positive associations between pollutants and GDM were robust to different model specifications. PM2.5 in the 2nd trimester was more strongly associated with GDM among mothers who were aged <35 years and not Medicaid recipients. NO2 in the 1st trimester was more strongly associated with GDM among overweight and parous women.ConclusionsIn this large cohort of singleton births in New York City, NO2 in the 1st trimester and PM2.5 in the 2nd trimester were associated with higher odds of GDM, while 1st trimester PM2.5 was weakly and inconsistently associated with lower odds of GDM.

Project description:Olfactory dysfunction affects millions of people worldwide. This sensory impairment is associated with neurodegenerative disease and significantly decreased quality of life. Exposure to airborne pollutants has been implicated in olfactory decline, likely due to the anatomic susceptibility of the olfactory nerve to the environment. Historically, studies have focused on occupational exposures, but more recent studies have considered effects from exposure to ambient air pollutants.To examine all relevant human data evaluating a link between ambient pollution exposure and olfaction and to review supporting animal data in order to examine potential mechanisms for pollution-associated olfactory loss.We identified and reviewed relevant articles from 1950 to 2015 using PubMed and Web of Science and focusing on human epidemiologic and pathophysiologic studies. Animal studies were included only to support pertinent data on humans. We reviewed findings from these studies evaluating a relationship between environmental pollutant exposure and olfactory function.We identified and reviewed 17 articles, with 1 additional article added from a bibliography search, for a total of 18 human studies. There is evidence in human epidemiologic and pathologic studies that increased exposure to ambient air pollutants is associated with olfactory dysfunction. However, most studies have used proxies for pollution exposure in small samples of convenience. Human pathologic studies, with supporting animal work, have also shown that air pollution can contact the olfactory epithelium, translocate to the olfactory bulb, and migrate to the olfactory cortex. Pollutants can deposit at each location, causing direct damage and disruption of tissue morphology or inducing local inflammation and cellular stress responses.Ambient air pollution may impact human olfactory function. Additional studies are needed to examine air pollution-related olfactory impacts on the general population using measured pollution exposures and to link pollution exposure with olfactory dysfunction and related pathology. Citation: Ajmani GS, Suh HH, Pinto JM. 2016. Effects of ambient air pollution exposure on olfaction: a review. Environ Health Perspect 124:1683-1693;?http://dx.doi.org/10.1289/EHP136.

Project description:Few epidemiologic studies have evaluated the effects of air pollution on the risk of Parkinson disease (PD).We investigated the associations of long-term residential concentrations of ambient particulate matter (PM) < 10 ?m in diameter (PM10) and < 2.5 ?m in diameter (PM2.5) and nitrogen dioxide (NO2) in relation to PD risk.Our nested case-control analysis included 1,556 self-reported physician-diagnosed PD cases identified between 1995 and 2006 and 3,313 controls frequency-matched on age, sex, and race. We geocoded home addresses reported in 1995-1996 and estimated the average ambient concentrations of PM10, PM2.5, and NO2 using a national fine-scale geostatistical model incorporating roadway information and other geographic covariates. Air pollutant exposures were analyzed as both quintiles and continuous variables, adjusting for matching variables and potential confounders.We observed no statistically significant overall association between PM or NO2 exposures and PD risk. However, in preplanned subgroup analyses, a higher risk of PD was associated with higher exposure to PM10 (ORQ5 vs. Q1 = 1.65; 95% CI: 1.11, 2.45; p-trend = 0.02) among women, and with higher exposure to PM2.5 (ORQ5 vs. Q1 = 1.29; 95% CI: 0.94, 1.76; p-trend = 0.04) among never smokers. In post hoc analyses among female never smokers, both PM2.5 (ORQ5 vs. Q1 = 1.79; 95% CI: 1.01, 3.17; p-trend = 0.05) and PM10 (ORQ5 vs. Q1 = 2.34; 95% CI: 1.29, 4.26; p-trend = 0.01) showed positive associations with PD risk. Analyses based on continuous exposure variables generally showed similar but nonsignificant associations.Overall, we found limited evidence for an association between exposures to ambient PM10, PM2.5, or NO2 and PD risk. The suggestive evidence that exposures to PM2.5 and PM10 may increase PD risk among female never smokers warrants further investigation. Citation: Liu R, Young MT, Chen JC, Kaufman JD, Chen H. 2016. Ambient air pollution exposures and risk of Parkinson disease. Environ Health Perspect 124:1759-1765;?http://dx.doi.org/10.1289/EHP135.

Project description:Study questionTo what extent are ambient concentrations of particulate matter <2.5 microns (PM2.5), nitrogen dioxide (NO2) and ozone (O3) associated with risk of self-reported physician-diagnosed uterine leiomyomata (UL)?Summary answerIn this large prospective cohort study of Black women, ambient concentrations of O3, but not PM2.5 or NO2, were associated with increased risk of UL.What is known alreadyUL are benign tumors of the myometrium that are the leading cause of gynecologic inpatient care among reproductive-aged women. Black women are clinically diagnosed at two to three times the rate of white women and tend to exhibit earlier onset and more severe disease. Two epidemiologic studies have found positive associations between air pollution exposure and UL risk, but neither included large numbers of Black women.Study design, size, durationWe conducted a prospective cohort study of 21 998 premenopausal Black women residing in 56 US metropolitan areas from 1997 to 2011.Participants/material, setting, methodsWomen reported incident UL diagnosis and method of confirmation (i.e. ultrasound, surgery) on biennial follow-up questionnaires. We modeled annual residential concentrations of PM2.5, NO2 and O3 throughout the study period. We used Cox proportional hazards regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for a one-interquartile range (IQR) increase in air pollutant concentrations, adjusting for confounders and co-pollutants.Main results and the role of chanceDuring 196 685 person-years of follow-up, 6238 participants (28.4%) reported physician-diagnosed UL confirmed by ultrasound or surgery. Although concentrations of PM2.5 and NO2 were not appreciably associated with UL (HRs for a one-IQR increase: 1.01 (95% CI: 0.93, 1.10) and 1.05 (95% CI: 0.95, 1.16), respectively), O3 concentrations were associated with increased UL risk (HR for a one-IQR increase: 1.19, 95% CI: 1.07, 1.32). The association was stronger among women age <35 years (HR: 1.26, 95% CI: 0.98, 1.62) and parous women (HR: 1.28, 95% CI: 1.11, 1.48).Limitations, reasons for cautionOur measurement of air pollution is subject to misclassification, as monitoring data are not equally spatially distributed and we did not account for time-activity patterns. Our outcome measure was based on self-report of a physician diagnosis, likely resulting in under-ascertainment of UL. Although we controlled for several individual- and neighborhood-level confounding variables, residual confounding remains a possibility.Wider implications of the findingsInequitable burden of air pollution exposure has important implications for racial health disparities, and may be related to disparities in UL. Our results emphasize the need for additional research focused on environmental causes of UL.Study funding/competing interest(s)This research was funded by the National Cancer Institute (U01-CAA164974) and the National Institute of Environmental Health Sciences (R01-ES019573). L.A.W. is a fibroid consultant for AbbVie, Inc. and accepts in-kind donations from Swiss Precision Diagnostics, Sandstone Diagnostics, FertilityFriend.com and Kindara.com for primary data collection in Pregnancy Study Online (PRESTO). M.J. declares consultancy fees from the Health Effects Institute (as a member of the review committee). The remaining authors declare they have no actual or potential competing financial interests.Trial registration numberN/A.

Dataset Information

Differential Effect of Ambient Air Pollution Exposure on Risk of Gestational Hypertension and Preeclampsia.

Publications

Differential Effect of Ambient Air Pollution Exposure on Risk of Gestational Hypertension and Preeclampsia.

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