Dataset Information

Exposures to Air Pollution and Risk of Acute-onset Placental Abruption: A Case-crossover Study.

ABSTRACT: BACKGROUND:Despite abruption's elusive etiology, knowledge of triggers that precede it by just a few days prior to delivery may help to understand the underpinnings of this acute obstetrical complication. We examine whether air pollution exposures immediately preceding delivery are associated with acute-onset abruptions. METHODS:We applied a bidirectional, time-stratified, case-crossover design to births with an abruption diagnosis in New York City, 2008-2014. We measured ambient fine particulate matter (PM2.5) and nitrogen dioxide (NO2). We fit distributed lag nonlinear models based on conditional logistic regression to evaluate individual exposure and cumulative exposures over lags 0-7 days before abruption, adjusted for temperature and relative humidity (similar lags to the main exposures). RESULTS:We identified 1,190 abruption cases. We observed increased odds of abruption for exposure to PM2.5 (per 10 ?g/m) on lag day 3 (odds ratio [OR] 1.19, 95% confidence interval [CI] = 0.98, 1.43), lag day 4 (OR 1.21, 95% CI = 1.01, 1.46), and lag day 5 (OR 1.17, 95% CI = 1.03, 1.33). Similarly, the odds of abruption increased with exposure to NO2 (per 5 ppb) on lag day 3 (OR 1.16, 95% CI = 0.98, 1.37), lag day 4 (OR 1.19, 95% CI = 1.02, 1.39), and lag day 5 (OR 1.16, 95% CI = 1.05, 1.27). Exposures to PM2.5 and NO2 at other lags, or cumulative exposures, were not associated with abruption of acute onset. CONCLUSIONS:This case-crossover study showed evidence of an association between short-term ambient air pollution exposures and increased abruption risk of acute onset.

SUBMITTER: Ananth CV

PROVIDER: S-EPMC6066409 | biostudies-literature | 2018 Sep

REPOSITORIES: biostudies-literature

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Exposures to Air Pollution and Risk of Acute-onset Placental Abruption: A Case-crossover Study.

Ananth Cande V CV Kioumourtzoglou Marianthi-Anna MA Huang Yongmei Y Ross Zev Z Friedman Alexander M AM Williams Michelle A MA Wang Shuang S Mittleman Murray A MA Schwartz Joel J

Epidemiology (Cambridge, Mass.) 20180901 5

<h4>Background</h4>Despite abruption's elusive etiology, knowledge of triggers that precede it by just a few days prior to delivery may help to understand the underpinnings of this acute obstetrical complication. We examine whether air pollution exposures immediately preceding delivery are associated with acute-onset abruptions.<h4>Methods</h4>We applied a bidirectional, time-stratified, case-crossover design to births with an abruption diagnosis in New York City, 2008-2014. We measured ambient ...[more]

PMID: 29863531

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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:BackgroundFew studies have explored the relationship between air pollution and arrhythmia onset at the hourly level. We aimed to examine the association of exposure to air pollution with the onset of acute symptomatic arrhythmia at an hourly level.MethodsWe conducted a nationwide, time-stratified, case-crossover study in China between 2015 and 2021. We obtained hourly information on the onset of symptomatic arrhythmia (including atrial fibrillation, atrial flutter, atrial and ventricular premature beats and supraventricular tachycardia) from the Chinese Cardiovascular Association Database - Chest Pain Center (including 2025 certified hospitals in 322 cities). We obtained data on hourly concentrations of 6 air pollutants from the nearest monitors, including fine particles (PM2.5), coarse particles (PM2.5-10), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (CO) and ozone. For each patient, we matched the case period to 3 or 4 control periods during the same hour, day of week, month and year. We used conditional logistic regression models to analyze the data.ResultsWe included a total of 190 115 patients with acute onset of symptomatic arrhythmia. Air pollution was associated with increased risk of onset of symptomatic arrhythmia within the first few hours of exposure; this risk attenuated substantially after 24 hours. An interquartile range increase in PM2.5, NO2, SO2 and CO in the first 24 hours after exposure (i.e., lag period 0-24 h) was associated with significantly higher odds of atrial fibrillation (1.7%-3.4%), atrial flutter (8.1%-11.4%) and supraventricular tachycardia (3.4%-8.9%). Exposure to PM2.5-10 was associated with significantly higher odds of atrial flutter (8.7%) and supraventricular tachycardia (5.4%), and exposure to ozone was associated with higher odds of supraventricular tachycardia (3.4%). The exposure-response relationships were approximately linear, without discernible concentration thresholds.InterpretationExposure to air pollution was associated with the onset of symptomatic arrhythmia shortly after exposure. This finding highlights the importance of further reducing air pollution and taking prompt protective measures for susceptible populations during periods of elevated levels of air pollutants.

Dataset Information

Exposures to Air Pollution and Risk of Acute-onset Placental Abruption: A Case-crossover Study.

Publications

Exposures to Air Pollution and Risk of Acute-onset Placental Abruption: A Case-crossover Study.

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