Dataset Information

Wildfire-specific Fine Particulate Matter and Risk of Hospital Admissions in Urban and Rural Counties.

ABSTRACT: The health impacts of wildfire smoke, including fine particles (PM2.5), are not well understood and may differ from those of PM2.5 from other sources due to differences in concentrations and chemical composition.First, for the entire Western United States (561 counties) for 2004-2009, we estimated daily PM2.5 concentrations directly attributable to wildfires (wildfires-specific PM2.5), using a global chemical transport model. Second, we defined smoke wave as ?2 consecutive days with daily wildfire-specific PM2.5 > 20 ?g/m, with sensitivity analysis considering 23, 28, and 37 ?g/m. Third, we estimated the risk of cardiovascular and respiratory hospital admissions associated with smoke waves for Medicare enrollees. We used a generalized linear mixed model to estimate the relative risk of hospital admissions on smoke wave days compared with matched comparison days without wildfire smoke.We estimated that about 46 million people of all ages were exposed to at least one smoke wave during 2004 to 2009 in the Western United States. Of these, 5 million are Medicare enrollees (?65 years). We found a 7.2% (95% confidence interval: 0.25%, 15%) increase in risk of respiratory admissions during smoke wave days with high wildfire-specific PM2.5 (>37 ?g/m) compared with matched non smoke wave days. We did not observe an association between smoke wave days with wildfire-specific PM2.5 ? 37 ?g/mand respiratory or cardiovascular admissions. Respiratory effects of wildfire-specific PM2.5 may be stronger than that of PM2.5 from other sources.Short-term exposure to wildfire-specific PM2.5was associated with risk of respiratory diseases in the elderly population in the Western United States during severe smoke days. See video abstract at, http://links.lww.com/EDE/B137.

SUBMITTER: Liu JC

PROVIDER: S-EPMC5130603 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Wildfire-specific Fine Particulate Matter and Risk of Hospital Admissions in Urban and Rural Counties.

Liu Jia Coco JC Wilson Ander A Mickley Loretta J LJ Dominici Francesca F Ebisu Keita K Wang Yun Y Sulprizio Melissa P MP Peng Roger D RD Yue Xu X Son Ji-Young JY Anderson G Brooke GB Bell Michelle L ML

Epidemiology (Cambridge, Mass.) 20170101 1

<h4>Background</h4>The health impacts of wildfire smoke, including fine particles (PM2.5), are not well understood and may differ from those of PM2.5 from other sources due to differences in concentrations and chemical composition.<h4>Methods</h4>First, for the entire Western United States (561 counties) for 2004-2009, we estimated daily PM2.5 concentrations directly attributable to wildfires (wildfires-specific PM2.5), using a global chemical transport model. Second, we defined smoke wave as ≥2 ...[more]

PMID: 27648592

Similar Datasets

Project description:Exposures to ambient particulate matter (PM) are associated with increased morbidity and mortality. PM2.5 (<2.5 μm) and ozone exposures have been shown to associate with carotid intima media thickness in humans. Animal studies support a causal relationship between air pollution and atherosclerosis and identified adverse PM effects on HDL functionality. We aimed to determine whether brief exposures to PM2.5 and/or ozone could induce effects on HDL anti-oxidant and anti-inflammatory capacity in humans.Subjects were exposed to fine concentrated ambient fine particles (CAP) with PM2.5 targeted at 150 μg/m(3), ozone targeted at 240 μg/m(3) (120 ppb), PM2.5 plus ozone targeted at similar concentrations, and filtered air (FA) for 2 h, on 4 different occasions, at least two weeks apart, in a randomized, crossover study. Blood was obtained before exposures (baseline), 1 h after and 20 h after exposures. Plasma HDL anti-oxidant/anti-inflammatory capacity and paraoxonase activity were determined. HDL anti-oxidant/anti-inflammatory capacity was assessed by a cell-free fluorescent assay and expressed in units of a HDL oxidant index (HOI). Changes in HOI (ΔHOI) were calculated as the difference in HOI from baseline to 1 h after or 20 h after exposures.There was a trend towards bigger ΔHOI between PM2.5 and FA 1 h after exposures (p = 0.18) but not 20 h after. This trend became significant (p <0.05) when baseline HOI was lower (<1.5 or <2.0), indicating decreased HDL anti-oxidant/anti-inflammatory capacity shortly after the exposures. There were no significant effects of ozone alone or in combination with PM2.5 on the change in HOI at both time points. The change in HOI due to PM2.5 showed a positive trend with particle mass concentration (p = 0.078) and significantly associated with the slope of systolic blood pressure during exposures (p = 0.005).Brief exposures to concentrated PM2.5 elicited swift effects on HDL anti-oxidant/anti-inflammatory functionality, which could indicate a potential mechanism for how particulate air pollution induces harmful cardiovascular effects.

Project description:BACKGROUND:The effects of exposure to fine particulate matter ([Formula: see text]) during wildland fires are not well understood in comparison with [Formula: see text] exposures from other sources. OBJECTIVES:We examined the cardiopulmonary effects of short-term exposure to [Formula: see text] on smoke days in the United States to evaluate whether health effects are consistent with those during non-smoke days. METHODS:We examined cardiopulmonary hospitalizations among adults [Formula: see text] y of age, in U.S. counties ([Formula: see text]) within [Formula: see text] of 123 large wildfires during 2008-2010. We evaluated associations during smoke and non-smoke days and examined variability with respect to modeled and observed exposure metrics. Poisson regression was used to estimate county-specific effects at lag days 0-6 (L0-6), adjusted for day of week, temperature, humidity, and seasonal trend. We used meta-analyses to combine county-specific effects and estimate overall percentage differences in hospitalizations expressed per [Formula: see text] increase in [Formula: see text]. RESULTS:Exposure to [Formula: see text], on all days and locations, was associated with increased hospitalizations on smoke and non-smoke days using modeled exposure metrics. The estimated effects persisted across multiple lags, with a percentage increase of 1.08% [95% confidence interval (CI): 0.28, 1.89] on smoke days and 0.67% (95% CI: [Formula: see text], 1.44) on non-smoke days for respiratory and 0.61% (95% CI: 0.09, 1.14) on smoke days and 0.69% (95% CI: 0.19, 1.2) on non-smoke days for cardiovascular outcomes on L1. For asthma-related hospitalizations, the percentage increase was greater on smoke days [6.9% (95% CI: 3.71, 10.11)] than non-smoke days [1.34% (95% CI: [Formula: see text], 3.77)] on L1. CONCLUSIONS:The increased risk of [Formula: see text]-related cardiopulmonary hospitalizations was similar on smoke and non-smoke days across multiple lags and exposure metrics, whereas risk for asthma-related hospitalizations was higher during smoke days. https://doi.org/10.1289/EHP3860.

Project description:BACKGROUND:Previous work reported increased rates of acute cardiovascular hospitalizations associated with increased PM2.5 concentrations in the previous few days across urban centers in New York State from 2005 to 2016. These relative rates were higher after air quality policies and economic changes resulted in decreased PM2.5 concentrations and changes in PM composition (e.g. increased secondary organic carbon), compared to before and during these changes. Changes in PM composition and sources may explain this difference. OBJECTIVES:To estimate the rate of acute cardiovascular hospitalizations associated with increases in source specific PM2.5 concentrations. METHODS:Using source apportioned PM2.5 concentrations at the same NYS urban sites, a time-stratified case-crossover design, and conditional logistic regression models adjusting for ambient temperature and relative humidity, we estimated the rate of these acute cardiovascular hospitalizations associated with increases in mean source specific PM2.5 concentrations in the previous 1, 4, and 7?days. RESULTS:Interquartile range (IQR) increases in spark-ignition emissions (GAS) concentrations were associated with increased excess rates of cardiac arrhythmia hospitalizations (2.3%; 95% CI?=?0.4%, 4.2%; IQR?=?2.56??g/m3) and ischemic stroke hospitalizations (3.7%; 95% CI?=?1.1%, 6.4%; 2. 73??g/m3) over the next day. IQR increases in diesel (DIE) concentrations were associated with increased rates of congestive heart failure hospitalizations (0.7%; 95% CI?=?0.2% 1.3%; 0.51??g/m3) and ischemic heart disease hospitalizations (0.8%; 95% CI?=?0.3%, 1.3%; 0.60??g/m3) over the next day, as hypothesized. However, secondary sulfate PM2.5 (SS) was not. Increased acute cardiovascular hospitalization rates were also associated with IQR increases in concentrations of road dust (RD), residual oil (RO), and secondary nitrate (SN) over the previous 1, 4, and 7?days, but not other sources. CONCLUSIONS:These findings suggest a role of several sources of PM2.5 in New York State (i.e. traffic emissions, non-traffic emissions such as brake and tire wear, residual oil, and nitrate that may also reflect traffic emissions) in the triggering of acute cardiovascular events.

Dataset Information

Wildfire-specific Fine Particulate Matter and Risk of Hospital Admissions in Urban and Rural Counties.

Publications

Wildfire-specific Fine Particulate Matter and Risk of Hospital Admissions in Urban and Rural Counties.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets