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Wildland fire smoke risks are not uniformly distributed across people and places, and the most vulnerable communities are often disproportionately impacted. This study develops a county level community health vulnerability index (CHVI) for the Contiguous United States (CONUS) using three major vulnerability components: adaptive capacity, sensitivity, and exposure at the national and regional level. We first calculated sensitivity and adaptive capacity sub-indices using nine sensitivity and twenty adaptive capacity variables. These sub-indices were then combined with an exposure sub-index, which is based on the Community Multiscale Air Quality data (2008-2018), to develop CHVI. Finally, we conducted several analyses with the derived indices to: 1) explore associations between the level of fine particulate matter from wildland fires (fire-PM 2.5 ) and the sub-indices/CHVI; 2) measure the impact of fire-PM 2.5 on the increase in the annual number of days with 12-35 μg/m 3 (moderate) and >35 μg/m 3 (at or above unhealthy for sensitive groups) based on the US EPA Air Quality Index categories, and 3) calculate population size in different deciles of the sub-indices/CHVI. This study has three main findings. First, we showed that the counties with higher daily fire-PM 2.5 concentration tend to have lower adaptive capacity and higher sensitivity and vulnerability. Relatedly, the counties at high risk tended to experience a greater increase in the annual number of days with 12-35 μg/m 3 and >35 μg/m 3 than their counterparts. Second, we found that 16.1, 12.0, and 17.6 million people out of 332 million in CONUS reside in the counties in the lowest adaptive capacity decile, highest sensitivity decile, and highest vulnerability decile, respectively. Third, we identified that the US Northwest, California, and Southern regions tended to have higher vulnerability than others. Accurately identifying a community's vulnerability to wildfire smoke can help individuals, researchers, and policymakers better understand, prepare for, and respond to future wildland fire events., Competing Interests: Declaration of competing interest The authors declare there are no competing or conflicts of interest., (Copyright © 2023 The Author(s). Published by Elsevier B.V. All rights reserved.)

Background: Fine particulate matter (PM 2.5 ) related mild inflammation, altered autonomic control of cardiovascular function, and changes to cell function have been observed in controlled human exposure studies., Methods: To measure the systemic and cardiopulmonary impacts of low-level PM exposure, we exposed 20 healthy, young volunteers to PM 2.5 , in the form of concentrated ambient particles (mean: 37.8 μg/m 3 , SD 6.5), and filtered air (mean: 2.1 μg/m 3 , SD 2.6). In this double-blind, crossover study the exposure order was randomized. During the 4 h exposure, volunteers (7 females and 13 males) underwent light intensity exercise to regulate ventilation rate. We measured pulmonary, cardiac, and hematologic end points before exposure, 1 h after exposure, and again 20 h after exposure., Results: Low-level PM 2.5 resulted in both pulmonary and extra-pulmonary changes characterized by alterations in systematic inflammation markers, cardiac repolarization, and decreased pulmonary function. A mean increase in PM 2.5 concentration (37.8 μg/m 3 ) significantly increased serum amyloid A (SAA), C-reactive protein (CRP), soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1), 1 h after exposure by 8.7, 9.1, 10.7, and 6.6%, respectively, relative to the filtered air control. SAA remained significantly elevated (34.6%) 20 h after PM 2.5 exposure which was accompanied by a 5.7% decrease in percent neutrophils. Decreased pulmonary function was observed 1 h after exposure through a 0.8 and 1.2% decrease in forced expiratory volume in 1 s (FEV 1 ) and FEV 1 / forced vital capacity (FEV 1 /FVC) respectively. Additionally, sex specific changes were observed in repolarization outcomes following PM 2.5 exposure. In males, P-wave and QRS complex were increased by 15.4 and 5.4% 1 h after exposure., Conclusions: This study is the first controlled human exposure study to demonstrate biological effects in response to exposure to concentrated ambient air PM 2.5 particles at levels near the PM 2.5 US NAAQS standard., Clinical Trial Registration Information: clinicaltrials.gov ; Identifier: NCT03232086 . The study was registered retrospectively on July 25, 2017, prior to final data collection on October 25, 2017 and data analysis.

Background: Wildfires are increasingly a significant source of fine particulate matter (PM 2.5 ), which has been linked to adverse health effects and increased mortality. ESKD patients are potentially susceptible to this environmental stressor., Methods: We conducted a retrospective time-series analysis of the association between daily exposure to wildfire PM 2.5 and mortality in 253 counties near a major wildfire between 2008 and 2012. Using quasi-Poisson regression models, we estimated rate ratios (RRs) for all-cause mortality on the day of exposure and up to 30 days following exposure, adjusted for background PM 2.5 , day of week, seasonality, and heat. We stratified the analysis by causes of death (cardiac, vascular, infectious, or other) and place of death (clinical or nonclinical setting) for differential PM 2.5 exposure and outcome classification., Results: We found 48,454 deaths matched to the 253 counties. A 10- μ g/m 3 increase in wildfire PM 2.5 associated with a 4% increase in all-cause mortality on the same day (RR, 1.04; 95% confidence interval [95% CI], 1.01 to 1.07) and 7% increase cumulatively over 30 days following exposure (RR, 1.07; 95% CI, 1.01 to 1.12). Risk was elevated following exposure for deaths occurring in nonclinical settings (RR, 1.07; 95% CI, 1.02 to 1.12), suggesting modification of exposure by place of death. "Other" deaths (those not attributed to cardiac, vascular, or infectious causes) accounted for the largest portion of deaths and had a strong same-day effect (RR, 1.08; 95% CI, 1.03 to 1.12) and cumulative effect over the 30-day period. On days with a wildfire PM 2.5 contribution >10 μ g/m 3 , exposure accounted for 8.4% of mortality., Conclusions: Wildfire smoke exposure was positively associated with all-cause mortality among patients receiving in-center hemodialysis., (Copyright © 2020 by the American Society of Nephrology.)

Background: Reductions in ambient concentrations of fine particulate matter ( PM 2.5 ) have contributed to reductions in cardiovascular (CV) mortality., Objectives: We examined changes in CV mortality attributed to reductions in emissions from mobile, point, areal, and nonroad sources through changes in concentrations of PM 2.5 and its major components [nitrates, sulfates, elemental carbon (EC), and organic carbon (OC)] in 2,132 U.S. counties between 1990 and 2010., Methods: Using Community Multiscale Air Quality model estimated PM 2.5 total and component concentrations, we calculated population-weighted annual averages for each county. We estimated PM 2.5 total- and component-related CV mortality, adjusted for county-level population characteristics and baseline PM 2.5 concentrations. Using the index of Emission Mitigation Efficiency for primary emission-to-particle pathways, we expressed changes in particle-related mortality in terms of precursor emissions by each sector., Results: PM 2.5 reductions represented 5.7% of the overall decline in CV mortality. Large point source emissions of sulfur dioxide accounted for 6.685 [95% confidence interval (CI): 5.703, 7.667] fewer sulfate-related CV deaths per 100,000 people. Mobile source emissions of primary EC and nitrous oxides accounted for 3.396 (95% CI: 2.772, 4.020) and 3.984 (95% CI: 2.472, 5.496) fewer CV deaths per 100,000 people respectively. Increased EC and OC emissions from areal sources increased carbon-related CV mortality by 0.788 (95% CI: - 0.540 , 2.116) and 0.245 (95% CI: - 0.697 , 1.187) CV deaths per 100,000 people., Discussion: In a nationwide epidemiological study of emission sector contribution to PM 2.5 -related mortality, we found that reductions in sulfur-dioxide emissions from large point sources and nitrates and EC emissions from mobile sources contributed the largest reduction in particle-related mortality rates respectively. https://doi.org/10.1289/EHP5692.

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.

Background: Wildfire smoke is known to exacerbate respiratory conditions; however, evidence for cardiovascular and cerebrovascular events has been inconsistent, despite biological plausibility., Methods and Results: A population-based epidemiologic analysis was conducted for daily cardiovascular and cerebrovascular emergency department (ED) visits and wildfire smoke exposure in 2015 among adults in 8 California air basins. A quasi-Poisson regression model was used for zip code-level counts of ED visits, adjusting for heat index, day of week, seasonality, and population. Satellite-imaged smoke plumes were classified as light, medium, or dense based on model-estimated concentrations of fine particulate matter. Relative risk was determined for smoky days for lag days 0 to 4. Rates of ED visits by age- and sex-stratified groups were also examined. Rates of all-cause cardiovascular ED visits were elevated across all lags, with the greatest increase on dense smoke days and among those aged ≥65 years at lag 0 (relative risk 1.15, 95% confidence interval [1.09, 1.22]). All-cause cerebrovascular visits were associated with smoke, especially among those 65 years and older, (1.22 [1.00, 1.49], dense smoke, lag 1). Respiratory conditions were also increased, as anticipated (1.18 [1.08, 1.28], adults >65 years, dense smoke, lag 1). No association was found for the control condition, acute appendicitis. Elevated risks for individual diagnoses included myocardial infarction, ischemic heart disease, heart failure, dysrhythmia, pulmonary embolism, ischemic stroke, and transient ischemic attack., Conclusions: Analysis of an extensive wildfire season found smoke exposure to be associated with cardiovascular and cerebrovascular ED visits for all adults, particularly for those over aged 65 years., (© 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.)

Identifying communities vulnerable to adverse health effects from exposure to wildfire smoke may help prepare responses, increase the resilience to smoke and improve public health outcomes during smoke days. We developed a Community Health-Vulnerability Index (CHVI) based on factors known to increase the risks of health effects from air pollution and wildfire smoke exposures. These factors included county prevalence rates for asthma in children and adults, chronic obstructive pulmonary disease, hypertension, diabetes, obesity, percent of population 65 years of age and older, and indicators of socioeconomic status including poverty, education, income and unemployment. Using air quality simulated for the period between 2008 and 2012 over the continental U.S. we also characterized the population size at risk with respect to the level and duration of exposure to fire-originated fine particulate matter (fire-PM 2.5 ) and CHVI. We estimate that 10% of the population (30.5 million) lived in the areas where the contribution of fire-PM 2.5 to annual average ambient PM 2.5 was high (>1.5 μg/m 3 ) and that 10.3 million individuals experienced unhealthy air quality levels for more than 10 days due to smoke. Using CHVI we identified the most vulnerable counties and determined that these communities experience more smoke exposures in comparison to less vulnerable communities.

BACKGROUND: Air pollution risk assessments do not generally quantify health impacts using multipollutant risk estimates, but instead use results from single-pollutant or copollutant models. Multipollutant epidemiological models account for pollutant interactions and joint effects but can be computationally complex and data intensive. Risk estimates from multipollutant studies are therefore challenging to implement in the quantification of health impacts. OBJECTIVES: Our objective was to conduct a case study using a developmental multipollutant version of the Environmental Benefits Mapping and Analysis Program—Community Edition (BenMAP-CE) to estimate the health impact associated with changes in multiple air pollutants using both a single and multipollutant approach. METHODS: BenMAP-CE was used to estimate the change in the number of pediatric asthma emergency department (ED) visits attributable to simulated changes in air pollution between 2011 and 2025 in Atlanta, Georgia, applying risk estimates from an epidemiological study that examined shortterm single-pollutant and multipollutant (with and without first-order interactions) exposures. Analyses examined individual pollutants (i.e., ozone, fine particulate matter, carbon monoxide, nitrogen dioxide (NO2), sulfur dioxide, and particulate matter components) and combinations of these pollutants meant to represent shared properties or predefined sources (i.e., oxidant gases, secondary pollutants, traffic, power plant, and criteria pollutants). Comparisons were made between multipollutant health impact functions (HIF) and the sum of single-pollutant HIFs for the individual pollutants that constitute the respective pollutant groups. RESULTS: Photochemical modeling predicted large decreases in most of the examined pollutant concentrations between 2011 and 2025 based on sector specific (i.e., source-based) estimates of growth and anticipated controls. Estimated number of avoided asthma ED visits attributable to any given multipollutant group were generally higher when using results from models that included interaction terms in comparison with those that did not. We estimated the greatest number of avoided pediatric asthma ED visits for pollutant groups that include NO2 (i. e., criteria pollutants, oxidants, and traffic pollutants). In models that accounted for interaction, year-round estimates for pollutant groups that included NO2 ranged from 27.1 [95% confidence interval (CI): 1.6, 52.7; traffic pollutants] to 55.4 (95% CI: 41.8, 69.0; oxidants) avoided pediatric asthma ED visits. Year-round results using multipollutant risk estimates with interaction were comparable to the sum of the single-pollutant results corresponding to most multipollutant groups [e.g., 52.9 (95% CI: 43.6, 62.2) for oxidants] but were notably lower than the sum of the single-pollutant results for some pollutant groups [e.g., 77.5 (95% CI: 66.0, 89.0) for traffic pollutants]. DISCUSSION: Performing a multipollutant health impact assessment is technically feasible but computationally complex. It requires time, resources, and detailed input parameters not commonly reported in air pollution epidemiological studies. Results estimated using the sum of single-pollutant models are comparable to those quantified using a multipollutant model. Although limited to a single study and location, assessing the trade-offs between a multipollutant and single-pollutant approach is warranted. [ABSTRACT FROM AUTHOR]

Rationale: Exposure to air pollution is associated with adverse respiratory effects. Polyunsaturated omega 3 (n-3) fatty acids (FAs) appear to attenuate the health effects of air pollution. Objectives: This panel study evaluated whether n-3 FA intake and blood levels of polyunsaturated omega 6 (n-6) FAs can modulate the associations between respiratory effects and short-term exposure to ambient air pollution in healthy adults. Methods: Sixty-two healthy adults were enrolled into either high or low n-3 FA groups on the basis of n-3 FA intake and erythrocyte n-3 FA concentrations. Low and high n-6 FA groups were dichotomized on the basis of blood n-6 FA levels. Participants underwent three to five testing sessions separated by at least 7 days. At each session, the forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), and plasma markers of inflammation (IL-6 [interleukin-6]) and oxidative stress (ox-LDL [oxidized low-density lipoprotein]) were measured. Associations between the ambient ozone and fine particulate matter (PM) (PM with an aerodynamic diameter ⩽2.5 μm [PM2.5]) levels and the lung function and blood markers were assessed by using mixed-effect models stratified by FA levels. Results: Average levels of ozone (40.8 ± 11.1 ppb) and PM2.5 (10.2 ± 4.1 μg/m3) were below national ambient air quality standards during the study period. FVC was positively associated with ozone at a lag of 0 days (lag0) in the high n-3 FA group, whereas the association was null in the low n-3 FA group (for an interquartile range increase in ozone of 1.8% [95% confidence interval (CI): 0.5% to 3.2%] vs. 0.0% [95% CI: -1.4% to 1.5%]); however, the association shifted to being negative at lag4 (-1.9% [95% CI: -3.2 to -0.5] vs. 0.2% [95% CI: -1.2% to 1.5%]) and lag5 (-1.2% [95% CI: -2.4% to 0.0%] vs. 0.9% [95% CI: -0.4% to 2.3%]). A similar pattern was observed in the low n-6 FA group compared with the high n-6 FA group (lag0: 1.7% [95% CI: 0.3% to 3.0%] vs. 0.5% [95% CI: -0.9% to 2.0%] and lag4: -1.4% [95% CI: -2.8% to 0.0%] vs. -0.5% [95% CI: -1.8% to 0.9%]). The associations between FEV1 and ozone and between FVC and PM2.5 also followed a similar pattern. Elevated ozone levels were associated with an immediate decrease in ox-LDL in the high n-3 FA group at lag0 (-12.3% [95% CI: -24.8% to 0.1%]), whereas there was no change in the low n-3 FA group (-7.5% [95% CI: -21.4% to 6.5%]) and there was a delayed increase in IL-6 in the high n-3 FA group compared with the low n-3 FA group (lag4: 66.9% [95% CI: 27.9% to 106.0%] vs. 8.9% [95% CI: -31.8% to 49.6%], lag5: 58.2% [95% CI: 22.4% to 94.1%] vs. -7.4% [95% CI: -48.8% to 34.0%], and lag6: 45.8% [95% CI: 8.7% to 82.9%] vs. -8.5% [95% CI: -49.7% to 32.6%]). Conclusions: We observed lag-dependent associations between short-term ambient air pollutants and lung function that were differentially modulated by n-3 and n-6 FAs, suggesting that n-3 and n-6 FAs counteract the respiratory response to low levels of ambient air pollution in healthy adults.Clinical trial registered with clinicaltrials.gov (NCT02921048). [ABSTRACT FROM AUTHOR]

Objective(s): This study explored the feasibility, acceptability, preliminary impact, and functionality of two risk reduction mobile application (app) interventions on asthma outcomes as compared to a control arm during wildfire season. Design: Three‐arm, 8‐week randomized clinical trial. Sample: Sixty‐seven young adults with asthma were enrolled. Measurements: The Asthma Control Test, forced expiratory volume in one second (FEV1) and the System Usability Scale were measured at baseline, 4, and 8 weeks. The Research Attitude Scale was administered at 8 weeks. Twenty participants from the two intervention arms completed an optional survey and six were interviewed after completing the study. Intervention: Both intervention arms could access Smoke Sense Urbanova, an app that supports reducing risks from breathing wildfire smoke. The Smoke Sense Urbanova Plus arm also monitored their daily FEV1, received air quality notifications, and accessed preventive tips and a message board. Results: Most participants agreed the app and spirometer were usable and their privacy and confidentiality were maintained. No adverse events were reported. Conclusions: Participant‐identified recommendations will support intervention refinement and testing. This research supports asthma self‐management tools that public health nurses and community health workers can recommend for at‐risk populations. [ABSTRACT FROM AUTHOR]

Exposure to wildfire smoke increases the risk of respiratory and cardiovascular hospital admissions. Health impact assessments, used to inform decision‐making processes, characterize the health impacts of environmental exposures by combining preexisting epidemiological concentration–response functions (CRFs) with estimates of exposure. These two key inputs influence the magnitude and uncertainty of the health impacts estimated, but for wildfire‐related impact assessments the extent of their impact is largely unknown. We first estimated the number of respiratory, cardiovascular, and asthma hospital admissions attributable to fire‐originated PM2.5 exposure in central California during the October 2017 wildfires, using Monte Carlo simulations to quantify uncertainty with respect to the exposure and epidemiological inputs. We next conducted sensitivity analyses, comparing four estimates of fire‐originated PM2.5 and two CRFs, wildfire and nonwildfire specific, to understand their impact on the estimation of excess admissions and sources of uncertainty. We estimate the fires accounted for an excess 240 (95% CI: 114, 404) respiratory, 68 (95% CI: −10, 159) cardiovascular, and 45 (95% CI: 18, 81) asthma hospital admissions, with 56% of admissions occurring in the Bay Area. Although differences between impact assessment methods are not statistically significant, the admissions estimates' magnitude is particularly sensitive to the CRF specified while the uncertainty is most sensitive to estimates of fire‐originated PM2.5. Not accounting for the exposure surface's uncertainty leads to an underestimation of the uncertainty of the health impacts estimated. Employing context‐specific CRFs and using accurate exposure estimates that combine multiple data sets generates more certain estimates of the acute health impacts of wildfires. Plain Language Summary: Health impact assessments are public health decision‐making tools that quantify the health impacts of environmental exposures by combining two key pieces of information: estimates of the population's level of exposure and a function describing the relationship between exposure and the risk of adverse health outcome(s). For wildfire smoke, an environmental exposure of increasing importance, it is largely unknown how different choices for these two inputs impact the magnitude and uncertainty of the health impacts estimated. To understand this, we evaluated the sensitivity of an impact assessment, which estimated the number of hospital admissions attributable to smoke exposure during the October 2017 California wildfires, to four different estimates of smoke exposure and two different health risk functions. We find that smoke exposure accounted for an estimated 308 excess respiratory and cardiovascular admissions. The health impact assessment is sensitive to the inputs selected, with the admissions estimates' magnitude most impacted by the health risk function and the uncertainty most impacted by the estimates of exposure. In order to estimate the health impacts of wildfires with greater certainty, we recommend using more informed and accurate estimates of smoke exposure and health risk functions that are specific to wildfire smoke. Key Points: PM2.5 exposure during the 2017 California fires accounted for an estimated 308 excess respiratory and cardiovascular hospital admissionsHealth impact assessments, used to inform decision‐making processes, are sensitive to the exposure and epidemiologic inputs specifiedAccurate exposure estimates and context‐specific health risk functions estimate fire‐attributable health impacts with greater certainty [ABSTRACT FROM AUTHOR]

BACKGROUND: Exposure to ambient particulate matter (PM) induces endothelial dysfunction, a risk factor for cardiovascular disease. Olive oil (OO) and fish oil (FO) supplements have beneficial effects on endothelial function. OBJECTIVE: In this study we evaluated the potential efficacy of OO and FO in mitigating endothelial dysfunction and disruption of hemostasis caused by exposure to particulate matter (PM). METHODS AND RESULTS: Forty-two participants (58 ± 1 years of age) received either 3 g/day of OO or FO, or no supplements (naive) for 4 weeks prior to undergoing 2-hr exposures to filtered air and concentrated ambient particulate matter (CAP; mean, 253 ± 16 µg/m³). Endothelial function was assessed by flow-mediated dilation (FMD) of the brachial artery preexposure, immediately postexposure, and 20 hr postexposure. Levels of endothelin-1 and markers of fibrinolysis and inflammation were also measured. The FMD was significantly lower after CAP exposure in the naive (-19.4%; 95% CI: -36.4, -2.3 per 100 µg/m³ CAP relative to baseline; p = 0.03) and FO groups (-13.7%; 95% CI: -24.5, -2.9; p = 0.01), but not in the OO group (-7.6%; 95% CI: --21.5, 6.3; p = 0.27). Tissue plasminogen activator levels were significantly increased immediately after (11.6%; 95% CI: 0.8, 22.2; p = 0.04) and 20 hr after CAP exposure in the OO group. Endothelin-1 levels were significantly increased 20 hr after CAP exposure in the naive group only (17.1%; 95% CI: 2.2, 32.0;p = 0.03). CONCLUSIONS: Short-term exposure to CAP induced vascular endothelial dysfunction. OO supplementation attenuated CAP-induced reduction of FMD and changes in blood markers associated with vasoconstriction and fibrinolysis, suggesting that OO supplementation may be an efficacious intervention to protect against vascular effects of exposure to PM. [ABSTRACT FROM AUTHOR]

Background: Air pollution epidemiologic studies, often conducted in large metropolitan areas because of proximity to regulatory monitors, are limited in their ability to examine potential associations between air pollution exposures and health effects in rural locations. Methods: Using a time-stratified case-crossover framework, we examined associations between asthma emergency department (ED) visits in North Carolina (2006-2008), collected by a surveillance system, and short-term ozone (O3) exposures using predicted concentrations from the Community Multiscale Air Quality (CMAQ) model. We estimated associations by county groupings based on four urbanicity classifications (representative of county size and urban proximity) and county health. Results: O3 was associated with asthma ED visits in all-year and warm season (April-October) analyses [odds ratio (OR) = 1.019; 95% CI: 0.998, 1.040; OR = 1.020; 95% CI: 0.997, 1.044, respectively, for a 20-ppb increase in lag 0-2 days O3]. The association was strongest in Less Urbanized counties, with no evidence of a positive association in Rural counties. Associations were similar when adjusted for fine particulate matter in copollutant models. Associations were stronger for children (5-17 years of age) compared with other age groups, and for individuals living in counties identified with poorer health status compared with counties that had the highest health rankings, although estimated associations for these subgroups had larger uncertainty. Conclusions: Associations between short-term O3 exposures and asthma ED visits differed by overall county health and urbanicity, with stronger associations in Less Urbanized counties, and no positive association in Rural counties. Results also suggest that children are at increased risk of O3-related respiratory effects. [ABSTRACT FROM AUTHOR]

Background: In June 2008, burning peat deposits produced haze and air pollution far in excess of National Ambient Air Quality Standards, encroaching on rural communities of eastern North Carolina. Although the association of mortality and morbidity with exposure to urban air pollution is well established, the health effects associated with exposure to wildfire emissions are less well understood. Objective: We investigated the effects of exposure on cardiorespiratory outcomes in the population affected by the fire. Methods: We performed a population-based study using emergency department (ED) visits reported through the syndromic surveillance program NC DETECT (North Carolina Disease Event Tracking and Epidemiologic Collection Tool). We used aerosol optical depth measured by a satellite to determine a high-exposure window and distinguish counties most impacted by the dense smoke plume from surrounding referent counties. Poisson log-linear regression with a 5-day distributed lag was used to estimate changes in the cumulative relative risk (RR). Results: In the exposed counties, significant increases in cumulative RR for asthma [1.65 (95% confidence interval, 1.25-2.1)], chronic obstructive pulmonary disease [1.73 (1.06-2.83)], and pneumonia and acute bronchitis [1.59 (1.07-2.34)] were observed. ED visits associated with cardio- pulmonary symptoms [1.23 (1.06-1.43)] and heart failure [1.37 (1.01-1.85)] were also significantly increased. Conclusions: Satellite data and syndromic surveillance were combined to assess the health impacts of wildfire smoke in rural counties with sparse air-quality monitoring. This is the first study to demonstrate both respiratory and cardiac effects after brief exposure to peat wildfire smoke. [ABSTRACT FROM AUTHOR]