Importance The Environmental Protection Agency (EPA) is required to re-examine its National Ambient Air Quality Standards (NAAQS) every 5 years, but evidence of mortality risk is lacking at air pollution levels below the current daily NAAQS, in unmonitored areas and for sensitive subgroups. Objective To estimate the association between short-term exposures to ambient PM2.5 and ozone and at levels below the current daily NAAQS and mortality in the continental US. Design, Setting, and Participants Case-crossover design and conditional logistic regression to estimate the association between short-term exposures to PM2.5 and ozone (mean of daily exposure on the same day of death and one day prior) and mortality in 2-pollutant models. The study included the entire Medicare population from January 1, 2000 to December 31, 2012 residing in 39,182 zip codes. Exposures Daily PM2.5 and ozone levels in a 1 km × 1 km grid were estimated using published and validated air pollution prediction models based on land use, chemical transport modeling, and satellite remote sensing data. From these gridded exposures, daily exposures were calculated for every zip code in the US. Warm-season ozone was defined as ozone levels for the months April to September of each year. Main Outcome and Measure All-cause mortality in the entire Medicare population from 2000 to 2012. Results During the study period, there were 22,433,862 million case days and 76,143,209 control days. Of all case and control days, 93.6% had PM2.5 levels below 25 μg/m3, during which 95% of deaths occurred (21,353,817 of 22,433,862), and 91.1% of days had ozone levels below 60 ppb, during which 93.4% of deaths occurred (20,955,387 of 22,433,862). The baseline daily mortality rate was 137.33 and 129.44 (per 1 million persons at risk per day) for the entire year and for the warm season, respectively. Each short-term increase of 10 μg/m3 in PM2.5 (adjusted by ozone) and 10 ppb (parts-per-billion, 10−9) in warm-season ozone (adjusted by PM2.5) were statistically significantly associated with a relative increase of 1.05% (95% confidence interval [CI]: 0.95%, 1.15%) and 0.51% (95% CI: 0.41%, 0.61%) in daily mortality rate, respectively. Absolute risk differences in daily mortality rate were 1.42 (95% CI: 1.29, 1.56) and 0.66 (95% CI: 0.53, 0.78) per 1 million persons at risk per day. There was no evidence of a threshold in the exposure-response relationship. Conclusions and Relevance In the US Medicare population from 2000-2012, short-term exposures to PM2.5 and warm-season ozone were significantly associated with increased risk of mortality. This risk occurred at levels below current national air quality standards, suggesting that these standards may need to be reevaluated.

Background: Epidemiological studies have examined the association between PM2.5 and mortality, but uncertainty remains about the seasonal variations in PM2.5-related effects and the relative importance of species.Objectives: We estimated the effects of PM2.5 species on mortality and how infiltration rates may modify the association.Methods: Using city–season specific Poisson regression, we estimated PM2.5 effects on approximately 4.5 million deaths for all causes, cardiovascular disease (CVD), myocardial infarction (MI), stroke, and respiratory diseases in 75 U.S. cities for 2000–2006. We added interaction terms between PM2.5 and monthly average species-to-PM2.5 proportions of individual species to determine the relative toxicity of each species. We combined results across cities using multivariate meta-regression, and controlled for infiltration.Results: We estimated a 1.18% (95% CI: 0.93, 1.44%) increase in all-cause mortality, a 1.03% (95% CI: 0.65, 1.41%) increase in CVD, a 1.22% (95% CI: 0.62, 1.82%) increase in MI, a 1.76% (95% CI: 1.01, 2.52%) increase in stroke, and a 1.71% (95% CI: 1.06, 2.35%) increase in respiratory deaths in association with a 10-μg/m3 increase in 2-day averaged PM2.5 concentration. The associations were largest in the spring. Silicon, calcium, and sulfur were associated with more all-cause mortality, whereas sulfur was related to more respiratory deaths. County-level smoking and alcohol were associated with larger estimated PM2.5 effects.Conclusions: Our study showed an increased risk of mortality associated with PM2.5, which varied with seasons and species. The results suggest that mass alone might not be sufficient to evaluate the health effects of particles.Citation: Dai L, Zanobetti A, Koutrakis P, Schwartz JD. 2014. Associations of fine particulate matter species with mortality in the United States: a multicity time-series analysis. Environ Health Perspect 122:837–842; http://dx.doi.org/10.1289/ehp.1307568

The authors conducted a time-series analysis to examine seasonal variation of mortality risk in association with particulate matter less than 2.5 μm in aerodynamic diameter (PM(2.5)) and chemical species in Xi'an, China, using daily air pollution and all-cause and cause-specific mortality data (2004-2008). Poisson regression incorporating natural splines was used to estimate mortality risks of PM(2.5) and its chemical components, adjusting for day of the week, time trend, and meteorologic effects. Increases of 2.29% (95% confidence interval: 0.83, 3.76) for all-cause mortality and 3.08% (95% confidence interval: 0.94, 5.26) for cardiovascular mortality were associated with an interquartile range increase of 103.0 μg/m(3) in lagged 1-2 day PM(2.5) exposure. Stronger effects were observed for the elderly (≥65 years), males, and cardiovascular diseases groups. Secondary components (sulfate and ammonium), combustion species (elemental carbon, sulfur, chlorine), and transition metals (chromium, lead, nickel, and zinc) appeared most responsible for increased risk, particularly in the cold months. The authors concluded that differential association patterns observed across species and seasons indicated that PM(2.5)-related effects might not be sufficiently explained by PM(2.5) mass alone. Future research is needed to examine spatial and temporal varying factors that might play important roles in modifying the PM(2.5)-mortality association.

Background and objectives: Epidemiologic studies have attributed adverse health effects to air pollution; however, controversy remains regarding the relationship between ambient oxidants [ozone (O3) and nitrogen dioxide (NO2)] and mortality, especially in Asia. We conducted a four-city time-series study to investigate acute effects of O3 and NO2 in the Pearl River Delta (PRD) of southern China, using data from 2006 through 2008.Methods: We used generalized linear models with Poisson regression incorporating natural spline functions to analyze acute mortality in association with O3 and NO2, with PM10 (particulate matter ≤ 10 μm in diameter) included as a major confounder. Effect estimates were determined for individual cities and for the four cities as a whole. We stratified the analysis according to high- and low- exposure periods for O3.Results: We found consistent positive associations between ambient oxidants and daily mortality across the PRD cities. Overall, 10-μg/m3 increases in average O3 and NO2 concentrations over the previous 2 days were associated with 0.81% [95% confidence interval (CI): 0.63%, 1.00%] and 1.95% (95% CI: 1.62%, 2.29%) increases in total mortality, respectively, with stronger estimated effects for cardiovascular and respiratory mortality. After adjusting for PM10, estimated effects of O3 on total and cardiovascular mortality were stronger for exposure during high-exposure months (September through November), whereas respiratory mortality was associated with O3 exposure during nonpeak exposure months only.Conclusions: Our findings suggest significant acute mortality effects of O3 and NO2 in the PRD and strengthen the rationale for further limiting the ambient pollution levels in the area.