Background

Exceptional aging, defined as reaching age 85 years, shows geographic inequalities that may depend on local environmental conditions. Links between particulate pollution-a well-recognized environmental risk factor-and exceptional aging have not been investigated.

Objectives

We conducted a nationwide analysis of ~28 million adults in 3,034 United States counties to determine whether local PM2.5 levels (particulate matter < 2.5 μm in aerodynamic diameter) affected the probability of becoming 85- to 94-year-olds or centenarians (100- to 104-year-olds) in 2010 for individuals who were 55-64 or 70-74 years old, respectively, in 1980.

Methods

We used population-weighted regression models including county-level PM2.5 from hybrid land-use regression and geostatistical interpolation, smoking, obesity, sociodemographic, and age-specific migration variables.

Results

On average, 2,295 and 71.4 per 10,000 of the 55- to 64- and 70- to 74-year-olds in 1980, respectively, remained in the 85- to 94- and 100- to 104-year-old population in 2010. An interquartile range (4.19 μg/m3) increase in PM2.5 was associated with 93.7 fewer 85- to 94-year-olds (p < 0.001) and 3.5 fewer centenarians (p < 0.05). These associations were nearly linear, were stable to model specification, and were detectable below the annual PM2.5 national standard. Exceptional aging was strongly associated with smoking, with an interquartile range (4.77%) increase in population who smoked associated with 181.9 fewer 85- to 94-year-olds (p < 0.001) and 6.4 fewer centenarians (p < 0.001). Exceptional aging was also associated with obesity rates and median income.

Conclusions

Communities with the most exceptional aging have low ambient air pollution and low rates of smoking, poverty, and obesity. Improvements in these determinants may contribute to increasing exceptional aging. Citation: Baccarelli AA, Hales N, Burnett RT, Jerrett M, Mix C, Dockery DW, Pope CA III. 2016. Particulate air pollution, exceptional aging, and rates of centenarians: a nationwide analysis of the United States, 1980-2010. Environ Health Perspect 124:1744-1750; http://dx.doi.org/10.1289/EHP197.

While laboratory studies show that air pollutants can potentiate insulin resistance, the epidemiologic evidence regarding the association of air pollution with diabetes incidence is conflicting. The purpose of the present study was to assess the association of the traffic-related nitrogen dioxide (NO2) with the incidence of diabetes in a longitudinal cohort study of African American women. We used Cox proportional hazards models to calculate hazard ratios and 95% confidence intervals (CI) for diabetes associated with exposure to NO2 among 43,003 participants in the Black Women's Health Study (BWHS). Pollutant levels at participant residential locations were estimated with 1) a land use regression model for participants living in 56 metropolitan areas, and 2) a dispersion model for participants living in 27 of the cities. From 1995 to 2011, 4387 cases of diabetes occurred. The hazard ratios per interquartile range of NO2 (9.7 ppb), adjusted for age, metropolitan area, education, vigorous exercise, body mass index, smoking, and diet, were 0.96 (95% CI 0.88-1.06) using the land use regression model estimates and 0.94 (95% CI 0.80, 1.10) using the dispersion model estimates. The present results do not support the hypothesis that exposure to NO2 contributes to diabetes incidence in African American women.

Background

Fine particulate matter (PM2.5) air pollution exposure has been identified as a global health threat. However, the types and sources of particles most responsible are not yet known.

Objectives

We sought to identify the causal characteristics and sources of air pollution underlying past associations between long-term PM2.5 exposure and ischemic heart disease (IHD) mortality, as established in the American Cancer Society's Cancer Prevention Study-II cohort.

Methods

Individual risk factor data were evaluated for 445,860 adults in 100 U.S. metropolitan areas followed from 1982 through 2004 for vital status and cause of death. Using Cox proportional hazard models, we estimated IHD mortality hazard ratios (HRs) for PM2.5, trace constituents, and pollution source-associated PM2.5, as derived from air monitoring at central stations throughout the nation during 2000-2005.

Results

Associations with IHD mortality varied by PM2.5 mass constituent and source. A coal combustion PM2.5 IHD HR = 1.05 (95% CI: 1.02, 1.08) per microgram/cubic meter, versus an IHD HR = 1.01 (95% CI: 1.00, 1.02) per microgram/cubic meter PM2.5 mass, indicated a risk roughly five times higher for coal combustion PM2.5 than for PM2.5 mass in general, on a per microgram/cubic meter PM2.5 basis. Diesel traffic-related elemental carbon (EC) soot was also associated with IHD mortality (HR = 1.03; 95% CI: 1.00, 1.06 per 0.26-μg/m3 EC increase). However, PM2.5 from both wind-blown soil and biomass combustion was not associated with IHD mortality.

Conclusions

Long-term PM2.5 exposures from fossil fuel combustion, especially coal burning but also from diesel traffic, were associated with increases in IHD mortality in this nationwide population. Results suggest that PM2.5-mortality associations can vary greatly by source, and that the largest IHD health benefits per microgram/cubic meter from PM2.5 air pollution control may be achieved via reductions of fossil fuel combustion exposures, especially from coal-burning sources.

Citation

Thurston GD, Burnett RT, Turner MC, Shi Y, Krewski D, Lall R, Ito K, Jerrett M, Gapstur SM, Diver WR, Pope CA III. 2016. Ischemic heart disease mortality and long-term exposure to source-related components of U.S. fine particle air pollution. Environ Health Perspect 124:785-794; http://dx.doi.org/10.1289/ehp.1509777.

Rationale: Evidence linking outdoor air pollution with coronavirus disease (COVID-19) incidence and mortality is largely based on ecological comparisons between regions that may differ in factors such as access to testing and control measures that may not be independent of air pollution concentrations. Moreover, studies have yet to focus on key mechanisms of air pollution toxicity such as oxidative stress. Objectives: To conduct a within-city analysis of spatial variations in COVID-19 incidence and the estimated generation of reactive oxygen species (ROS) in lung lining fluid attributable to fine particulate matter (particulate matter with an aerodynamic diameter ⩽2.5 μm [PM_2.5]). Methods: Sporadic and outbreak-related COVID-19 case counts, testing data, population data, and sociodemographic data for 140 neighborhoods were obtained from the City of Toronto. ROS estimates were based on a mathematical model of ROS generation in lung lining fluid in response to iron and copper in PM_2.5. Spatial variations in long-term average ROS were predicted using a land-use regression model derived from measurements of iron and copper in PM_2.5. Data were analyzed using negative binomial regression models adjusting for covariates identified using a directed acyclic graph and accounting for spatial autocorrelation. Measurements and Main Results: A significant positive association was observed between neighborhood-level ROS and COVID-19 incidence (incidence rate ratio = 1.07; 95% confidence interval, 1.01-1.15 per interquartile range ROS). Effect modification by neighborhood-level measures of racialized group membership and socioeconomic status was also identified. Conclusions: Examination of neighborhood characteristics associated with COVID-19 incidence can identify inequalities and generate hypotheses for future studies.

Ambient fine particulate matter (PM2.5) is the worlds leading environmental health risk factor. Quantification is needed of regional contributions to changes in global PM2.5 exposure. Here we interpret satellite-derived PM2.5 estimates over 1998-2019 and find a reversal of previous growth in global PM2.5 air pollution, which is quantitatively attributed to contributions from 13 regions. Global population-weighted (PW) PM2.5 exposure, related to both pollution levels and population size, increased from 1998 (28.3 μg/m3) to a peak in 2011 (38.9 μg/m3) and decreased steadily afterwards (34.7 μg/m3 in 2019). Post-2011 change was related to exposure reduction in China and slowed exposure growth in other regions (especially South Asia, the Middle East and Africa). The post-2011 exposure reduction contributes to stagnation of growth in global PM2.5-attributable mortality and increasing health benefits per µg/m3 marginal reduction in exposure, implying increasing urgency and benefits of PM2.5 mitigation with aging population and cleaner air.

Background Long-term exposure to outdoor fine particulate matter (PM_2.5) is the leading environmental risk factor for premature mortality worldwide. Characterizing important pathways through which PM_2.5 increases individuals' mortality risk can clarify the PM_2.5-mortality relationship and identify possible points of interventions. Recent evidence has linked PM_2.5 to the onset of diabetes and cardiovascular disease, but to what extent these associations contribute to the effect of PM_2.5 on mortality remains poorly understood. Methods and Results We conducted a population-based cohort study to investigate how the effect of PM_2.5 on nonaccidental mortality is mediated by its impacts on incident diabetes, acute myocardial infarction, and stroke. Our study population comprised ≈200 000 individuals aged 20 to 90 years who participated in population-based health surveys in Ontario, Canada, from 1996 to 2014. Follow-up extended until December 2017. Using causal mediation analyses with Aalen additive hazards models, we decomposed the total effect of PM_2.5 on mortality into a direct effect and several path-specific indirect effects mediated by diabetes, each cardiovascular event, or both combined. A series of sensitivity analyses were also conducted. After adjusting for various individual- and neighborhood-level covariates, we estimated that for every 1000 adults, each 10 μg/m³ increase in PM_2.5 was associated with ≈2 incident cases of diabetes, ≈1 major cardiovascular event (acute myocardial infarction and stroke combined), and ≈2 deaths annually. Among PM_2.5-related deaths, 31.7% (95% CI, 17.2%-53.2%) were attributable to diabetes and major cardiovascular events in relation to PM_2.5. Specifically, 4.5% were explained by PM_2.5-induced diabetes, 22.8% by PM_2.5-induced major cardiovascular events, and 4.5% through their interaction. Conclusions This study suggests that a significant portion of the estimated effect of long-term exposure to PM_2.5 on deaths can be attributed to its effect on diabetes and cardiovascular diseases, highlighting the significance of PM_2.5 on deteriorating cardiovascular health. Our findings should raise awareness among professionals that improving metabolic and cardiovascular health may reduce mortality burden in areas with higher exposure to air pollution.

Background

Ozone is a ubiquitous air pollutant with increasing concentrations in many populous regions. Toxicological studies show that ozone can cause oxidative stress and increase insulin resistance. These pathways may contribute to metabolic changes and diabetes formation. In this paper, we investigate the association between ozone and incident type 2 diabetes in a large cohort of African American women.

Methods

We used Cox proportional hazards models to calculate hazard ratios (HRs) for incident type 2 diabetes associated with exposure to ozone in a cohort of 45,231 African American women living in 56 metropolitan areas across the United States. Ozone levels were estimated using the U.S. EPA Models-3/Community Multiscale Air Quality (CMAQ) predictions fused with ground measurements at a resolution of 12km for the years 2007-2008.

Results

The HR per interquartile range increment of 6.7ppb of ozone was 1.18 (95% CI 1.04-1.34) for incident diabetes in adjusted models. This association was unaltered in models that controlled for fine particulate matter with diameter <2.5μm (PM_2.5). Associations were modified by nitrogen dioxide (NO₂) levels, such that HRs for ozone levels were larger in areas of lower NO₂.

Conclusions

Our results provide initial evidence of a positive association between O₃ and incident diabetes in African American women. Given the ubiquity of ozone exposure and the importance of diabetes on quality of life and survival, these results may have important implications for the protection of public health.

Background Exposure to road traffic noise has been linked to cardiometabolic complications, such as elevated blood pressure and glucose dysregulation. However, epidemiologic evidence linking road traffic noise to diabetes mellitus and hypertension remains scarce. We examined associations between road traffic noise and the incidence of diabetes mellitus and hypertension in Toronto, Canada. Methods and Results Using the Ontario Population Health and Environment Cohort, we conducted a retrospective, population-based cohort study of long-term residents of Toronto, aged 35 to 100 years, who were registered for provincial publicly funded health insurance, and were without a history of hypertension (n=701 174) or diabetes mellitus (n=914 607). Road traffic noise exposure levels were assessed by the equivalent continuous A-weighted sound pressure level (dBA) for the 24-hour day and the equivalent continuous A-weighted sound pressure level for the night (11 pm-7am). Noise exposures were assigned to subjects according to their annual residential postal codes during the 15-year follow-up. We used random-effect Cox proportional hazards models adjusting for personal and area-level characteristics. From 2001 to 2015, each interquartile range increase in the equivalent continuous A-weighted sound pressure level (dBA) for the 24-hour day (10.0 dBA) was associated with an 8% increase in incident diabetes mellitus (95% CI, 1.07-1.09) and a 2% increase in hypertension (95% CI, 1.01-1.03). We obtained similar estimates with the equivalent continuous A-weighted sound pressure level for the night (11 pm-7am). These results were robust to all sensitivity analyses conducted, including further adjusting for traffic-related air pollutants (ultrafine particles and nitrogen dioxide). For both hypertension and diabetes mellitus, we observed stronger associations with the equivalent continuous A-weighted sound pressure level (dBA) for the 24-hour day among women and younger adults (aged <60 years). Conclusions Long-term exposure to road traffic noise was associated with an increased incidence of diabetes mellitus and hypertension in Toronto.

Background

The International Agency for Research on Cancer classified both outdoor air pollution and airborne particulate matter as carcinogenic to humans (Group 1) for lung cancer. There may be associations with cancer at other sites; however, the epidemiological evidence is limited.

Objective

The aim of this study was to clarify whether ambient air pollution is associated with specific types of cancer other than lung cancer by examining associations of ambient air pollution with nonlung cancer death in the Cancer Prevention Study II (CPS-II).

Methods

Analysis included 623,048 CPS-II participants who were followed for 22 y (1982-2004). Modeled estimates of particulate matter with aerodynamic diameter <2.5µm (PM_2.5) (1999-2004), nitrogen dioxide (NO₂) (2006), and ozone (O₃) (2002-2004) concentrations were linked to the participant residence at enrollment. Cox proportional hazards models were used to estimate associations per each fifth percentile-mean increment with cancer mortality at 29 anatomic sites, adjusted for individual and ecological covariates.

Results

We observed 43,320 nonlung cancer deaths. PM_2.5 was significantly positively associated with death from cancers of the kidney {adjusted hazard ratio (HR) per 4.4 μg/m³=1.14 [95% confidence interval (CI): 1.03, 1.27]} and bladder [HR=1.13 (95% CI: 1.03, 1.23)]. NO₂ was positively associated with colorectal cancer mortality [HR per 6.5 ppb=1.06 (95% CI: 1.02, 1.10). The results were similar in two-pollutant models including PM_2.5 and NO₂ and in three-pollutant models with O₃. We observed no statistically significant positive associations with death from other types of cancer based on results from adjusted models.

Conclusions

The results from this large prospective study suggest that ambient air pollution was not associated with death from most nonlung cancers, but associations with kidney, bladder, and colorectal cancer death warrant further investigation. https://doi.org/10.1289/EHP1249.

Background

Recent evidence links ambient air pollution to COVID-19 incidence, severity, and death, but few studies have analyzed individual-level mortality data with high quality exposure models.

Methods

We sought to assess whether higher air pollution exposures led to greater risk of death during or after hospitalization in confirmed COVID-19 cases among patients who were members of the Kaiser Permanente Southern California (KPSC) healthcare system (N=21,415 between 06-01-2020 and 01-31-2022 of whom 99.85 % were unvaccinated during the study period). We used 1 km resolution chemical transport models to estimate ambient concentrations of several common air pollutants, including ozone, nitrogen dioxide, and fine particle matter (PM_2.5). We also derived estimates of pollutant exposures from ultra-fine particulate matter (PM_0.1), PM chemical species, and PM sources. We employed Cox proportional hazards models to assess associations between air pollution exposures and death from COVID-19 among hospitalized patients.

Findings

We found significant associations between COVID-19 death and several air pollution exposures, including: PM_2.5 mass, PM_0.1 mass, PM_2.5 nitrates, PM_2.5 elemental carbon, PM_2.5 on-road diesel, and PM_2.5 on-road gasoline. Based on the interquartile (IQR) exposure increment, effect sizes ranged from hazard ratios (HR) = 1.12 for PM_2.5 mass and PM_2.5 nitrate to HR ∼ 1.06-1.07 for other species or source markers. Humidity and temperature in the month of diagnosis were also significant negative predictors of COVID-19 death and negative modifiers of the air pollution effects.

Interpretation

Air pollution exposures and meteorology were associated the risk of COVID-19 death in a cohort of patients from Southern California. These findings have implications for prevention of death from COVID-19 and for future pandemics.