Outdoor air pollution and cancer: An overview of the current evidence and public health recommendations.

Outdoor air pollution is a major contributor to the burden of disease worldwide. Most of the global population resides in places where air pollution levels, because of emissions from industry, power generation, transportation, and domestic burning, considerably exceed the World Health Organization's health-based air-quality guidelines. Outdoor air pollution poses an urgent worldwide public health challenge because it is ubiquitous and has numerous serious adverse human health effects, including cancer. Currently, there is substantial evidence from studies of humans and experimental animals as well as mechanistic evidence to support a causal link between outdoor (ambient) air pollution, and especially particulate matter (PM) in outdoor air, with lung cancer incidence and mortality. It is estimated that hundreds of thousands of lung cancer deaths annually worldwide are attributable to PM air pollution. Epidemiological evidence on outdoor air pollution and the risk of other types of cancer, such as bladder cancer or breast cancer, is more limited. Outdoor air pollution may also be associated with poorer cancer survival, although further research is needed. This report presents an overview of outdoor air pollutants, sources, and global levels, as well as a description of epidemiological evidence linking outdoor air pollution with cancer incidence and mortality. Biological mechanisms of air pollution-derived carcinogenesis are also described. This report concludes by summarizing public health/policy recommendations, including multilevel interventions aimed at individual, community, and regional scales. Specific roles for medical and health care communities with regard to prevention and advocacy and recommendations for further research are also described.

Cardiopulmonary Mortality and Fine Particulate Air Pollution by Species and Source in a National U.S. Cohort.

The purpose of this study was to estimate cardiopulmonary mortality associations for long-term exposure to PM2.5 species and sources (i.e., components) within the U.S. National Health Interview Survey cohort. Exposures were estimated through a chemical transport model for six species (i.e., elemental carbon (EC), primary organic aerosols (POA), secondary organic aerosols (SOA), sulfate (SO4), ammonium (NH4), nitrate (NO3)) and five sources of PM2.5 (i.e., vehicles, electricity-generating units (EGU), non-EGU industrial sources, biogenic sources (bio), "other" sources). In single-pollutant models, we found positive, significant (p < 0.05) mortality associations for all components, except POA. After adjusting for remaining PM2.5 (total PM2.5 minus component), we found significant mortality associations for EC (hazard ratio (HR) = 1.36; 95% CI [1.12, 1.64]), SOA (HR = 1.11; 95% CI [1.05, 1.17]), and vehicle sources (HR = 1.06; 95% CI [1.03, 1.10]). HRs for EC, SOA, and vehicle sources were significantly larger in comparison to those for remaining PM2.5 (per unit µg/m3). Our findings suggest that cardiopulmonary mortality associations vary by species and source, with evidence that EC, SOA, and vehicle sources are important contributors to the PM2.5 mortality relationship. With further validation, these findings could facilitate targeted pollution regulations that more efficiently reduce air pollution mortality.

Designing health impact functions to assess marginal changes in outdoor fine particulate matter.

Estimating health benefits from improvements in ambient air quality requires the characterization of the magnitude and shape of the association between marginal changes in exposure and marginal changes in risk, and its uncertainty. Several attempts have been made to do this, each requiring different assumptions. These include the Log-Linear(LL), IntegratedExposure-Response(IER), and GlobalExposureMortalityModel(GEMM). In this paper we develop an improved relative risk model suitable for use in health benefits analysis that incorporates features of existing models while addressing limitations in each model. We model the derivative of the relative risk function within a meta-analytic framework; a quantity directly applicable to benefits analysis, incorporating a Fusion of algebraic functions used in previous models. We assume a constant derivative in concentration over low exposures, like the LL model, a declining derivative over moderate exposures observed in cohort studies, and a derivative declining as the inverse of concentration over high global exposures in a similar manner to the GEMM. The model properties are illustrated with examples of fitting it to data for the six specific causes of death previously examined by the GlobalBurdenofDisease program with ambient fine particulate matter (PM2.5). In a test case analysis assuming a 1% (benefits analysis) or 100% (burden analysis), reduction in country-specific fine particulate matter concentrations, corresponding estimated global attributable deaths using the Fusion model were found to lie between those of the IER and LL models, with the GEMM estimates similar to those based on the LL model.

Dose-response association of aerobic and muscle-strengthening physical activity with mortality: a national cohort study of 416 420 US adults.

OBJECTIVES: To investigate the dose-response association of aerobic physical activity (PA) and muscle-strengthening exercise (MSE) with all-cause mortality. METHODS: National Health Interview Survey data (1997-2014) were linked to the National Death Index through 2015, which produced a cohort of 416 420 US adults. Cox proportional-hazard models were used to estimate HRs and 95% CIs for the associations of moderate aerobic PA (MPA), vigorous aerobic PA (VPA) and MSE with mortality risk. Models controlled for age, sex, race-ethnicity, income, education, marital status, survey year, smoking status, body mass index and chronic conditions. RESULTS: Relative to those who engaged in no aerobic PA, substantial mortality risk reduction was associated with 1 hour/week of aerobic PA (HR: 0.85, 95% CI: 0.83 to 0.86) and levelled off at 3 hours/week of aerobic PA (0.73, 0.71 to 0.75). Similar results were observed for men and women and for individuals younger and older than 60 years. MSE conferred additional mortality risk reduction at 1 time/week (0.89, 0.81 to 0.97) and appeared no longer beneficial at 7 times/week (0.99, 0.94 to 1.04). CONCLUSION: The minimum effective dose of aerobic PA for significant mortality risk reduction was 1 hour/week of MPA or VPA, with additional mortality risk reduction observed up to 3 hours/week. For older adults, only small decreases in mortality risk were observed beyond this duration. Completing MSE in combination with aerobic PA conferred additional mortality risk reduction, with a minimum effective dose of 1-2 times/week.

Global estimates of mortality associated with long-term exposure to outdoor fine particulate matter.

Exposure to ambient fine particulate matter (PM2.5) is a major global health concern. Quantitative estimates of attributable mortality are based on disease-specific hazard ratio models that incorporate risk information from multiple PM2.5 sources (outdoor and indoor air pollution from use of solid fuels and secondhand and active smoking), requiring assumptions about equivalent exposure and toxicity. We relax these contentious assumptions by constructing a PM2.5-mortality hazard ratio function based only on cohort studies of outdoor air pollution that covers the global exposure range. We modeled the shape of the association between PM2.5 and nonaccidental mortality using data from 41 cohorts from 16 countries-the Global Exposure Mortality Model (GEMM). We then constructed GEMMs for five specific causes of death examined by the global burden of disease (GBD). The GEMM predicts 8.9 million [95% confidence interval (CI): 7.5-10.3] deaths in 2015, a figure 30% larger than that predicted by the sum of deaths among the five specific causes (6.9; 95% CI: 4.9-8.5) and 120% larger than the risk function used in the GBD (4.0; 95% CI: 3.3-4.8). Differences between the GEMM and GBD risk functions are larger for a 20% reduction in concentrations, with the GEMM predicting 220% higher excess deaths. These results suggest that PM2.5 exposure may be related to additional causes of death than the five considered by the GBD and that incorporation of risk information from other, nonoutdoor, particle sources leads to underestimation of disease burden, especially at higher concentrations.

Cancer mortality risk, fine particulate air pollution, and smoking in a large, representative cohort of US adults.

PURPOSE: Air pollution and smoking are associated with various types of mortality, including cancer. The current study utilizes a publicly accessible, nationally representative cohort to explore relationships between fine particulate matter (PM2.5) exposure, smoking, and cancer mortality. METHODS: National Health Interview Survey and mortality follow-up data were combined to create a study population of 635,539 individuals surveyed from 1987 to 2014. A sub-cohort of 341,665 never-smokers from the full cohort was also created. Individuals were assigned modeled PM2.5 exposure based on average exposure from 1999 to 2015 at residential census tract. Cox Proportional Hazard models were utilized to estimate hazard ratios for cancer-specific mortality controlling for age, sex, race, smoking status, body mass, income, education, marital status, rural versus urban, region, and survey year. RESULTS: The risk of all cancer mortality was adversely associated with PM2.5 (per 10 µg/m3 increase) in the full cohort (hazard ratio [HR] 1.15, 95% confidence interval [CI] 1.08-1.22) and the never-smokers' cohort (HR 1.19, 95% CI 1.06-1.33). PM2.5-morality associations were observed specifically for lung, stomach, colorectal, liver, breast, cervix, and bladder, as well as Hodgkin lymphoma, non-Hodgkin lymphoma, and leukemia. The PM2.5-morality association with lung cancer in never-smokers was statistically significant adjusting for multiple comparisons. Cigarette smoking was statistically associated with mortality for many cancer types. CONCLUSIONS: Exposure to PM2.5 air pollution contributes to lung cancer mortality and may be a risk factor for other cancer types. Cigarette smoking has a larger impact on cancer mortality than PM2.5 , but is associated with similar cancer types.

Fine particulate air pollution and human mortality: 25+ years of cohort studies.

Much of the key epidemiological evidence that long-term exposure to fine particulate matter air pollution (PM2.5) contributes to increased risk of mortality comes from survival studies of cohorts of individuals. Although the first two of these studies, published in the mid-1990s, were highly controversial, much has changed in the last 25 + years. The objectives of this paper are to succinctly compile and summarize the findings of these cohort studies using meta-analytic tools and to address several of the key controversies. Independent reanalysis and substantial extended analysis of the original cohort studies have been conducted and many additional studies using a wide variety of cohorts, including cohorts constructed from public data and leveraging natural experiments have been published. Meta-analytic estimates of the mean of the distribution of effects from cohort studies that are currently available, provide substantial evidence of adverse air pollution associations with all-cause, cardiopulmonary, and lung cancer mortality.

Particulate matter air pollution and national and county life expectancy loss in the USA: A spatiotemporal analysis.

BACKGROUND: Exposure to fine particulate matter pollution (PM2.5) is hazardous to health. Our aim was to directly estimate the health and longevity impacts of current PM2.5 concentrations and the benefits of reductions from 1999 to 2015, nationally and at county level, for the entire contemporary population of the contiguous United States. METHODS AND FINDINGS: We used vital registration and population data with information on sex, age, cause of death, and county of residence. We used four Bayesian spatiotemporal models, with different adjustments for other determinants of mortality, to directly estimate mortality and life expectancy loss due to current PM2.5 pollution and the benefits of reductions since 1999, nationally and by county. The covariates included in the adjusted models were per capita income; percentage of population whose family income is below the poverty threshold, who are of Black or African American race, who have graduated from high school, who live in urban areas, and who are unemployed; cumulative smoking; and mean temperature and relative humidity. In the main model, which adjusted for these covariates and for unobserved county characteristics through the use of county-specific random intercepts, PM2.5 pollution in excess of the lowest observed concentration (2.8 µg/m3) was responsible for an estimated 15,612 deaths (95% credible interval 13,248-17,945) in females and 14,757 deaths (12,617-16,919) in males. These deaths would lower national life expectancy by an estimated 0.15 years (0.13-0.17) for women and 0.13 years (0.11-0.15) for men. The life expectancy loss due to PM2.5 was largest around Los Angeles and in some southern states such as Arkansas, Oklahoma, and Alabama. At any PM2.5 concentration, life expectancy loss was, on average, larger in counties with lower income and higher poverty rate than in wealthier counties. Reductions in PM2.5 since 1999 have lowered mortality in all but 14 counties where PM2.5 increased slightly. The main limitation of our study, similar to other observational studies, is that it is not guaranteed for the observed associations to be causal. We did not have annual county-level data on other important determinants of mortality, such as healthcare access and quality and diet, but these factors were adjusted for with use of county-specific random intercepts. CONCLUSIONS: According to our estimates, recent reductions in particulate matter pollution in the USA have resulted in public health benefits. Nonetheless, we estimate that current concentrations are associated with mortality impacts and loss of life expectancy, with larger impacts in counties with lower income and higher poverty rate.

Short-Term Elevation of Fine Particulate Matter Air Pollution and Acute Lower Respiratory Infection.

RATIONALE: Nearly 60% of U.S. children live in counties with particulate matter less than or equal to 2.5 µm in aerodynamic diameter (PM2.5) concentrations above air quality standards. Understanding the relationship between ambient air pollution exposure and health outcomes informs actions to reduce exposure and disease risk. OBJECTIVES: To evaluate the association between ambient PM2.5 levels and healthcare encounters for acute lower respiratory infection (ALRI). METHODS: Using an observational case-crossover design, subjects (n = 146,397) were studied if they had an ALRI diagnosis and resided on Utah's Wasatch Front. PM2.5 air pollution concentrations were measured using community-based air quality monitors between 1999 and 2016. Odds ratios for ALRI healthcare encounters were calculated after stratification by ages 0-2, 3-17, and 18 or more years. MEASUREMENTS AND MAIN RESULTS: Approximately 77% (n = 112,467) of subjects were 0-2 years of age. The odds of ALRI encounter for these young children increased within 1 week of elevated PM2.5 and peaked after 3 weeks with a cumulative 28-day odds ratio of 1.15 per +10 µg/m3 (95% confidence interval, 1.12-1.19). ALRI encounters with diagnosed and laboratory-confirmed respiratory syncytial virus and influenza increased following elevated ambient PM2.5 levels. Similar elevated odds for ALRI were also observed for older children, although the number of events and precision of estimates were much lower. CONCLUSIONS: In this large sample of urban/suburban patients, short-term exposure to elevated PM2.5 air pollution was associated with greater healthcare use for ALRI in young children, older children, and adults. Further exploration is needed of causal interactions between PM2.5 and ALRI.

Estimates and 25-year trends of the global burden of disease attributable to ambient air pollution: an analysis of data from the Global Burden of Diseases Study 2015.

BACKGROUND: Exposure to ambient air pollution increases morbidity and mortality, and is a leading contributor to global disease burden. We explored spatial and temporal trends in mortality and burden of disease attributable to ambient air pollution from 1990 to 2015 at global, regional, and country levels. METHODS: We estimated global population-weighted mean concentrations of particle mass with aerodynamic diameter less than 2·5 µm (PM2·5) and ozone at an approximate 11 km × 11 km resolution with satellite-based estimates, chemical transport models, and ground-level measurements. Using integrated exposure-response functions for each cause of death, we estimated the relative risk of mortality from ischaemic heart disease, cerebrovascular disease, chronic obstructive pulmonary disease, lung cancer, and lower respiratory infections from epidemiological studies using non-linear exposure-response functions spanning the global range of exposure. FINDINGS: Ambient PM2·5 was the fifth-ranking mortality risk factor in 2015. Exposure to PM2·5 caused 4·2 million (95% uncertainty interval [UI] 3·7 million to 4·8 million) deaths and 103·1 million (90·8 million 115·1 million) disability-adjusted life-years (DALYs) in 2015, representing 7·6% of total global deaths and 4·2% of global DALYs, 59% of these in east and south Asia. Deaths attributable to ambient PM2·5 increased from 3·5 million (95% UI 3·0 million to 4·0 million) in 1990 to 4·2 million (3·7 million to 4·8 million) in 2015. Exposure to ozone caused an additional 254 000 (95% UI 97 000-422 000) deaths and a loss of 4·1 million (1·6 million to 6·8 million) DALYs from chronic obstructive pulmonary disease in 2015. INTERPRETATION: Ambient air pollution contributed substantially to the global burden of disease in 2015, which increased over the past 25 years, due to population ageing, changes in non-communicable disease rates, and increasing air pollution in low-income and middle-income countries. Modest reductions in burden will occur in the most polluted countries unless PM2·5 values are decreased substantially, but there is potential for substantial health benefits from exposure reduction. FUNDING: Bill & Melinda Gates Foundation and Health Effects Institute.

Exposure to Fine Particulate Air Pollution Is Associated With Endothelial Injury and Systemic Inflammation.

RATIONALE: Epidemiological evidence indicates that exposures to fine particulate matter air pollution (PM2.5) contribute to global burden of disease, primarily as a result of increased risk of cardiovascular morbidity and mortality. However, mechanisms by which PM2.5 exposure induces cardiovascular injury remain unclear. PM2.5-induced endothelial dysfunction and systemic inflammation have been implicated, but direct evidence is lacking. OBJECTIVE: To examine whether acute exposure to PM2.5 is associated with endothelial injury and systemic inflammation. METHODS AND RESULTS: Blood was collected from healthy, nonsmoking, young adults during 3 study periods that included episodes of elevated PM2.5 levels. Microparticles and immune cells in blood were measured by flow cytometry, and plasma cytokine/growth factors were measured using multiplexing laser beads. PM2.5 exposure was associated with the elevated levels of endothelial microparticles (annexin V+/CD41-/CD31+), including subtypes expressing arterial-, venous-, and lung-specific markers, but not microparticles expressing CD62+. These changes were accompanied by suppressed circulating levels of proangiogenic growth factors (EGF [epidermal growth factor], sCD40L [soluble CD40 ligand], PDGF [platelet-derived growth factor], RANTES [regulated on activation, normal T-cell-expressed and secreted], GROα [growth-regulated protein α], and VEGF [vascular endothelial growth factor]), and an increase in the levels of antiangiogenic (TNFα [tumor necrosis factor α], IP-10 [interferon γ-induced protein 10]), and proinflammatory cytokines (MCP-1 [monocyte chemoattractant protein 1], MIP-1α/ß [macrophage inflammatory protein 1α/ß], IL-6 [interleukin 6], and IL-1ß [interleukin 1ß]), and markers of endothelial adhesion (sICAM-1 [soluble intercellular adhesion molecule 1] and sVCAM-1 [soluble vascular cellular adhesion molecule 1]). PM2.5 exposure was also associated with an inflammatory response characterized by elevated levels of circulating CD14+, CD16+, CD4+, and CD8+, but not CD19+ cells. CONCLUSIONS: Episodic PM2.5 exposures are associated with increased endothelial cell apoptosis, an antiangiogenic plasma profile, and elevated levels of circulating monocytes and T, but not B, lymphocytes. These changes could contribute to the pathogenic sequelae of atherogenesis and acute coronary events.

Relationships between fine particulate air pollution, cardiometabolic disorders, and cardiovascular mortality.

RATIONALE: Growing evidence suggests that long-term exposure to fine particulate matter (PM2.5) air pollution contributes to risk of cardiovascular disease (CVD) morbidity and mortality. There is uncertainty about who are most susceptible. Individuals with underlying cardiometabolic disorders, including hypertension, diabetes mellitus, and obesity, may be at greater risk. PM2.5 pollution may also contribute to cardiometabolic disorders, augmenting CVD risk. OBJECTIVE: This analysis evaluates relationships between long-term PM2.5 exposure and cardiometabolic disease on risk of death from CVD and cardiometabolic conditions. METHODS AND RESULTS: Data on 669 046 participants from the American Cancer Society Cancer Prevention Study II cohort were linked to modeled PM2.5 concentrations at geocoded home addresses. Cox proportional hazards regression models were used to estimate adjusted hazards ratios for death from CVD and cardiometabolic diseases based on death-certificate information. Effect modification by pre-existing cardiometabolic risk factors on the PM2.5-CVD mortality association was examined. PM2.5 exposure was associated with CVD mortality, with the hazards ratios (95% confidence interval) per 10 µg/m(3) increase in PM2.5 equal to 1.12 (1.10-1.15). Deaths linked to hypertension and diabetes mellitus (mentioned on death certificate as either primary or contributing cause of death) were also associated with PM2.5. There was no consistent evidence of effect modification by cardiometabolic disease risk factors on the PM2.5-CVD mortality association. CONCLUSIONS: Pollution-induced CVD mortality risk is observed for those with and without existing cardiometabolic disorders. Long-term exposure may also contribute to the development or exacerbation of cardiometabolic disorders, increasing risk of CVD, and cardiometabolic disease mortality.

Interactions between cigarette smoking and ambient PM2.5 for cardiovascular mortality.

Associations between long-term exposure to ambient fine particulate matter (PM2.5) and all-cause and cardiovascular mortality are well documented however less is known regarding possible interactions with cigarette smoking. We previously reported a supra-additive synergistic relationship between PM2.5 and cigarette smoking for lung cancer mortality. Here we examine interactions for all-cause and cardiovascular mortality among 429,406 current or never smoking participants in the prospective American Cancer Society Cancer Prevention Study-II with modeled PM2.5 concentrations. Cox proportional and additive hazards models were used to estimate mortality associations and interactions on the multiplicative and additive scales. A total of 146,495 all-cause and 64,339 cardiovascular (plus diabetes) deaths were observed. The hazard ratio (HR) (95% confidence interval (CI)) for cardiovascular mortality for high vs. low PM2.5 exposure (>14.44µg/m3 vs ≤10.59µg/m3, 75th vs 25th percentile) was 1.09 (95% CI 1.05, 1.12) in never smokers. The HR for cigarette smoking was 1.89 (95% CI 1.82, 1.96) in those with low PM2.5. The HR for both high PM2.5 and cigarette smoking was 2.08 (95% CI 2.00, 2.17). A small significant excess relative risk due to interaction (0.10; 95% CI 0.02, 0.19) was observed. Quantification of the public health burden attributed to the interaction between PM2.5 and cigarette smoking indicated a total of 32 (95% CI -6, 71) additional cardiovascular deaths per 100,000 person-years due to this interaction. In conclusion, PM2.5 was associated with all-cause and cardiovascular mortality in both smokers and never smokers, with some evidence for a small additive interaction with cigarette smoking. Reductions in cigarette smoking will result in the greatest impact on reducing all-cause and cardiovascular death at the levels of PM2.5 observed in this study. However, reductions in PM2.5 will also contribute to preventing a proportion of mortality attributed to cigarette smoking.

Long-Term Ozone Exposure and Mortality in a Large Prospective Study.

RATIONALE: Tropospheric ozone (O3) is potentially associated with cardiovascular disease risk and premature death. Results from long-term epidemiological studies on O3 are scarce and inconclusive. OBJECTIVES: In this study, we examined associations between chronic ambient O3 exposure and all-cause and cause-specific mortality in a large cohort of U.S. adults. METHODS: Cancer Prevention Study II participants were enrolled in 1982. A total of 669,046 participants were analyzed, among whom 237,201 deaths occurred through 2004. We obtained estimates of O3 concentrations at the participant's residence from a hierarchical Bayesian space-time model. Estimates of fine particulate matter (particulate matter with an aerodynamic diameter of up to 2.5 µm [PM2.5]) and NO2 concentrations were obtained from land use regression. Cox proportional hazards regression models were used to examine mortality associations adjusted for individual- and ecological-level covariates. MEASUREMENTS AND MAIN RESULTS: In single-pollutant models, we observed significant positive associations between O3, PM2.5, and NO2 concentrations and all-cause and cause-specific mortality. In two-pollutant models adjusted for PM2.5, significant positive associations remained between O3 and all-cause (hazard ratio [HR] per 10 ppb, 1.02; 95% confidence interval [CI], 1.01-1.04), circulatory (HR, 1.03; 95% CI, 1.01-1.05), and respiratory mortality (HR, 1.12; 95% CI, 1.08-1.16) that were unchanged with further adjustment for NO2. We also observed positive mortality associations with both PM2.5 (both near source and regional) and NO2 in multipollutant models. CONCLUSIONS: Findings derived from this large-scale prospective study suggest that long-term ambient O3 contributes to risk of respiratory and circulatory mortality. Substantial health and environmental benefits may be achieved by implementing further measures aimed at controlling O3 concentrations.

Kawasaki Disease and Exposure to Fine Particulate Air Pollution.

OBJECTIVE: To analyze associations of short-term exposure to fine particulate matter (diameter ≤ 2.5 µm [PM2.5]), a measurable component of urban pollution, with the event date of fever onset for patients with Kawasaki disease (KD) residing in 7 metropolitan regions. STUDY DESIGN: A case-crossover study design was used. Time trends, seasonality, month, and weekday were controlled for by matching. We assembled PM2.5 exposure measurements from urban monitors and imputed PM2.5 to provide day-to-day temporal variability and resolution for time series indexes of exposures. Selected exposure windows (to 14 days) of PM2.5 were examined. RESULTS: A total of 3009 KD events were included for which the subject resided within a study metropolitan area and the event date occurred during years with available PM2.5. The estimated ORs (with 95% CIs) of an event of KD associated with a 10 µg/m(3) PM2.5 lagged moving average concentration of lagged exposure period (ie, concurrent, preceding day[s]) revealed no evidence of a consistent, statistically significant, positive association between elevated PM2.5 exposure and increased risk of KD. Extended analysis with stratification by city, sex, age, ethnic origin, incomplete or complete clinical manifestations, the presence of coronary aneurysm, and intravenous immunoglobulin resistance did not provide evidence of a consistent, statistically significant, positive association between elevated exposure to PM2.5 and increased risk of KD for any of the strata studied. CONCLUSIONS: This multicity study failed to establish a risk of the event of KD with short-term fine particulate exposure. Our negative findings add to the growing field of environmental epidemiology research of KD.

"What We Breathe Impacts Our Health: Improving Understanding of the Link between Air Pollution and Health".

Air pollution contributes to the premature deaths of millions of people each year around the world, and air quality problems are growing in many developing nations. While past policy efforts have succeeded in reducing particulate matter and trace gases in North America and Europe, adverse health effects are found at even these lower levels of air pollution. Future policy actions will benefit from improved understanding of the interactions and health effects of different chemical species and source categories. Achieving this new understanding requires air pollution scientists and engineers to work increasingly closely with health scientists. In particular, research is needed to better understand the chemical and physical properties of complex air pollutant mixtures, and to use new observations provided by satellites, advanced in situ measurement techniques, and distributed micro monitoring networks, coupled with models, to better characterize air pollution exposure for epidemiological and toxicological research, and to better quantify the effects of specific source sectors and mitigation strategies.

Countervailing effects of income, air pollution, smoking, and obesity on aging and life expectancy: population-based study of U.S. Counties.

BACKGROUND: Income, air pollution, obesity, and smoking are primary factors associated with human health and longevity in population-based studies. These four factors may have countervailing impacts on longevity. This analysis investigates longevity trade-offs between air pollution and income, and explores how relative effects of income and air pollution on human longevity are potentially influenced by accounting for smoking and obesity. METHODS: County-level data from 2,996 U.S. counties were analyzed in a cross-sectional analysis to investigate relationships between longevity and the four factors of interest: air pollution (mean 1999-2008 PM2.5), median income, smoking, and obesity. Two longevity measures were used: life expectancy (LE) and an exceptional aging (EA) index. Linear regression, generalized additive regression models, and bivariate thin-plate smoothing splines were used to estimate the benefits of living in counties with higher incomes or lower PM2.5. Models were estimated with and without controls for smoking, obesity, and other factors. RESULTS: Models which account for smoking and obesity result in substantially smaller estimates of the effects of income and pollution on longevity. Linear regression models without these two variables estimate that a $1,000 increase in median income (1 µg/m(3) decrease in PM2.5) corresponds to a 27.39 (33.68) increase in EA and a 0.14 (0.12) increase in LE, whereas models that control for smoking and obesity estimate only a 12.32 (20.22) increase in EA and a 0.07 (0.05) increase in LE. Nonlinear models and thin-plate smoothing splines also illustrate that, at higher levels of income, the relative benefits of the income-pollution tradeoff changed-the benefit of higher incomes diminished relative to the benefit of lower air pollution exposure. CONCLUSIONS: Higher incomes and lower levels of air pollution both correspond with increased human longevity. Adjusting for smoking and obesity reduces estimates of the benefits of higher income and lower air pollution exposure. This adjustment also alters the tradeoff between income and pollution: increases in income become less beneficial relative to a fixed reduction in air pollution-especially at higher levels of income.

Meta-Analysis Methods to Estimate the Shape and Uncertainty in the Association Between Long-Term Exposure to Ambient Fine Particulate Matter and Cause-Specific Mortality Over the Global Concentration Range.

Estimates of excess mortality associated with exposure to ambient concentrations of fine particulate matter have been obtained from either a single cohort study or pooling information from a small number of studies. However, standard frequentist methods of pooling are known to underestimate statistical uncertainty in the true risk distribution when the number of studies pooled is small. Alternatively, Bayesian pooling methods using noninformative priors yield unrealistically large amounts of uncertainty in this case. We present a new hybrid frequentist-bayesian framework for meta-analysis that incorporates features of both frequentist and Bayesian approaches, yielding estimated uncertainty distributions that are more useful for burden estimation. We also present an example of mortality risk due to long-term exposure to ambient fine particulate matter obtained from a small number of cohort studies conducted in the United States and Europe. We compare our new risk uncertainty distribution to that obtained by the integrated exposure-response (IER) model used in the Global Burden of Disease 2010 project for which risk was modeled over the entire global concentration range. We suggest a method to incorporate our new risk uncertainty distribution based on the relatively low concentrations observed in the United States and western Europe into the IER model, thus extending risk estimation to the global concentration range.

Chemical Composition of Fine Particulate Matter and Life Expectancy: In 95 US Counties Between 2002 and 2007.

BACKGROUND: In a previous study, we provided evidence that a decline in fine particulate matter (PM2.5) air pollution during the period between 2000 and 2007 was associated with increased life expectancy in 545 counties in the United States. In this article, we investigated which chemical constituents of PM2.5 were the main drivers of the observed association. METHODS: We estimated associations between temporal changes in seven major components of PM2.5 (ammonium, sulfate, nitrate, elemental carbon matter, organic carbon matter, sodium, and silicon) and temporal changes in life expectancy in 95 counties between 2002 and 2007. We included US counties that had adequate chemical components of PM2.5 mass data across all seasons. We fitted single pollutant and multiple pollutant linear models, controlling for available socioeconomic, demographic, and smoking variables and stratifying by urban and nonurban counties. RESULTS: In multiple pollutant models, we found that: (1) a reduction in sulfate was associated with an increase in life expectancy; and (2) reductions in ammonium and sodium ion were associated with increases in life expectancy in nonurban counties only. CONCLUSIONS: Our findings suggest that recent reductions in long-term exposure to sulfate, ammonium, and sodium ion between 2002 and 2007 are associated with improved public health.