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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.

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. 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). 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 ) (1999-2004), nitrogen dioxide (NO ) (2006), and ozone (O ) (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. We observed 43,320 nonlung cancer deaths. PM was significantly positively associated with death from cancers of the kidney {adjusted hazard ratio (HR) per 4.4 μg/m =1.14 [95% confidence interval (CI): 1.03, 1.27]} and bladder [HR=1.13 (95% CI: 1.03, 1.23)]. NO 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 and NO and in three-pollutant models with O . We observed no statistically significant positive associations with death from other types of cancer based on results from adjusted models. 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: Lung cancer and cardiovascular disease (CVD) mortality risks increase with smoking, secondhand smoke (SHS), and exposure to fine paniculate matter <2.5 µm in diameter (PM2.5) from ambient air pollution. Recent research indicates that the exposure-response relationship for CVD is nonlinear, with a steep increase in risk at low exposures and flattening out at higher exposures. Comparable estimates of the exposure-response relationship for lung cancer are required for disease burden estimates and related public health policy assessments. Objectives: We compared exposure-response relationships of PM2.5 with lung cancer and cardiovascular mortality and considered the implications of the observed differences for efforts to estimate the disease burden of PM2.5. Methods: Prospective cohort data for 1.2 million adults were collected by the American Cancer Society as part of the Cancer Prevention Study II. We estimated relative risks (RRs) for increments of cigarette smoking, adjusting for various individual risk factors. RRs were plotted against estimated daily dose of PM2.5 from smoking along with comparison estimates for ambient air pollution and SHS. Results: For lung cancer mortality, excess risk rose nearly linearly, reaching maximum RRs > 40 among long-term heavy smokers. Excess risks for CVD mortality increased steeply at low exposure levels and leveled off at higher exposures, reaching RRs of approximately 2-3 for cigarette smoking. Conclusions: The exposure-response relationship associated with PM2.5 is qualitatively different for lung cancer versus cardiovascular mortality. At low exposure levels, cardiovascular deaths are projected to account for most of the burden of disease, whereas at high levels of PM2.5, lung cancer becomes proportionately more important.

Estimating the burden of disease attributable to long-term exposure to fine particulate matter (PM2.5) in ambient air requires knowledge of both the shape and magnitude of the relative risk (RR) function. However, adequate direct evidence to identify the shape of the mortality RR functions at the high ambient concentrations observed in many places in the world is lacking. We developed RR functions over the entire global exposure range for causes of mortality in adults: ischemic heart disease (IHD), cerebrovascular disease (stroke), chronic obstructive pulmonary disease (COPD), and lung cancer (LC). We also developed RR functions for the incidence of acute lower respiratory infection (ALRI) that can be used to estimate mortality and lost-years of healthy life in children < 5 years of age. We fit an integrated exposure-response (IER) model by integrating available RR information from studies of ambient air pollution (AAP), second hand tobacco smoke, household solid cooking fuel, and active smoking (AS). AS exposures were converted to estimated annual PM2.5 exposure equivalents using inhaled doses of particle mass. We derived population attributable fractions (PAFs) for every country based on estimated worldwide ambient PM2.5 concentrations. The IER model was a superior predictor of RR compared with seven other forms previously used in burden assessments. The percent PAF attributable to AAP exposure varied among countries from 2 to 41 for IHD, 1 to 43 for stroke, < 1 to 21 for COPD, < 1 to 25 for LC, and < 1 to 38 for ALRI. We developed a fine particulate mass-based RR model that covered the global range of exposure by integrating RR information from different combustion types that generate emissions of particulate matter. The model can be updated as new RR information becomes available.

Background: In recent years (2000-2007), ambient levels of fine particulate matter (PM 2.5 ) have continued to decline as a result of interventions, but the decline has been at a slower rate than previous years (1980-2000). Whether these more recent and slower declines of PM 2.5 levels continue to improve life expectancy and whether they benefit all populations equally is unknown. Methods: We assembled a data set for 545 U.S. counties consisting of yearly county-specific average PM 2.5 , yearly county-specific life expectancy, and several potentially confounding variables measuring socioeconomic status, smoking prevalence, and demographic characteristics for the years 2000 and 2007. We used regression models to estimate the association between reductions in PM 2.5 and changes in life expectancy for the period from 2000 to 2007. Results: A decrease of 10 μg/m³ in the concentration of PM 2.5 was associated with an increase in mean life expectancy of 0.35 years (SD = 0.16 years, P = 0.033). This association was stronger in more urban and densely populated counties. Conclusions: Reductions in PM 2.5 were associated with improvements in life expectancy for the period from 2000 to 2007. Air pollution control in the last decade has continued to have a positive impact on public health.

Abstract 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.

Evidence indicates that air pollution contributes to cardiopulmonary mortality. There is ongoing debate regarding the size and shape of the pollution–mortality exposure–response relationship. There are also growing appeals for estimates of pollution–mortality relationships that use public data and are based on large, representative study cohorts. Our goal was to evaluate fine particulate matter air pollution ([Formula: see text]) and mortality using a large cohort that is representative of the U.S. population and is based on public data. Additional objectives included exploring model sensitivity, evaluating relative effects across selected subgroups, and assessing the shape of the [Formula: see text]–mortality relationship. National Health Interview Surveys (1986–2014), with mortality linkage through 2015, were used to create a cohort of 1,599,329 U.S. adults and a subcohort with information on smoking and body mass index (BMI) of 635,539 adults. Data were linked with modeled ambient [Formula: see text] at the census-tract level. Cox proportional hazards models were used to estimate [Formula: see text]–mortality hazard ratios for all-cause and specific causes of death while controlling for individual risk factors and regional and urban versus rural differences. Sensitivity and subgroup analyses were conducted and the shape of the [Formula: see text]–mortality relationship was explored. Estimated mortality hazard ratios, per [Formula: see text] long-term exposure to [Formula: see text], were 1.12 (95% CI: 1.08, 1.15) for all-cause mortality, 1.23 (95% CI: 1.17, 1.29) for cardiopulmonary mortality, and 1.12 (95% CI: 1.00, 1.26) for lung cancer mortality. In general, [Formula: see text]–mortality associations were consistently positive for all-cause and cardiopulmonary mortality across key modeling choices and across subgroups of sex, age, race-ethnicity, income, education levels, and geographic regions. This large, nationwide, representative cohort of U.S. adults provides robust evidence that long-term [Formula: see text] exposure contributes to cardiopulmonary mortality risk. The ubiquitous and involuntary nature of exposures and the broadly observed effects across subpopulations underscore the public health importance of breathing clean air. https://doi.org/10.1289/EHP4438.

The effect of long-term exposure to tropospheric ozone on air pollution–related mortality was examined in an analysis of data from almost 500,000 subjects over a period of 18 years. Ozone concentrations were not associated with the rate of death from any cause or, when concentrations of fine particulate matter were taken into account, with the rate of death from cardiopulmonary causes. However, ozone concentrations were significantly correlated with the rate of death from respiratory causes. Ozone concentrations were not associated with the rate of death from any cause or, when concentrations of fine particulate matter were taken into account, with the rate of death from cardiopulmonary causes. However, ozone concentrations were significantly correlated with the rate of death from respiratory causes. Studies conducted over the past 15 years have provided substantial evidence that long-term exposure to air pollution is a risk factor for cardiopulmonary disease and death. 1 – 5 Recent reviews of this literature suggest that fine particulate matter (particles that are ≤2.5 μm in aerodynamic diameter [PM 2.5 ]) has a primary role in these adverse health effects. 6 , 7 The particulate-matter component of air pollution includes complex mixtures of metals, black carbon, sulfates, nitrates, and other direct and indirect byproducts of incomplete combustion and high-temperature industrial processes. Ozone is a single, well-defined pollutant, yet the effect of exposure to ozone on . . .

Previous research has identified an association between fine particulate matter ( ) air pollution and lung cancer. Most of the evidence for this association, however, is based on research using lung cancer mortality, not incidence. Research that examines potential associations between and incidence of non-lung cancers is limited. The primary purpose of this study was to evaluate the association between the incidence of cancer and exposure to using cases of cancer incidences from U.S. registries. Secondary objectives include evaluating the sensitivity of the associations to model selection, spatial control, and latency period as well as estimating the exposure-response relationship for several cancer types. Surveillance, Epidemiology, and End Results (SEER) program data were used to calculate incidence rates for various cancer types in 607 U.S. counties. County-level concentrations were estimated using integrated empirical geographic regression models. Flexible semi-nonparametric regression models were used to estimate associations between and cancer incidence for selected cancers while controlling for important county-level covariates. Primary time-independent models using average incidence rates from 1992-2016 and average from 1988-2015 were estimated. In addition, time-varying models using annual incidence rates from 2002-2011 and lagged moving averages of annual estimates for were also estimated. The incidences of all cancer and lung cancer were consistently associated with . The incident rate ratios (IRRs), per increase in , for all and lung cancer were 1.09 (95% CI: 1.03, 1.14) and 1.19 (95% CI: 1.09, 1.30), respectively. Less robust associations were observed with oral, rectal, liver, skin, breast, and kidney cancers. Exposure to air pollution contributes to lung cancer incidence and is potentially associated with non-lung cancer incidence. https://doi.org/10.1289/EHP7246.

Particulate air pollution has been implicated as being responsible for deaths from any cause. This epidemiologic study examined the change in fine-particulate air pollution in 51 U.S. metropolitan areas between the late 1970s and the late 1990s. A decrease in fine-particulate air pollution was associated with increased life expectancy. This epidemiologic study examined the change in fine-particulate air pollution in U.S. metropolitan areas between the late 1970s and the late 1990s. A decrease in fine-particulate air pollution was associated with increased life expectancy. Since the 1970s, the United States has made substantial efforts and investments to improve air quality. As these efforts continue, a fundamental question remains: Do improvements in air quality result in measurable improvements in human health and longevity? Associations between long-term exposure to fine-particulate air pollution and mortality have been observed in population-based studies 1 – 3 and, more recently, in cohort-based studies. 4 – 11 Daily time-series and related studies, 12 – 15 natural intervention studies, 16 – 18 and cohort studies 10 , 19 all support the view that relatively prompt and sustained health benefits are derived from improved air quality. We directly assessed associations between life expectancy . . .