Summary Background Emerging evidence suggests that living near major roads might adversely affect cognition. However, little is known about its relationship with the incidence of dementia, ...Parkinson's disease, and multiple sclerosis. We aimed to investigate the association between residential proximity to major roadways and the incidence of these three neurological diseases in Ontario, Canada. Methods In this population-based cohort study, we assembled two population-based cohorts including all adults aged 20–50 years (about 4·4 million; multiple sclerosis cohort) and all adults aged 55–85 years (about 2·2 million; dementia or Parkinson's disease cohort) who resided in Ontario, Canada on April 1, 2001. Eligible patients were free of these neurological diseases, Ontario residents for 5 years or longer, and Canadian-born. We ascertained the individual's proximity to major roadways based on their residential postal-code address in 1996, 5 years before cohort inception. Incident diagnoses of dementia, Parkinson's disease, and multiple sclerosis were ascertained from provincial health administrative databases with validated algorithms. We assessed the associations between traffic proximity and incident dementia, Parkinson's disease, and multiple sclerosis using Cox proportional hazards models, adjusting for individual and contextual factors such as diabetes, brain injury, and neighbourhood income. We did various sensitivity analyses, such as adjusting for access to neurologists and exposure to selected air pollutants, and restricting to never movers and urban dwellers. Findings Between 2001, and 2012, we identified 243 611 incident cases of dementia, 31 577 cases of Parkinson's disease, and 9247 cases of multiple sclerosis. The adjusted hazard ratio (HR) of incident dementia was 1·07 for people living less than 50 m from a major traffic road (95% CI 1·06–1·08), 1·04 (1·02–1·05) for 50–100 m, 1·02 (1·01–1·03) for 101–200 m, and 1·00 (0·99–1·01) for 201–300 m versus further than 300 m ( p for trend=0·0349). The associations were robust to sensitivity analyses and seemed stronger among urban residents, especially those who lived in major cities (HR 1·12, 95% CI 1·10–1·14 for people living <50 m from a major traffic road), and who never moved (1·12, 1·10–1·14 for people living <50 m from a major traffic road). No association was found with Parkinson's disease or multiple sclerosis. Interpretation In this large population-based cohort, living close to heavy traffic was associated with a higher incidence of dementia, but not with Parkinson's disease or multiple sclerosis. Funding Health Canada (MOA-4500314182).
An accurate fine-resolution surface of the chemical composition of fine particulate matter (PM2.5) would offer valuable information for epidemiological studies and health impact assessments. We ...develop geoscience-derived estimates of PM2.5 composition from a chemical transport model (GEOS-Chem) and satellite observations of aerosol optical depth, and statistically fuse these estimates with ground-based observations using a geographically weighted regression over North America to produce a spatially complete representation of sulfate, nitrate, ammonium, black carbon, organic matter, mineral dust, and sea-salt over 2000–2016. Significant long-term agreement is found with cross-validation sites over North America (R2 = 0.570.96), with the strongest agreement for sulfate (R2 = 0.96), nitrate (R2 = 0.90), and ammonium (R2 = 0.86). We find that North American decreases in population-weighted fine particulate matter (PM2.5) concentrations since 2000 have been most heavily influenced by regional changes in sulfate and organic matter. Regionally, the relative importance of several chemical components are found to change with PM2.5 concentration, such as higher PM2.5 concentrations having a larger proportion of nitrate and a smaller proportion of sulfate. This data set offers information for research into the health effects of PM2.5 chemical components.
Cohort studies in North America and western Europe have reported increased risk of mortality associated with long-term exposure to fine particles (PM
), but to date, no such studies have been ...reported in China, where higher levels of exposure are experienced.
We estimated the association between long-term exposure to PM
with nonaccidental and cause-specific mortality in a cohort of Chinese men.
We conducted a prospective cohort study of 189,793 men 40 y old or older during 1990-91 from 45 areas in China. Annual average PM
levels for the years 1990, 1995, 2000, and 2005 were estimated for each cohort location using a combination of satellite-based estimates, chemical transport model simulations, and ground-level measurements developed for the Global Burden of Disease (GBD) 2013 study. A Cox proportional hazards regression model was used to estimate hazard ratios (HR) for nonaccidental cardiovascular disease (CVD), chronic obstructive pulmonary disease (COPD), and lung-cancer mortality. We also assessed the shape of the concentration-response relationship and compared the risk estimates with those predicted by Integrated Exposure-Response (IER) function, which incorporated estimates of mortality risk from previous cohort studies in western Europe and North America.
The mean level of PM
exposure during 2000-2005 was 43.7 μg/m
(ranging from 4.2 to 83.8 μg/m
). Mortality HRs (95% CI) per 10-μg/m
increase in PM
were 1.09 (1.08, 1.09) for nonaccidental causes; 1.09 (1.08, 1.10) for CVD, 1.12 (1.10, 1.13) for COPD; and 1.12 (1.07, 1.14) for lung cancer. The HR estimate from our cohort was consistently higher than IER predictions.
Long-term exposure to PM
was associated with nonaccidental, CVD, lung cancer, and COPD mortality in China. The IER estimator may underestimate the excess relative risk of cause-specific mortality due to long-term exposure to PM
over the exposure range experienced in China and other low- and middle-income countries. https://doi.org/10.1289/EHP1673.
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CEKLJ, DOBA, IZUM, KILJ, NUK, OILJ, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK, VSZLJ
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.
•Cohort studies link PM2.5 air pollution with excess mortality risk.•25+ years of re-analyses, extended analyses, many replicative analyses.•Evidence from many studies from North America, Europe, and Asia.•Meta-estimates indicate robust PM2.5-mortality associations with heterogeneity.•PM2.5 associated with all-cause, cardiopulmonary and lung-cancer mortality.
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.
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.
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.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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CEKLJ, DOBA, IZUM, KILJ, NUK, OILJ, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK, VSZLJ
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 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.
Current evidence on the relationship between long-term exposure to air pollution and new onset of chronic lung disease is inconclusive.
To examine associations of incident chronic obstructive ...pulmonary disease (COPD) and adult-onset asthma with past exposure to fine particulate matter ≤ 2.5 μm in diameter (PM
), nitrogen dioxide (NO
), ozone (O
), and the redox-weighted average of NO
and O
(O
) and characterize the concentration-response relationship.
We conducted a population-based cohort study of all Ontarians, aged 35-85 years, from 2001 to 2015. A 3-year moving average of residential exposures to selected pollutants with a 1-year lag were estimated during follow-up. We used Cox proportional hazard models and Aalen additive-hazard models to quantify the pollution-disease associations and characterized the shape of these relationships using newly developed nonlinear risk models.
Among 5.1 million adults, we identified 340,733 and 218,005 incident cases of COPD and asthma, respectively. We found positive associations of COPD with PM
per interquartile-range (IQR) increase of 3.4 μg/m
(hazard ratio, 1.07; 95% confidence interval, 1.06-1.08), NO
per IQR increase of 13.9 ppb (1.04; 1.02-1.05), O
per IQR increase of 6.3 ppb (1.04; 1.03-1.04), and O
per IQR increase of 4.4 ppb (1.03; 1.03-1.03). By contrast, we did not find strong evidence linking these pollutants to adult-onset asthma. In addition, we quantified that each IQR increase in pollution exposure yielded 3.0 (2.4-3.6), 3.2 (2.0-4.3), 1.9 (1.3-2.5), and 2.3 (1.7-2.9) excess cases of COPD per 100,000 adults for PM
, NO
, O
, and O
, respectively. Furthermore, most pollutant-COPD relationships exhibited supralinear shapes.
Air pollution was associated with a higher incidence of COPD but was not associated with a higher incidence of adult-onset asthma.
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.
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CEKLJ, DOBA, IZUM, KILJ, NUK, OILJ, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK, VSZLJ
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