Long-Term Exposure to Ozone and Cause-Specific Mortality Risk in the United States.
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ABSTRACT:
SUBMITTER: Lim CC
PROVIDER: S-EPMC6794108 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Although many studies have linked elevations in tropospheric ozone to adverse health outcomes, the effect of long-term exposure to ozone on air pollution-related mortality remains uncertain. We examined the potential contribution of exposure to ozone to the risk of death from cardiopulmonary causes and specifically to death from respiratory causes.Data from the study cohort of the American Cancer Society Cancer Prevention Study II were correlated with air-pollution data from 96 metropolitan statistical areas in the United States. Data were analyzed from 448,850 subjects, with 118,777 deaths in an 18-year follow-up period. Data on daily maximum ozone concentrations were obtained from April 1 to September 30 for the years 1977 through 2000. Data on concentrations of fine particulate matter (particles that are < or = 2.5 microm in aerodynamic diameter [PM(2.5)]) were obtained for the years 1999 and 2000. Associations between ozone concentrations and the risk of death were evaluated with the use of standard and multilevel Cox regression models.In single-pollutant models, increased concentrations of either PM(2.5) or ozone were significantly associated with an increased risk of death from cardiopulmonary causes. In two-pollutant models, PM(2.5) was associated with the risk of death from cardiovascular causes, whereas ozone was associated with the risk of death from respiratory causes. The estimated relative risk of death from respiratory causes that was associated with an increment in ozone concentration of 10 ppb was 1.040 (95% confidence interval, 1.010 to 1.067). The association of ozone with the risk of death from respiratory causes was insensitive to adjustment for confounders and to the type of statistical model used.In this large study, we were not able to detect an effect of ozone on the risk of death from cardiovascular causes when the concentration of PM(2.5) was taken into account. We did, however, demonstrate a significant increase in the risk of death from respiratory causes in association with an increase in ozone concentration.
| S-EPMC4105969 | biostudies-literature
Project description:We examined the association of long-term, daily 1-h maximum O3 (ozone) exposures on cause-specific mortality for 22.2 million US Medicare beneficiaries between 2000-2008. We modeled the association between O3 and mortality using age-gender-race stratified log-linear regression models, adjusted for state of residence. We examined confounding by (1) adjusting for PM2.5 (particles with aerodynamic diameters <2.5 μm) and NO2 (nitrogen dioxide) exposures, temperature, and neighborhood-level characteristics and behaviors, and (2) decomposing O3 into its temporal and spatio-temporal components and comparing estimated risk ratios. We also examined sensitivity of our results to alternate exposure measures based on warm-season 8-h daily maximum and 24-h average exposures. We found increased risks from long-term O3 exposures to be strongest and most consistent for mortality from respiratory disease (1.030, 95% CI: 1.027, 1.034) (including COPD (chronic obstructive pulmonary disease)), CHF (congestive heart failure), and lung cancer (1.015, 95% CI: 1.010, 1.020), with no evidence of confounding by PM2.5, NO2, and temperature and with results similar across O3 exposure measures. While significant, associations between long-term O3 exposures and CVD (cardiovascular)-related mortality (1.005, 95% CI: 1.003, 1.007) were confounded by PM2.5 and varied with the exposure measure, with associations no longer significantly positive when warm-season 8-h maximum or 24-h average O3 was used to assess exposures. In this large study, we provide strong evidence that O3 exposure is associated with mortality from respiratory-related causes and for the first-time, lung cancer, but raise questions regarding O3-related impacts on CVD mortality. Our findings demonstrate the need to further identify potential confounders.
| S-EPMC7197379 | biostudies-literature
Project description: Not available
| S-EPMC6794103 | biostudies-literature
Project description:BackgroundFrailty is a common condition among older adults increasing risk of adverse outcomes including mortality; however, little is known about the incidence or risk of specific causes of death among frail individuals.MethodsData came from the Health and Retirement Study (HRS; 2004-2012), linked to underlying cause-of-death information from the National Death Index (NDI). Community-dwelling HRS participants aged 65 and older who completed a general health interview and physical measurements (n = 10,490) were included in analysis. Frailty was measured using phenotypic model criteria-exhaustion, low weight, low energy expenditure, slow gait, and weakness. Underlying causes of death were determined using International Classification of Diseases, Version 10 codes. We used Cox proportional hazards and competing risks regression models to calculate and compare incidence of cause-specific mortality by frailty status.ResultsDuring follow-up, prefrail and frail older adults had significantly greater hazard of all-cause mortality compared to individuals without symptoms (adjusted hazard ratio [HR] prefrail: 1.85, 95% CI: 1.51, 2.25; HR frail: 2.75, 95% CI: 2.14, 3.53). Frailty was associated with 2.96 (95% CI: 2.17, 4.03), 2.82 (95% CI: 2.02, 3.94), 3.48 (95% CI: 2.17, 5.59), and 2.87 (95% CI: 1.47, 5.59) times greater hazard of death from heart disease, cancer, respiratory illness, and dementia, respectively.ConclusionsSignificantly greater risk of mortality from several different causes should be considered alongside the potential costs of screening and intervention for frailty in subspecialty and general geriatric clinical practice. Findings may help investigators estimate the potential impact of frailty reduction approaches on mortality.
| S-EPMC7518553 | biostudies-literature
Project description:BackgroundSince 1971, the annual National Ambient Air Quality Standard (NAAQS) for nitrogen dioxide (NO2) has remained at 53 ppb, the impact of long-term NO2 exposure on mortality is poorly understood.ObjectivesWe examined associations between long-term NO2 exposure (12-month moving average of NO2) below the annual NAAQS and cause-specific mortality among the older adults in the U.S.MethodsCox proportional-hazard models were used to estimate Hazard Ratio (HR) for cause-specific mortality associated with long-term NO2 exposures among about 50 million Medicare beneficiaries living within the conterminous U.S. from 2001 to 2008.ResultsA 10 ppb increase in NO2 was associated with increased mortality from all-cause (HR: 1.06; 95% CI: 1.05-1.06), cardiovascular (HR: 1.10; 95% CI: 1.10-1.11), respiratory disease (HR: 1.09; 95% CI: 1.08-1.11), and cancer (HR: 1.01; 95% CI: 1.00-1.02) adjusting for age, sex, race, ZIP code as strata ZIP code- and state-level socio-economic status (SES) as covariates, and PM2.5 exposure using a 2-stage approach. NO2 was also associated with elevated mortality from ischemic heart disease, cerebrovascular disease, congestive heart failure, chronic obstructive pulmonary disease, pneumonia, and lung cancer. We found no evidence of a threshold, with positive and significant HRs across the range of NO2 exposures for all causes of death examined. Exposure-response curves were linear for all-cause, supra-linear for cardiovascular-, and sub-linear for respiratory-related mortality. HRs were highest consistently among Black beneficiaries.ConclusionsLong-term NO2 exposure is associated with elevated risks of death by multiple causes, without evidence of a threshold response. Our findings raise concerns about the sufficiency of the annual NAAQS for NO2.
| S-EPMC8810665 | biostudies-literature
Project description:BackgroundHuman exposure to silica dust is very common in both working and living environments. However, the potential long-term health effects have not been well established across different exposure situations.Methods and findingsWe studied 74,040 workers who worked at 29 metal mines and pottery factories in China for 1 y or more between January 1, 1960, and December 31, 1974, with follow-up until December 31, 2003 (median follow-up of 33 y). We estimated the cumulative silica dust exposure (CDE) for each worker by linking work history to a job-exposure matrix. We calculated standardized mortality ratios for underlying causes of death based on Chinese national mortality rates. Hazard ratios (HRs) for selected causes of death associated with CDE were estimated using the Cox proportional hazards model. The population attributable risks were estimated based on the prevalence of workers with silica dust exposure and HRs. The number of deaths attributable to silica dust exposure among Chinese workers was then calculated using the population attributable risk and the national mortality rate. We observed 19,516 deaths during 2,306,428 person-years of follow-up. Mortality from all causes was higher among workers exposed to silica dust than among non-exposed workers (993 versus 551 per 100,000 person-years). We observed significant positive exposure-response relationships between CDE (measured in milligrams/cubic meter-years, i.e., the sum of silica dust concentrations multiplied by the years of silica exposure) and mortality from all causes (HR 1.026, 95% confidence interval 1.023-1.029), respiratory diseases (1.069, 1.064-1.074), respiratory tuberculosis (1.065, 1.059-1.071), and cardiovascular disease (1.031, 1.025-1.036). Significantly elevated standardized mortality ratios were observed for all causes (1.06, 95% confidence interval 1.01-1.11), ischemic heart disease (1.65, 1.35-1.99), and pneumoconiosis (11.01, 7.67-14.95) among workers exposed to respirable silica concentrations equal to or lower than 0.1 mg/m(3). After adjustment for potential confounders, including smoking, silica dust exposure accounted for 15.2% of all deaths in this study. We estimated that 4.2% of deaths (231,104 cases) among Chinese workers were attributable to silica dust exposure. The limitations of this study included a lack of data on dietary patterns and leisure time physical activity, possible underestimation of silica dust exposure for individuals who worked at the mines/factories before 1950, and a small number of deaths (4.3%) where the cause of death was based on oral reports from relatives.ConclusionsLong-term silica dust exposure was associated with substantially increased mortality among Chinese workers. The increased risk was observed not only for deaths due to respiratory diseases and lung cancer, but also for deaths due to cardiovascular disease. Please see later in the article for the Editors' Summary.
| S-EPMC3328438 | biostudies-literature
Project description:This study illuminates the association between cigarette smoking and adult mortality in the contemporary United States. Recent studies have estimated smoking-attributable mortality using indirect approaches or with sample data that are not nationally representative and that lack key confounders. We use the 1990-2011 National Health Interview Survey Linked Mortality Files to estimate relative risks of all-cause and cause-specific mortality for current and former smokers compared with never smokers. We examine causes of death established as attributable to smoking as well as additional causes that appear to be linked to smoking but have not yet been declared by the U.S. Surgeon General to be caused by smoking. Mortality risk is substantially elevated among smokers for established causes and moderately elevated for additional causes. We also decompose the mortality disadvantage among smokers by cause of death and estimate the number of smoking-attributable deaths for the U.S. adult population ages 35+, net of sociodemographic and behavioral confounders. The elevated risks translate to 481,887 excess deaths per year among current and former smokers compared with never smokers, 14 % to 15 % of which are due to the additional causes. The additional causes of death contribute to the health burden of smoking and should be considered in future studies of smoking-attributable mortality. This study demonstrates that smoking-attributable mortality must remain a top population health priority in the United States and makes several contributions to further underscore the human costs of this tragedy that has ravaged American society for more than a century.
| S-EPMC6219821 | biostudies-literature
Project description:BackgroundFew studies have examined the impact of treatment-related morbidity on long-term, cause-specific mortality in Hodgkin lymphoma (HL) patients.MethodsThis multicenter cohort included 4919 HL patients, treated before age 51 years between 1965 and 2000, with a median follow-up of 20.2 years. Standardized mortality ratios, absolute excess mortality (AEM) per 10 000 person-years, and cause-specific cumulative mortality by stage and primary treatment, accounting for competing risks, were calculated.ResultsHL patients experienced a 5.1-fold (AEM = 123 excess deaths per 10 000 person-years) higher risk of death due to causes other than HL. This risk remained increased in 40-year survivors (standardized mortality ratio = 5.2, 95% confidence interval [CI] = 4.2 to 6.5, AEM = 619). At age 54 years, HL survivors experienced similar cumulative mortality (20.0%) from causes other than HL to 71-year-old individuals from the general population. Whereas HL mortality statistically significantly decreased over the calendar period (P < .001), solid tumor mortality did not change in the most recent treatment era. Patients treated in 1989-2000 had lower 25-year cardiovascular disease mortality than patients treated in 1965-1976 (4.3% vs 5.7%; subdistribution hazard ratio = 0.65, 95% CI = 0.46 to 0.93). Infectious disease mortality was not only increased after splenectomy but also after spleen irradiation (hazard ratio = 2.81, 95% CI = 1.55 to 5.07). For stage I-II, primary treatment with chemotherapy (CT) alone was associated with statistically significantly higher HL mortality (P < .001 for CT vs radiotherapy [RT]; P = .04 for CT vs RT+CT) but lower 30-year mortality from causes other than HL (15.8%, 95% CI = 9.7% to 23.3%) compared with RT alone (36.9%, 95% CI = 34.0% to 39.8%, P = .001) and RT and CT combined (29.8%, 95% CI = 26.8% to 32.9%, P = .02).ConclusionsCompared with the general population, HL survivors have a substantially reduced life expectancy. Optimal selection of patients for primary CT is crucial, weighing risks of HL relapse and long-term toxicity.
| S-EPMC8168246 | biostudies-literature
Project description:BackgroundLong-term exposure to fine particulate matter (PM2.5) mass has been associated with adverse health effects. However, the health effects of PM2.5 components have been less studied. There is a pressing need to better understand the relative contribution of components of PM2.5, which can lay the scientific basis for designing effective policies and targeted interventions.MethodsWe conducted a population-based cohort study, comprising all Medicare enrollees aged 65 or older in the southeastern United States from 2000 to 2016, to explore the associations between long-term exposure to PM2.5 major components and all-cause mortality among the elderly. Based on well-validated prediction models, we estimated ZIP code-level annual mean concentrations for five major PM2.5 components, including black carbon (BC), nitrate (NIT), organic matter (OM), sulfate (SO4), and soil particles. Data were analyzed using Cox proportional hazards models, adjusting for potential confounders.ResultsThe cohort comprised 13,590,387 Medicare enrollees and a total of 107,191,652 person-years. In single-component models, all five major PM2.5 components were significantly associated with elevated all-cause mortality. The hazard ratios (HR) per interquartile range (IQR) increase in exposure were 1.027 (95% CI: 1.025-1.030), 1.012 (95% CI: 1.010-1.013), 1.018 (95% CI: 1.017-1.020), 1.021 (95% CI: 1.017-1.024), and 1.004 (95% CI: 1.003-1.006) for BC, NIT, OM, SO4, and soil particles, respectively. While the effect estimate of soil component was statistically significant, it is much smaller than those of combustion-related components.ConclusionOur study provides epidemiological evidence that long-term exposure to major PM2.5 components is significantly associated with elevated mortality.
| S-EPMC9190768 | biostudies-literature
Project description:Despite the growing evidence on the health effects of short-term exposure to wildfire smoke fine particles (PM2.5), the impacts of long-term wildfire smoke PM2.5 exposure remain unclear. We investigated the association between long-term exposure to wildfire smoke PM2.5 and all-cause mortality and mortality from a wide range of specific causes in all 3,108 counties in the contiguous U.S., 2007-2020. Monthly county-level mortality data were collected from the National Center for Health Statistics. Wildfire smoke PM2.5 concentration was derived from a 10×10 km2 resolution spatiotemporal model. Controlling for non-smoke PM2.5, air temperature, and unmeasured spatial and temporal confounders, we found a non-linear association between 12-month moving average concentration of smoke PM2.5 and monthly all-cause mortality rate. Relative to a month with the long-term smoke PM2.5 exposure below 0.1 μg/m3, all-cause mortality increased by 0.40-1.54 and 3.65 deaths per 100,000 people per month when the 12-month moving average of PM2.5 concentration was of 0.1-5 and 5+ μg/m3, respectively. Cardiovascular, ischemic heart disease, digestive, endocrine, diabetes, mental, suicide, and chronic kidney disease mortality were all found to be associated with long-term wildfire smoke PM2.5 exposure. Smoke PM2.5 contributed to approximately 30,180 all-cause deaths/year (95% CI: 21,449, 38,910) in the contiguous U.S. Higher smoke PM2.5-related increases in mortality rates were found for people aged 65 above and racial minority populations. Positive interaction effects with extreme heat were also observed. Our study identified the detrimental effects of long-term exposure to wildfire smoke PM2.5 on a wide range of mortality outcomes, underscoring the need for public health actions and communication to prepare communities and individuals to mitigate smoke exposure.
| S-EPMC9915814 | biostudies-literature