Mortality burdens in California due to air pollution attributable to local and nonlocal emissions.
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ABSTRACT:
SUBMITTER: Wang T
PROVIDER: S-EPMC7145419 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Exposure to ozone and fine particulate matter (PM2.5) can cause adverse health effects, including premature mortality due to cardiopulmonary diseases and lung cancer. Recent studies quantify global air pollution mortality but not the contribution of different emissions sectors, or they focus on a specific sector.We estimated the global mortality burden of anthropogenic ozone and PM2.5, and the impact of five emissions sectors, using a global chemical transport model at a finer horizontal resolution (0.67° × 0.5°) than previous studies.We performed simulations for 2005 using the Model for Ozone and Related Chemical Tracers, version 4 (MOZART-4), zeroing out all anthropogenic emissions and emissions from specific sectors (All Transportation, Land Transportation, Energy, Industry, and Residential and Commercial). We estimated premature mortality using a log-linear concentration-response function for ozone and an integrated exposure-response model for PM2.5.We estimated 2.23 (95% CI: 1.04, 3.33) million deaths/year related to anthropogenic PM2.5, with the highest mortality in East Asia (48%). The Residential and Commercial sector had the greatest impact globally-675 (95% CI: 428, 899) thousand deaths/year-and in most regions. Land Transportation dominated in North America (32% of total anthropogenic PM2.5 mortality), and it had nearly the same impact (24%) as Residential and Commercial (27%) in Europe. Anthropogenic ozone was associated with 493 (95% CI: 122, 989) thousand deaths/year, with the Land Transportation sector having the greatest impact globally (16%).The contributions of emissions sectors to ambient air pollution-related mortality differ among regions, suggesting region-specific air pollution control strategies. Global sector-specific actions targeting Land Transportation (ozone) and Residential and Commercial (PM2.5) sectors would particularly benefit human health. Citation: Silva RA, Adelman Z, Fry MM, West JJ. 2016. The impact of individual anthropogenic emissions sectors on the global burden of human mortality due to ambient air pollution. Environ Health Perspect 124:1776-1784;?http://dx.doi.org/10.1289/EHP177.
| S-EPMC5089880 | biostudies-other
Project description: Not available
| S-EPMC6150471 | biostudies-literature
Project description:BackgroundAmbient air pollution and tuberculosis (TB) have an impact on public health worldwide, yet associations between the two remain uncertain.ObjectiveWe determined the impact of residential traffic on mortality during treatment of active TB.MethodsFrom 2000-2012, we enrolled 32,875 patients in California with active TB and followed them throughout treatment. We obtained patient data from the California Tuberculosis Registry and calculated traffic volumes and traffic densities in 100- to 400-m radius buffers around residential addresses. We used Cox models to determine mortality hazard ratios, controlling for demographic, socioeconomic, and clinical potential confounders. We categorized traffic exposures as quintiles and determined trends using Wald tests.ResultsParticipants contributed 22,576 person-years at risk. There were 2,305 deaths during treatment for a crude mortality rate of 1,021 deaths per 10,000 person-years. Traffic volumes and traffic densities in all buffers around patient residences were associated with increased mortality during TB treatment, although the findings were not statistically significant in all buffers. As the buffer size decreased, fifth-quintile mortality hazards increased, and trends across quintiles of traffic exposure became more statistically significant. Increasing quintiles of nearest-road traffic volumes in the 100-m buffer were associated with 3%, 14%, 19%, and 28% increased risk of death during TB treatment [first quintile, referent; second quintile hazard ratio (HR)=1.03 [95% confidence interval (CI): 0.86, 1.25]; third quintile HR=1.14 (95% CI: 0.95, 1.37); fourth quintile HR=1.19 (95% CI: 0.99, 1.43); fifth quintile HR=1.28 (95% CI: 1.07, 1.53), respectively; p-trend=0.002].ConclusionsResidential proximity to road traffic volumes and traffic density were associated with increased all-cause mortality in patients undergoing treatment for active tuberculosis even after adjusting for multiple demographic, socioeconomic, and clinical factors, suggesting that TB patients are susceptible to the adverse health effects of traffic-related air pollution. https://doi.org/10.1289/EHP1699.
| S-EPMC5915191 | biostudies-literature
Project description:Background: Exposure to 2.5-micron diameter air pollutants (PM 2.5) has been associated with an increased risk of illness and death worldwide; however, in Latin American health impacts assessment of this risk factor is scarce. Medellín is one of the most polluted cities in the region, with a population growth rate that is twice as high as that of other Colombian cities, which implies a growing population at risk. Methods: A descriptive study of the disease burden was carried out using the city as the unit of observation. Health events were selected based on epidemiologic evidence and the availability of the population attributable fraction associated with PM 2.5. The mortality records were taken from the module of deceased of the Single Registry of Affiliates of the Health System; the morbidity records were taken from the Individual Health Services Registries. For the estimation of the burden of disease, the current Global Burden of Disease guidelines were followed. Results: Attributable disability-adjusted life years to exposure to ambient PM 2.5 pollution (DALYs PM2.5) constituted 13.8% of total burden of the city. Males showed the greatest loss of DALYs PM2.5 due to acute events, while in women the greatest loss was due to chronic events. Ischemic heart disease, chronic diseases of the lower respiratory tract, and influenza and pneumonia were the events that contributed the most to DALYs PM2.5. 71.4% of the DALYs PM2.5 corresponded to mortality, mainly in the population over 65 years of age. Regarding attributable morbidity, acute events were more prevalent in both sexes, especially due to respiratory diseases Conclusion: Premature death among the elderly population has the greatest weight on burden of disease attributable to ambient PM 2.5 pollution, mainly due to respiratory and cardiovascular diseases, without significant differences according to gender.
| S-EPMC8564742 | biostudies-literature
Project description:BACKGROUND: Long-term exposures to particulate matter air pollution (PM2.5 and PM10) and high traffic load have been associated with markers of systemic inflammation. Epidemiological investigations have focused primarily on total PM, which represents a mixture of pollutants originating from different sources. OBJECTIVE: We investigated associations between source-specific PM and high-sensitive C-reactive protein (hs-CRP), an independent predictor of cardiovascular disease. METHODS: We used data from the first (2000-2003) and second examination (2006-2008) of the Heinz Nixdorf Recall study, a prospective population-based German cohort of initially 4,814 participants (45-75 years of age). We estimated residential long-term exposure to local traffic- and industry-specific fine particulate matter (PM2.5) at participants' residences using a chemistry transport model. We used a linear mixed model with a random participant intercept to estimate associations of source-specific PM and natural log-transformed hs-CRP, controlling for age, sex, education, body mass index, low- and high-density lipoprotein cholesterol, smoking variables, physical activity, season, humidity, and city (8,204 total observations). RESULTS: A 1-?g/m3 increase in total PM2.5 was associated with a 4.53% increase in hs-CRP concentration (95% CI: 2.76, 6.33%). hs-CRP was 17.89% (95% CI: 7.66, 29.09%) and 7.96% (95% CI: 3.45, 12.67%) higher in association with 1-?g/m3 increases in traffic- and industry-specific PM2.5, respectively. RESULTS for PM10 were similar. CONCLUSIONS: Long-term exposure to local traffic-specific PM (PM2.5, PM10) was more strongly associated with systemic inflammation than total PM. Associations of local industry-specific PM were slightly stronger but not significantly different from associations with total PM.
| S-EPMC4080540 | biostudies-literature
Project description:Few studies have investigated the chronic obstructive pulmonary disease (COPD) mortality fraction attributable to air pollution and modification by individual characteristics of air pollution effects. We applied distributed lag non-linear models to assess the associations between air pollution and COPD mortality in 2007-2011 in Guangzhou, China, and the total COPD mortality fraction attributable to air pollution was calculated as well. We found that an increase of 10 μg/m(3) in particulate matter with an aerodynamic diameter of 10 μm or less (PM10), sulfur dioxide (SO2) and nitrogen dioxide (NO2) was associated with a 1.58% (95% confidence interval (CI): 0.12-3.06%), 3.45% (95% CI: 1.30-5.66%) and 2.35% (95% CI: 0.42-4.32%) increase of COPD mortality over a lag of 0-15 days, respectively. Greater air pollution effects were observed in the elderly, males and residents with low educational attainment. The results showed 10.91% (95% CI: 1.02-9.58%), 12.71% (95% CI: 5.03-19.85%) and 13.38% (95% CI: 2.67-22.84%) COPD mortality was attributable to current PM10, SO2 and NO2 exposure, respectively. In conclusion, the associations between air pollution and COPD mortality differed by individual characteristics. There were remarkable COPD mortality burdens attributable to air pollution in Guangzhou.
| S-EPMC4872534 | biostudies-literature
Project description:BackgroundAmbient nitrogen dioxide (NO2) and fine particulate matter with aerodynamic diameter ≤2.5μm (PM2.5) threaten public health in the US, and systemic racism has led to modern-day disparities in the distribution and associated health impacts of these pollutants.ObjectivesMany studies on environmental injustices related to ambient air pollution focus only on disparities in pollutant concentrations or provide only an assessment of pollution or health disparities at a snapshot in time. In this study, we compare injustices in NO2- and PM2.5-attributable health burdens, considering NO2-attributable health impacts across the entire US; document changing disparities in these health burdens over time (2010-2019); and evaluate how more stringent air quality standards would reduce disparities in health impacts associated with these pollutants.MethodsThrough a health impact assessment, we quantified census tract-level variations in health outcomes attributable to NO2 and PM2.5 using health impact functions that combine demographic data from the US Census Bureau; two spatially resolved pollutant datasets, which fuse satellite data with physical and statistical models; and epidemiologically derived relative risk estimates and incidence rates from the Global Burden of Disease study.ResultsDespite overall decreases in the public health damages associated with NO2 and PM2.5, racial and ethnic relative disparities in NO2-attributable pediatric asthma and PM2.5-attributable premature mortality have widened in the US during the last decade. Racial relative disparities in PM2.5-attributable premature mortality and NO2-attributable pediatric asthma have increased by 16% and 19%, respectively, between 2010 and 2019. Similarly, ethnic relative disparities in PM2.5-attributable premature mortality have increased by 40% and NO2-attributable pediatric asthma by 10%.DiscussionEnacting and attaining more stringent air quality standards for both pollutants could preferentially benefit the most marginalized and minoritized communities by greatly reducing racial and ethnic relative disparities in pollution-attributable health burdens in the US. Our methods provide a semi-observational approach to track changes in disparities in air pollution and associated health burdens across the US. https://doi.org/10.1289/EHP11900.
| S-EPMC10916678 | biostudies-literature
Project description:BackgroundThe International Agency for Research on Cancer has classified outdoor air pollution (fine particulate matter [PM2.5]) as a Group 1 lung carcinogen in humans. We aimed to estimate the proportion of lung cancer cases attributable to PM2.5 exposure in Alberta in 2012.MethodsAnnual average concentrations of PM2.5 in 2011 for 22 communities across Alberta were extracted from the Clean Air Strategic Alliance Data Warehouse and were population-weighted across the province. Using 7.5 µg/m3 and 3.18 µg/m3 as the annual average theoretical minimum risk concentrations of PM2.5, we estimated the proportion of the population above this cut-off to determine the population attributable risk of lung cancer due to PM2.5 exposure.ResultsThe mean population-weighted concentration of PM2.5 for Alberta in 2011 was 10.03 µg/m3. We estimated relative risks of 1.02 and 1.06 for theoretical minimum risk PM2.5 concentration thresholds of 7.5 µg/m3 and 3.18 µg/m3, respectively. About 1.87%-5.69% of incident lung cancer cases in Alberta were estimated to be attributable to PM2.5 exposure.InterpretationOur estimate of attributable burden is low compared to that reported in studies in other areas of the world owing to the relatively low levels of PM2.5 recorded in Alberta. Reducing PM2.5 emissions in Alberta should continue to be a priority to help decrease the burden of lung cancer in the population.
| S-EPMC5498315 | biostudies-literature
Project description:Zinc (Zn) is a major elemental component of respirable ambient particulate matter (PM) detected often at alarming levels in urban air. Exposure to PM has been widely associated with increased cardiovascular morbidity and mortality, however, it is not known what components or sources of PM are causative. We recently demonstrated that long-term episodic inhalation of combustion PM, having similar amount of Zn found in urban PM, caused myocardial lesions in rats. We further demonstrated that a single pulmonary exposure to Zn at high concentration is associated with disturbances in cardiac mitochondrial function, ion channel regulation, calcium homeostasis, and cell signaling. Therefore, in this study we investigated the role of PM-associated Zn in cardiac injury using multiple exposure scenarios. Male Wistar-Kyoto (WKY) rats of 12-14 wks age were intratracheally exposed (once per wk x 8 or16 wks) to either (1) saline (control); (2) PM having no soluble Zn; (3) combustion PM suspension containing 14.5 ug/mg water-soluble Zn at high and (4) low dose levels, (5) the aqueous fraction of this suspension devoid of solid insoluble particulate fraction (14.5 ug/mg soluble Zn), or (6) Zn sulfate. Zn concentrations were identical in groups 3, 5 and 6. Pulmonary toxicity was apparent in all exposure groups when compared to saline as determined by recovery of cells in bronchoalveolar lavage fluid. Long-term exposure to PM with or without soluble Zn, or Zn sulfate caused distinct myocardial lesions characterized by subepicardial and randomly distributed myocardial inflammation, degeneration, and fibrosis. The lesion severity was higher in those groups receiving Zn PM. Because cardiac mitochondria are likely the primary target of inhaled metal or other absorbed PM components, we analyzed mitochondrial DNA damage using QPCR and found that all exposure groups except those exposed to PM without Zn caused variable degree of damage. Aconitase activity, sensitive to inhibition by oxidative stress was inhibited slightly but significantly in rats receiving zinc sulfate. Although modest, microarray (Affymetrix) analysis revealed expression changes in the heart reflective of effects on cell signaling, inflammation/oxidative stress, mitochondrial fatty acid metabolisms and cell cycle regulation in rats exposed to zinc sulfate. However, these changes were minimal following exposure to PM devoid of soluble metals. We demonstrate that episodic subchronic pulmonary exposure to zinc sulfate causes cardiac injury and mitochondrial DNA damage. Thus, water-soluble PM-associated zinc may be one of the PM components responsible for cardiovascular morbidity. Experiment Overall Design: Group 1 received Saline to serve as a control. Group 2 received Mount St. Helenâs ash, which does not contain any water-soluble zinc or other metals such that we can delineate any cardiac effect secondary to pulmonary deposition of these particles as these fine mode particles themselves are not likely to translocate to the heart. Group 3 received whole saline suspension of the same fugitive oil combustion particle sample used in the previous study, which contained insoluble components plus water-soluble zinc (Kodavanti et al., 2003; 14.5 ug/mg zinc) and also a small amount of water-soluble nickel (3.0 µg/mg). Elemental composition of this PM is comparable to Ottawa urban PM (Kodavanti et al., 2003). Group 4 also received same particle sample but at half the dose than group 3. Group 5 received saline-soluble or leachable fraction of PM-HD devoid of any solid material but contained soluble components including zinc and nickel. And, group 6 received zinc sulfate at concentration that was present in groups 3 or 5. This design allowed us to test if cardiac injury in rats was due to leached of zinc or solid particles. There were 4 replicates per treatment group.
2008-06-14 | E-GEOD-6541 | biostudies-arrayexpress
Project description:Accelerating growth due to industrialization and urbanization has improved the Indian economy but simultaneously has deteriorated human health, environment, and ecosystem. In the present study, the associated health risk mortality (age > 25) and welfare loss for the year 2017 due to excess PM2.5 concentration in ambient air for 31 major million-plus non-attainment cities (NACs) in India is assessed. The cities for the assessment are prioritised based on population and are classified as 'X' (> 5 million population) and 'Y' (1-5 million population) class cities. Ground-level PM2.5 concentration retrieved from air quality monitoring stations for the NACs ranged from 33 to 194 µg/m3. Total PM2.5 attributable premature mortality cases estimated using global exposure mortality model was 80,447 [95% CI 70,094-89,581]. Ischemic health disease was the leading cause of death accounting for 47% of total mortality, followed by chronic obstructive pulmonary disease (COPD-17%), stroke (14.7%), lower respiratory infection (LRI-9.9%) and lung cancer (LC-1.9%). 9.3% of total mortality is due to other non-communicable diseases (NCD-others). 7.3-18.4% of total premature mortality for the NACs is attributed to excess PM2.5 exposure. The total economic loss of 90,185.6 [95% CI 88,016.4-92,411] million US$ (as of 2017) was assessed due to PM2.5 mortality using the value of statistical life approach. The highest mortality (economic burden) share of 61.3% (72.7%) and 30.1% (42.7%) was reported for 'X' class cities and North India zone respectively. Compared to the base year 2017, an improvement of 1.01% and 0.7% is observed in premature mortality and economic loss respectively for the year 2024 as a result of policy intervention through National Clean Air Action Programme. The improvement among 31 NACs was found inconsistent, which may be due to a uniform targeted policy, which neglects other socio-economic factors such as population, the standard of living, etc. The study highlights the need for these parameters to be incorporated in the action plans to bring in a tailored solution for each NACs for better applicability and improved results of the programme facilitating solutions for the complex problem of air pollution in India.
| S-EPMC8640062 | biostudies-literature