Contribution of climate and air pollution to variation in coronary heart disease mortality rates in England.
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ABSTRACT:
SUBMITTER: Scarborough P
PROVIDER: S-EPMC3299689 | biostudies-other | 2012
REPOSITORIES: biostudies-other
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Project description:Emerging evidence indicates that the near-roadway air pollution (NRAP) mixture contributes to CHD, yet few studies have evaluated the associated costs.We integrated an assessment of NRAP-attributable CHD in Southern California with new methods to value the associated mortality and hospitalizations.Based on population-weighted residential exposure to NRAP (traffic density, proximity to a major roadway and elemental carbon), we estimated the inflation-adjusted value of NRAP-attributable mortality and costs of hospitalizations that occurred in 2008. We also estimated anticipated costs in 2035 based on projected changes in population and in NRAP exposure associated with California's plans to reduce greenhouse gas emissions. For comparison, we estimated the value of CHD mortality attributable to PM less than 2.5?m in diameter (PM2.5) in both 2008 and 2035.The value of CHD mortality attributable to NRAP in 2008 was between $3.8 and $11.5 billion, 23% (major roadway proximity) to 68% (traffic density) of the $16.8 billion attributable to regulated regional PM2.5. NRAP-attributable costs were projected to increase to $10.6 to $22 billion in 2035, depending on the NRAP metric. Cost of NRAP-attributable hospitalizations for CHD in 2008 was $48.6 million and was projected to increase to $51.4 million in 2035.We developed an economic framework that can be used to estimate the benefits of regulations to improve air quality. CHD attributable to NRAP has a large economic impact that is expected to increase by 2035, largely due to an aging population. PM2.5-attributable costs may underestimate total value of air pollution-attributable CHD.
| S-EPMC5769477 | biostudies-literature
Project description: Not available
| S-EPMC6150471 | biostudies-literature
Project description:BACKGROUND:Socioeconomically disadvantaged populations often have higher exposures to particulate air pollution, which can be expected to contribute to differentials in life expectancy. We examined socioeconomic differentials in exposure and air pollution-related mortality relating to larger scale (5 km resolution) variations in background concentrations of selected pollutants across England. METHODS:Ozone and particulate matter (sub-divided into PM10, PM2.5, PM2.5-10, primary, nitrate and sulphate PM2.5) were simulated at 5 km horizontal resolution using an atmospheric chemistry transport model (EMEP4UK). Annual mean concentrations of these pollutants were assigned to all 1,202,578 residential postcodes in England, which were classified by urban-rural status and socioeconomic deprivation based on the income and employment domains of the 2010 English Index of Multiple Deprivation for the Lower-level Super Output Area of residence. We used life table methods to estimate PM2.5-attributable life years (LYs) lost in both relative and absolute terms. RESULTS:Concentrations of the most particulate fractions, but not of nitrate PM2.5 or ozone, were modestly higher in areas of greater socioeconomic deprivation. Relationships between pollution level and socioeconomic deprivation were non-linear and varied by urban-rural status. The pattern of PM2.5 concentrations made only a small contribution to the steep socioeconomic gradient in LYs lost due to PM2.5 per 103 population, which primarily was driven by the steep socioeconomic gradient in underlying mortality rates. In rural areas, the absolute burden of air pollution-related LYs lost was lowest in the most deprived deciles. CONCLUSIONS:Air pollution shows modest socioeconomic patterning at 5 km resolution in England, but absolute attributable mortality burdens are strongly related to area-level deprivation because of underlying mortality rates. Measures that cause a general reduction in background concentrations of air pollution may modestly help narrow socioeconomic differences in health.
| S-EPMC6389046 | 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:Recent studies suggested a link between long-term exposure to air-pollution and COVID-19 mortality. However, due to their ecological design based on large spatial units, they neglect the strong localised air-pollution patterns, and potentially lead to inadequate confounding adjustment. We investigated the effect of long-term exposure to NO2 and PM2.5 on COVID-19 mortality in England using high geographical resolution. In this nationwide cross-sectional study in England, we included 38,573 COVID-19 deaths up to June 30, 2020 at the Lower Layer Super Output Area level (n = 32,844 small areas). We retrieved averaged NO2 and PM2.5 concentration during 2014-2018 from the Pollution Climate Mapping. We used Bayesian hierarchical models to quantify the effect of air-pollution while adjusting for a series of confounding and spatial autocorrelation. We find a 0.5% (95% credible interval: -0.2%, 1.2%) and 1.4% (95% CrI: -2.1%, 5.1%) increase in COVID-19 mortality risk for every 1 μg/m3 increase in NO2 and PM2.5 respectively, after adjusting for confounding and spatial autocorrelation. This corresponds to a posterior probability of a positive effect equal to 0.93 and 0.78 respectively. The spatial relative risk at LSOA level revealed strong patterns, similar for the different pollutants. This potentially captures the spread of the disease during the first wave of the epidemic. Our study provides some evidence of an effect of long-term NO2 exposure on COVID-19 mortality, while the effect of PM2.5 remains more uncertain.
| S-EPMC7786642 | biostudies-literature
Project description:Recent studies suggested a link between long-term exposure to air-pollution and COVID-19 mortality. However, due to their ecological design, based on large spatial units, they neglect the strong localised air-pollution patterns, and potentially lead to inadequate confounding adjustment. We investigated the effect of long-term exposure to NO2 and PM2.5 on COVID-19 deaths up to June 30, 2020 in England using high geographical resolution. We included 38 573 COVID-19 deaths up to June 30, 2020 at the Lower Layer Super Output Area level in England (n=32 844 small areas). We retrieved averaged NO2 and PM2.5 concentration during 2014-2018 from the Pollution Climate Mapping. We used Bayesian hierarchical models to quantify the effect of air-pollution while adjusting for a series of confounding and spatial autocorrelation. We find a 0.5% (95% credible interval: -0.2%-1.2%) and 1.4% (-2.1%-5.1%) increase in COVID-19 mortality rate for every 1μg/m3 increase in NO2 and PM2.5 respectively, after adjusting for confounding and spatial autocorrelation. This corresponds to a posterior probability of a positive effect of 0.93 and 0.78 respectively. The spatial relative risk at LSOA level revealed strong patterns, similar for the different pollutants. This potentially captures the spread of the disease during the first wave of the epidemic. Our study provides some evidence of an effect of long-term NO2 exposure on COVID-19 mortality, while the effect of PM2.5 remains more uncertain. Medical Research Council, Wellcome Trust, Environmental Protection Agency and National Institutes of Health.
| S-EPMC7430619 | biostudies-literature
Project description:Epidemiological findings concerning the seasonal variation in the acute effect of particulate matter (PM) are inconsistent. We investigated the seasonality in the association between PM with an aerodynamic diameter of less than 10 ?m (PM10) and daily mortality in 17 Chinese cities. We fitted the "main" time-series model after adjustment for time-varying confounders using smooth functions with natural splines. We established a "seasonal" model to obtain the season-specific effect estimates of PM10, and a "harmonic" model to show the seasonal pattern that allows PM10 effects to vary smoothly with the day in a year. At the national level, a 10 ?g/m(3) increase in the two-day moving average concentrations (lag 01) of PM10 was associated with 0.45% [95% posterior interval (PI), 0.15% to 0.76%], 0.17% (95% PI, -0.09% to 0.43%), 0.55% (95% PI, 0.15% to 0.96%) and 0.25% (95%PI, -0.05% to 0.56%) increases in total mortality for winter, spring, summer and fall, respectively. For the smoothly-varying plots of seasonality, we identified a two-peak pattern in winter and summer. The observed seasonal pattern was generally insensitive to model specifications. Our analyses suggest that the acute effect of particulate air pollution could vary by seasons with the largest effect in winter and summer in China. To our knowledge, this is the first multicity study in developing countries to analyze the seasonal variations of PM-related health effects.
| S-EPMC3885864 | biostudies-literature
Project description:In December 2019, a novel disease, coronavirus disease 19 (COVID-19), emerged in Wuhan, People's Republic of China. COVID-19 is caused by a novel coronavirus (SARS-CoV-2) presumed to have jumped species from another mammal to humans. This virus has caused a rapidly spreading global pandemic. To date, over 300,000 cases of COVID-19 have been reported in England and over 40,000 patients have died. While progress has been achieved in managing this disease, the factors in addition to age that affect the severity and mortality of COVID-19 have not been clearly identified. Recent studies of COVID-19 in several countries identified links between air pollution and death rates. Here, we explored potential links between major fossil fuel-related air pollutants and SARS-CoV-2 mortality in England. We compared current SARS-CoV-2 cases and deaths from public databases to both regional and subregional air pollution data monitored at multiple sites across England. After controlling for population density, age and median income, we show positive relationships between air pollutant concentrations, particularly nitrogen oxides, and COVID-19 mortality and infectivity. Using detailed UK Biobank data, we further show that PM2.5 was a major contributor to COVID-19 cases in England, as an increase of 1 m3 in the long-term average of PM2.5 was associated with a 12% increase in COVID-19 cases. The relationship between air pollution and COVID-19 withstands variations in the temporal scale of assessments (single-year vs 5-year average) and remains significant after adjusting for socioeconomic, demographic and health-related variables. We conclude that a small increase in air pollution leads to a large increase in the COVID-19 infectivity and mortality rate in England. This study provides a framework to guide both health and emissions policies in countries affected by this pandemic.
| S-EPMC7571423 | biostudies-literature
Project description:IntroductionLong-term air pollution exposure contributes to mortality but there are few studies examining effects of very long-term (>25 years) exposures.MethodsThis study investigated modelled air pollution concentrations at residence for 1971, 1981, 1991 (black smoke (BS) and SO2) and 2001 (PM10) in relation to mortality up to 2009 in 367,658 members of the longitudinal survey, a 1% sample of the English Census. Outcomes were all-cause (excluding accidents), cardiovascular (CV) and respiratory mortality.ResultsBS and SO2 exposures remained associated with mortality decades after exposure-BS exposure in 1971 was significantly associated with all-cause (OR 1.02 (95% CI 1.01 to 1.04)) and respiratory (OR 1.05 (95% CI 1.01 to 1.09)) mortality in 2002-2009 (ORs expressed per 10 μg/m(3)). Largest effect sizes were seen for more recent exposures and for respiratory disease. PM10 exposure in 2001 was associated with all outcomes in 2002-2009 with stronger associations for respiratory (OR 1.22 (95% CI 1.04 to 1.44)) than CV mortality (OR 1.12 (95% CI 1.01 to 1.25)). Adjusting PM10 for past BS and SO2 exposures in 1971, 1981 and 1991 reduced the all-cause OR to 1.16 (95% CI 1.07 to 1.26) while CV and respiratory associations lost significance, suggesting confounding by past air pollution exposure, but there was no evidence for effect modification. Limitations include limited information on confounding by smoking and exposure misclassification of historic exposures.ConclusionsThis large national study suggests that air pollution exposure has long-term effects on mortality that persist decades after exposure, and that historic air pollution exposures influence current estimates of associations between air pollution and mortality.
| S-EPMC4819629 | biostudies-literature
Project description:BackgroundMagnitudes, geographic and racial variation in trends in coronary heart disease (CHD) mortality within the US require updating for health services and health disparities research. Therefore the aim of this study is to present data on these trends through 2007.MethodsData for CHD were analyzed using the US mortality files for 1999-2007 obtained from the US Centers for Disease Control and Prevention. Age-adjusted annual death rates were computed for non-Hispanic African Americans (AA) and European Americans (EA) aged 35-84 years. The direct method was used to standardize rates by age, using the 2000 US standard population. Joinpoint regression models were used to evaluate trends, expressed as annual percent change (APC).ResultsFor both AA men and women the magnitude in CHD mortality is higher compared to EA men and women, respectively. Between 1999 and 2007 the rate declined both in AA and in EA of both sexes in every geographic division; however, relative declines varied. For example, among men, relative average annual declines ranged from 3.2% to 4.7% in AA and from 4.4% to 5.5% in EA among geographic divisions. In women, rates declined more in later years of the decade and in women over 54 years. In 2007, age-adjusted death rate per 100,000 for CHD ranged from 93 in EA women in New England to 345 in AA men in the East North Central division. In EA, areas near the Ohio and lower Mississippi Rivers had above average rates. Disparities in trends by urbanization level were also found. For AA in the East North Central division, the APC was similar in large central metro (-4.2), large fringe metro (-4.3), medium metro urbanization strata (-4.4), and small metro (-3.9). APC was somewhat higher in the micropolitan/non-metro (-5.3), and especially the non-core/non-metro (-6.5). For EA in the East South Central division, the APC was higher in large central metro (-5.3), large fringe metro (-4.3) and medium metro urbanization strata (-5.1) than in small metro (-3.8), micropolitan/non-metro (-4.0), and non-core/non-metro (-3.3) urbanization strata.ConclusionsBetween 1999 and 2007, the level and rate of decline in CHD mortality displayed persistent disparities. Declines were greater in EA than AA racial groups. Rates were greater in the Ohio and Mississippi River than other geographic regions.
| S-EPMC3532343 | biostudies-literature