Air pollution and mortality in a large, representative U.S. cohort: multiple-pollutant analyses, and spatial and temporal decompositions.
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ABSTRACT:
SUBMITTER: Lefler JS
PROVIDER: S-EPMC6873509 | biostudies-literature | 2019 Nov
REPOSITORIES: biostudies-literature
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Project description:BackgroundEvidence 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.ObjectivesOur 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.MethodsNational 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.ResultsEstimated 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.DiscussionThis 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.
| S-EPMC6792459 | biostudies-literature
Project description:While recent assessments have quantified the burden of air pollution at the national scale in China, air quality managers would benefit from assessments that disaggregate health impacts over regions and over time. We took advantage of a new 10×10km satellite-based PM2.5 dataset to analyze spatial and temporal trends of air pollution health impacts in China, from 2004 to 2012. Results showed that national PM2.5 related deaths from stroke, ischemic heart disease and lung cancer increased from approximately 800,000 cases in 2004 to over 1.2 million cases in 2012. The health burden exhibited strong spatial variations, with high attributable deaths concentrated in regions including the Beijing-Tianjin Metropolitan Region, Yangtze River Delta, Pearl River Delta, Sichuan Basin, Shandong, Wuhan Metropolitan Region, Changsha-Zhuzhou-Xiangtan, Henan, and Anhui, which have heavy air pollution, high population density, or both. Increasing trends were found in most provinces, but with varied growth rates. While there was some evidence for improving air quality in recent years, this was offset somewhat by the countervailing influences of in-migration together with population growth. We recommend that priority areas for future national air pollution control policies be adjusted to better reflect the spatial hotspots of health burdens. Satellite-based exposure and health impact assessments can be a useful tool for tracking progress on both air quality and population health burden reductions.
| S-EPMC5479577 | biostudies-literature
Project description:China has had a rapid increase in its economy over the past three decades. However, the economic boom came at a certain cost of depleting air quality. In the study, we aimed to examine the burden of air pollution and its association with climatic factors and health outcomes using data from Chinese national and city-level air quality and public health surveillance systems. City-level daily air pollution index (API, a sum weighted index of SO2, NO2, PM10, CO, and Ozone) in 120 cities in 2012 and 2013, and its association with climate factors were analyzed using multiple linear regression analysis, spatial autocorrelation analysis, and panel fixed models. City-level ecological association between annual average API and total mortality were examined using univariate and partial correlation analysis. Sensitivity analysis was conducted by taking the consideration of time-lag effect between exposures and outcomes. The results show that among the 120 cities, annual average API significantly increased from 2012 to 2013 (65.05 vs. 75.99, p < 0.0001). The highest average API was in winter, and the lowest in summer. A significantly spatial clustering of elevated API was observed, with the highest API in northwest China in 2012 and with the highest in east China in 2013. In 2012, 5 (4%) of the 120 cities had ≥60 days with API >100 (defined as "slightly polluted"), however, it increased to 21 cities (18%) that experienced API >100 for ≥60 days in 2013. Furthermore, 16 cities (13%) in 2012 and 35 (29%) in 2013 experienced a maximum API >300 (defined as "severely polluted"). API was negatively and significantly correlated with heat index, precipitation, and sunshine hours, but positively with air pressure. Cities with higher API concentrations had significantly higher total mortality rates than those with lower API. About a 4-7% of the variation in total mortality could be explained by the difference in API across the nation. In conclusion, the study highlights an increased trend of air pollution from 2012 to 2013 in China. The magnitude of air pollution varied by seasons and regions and correlated with climatic factors and total mortality across the country.
| S-EPMC4947578 | biostudies-literature
Project description:We introduce a Bayesian spatial-temporal hierarchical multivariate probit regression model that identifies weeks during the first trimester of pregnancy which are impactful in terms of cardiac congenital anomaly development. The model is able to consider multiple pollutants and a multivariate cardiac anomaly grouping outcome jointly while allowing the critical windows to vary in a continuous manner across time and space. We utilize a dataset of numerical chemical model output which contains information regarding multiple species of PM2.5. Our introduction of an innovative spatial-temporal semiparametric prior distribution for the pollution risk effects allows for greater flexibility to identify critical weeks during pregnancy which are missed when more standard models are applied. The multivariate kernel stick-breaking prior is extended to include space and time simultaneously in both the locations and the masses in order to accommodate complex data settings. Simulation study results suggest that our prior distribution has the flexibility to outperform competitor models in a number of data settings. When applied to the geo-coded Texas birth data, weeks 3, 7 and 8 of the pregnancy are identified as being impactful in terms of cardiac defect development for multiple pollutants across the spatial domain.
| S-EPMC3589577 | biostudies-literature
Project description:Hundreds of millions of visitors travel to U.S. national parks every year to visit America's iconic landscapes. Concerns about air quality in these areas have led to strict, yet controversial pollution control policies. We document pollution trends in U.S. national parks and estimate the relationship between pollution and park visitation. From 1990 to 2014, average ozone concentrations in national parks were statistically indistinguishable from the 20 largest U.S. metropolitan areas. Further, relative to U.S. cities, national parks have seen only modest reductions in days with ozone concentrations exceeding levels deemed unhealthy by the U.S. Environmental Protection Agency. We find a robust, negative relationship between in-park ozone concentrations and park visitation. Still, 35% of all national park visits occur when ozone levels are elevated.
| S-EPMC6051738 | biostudies-literature
Project description:Traffic activity encompasses the number, mix, speed and acceleration of vehicles on roadways. The temporal pattern and variation of traffic activity reflects vehicle use, congestion and safety issues, and it represents a major influence on emissions and concentrations of traffic-related air pollutants. Accurate characterization of vehicle flows is critical in analyzing and modeling urban and local-scale pollutants, especially in near-road environments and traffic corridors. This study describes methods to improve the characterization of temporal variation of traffic activity. Annual, monthly, daily and hourly temporal allocation factors (TAFs), which describe the expected temporal variation in traffic activity, were developed using four years of hourly traffic activity data recorded at 14 continuous counting stations across the Detroit, Michigan, U.S. region. Five sites also provided vehicle classification. TAF-based models provide a simple means to apportion annual average estimates of traffic volume to hourly estimates. The analysis shows the need to separate TAFs for total and commercial vehicles, and weekdays, Saturdays, Sundays and observed holidays. Using either site-specific or urban-wide TAFs, nearly all of the variation in historical traffic activity at the street scale could be explained; unexplained variation was attributed to adverse weather, traffic accidents and construction. The methods and results presented in this paper can improve air quality dispersion modeling of mobile sources, and can be used to evaluate and model temporal variation in ambient air quality monitoring data and exposure estimates.
| S-EPMC4380130 | 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:Vehicle emissions represent one of the most important air pollution sources in most urban areas, and elevated concentrations of pollutants found near major roads have been associated with many adverse health impacts. To understand these impacts, exposure estimates should reflect the spatial and temporal patterns observed for traffic-related air pollutants. This paper evaluates the spatial resolution and zonal systems required to estimate accurately intraurban and near-road exposures of traffic-related air pollutants. The analyses use the detailed information assembled for a large (800 km2) area centered on Detroit, Michigan, USA. Concentrations of nitrogen oxides (NOx) due to vehicle emissions were estimated using hourly traffic volumes and speeds on 9,700 links representing all but minor roads in the city, the MOVES2010 emission model, the RLINE dispersion model, local meteorological data, a temporal resolution of 1 hr, and spatial resolution as low as 10 m. Model estimates were joined with the corresponding shape files to estimate residential exposures for 700,000 individuals at property parcel, census block, census tract, and ZIP code levels. We evaluate joining methods, the spatial resolution needed to meet specific error criteria, and the extent of exposure misclassification. To portray traffic-related air pollutant exposure, raster or inverse distance-weighted interpolations are superior to nearest neighbor approaches, and interpolations between receptors and points of interest should not exceed about 40 m near major roads, and 100 m at larger distances. For census tracts and ZIP codes, average exposures are overestimated since few individuals live very near major roads, the range of concentrations is compressed, most exposures are misclassified, and high concentrations near roads are entirely omitted. While smaller zones improve performance considerably, even block-level data can misclassify many individuals. To estimate exposures and impacts of traffic-related pollutants accurately, data should be geocoded or estimated at the most-resolved spatial level; census tract and larger zones have little if any ability to represent intraurban variation in traffic-related air pollutant concentrations. These results are based on one of the most comprehensive intraurban modeling studies in the literature and results are robust. Recommendations address the value of dispersion models to portray spatial and temporal variation of air pollutants in epidemiology and other studies; techniques to improve accuracy and reduce the computational burden in urban scale modeling; the necessary spatial resolution for health surveillance, demographic, and pollution data; and the consequences of low resolution data in terms of exposure misclassification.
| S-EPMC4131205 | 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. Keywords: Pulmonary exposure, Cardiac gene expression
2007-11-15 | GSE6541 | GEO
Project description:Relatively few studies have characterized differences in intra- and inter-neighborhood traffic-related air pollutant (TRAP) concentrations and distance-decay gradients in along an urban highway for the purposes of exposure assessment. The goal of this work was to determine the extent to which intra- and inter-neighborhood differences in TRAP concentrations can be explained by traffic and meteorology in three pairs of neighborhoods along Interstate 93 (I-93) in the metropolitan Boston area (USA). We measured distance-decay gradients of seven TRAPs (PNC, pPAH, NO, NOX, BC, CO, PM2.5) in near-highway (<400 m) and background areas (>1 km) in Somerville, Dorchester/South Boston, Chinatown and Malden to determine whether (1) spatial patterns in concentrations and inter-pollutant correlations differ between neighborhoods, and (2) variation within and between neighborhoods can be explained by traffic and meteorology. The neighborhoods ranged in area from 0.5 to 2.3 km2. Mobile monitoring was performed over the course of one year in each pair of neighborhoods (one pair of neighborhoods per year in three successive years; 35-47 days of monitoring in each neighborhood). Pollutant levels generally increased with highway proximity, consistent with I-93 being a major source of TRAP; however, the slope and extent of the distance-decay gradients varied by neighborhood as well as by pollutant, season and time of day. Correlations among pollutants differed between neighborhoods (e.g., ? = 0.35-0.80 between PNC and NOX and ? = 0.11-0.60 between PNC and BC) and were generally lower in Dorchester/South Boston than in the other neighborhoods. We found that the generalizability of near-road gradients and near-highway/urban background contrasts was limited for near-highway neighborhoods in a metropolitan area with substantial local street traffic. Our findings illustrate the importance of measuring gradients of multiple pollutants under different ambient conditions in individual near-highway neighborhoods for health studies involving inter-neighborhood comparisons.
| S-EPMC4212216 | biostudies-literature