Causal Effects of Air Pollution on Mortality Rate in Massachusetts.
Ontology highlight
ABSTRACT:
SUBMITTER: Wei Y
PROVIDER: S-EPMC7604530 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:BackgroundWe previously found additive effects of long- and short-term exposures to fine particulate matter (PM2.5), ozone (O3), and nitrogen dioxide (NO2) on all-cause mortality rate using a generalized propensity score (GPS) adjustment approach. The study addressed an important question of how many early deaths were caused by each exposure. However, the study was computationally expensive, did not capture possible interactions and high-order nonlinearities, and omitted potential confounders.MethodsWe proposed two new methods and reconducted the analysis using the same cohort of Medicare beneficiaries in Massachusetts during 2000-2012, which consisted of 1.5 million individuals with 3.8 billion person-days of follow-up. The first method, weighted least squares (WLS), leveraged large volume of data by aggregating person-days, which gave equivalent results to the linear probability model (LPM) method in the previous analysis but significantly reduced computational burden. The second method, m-out-of-n random forests (moonRF), implemented scaling random forests that captured all possible interactions and nonlinearities in the GPS model. To minimize confounding bias, we additionally controlled relative humidity and health care utilizations that were not included previously. Further, we performed low-level analysis by restricting to person-days with exposure levels below increasingly stringent thresholds.ResultsWe found consistent results between LPM/WLS and moonRF: all exposures were positively associated with mortality rate, even at low levels. For long-term PM2.5 and O3, the effect estimates became larger at lower levels. Long-term exposure to PM2.5 posed the highest risk: 1 μg/m3 increase in long-term PM2.5 was associated with 1053 (95% confidence interval [CI]: 984, 1122; based on LPM/WLS methods) or 1058 (95% CI: 988, 1127; based on moonRF method) early deaths each year among the Medicare population in Massachusetts.ConclusionsThis study provides more rigorous causal evidence between PM2.5, O3, and NO2 exposures and mortality, even at low levels. The largest effect estimate for long-term PM2.5 suggests that reducing PM2.5 could gain the most substantial benefits. The consistency between LPM/WLS and moonRF suggests that there were not many interactions and high-order nonlinearities. In the big data context, the proposed methods will be useful for future scientific work in estimating causality on an additive scale.
| S-EPMC7903765 | biostudies-literature
Project description:Individual housing characteristics can modify outdoor ambient air pollution infiltration through air exchange rate (AER). Time and labor-intensive methods needed to measure AER has hindered characterization of AER distributions across large geographic areas. Using publicly-available data and regression models associating AER with housing characteristics, we estimated AER for all Massachusetts residential parcels. We conducted an exposure disparities analysis, considering ambient PM2.5 concentrations and residential AERs. Median AERs (h-1) with closed windows for winter and summer were 0.74 (IQR: 0.47-1.09) and 0.36 (IQR: 0.23-0.57), respectively, with lower AERs for single family homes. Across residential parcels, variability of indoor PM2.5 concentrations of ambient origin was twice that of ambient PM2.5 concentrations. Housing parcels above the 90th percentile of both AER and ambient PM2.5 (i.e., the leakiest homes in areas of highest ambient PM2.5)-vs. below the 10 percentile-were located in neighborhoods with higher proportions of Hispanics (20.0% vs. 2.0%), households with an annual income of less than $20,000 (26.0% vs. 7.5%), and individuals with less than a high school degree (23.2% vs. 5.8%). Our approach can be applied in epidemiological studies to estimate exposure modifiers or to characterize exposure disparities that are not solely based on ambient concentrations.
| S-EPMC6428635 | biostudies-literature
Project description:Mounting evidence over the past several decades has demonstrated inequitable distribution of pollutants of ambient origin between sociodemographic groups in the United States. Most environmental inequality studies to date are cross-sectional and used proximity-based methods rather than modeled air pollution concentrations, limiting the ability to examine trends over time or the factors that drive exposure inequalities. In this paper, we use 1km2 modeled PM2.5 and NO2 concentrations in Massachusetts over an 8-year period and Census demographic data to quantify inequality between sociodemographic groups and to develop a more nuanced understanding of the drivers and trends in longitudinal air pollution inequality. Annual-average population-weighted PM2.5 and NO2 concentrations were highest for urban non-Hispanic black populations (11.8µg/m3 in 2003 and 8.4µg/m3 in 2010, vs. 11.3µg/m3 and 8.1µg/m3 for urban non-Hispanic whites) and urban Hispanic populations (15.9 ppb in 2005 and 13.0 ppb in 2010, vs. 13.0 ppb and 10.2 ppb for urban non-Hispanic whites), respectively. While population groups experienced similar absolute decreases in exposure over time, disparities in population-weighted concentrations increased over time when quantified by the Atkinson Index, a relative inequality measure. Exposure inequalities were approximately one order of magnitude greater for NO2 compared to PM2.5, were more pronounced in urban compared to rural geographies, and between racial/ethnic groups compared to income and educational attainment groups. Our results also revealed similar longitudinal PM2.5 and NO2 inequality trends using Census 2000 and Census 2010 data, indicating that spatio-temporal shifts in air pollution may best explain observed trends in inequality. These findings enhance our understanding of factors that contribute to persistent inequalities and underscore the importance of targeted exposure reduction strategies aimed at vulnerable populations and neighborhoods.
| S-EPMC5761067 | 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:Exposures to particulate matter with diameter of 2.5µm or less (PM2.5) may influence risk of birth defects. We estimated associations between maternal exposure to prenatal traffic-related air pollution and risk of cardiac, orofacial, and neural tube defects among Massachusetts births conceived 2001 through 2008. Our analyses included 2729 cardiac, 255 neural tube, and 729 orofacial defects. We used satellite remote sensing, meteorological and land use data to assess PM2.5 and traffic-related exposures (distance to roads and traffic density) at geocoded birth addresses. We calculated adjusted odds ratios (OR) and confidence intervals (CI) using logistic regression models. Generalized additive models were used to assess spatial patterns of birth defect risk. There were positive but non-significant associations for a 10µg/m(3) increase in PM2.5 and perimembranous ventricular septal defects (OR=1.34, 95% CI: 0.98, 1.83), patent foramen ovale (OR=1.19, 95% CI: 0.92, 1.54) and patent ductus arteriosus (OR=1.20, 95% CI: 0.95, 1.62). There was a non-significant inverse association between PM2.5 and cleft lip with or without palate (OR=0.76, 95% CI: 0.50, 1.10), cleft palate only (OR=0.89, 95% CI: 0.54, 1.46) and neural tube defects (OR=0.77, 95% CI: 0.46, 1.05). Results for traffic related exposure were similar. Only ostium secundum atrial septal defects displayed significant spatial variation after accounting for known risk factors.
| S-EPMC4761511 | biostudies-literature
Project description:In this study, we modeled early life air pollution exposure using C57BL/6J male mice on a controlled chow diet, exposed to real-world inhaled concentrated PM2.5 (~10x ambient level/ ~60-120g/m3) or filtered air (FA) over 14 weeks. We investigated PM2.5 effects on phenotype, transcriptome and chromatin accessibility, compared the effects with a prototypical high-fat diet (HFD) stimulus, and examined the effects of cessation of exposure on reversibility of phenotype/genotype.
2020-11-05 | GSE145840 | GEO
Project description:Large national-level electronic health record (EHR) datasets offer new opportunities for disentangling the role of genes and environment through deep phenotype information and approximate pedigree structures. Here we use the approximate geographical locations of patients as a proxy for spatially correlated community-level environmental risk factors. We develop a spatial mixed linear effect (SMILE) model that incorporates both genetics and environmental contribution. We extract EHR and geographical locations from 257,620 nuclear families and compile 1083 disease outcome measurements from the MarketScan dataset. We augment the EHR with publicly available environmental data, including levels of particulate matter 2.5 (PM2.5), nitrogen dioxide (NO2), climate, and sociodemographic data. We refine the estimates of genetic heritability and quantify community-level environmental contributions. We also use wind speed and direction as instrumental variables to assess the causal effects of air pollution. In total, we find PM2.5 or NO2 have statistically significant causal effects on 135 diseases, including respiratory, musculoskeletal, digestive, metabolic, and sleep disorders, where PM2.5 and NO2 tend to affect biologically distinct disease categories. These analyses showcase several robust strategies for jointly modeling genetic and environmental effects on disease risk using large EHR datasets and will benefit upcoming biobank studies in the era of precision medicine.
| S-EPMC11199552 | 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:The health, economic, and social impact of COVID-19 has been significant across the world. Our objective was to evaluate the association between air pollution (through NO2 and PM2.5 levels) and COVID-19 mortality in Spanish provinces from February 3, 2020, to July 14, 2020, adjusting for climatic parameters. An observational and ecological study was conducted with information extracted from Datadista repository (Datadista, 2020). Air pollutants (NO2 and PM2.5 levels) were analyzed as potential determinants of COVID-19 mortality. Multilevel Poisson regression models were used to analyze the risk of mortality after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Models were adjusted by four climatic variables (hours of solar radiation, precipitation, daily temperature and wind speed) and population size. The mean levels of PM2.5 and NO2 across all provinces and time in Spain were 8.7 μg/m3 (SD 9.7) and 8.7 μg/m3 (SD 6.2), respectively. High levels of PM2.5 (IRR = 1.016, 95% CI: 1.007-1.026), NO2 (IRR = 1.066, 95% CI: 1.058-1.075) and precipitation (IRRNO2 = 0.989, 95% CI: 0.981-0.997) were positively associated with COVID-19 mortality, whereas temperature (IRRPM2.5 = 0.988, 95% CI: 0.976-1.000; and IRRNO2 = 0.771, 95% CI: 0.761-0.782, respectively) and wind speed (IRRNO2 = 1.095, 95% CI: 1.061-1.131) were negatively associated with COVID-19 mortality. Air pollution can be a key factor to understand the mortality rate for COVID-19 in Spain. Furthermore, climatic variables could be influencing COVID-19 progression. Thus, air pollution and climatology ought to be taken into consideration in order to control the pandemic.Supplementary informationThe online version contains supplementary material available at 10.1007/s11869-021-01062-2.
| S-EPMC8310774 | biostudies-literature
Project description:We examine the relationship between contemporaneous fine particulate matter exposure and COVID-19 morbidity and mortality using an instrumental variable approach. Harnessing daily changes in county-level wind direction, we show that arguably exogenous fluctuations in local air quality impact the incidence of confirmed COVID-19 cases and deaths. We find that a one μ g/m 3 increase in PM 2.5, or 15% of the average PM 2.5 concentration in a county, increases the number of same-day confirmed cases by 1.8% from the mean case incidence in a county. A one μ g/m 3 increase in PM 2.5 increases the same-day death rate by just over 4% from the mean. These effects tend to increase in magnitude over longer time horizons and are robust to a host of sensitivity tests. When analyzing potential mechanisms, we also demonstrate that an additional unit of PM 2.5 increases COVID-19-related hospitalizations by 0.8% and use of intensive care units by 0.5% on the same day. Using individual case records, we also show that higher PM 2.5 exposure at the time of case confirmation increases risk of later mechanical ventilation and mortality. These results suggest that air pollution plays an important role in mediating the severity of respiratory syndromes such as COVID-19.
| S-EPMC10073864 | biostudies-literature