Independent and Joint Contributions of Fine Particulate Matter Exposure and Population Vulnerability to Mortality in the Detroit Metropolitan Area.
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ABSTRACT:
SUBMITTER: Schulz AJ
PROVIDER: S-EPMC6024972 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundGiven that fine particulate matter (≤ 2.5 μm; PM2.5) is a mixture of multiple components, it has been of high interest to identify its specific health-relevant physical and/or chemical features.ObjectivesWe conducted a time-series study of PM2.5 and cardiorespiratory emergency department (ED) visits in the St. Louis, Missouri-Illinois metropolitan area, using 2 years of daily PM2.5 and PM2.5 component measurements (including ions, carbon, particle-phase organic compounds, and elements) made at the St. Louis-Midwest Supersite, a monitoring site of the U.S. Environmental Protection Agency Supersites ambient air monitoring research program.MethodsUsing Poisson generalized linear models, we assessed short-term associations between daily cardiorespiratory ED visit counts and daily levels of 24 selected pollutants. Associations were estimated for interquartile range changes in each pollutant. To allow comparison of relationships among multiple pollutants and outcomes with potentially different lag structures, we used 3-day unconstrained distributed lag models controlling for time trends and meteorology.ResultsConsidering results of our primary models, as well as sensitivity analyses and models assessing co-pollutant confounding, we observed robust associations of cardiovascular disease visits with 17α(H),21β(H)-hopane and congestive heart failure visits with elemental carbon. We also observed a robust association of respiratory disease visits with ozone. For asthma/wheeze, associations were strongest with ozone and nitrogen dioxide; observed associations of asthma/wheeze with PM2.5 and its components were attenuated in two-pollutant models with these gases. Differential measurement error due to differential patterns of spatiotemporal variability may have influenced patterns of observed associations across pollutants.ConclusionsOur findings add to the growing field examining the health effects of PM2.5 components. Combustion-related components of the pollutant mix showed particularly strong associations with cardiorespiratory ED visit outcomes.
| S-EPMC4421761 | biostudies-literature
Project description:Recent changes of surface particulate matter (PM) concentration in the Seoul Metropolitan Area (SMA), South Korea, are puzzling. The long-term trend of surface PM concentration in the SMA declined in the 2000s, but since 2012 its concentrations have tended to incline, which is coincident with frequent severe hazes in South Korea. This increase puts the Korean government's emission reduction efforts in jeopardy. This study reports that interannual variation of surface PM concentration in South Korea is closely linked with the interannual variations of wind speed. A 12-year (2004-2015) regional air quality simulation was conducted over East Asia (27-km) and over South Korea (9-km) to assess the impact of meteorology under constant anthropogenic emissions. Simulated PM concentrations show a strong negative correlation (i.e. R?=?-0.86) with regional wind speed, implying that reduced regional ventilation is likely associated with more stagnant conditions that cause severe pollutant episodes in South Korea. We conclude that the current PM concentration trend in South Korea is a combination of long-term decline by emission control efforts and short-term fluctuation of regional wind speed interannual variability. When the meteorology-driven variations are removed, PM concentrations in South Korea have declined continuously even after 2012.
| S-EPMC5498658 | biostudies-literature
Project description:BackgroundEpidemiological studies report fairly consistent associations between various air pollution metrics and autism spectrum disorder (ASD), with some elevated risks reported for different prenatal and postnatal periods.ObjectivesTo examine associations between ASD and ambient fine particulate matter (PM2.5) and ozone concentrations during the prenatal period through the second year of life in a case-control study.MethodsASD cases (n = 428) diagnosed at Cincinnati Children's Hospital Medical Center were frequency matched (15:1) to 6420 controls from Ohio birth records. We assigned daily PM2.5 and ozone estimates for 2005-2012 from US EPA's Fused Air Quality Surface Using Downscaling model to each participant for each day based on the mother's census tract of residence at birth. We calculated adjusted odds ratios (aORs) using logistic regression across continuous and categorical exposure window averages (trimesters, first and second postnatal years, and cumulative measure), adjusting for maternal- and birth-related confounders, both air pollutants, and multiple temporal exposure windows.ResultsWe detected elevated aORs for PM2.5 during the 2nd trimester, 1st year of life, and a cumulative period from pregnancy through the 2nd year (aOR ranges across categories: 1.41-1.44, 1.54-1.84, and 1.41-1.52 respectively), and for ozone in the 2nd year of life (aOR range across categories: 1.29-1.42). Per each change in IQR, we observed elevated aORs for ozone in the 3rd trimester, 1st and 2nd years of life, and the cumulative period (aOR range: 1.19-1.27) and for PM2.5 in the 2nd trimester, 1st year of life, and the cumulative period (aOR range: 1.11-1.17).DiscussionWe saw limited evidence of linear exposure-response relationships for ASD with increasing air pollution, but the elevated aORs detected for PM2.5 in upper exposure categories and per IQR unit increases were similar in magnitude to those reported in previous studies, especially for postnatal exposures.
| S-EPMC7232936 | biostudies-literature
Project description:Recently, the population of Seoul has been affected by particulate matter in the atmosphere. This problem can be addressed by developing an elaborate forecasting model to estimate the concentration of fine dust in the metropolitan area. We present a forecasting model of the fine dust concentration with an extended range of input variables, compared to existing models. The model takes inputs from holistic perspectives such as topographical features on the surface, chemical sources of the fine dusts, traffic and the human activities in sub-areas, and meteorological data such as wind, temperature, and humidity, of fine dust. Our model was evaluated by the index-of-agreement (IOA) and the root mean-squared error (RMSE) in predicting PM2.5 and PM10 over three subsequent days. Our model variations consist of linear regressions, ARIMA, and Gaussian process regressions (GPR). The GPR showed the best performance in terms of IOA that is over 0.6 in the three-day predictions.
| S-EPMC7412375 | biostudies-literature
Project description:Objectives: The primary purpose of this study is to analyze the relationship between the first occurrence of hospitalization for cardiovascular disease (CVD) and particulate matter less than 2.5 μm in diameter (PM2.5) exposure, considering average PM2.5 concentration and the frequency of high PM2.5 concentration simultaneously. Methods: We used large-scale cohort data from seven metropolitan cities in South Korea. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) using the Cox proportional-hazards model, including annual average PM2.5 and annual hours of PM2.5 concentration exceeding 55.5 μg/m3 (FH55). Results: We found that the risk was elevated by 11.6% (95% CI, 9.7-13.6) for all CVD per 2.9 μg/m3 increase of average PM2.5. In addition, a 94-h increase in FH55 increased the risk of all CVD by 3.8% (95% CI, 2.8-4.7). Regarding stroke, we found that people who were older and had a history of hypertension were more vulnerable to PM2.5 exposure. Conclusion: Based on the findings, we conclude that accurate forecasting, information dissemination, and timely warning of high concentrations of PM2.5 at the national level may reduce the risk of CVD occurrence.
| S-EPMC9149776 | biostudies-literature
Project description:BackgroundPolycystic ovary morphology (PCOM) is an ultrasonographic finding that can be present in women with ovulatory disorder and oligomenorrhea due to hypothalamic, pituitary, and ovarian dysfunction. While air pollution has emerged as a possible disrupter of hormone homeostasis, limited research has been conducted on the association between air pollution and PCOM.MethodsWe conducted a longitudinal cohort study using electronic medical records data of 5,492 women with normal ovaries at the first ultrasound that underwent a repeated pelvic ultrasound examination during the study period (2004-2016) at Boston Medical Center. Machine learning text algorithms classified PCOM by ultrasound. We used geocoded home address to determine the ambient annual average PM2.5 exposures and categorized into tertiles of exposure. We used Cox Proportional Hazards models on complete data (n = 3,994), adjusting for covariates, and additionally stratified by race/ethnicity and body mass index (BMI).ResultsCumulative exposure to PM2.5 during the study ranged from 4.9 to 17.5 µg/m3 (mean = 10.0 μg/m3). On average, women were 31 years old and 58% were Black/African American. Hazard ratios and 95% confidence intervals (CI) comparing the second and third PM2.5 exposure tertile vs. the reference tertile were 1.12 (0.88, 1.43) and 0.89 (0.62, 1.28), respectively. No appreciable differences were observed across race/ethnicity. Among women with BMI ≥ 30 kg/m2, we observed weak inverse associations with PCOM for the second (HR: 0.93, 95% CI: 0.66, 1.33) and third tertiles (HR: 0.89, 95% CI: 0.50, 1.57).ConclusionsIn this study of reproductive-aged women, we observed little association between PM2.5 concentrations and PCOM incidence. No dose response relationships were observed nor were estimates appreciably different across race/ethnicity within this clinically sourced cohort.
| S-EPMC8855564 | biostudies-literature
Project description:Toxicological evidence has shown that fine particulate matter (PM2.5) may affect distant organs, including kidneys, over the short term. However, epidemiological evidence is limited.ObjectivesWe investigated associations between short-term exposure to PM2.5, major PM2.5 components [elemental carbon (EC), organic carbon (OC), sulfate, and nitrate], and gaseous co-pollutants (O3, CO, SO2, NO2, and NOx) and emergency department (ED) visits for kidney diseases during 2002-2008 in Atlanta, Georgia.MethodsLog-linear time-series models were fitted to estimate the acute effects of air pollution, with single-day and unconstrained distributed lags, on rates of ED visits for kidney diseases [all renal diseases and acute renal failure (ARF)], controlling for meteorology (maximum air and dew-point temperatures) and time (season, day of week, holidays, and long-term time trend).ResultsFor all renal diseases, we observed positive associations for most air pollutants, particularly 8-day cumulative exposure to OC [rate ratio (RR) = 1.018, (95% confidence interval [CI]: 1.003, 1.034)] and EC [1.016 (1.000, 1.031)] per interquartile range increase exposure. For ARF, we observed positive associations particularly for 8-day exposure to OC [1.034 (1.005, 1.064)], EC [1.032 (1.002, 1.063)], nitrate [1.032 (0.996, 1.069)], and PM2.5 [1.026 (0.997, 1.057)] per interquartile range increase exposure. We also observed positive associations for most criteria gases. The RR estimates were generally higher for ARF than all renal diseases.ConclusionsWe observed positive associations between short-term exposure to fine particulate air pollution and kidney disease outcomes. This study adds to the growing epidemiological evidence that fine particles may impact distant organs (e.g., kidneys) over the short term.
| S-EPMC8367053 | biostudies-literature
Project description:Several studies have pointed to fine particulate matter (PM2.5) as the main responsible for air pollution toxic effects. Indeed, PM2.5 may not only cause respiratory and cardiovascular abnormalities but it may also affect other organs such as the liver. Be that as it may, only a few studies have evaluated the PM2.5 effects on hepatic tissue. Moreover, most of them have not analyzed the relationship between particles composition and toxicological effects. In this study, healthy rats were subjected to urban levels of PM2.5 particles in order to assess their structural and functional effects on the liver. During the exposure periods, mean PM2.5 concentrations were slightly higher than the value suggested by the daily guideline of the World Health Organization. The exposed rats showed a hepatic increase of Cr, Zn, Fe, Ba, Tl and Pb levels. This group also showed leukocyte infiltration, sinusoidal dilation, hydropic inclusions and alterations in carbohydrates distribution. These histologic lesions were accompanied by serological changes, such as increase of total cholesterol and triglycerides, as well as genotoxic damage in their nuclei. We also observed significant associations between several biomarkers and PM2.5 composition. Our results show that exposure to low levels of PM2.5 might cause histologic and serological changes in liver tissue, suggesting that PM2.5 toxicity is influenced not only by their concentration but also by their composition and the exposure frequency.
| S-EPMC7099102 | biostudies-literature
Project description:We evaluate fine particulate matter (PM2.5) exposure-response models to propose a consistent set of global effect factors for product and policy assessments across spatial scales and across urban and rural environments. Relationships among exposure concentrations and PM2.5-attributable health effects largely depend on location, population density, and mortality rates. Existing effect factors build mostly on an essentially linear exposure-response function with coefficients from the American Cancer Society study. In contrast, the Global Burden of Disease analysis offers a nonlinear integrated exposure-response (IER) model with coefficients derived from numerous epidemiological studies covering a wide range of exposure concentrations. We explore the IER, additionally provide a simplified regression as a function of PM2.5 level, mortality rates, and severity, and compare results with effect factors derived from the recently published global exposure mortality model (GEMM). Uncertainty in effect factors is dominated by the exposure-response shape, background mortality, and geographic variability. Our central IER-based effect factor estimates for different regions do not differ substantially from previous estimates. However, IER estimates exhibit significant variability between locations as well as between urban and rural environments, driven primarily by variability in PM2.5 concentrations and mortality rates. Using the IER as the basis for effect factors presents a consistent picture of global PM2.5-related effects for use in product and policy assessment frameworks.
| S-EPMC6613786 | biostudies-literature
Project description:Fine particulate matter (PM2.5) is a complex mixture of components with diverse chemical and physical characteristics associated with increased respiratory and cardiovascular diseases mortality. Our study aimed to investigate the effects of exposure to concentrated PM2.5 on LPS-induced lung injury onset. BALB/c male mice were exposed to either filtered air or ambient fine PM2.5 in an ambient particle concentrator for 5 weeks. Then, an acute lung injury was induced with nebulized LPS. The animals were euthanized 24 h after the nebulization to either LPS or saline. Inflammatory cells and cytokines (IL-1β, IL-4, IL-5, IL-6, IL-10, IL-17, TNF) were assessed in the blood, bronchoalveolar lavage fluid (BALF), and lung tissue. In addition, lung morphology was assessed by stereological methods. Our results showed that the PM+LPS group showed histological evidence of injury, leukocytosis with increased neutrophils and macrophages, and a mixed inflammatory response profile, with increased KC, IL-6, IL-1β, IL-4, and IL-17. Our analysis shows that there is an interaction between the LPS nebulization and PM2.5 exposure, differently modulating the inflammatory response, with a distinct response pattern as compared to LPS or PM2.5 exposure alone. Further studies are required to explain the mechanism of immune modulation caused by PM2.5 exposure.
| S-EPMC8998903 | biostudies-literature