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A framework for estimating the US mortality burden of fine particulate matter exposure attributable to indoor and outdoor microenvironments.

ABSTRACT: Exposure to fine particulate matter (PM_2.5) is associated with increased mortality. Although epidemiology studies typically use outdoor PM_2.5 concentrations as surrogates for exposure, the majority of PM_2.5 exposure in the US occurs in microenvironments other than outdoors. We develop a framework for estimating the total US mortality burden attributable to exposure to PM_2.5 of both indoor and outdoor origin in the primary non-smoking microenvironments in which people spend most of their time. The framework utilizes an exposure-response function combined with adjusted mortality effect estimates that account for underlying exposures to PM_2.5 of outdoor origin that likely occurred in the original epidemiology populations from which effect estimates are derived. We demonstrate the framework using several different scenarios to estimate the potential magnitude and bounds of the US mortality burden attributable to total PM_2.5 exposure across all non-smoking environments under a variety of assumptions. Our best estimates of the US mortality burden associated with total PM_2.5 exposure in the year 2012 range from ~230,000 to ~300,000 deaths. Indoor exposure to PM_2.5 of outdoor origin is typically the largest total exposure, accounting for ~40-60% of total mortality, followed by residential exposure to indoor PM_2.5 sources, which also drives the majority of variability in each scenario.

SUBMITTER: Azimi P

PROVIDER: S-EPMC7039807 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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A framework for estimating the US mortality burden of fine particulate matter exposure attributable to indoor and outdoor microenvironments.

Azimi Parham P Stephens Brent B

Journal of exposure science & environmental epidemiology 20181205 2

Exposure to fine particulate matter (PM2.5) is associated with increased mortality. Although epidemiology studies typically use outdoor PM2.5 concentrations as surrogates for exposure, the majority of PM2.5 exposure in the US occurs in microenvironments other than outdoors. We develop a framework for estimating the total US mortality burden attributable to exposure to PM2.5 of both indoor and outdoor origin in the primary non-smoking microenvironments ...[more]

PMID: 30518794

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Project description:ObjectiveAmbient fine particulate matter (PM2.5) pollution is currently a major public health concern in Chinese urban areas. However, PM2.5 exposure primarily occurs indoors. Given such, we conducted this study to characterize the indoor-outdoor relationship of PM2.5 mass concentrations for urban residences in Beijing.MethodsIn this study, 24-h real-time indoor and ambient PM2.5 mass concentrations were concurrently collected for 41 urban residences in the non-heating season. The diurnal variation of pollutant concentrations was characterized. Pearson correlation analysis was used to examine the correlation between indoor and ambient PM2.5 mass concentrations. Regression analysis with ordinary least square was employed to characterize the influences of a variety of factors on PM2.5 mass concentration.ResultsHourly ambient PM2.5 mass concentrations were 3-280 ?g/m3 with a median of 58 ?g/m3, and hourly indoor counterpart were 4-193 ?g/m3 with a median of 34 ?g/m3. The median indoor/ambient ratio of PM2.5 mass concentration was 0.62. The diurnal variation of residential indoor and ambient PM2.5 mass concentrations tracked with each other well. Strong correlation was found between indoor and ambient PM2.5 mass concentrations on the community basis (coefficients: r ? 0.90, p < 0.0001), and the ambient data explained ? 84% variance of the indoor data. Regression analysis suggested that the variables, such as traffic conditions, indoor smoking activities, indoor cleaning activities, indoor plants and number of occupants, had significant influences on the indoor PM2.5 mass concentrations.ConclusionsPM2.5 of ambient origin made dominant contribution to residential indoor PM2.5 exposure in the non-heating season under the high ambient fine particle pollution condition. Nonetheless, the large inter-residence variability of infiltration factor of ambient PM2.5 raised the concern of exposure misclassification when using ambient PM2.5 mass concentrations as exposure surrogates. PM2.5 of indoor origin still had minor influence on indoor PM2.5 mass concentrations, particularly at 11:00-13:00 and 22:00-0:00. The predictive models suggested that particles from traffic emission, secondary aerosols, particles from indoor smoking, resuspended particles due to indoor cleaning and particles related to indoor plants contributed to indoor PM2.5 mass concentrations in this study. Real-time ventilation measurements and improvement of questionnaire design to involve more variables subject to built environment were recommended to enhance the performance of the predictive models.

Project description:ObjectiveTo quantitate the 2016 global and national burden of chronic kidney disease (CKD) attributable to ambient fine particulate matter air pollution ≤ 2.5 μm in aerodynamic diameter (PM2.5).DesignWe used the Global Burden of Disease (GBD) study data and methodologies to estimate the 2016 burden of CKD attributable to PM2.5 in 194 countries and territories. Population-weighted PM2.5 levels and incident rates of CKD for each country were curated from the GBD study publicly available data sources.SettingGBD global and national data on PM2.5 and CKD.Participants194 countries and territories.Main outcome measuresWe estimated the attributable burden of disease (ABD), years living with disability (YLD), years of life lost (YLL) and disability-adjusted life-years (DALYs).ResultsThe 2016 global burden of incident CKD attributable to PM2.5 was 6 950 514 (95% uncertainty interval: 5 061 533-8 914 745). Global YLD, YLL and DALYs of CKD attributable to PM2.5 were 2 849 311 (1 875 219-3 983 941), 8 587 735 (6 355 784-10 772 239) and 11 445 397 (8 380 246-14 554 091), respectively. Age-standardised ABD, YLL, YLD and DALY rates varied substantially among geographies. Populations in Mesoamerica, Northern Africa, several countries in the Eastern Mediterranean region, Afghanistan, Pakistan, India and several countries in Southeast Asia were among those with highest age-standardised DALY rates. For example, age-standardised DALYs per 100 000 were 543.35 (391.16-707.96) in El Salvador, 455.29 (332.51-577.97) in Mexico, 408.41 (283.82-551.84) in Guatemala, 238.25 (173.90-303.98) in India and 178.26 (125.31-238.47) in Sri Lanka, compared with 5.52 (0.82-11.48) in Sweden, 6.46 (0.00-14.49) in Australia and 12.13 (4.95-21.82) in Canada. Frontier analyses showed that Mesoamerican countries had significantly higher CKD DALY rates relative to other countries with comparable sociodemographic development.ConclusionsOur results demonstrate that the global toll of CKD attributable to ambient air pollution is significant and identify several endemic geographies where air pollution may be a significant driver of CKD burden. Air pollution may need to be considered in the discussion of the global epidemiology of CKD.

Project description:Concurrent indoor and outdoor measurements of fine particulate matter (PM2.5) were conducted at three retirement homes in the Los Angeles Basin during two separate phases (cold and warm) between 2005 and 2006. Indoor-to-outdoor relationships of PM2.5 chemical constituents were determined and sources of indoor and outdoor PM2.5 were evaluated using a molecular marker-based chemical mass balance (MM-CMB) model. Indoor levels of elemental carbon (EC) along with metals and trace elements were found to be significantly affected by outdoor sources. EC, in particular, displayed very high indoor-to-outdoor (I/O) mass ratios accompanied by strong I/O correlations, illustrating the significant impact of outdoor sources on indoor levels of EC. Similarly, indoor levels of polycyclic aromatic hydrocarbons (PAHs), hopanes, and steranes were strongly correlated with their outdoor components and displayed I/O ratios close to unity. On the other hand, concentrations of n-alkanes and organic acids inside the retirement communities were dominated by indoor sources (e.g. food cooking and consumer products), as indicated by their I/O ratios, which exceeded unity. Source apportionment results revealed that vehicular emissions were the major contributor to both indoor and outdoor PM2.5, accounting for 39 and 46% of total mass, respectively. Moreover, the contribution of vehicular sources to indoor levels was generally comparable to its corresponding outdoor estimate. Other water-insoluble organic matter (other WIOM), which accounts for emissions from uncharacterized primary biogenic sources, displayed a wider range of contributions, varying from 2 to 73% of PM2.5, across all sites and phases of the study. Lastly, higher indoor than outdoor contribution of other water-soluble organic matter (other WSOM) was evident at some of the sites, suggesting the production of secondary aerosols as well as direct emissions from primary sources (including cleaning or other consumer products) at the indoor environments.

Project description:ImportanceOutdoor particulate matter 2.5 μm or less in diameter (PM2.5) is a ubiquitous environmental neurotoxicant that may affect the developing brain. Little is known about associations between PM2.5 and white matter connectivity.ObjectivesTo assess associations between annual residential PM2.5 exposure and white matter microstructure health in a US sample of children 9 to 10 years of age and to examine whether associations are specific to certain white matter pathways or vary across neuroimaging diffusion markers reflective of intracellular and extracellular microstructural processes.Design, setting, and participantsThis cross-sectional study, the Adolescent Brain and Cognitive Development (ABCD) Study, was composed of 21 study sites across the US and used baseline data collected from children 9 to 10 years of age from September 1, 2016, to October 15, 2018. Data analysis was performed from September 15, 2020, to June 30, 2021.ExposuresAnnual mean PM2.5 exposure estimated by ensemble-based models and assigned to the primary residential addresses at baseline.Main outcomes and measuresDiffusion-weighted imaging (DWI) and tractography were used to delineate white matter tracts. The biophysical modeling technique of restriction spectrum imaging (RSI) was implemented to examine total hindered diffusion and restricted isotropic and anisotropic intracellular diffusion in each tract. Hierarchical mixed-effects models with natural splines were used to analyze the associations between PM2.5 exposure and DWI.ResultsIn a study population of 7602 children (mean [SD] age, 119.1 [7.42] months; 3955 [52.0%] female; 160 [ 21.%] Asian, 1025 [13.5%] Black, 1616 [21.3%] Hispanic, 4025 [52.9%] White, and 774 [10.2%] other [identified by parents as American Indian/Native American or Alaska Native; Native Hawaiian, Guamanian, Samoan, other Pacific Islander; Asian Indian, Chinese, Filipino, Japanese, Korean, Vietnamese, or other Asian; or other race]), associations were seen between annual ambient PM2.5 and hemispheric differences in white matter microstructure. Hemisphere-stratified models revealed significant associations between PM2.5 exposure and restricted isotropic intracellular diffusion in the left cingulum, in the left superior longitudinal fasciculus, and bilaterally in the fornix and uncinate fasciculus. In tracts with strong positive associations, a PM2.5 increase from 8 to 12 μg/m3 was associated with increases of 2.16% (95% CI, 0.49%-3.84%) in the left cingulum, 1.95% (95% CI, 0.43%-3.47%) in the left uncinate, and 1.68% (95% CI, 0.01%-3.34%) in the right uncinate. Widespread negative associations were observed between PM2.5 and mean diffusivity.Conclusions and relevanceThe findings of this cross-sectional study suggest that annual mean PM2.5 exposure during childhood is associated with increased restricted isotropic diffusion and decreased mean diffusivity of specific white matter tracts, potentially reflecting differences in the composition of white matter microarchitecture.

Project description:This study aimed to investigate the short-term effect of exposure to indoor fine particulate matter (PM2.5) on atopic dermatitis (AD) symptoms in children. Sixty-four children (40 boys and 24 girls) with moderate-to-severe AD, aged under 18 years were enrolled in the study. They were followed up from February 2019 through November 2020. Exposure to indoor PM2.5 in each household of the enrolled children and their AD symptoms were measured daily. The generalized linear mixed model was utilized for statistical analysis. Subdivision analysis was performed by stratifying the patients by age, sex, season, severity, the presence of family allergic diseases, sensitization, and indoor environment conditions including temperature and relative humidity. A total of 9,321 person-days of AD symptom data were collected. The average PM2.5 concentration was 28.7 ± 24.3 µg/m3, with the highest value in winter (47.1 ± 29.6 µg/m3). The overall effect of PM2.5 on AD symptoms was not statistically significant. However, an increase of 10 µg/m3 in indoor PM2.5 concentration increased AD symptom scores by 16.5% (95% CI: 6.5, 27.5) in spring and12.6% (95% CI: 4.3, 21.5) in winter, 6.7% (95% CI: 2.3, 11.3) at indoor temperatures of <25.5 °C, and by 15.0% (95% CI: 3.5, 27.7) with no use of an air purifier. The harmful effect of PM2.5 in boys, in children aged ≥6 years, and in children with inhalant allergen sensitization was significant, showing an increase in AD symptoms of 4.9% (95% CI: 1.4, 8.6), 12.0% (95% CI: 5.3, 19.1), and 7.0% (95% CI: 1.9, 12.3) per 10 µg/m3 of PM2.5, respectively. Furthermore, children with inhalant allergen sensitization plus severe symptoms (SCORing Atopic Dermatitis, SCORAD ≥ 30.7, median value) showed more harmful effects from exposure to PM2.5 (15.7% (95% CI: 4.5, 28.1) increase in AD symptom scores per 10 µg/m3 of PM2.5 increase). Indoor exposure to PM2.5 exacerbated AD symptoms in children in spring, winter, and at indoor temperatures of < 25.5 °C. In particular, this harmful effect was prominent in children with inhalant allergen sensitization and severe symptoms. Minimizing exposure to indoor PM2.5 is needed for the proper management of AD.

Dataset Information

A framework for estimating the US mortality burden of fine particulate matter exposure attributable to indoor and outdoor microenvironments.

Publications

A framework for estimating the US mortality burden of fine particulate matter exposure attributable to indoor and outdoor microenvironments.

Similar Datasets

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