Research report (Health Effects Institute)最新文献

{"title":"Social Susceptibility to Multiple Air Pollutants in Cardiovascular Disease.","authors":"J E Clougherty,&nbsp;J L Humphrey,&nbsp;E J Kinnee,&nbsp;L F Robinson,&nbsp;L A McClure,&nbsp;L D Kubzansky,&nbsp;C E Reid","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>Cardiovascular disease (CVD) is the leading cause of death in the United States, and substantial research has linked ambient air pollution to elevated rates of CVD etiology and events. Much of this research identified increased effects of air pollution in lower socioeconomic position (SEP) communities, where pollution exposures are also often higher. The complex spatial confounding between air pollution and SEP makes it very challenging, however, to disentangle the impacts of these very different exposure types and to accurately assess their interactions. The specific causal components (i.e., specific social stressors) underlying this SEP-related susceptibility remain unknown, because there are myriad pathways through which poverty and/or lower-SEP conditions may influence pollution susceptibility - including diet, smoking, coexposures in the home and occupational environments, health behaviors, and healthcare access. Growing evidence suggests that a substantial portion of SEP-related susceptibility may be due to chronic psychosocial stress - given the known wide-ranging impacts of chronic stress on immune, endocrine, and metabolic function - and to a higher prevalence of unpredictable chronic stressors in many lower-SEP communities, including violence, job insecurity, and housing instability. As such, elucidating susceptibility to pollution in the etiology of CVD, and in the risk of CVD events, has been identified as a research priority. This interplay among social and environmental conditions may be particularly relevant for CVD, because pollution and chronic stress both impact inflammation, metabolic function, oxidative stress, hypertension, atherosclerosis, and other processes relevant to CVD etiology. Because pollution exposures are often spatially patterned by SEP, disentangling their effects - and quantifying any interplay - is especially challenging. Doing so, however, would help to improve our ability to identify and characterize susceptible populations and to improve our understanding of how community stressors may alter responses to multiple air pollutants. More clearly characterizing susceptible populations will improve our ability to design and target interventions more effectively (and cost-effectively) and may reveal greater benefits of pollution reduction in susceptible communities, strengthening cost-benefit and accountability analyses, ultimately reducing the disproportionate burden of CVD and reducing health disparities.</p><p><strong>Methods: </strong>In the current study, we aimed to quantify combined effects of multiple pollutants and stressor exposures on CVD events, using a number of unique datasets we have compiled and verified, including the following. 1. Poverty metrics, violent crime rates, a composite socioeconomic deprivation index (SDI), an index of racial and economic segregation, noise disturbance metrics, and three composite spatial factors produced from a factor analysis of 27 c","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 206","pages":"1-71"},"PeriodicalIF":0.0,"publicationDate":"2021-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9403800/pdf/hei-2021-206.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9999831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improvements in Air Quality and Health Outcomes Among California Medicaid Enrollees Due to Goods Movement Actions.","authors":"Y-Y Meng,&nbsp;J G Su,&nbsp;X Chen,&nbsp;J Molitor,&nbsp;D Yue,&nbsp;M Jerrett","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>In 2006, the California Air Resources Board (CARB) and local air quality management districts implemented an Emission Reduction Plan for Ports and Goods Movement program (referred to hereinafter as GM policy actions) (CARB 2006). The GM policy actions comprise approximately 200 actions with an estimated investment value of $6 to $10 billion. These actions targeted the major sources and polluters related to goods movements, such as highways; ports and railyard trucks; ship fuel and shore power; cargo equipment; and locomotives. These actions aimed to reduce total statewide domestic GM emissions to 2001 levels or lower by the year 2010; to reduce the statewide diesel particulate matter (DPM) health risk from GM by 85% by the year 2020; and to reduce the nitrogen oxides (NO_x) emissions from international GM in the South Coast Air Basin by 30% from projected 2015 levels and 50% from projected 2020 levels. The years 2006 and 2007 marked an important milestone in starting to regulate GM polluters and adopting stricter standards for traffic-related air pollution.</p><p><p>This project aimed to examine the impact of the GM policy actions on reductions in ambient air pollution and subsequent improvements in health outcomes of Medi-Cal fee-for-service (FFS) beneficiaries with chronic conditions in 10 counties in California. Specifically, we examined whether the GM policy actions reduced air pollution near GMC corridors more than in control areas. We subsequently assessed whether there were greater decreases in emergency room (ER) visits and hospitalizations for enrollees with chronic conditions who lived in the GM corridors (GMCs) than for those who lived in other areas.</p><p><strong>Methods: </strong>The study used a quasi-experimental design. We defined areas within 500 m of truck-permitted freeways and ports as GMCs. We further defined non-goods movement corridors (NGMCs) as locations within 500 m of truck-prohibited freeways or 300 m of a connecting roadway, and areas out of GMCs and NGMCs as controls (CTRLs). We defined years 2004-2007 as the pre-policy period and years 2008-2010 as the post-policy period. We developed linear mixed-effects land use regression models and created annual air pollution surfaces for nitrogen dioxide (NO₂), fine particulate matter (PM_2.5), and ozone (O₃) across California for years 2004-2010 at a spatial resolution of 30 m, then assigned them to enrollees' home addresses.</p><p><p>We used a retrospective cohort of 23,000 California Medicaid (Medi-Cal) FFS adult beneficiaries living in 10 California counties with six years of data (September 1, 2004, to August 31, 2010). Cohort beneficiaries had at least one of four chronic conditions, including asthma, chronic obstructive pulmonary disease (COPD), diabetes, and heart disease.</p><p><p>We used a difference-in-differences (DiD) model to assess whether air pollutant concentration and health care uti","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 205","pages":"1-61"},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9314313/pdf/hei-2021-205.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10011323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel Mechanisms of Ozone-Induced Pulmonary Inflammation and Resolution, and the Potential Protective Role of Scavenger Receptor BI.","authors":"K M Gowdy,&nbsp;B Kilburg-Basnyat,&nbsp;M X Hodge,&nbsp;S W Reece,&nbsp;V Yermalitsk,&nbsp;S S Davies,&nbsp;J Manke,&nbsp;M L Armstrong,&nbsp;N Reisdorph,&nbsp;R M Tighe,&nbsp;S R Shaikh","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>Increases in ambient levels of ozone (O₃), a criteria air pollutant, have been associated with increased susceptibility and exacerbations of chronic pulmonary diseases through lung injury and inflammation. O₃ induces pulmonary inflammation, in part by generating damage-associated molecular patterns (DAMPs), which are recognized by pattern recognition receptors (PRRs), such as toll-like receptors (TLRs) and scavenger receptors (SRs). This inflammatory response is mediated in part by alveolar macrophages (AMs), which highly express PRRs, including scavenger receptor BI (SR-BI). Once pulmonary inflammation has been induced, an active process of resolution occurs in order to prevent secondary necrosis and to restore tissue homeostasis. The processes known to promote the resolution of inflammation include the clearance by macrophages of apoptotic cells, known as efferocytosis, and the production of specialized pro-resolving mediators (SPMs). Impaired efferocytosis and production of SPMs have been associated with the pathogenesis of chronic lung diseases; however, these impairments have yet to be linked with exposure to air pollutants.</p><p><strong>Specific aims: </strong>The primary goals of this study were: Aim 1 - to define the role of SR-BI in O₃-derived pulmonary inflammation and resolution of injury; and Aim 2 - to determine if O₃ exposure alters pulmonary production of SPMs and processes known to promote the resolution of pulmonary inflammation and injury.</p><p><strong>Methods: </strong>To address Aim 1, female wild-type (WT) and SR-BI-deficient, or knock-out (SR-BI KO), mice were exposed to either O₃ or filtered air. In one set of experiments mice were instilled with an oxidized phospholipid (oxPL). Bronchoalveolar lavage fluid (BALF) and lung tissue were collected for the analyses of inflammatory and injury markers and oxPL. To estimate efferocytosis, mice were administered apoptotic cells (derived from the Jurkat T cell line) after O₃ or filtered air exposure.</p><p><p>To address Aim 2, male WT mice were exposed to either O₃ or filtered air, and levels of SPMs were assessed in the lung, as well as markers of inflammation and injury in BALF. In some experiments SPMs were administered before exposure to O₃or filtered air, to determine whether SPMs could mitigate inflammatory or resolution responses. Efferocytosis was measured as in Aim 1.</p><p><strong>Results: </strong>For Aim 1, SR-BI protein levels increased in the lung tissue of mice exposed to O₃, compared with mice exposed to filtered air. Compared with WT controls, SR-BI KO mice had a significant increase in the number of neutrophils in their airspace 24 hours post O₃ exposure. The oxPL levels increased in the airspace of both WT and SR-BI KO mice after O₃ exposure, compared with filtered air controls. Four hours after instillation o","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 204","pages":"1-49"},"PeriodicalIF":0.0,"publicationDate":"2021-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8126671/pdf/hei-2021-204.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9999272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding the Functional Impact of VOC-Ozone Mixtures on the Chemistry of RNA in Epithelial Lung Cells.","authors":"L M Contreras,&nbsp;J C Gonzalez-Rivera,&nbsp;K C Baldridge,&nbsp;D S Wang,&nbsp;Jcl Chuvalo-Abraham,&nbsp;L H Ruiz","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>Ambient air pollution is associated with premature death caused by heart disease, stroke, chronic obstructive pulmonary disease (COPD), and lung cancer. Recent studies have suggested that ribonucleic acid (RNA) oxidation is a sensitive environment-related biomarker that is implicated in pathogenesis.</p><p><strong>Aims and methods: </strong>We used a novel approach that integrated RNA-Seq analysis with detection by immunoprecipitation techniques of the prominent RNA oxidative modification 8-oxo-7,8-dihydroguanine (8-oxoG). Our goal was to uncover specific messenger RNA (mRNA) oxidation induced by mixtures of volatile organic compounds (VOCs) and ozone in healthy human epithelial lung cells. To this end, we exposed the BEAS-2B human epithelial lung cell line to the gas- and particle-phase products formed from reactions of 790 ppb acrolein (ACR) and 670 ppb methacrolein (MACR) with 4 ppm ozone.</p><p><strong>Results: </strong>Using this approach, we identified 222 potential direct targets of oxidation belonging to previously described pathways, as well as uncharacterized pathways, after air pollution exposures. We demonstrated the effect of our VOC-ozone mixtures on the morphology and actin cytoskeleton of lung cells, suggesting the influence of selective mRNA oxidation in members of pathways regulating physical components of the cells. In addition, we observed the influence of the VOC-ozone mixtures on metabolic cholesterol synthesis, likely implicated as a result of the incidence of mRNA oxidation and the deregulation of protein levels of squalene synthase (farnesyl-diphosphate farnesyltransferase 1 [FDFT1]), a key enzyme in endogenous cholesterol biosynthesis.</p><p><strong>Conclusions: </strong>Overall, our findings indicate that air pollution influences the accumulation of 8-oxoG in transcripts of epithelial lung cells that largely belong to stress-induced signaling and metabolic and structural pathways. A strength of the study was that it combined traditional transcriptome analysis with transcriptome-wide 8-oxoG mapping to facilitate the discovery of underlying processes not characterized by earlier approaches. Investigation of the processes mediated by air pollution oxidation of RNA molecules in primary cells and animal models needs to be explored in future studies. Our research has thus opened new avenues to further inform the relationship between atmospheric agents on the one hand and cellular responses on the other that are implicated in diseases.</p>","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 201","pages":""},"PeriodicalIF":0.0,"publicationDate":"2020-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7448316/pdf/hei-2020-201.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9998791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multicenter Ozone Study in oldEr Subjects (MOSES): Part 2. Effects of Personal and Ambient Concentrations of Ozone and Other Pollutants on Cardiovascular and Pulmonary Function.","authors":"D Q Rich,&nbsp;M W Frampton,&nbsp;J R Balmes,&nbsp;P A Bromberg,&nbsp;M Arjomandi,&nbsp;M J Hazucha,&nbsp;S W Thurston,&nbsp;N E Alexis,&nbsp;P Ganz,&nbsp;W Zareba,&nbsp;P Koutrakis,&nbsp;K Thevenet-Morrison","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>The Multicenter Ozone Study of oldEr Subjects (MOSES) was a multi-center study evaluating whether short-term controlled exposure of older, healthy individuals to low levels of ozone (O₃) induced acute changes in cardiovascular biomarkers. In MOSES Part 1 (MOSES 1), controlled O₃ exposure caused concentration-related reductions in lung function with evidence of airway inflammation and injury, but without convincing evidence of effects on cardiovascular function. However, subjects' prior exposures to indoor and outdoor air pollution in the few hours and days before each MOSES controlled O₃ exposure may have independently affected the study biomarkers and/or modified biomarker responses to the MOSES controlled O₃ exposures.</p><p><strong>Methods: </strong>MOSES 1 was conducted at three clinical centers (University of California San Francisco, University of North Carolina, and University of Rochester Medical Center) and included healthy volunteers 55 to 70 years of age. Consented participants who successfully completed the screening and training sessions were enrolled in the study. All three clinical centers adhered to common standard operating procedures and used common tracking and data forms. Each subject was scheduled to participate in a total of 11 visits: screening visit, training visit, and three sets of exposure visits consisting of the pre-exposure day, the exposure day, and the post-exposure day. After completing the pre-exposure day, subjects spent the night in a nearby hotel. On exposure days, the subjects were exposed for 3 hours in random order to 0 ppb O₃ (clean air), 70 ppb O₃, and 120 ppm O₃. During the exposure period the subjects alternated between 15 minutes of moderate exercise and 15 minutes of rest. A suite of cardiovascular and pulmonary endpoints was measured on the day before, the day of, and up to 22 hours after each exposure.</p><p><p>In MOSES Part 2 (MOSES 2), we used a longitudinal panel study design, cardiopulmonary biomarker data from MOSES 1, passive cumulative personal exposure samples (PES) of O₃ and nitrogen dioxide (NO₂) in the 72 hours before the pre-exposure visit, and hourly ambient air pollution and weather measurements in the 96 hours before the pre-exposure visit. We used mixed-effects linear regression and evaluated whether PES O₃ and NO₂ and these ambient pollutant concentrations in the 96 hours before the pre-exposure visit confounded the MOSES 1 controlled O₃ exposure effects on the pre- to post-exposure biomarker changes (Aim 1), whether they modified these pre- to post-exposure biomarker responses to the controlled O₃ exposures (Aim 2), whether they were associated with changes in biomarkers measured at the pre-exposure visit or morning of the exposure session (Aim 3), and whether they were associated with differences in the pre","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 192, Pt 2","pages":"1-90"},"PeriodicalIF":0.0,"publicationDate":"2020-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7325421/pdf/hei-2020-192-p2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10005060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhancing Models and Measurements of Traffic-Related Air Pollutants for Health Studies Using Dispersion Modeling and Bayesian Data Fusion.","authors":"S Batterman, V J Berrocal, C Milando, O Gilani, S Arunachalam, K M Zhang","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>The adverse health effects associated with exposure to traffic-related air pollutants (TRAPs) remain a key public health issue. Often, exposure assessments have not represented the small-scale variation and elevated concentrations found near major roads and in urban settings. This research explores approaches aimed at improving exposure estimates of TRAPs that can reduce exposure measurement error when used in health studies. We consider dispersion models designed specifically for the near-road environment, as well as spatiotemporal and data fusion models. These approaches are implemented and evaluated utilizing data collected in recent modeling, monitoring, and epidemiological studies conducted in Detroit, Michigan.</p><p><strong>Approach: </strong>Dispersion models, which estimate near-road pollutant concentrations and individual exposures based on first principles - and in particular, high fidelity models - can provide great flexibility and theoretical strength. They can represent the spatial variability of TRAP concentrations at locations not measured by conventional and spatially sparse air quality monitoring networks. A number of enhancements to dispersion modeling and mobile on-road emissions inventories were considered, including the representation of link-based road networks and updated estimates of temporal allocation of traffic activity, emission factors, and meteorological inputs. The recently developed Research LINE-source model (RLINE), a Gaussian line-source dispersion model specifically designed for the near-road environment, was used in an operational evaluation that compared predicted concentrations of nitrogen oxides (NO_x), carbon monoxide (CO), and PM_2.5 (particulate matter ≤ 2.5 µm in aerodynamic diameter) with observed concentrations at air quality monitoring stations located near high-traffic roads. Spatiotemporal and data fusion models provided additional and complementary approaches for estimating TRAP exposures. We formulated both nonstationary universal kriging models that exploit the spatial correlation in the monitoring data, and data fusion models that leverage the information contained in both the monitoring data and the output of numerical models, specifically RLINE. These models were evaluated using observations of nitric oxide (NO), NO_x, black carbon (BC), and PM_2.5 monitored along transects crossing major roads in Detroit. We also examined model assumptions, including the appropriateness of the covariance functions, errors in RLINE outputs, and the effects of jointly modeling two pollutants and using an updated emission inventory.</p><p><strong>Results: </strong>For CO and NO_x, dispersion model performance was best when monitoring sites were close to major roads, during downwind conditions, during weekdays, and during certain seasons. The ability to discern local and particularly the traffic-related portion of PM<sub>2.5</su","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 202","pages":"1-63"},"PeriodicalIF":0.0,"publicationDate":"2020-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7313251/pdf/hei-2020-202.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10053274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mortality-Air Pollution Associations in Low-Exposure Environments (MAPLE): Phase 1.","authors":"M Brauer, J R Brook, T Christidis, Y Chu, D L Crouse, A Erickson, P Hystad, C Li, R V Martin, J Meng, A J Pappin, L L Pinault, M Tjepkema, A van Donkelaar, S Weichenthal, R T Burnett","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>Fine particulate matter (particulate matter ≤2.5 μm in aerodynamic diameter, or PM_2.5) is associated with mortality, but the lower range of relevant concentrations is unknown. Novel satellite-derived estimates of outdoor PM_2.5 concentrations were applied to several large population-based cohorts, and the shape of the relationship with nonaccidental mortality was characterized, with emphasis on the low concentrations (<12 μg/m³) observed throughout Canada.</p><p><strong>Methods: </strong>Annual satellite-derived estimates of outdoor PM_2.5 concentrations were developed at 1-km² spatial resolution across Canada for 2000-2016 and backcasted to 1981 using remote sensing, chemical transport models, and ground monitoring data. Targeted ground-based measurements were conducted to measure the relationship between columnar aerosol optical depth (AOD) and ground-level PM_2.5. Both existing and targeted ground-based measurements were analyzed to develop improved exposure data sets for subsequent epidemiological analyses.</p><p><p>Residential histories derived from annual tax records were used to estimate PM_2.5 exposures for subjects whose ages ranged from 25 to 90 years. About 8.5 million were from three Canadian Census Health and Environment Cohort (CanCHEC) analytic files and another 540,900 were Canadian Community Health Survey (CCHS) participants. Mortality was linked through the year 2016. Hazard ratios (HR) were estimated with Cox Proportional Hazard models using a 3-year moving average exposure with a 1-year lag, with the year of follow-up as the time axis. All models were stratified by 5-year age groups, sex, and immigrant status. Covariates were based on directed acyclical graphs (DAG), and included contextual variables (airshed, community size, neighborhood dependence, neighborhood deprivation, ethnic concentration, neighborhood instability, and urban form). A second model was examined including the DAG-based covariates as well as all subject-level risk factors (income, education, marital status, indigenous identity, employment status, occupational class, and visible minority status) available in each cohort. Additional subject-level behavioral covariates (fruit and vegetable consumption, leisure exercise frequency, alcohol consumption, smoking, and body mass index [BMI]) were included in the CCHS analysis.</p><p><p>Sensitivity analyses evaluated adjustment for covariates and gaseous copollutants (nitrogen dioxide [NO₂] and ozone [O₃]), as well as exposure time windows and spatial scales. Estimates were evaluated across strata of age, sex, and immigrant status. The shape of the PM_2.5-mortality association was examined by first fitting restricted cubic splines (RCS) with a large number of knots and then fitting the shape-constrained health impact function (SCHIF) to the RCS predictions and their standard erro","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 203","pages":"1-87"},"PeriodicalIF":0.0,"publicationDate":"2019-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7334864/pdf/hei-2019-203.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9998749","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing Adverse Health Effects of Long-Term Exposure to Low Levels of Ambient Air Pollution: Phase 1.","authors":"F Dominici, J Schwartz, Q Di, D Braun, C Choirat, A Zanobetti","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>This report provides a summary of major findings and key conclusions supported by a Health Effects Institute grant aimed at \"Assessing Adverse Health Effects of Long-Term Exposure to Low Levels of Ambient Pollution.\" Our study was designed to advance four critical areas of inquiry and methods development.</p><p><strong>Methods: </strong>First, our work focused on predicting short- and long-term exposures to ambient PM_2.5 mass (particulate matter ≤ 2.5μm in aerodynamic diameter) and ozone (O₃) at high spatial resolution (1 km × 1 km) for the continental United States during the period 2000-2012 and linking these predictions to health data. Second, we developed new causal inference methods for exposure-response (ER) that account for exposure error and adjust for measured confounders. We applied these methods to data from the New England region. Third, we applied standard regression methods using Medicare claims data to estimate health effects that are associated with short- and long-term exposure to low levels of ambient air pollution. We conducted sensitivity analyses to assess potential confounding bias due to lack of extensive information on behavioral risk factors in the Medicare population using the Medicare Current Beneficiary Survey (MCBS) (nationally representative sample of approximately 15,000 Medicare enrollees per year), which includes abundant data on individual-level risk factors including smoking. Finally, we have begun developing tools for reproducible research - including approaches for data sharing, record linkage, and statistical software.</p><p><strong>Results: </strong>Our HEI-funded work has supported an extensive portfolio of analysis and the development of statistical methods that can be used to robustly understand the health effects of long- and short-term exposure to low levels of ambient air pollution. This report provides a high-level overview of statistical methods, data analysis, and key findings, as grouped into the following four areas: (1) Exposure assessment and data access; (2) Epidemiological studies of ambient exposures to air pollution at low levels; (3) Methodological contributions in causal inference; and (4) Open science research data platform.</p><p><strong>Conclusion: </strong>Our body of work, advanced by HEI, lends extensive evidence that short- and long-term exposure to PM_2.5 and O₃ is harmful to human health, increasing the risks of hospitalization and death, even at levels that are well below the National Ambient Air Quality Standards (NAAQS).</p>","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 200","pages":"1-51"},"PeriodicalIF":0.0,"publicationDate":"2019-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7300216/pdf/hei-2019-200.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9998751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding the Early Biological Effects of Isoprene-Derived Particulate Matter Enhanced by Anthropogenic Pollutants.","authors":"J D Surratt,&nbsp;Y-H Lin,&nbsp;M Arashiro,&nbsp;W G Vizuete,&nbsp;Z Zhang,&nbsp;A Gold,&nbsp;I Jaspers,&nbsp;R C Fry","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>Airborne fine particulate matter (PM_2.5; particulate matter ≤ 2.5 μm in aerodynamic diameter) plays a key role in air quality, climate, and public health. Globally, the largest mass fraction of PM_2.5 is organic, dominated by secondary organic aerosol (SOA) formed from atmospheric oxidation of volatile organic compounds (VOCs). Isoprene from vegetation is the most abundant nonmethane VOC emitted into Earth's atmosphere. Isoprene has been recently recognized as one of the major sources of global SOA production that is enhanced by the presence of anthropogenic pollutants, such as acidic sulfate derived from sulfur dioxide (SO₂), through multiphase chemistry of its oxidation products. Considering the abundance of isoprene-derived SOA in the atmosphere, understanding mechanisms of adverse health effects through inhalation exposure is critical to mitigating its potential impact on public health. Although previous studies have examined the toxicological effects of certain isoprene-derived gas-phase oxidation products, to date, no systematic studies have examined the potential toxicological effects of isoprene-derived SOA, its constituents, or its SOA precursors on human lung cells.</p><p><strong>Specific aims: </strong>The overall objective of this study was to investigate the early biological effects of isoprene-derived SOA and its subtypes on BEAS-2B cells (a human bronchial epithelial cell line), with a particular focus on the alteration of oxidative stress- and inflammation-related genes. To achieve this objective, there were two specific aims.</p><p><p>1. Examine toxicity and early biological effects of SOA derived from the photochemical oxidation of isoprene, considering both urban and downwind-urban types of chemistry.</p><p><p>2. Examine toxicity and early biological effects of SOA derived directly from downstream oxidation products of isoprene (i.e., epoxides and hydroperoxides).</p><p><strong>Methods: </strong>Isoprene-derived SOA was first generated by photooxidation of isoprene under natural sunlight in the presence of nitric oxide (NO) and acidified sulfate aerosols. Experiments were conducted in a 120-m³ outdoor Teflon-film chamber located on the roof of the Gillings School of Global Public Health, University of North Carolina at Chapel Hill (UNC-Chapel Hill). BEAS-2B cells were exposed to chamber- generated isoprene-derived SOA using the Electrostatic Aerosol in Vitro Exposure System (EAVES). This approach allowed us to generate atmospherically relevant compositions of isoprene-derived SOA and to examine its toxicity through in vitro exposures at an air-liquid interface, providing a more biologically relevant exposure model. Isoprene-derived SOA samples were also collected, concurrently with EAVES sampling, onto Teflon membrane filters for in vitro resuspension exposures and for analysis of aerosol chemical composition by gas chromatography/electron ionization-q","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 198","pages":"1-54"},"PeriodicalIF":0.0,"publicationDate":"2019-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7271660/pdf/hei-2019-198.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10007802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cellular and Acellular Assays for Measuring Oxidative Stress Induced by Ambient and Laboratory-Generated Aerosols.","authors":"N L Ng, W Y Tuet, Y Chen, S Fok, D Gao, M S Tagle Rodriguez, M Klein, A Grosberg, R J Weber, J A Champion","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>Many studies have established associations between exposure to air pollution, or atmospheric particulate matter (PM), and adverse health effects. An increasing array of studies have suggested oxidative stress as a possible mechanism by which PM-induced health effects arise, and as a result, many chemical and cellular assays have been developed to study PM-induced oxidant production. Although significant progress has been made in recent years, there are still many gaps in this area of research that have not been addressed. Many prior studies have focused on the aerosol of primary origin (e.g., the aerosol emitted from combustion engines) although the aerosol formed from the oxidation of volatile species, secondary organic aerosol (SOA), has been shown to be the predominant type of aerosol even in urban areas. Current SOA health studies are limited in number, and as such, the health effects of SOA are poorly characterized. Also, there is a lack of perspective in terms of the relative toxicities of different SOA systems. Additionally, although chemical assays have identified some SOA constituents associated with adverse health endpoints, the applicability of these results to cellular responses has not been well established.</p><p><strong>Specific aims: </strong>The overall objective of this study was to better understand the oxidative properties of different types and components of PM mixtures (especially SOA) through systematic laboratory chamber experiments and ambient field studies. The study had four specific aims.</p><p><p>1 To develop a cellular assay optimized for measuring reactive oxygen and nitrogen species (ROS/RNS) production resulting from PM exposure and to identify a robust parameter that could represent ROS/RNS levels for comparison with different endpoints.</p><p><p>2 To identify ambient PM components associated with ROS/RNS production and evaluate whether results from chemical assays represented cellular responses in terms of ROS/RNS production.</p><p><p>3 To investigate and provide perspective on the relative toxicities of SOA formed from common biogenic and anthropogenic precursors under different conditions (e.g., humidity, nitrogen oxides [NO_x], and redox-active metals) and identify bulk aerosol properties associated with cellular responses.</p><p><p>4 To investigate the effects of photochemical aging on aerosol toxicity.</p><p><strong>Methods: </strong>Ambient PM samples were collected from urban and rural sites in the greater Atlanta area as part of the Southeastern Center for Air Pollution and Epidemiology (SCAPE) study between June 2012 and October 2013. The concentrations of water-soluble species (e.g., water-soluble organic carbon [WSOC], brown carbon [Br C], and metals) were characterized using a variety of instruments. Samples for this study were chosen to span the observed range of dithiothreitol (DTT) activities.</p><p><p>Laboratory studies were conducted in the Georgia Tec","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 197","pages":"1-57"},"PeriodicalIF":0.0,"publicationDate":"2019-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7266377/pdf/hei-2019-197.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10010209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}