Research report (Health Effects Institute)最新文献

{"title":"Impacts of Regulations on Air Quality and Emergency Department Visits in the Atlanta Metropolitan Area, 1999-2013.","authors":"A G Russell, P Tolbert, Lrf Henneman, J Abrams, C Liu, M Klein, J Mulholland, S E Sarnat, Y Hu, H H Chang, T Odman, M J Strickland, H Shen, A Lawal","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>The United States and Western Europe have seen great improvements in air quality, presumably in response to various regulations curtailing emissions from the broad range of sources that have contributed to local, regional, and global pollution. Such regulations, and the ensuing controls, however, have not come without costs, which are estimated at tens of billions of dollars per year. These costs motivate accountability-related questions such as, to what extent do regulations lead to emissions changes? More important, to what degree have the regulations provided the expected human health benefits?</p><p><p>Here, the impacts of specific regulations on both electricity generating unit (EGU) and on-road mobile sources are examined through the classical accountability process laid out in the 2003 Health Effects Institute report linking regulations to emissions to air quality to health effects, with a focus on the 1999-2013 period. This analysis centers on regulatory actions in the southeastern United States and their effects on health outcomes in the 5-county Atlanta metropolitan area. The regulations examined are largely driven by the 1990 Clean Air Act Amendments (C). This work investigates regulatory actions and controls promulgated on EGUs: the Acid Rain Program (ARP), the NO<sub>x</sub> Budget Trading Program (NBP), and the Clean Air Interstate Rule (CAIR) - and mobile sources: Tier 2 Gasoline Vehicle Standards and the 2007 Heavy Duty Diesel Rule.</p><p><strong>Methods: </strong>Each step in the classic accountability process was addressed using one or more methods. Linking regulations to emissions was accomplished by identifying major federal regulations and the associated state regulations, along with analysis of individual facility emissions and control technologies and emissions modeling (e.g., using the U.S. Environmental Protection Agency's [U.S. EPA's] MOtor Vehicle Emissions Simulator [MOVES] mobile-source model). Regulators, including those from state environmental and transportation agencies, along with the public service commissions, play an important role in implementing federal rules and were involved along with other regional stakeholders in the study. We used trend analysis, air quality modeling, satellite data, and a ratio-of-ratios technique to investigate a critical current issue, a potential large bias in mobile-source oxides of nitrogen (NO<sub>x</sub>) emissions estimates.</p><p><p>The second link, emissions-air quality relationships, was addressed using both empirical analyses as well as chemical transport modeling employing the Community Multiscale Air Quality (CMAQ) model. Kolmogorov-Zurbenko filtering accounting for day of the year was used to separate the air quality signal into long-term, seasonal, weekday-holiday, and short-term meteorological signals. Regression modeling was then used to link emissions and meteorology to ambient concentrations for each of the species examined (ozone ","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 195","pages":"1-93"},"PeriodicalIF":0.0,"publicationDate":"2018-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7266381/pdf/hei-2018-195.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10012328","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":"Developing Multipollutant Exposure Indicators of Traffic Pollution: The Dorm Room Inhalation to Vehicle Emissions (DRIVE) Study.","authors":"J A Sarnat,&nbsp;A Russell,&nbsp;D Liang,&nbsp;J L Moutinho,&nbsp;R Golan,&nbsp;R J Weber,&nbsp;D Gao,&nbsp;S E Sarnat,&nbsp;H H Chang,&nbsp;R Greenwald,&nbsp;T Yu","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>The Dorm Room Inhalation to Vehicle Emissions (DRIVE²) study was conducted to measure traditional single-pollutant and novel multipollutant traffic indicators along a complete emission-to-exposure pathway. The overarching goal of the study was to evaluate the suitability of these indicators for use as primary traffic exposure metrics in panel-based and small-cohort epidemiological studies.</p><p><strong>Methods: </strong>Intensive field sampling was conducted on the campus of the Georgia Institute of Technology (GIT) between September 2014 and January 2015 at 8 monitoring sites (2 indoors and 6 outdoors) ranging from 5 m to 2.3 km from the busiest and most congested highway artery in Atlanta. In addition, 54 GIT students living in one of two dormitories either near (20 m) or far (1.4 km) from the highway were recruited to conduct personal exposure sampling and weekly biomonitoring. The pollutants measured were selected to provide information about the heterogeneous particulate and gaseous composition of primary traffic emissions, including the traditional traffic-related species (e.g., carbon monoxide [CO], nitrogen dioxide [NO₂], nitric oxide [NO], fine particulate matter [PM_2.5], and black carbon [BC]), and of secondary species (e.g., ozone [O₃] and sulfate as well as organic carbon [OC], which is both primary and secondary) from traffic and other sources. Along with these pollutants, we also measured two multipollutant traffic indicators: integrated mobile source indicators (IMSIs) and fine particulate matter oxidative potential (FPMOP). IMSIs are derived from elemental carbon (EC), CO, and nitrogen oxide (NO_x) concentrations, along with the fractions of these species emitted by gasoline and diesel vehicles, to construct integrated estimates of gasoline and diesel vehicle impacts. Our FPMOP indicator was based on an acellular assay involving the depletion of dithiothreitol (DTT), considering both water-soluble and insoluble components (referred to as FPMOP^total-DTT). In addition, a limited assessment of 18 low-cost sensors was added to the study to supplement the four original aims.</p><p><strong>Results: </strong>Pollutant levels measured during the study showed a low impact by this highway hotspot source on its surrounding vicinity. These findings are broadly consistent with results from other studies throughout North America showing decreased relative contributions to urban air pollution from primary traffic emissions. We view these reductions as an indication of a changing near-road environment, facilitated by the effectiveness of mobile source emission controls. Many of the primary pollutant species, including NO, CO, and BC, decreased to near background levels by 20 to 30 m from the highway source. Patterns of correlation among the sites also varied by pollutant and time of day. NO₂ exhibited spatial trends that differed from th","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 196","pages":"3-75"},"PeriodicalIF":0.0,"publicationDate":"2018-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7266376/pdf/hei-2018-196.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10007804","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":"A Dynamic Three-Dimensional Air Pollution Exposure Model for Hong Kong.","authors":"B Barratt, M Lee, P Wong, R Tang, T H Tsui, W Cheng, Y Yang, P-C Lai, L Tian, T-Q Thach, R Allen, M Brauer","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>High-density high-rise cities have become a more prominent feature globally. Air quality is a significant public health risk in many of these cities. There is a need to better understand the extent to which vertical variation in air pollution and population mobility in such cities affect exposure and exposure-response relationships in epidemiological studies.</p><p><strong>Methods: </strong>We used a novel strategy to execute a staged model development that incorporated horizontal and vertical pollutant dispersion, building infiltration, and population mobility patterns in estimating traffic-related air pollution (TRAP) exposures in the Hong Kong Special Administrative Region (HK SAR).</p><p><p>Two street-level spatial monitoring campaigns were undertaken to facilitate the creation of a two-dimensional land-use regression (LUR) model. A network of approximately 100 passive nitric oxide-nitrogen dioxide (NO-NO₂) monitors was deployed for two-week periods during the cool and warm seasons. Sampling locations were selected based on population and road network density with a range of physical and geographical characteristics represented. Eight sets of portable monitors for black carbon (BC) and particulate matter ≤2.5 μm in aerodynamic diameter (PM_2.5) were rotated so as to be deployed at 80 locations for a 24-hour period. Land-use, geographical, and emissions layers were combined with the spatial monitoring campaign results to create spatiotemporal exposure models.</p><p><p>Vertical air pollution monitoring was carried out at six strategic locations for two weeks in the warm season and two weeks in the cool season. Continuous measurements were carried out at four different heights of a residential building and on both sides of a street canyon. The heights ranged from as close to street level as practically possible up to a maximum of 50 meters (i.e., below the 20th floor). Paired indoor monitoring was included to allow the calculation of infiltration coefficients to feed into the dynamic component of the exposure model.</p><p><p>The final phase of model development addressed population mobility. A population-representative travel behavior survey (<i>n</i> = 89,358) was used to produce the dynamic component of the model, with time-weighted exposure estimates split between home and work or school. Transport microenvironment exposures were taken from published literature. Time-activity exposure estimates were split by age, sex, and employment status.</p><p><p>Development of the exposure model in distinct packages allowed the application of a staged approach to an existing cohort data set. Mortality risk estimates for an elderly cohort of 66,000 Hong Kong residents were calculated using increasing exposure model complexity.</p><p><strong>Results: </strong>The street-level (2-dimensional [2D]) LUR modeling captured important spatial parameters and represented spatial patterns of air quality in Hong K","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 194","pages":"1-65"},"PeriodicalIF":0.0,"publicationDate":"2018-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7266374/pdf/hei-2018-194.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10010205","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":"Particulate Air Pollutants, Brain Structure, and Neurocognitive Disorders in Older Women.","authors":"J-C Chen, X Wang, M Serre, S Cen, M Franklin, M Espeland","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>An increasing number of studies have suggested that exposure to particulate matter (PM) may represent a novel - and potentially amendable - environmental determinant of brain aging. The current longitudinal environmental epidemiological study addressed some important knowledge gaps in this emerging field, which combines the study of air pollution and neuroepidemiology. The investigators hypothesized that long-term PM exposure adversely influences global brain volume and brain regions (e.g., frontal lobe or hippocampus) that are critical to memory and complex cognitive processing or that are affected by neuropathological changes in dementia. It was also hypothesized that long-term PM exposure results in neurovascular damage and may increase the risk of mild cognitive impairment (MCI) and -dementia.</p><p><strong>Methods: </strong>The investigators selected a well-characterized and geographically diverse population of older women (<i>N</i> = 7,479; average age = 71.0 ± 3.8 years at baseline) in the Women's Health Initiative (WHI) Memory Study (WHIMS) cohort (1996-2007), which included a subcohort (<i>n</i> = 1,403) enrolled in the WHIMS-Magnetic Resonance Imaging (WHIMS-MRI) study (2005-2006). Residence-specific yearly exposures to PM ≤ 2.5 µm in aerodynamic diameter (PM₂.₅) were estimated using a Bayesian maximum entropy spatiotemporal model of annual monitoring data (1999-2007) recorded in the U.S. Environmental Protection Agency (U.S. EPA) Air Quality System (AQS). Annual exposures (1996-2005) to diesel PM (DPM) were assigned to each residential census tract in a nationwide spatiotemporal mapping, based on a generalized additive model (GAM), to conduct census tract-specific temporal interpolation of DPM on-road estimates given by the U.S. EPA National-Scale Air Toxics Assessment Program. Multiple linear regression and multicovariate-adjusted Cox models were used to examine the associations, with statistical adjustment for multiple potential confounders.</p><p><strong>Results: </strong>The investigators found that participants had smaller brain volumes, especially in the normal-appearing white matter (WM), if they lived in locations with higher levels of cumulative exposure (1999-2006) to PM ₂.₅ before the brain MRI scans were performed. The associations were not explained by sociodemographic factors, socioeconomic status, lifestyle factors, or other clinical characteristics. Analyses showed that the adverse effect on brain structure in the participants was driven primarily by the smaller WM volumes associated with cumulative PM₂.₅ exposures, which were present in the WM divisions of the association brain area (frontal, parietal, and temporal lobes) and corpus callosum. Increased DPM exposures were associated with larger ventricular volume, suggesting an overall atrophic effect on the aging brains. The participants tended to have smaller gray matter (GM) volumes if they lived in areas with the highest (i.e., four","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 193","pages":"1-65"},"PeriodicalIF":0.0,"publicationDate":"2017-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7266369/pdf/hei-2017-193.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9998754","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 1. Effects of Exposure to Low Concentrations of Ozone on Respiratory and Cardiovascular Outcomes.","authors":"M W Frampton,&nbsp;J R Balmes,&nbsp;P A Bromberg,&nbsp;P Stark,&nbsp;M Arjomandi,&nbsp;M J Hazucha,&nbsp;D Q Rich,&nbsp;D Hollenbeck-Pringle,&nbsp;N Dagincourt,&nbsp;N Alexis,&nbsp;P Ganz,&nbsp;W Zareba,&nbsp;M G Costantini","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>Exposure to air pollution is a well-established risk factor for cardiovascular morbidity and mortality. Most of the evidence supporting an association between air pollution and adverse cardiovascular effects involves exposure to particulate matter (PM). To date, little attention has been paid to acute cardiovascular responses to ozone, in part due to the notion that ozone causes primarily local effects on lung function, which are the basis for the current ozone National Ambient Air Quality Standards (NAAQS). There is evidence from a few epidemiological studies of adverse health effects of chronic exposure to ambient ozone, including increased risk of mortality from cardiovascular disease. However, in contrast to the well-established association between ambient ozone and various nonfatal adverse respiratory effects, the observational evidence for impacts of acute (previous few days) increases in ambient ozone levels on total cardiovascular mortality and morbidity is mixed.</p><p><p>Ozone is a prototypic oxidant gas that reacts with constituents of the respiratory tract lining fluid to generate reactive oxygen species (ROS) that can overwhelm antioxidant defenses and cause local oxidative stress. Pathways by which ozone could cause cardiovascular dysfunction include alterations in autonomic balance, systemic inflammation, and oxidative stress. These initial responses could lead ultimately to arrhythmias, endothelial dysfunction, acute arterial vasoconstriction, and procoagulant activity. Individuals with impaired antioxidant defenses, such as those with the null variant of glutathione S-transferase mu 1 (GSTM1), may be at increased risk for acute health effects.</p><p><p>The Multicenter Ozone Study in oldEr Subjects (MOSES) was a controlled human exposure study designed to evaluate whether short-term exposure of older, healthy individuals to ambient levels of ozone induces acute cardiovascular responses. The study was designed to test the a priori hypothesis that short-term exposure to ambient levels of ozone would induce acute cardiovascular responses through the following mechanisms: autonomic imbalance, systemic inflammation, and development of a prothrombotic vascular state. We also postulated a priori the confirmatory hypothesis that exposure to ozone would induce airway inflammation, lung injury, and lung function decrements. Finally, we postulated the secondary hypotheses that ozone-induced acute cardiovascular responses would be associated with: (a) increased systemic oxidative stress and lung effects, and (b) the GSTM1-null genotype.</p><p><strong>Methods: </strong>The study was conducted at three clinical centers with a separate Data Coordinating and Analysis Center (DCAC) using a common protocol. All procedures were approved by the institutional review boards (IRBs) of the participating centers. Healthy volunteers 55 to 70 years of age were recruited. Consented participants who successfully completed the","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 192, Pt 1","pages":"1-107"},"PeriodicalIF":0.0,"publicationDate":"2017-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7266375/pdf/hei-2017-192-p1.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10010208","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":"Protective Role of Eosinophils and TNFa after Ozone Inhalation.","authors":"Allison D Fryer,&nbsp;David B Jacoby,&nbsp;Sarah A Wicher","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>Exposure to ozone induces deleterious responses\u0000in the airways that include shortness of breath,\u0000inflammation, and bronchoconstriction. People\u0000with asthma have increased airway sensitivity to\u0000ozone and other irritants. Dr. Allison Fryer and\u0000colleagues addressed how exposure to ozone affects\u0000the immune and physiological responses in\u0000guinea pigs. Guinea pigs are considered a useful\u0000animal model for studies of respiratory and physiological\u0000responses in humans; their response to\u0000airborne allergens is similar to that in humans and\u0000shares some features of allergic asthma.\u0000Fryer and colleagues had previously observed\u0000that within 24 hours of exposure, ozone not only\u0000induced bronchoconstriction but also stimulated\u0000the production of new cells in the bone marrow,\u0000where all white blood cells develop. As a result\u0000of ozone exposure, increased numbers of newly\u0000synthesized white blood cells, particularly eosinophils,\u0000moved into the blood and lungs.\u0000The central hypothesis of the current study was\u0000that newly synthesized eosinophils recruited to\u0000the lungs 3 days after ozone exposure were beneficial\u0000to the animals because they reduced ozoneinduced\u0000bronchoconstriction. The investigators\u0000also hypothesized that the beneficial effect seen\u0000in normal (nonsensitized) animals was lost in animals\u0000that had been injected with an allergen, ovalbumin\u0000(sensitized). They also planned to explore\u0000the effects of inhibitors of certain cytokines (cellsignaling\u0000molecules).\u0000Immune responses in sensitized animals are\u0000dominated by a Th2 pattern, which is characterized\u0000by the synthesis of cytokines (interleukin\u0000[IL]-4, IL-5, and IL-13) and the Th2 subset of CD4+\u0000T lymphocytes and the cells they activate (predominantly\u0000eosinophils, and B lymphocytes that\u0000switch to making immunoglobulin E [IgE]). Thus,\u0000sensitized animals were used as a model of allergic\u0000humans, whose immune responses tend to be\u0000dominated by IgE.</p><p><strong>Approach: </strong>Fryer and colleagues exposed normal and sensitized\u0000(allergic) guinea pigs to 2 ppm ozone or filtered\u0000air for 4 hours and measured changes in cell\u0000numbers and airway responses 1 or 3 days later.\u0000They counted the numbers of eosinophils and other\u0000white blood cells (macrophages, neutrophils, and\u0000lymphocytes) in bone marrow, blood, and bronchoalveolar\u0000lung lavage fluid. The investigators\u0000also measured important physiological responses,\u0000including bronchoconstriction. Some animals were\u0000pretreated with etanercept and monoclonal anti-IL-5,\u0000which block tumor necrosis factor-a (TNFa) and IL-5,\u0000respectively. TNFa and IL-5 blockers have been used\u0000to treat patients with asthma.\u0000A key feature of the study was a technique to distinguish\u0000which white blood cells were synthesized after\u0000exposure from those that already existed, by injecting\u0000animals with bromodeoxyuridine (BrdU). BrdU\u0000is a thymidine analogue that is incorporated into the\u0000DNA of dividing cells, serving as a marker of newly\u0000produced cells. Therefore, a snapshot can be obtain","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 191","pages":"1-41"},"PeriodicalIF":0.0,"publicationDate":"2017-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7266380/pdf/hei-2017-191.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10007748","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":"The Effects of Policy-Driven Air Quality Improvements on Children's Respiratory Health.","authors":"F Gilliland,&nbsp;E Avol,&nbsp;R McConnell,&nbsp;K Berhane,&nbsp;W J Gauderman,&nbsp;F W Lurmann,&nbsp;R Urman,&nbsp;R Chang,&nbsp;E B Rappaport,&nbsp;S Howland","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>Ambient air pollution causes substantial morbidity and mortality in the United States and worldwide. To reduce this burden of adverse health effects, a broad array of strategies to reduce ambient air pollution has been developed and applied over past decades to achieve substantial reductions in ambient air pollution levels. This has been especially true in California, where the improvement of air quality has been a major focus for more than 50 years. Direct links between regulatory policies, changes in ambient pollutant concentrations, and improvements in public health have not been extensively documented. Data from the Children's Health Study (CHS), a multiyear study of children's respiratory health development, offered a unique opportunity to evaluate the effects of long-term reductions in air pollution on children's health.</p><p><strong>Methods: </strong>We assessed whether changes in ambient air quality and emissions were reflected in three important indices of children's respiratory health: lung-function growth, lung-function level, and bronchitic symptoms. To make the best use of available data, these analyses were performed across the longest chronological period and largest CHS population available for the respective lung-function or bronchitic symptoms data sets. During field study operations over the course of the CHS, children's health status was documented annually by testing lung-function performance and the completion of standardized questionnaires covering a broad range of respiratory symptoms. Air quality data for the periods of interest were obtained from community monitoring stations, which operated in collaboration with regional air monitoring networks over the 20-year study time frame. Over the 20-year sampling period, common protocols were applied to collect data across the three cohorts of children. Each cohort's data set was assessed to investigate the relationship between temporal changes in lung-function development, prevalence of bronchitic symptoms, and ambient air pollution concentrations during a similar, vulnerable adolescent growth period (age 11 to 15 years). Analyses were performed separately for particulate matter ≤10 µm in aerodynamic diameter (PM₁₀), particulate matter ≤2.5 µm in aerodynamic diameter (PM₂.₅), ozone (O₃), and nitrogen dioxide (NO₂). Emissions data and regulatory policies were collected from the staff of state and regional regulatory agencies, modeling estimates, and archived reports.</p><p><strong>Results: </strong>Emissions in the regions of California studied during the 20-year period decreased by 54% for oxides of nitrogen (NOₓ), 65% for reactive organic gases (ROG), 21% for PM₂.₅, and 15% for PM₁₀. These reductions occurred despite a concurrent 22% increase in population and a 38% increase in motor vehicle miles driven during that time frame. Air quality improved over the same time frame, with reductions in NO₂ and PM₂.₅ in virtually all of the CHS communit","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 190","pages":"1-75"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7266378/pdf/hei-2017-190.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10005050","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":"Ambient Air Pollution and Adverse Pregnancy Outcomes in Wuhan, China.","authors":"Zhengmin Qian,&nbsp;Bin Zhang,&nbsp;Shengwen Liang,&nbsp;Jing Wang,&nbsp;Shaoping Yang,&nbsp;Ke Hu,&nbsp;Edwin Trevathan,&nbsp;Rong Yang,&nbsp;Qijie Li,&nbsp;Louise H Flick,&nbsp;Ronghua Hu,&nbsp;Zhen Huang,&nbsp;Yimin Zhang,&nbsp;Shixiang Hu,&nbsp;Jing Wang,&nbsp;Longjiao Shen,&nbsp;Yuan Lu,&nbsp;Hui Peng,&nbsp;Yuzhen Yu,&nbsp;Li Yang,&nbsp;Wei Chen,&nbsp;Wenjin Liu,&nbsp;Wei Zhang","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Background: </strong>Several recent studies have suggested that maternal\u0000exposures to air pollution and temperature extremes\u0000might contribute to low birth weight (LBW),\u0000preterm birth (PTB), and other outcomes that can adversely\u0000affect infant health. At the time the current\u0000study began, most other studies had been conducted\u0000in the United States or Europe. Dr. Zhengmin Qian\u0000proposed to extend work he had done on ambient\u0000particulate air pollution and daily mortality in\u0000Wuhan, China (Qian et al. 2010), as part of the HEIsponsored\u0000Public Health and Air Pollution in Asia\u0000program, to study adverse birth outcomes. Wuhan is\u0000the capital city of Hubei province, has a large population\u0000of about 6.4 million within the urban study area,\u0000experiences temperature extremes, and generally has\u0000higher air pollution levels than those observed in the\u0000United States and Europe, thus providing a good opportunity\u0000to explore questions about air pollution\u0000and health.</p><p><strong>Approach: </strong>Qian and colleagues planned a cohort and nested\u0000case–control design with four specific aims, examining\u0000whether increased exposures to air pollutants\u0000(PM2.5, PM10, SO2, NO2, O3, and CO) during vulnerable\u0000pregnancy periods were associated with\u0000increased rates of PTB, LBW (<2500 g), or intrauterine\u0000growth retardation (IUGR, defined as having\u0000a birth weight below the 10th percentile of singleton\u0000live births in Wuhan) after adjusting for major risk\u0000factors and whether the associations were confounded\u0000by copollutant exposures, affected by\u0000residual confounding, or modified by temperature\u0000extremes, socioeconomic status (SES), or secondhand\u0000smoke (SHS) exposure.\u0000The cohort study included 95,911 births that\u0000occurred from June 10, 2011, to June 9, 2013, and\u0000met typical prespecified inclusion criteria used in\u0000other birth outcome studies. The case–control\u0000study included 3146 cases (PTB, LBW, or both, but\u0000not IUGR) and 4263 controls (matched to the cases\u0000by birth month) for whom investigators were able to\u0000complete home visits and questionnaires.\u0000The investigators obtained air pollution and daily\u0000weather data for August 2010 to June 2013 from nine\u0000monitoring stations representing background air pollution\u0000sites in seven Wuhan inner-city districts. Only\u0000two of these stations provided PM2.5 data. For the\u0000cohort study, the investigators assigned exposures to\u0000mothers according to the daily mean concentrations\u0000from the monitor nearest the residential community\u0000in which the mother lived at the time of the birth. For\u0000the case–control study, they assigned exposures\u0000based on the inverse distance weighted average of\u0000daily mean concentrations from the three nearest\u0000monitors, for all but PM2.5 for which the method was\u0000not specified.\u0000They also collected data on various factors that\u0000might confound or modify the impact of the pollutants\u0000on the adverse outcomes, including data collected\u0000in the cohort from mothers at the time of delivery\u0000and, in the case–control study, from questionnaires\u0000administered ","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 189","pages":"1-65"},"PeriodicalIF":0.0,"publicationDate":"2016-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36015351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ambient and Controlled Particle Exposures as Triggers for Acute ECG Changes.","authors":"David Q Rich,&nbsp;Annette Peters,&nbsp;Alexandra Schneider,&nbsp;Wojciech Zareba,&nbsp;Susanne Breitner,&nbsp;David Oakes,&nbsp;Jelani Wiltshire,&nbsp;Cathleen Kane,&nbsp;Mark W Frampton,&nbsp;Regina Hampel,&nbsp;Philip K Hopke,&nbsp;Josef Cyrys,&nbsp;Mark J Utell","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>Previous studies have examined changes in heart rate variability (HRV*) and repolarization associated with increased particulate matter (PM) concentrations on the same and previous few days. However, few studies have examined whether these health responses to PM occur within a few hours or even less. Moreover, it is not clear whether exposure of subjects to ambient or-controlled PM concentrations both lead to similar health effects or whether any of the subjects' individual characteristics modify any of their responses to PM. The aims of the cur- rent study were to investigate whether exposure to PM was associated with rapid changes (< 60 minutes or con- current hour up to a delay of 6 hours) in markers of car- diac rhythni or changes in total antioxidant capacity (a marker of protection against oxidative stress) and whether any PM effects on cardiac rhythm markers were modified by total antioxidant capacity, age, obesity, smoking, hypertension, exertion, prior myocardial infarction (MI), or medication.</p><p><strong>Methods: </strong>We obtained data from a completed study in Augsburg, Germany (a panel study in N= 109 subjects, including a group with type 2 diabetes or impaired glucose tolerance [IGT; also known as prediabetes]) and a group of other- wise healthy subjects with a potential genetic susceptibil- ity to detoxifying and inflammatory pathways (Hampel et al. 2012b), as well as three completed studies in Rochester, New York (the REHAB panel study of N= 76 postinfarction patients in a cardiac rehabilitation pro- gram [Rich et al. 2012b]; the UPDIABETES study of con- trolled exposure to ultrafine particles [UFPs, particles with an aerodynamic diameter < 100 nm] of N = 19 patients with type 2 diabetes [Stewart et al. 2010; Vora et al. 2014j; and the UPCON controlled-exposure study of concentrated UFP exposure in N = 20 young, healthy, life- time nonsmokers). Data included 5-minute and 1-hour values for HRV and repolarization parameters from elec- trocardiogram (ECG) recordings and total antioxidant capacity measured in stored blood samples. Ambient con- centrations of UFPs, accumulation-mode particles (AMP, particles with an aerodynamic diameter of 100-500 nm), fine PM (PM2.5, particles with an aerodynamic diameter 2.5 pm), and black carbon (BC) were also available. We first conducted factor analyses in each study to find subgroups of correlated ECG outcomes and to reduce the number of outcomes examined in our statistical models. We then restricted the statistical analyses to the factors and representative.outcomes that were common to all four studies, including total HRV (measured as the standard deviation of normal-to-normal [NN] beat intervals [SDNNj), parasympathetic modulation (measured as the root mean square of the successive differences [RMSSD between adjacent NN beat intervals), and T-wave morphol- ogy (measured as T-wave complexity). Next, we used addi- tive mixed models to estimate the change in","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 186","pages":"5-75"},"PeriodicalIF":0.0,"publicationDate":"2016-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35128972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causal Inference Methods for Estimating Long-Term Health Effects of Air Quality Regulations.","authors":"Corwin Matthew Zigler,&nbsp;Chanmin Kim,&nbsp;Christine Choirat,&nbsp;John Barrett Hansen,&nbsp;Yun Wang,&nbsp;Lauren Hund,&nbsp;Jonathan Samet,&nbsp;Gary King,&nbsp;Francesca Dominici","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>The regulatory and policy environment surrounding air quality management warrants new types of epidemiological evidence. Whereas air pollution epidemiology has typically informed previous policies with estimates of exposure-response relationships between pollution and health outcomes, new types of evidence can inform current debates about the actual health impacts of air quality regulations. Directly evaluating specific regulatory strategies is distinct from and complements estimating exposure-response relationships; increased emphasis on assessing the effectiveness of well-defined regulatory interventions will enhance the evidence supporting policy decisions. The goal of this report is to provide new analytic perspectives and statistical methods for what we refer to as \"direct\"-accountability assessment of the effectiveness of specific air quality regulatory interventions. Toward this end, we sharpened many of the distinctions surrounding accountability assessment initially raised by the HEI Accountability Working Group (2003) through discussion, development, and deployment of statistical methods for drawing causal inferences from observational data. The methods and analyses presented here are unified in their focus on anchoring accountability assessment to the estimation of the causal consequences of well-defined actions or interventions. These analytic perspectives are discussed in the context of two direct-accountability case studies pertaining to four different links in the so-called chain of accountability, the related series of events leading from the intervention to the expected outcomes (see Preface; HEI Accountability Working Group 2003).</p><p><strong>Methods: </strong>The statistical methods described in this report consist of both established methods for drawing causal inferences from observational data and newly developed methods for assessing causal accountability. We have sharpened the analytic distinctions between studies that directly evaluated the effectiveness of specific policies and those that estimated exposure-response relationships between pollution and health. We emphasized how a potential-outcomes paradigm for causal inference can elevate policy debates by means of more direct evidence of the extent to which complex regulatory interventions affect pollution and health outcomes. We also outlined the potential-outcomes perspective and promoted its use as a means to frame observational studies as approximate randomized experiments. Our newly developed methods for assessing causal accountability draw on propensity scores, principal stratification, causal mediation analysis, spatial hierarchical models, and Bayesian estimation. The first case study made use of health outcomes among approximately four million Medicare beneficiaries living in the Western United States to estimate the causal health impacts of areas designated as being in nonattainment for particulate matter ≤10 μm in aerodynami","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 187","pages":"5-49"},"PeriodicalIF":0.0,"publicationDate":"2016-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34309400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}