Research report (Health Effects Institute)最新文献

{"title":"Accountability analysis of title IV phase 2 of the 1990 Clean Air Act Amendments.","authors":"Richard D Morgenstern,&nbsp;Winston Harrington,&nbsp;Jhih-Shyang Shih,&nbsp;Michelle L Bell","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In this study, we sought to assess what portion, if any, of the reductions in ambient concentrations of particulate matter (PM*) < or = 2.5 microm in aerodynamic diameter (PM2.5) that occurred in the United States between the years 1999 and 2006 can be attributed to reductions in emissions of sulfur dioxide (SO2) and nitrogen oxides (NOx) resulting from implementation of Phase 2 of Title IV of the 1990 Clean Air Act Amendments. To this end, a detailed statistical model linking sources and monitors over time and space was used to estimate associations between the observed emissions reductions and improvements in air quality. Overall, it turned out to be quite feasible to use relatively transparent statistical methods to assess these outcomes of the Phase 2 program, which was designed to reduce long-range transport of emissions. Associations between changes in emissions from individual power plants and monitor-specific estimates of changes in concentrations of PM2.5, our indicator pollutant, were highly significant and were mostly of the expected relative magnitudes with respect to distances and directions from sources. Originally estimated on monthly data for a set of 193 monitors between 1999 and 2005, our preferred model performed equally well using data for the same 193 monitors for 2006 as well as for an additional 217 monitors not in the original set in 2006. Although substantial model uncertainty was observed, we were able to estimate that the Title IV Phase 2 emissions reduction program implemented between 1999 and 2005 reduced PM2.5 concentrations in the eastern United States by an average of 1.07 microg/m3 (standard deviation [SD] = 0.11 microg/m3) compared with a counterfactual case defined as there having been no change in emission rates per unit of energy input (1 million British thermal units [BTUs]). On a population-weighted basis, the comparable reduction in PM2.5 was 0.89 microg/m3. Compared with the air quality fate and transport models used by the U.S. Environmental Protection Agency (EPA) to estimate air quality improvements associated with the Clean Air Interstate Rule (CAIR) for 2010 and 2015, when baseline PM2.5 concentrations were expected to be about one-third lower, our statistical model yielded roughly similar results per ton of SO2 reduced, well within the estimated confidence intervals of the models. We have proposed a number of steps to advance air quality outcomes research using statistical methods. Specifically, we have emphasized the value of updating our analysis with post-2005 data to try to corroborate our findings. We have also recommended extending the work on air quality outcomes to include changes in health outcomes that might be associated with the implementation of Title IV Phase 2.</p>","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 168","pages":"5-35"},"PeriodicalIF":0.0,"publicationDate":"2012-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31330043","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":"Multicity study of air pollution and mortality in Latin America (the ESCALA study).","authors":"Isabelle Romieu,&nbsp;Nelson Gouveia,&nbsp;Luis A Cifuentes,&nbsp;Antonio Ponce de Leon,&nbsp;Washington Junger,&nbsp;Jeanette Vera,&nbsp;Valentina Strappa,&nbsp;Magali Hurtado-Díaz,&nbsp;Victor Miranda-Soberanis,&nbsp;Leonora Rojas-Bracho,&nbsp;Luz Carbajal-Arroyo,&nbsp;Guadalupe Tzintzun-Cervantes","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>The ESCALA* project (Estudio de Salud y Contaminación del Aire en Latinoamérica) is an HEI-funded study that aims to examine the association between exposure to outdoor air pollution and mortality in nine Latin American cities, using a common analytic framework to obtain comparable and updated information on the effects of air pollution on several causes of death in different age groups. This report summarizes the work conducted between 2006 and 2009, describes the methodologic issues addressed during project development, and presents city-specific results of meta-analyses and meta-regression analyses.</p><p><strong>Methods: </strong>The ESCALA project involved three teams of investigators responsible for collection and analysis of city-specific air pollution and mortality data from three different countries. The teams designed five different protocols to standardize the methods of data collection and analysis that would be used to evaluate the effects of air pollution on mortality (see Appendices B-F). By following the same protocols, the investigators could directly compare the results among cities. The analysis was conducted in two stages. The first stage included analyses of all-natural-cause and cause-specific mortality related to particulate matter < or = 10 pm in aerodynamic diameter (PM10) and to ozone (O3) in cities of Brazil, Chile, and México. Analyses for PM10 and O3 were also stratified by age group and O3 analyses were stratified by season. Generalized linear models (GLM) in Poisson regression were used to fit the time-series data. Time trends and seasonality were modeled using natural splines with 3, 6, 9, or 12 degrees of freedom (df) per year. Temperature and humidity were also modeled using natural splines, initially with 3 or 6 df, and then with degrees of freedom chosen on the basis of residual diagnostics (i.e., partial autocorrelation function [PACF], periodograms, and a Q-Q plot) (Appendix H, available on the HEI Web site). Indicator variables for day-of-week and holidays were used to account for short-term cyclic fluctuations. To assess the association between exposure to air pollution and risk of death, the PM10 and O3 data were fit using distributed lag models (DLMs). These models are based on findings indicating that the health effects associated with air pollutant concentrations on a given day may accumulate over several subsequent days. Each DLM measured the cumulative effect of a pollutant concentration on a given day (day 0) and that day's contribution to the effect of that pollutant on multiple subsequent (lagged) days. For this study, exposure lags of up to 3, 5, and 10 days were explored. However, only the results of the DLMs using a 3-day lag (DLM 0-3) are presented in this report because we found a decreasing association with mortality in various age-cause groups for increasing lag effects from 3 to 5 days for both PM10 and O3. The potential modifying effect of socioeconomic st","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 171","pages":"5-86"},"PeriodicalIF":0.0,"publicationDate":"2012-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31154691","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":"Part 1. Biologic responses in rats and mice to subchronic inhalation of diesel exhaust from U.S. 2007-compliant engines: report on 1-, 3-, and 12-month exposures in the ACES bioassay.","authors":"Jacob D Mcdonald,&nbsp;Melanie Doyle-Eisele,&nbsp;Andrew Gigliotti,&nbsp;Rodney A Miller,&nbsp;Steve Seilkop,&nbsp;Joe L Mauderly,&nbsp;JeanClare Seagrave,&nbsp;Judith Chow,&nbsp;Barbara Zielinska","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The Health Effects Institute and its partners conceived and funded a program to characterize the emissions from heavy-duty diesel engines compliant with the 2007 and 2010 on-road emissions standards in the United States and to evaluate indicators of lung toxicity in rats and mice exposed repeatedly to diesel exhaust (DE*) from 2007-compliant engines. The preliminary hypothesis of this Advanced Collaborative Emissions Study (ACES) was that 2007-compliant on-road diesel emissions \". . . will not cause an increase in tumor formation or substantial toxic effects in rats and mice at the highest concentration of exhaust that can be used . . . although some biological effects may occur.\" This hypothesis is being tested at the Lovelace Respiratory Research Institute (LRRI) by exposing rats by chronic inhalation as a carcinogenicity bioassay, measuring indicators of pulmonary toxicity in rats after 1, 3, 12, and 24-30 months of exposure (final time point depends on the survival of animals), and measuring similar indicators of pulmonary toxicity in mice after 1 and 3 months of exposure. This report provides results of exposures through 3 months in rats and mice. Emissions from a 2007-compliant, 500-horsepower-class engine and aftertreatment system operated on a variable-duty cycle were used to generate the animal inhalation test atmospheres. Four treatment groups were exposed to one of three concentrations (dilutions) of exhaust combined with crankcase emissions, or to clean air as a negative control. Dilutions of exhaust were set to yield average integrated concentrations of 4.2, 0.8, and 0.1 ppm nitrogen dioxide (NO2). Exposure atmospheres were analyzed by daily measurements of key components and periodic detailed physical-chemical characterizations. Exposures were conducted 16 hr/dy (overnight), 5 dy/wk. Rats were evaluated for hematology, serum chemistry, bronchoalveolar lavage (BAL), lung cell proliferation, and histopathology after 1 month of exposure, and the same indicators plus pulmonary function after 3 months. Mice were evaluated for BAL, lung cell proliferation, and respiratory tract histopathology after 1 month of exposure, and the same indicators plus hematology and serum chemistry after 3 months. Samples from both species were collected for ancillary studies performed by investigators who were not at LRRI and were funded separately. Exposures were accomplished as planned, with average integrated exposure concentrations within 20% of the target dilutions. The major components were the gaseous inorganic compounds, nitrogen monoxide (NO), NO2, and carbon monoxide (CO). Minor components included low concentrations of diesel particulate matter (DPM) and volatile and semivolatile organic compounds (VOCs and SVOCs). There were no exposure-related differences in mortality or clinically evident morbidity. Among the more than 100 biologic response variables evaluated, the majority showed no significant difference from control as a result of expo","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 166","pages":"9-120"},"PeriodicalIF":0.0,"publicationDate":"2012-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31054082","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":"Part 2. Assessment of genotoxicity after exposure to diesel exhaust from U.S. 2007-compliant diesel engines: report on 1- and 3-month exposures in the ACES bioassay.","authors":"Jeffrey C Bemis,&nbsp;Dorothea K Torous,&nbsp;Stephen D Dertinger","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Micronucleus (MN*) formation is a well-established endpoint in genetic toxicology; studies designed to examine MN formation in vivo have been conducted for decades. Conditions that cause double-strand breaks or disrupt the proper segregation of chromosomes during division result in an increase in MN frequency. Thus this endpoint is commonly employed in preclinical studies designed to assess the potential risks of human exposure to a myriad of chemical and physical agents, including inhaled diesel exhaust (DE). As part of the Advanced Collaborative Emissions Study (ACES) this investigation examined the potential of inhaled DE to induce chromosome damage in chronically exposed rodents. The ACES design included exposure of both rats and mice to DE derived from 2007-compliant heavy-duty engines. The exposure conditions consisted of air control and dilutions of DE resulting in three levels of exposure. At specified times, blood samples were collected, fixed, and shipped by the bioassay staff to Litron Laboratories for further processing and analysis. Significant improvements have been made to MN scoring by using objective, automated methods such as flow cytometry, which allows for the detection of micronucleated reticulocytes (MN-RET), micronucleated normochromatic erythrocytes (MN-NCE), and reticulocytes (RETs) in peripheral blood samples from mice and rats. By using a simple staining procedure coupled with rapid and efficient analysis, many more cells were examined in less time than was possible in traditional, microscopy-based MN assays. Thus, for each sample, 20,000 RETs were scored for the presence of MN. In the chronic-exposure bioassay, blood samples were obtained from independent groups of exposed animals at specific time points throughout the course of the entire study. This automated method is supported by numerous regulatory guidelines and meets the requirements for an Organization of Economic Cooperation and Development (OECD)-compliant assay for genotoxicity. Statistical approaches employed analysis of variance (ANOVA) to compare effects of sex, exposure condition, and duration, as well as their interactions. This initial assessment of MN was performed on both mouse and rat blood samples from the 1-month and 3-month exposures. The data from mice demonstrate the well established, sex-based difference in MN-RET and MN-NCE frequencies regularly observed in this species, with females exhibiting slightly lower frequencies. There were no sex-based differences observed in rats. An examination of the mean frequencies across the exposure groups and durations of exposure did not show an appreciable induction of MN at the 1- or 3-month exposures in either species. Further statistical analyses did not reveal any significant exposure-related effects. An examination of the potential genotoxic effects of DE is clearly valuable as part of a large-scale chronic-exposure bioassay. The data and observations from the 1-and 3-month exposure studies will","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 166","pages":"125-57"},"PeriodicalIF":0.0,"publicationDate":"2012-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31054083","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":"Part 4. Effects of subchronic diesel engine emissions exposure on plasma markers in rodents: report on 1- and 3-month exposures in the ACES bioassay.","authors":"Daniel J Conklin,&nbsp;Maiying Kong","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Although epidemiologic and experimental studies suggest that exposure to diesel exhaust (DE*) emissions causes adverse cardiovascular effects, neither the specific components of DE nor the mechanisms by which DE exposure could induce cardiovascular dysfunction and exacerbate cardiovascular disease (CVD) are known. Moreover, because the advance of new technologies has resulted in cleaner fuels and decreased engine emissions, there is even more uncertainty about the relationship between DE exposure and cardiovascular health effects. To address this ever-changing baseline of engine emissions, we tested for exposure-, sex- and duration-dependent alterations in plasma markers following subchronic exposure of mice and rats to DE emissions from a 2007-compliant diesel engine. Many plasma markers--several recognized as known human CVD risk factors--were measured in the plasma of rodents exposed to 1 or 3 months of air (the control) or DE emissions. Few changes in plasma markers resulted from exposure to DE, although significant exposure-level-dependent increases in total cholesterol and high-density lipoprotein (HDL) cholesterol were observed in male rats after 1 month of DE exposure, an effect that was neither sustained nor observed in any other group. These data indicate that DE emissions from a 2007-compliant diesel engine as tested in this study had little adverse effect on CVD markers in rodents.</p>","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 166","pages":"189-223"},"PeriodicalIF":0.0,"publicationDate":"2012-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31054564","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":"Part 3. Assessment of genotoxicity and oxidative stress after exposure to diesel exhaust from U.S. 2007-compliant diesel engines: report on 1- and 3-month exposures in the ACES bioassay.","authors":"L M Hallberg,&nbsp;J B Ward,&nbsp;C Hernandez,&nbsp;B T Ameredes,&nbsp;J K Wickliffe","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Human health hazards due to diesel exhaust (DE*) exposure have been associated with both solvent and combustion components. In the past, diesel engine exhaust components have been linked to increased mutagenicity in cultures of Salmonella typhimurium and mammalian cells (Tokiwa and Ohnishi 1986). In addition, DE has been shown to increase both the incidence of tumors and the induction of 8-hydroxy-deoxyguanosine adducts (8-OHdG) in ICR mice (Ichinose et al. 1997). Furthermore, DE is composed of a complex mixture of polycyclic aromatic hydrocarbons (PAHs) and particulates. One such PAH, 3-nitrobenzanthrone (3-NBA), has been identified in DE and found in urban air. 3-NBA has been observed to induce micronucleus formation in DNA of human hepatoma cells (Lamy et al. 2004). The purpose of the current research, which is part of the Advanced Collaborative Emissions Study (ACES), a multidisciplinary program being carried out by the Health Effects Institute and the Coordinating Research Council, is to determine whether improvements in the engineering of heavy-duty diesel engines reduce the oxidative stress and genotoxic risk associated with exposure to DE components. To this end, the genotoxicity and oxidative stress of DE from an improved diesel engine was evaluated in bioassays of tissues from Wistar Han rats and C57BL/6 mice exposed to DE. Genotoxicity was measured as strand breaks using an alkaline-modified comet assay. To correlate possible DNA damage found by the comet assay, measurement of DNA-adduct formation was evaluated by a competitive enzyme-linked immunosorbent assay (ELISA) to determine the levels of free 8-OHdG found in the serum of the animals exposed to DE. 8-OHdG is a specific modified base indicating an oxidative type of DNA damage to DNA nucleotides. In addition, a thiobarbituric acid reactive substances (TBARS) assay was used to assess oxidative stress and damage in the form of lipid peroxidation in the hippocampus region of the brains of DE-exposed animals. Results from the comet assay showed no significant differences in rats between the control and exposed groups (P = 0.53, low exposure; P = 0.92, medium exposure; P = 0.77, high exposure) after 1 month of DE exposure. There were no differences between sexes in the responses of rats to these exposures. Likewise, there were no significant differences found after 3 months of exposure. Similarly, no significant differences were found between the mice exposed for 1 and 3 months to DE, nor were any differences found between sexes. Measurements of 8-OHdG in both mice and rats showed no significant difference among DE exposure groups (P = 0.46, mice; P = 0.86, rats). In mice, measured 8-OHdG was lower in the 3-month group than the 1-month group. In rats, the inverse was true. In mice, no significant differences in the levels of lipid peroxidation, as measured by TBARS, were found between the controls and DE exposure groups (P = 0.92), nor were there any differences between sexes. In","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 166","pages":"163-84"},"PeriodicalIF":0.0,"publicationDate":"2012-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31054084","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":"Impact of the 1990 Hong Kong legislation for restriction on sulfur content in fuel.","authors":"Chit-Ming Wong,&nbsp;Ari Rabl,&nbsp;Thuan Q Thach,&nbsp;Yuen Kwan Chau,&nbsp;King Pan Chan,&nbsp;Benjamin J Cowling,&nbsp;Hak Kan Lai,&nbsp;Tai Hing Lam,&nbsp;Sarah M McGhee,&nbsp;H Ross Anderson,&nbsp;Anthony J Hedley","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Introduction: </strong>After the implementation of a regulation restricting sulfur to 0.5% by weight in fuel on July 1, 1990, in Hong Kong, sulfur dioxide (SO2*) levels fell by 45% on average and as much as 80% in the most polluted districts (Hedley et al. 2002). In addition, a reduction of respiratory symptoms and an improvement in bronchial hyperresponsiveness in children were observed (Peters et al. 1996; Wong et al. 1998). A recent time-series study (Hedley et al. 2002) found an immediate reduction in mortality during the cool season at six months after the intervention, followed by an increase in cool-season mortality in the second and third years, suggesting that the reduction in pollution was associated with a delay in mortality. Proportional changes in mortality trends between the 5-year periods before and after the intervention were measured as relative risks and used to assess gains in life expectancy using the life table method (Hedley et al. 2002). To further explore the relation between changes in pollution-related mortality before and after the intervention, our study had three objectives: (1) to evaluate the short-term effects on mortality of changes in the pollutant mix after the Hong Kong sulfur intervention, particularly with changes in the particulate matter (PM) chemical species; (2) to improve the methodology for assessment of the health impact in terms of changes in life expectancy using linear regression models; and (3) to develop an approach for analyzing changes in life expectancy from Poisson regression models. A fourth overarching objective was to determine the relation between short- and long-term benefits due to an improvement in air quality.</p><p><strong>Methods: </strong>For an assessment of the short-term effects on mortality due to changes in the pollutant mix, we developed Poisson regression Core Models with natural spline smoothers to control for long-term and seasonal confounding variations in the mortality counts and with covariates to adjust for temperature (T) and relative humidity (RH). We assessed the adequacy of the Core Models by evaluating the results against the Akaike Information Criterion, which stipulates that, at a minimum, partial autocorrelation plots should be between -0.1 and 0.1, and by examining the residual plots to make sure they were free from patterns. We assessed the effects for gaseous pollutants (NO2, SO2, and O3), PM with an aerodynamic diameter < or = 10 microm (PM10), and its chemical species (aluminum [Al], iron [Fe], manganese [Mn], nickel [Ni], vanadium [V], lead [Pb], and zinc [Zn]) using the Core Models, which were developed for the periods 5 years (or 2 years in the case of the sensitivity analysis) before and 5 years after the intervention, as well as in the10-year (or 7-year in the case of the sensitivity analysis) period pre- and post-intervention. We also included an indicator to separate the pre- and post-intervention periods, as well as the product of the ind","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 170","pages":"5-91"},"PeriodicalIF":0.0,"publicationDate":"2012-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31159774","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":"Effects of short-term exposure to air pollution on hospital admissions of young children for acute lower respiratory infections in Ho Chi Minh City, Vietnam.","authors":"Truong Giang Le,&nbsp;Long Ngo,&nbsp;Sumi Mehta,&nbsp;Van Dzung Do,&nbsp;T Q Thach,&nbsp;Xuan Dan Vu,&nbsp;Dinh Tuan Nguyen,&nbsp;Aaron Cohen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>There is emerging evidence, largely from studies in Europe and North America, that economic deprivation increases the magnitude of morbidity and mortality related to air pollution. Two major reasons why this may be true are that the poor experience higher levels of exposure to air pollution, and they are more vulnerable to its effects--in other words, due to poorer nutrition, less access to medical care, and other factors, they experience more health impact per unit of exposure. The relations among health, air pollution, and poverty are likely to have important implications for public health and social policy, especially in areas such as the developing countries of Asia where air pollution levels are high and many live in poverty. The aims of this study were to estimate the effect of exposure to air pollution on hospital admissions of young children for acute lower respiratory infection (ALRI*) and to explore whether such effects differed between poor children and other children. ALRI, which comprises pneumonia and bronchiolitis, is the largest single cause of mortality among young children worldwide and is responsible for a substantial burden of disease among young children in developing countries. To the best of our knowledge, this is the first study of the health effects of air pollution in Ho Chi Minh City (HCMC), Vietnam. For these reasons, the results of this study have the potential to make an important contribution to the growing literature on the health effects of air pollution in Asia. The study focused on the short-term effects of daily average exposure to air pollutants on hospital admissions of children less than 5 years of age for ALRI, defined as pneumonia or bronchiolitis, in HCMC during 2003, 2004, and 2005. Admissions data were obtained from computerized records of Children's Hospital 1 and Children's Hospital 2 (CH1 and CH2) in HCMC. Nearly all children hospitalized for respiratory illnesses in the city are admitted to one of these two pediatric hospitals. Daily citywide 24-hour average concentrations of particulate matter (PM) < or =10 microm in aerodynamic diameter (PM10), nitrogen dioxide (NO2), and sulfur dioxide (SO2) and 8-hour maximum average concentrations of ozone (O3) were estimated from the HCMC Environmental Protection Agency (HEPA) ambient air quality monitoring network. Daily meteorologic information including temperature and relative humidity were collected from KTTV NB, the Southern Regional Hydro-Meteorological Center. An individual-level indicator of socioeconomic position (SEP) was based on the degree to which the patient was exempt from payment according to hospital financial records. A group-level indicator of SEP was based on estimates of poverty prevalence in the districts of HCMC in 2004, obtained from a poverty mapping project of the Institute of Economic Research in HCMC, in collaboration with the General Statistics Office of Vietnam and the World Bank. Poverty prevalence was defined using the po","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 169","pages":"5-72; discussion 73-83"},"PeriodicalIF":0.0,"publicationDate":"2012-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30801669","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":"Assessment and statistical modeling of the relationship between remotely sensed aerosol optical depth and PM2.5 in the eastern United States.","authors":"Christopher J Paciorek,&nbsp;Yang Liu","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Research in scientific, public health, and policy disciplines relating to the environment increasingly makes use of high-dimensional remote sensing and the output of numerical models in conjunction with traditional observations. Given the public health and resultant public policy implications of the potential health effects of particulate matter (PM*) air pollution, specifically fine PM with an aerodynamic diameter < or = 2.5 pm (PM2.5), there has been substantial recent interest in the use of remote-sensing information, in particular aerosol optical depth (AOD) retrieved from satellites, to help characterize variability in ground-level PM2.5 concentrations in space and time. While the United States and some other developed countries have extensive PM monitoring networks, gaps in data across space and time necessarily occur; the hope is that remote sensing can help fill these gaps. In this report, we are particularly interested in using remote-sensing data to inform estimates of spatial patterns in ambient PM2.5 concentrations at monthly and longer time scales for use in epidemiologic analyses. However, we also analyzed daily data to better disentangle spatial and temporal relationships. For AOD to be helpful, it needs to add information beyond that available from the monitoring network. For analyses of chronic health effects, it needs to add information about the concentrations of long-term average PM2.5; therefore, filling the spatial gaps is key. Much recent evidence has shown that AOD is correlated with PM2.5 in the eastern United States, but the use of AOD in exposure analysis for epidemiologic work has been rare, in part because discrepancies necessarily exist between satellite-retrieved estimates of AOD, which is an atmospheric-column average, and ground-level PM2.5. In this report, we summarize the results of a number of empirical analyses and of the development of statistical models for the use of proxy information, in particular satellite AOD, in predicting PM2.5 concentrations in the eastern United States. We analyzed the spatiotemporal structure of the relationship between PM2.5 and AOD, first using simple correlations both before and after calibration based on meteorology, as well as large-scale spatial and temporal calibration to account for discrepancies between AOD and PM2.5. We then used both raw and calibrated AOD retrievals in statistical models to predict PM2.5 concentrations, accounting for AOD in two ways: primarily as a separate data source contributing a second likelihood to a Bayesian statistical model, as well as a data source on which we could directly regress. Previous consideration of satellite AOD has largely focused on the National Aeronautics and Space Administration (NASA) moderate resolution imaging spectroradiometer (MODIS) and multiangle imaging spectroradiometer (MISR) instruments. One contribution of our work is more extensive consideration of AOD derived from the Geostationary Operational Environmental","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 167","pages":"5-83; discussion 85-91"},"PeriodicalIF":0.0,"publicationDate":"2012-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30794149","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":"Allergic inflammation in the human lower respiratory tract affected by exposure to diesel exhaust.","authors":"Marc A Riedl,&nbsp;David Diaz-Sanchez,&nbsp;William S Linn,&nbsp;Henry Gong,&nbsp;Kenneth W Clark,&nbsp;Richard M Effros,&nbsp;J Wayne Miller,&nbsp;David R Cocker,&nbsp;Kiros T Berhane","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>To improve understanding of human health risks from exposure to diesel exhaust particles (DEP*), we tested whether immunologic effects previously observed in the human nose also occur in the lower airways. Our overall hypothesis was that cell influx and production of cytokines, chemokines, immunoglobulin E (IgE), and other mediators, which would be measurable in sputum and blood, occur in people with asthma after realistic controlled exposures to diesel exhaust (DE). In Phase 1 we tested for direct effects of DE in subjects with clinically undifferentiated mild asthma. In Phase 2 we tested whether DE exposure would exacerbate response to inhaled cat allergen in subjects with both asthma and cat sensitivity. The exposure facility was a controlled-environment chamber supplied with DE from an idling medium-duty truck with ultra-low-sulfur fuel and no catalytic converter. We exposed volunteers for 2 hours with intermittent exercise to exhaust with DEP mass concentration near 100 microg/m3. Exposures to nitrogen dioxide (NO2) near 0.35 ppm (similar to its concentration in DE) and to filtered air (FA) served as controls. Blood was drawn before exposure on day 1 and again the next morning (day 2). Sputum was induced only on day 2. Bronchial reactivity was measured -1 hour after exposure ended. Supplementary endpoints included measures of blood coagulation status, cardiopulmonary physiology, and symptoms. Each phase employed 15 subjects with asthma; 3 subjects participated in both phases. In Phase 1, airway reactivity was measured with inhaled methacholine; in Phase 2, with inhaled cat allergen. We found little biologic response to DE exposure compared with exposure to control atmospheres. In Phase 1, interleukin 4 (IL-4) in sputum showed an estimated 1.7-fold increase attributable to DE exposure, which was close to statistical significance; airway resistance increased modestly but significantly on day 2 after DE exposure; and nonspecific symptom scores increased significantly during DE exposure. In Phase 2, indicators of airway inflammation in sputum showed a possibly meaningful response: polymorphonuclear leukocytes (PMNs) and eosinophils increased after DE exposure, whereas macrophages decreased. IgE in sputum and the bronchoconstrictive response to cat allergen varied significantly between atmospheres, but not in patterns consistent with our primary hypothesis. Symptom score changes relatable to DE exposure were smaller than those in Phase 1 and not statistically significant. Controlled exposures, lasting 2 hours with intermittent exercise, to diluted DE at a particle mass concentration of 100 microg/m3 did not evoke clear and consistent lower-airway or systemic immunologic or inflammatory responses in mildly asthmatic subjects, with or without accompanying challenge with cat allergen. Likewise, these DE exposures did not significantly increase nonspecific or allergen-specific bronchial reactivity. A few isolated statistically significant or ne","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 165","pages":"5-43; discussion 45-64"},"PeriodicalIF":0.0,"publicationDate":"2012-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30803708","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}