Research report (Health Effects Institute)最新文献

{"title":"Assessment of the health impacts of particulate matter characteristics.","authors":"Michelle L Bell","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>While numerous studies have demonstrated that shortterm exposure to particulate matter (PM*) is associated with adverse health effects, the characteristics of PM that cause harm are not well understood, and PM toxicity may vary by its chemical composition. This study investigates whether spatial and temporal patterns in PM health effect estimates based on total mass can be explained by spatial and temporal heterogeneity in the chemical composition of the particles. A database of 52 chemical components of PM with an aerodynamic diameter < or = 2.5 pm (PM2.5) was constructed for 187 U.S. counties, for 2000 through 2005, based on data from U.S. Environmental Protection Agency (U.S. EPA) monitoring networks. Components that covary with PM2.5 total mass and/or are large contributors to PM2.5, total mass were identified using actual and seasonally detrended data. Using Bayesian hierarchical modeling, seasonal and temporal variation in PM2.5 and the risk of total, cardiovascular, and respiratory hospital admissions were investigated for persons > or = 65 years in 202 U.S. counties for 1999 through 2005. Seasonal variation was investigated using three model structures with different underlying assumptions about the relationship between PM2.5 and hospitalizations. The findings of this study indicate higher effects in winter for both causes of hospitalization, and higher effects in the Northeast for cardiovascular admissions, although 53% of the counties were in this region. Higher PM2.5 effect estimates for cardiovascular or respiratory hospitalizations were observed in seasons and counties with a higher PM2.5 content of nickel (Ni), vanadium (V), or EC. Mortality effect estimates for PM with an aerodynamic diameter < or = 10 pm (PM10) were higher in seasons and counties with higher PM2.5 Ni content. The association between the Ni content of PM2.5 and effect estimates for cardiovascular hospitalization was robust to adjustment by EC, V, or both EC and V. An interquartile range (IQR) increase in the fraction of PM2.5 that is Ni was associated with a 14.9% (PI, 3.4-26.4) increase in the relative rates of cardiovascular hospital admissions associated with PM2.5 total mass adjusted for EC and V. No associations were observed between PM total mass health effect estimates and community-level variables for socioeconomic status, racial composition, or urbanicity. Communities with a higher prevalence of central AC had lower PM2.5 effect estimates for cardiovascular hospital admissions. The findings of this study indicate strong spatial and temporal variation in the chemical composition of the particle mixture and in the regional and seasonal variation in health effect estimates for PM2.5 total mass. The chemical composition of particles partially explained the heterogeneity of effect estimates. Observed associations could be related to the components themselves, to other components, or to a combination of components that share similar sources. The findings d","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 161","pages":"5-38"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40142961","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":"Assessing the impact of a wood stove replacement program on air quality and children's health.","authors":"Curtis W Noonan,&nbsp;Tony J Ward,&nbsp;William Navidi,&nbsp;Lianne Sheppard,&nbsp;Megan Bergauff,&nbsp;Chris Palmer","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Many rural mountain valley communities experience elevated ambient levels of fine particulate matter (PM*) in the winter, because of contributions from residential wood-burning appliances and sustained temperature inversion periods during the cold season. A wood stove change-out program was implemented in a community heavily affected by wood-smoke-derived PM2.5 (PM < or = 2.5 microm in aerodynamic diameter). The objectives of this study were to evaluate the impact of this intervention program on ambient and indoor PM2.5 concentrations and to identify possible corresponding changes in the frequency of childhood respiratory symptoms and infections and illness-related school absences. Over 1100 old wood stoves were replaced with new EPA-certified wood stoves or other heating sources. Ambient PM2.5 concentrations were 30% lower in the winter after the changeout program, compared with baseline winters, which brought the community's ambient air within the PM2.5 standards of the U.S. Environmental Protection Agency (U.S. EPA). The installation of a new wood stove resulted in an overall reduction in indoor PM2.5 concentrations in a small sample of wood-burning homes, but the effects were highly variable across homes. Community-level reductions in wood-smoke-derived PM2.5 concentration were associated with decreased reports of childhood wheeze and of other childhood respiratory health conditions. The association was not limited to children living in homes with wood stoves nor does it appear to be limited to susceptible children (e.g., children with asthma). Community-level reductions in wood-smoke-derived PM2.5 concentration were also associated with lower illness-related school absences among older children, but this finding was not consistent across all age-groups. This community-level intervention provided a unique opportunity to prospectively observe exposure and outcome changes resulting from a targeted air pollution reduction strategy.</p>","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 162","pages":"3-37; discussion 39-47"},"PeriodicalIF":0.0,"publicationDate":"2011-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30803707","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":"Pulmonary particulate matter and systemic microvascular dysfunction.","authors":"Timothy R Nurkiewicz,&nbsp;Dale W Porter,&nbsp;Ann F Hubbs,&nbsp;Samuel Stone,&nbsp;Amy M Moseley,&nbsp;Jared L Cumpston,&nbsp;Adam G Goodwill,&nbsp;Stephanie J Frisbee,&nbsp;Peter L Perrotta,&nbsp;Robert W Brock,&nbsp;Jefferson C Frisbee,&nbsp;Matthew A Boegehold,&nbsp;David G Frazer,&nbsp;Bean T Chen,&nbsp;Vincent Castranova","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Pulmonary particulate matter (PM) exposure has been epidemiologically associated with an increased risk of cardiovascular morbidity and mortality, but the mechanistic foundations for this association are unclear. Exposure to certain types of PM causes changes in the vascular reactivity of several macrovascular segments. However, no studies have focused upon the systemic microcirculation, which is the primary site for the development of peripheral resistance and, typically, the site of origin for numerous pathologies. Ultrafine PM--also referred to as nanoparticles, which are defined as ambient and engineered particles with at least one physical dimension less than 100 nm (Oberdorster et al. 2005)--has been suggested to be more toxic than its larger counterparts by virtue of a larger surface area per unit mass. The purpose of this study was fourfold: (1) determine whether particle size affects the severity of postexposure microvascular dysfunction; (2) characterize alterations in microvascular nitric oxide (NO) production after PM exposure; (3) determine whether alterations in microvascular oxidative stress are associated with NO production, arteriolar dysfunction, or both; and (4) determine whether circulating inflammatory mediators, leukocytes, neurologic mechanisms, or a combination of these play a fundamental role in mediating pulmonary PM exposure and peripheral microvascular dysfunction. To achieve these goals, we created an inhalation chamber that generates stable titanium dioxide (TiO2) aerosols at concentrations up to 20 mg/m3. TiO2 is a well-characterized particle devoid of soluble metals. Sprague Dawley and Fischer 344 (F-344) rats were exposed to fine or nano-TiO2 PM (primary count modes of approximately 710 nm and approximately 100 nm in diameter, respectively) at concentrations of 1.5 to 16 mg/m3 for 4 to 12 hours to produce pulmonary loads of 7 to 150 microg in each rat. Twenty-four hours after pulmonary exposure, the following procedures were performed: the spinotrapezius muscle was prepared for in vivo microscopy, blood samples were taken from an arterial line, and various tissues were harvested for histologic and immunohistochemical analyses. Some rats received a bolus dose of cyclophosphamide 3 days prior to PM exposure to deplete circulating neutrophils and bronchoalveolar lavage (BAL) was performed in separate groups of rats exposed to identical TiO2 loads. No significant differences in BAL fluid composition based on PM size or load were found in these rats. Plasma levels of interleukin (IL)-2, IL-18, IL-13, and growth-related oncogene (GRO) (also known as keratinocyte-derived-chemokine [KC]) were altered after PM exposure. In rats exposed to fine TiO2, endothelium-dependent arteriolar dilation was significantly decreased, and this dysfunction was robustly augmented in rats exposed to nano-TiO2. This effect was not related to an altered smooth-muscle responsiveness to NO because arterioles in both groups dilated comparab","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 164","pages":"3-48"},"PeriodicalIF":0.0,"publicationDate":"2011-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30455120","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":"The London low emission zone baseline study.","authors":"Frank Kelly,&nbsp;Ben Armstrong,&nbsp;Richard Atkinson,&nbsp;H Ross Anderson,&nbsp;Ben Barratt,&nbsp;Sean Beevers,&nbsp;Derek Cook,&nbsp;Dave Green,&nbsp;Dick Derwent,&nbsp;Ian Mudway,&nbsp;Paul Wilkinson","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>On February 4, 2008, the world's largest low emission zone (LEZ) was established. At 2644 km2, the zone encompasses most of Greater London. It restricts the entry of the oldest and most polluting diesel vehicles, including heavy-goods vehicles (haulage trucks), buses and coaches, larger vans, and minibuses. It does not apply to cars or motorcycles. The LEZ scheme will introduce increasingly stringent Euro emissions standards over time. The creation of this zone presented a unique opportunity to estimate the effects of a stepwise reduction in vehicle emissions on air quality and health. Before undertaking such an investigation, robust baseline data were gathered on air quality and the oxidative activity and metal content of particulate matter (PM) from air pollution monitors located in Greater London. In addition, methods were developed for using databases of electronic primary-care records in order to evaluate the zone's health effects. Our study began in 2007, using information about the planned restrictions in an agreed-upon LEZ scenario and year-on-year changes in the vehicle fleet in models to predict air pollution concentrations in London for the years 2005, 2008, and 2010. Based on this detailed emissions and air pollution modeling, the areas in London were then identified that were expected to show the greatest changes in air pollution concentrations and population exposures after the implementation of the LEZ. Using these predictions, the best placement of a pollution monitoring network was determined and the feasibility of evaluating the health effects using electronic primary-care records was assessed. To measure baseline pollutant concentrations before the implementation of the LEZ, a comprehensive monitoring network was established close to major roadways and intersections. Output-difference plots from statistical modeling for 2010 indicated seven key areas likely to experience the greatest change in concentrations of nitrogen dioxide (NO2) (at least 3 microg/m3) and of PM with an aerodynamic diameter < or = 10 microm (PM10) (at least 0.75 microg/m3) as a result of the LEZ; these suggested that the clearest signals of change were most likely to be measured near roadsides. The seven key areas were also likely to be of importance in carrying out a study to assess the health outcomes of an air quality intervention like the LEZ. Of the seven key areas, two already had monitoring sites with a full complement of equipment, four had monitoring sites that required upgrades of existing equipment, and one required a completely new installation. With the upgrades and new installations in place, fully ratified (verified) pollutant data (for PM10, PM with an aerodynamic diameter < or = 2.5 microm [PM2.5], nitrogen oxides [NOx], and ozone [O3] at all sites as well as for particle number, black smoke [BS], carbon monoxide [CO], and sulfur dioxide [SO2] at selected sites) were then collected for analysis. In addition, the seven key monitoring s","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 163","pages":"3-79"},"PeriodicalIF":0.0,"publicationDate":"2011-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30443999","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":"Personal and ambient exposures to air toxics in Camden, New Jersey.","authors":"Paul J Lioy,&nbsp;Zhihua Fan,&nbsp;Junfeng Zhang,&nbsp;Panos Georgopoulos,&nbsp;Sheng-Wei Wang,&nbsp;Pamela Ohman-Strickland,&nbsp;Xiangmei Wu,&nbsp;Xianlei Zhu,&nbsp;Jason Harrington,&nbsp;Xiaogang Tang,&nbsp;Qingyu Meng,&nbsp;Kyung Hwa Jung,&nbsp;Jaymin Kwon,&nbsp;Marta Hernandez,&nbsp;Linda Bonnano,&nbsp;Joann Held,&nbsp;John Neal","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Personal exposures and ambient concentrations of air toxics were characterized in a pollution \"hot spot\" and an urban reference site, both in Camden, New Jersey. The hot spot was the city's Waterfront South neighborhood; the reference site was a neighborhood, about 1 km to the east, around the intersection of Copewood and Davis streets. Using personal exposure measurements, residential ambient air measurements, statistical analyses, and exposure modeling, we examined the impact of local industrial and mobile pollution sources, particularly diesel trucks, on personal exposures and ambient concentrations in the two neighborhoods. Presented in the report are details of our study design, sample and data collection methods, data- and model-analysis approaches, and results and key findings of the study. In summary, 107 participants were recruited from nonsmoking households, including 54 from Waterfront South and 53 from the Copewood-Davis area. Personal air samples were collected for 24 hr and measured for 32 target compounds--11 volatile organic compounds (VOCs*), four aldehydes, 16 polycyclic aromatic hydrocarbons (PAHs), and particulate matter (PM) with an aerodynamic diameter < or = 2.5 microm (PM2.5). Simultaneously with the personal monitoring, ambient concentrations of the target compounds were measured at two fixed monitoring sites, one each in the Waterfront South and Copewood-Davis neighborhoods. To understand the potential impact of local sources of air toxics on personal exposures caused by temporal (weekdays versus weekend days) and seasonal (summer versus winter) variations in source intensities of the air toxics, four measurements were made of each subject, two in summer and two in winter. Within each season, one measurement was made on a weekday and the other on a weekend day. A baseline questionnaire and a time diary with an activity questionnaire were administered to each participant in order to obtain information that could be used to understand personal exposure to specific air toxics measured during each sampling period. Given the number of emission sources of air toxics in Waterfront South, a spatial variation study consisting of three saturation-sampling campaigns was conducted to characterize the spatial distribution of VOCs and aldehydes in the two neighborhoods. Passive samplers were used to collect VOC and aldehyde samples for 24- and 48-hr sampling periods simultaneously at 22 and 16 grid-based sampling sites in Waterfront South and Copewood-Davis, respectively. Results showed that measured ambient concentrations of some target pollutants (mean +/- standard deviation [SD]), such as PM2.5 (31.3 +/- 12.5 microg/m3), toluene (4.24 +/- 5.23 microg/m3), and benzo[a]pyrene (0.36 +/- 0.45 ng/m3), were significantly higher (P < 0.05) in Waterfront South than in Copewood-Davis, where the concentrations of PM2.5, toluene, and benzo[a]pyrene were 25.3 +/- 11.9 microg/m3, 2.46 +/- 3.19 microg/m3, and 0.21 +/- 0.26 ng/m3, respectiv","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 160","pages":"3-127; discussion 129-51"},"PeriodicalIF":0.0,"publicationDate":"2011-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30120776","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":"Air toxics exposure from vehicle emissions at a U.S. border crossing: Buffalo Peace Bridge Study.","authors":"John Spengler, Jamson Lwebuga-Mukasa, Jose Vallarino, Steve Melly, Steve Chillrud, Joel Baker, Taeko Minegishi","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The Peace Bridge in Buffalo, New York, which spans the Niagara River at the east end of Lake Erie, is one of the busiest U.S. border crossings. The Peace Bridge plaza on the U.S. side is a complex of roads, customs inspection areas, passport control areas, and duty-free shops. On average 5000 heavy-duty diesel trucks and 20,000 passenger cars traverse the border daily, making the plaza area a potential \"hot spot\" for emissions from mobile sources. In a series of winter and summer field campaigns, we measured air pollutants, including many compounds considered by the U.S. Environmental Protection Agency (EPA*) as mobile-source air toxics (MSATs), at three fixed sampling sites: on the shore of Lake Erie, approximately 500 m upwind (under predominant wind conditions) of the Peace Bridge plaza; immediately downwind of (adjacent to) the plaza; and 500 m farther downwind, into the community of west Buffalo. Pollutants sampled were particulate matter (PM) < or = 10 microm (PM10) and < or = 2.5 microm (PM2.5) in aerodynamic diameter, elemental carbon (EC), 28 elements, 25 volatile organic compounds (VOCs) including 3 carbonyls, 52 polycyclic aromatic hydrocarbons (PAHs), and 29 nitrogenated polycyclic aromatic hydrocarbons (NPAHs). Spatial patterns of counts of ultrafine particles (UFPs, particles < 0.1 microm in aerodynamic diameter) and of particle-bound PAH (pPAH) concentrations were assessed by mobile monitoring in the neighborhood adjacent to the Peace Bridge plaza using portable instruments and Global Positioning System (GPS) tracking. The study was designed to assess differences in upwind and downwind concentrations of MSATs, in areas near the Peace Bridge plaza on the U.S. side of the border. The Buffalo Peace Bridge Study featured good access to monitoring locations proximate to the plaza and in the community, which are downwind with the dominant winds from the direction of Lake Erie and southern Ontario. Samples from the lakeside Great Lakes Center (GLC), which is upwind of the plaza with dominant winds, were used to characterize contaminants in regional air masses. On-site meteorologic measurements and hourly truck and car counts were used to assess the role of traffic on UFP counts and pPAH concentrations. The array of parallel and perpendicular residential streets adjacent to the plaza provided a grid on which to plot the spatial patterns of UFP counts and pPAH concentrations to determine the extent to which traffic emissions from the Peace Bridge plaza might extend into the neighboring community. For lake-wind conditions (southwest to northwest) 12-hour integrated daytime samples showed clear evidence that vehicle-related emissions at the Peace Bridge plaza were responsible for elevated downwind concentrations of PM2.5, EC, and benzene, toluene, ethylbenzene, and xylenes (BTEX), as well as 1,3-butadiene and styrene. The chlorinated VOCs and aldehydes were not differentially higher at the downwind site. Several metals (aluminum, calciu","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 158","pages":"5-132"},"PeriodicalIF":0.0,"publicationDate":"2011-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8941851/pdf/nihms-1780888.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30137799","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":"Role of neprilysin in airway inflammation induced by diesel exhaust emissions.","authors":"Simon S Wong,&nbsp;Nina N Sun,&nbsp;Cynthia D Fastje,&nbsp;Mark L Witten,&nbsp;R Clark Lantz,&nbsp;Bao Lu,&nbsp;Duane L Sherrill,&nbsp;Craig J Gerard,&nbsp;Jefferey L Burgess","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In this study, we examined the role of neprilysin (NEP), a key membrane-bound endopeptidase, in the inflammatory response induced by diesel exhaust emissions (DEE) in the airways through a number of approaches: in vitro, animal, and controlled human exposure. Our specific aims were (1) to examine the role of NEP in inflammatory injury induced by diesel exhaust particles (DEP) using Nep-intact (wild-type) and Nep-null mice; (2) to examine which components of DEP are associated with NEP downregulation in vitro; (3) to determine the molecular impact of DEP exposure and decreased NEP expression on airway epithelial cells' gene expression in vitro, using a combination of RNA interference (RNAi) and microarray approaches; and (4) to evaluate the effects on NEP activity of human exposure to DEE. We report four main results: First, we found that exposure of normal mice to DEP consisting of standard reference material (SRM) 2975 via intratracheal installation can downregulate NEP expression in a concentration-dependent manner. The changes were accompanied by increases in the number of macrophages and epithelial cells, as well as proinflammatory cytokines, examined in bronchoalveolar lavage (BAL) fluid and cells. Nep-null mice displayed increased and/or additional inflammatory responses when compared with wild-type mice, especially in response to exposure to the higher dose of DEP that we used. These in vivo findings suggest that loss of NEP in mice could cause increased susceptibility to injury or exacerbate inflammatory responses after DEP exposure via release of specific cytokines from the lungs. Second, we found evidence, using in vitro studies, that downregulation of NEP by DEP in cultured human epithelial BEAS-2B cells was mostly attributable to DEP-adsorbed organic compounds, whereas the carbonaceous core and transition metal components of DEP had little or no effect on NEP messenger RNA (mRNA) expression. This NEP downregulation was not a specific response to DEP or its contents because the change also occurred after exposure to urban dust (SRM 1649a), which differs in physical and chemical composition from DEP. Third, we also collected the transcriptome profiles of the concentration-effects of SRM 2975 in cultured BEAS-2B cells through a 2 X 3 factorial design. DEP exposure upregulated 151 genes and downregulated 59 genes. Cells with decreased NEP expression (accomplished by transfecting an NEP-specific small interfering RNA [siRNA]) substantially altered the expression of genes (upregulating 17 and downregulating 14) associated with DNA/protein binding, calcium channel activities, and the cascade of intracellular signaling by cytokines. Data generated from the combined RNAi and microarray approaches revealed that there is a complex molecular cascade mediated by NEP in different subcellular compartments, possibly influencing the inflammatory response. Fourth, in a controlled human exposure study, we observed significant increases in soluble ","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 159","pages":"3-40"},"PeriodicalIF":0.0,"publicationDate":"2011-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4751866/pdf/nihms441201.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30107206","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 impact of the congestion charging scheme on air quality in London. Part 2. Analysis of the oxidative potential of particulate matter.","authors":"Frank Kelly,&nbsp;H Ross Anderson,&nbsp;Ben Armstrong,&nbsp;Richard Atkinson,&nbsp;Ben Barratt,&nbsp;Sean Beevers,&nbsp;Dick Derwent,&nbsp;David Green,&nbsp;Ian Mudway,&nbsp;Paul Wilkinson","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>There is growing scientific consensus that the ability of inhaled particulate matter (PM*) to elicit oxidative stress both at the air-lung interface and systemically might underpin many of the acute and chronic respiratory and cardiovascular responses observed in exposed populations. In the current study (which is part two of a two-part HEI study of a congestion charging scheme [CCS] introduced in London, United Kingdom, in 2003), we tested the hypothesis that the reduction in vehicle numbers and changes in traffic composition resulting from the introduction of the CCS would result in decreased concentrations of traffic-specific emissions, both from vehicle exhaust and other sources (brake wear and tire wear), and an associated reduction in the oxidative potential of PM with an aerodynamic diameter < or = 10 microm (PM10). To test this hypothesis, we obtained, extracted, and analyzed tapered element oscillating microbalance (TEOM) PM10 filters from six monitoring sites within, bordering, or outside the area of the congestion charging zone (CCZ) for the 3 years before and after the introduction of the scheme. In addition, from January 2005, TEOM PM10 filters were obtained from an additional 10 sites outside the zone in order to perform the first-ever assessment of within-city spatial variability in the oxidative potential of PM10. Although London's PM10 was found to have remarkably high oxidative potential, it varied markedly between the studied sites, with evidence of increased potential at roadside locations compared with urban background locations. This difference appeared to reflect increased concentrations of copper (Cu), barium (Ba), and bioavailable iron (Fe) in PM10 collected at the roadside sites. PM10's oxidative potential after the introduction of the CCS did not change at the one urban background site within the zone. Yet compositional changes in PM10 were noted at the same site, including significant decreases in Cu and zinc (Zn) content, probably reflecting brake and tire wear (compared with increases in these metals at all sites outside the zone in the 3 years since the scheme's introduction). This pattern of results is consistent with observations of increased vehicle use throughout London in recent years and decreases in the number of vehicles entering the zone since the scheme's introduction.</p>","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 155","pages":"73-144"},"PeriodicalIF":0.0,"publicationDate":"2011-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29923424","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":"The impact of the congestion charging scheme on air quality in London. Part 1. Emissions modeling and analysis of air pollution measurements.","authors":"Frank Kelly,&nbsp;H Ross Anderson,&nbsp;Ben Armstrong,&nbsp;Richard Atkinson,&nbsp;Ben Barratt,&nbsp;Sean Beevers,&nbsp;Dick Derwent,&nbsp;David Green,&nbsp;Ian Mudway,&nbsp;Paul Wilkinson","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>On February 17, 2003, a congestion charging scheme (CCS*) was introduced in central London along with a program of traffic management measures. The scheme operated Monday through Friday, 7 AM to 6 PM. This program resulted in an 18% reduction in traffic volume and a 30% reduction in traffic congestion in the first year (2003). We developed methods to evaluate the possible effects of the scheme on air quality: We used a temporal-spatial design in which modeled and measured air quality data from roadside and background monitoring stations were used to compare time periods before (2001-2002) and after (2003-2004) the CCS was introduced and to compare the spatial area of the congestion charging zone (CCZ) with the rest of London. In the first part of this project, we modeled changes in concentrations of oxides of nitrogen (NOx), nitrogen dioxide (NO2), and PM10 (particles with a mass median aerodynamic diameter < or = 10 microm) across the CCZ and in Greater London under different traffic and emission scenarios for the periods before and after CCS introduction. Comparing model results within and outside the zone suggested that introducing the CCS would be associated with a net 0.8-microg/m3 decrease in the mean concentration of PM10 and a net 1.7-ppb decrease in the mean concentration of NOx within the CCZ. In contrast, a net 0.3-ppb increase in the mean concentration of NO2 was predicted within the zone; this was partly explained by an expected increase in primary NO2 emissions due to the introduction of particle traps on diesel buses (one part of the improvements in public transport associated with the CCS). In the second part of the project, we established a CCS Study Database from measurements obtained from the London Air Quality Network (LAQN) for air pollution monitors sited to measure roadside and urban background concentrations. Fully ratified (validated) 15-minute mean carbon monoxide (CO), nitric oxide (NO), NO2, NOx, PM10, and PM2.5 data from each chosen monitoring site for the period from February 17, 2001, to February 16, 2005, were transferred from the LAQN database. In the third part of our project, these data were used to compare geometric means for the 2 years before and the 2 years after the CCS was introduced. Temporal changes within the CCZ were compared with changes, over the same period, at similarly sited (roadside or background) monitors in a control area 8 km distant from the center of the CCZ. The analysis was confined to measurements obtained during the hours and days on which the scheme was in operation and focused on pollutants derived from vehicles (NO, NO2, NOx, PM10, and CO). This set of analyses was based on the limited data available from within the CCZ. When compared with data from outside the zone, we did not find evidence of temporal changes in roadside measurements of NOx, NO, and NO2, nor in urban background concentrations of NOx. (The latter result, however, concealed divergent trends in NO, which fell, a","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 155","pages":"5-71"},"PeriodicalIF":0.0,"publicationDate":"2011-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29923423","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. Short-term effects of air pollution on mortality: results from a time-series analysis in Chennai, India.","authors":"Kalpana Balakrishnan,&nbsp;Bhaswati Ganguli,&nbsp;Santu Ghosh,&nbsp;S Sankar,&nbsp;Vijaylakshmi Thanasekaraan,&nbsp;V N Rayudu,&nbsp;Harry Caussy","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This report describes the results of a time-series analysis of the effect of short-term exposure to particulate matter with an aerodynamic diameter < or = 10 pm (PM10) on mortality in metropolitan Chennai, India (formerly Madras). This was one of three sites in India chosen by HEI as part of its Public Health and Air Pollution in Asia (PAPA) initiative. The study involved integration and analysis of retrospective data for the years 2002 through 2004. The data were obtained from relevant government agencies in charge of routine data collection. Data on meteorologic confounders (including temperature, relative humidity, and dew point) were available on all days of the study period. Data on mortality were also available on all days, but information on cause-of-death (including accidental deaths) could not be reliably ascertained. Hence, only all-cause daily mortality was used as the major outcome for the time-series analyses. Data on PM10, nitrogen dioxide (NO2), and sulfur dioxide (SO2) were limited to a much smaller number of days, but spanned the full study period. Data limitations resulting from low sensitivity of gaseous pollutant measurements led to using only PM10 in the main analysis. Of the eight operational ambient air quality monitor (AQM) stations in the city, seven met the selection criteria set forth in the common protocol developed for the three PAPA studies in India. In addition, all raw data used in the analysis were subjected to additional quality assurance (QA) and quality control (QC) criteria to ensure the validity of the measurements. Two salient features of the PM10 data set in Chennai were a high percentage of missing readings and a low correlation among daily data recorded by the AQMs. The latter resulted partly because each AQM had a small footprint (approximate area over which the air pollutant measurements recorded in the AQM are considered valid), and partly because of differences in source profiles among the 10 zones within the city. The zones were defined by the Chennai Corporation based on population density. Alternative exposure series were developed to control for these data features. We first developed exposure series based on data from single AQMs and multiple AQMs. Because neither was found to satisfactorily represent population exposures, we subsequently developed an exposure series that disaggregated pollutant data to individual zones within the city boundary. The zonal series, despite some uncertainties, was found to best represent population exposures among other available choices. The core model was thus a zonal model developed using disaggregated mortality and pollutant data from individual zones. We used quasi-Poisson generalized additive models (GAMs) with smooth functions of time, temperature, and relative humidity modeled using penalized splines. The degrees of freedom (df) for these confounders were selected to maximize the precision with which the relative risk for PM10 was estimated. This is a ","PeriodicalId":74687,"journal":{"name":"Research report (Health Effects Institute)","volume":" 157","pages":"7-44"},"PeriodicalIF":0.0,"publicationDate":"2011-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29919328","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}