Abstract  The goal of this study is to describe linkages between the National Health Interview Survey (NHIS) and Environmental Protection Agency (EPA) air monitoring data, specifically how the linkage method affects characteristics and exposure estimates of study samples and estimated associations between exposure and health. In the USA, nationally representative health data are collected in the NHIS and annual air quality data are collected by the EPA. The linkage of these data for research is not straightforward and the choices made may introduce bias into results. The 2000-2003 NHIS and air quality data for six air pollutants were linked by residential block group and monitor location, which differ by pollutants. For each pollutant, three annual exposure variables were assigned to respondents: (1) average of all monitors in the county, (2) of monitors within a 5-mile radius of the distance between block group and monitor, and (3) within a 20-mile radius. Exposure estimates, study sample characteristics, and association between fine particle exposure and respondent-reported health status were compared for different geographic linkage methods. The results showed that study sample characteristics varied by geographic linkage method and pollutant linked. Generally, the fewer the NHIS respondents linked, the higher is the pollution exposure and lower is the percentage of non-Hispanic whites. After adjustment for sociodemographic and geographic factors, associations between fine particles and health status were generally comparable across study samples. Because exposure information is not available for all potential participants in an epidemiological study, selection effects should be considered when drawing inferences about air quality-health associations. With the current monitoring data system, the study sample is substantially reduced when linkage to multiple pollutants is performed.

Abstract  Background: A number of studies have shown associations between chronic exposure to particulate air pollution and increased mortality, particularly from cardiovascular disease, but fewer studies have examined the association between long-term exposure to fine particulate air pollution and specific cardiovascular events, such as acute myocardial infarction (AMI).
 Objective: We examined how long-term exposure to area particulate matter affects the onset of AMI, and we distinguished between area and local pollutants.
 Methods: Building on the Worcester Heart Attack Study, an ongoing community-wide investigation examining changes over time in myocardial infarction incidence in greater Worcester, Massachusetts, we conducted a case–control study of 4,467 confirmed cases of AMI diagnosed between 1995 and 2003 and 9,072 matched controls selected from Massachusetts resident lists. We used a prediction model based on satellite aerosol optical depth (AOD) measurements to generate both exposure to particulate matter ≤ 2.5 μm in diameter (PM2.5) at the area level (10 × 10 km) and the local level (100 m) based on local land use variables. We then examined the association between area and local particulate pollution and occurrence of AMI.
 Results: An interquartile range (IQR) increase in area PM2.5 (0.59 μg/m3) was associated with a 16% increase in the odds of AMI (95% CI: 1.04, 1.29). An IQR increase in total PM2.5 (area + local, 1.05 μg/m3) was weakly associated with a 4% increase in the odds of AMI (95% CI: 0.96, 1.11).
 Conclusions: Residential exposure to PM2.5 may best be represented by a combination of area and local PM2.5, and it is important to consider spatial gradients within a single metropolitan area when examining the relationship between particulate matter exposure and cardiovascular events.


Abstract  This study was undertaken to determine whether there was a correlation between fine particle (PM2.5) levels and hospital admissions for hemorrhagic stroke (HS) in Taipei, Taiwan. Hospital admissions for HS and ambient air pollution data for Taipei were obtained for the period 2006-2010. The relative risk of hospital admissions was estimated using a case-crossover approach, controlling for weather variables, day of the week, seasonality, and long-term time trends. For the single-pollutant model (without adjustment for other pollutants), increased HS admissions were significantly associated with PM2.5 levels both on warm days (>23°C) and cool days (<23°C), with an interquartile range rise associated with a 12% (95% CI = 7-18%) and 4% (95% CI = 0-8%) elevation in admissions for HS, respectively. In the two-pollutant models, PM2.5 remained significantly high after inclusion of SO2 or O3 on both warm and cool days. This study provides evidence that higher levels of PM2.5 increase the risk of hospital admissions for HS.

Abstract  Abstract This study was undertaken to determine whether there was an association between fine particles (PM2.5) levels and hospital admissions for congestive heart failure (CHF) in Taipei, Taiwan. Hospital admissions for CHF and ambient air pollution data for Taipei were obtained for the period 2006-2010. The relative risk of hospital admissions was estimated using a case-crossover approach, controlling for weather variables, day of the week, seasonality and long-term time trends. For the single pollutant model (without adjustment for other pollutants), increased CHF admissions were significantly associated with PM2.5 both on warm days (>23 °C) and cool days (<23 °C), with an interquartile range increase associated with a 13% (95% CI = 9-17%) and 3% (95% CI = 0-7%) increase in CHF admissions, respectively. In the two-pollutant models, PM2.5 remained significant after the inclusion of SO2 or O3 both on warm and cool days. This study provides evidence that higher levels of PM2.5 increase the risk of hospital admissions for CHF.

Abstract  Epidemiological studies have observed between city heterogeneity in PM2.5-mortality risk estimates. These differences could potentially be due to the use of central-site monitors as a surrogate for exposure which do not account for an individual's activities or ambient pollutant infiltration to the indoor environment. Therefore, relying solely on central-site monitoring data introduces exposure error in the epidemiological analysis. The amount of exposure error produced by using the central-site monitoring data may differ by city. The objective of this analysis was to cluster cities with similar exposure distributions based on residential infiltration and in-vehicle commuting characteristics. Factors related to residential infiltration and commuting were developed from the American Housing Survey (AHS) from 2001 to 2005 for 94 Core-Based Statistical Areas (CBSAs). We conducted two separate cluster analyses using a k-means clustering algorithm to cluster CBSAs based on these factors. The first only included residential infiltration factors (i.e. percent of homes with central air conditioning (AC) mean year home was built, and mean home size) while the second incorporated both infiltration and commuting (i.e. mean in-vehicle commuting time and mean in-vehicle commuting distance) factors. Clustering on residential infiltration factors resulted in 5 clusters, with two having distinct exposure distributions. Cluster 1 consisted of cities with older, smaller homes with less central AC while homes in Cluster 2 cities were newer, larger, and more likely to have central AC. Including commuting factors resulted in 10 clusters. Clusters with shorter in-vehicle commuting times had shorter in-vehicle commuting distances. Cities with newer homes also tended to have longer commuting times and distances. This is the first study to employ cluster analysis to group cities based on exposure factors. Identifying cities with similar exposure distributions may help explain city-to-city heterogeneity in PM2.5 mortality risk estimates.

Abstract  There are no reported studies on the effects of ambient air pollution on emergency department (ED) attendances in Sydney, Australia. This study aimed to determine associations between ambient air pollutants and ED attendances for cardiovascular disease (CVD) in those aged 65+ years. We constructed daily time series of hospital ED attendances, air pollutants and meteorological factors for the Sydney metropolitan area from 1 January 1997 to 31 December 2001. We used generalised linear models to determine associations between daily air pollution and daily ED attendances and controlled for the effects of long-term trends, seasonality, weather and other potential confounders. Increased ED attendances for all CVD, cardiac disease and ischaemic heart disease were seen with 24-h particulate pollution, 1-h NO(2), 8-h CO and 24-h SO(2). Air pollutants were associated with decreased ED attendances for stroke. The effects of air pollutants on CVD, cardiac disease and stroke attendances were generally greater in the cool period compared to the warm period. The single-pollutant effects of CO, O(3), NO(2) and SO(2) were essentially unchanged in two-pollutant models. Although air pollution levels in Sydney are relatively low compared to similar cities, we have demonstrated associations between ambient air pollutants and ED attendances for CVD in people aged 65+ years. Our study adds to the growing evidence for the effects of ambient air pollution on CVD outcomes even at relatively low ambient concentrations.

Abstract  RATIONALE: Several studies have linked long-term exposure to particulate air pollution with increased cardiopulmonary mortality; only two have also examined incident circulatory disease. OBJECTIVES: To examine associations of individualized long-term exposures to particulate and gaseous air pollution with incident myocardial infarction (MI) and stroke, as well as all-cause and cause-specific mortality. METHODS: We estimated long-term residential air pollution exposure for over 100,000 participants in the California Teachers Study, a prospective cohort of female public school professionals. We linked geocoded residential addresses with inverse distance-weighted monthly pollutant surfaces for two measures of particulate matter and for several gaseous pollutants. We examined associations between exposure to these pollutants and risks of incident MI and stroke, and of all-cause and cause-specific mortality, using Cox proportional hazards models. MEASUREMENTS AND MAIN RESULTS: We found elevated hazard ratios linking long-term exposure to fine particulate matter (PM2.5, scaled to an increment of 10 µg/m3) with mortality from ischemic heart disease (IHD) (1.20, 95% C.I. 1.02-1.41) and, particularly among post-menopausal women, incident stroke (1.19, 95% C.I. 1.02-1.38). Long-term exposure to particulate matter less than 10 µm aerodynamic diameter (PM10) was associated with elevated risks for IHD mortality (1.06, 95% C.I. 0.99-1.14) and incident stroke 1.06 (95% CI: 1.00-1.13), while nitrogen oxides were associated with elevated risks for cardiovascular as well as IHD mortality. CONCLUSIONS: Long-term exposures to PM2.5 and PM10 were associated with increased risks of incident stroke and death from IHD; exposures to nitrogen oxides were associated with all cardiovascular as well as IHD mortality.

Abstract  BACKGROUND: Epidemiologic studies have demonstrated that exposure to road traffic is associated with adverse cardiovascular outcomes. OBJECTIVES: To identify specific traffic-related air pollutants that are associated with the risk of coronary heart disease (CHD) morbidity and mortality to support evidence-based environmental policy making. METHODS: This population-based cohort study included a 5-year exposure period and a 4-year follow-up period. All residents aged 45-85 years who resided in Metropolitan Vancouver during the exposure period and without known CHD at baseline were included in this study (n = 452,735). Individual exposures to traffic-related air pollutants including black carbon, fine particles (aerodynamic diameter ≤2.5 µm; PM2.5), NO2, and NO were estimated at subjects' residences using land use regression models and integrating changes in residences during the exposure period. CHD hospitalizations and deaths during the follow-up period were identified from provincial hospitalization and death registration records. RESULTS: An interquartile range elevation in the average concentration of black carbon (0.94×10-5/m filter absorbance, equivalent to approximately 0.75 µg/m3 elemental carbon) was associated with a 3% increase in CHD hospitalization (95% confidence interval, 1-5%) and a 6% increase in CHD mortality (3-9%) after adjustment for age, sex, preexisting comorbidity, neighborhood socioeconomic status, and co-pollutants (PM2.5 and NO2). There were clear linear exposure-response relationships between black carbon and coronary events. CONCLUSIONS: Long-term exposure to traffic-related fine particulate air pollution, indicated by black carbon, may partly explain the observed associations between exposure to road traffic and adverse cardiovascular outcomes.

Abstract  BACKGROUND: Short-term changes in levels of fine ambient particulate matter (PM2.5) may increase the risk of acute ischemic stroke; however, results from prior studies have been inconsistent. We examined this hypothesis using data from a multicenter prospective stroke registry. METHODS: We analyzed data from 9202 patients hospitalized with acute ischemic stroke, having a documented date and time of stroke onset, and residing within 50 km of a PM2.5 monitor in 8 cities in Ontario, Canada. We evaluated the risk of ischemic stroke onset associated with PM2.5 in each city using a time-stratified case-crossover design, matching on day of week and time of day. We then combined these city-specific estimates using random-effects meta-analysis techniques. We examined whether the effects of PM2.5 differed across strata defined by patient characteristics and ischemic stroke etiology. RESULTS: Overall, PM2.5 was associated with a -0.7% change in ischemic stroke risk per 10-μg/m increase in PM2.5 (95% confidence interval = -6.3% to 5.1%). These overall negative results were robust to a number of sensitivity analyses. Among patients with diabetes mellitus, PM2.5 was associated with an 11% increase in ischemic stroke risk (1% to 22%). The association between PM2.5 and ischemic stroke risk varied according to stroke etiology, with the strongest associations observed for strokes due to large-artery atherosclerosis and small-vessel occlusion. CONCLUSIONS: These results do not support the hypothesis that short-term increases in PM2.5 levels are associated with ischemic stroke risk overall. However, specific patient subgroups may be at increased risk of particulate-related ischemic strokes.

Abstract  I used generalized additive models to analyze the time series of daily total nonaccidental deaths and deaths due to vascular disease over the period 1987-1995 in two major metropolitan areas, Cook County, Illinois, and Los Angeles County, California, in the United States. In both counties I had monitoring information on PM10, CO, SO2, NO2, and O3. In Los Angeles, monitoring information on PM2.5 was available as well. In addition to full-year analyses, I performed season-specific analyses. I present the results of both single- and multipollutant analyses. Although components of air pollution were associated with total nonaccidental and vascular disease mortality in both counties, the results indicate considerable heterogeneity of these associations in the two locations and also from season to season. In Los Angeles County, the gases, particularly CO and SO2 but not ozone, were more strongly associated with mortality than was particulate matter, which exhibited only weak and inconsistent associations with both mortality endpoints. Both PM10 and the gases were associated with total and vascular disease mortality in Cook County. The association of the gases with both mortality endpoints appeared to be stronger and more robust than that of PM10. Exposure-response analyses using flexible smoothers showed significant departures from linearity, particularly for PM effects.

Abstract  BACKGROUND: Relatively few studies have been conducted of the association between air pollution and emergency department (ED) visits, and most of these have been based on a small number of visits, for a limited number of health conditions and pollutants, and only daily measures of exposure and response. METHODS: A time-series analysis was conducted on nearly 400,000 ED visits to 14 hospitals in seven Canadian cities during the 1990 s and early 2000s. Associations were examined between carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), sulfur dioxide (SO2), and particulate matter (PM 10 and PM2.5), and visits for angina/myocardial infarction, heart failure, dysrhythmia/conduction disturbance, asthma, chronic obstructive pulmonary disease (COPD), and respiratory infections. Daily and 3-hourly visit counts were modeled as quasi-Poisson and analyses controlled for effects of temporal cycles, weather, day of week and holidays. RESULTS: 24-hour average concentrations of CO and NO2 lag 0 days exhibited the most consistent associations with cardiac conditions (2.1% (95% CI, 0.0-4.2%) and 2.6% (95% CI, 0.2-5.0%) increase in visits for myocardial infarction/angina per 0.7 ppm CO and 18.4 ppb NO2 respectively; 3.8% (95% CI, 0.7-6.9%) and 4.7% (95% CI, 1.2-8.4%) increase in visits for heart failure). Ozone (lag 2 days) was most consistently associated with respiratory visits (3.2% (95% CI, 0.3-6.2%), and 3.7% (95% CI, -0.5-7.9%) increases in asthma and COPD visits respectively per 18.4 ppb). Associations tended to be of greater magnitude during the warm season (April - September). In particular, the associations of PM 10 and PM2.5 with asthma visits were respectively nearly three- and over fourfold larger vs. all year analyses (14.4% increase in visits, 95% CI, 0.2-30.7, per 20.6 microg/m3 PM 10 and 7.6% increase in visits, 95% CI, 5.1-10.1, per 8.2 microg/m3 PM2.5). No consistent associations were observed between three hour average pollutant concentrations and same-day three hour averages of ED visits. CONCLUSION: In this large multicenter analysis, daily average concentrations of CO and NO2 exhibited the most consistent associations with ED visits for cardiac conditions, while ozone exhibited the most consistent associations with visits for respiratory conditions. PM 10 and PM2.5 were strongly associated with asthma visits during the warm season.

Abstract  We investigate the relationship between maternal exposure to benzene and birth weight outcomes for resident births in the United States in 1996 and 1999, taking advantage of a natural experiment afforded by the regulation of benzene content of gasoline in various American cities. Regression results show that a unit increase (μg/m(3)) in maternal exposure to benzene reduces birth weight by 16.5 g (95% CI, 17.6 to 15.4). A unit increase in benzene exposure increases the odds of a low birth weight event by 7%. Similarly, a 1 μg/m(3) increase in benzene concentration increases the odds of very low birth weight event by a multiplicative factor of 1.23 (95% CI, 1.19 to 1.28). Difference-in-differences analyses show that birth weight increased by 13.7 g (95% CI, 10.7 to 16.8) and the risk of low birth weight decreased by a factor of .95 (95% CI, .93 to .98) in counties experiencing a 25% decline in benzene concentrations from 1996 to 1999. Public health policy and economic implications of results are discussed.

Abstract  BACKGROUND: Maternal exposure to air pollution has been related to fetal growth in a number of recent scientific studies. The objective of this study was to assess the association between exposure to air pollution during pregnancy and anthropometric measures at birth in a cohort in Valencia, Spain. METHODS: Seven hundred and eighty-five pregnant women and their singleton newborns participated in the study. Exposure to ambient nitrogen dioxide (NO2) was estimated by means of land use regression. NO2 spatial estimations were adjusted to correspond to relevant pregnancy periods (whole pregnancy and trimesters) for each woman. Outcome variables were birth weight, length, and head circumference (HC), along with being small for gestational age (SGA). The association between exposure to residential outdoor NO2 and outcomes was assessed controlling for potential confounders and examining the shape of the relationship using generalized additive models (GAM). RESULTS: For continuous anthropometric measures, GAM indicated a change in slope at NO2 concentrations of around 40 mcg/m3. NO2 exposure >40 mcg/m3 during the first trimester was associated with a change in birth length of -0.27 cm (95% CI: -0.51 to -0.03) and with a change in birth weight of -40.3 grams (-96.3 to 15.6); the same exposure throughout the whole pregnancy was associated with a change in birth HC of -0.17 cm (-0.34 to -0.003). The shape of the relation was seen to be roughly linear for the risk of being SGA. A 10 mcg/m3 increase in NO2 during the second trimester was associated with being SGA-weight, OR: 1.37 (1.01-1.85). For SGA-length the estimate for the same comparison was OR: 1.42 (0.89-2.25). CONCLUSIONS: Prenatal exposure to traffic-related air pollution may reduce fetal growth. Findings from this study provide further evidence of the need for developing strategies to reduce air pollution in order to prevent risks to fetal health and development.

Abstract  Several studies have examined associations between particulate matter with aerodynamic diameter of 2.5 µm or less (PM2.5) and preterm birth, but it is uncertain whether results were affected by individual predispositions (e.g., genetic factors, social conditions) that might vary considerably between women. We tested the hypothesis that a woman is at greater risk of preterm delivery when she has had elevated exposure to ambient PM2.5 during a pregnancy than when she has not by comparing pregnancies in the same woman. From 271,204 births, we selected 29,175 women who had vaginal singleton livebirths at least twice in Connecticut in 2000-2006 (n = 61,688 births). Analyses matched pregnancies to the same woman. Adjusted odds ratios per interquartile range (2.33-µg/m(3)) increase in PM2.5 in the first trimester, second trimester, third trimester, and whole pregnancy were 1.07 (95% confidence interval (CI): 1.00, 1.15), 0.96 (95% CI: 0.90, 1.03), 1.03 (95% CI: 0.97, 1.08), and 1.13 (95% CI: 1.01, 1.28), respectively. Among Hispanic women, the odds ratio per interquartile range increase in whole-pregnancy exposure was 1.31 (95% CI: 1.00, 1.73). Pregnancies with elevated PM2.5 exposure were more likely to result in preterm birth than were other pregnancies to the same woman at lower exposure. Associations were most pronounced in the first trimester and among Hispanic women.

Abstract  RATIONALE: Although substantial scientific evidence suggests that chronic exposure to ambient air pollution contributes to premature mortality, uncertainties exist in the size and consistency of this association. Uncertainty may arise from inaccurate exposure assessment.

OBJECTIVES: To assess the associations of three types of air pollutants (fine particulate matter, ozone [O3], and nitrogen dioxide [NO2]) with the risk of mortality in a large cohort of California adults using individualized exposure assessments.

METHODS: For fine particulate matter and NO2, we used land use regression models to derive predicted individualized exposure at the home address. For O3, we estimated exposure with an inverse distance weighting interpolation. Standard and multilevel Cox survival models were used to assess the association between air pollution and mortality.

MEASUREMENTS AND MAIN RESULTS: Data for 73,711 subjects who resided in California were abstracted from the American Cancer Society Cancer Prevention II Study cohort, with baseline ascertainment of individual characteristics in 1982 and follow-up of vital status through to 2000. Exposure data were derived from government monitors. Exposure to fine particulate matter, O3, and NO2 was positively associated with ischemic heart disease mortality. NO2 (a marker for traffic pollution) and fine particulate matter were also associated with mortality from all causes combined. Only NO2 had significant positive association with lung cancer mortality.

CONCLUSIONS: Using the first individualized exposure assignments in this important cohort, we found positive associations of fine particulate matter, O3, and NO2 with mortality. The positive associations of NO2 suggest that traffic pollution relates to premature death.

Abstract  The purpose of this study was to determine the effects of road dust on human health. A PubMed search was used to extract references that included the words "road dust" and "health" or "fugitive dust" and "health" in the title or abstract. A total of 46 references were extracted and selected for review after the primary screening of 949 articles. The respiratory system was found to be the most affected system in the human body. Lead, platinum-group elements (platinum, rhodium, and bohrium), aluminum, zinc, vanadium, and polycyclic aromatic hydrocarbons were the components of road dust that were most frequently referenced in the articles reviewed. Road dust was found to have harmful effects on the human body, especially on the respiratory system. To determine the complex mechanism of action of various components of road dust on the human body and the results thereof, the authors recommend a further meta-analysis and extensive risk-assessment research into the health impacts of dust exposure.

Abstract  Background: Carbon monoxide (CO) is one of the primary components of emissions from light-duty vehicles, and reportedly comprises 77% of all pollutants emitted in terms of concentration. Exposure to CO aggravates cardiovascular disease and causes other health disorders. The study was aimed to assess the negative effects by injecting different amounts of CO concentration directly to human volunteers boarding in the car.

Methods: Human volunteers were exposed to CO concentrations of 0, 33.2, and 72.4 ppm, respectively during the first test and 0, 30.3, and 48.8 ppm respectively during the second test while seated in the car. The volunteers were exposed to each concentration for approximately 45 min. After exposure, blood pressure measurement, blood collection (carboxyhemoglobin [COHb] analysis), medical interview, echocardiography test, and cognitive reaction test were performed.

Result: In patients who were exposed to a mean concentration of CO for 72.4 +/- 1.4 ppm during the first exposure test and 48.8 +/- 3.7 ppm during the second exposure test, the COHb level exceeded 2%. Moreover, the diastolic blood pressure was decreased while increasing in CO concentration after exposure. The medical interview findings showed that the degree of fatigue was increased and the degree of concentration was reduced when the exposed concentration of CO was increased.

Conclusion: Although the study had a limited sample size, we found that even a low concentration of CO flowing into a car could have a negative influence on human health, such as change of blood pressure and degree of fatigue.

Abstract  Climate is a known modulator of disease, but its impact on hospital performance metrics remains unstudied. We assess the relationship between Köppen-Geiger climate classification and hospital performance metrics, specifically 30-day mortality, as reported in Hospital Compare, and collected for the period July 2013 through June 2014 (7/1/2013-06/30/2014). A hospital-level multivariate linear regression analysis was performed while controlling for known socioeconomic factors to explore the relationship between all-cause mortality and climate. Hospital performance scores were obtained from 4,524 hospitals belonging to 15 distinct Köppen-Geiger climates and 2,373 unique counties. Model results revealed that hospital performance metrics for mortality showed significant climate dependence (p < 0.001) after adjusting for socioeconomic factors. Climate is a significant factor in evaluating hospital 30-day mortality rates. These results demonstrate that climate classification is an important factor when comparing hospital performance across the United States.

Abstract  Both air pollution and meteorological factors in metropolitan areas increased emergency department (ED) visits from people with chronic obstructive pulmonary disease (COPD). Few studies investigated the associations between air pollution, meteorological factors, and COPD-related health disorders in Asian countries. This study aimed to investigate the relationship between the environmental factors and COPD-associated ED visits of susceptible elderly population in the largest Taiwanese metropolitan area (Taipei area, including Taipei city and New Taipei city) between 2000 and 2013. Data of air pollutant concentrations (PM10, PM2.5, O3, SO2, NO2 and CO), meteorological factors (daily temperature, relative humidity and air pressure), and daily COPD-associated ED visits were collected from Taiwan Environmental Protection Administration air monitoring stations, Central Weather Bureau stations, and the Taiwan National Health Insurance database in Taipei area. We used a case-crossover study design and conditional logistic regression models with odds ratios (ORs), and 95% confidence intervals (CIs) for evaluating the associations between the environmental factors and COPD-associated ED visits. Analyses showed that PM2.5, O3, and SO2 had significantly greater lag effects (the lag was 4 days for PM2.5, and 5 days for O3 and SO2) on COPD-associated ED visits of the elderly population (65-79 years old). In warmer days, a significantly greater effect on elderly COPD-associated ED visits was estimated for PM2.5 with coexistence of O3. Additionally, either O3 or SO2 combined with other air pollutants increased the risk of elderly COPD-associated ED visits in the days of high relative humidity and air pressure difference, respectively. This study showed that joint effect of urban air pollution and meteorological factors contributed to the COPD-associated ED visits of the susceptible elderly population in the largest metropolitan area in Taiwan. Government authorities should review existing air pollution policies, and strengthen health education propaganda to ensure the health of the susceptible elderly population.

Abstract  BACKGROUND: Heart failure (HF) is a significant source of morbidity and mortality among African Americans. Ambient air pollution, including from traffic, is associated with HF, but the mechanisms remain unknown. The objectives of this study were to estimate the cross-sectional associations between residential distance to major roadways with markers of cardiac structure: left ventricular (LV) mass index, LV end-diastolic diameter, LV end-systolic diameter, and LV hypertrophy among African Americans.

METHODS: We studied baseline participants of the Jackson Heart Study (recruited 2000-2004), a prospective cohort of cardiovascular disease (CVD) among African Americans living in Jackson, Mississippi, USA. All cardiac measures were assessed from echocardiograms. We assessed the associations between residential distance to roads and cardiac structure indicators using multivariable linear regression or multivariable logistic regression, adjusting for potential confounders.

RESULTS: Among 4826 participants, residential distance to road was <150 m for 103 participants, 150-299 m for 158, 300-999 for 1156, and ≥1000 m for 3409. Those who lived <150 m from a major road had mean 1.2 mm (95% CI 0.2, 2.1) greater LV diameter at end-systole compared to those who lived ≥1000 m. We did not observe statistically significant associations between distance to roads and LV mass index, LV end-diastolic diameter, or LV hypertrophy. Results did not materially change after additional adjustment for hypertension and diabetes or exclusion of those with CVD at baseline; results strengthened when modeling distance to A1 roads (such as interstate highways) as the exposure of interest.

CONCLUSIONS: We found that residential distance to roads may be associated with LV end-systolic diameter, a marker of systolic dysfunction, in this cohort of African Americans, suggesting a potential mechanism by which exposure to traffic pollution increases the risk of HF.

Abstract  Systemic metabolic effects and toxicity mechanisms of ambient fine particulate matter (PM2.5) remain uncertain. In order to investigate the mechanisms in PM2.5 toxicity, we explored the endogenous metabolic changes and possible influenced metabolic pathways in rats after intratracheal instillation of PM2.5 by using a (1)H nuclear magnetic resonance (NMR)-based metabolomics approach. Liver and kidney histopathology examinations were also performed. Chemical characterization demonstrated that PM2.5 was a complex mixture of elements. Histopathology showed cellular edema in liver and glomerulus atrophy of the PM2.5 treated rats. We systematically analyzed the metabolites changes of serum and urine in rats using (1)H NMR techniques in combination with multivariate statistical analysis. Significantly reduced levels of lactate, alanine, dimethylglycine, creatine, glycine and histidine in serum, together with increased levels of citrate, arginine, hippurate, allantoin and decreased levels of allthreonine, lactate, alanine, acetate, succinate, trimethylamine, formate in urine were observed of PM2.5 treated rats. The mainly affected metabolic pathways by PM2.5 were glycine, serine and threonine metabolism, glyoxylate and dicarboxylate metabolism, citrate cycle (TCA cycle), nitrogen metabolism and methane metabolism. Our study provided important information on assessing the toxicity of PM2.5 and demonstrated that metabolomics approach can be employed as a tool to understand the toxicity mechanism of complicated environmental pollutants.

Abstract  Ozone reacts readily with many indoor materials, as well as with compounds in indoor air. These reactions lead to lower indoor than outdoor ozone concentrations when outdoor air is the major contributor to indoor ozone. However, the products of indoor ozone reactions may be irritating or harmful to building occupants. While active technologies exist to reduce indoor ozone concentrations (i.e, in-duct filtration using activated carbon), they can be cost-prohibitive for some and/or infeasible for dwellings that do not have heating, ventilating, and air-conditioning systems. In this study, the potential for passive reduction of indoor ozone by two different clay-based interior surface coatings was explored. These coatings were exposed to occupied residential indoor environments and tested bimonthly in environmental chambers for quantification of ozone reaction probabilities and reaction product emission rates over a 6-month period. Results indicate that clay-based coatings may be effective as passive removal materials, with relatively low by-product emission rates that decay rapidly within 2 months.

Abstract  We employed an in vivo assay system of Caenorhabditis elegans to determine if and which microRNAs (miRNAs) were dysregulated upon exposure to coal combustion related fine particulate matter (PM2.5) by profiling the miRNAs using SOLiD sequencing. From this, expression of 25 miRNAs was discovered to become dysregulated by exposure to PM2.5. Using the corresponding C. elegans deletion mutants, 5 miRNAs (mir-231, mir-232, mir-230, mir-251 and mir-35) were found to be involved in the control of PM2.5 toxicity. Furthermore, mutation of mir-231 or mir-232 induced a resistance to PM2.5 toxicity, whereas mutation of mir-230, mir-251, or mir-35 induced a susceptibility to PM2.5 toxicity. SMK-1, an ortholog of the mammalian SMEK protein, was identified as a molecular target for mir-231 in the regulation of PM2.5 toxicity. In addition, the genes of sod-3, sod-4 and ctl-3, which are necessary for protection against oxidative stress, were determined to be important downstream targets of smk-1 in the regulation of PM2.5 toxicity. The triggering of this mir-231-SMK-1-SOD-3/SOD-4/CTL-3 signaling pathway may be a critical molecular basis for the role of oxidative stress in the induction of coal combustion related PM2.5 toxicity.