Abstract  BACKGROUND: Few recent studies examined acute effects on health of individual chemical species in the particulate matter (PM) mixture, and most of them have been conducted in North America. Studies in Southern Europe are scarce. The aim of this study is to examine the relationship between particulate matter constituents and daily hospital admissions and mortality in five cities in Southern Europe.

METHODS: The study included five cities in Southern Europe, three cities in Spain: Barcelona (2003-2010), Madrid (2007-2008) and Huelva (2003-2010); and two cities in Italy: Rome (2005-2007) and Bologna (2011-2013). A case-crossover design was used to link cardiovascular and respiratory hospital admissions and total, cardiovascular and respiratory mortality with a pre-defined list of 16 PM10 and PM2.5 constituents. Lags 0 to 2 were examined. City-specific results were combined by random-effects meta-analysis.

RESULTS: Most of the elements studied, namely EC, SO4(2-), SiO2, Ca, Fe, Zn, Cu, Ti, Mn, V and Ni, showed increased percent changes in cardiovascular and/or respiratory hospitalizations, mainly at lags 0 and 1. The percent increase by one interquartile range (IQR) change ranged from 0.69% to 3.29%. After adjustment for total PM levels, only associations for Mn, Zn and Ni remained significant. For mortality, although positive associations were identified (Fe and Ti for total mortality; EC and Mg for cardiovascular mortality; and NO3(-) for respiratory mortality) the patterns were less clear.

CONCLUSIONS: The associations found in this study reflect that several PM constituents, originating from different sources, may drive previously reported results between PM and hospital admissions in the Mediterranean area.

Abstract  Several papers reported associations between airborne fine particulate matter (PM2.5) and birth weight, though findings are inconsistent across studies. Conflicting results might be due to (1) different PM2.5 chemical structure across locations, and (2) various exposure assignment methods across studies even among the studies that use ambient monitors to assess exposure. We investigated associations between birth weight and PM2.5 chemical constituents, considering issues arising from choice of buffer size (i.e. distance between residence and pollution monitor). We estimated the association between each pollutant and term birth weight applying buffers of 5 to 30 km in Connecticut (2000-2006), in the New England region of the USA. We also investigated the implication of the choice of buffer size in relation to population characteristics, such as socioeconomic status. Results indicate that some PM2.5 chemical constituents, such as nitrate, are associated with lower birth weight and appear more harmful than other constituents. However, associations vary with buffer size and the implications of different buffer sizes may differ by pollutant. A homogeneous pollutant level within a certain distance is a common assumption in many environmental epidemiology studies, but the validity of this assumption may vary by pollutant. Furthermore, we found that areas close to monitors reflect more minority and lower socio-economic populations, which implies that different exposure approaches may result in different types of study populations. Our findings demonstrate that choosing an exposure method involves key tradeoffs of the impacts of exposure misclassification, sample size, and population characteristics.

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  Rationale: Growing evidence suggests that long-term exposure to fine particulate matter (PM2.5) air pollution contributes to risk of cardiovascular disease (CVD) morbidity and mortality. There is uncertainty regarding who are most susceptible. Individuals with underlying cardiometabolic disorders, including hypertension, diabetes, and obesity, may be at greater risk. PM2.5 pollution may also contribute to cardiometabolic disorders, augmenting CVD risk. Objective: This analysis evaluates relationships between long-term PM2.5 exposure and cardiometabolic disease on risk of death from CVD and cardiometabolic conditions. Methods and Results: Data on 669,046 participants from the American Cancer Society, Cancer Prevention Study II cohort were linked to modeled PM2.5 concentrations at geocoded home addresses. Cox proportional hazards regression models were used to estimate adjusted hazards ratios (HR) for death from CVD and cardiometabolic diseases based on death-certificate information. Effect modification by pre-existing cardiometabolic risk factors on the PM2.5-CVD mortality association was examined. PM2.5 exposure was associated with CVD mortality, with the HR (95% CI) per 10 µg/m(3) increase in PM2.5 equal to 1.12 (1.10-1.15). Deaths linked to hypertension and/or diabetes (mentioned on death certificate as either primary or contributing cause of death) were also associated with PM2.5. There was no consistent evidence of effect modification by cardiometabolic disease risk factors on the PM2.5-CVD mortality association. Conclusions: Pollution-induced CVD mortality risk is observed for those with and without existing cardiometabolic disorders. Long-term exposure may also contribute to the development or exacerbation of cardiometabolic disorders, increasing risk of CVD and cardiometabolic disease mortality.

Abstract  There is interest in determining the relationship between fine particulate matter air pollution and various health outcomes, including birth outcomes such as term low birth weight. Previous studies have come to different conclusions. In this study we consider whether the effect may vary by location and gestational period. We also compare results when using different spatial resolutions for the air concentration estimates. Among the seven states considered, New Jersey and New York had the highest PM2.5 levels (average full gestation period exposures of 13µg/m(3)) and the largest rate of low birth weight births (2.6 and 2.8%, respectively); conversely Utah and Minnesota had the lowest PM2.5 levels (9µg/m(3)) and the lowest rates of low birth weight births (2.1 and1.9%, respectively). There is an association between PM2.5 exposure and low birth weight in New York for the full gestation period and all three trimesters, in Minnesota for the full gestation period and the first and third trimesters, and in New Jersey for the full gestation period and the first trimester. When we pooled the data across states, the OR for the full gestation period was 1.030 (95% CI: 1.022-1.037) and it was highest for the first trimester (OR 1.018; CI: 1.013-1.022) and decreasing during the later trimesters. When we used a finer spatial resolution, the strengths of the associations tended to diminish and were no longer statistically significant. We consider reasons why these differences may occur and their implications for evaluating the effects of PM2.5 on birth outcomes.

Abstract  BACKGROUND: While several cohort studies report associations between chronic exposure to fine particles (PM2.5) and mortality, few have studied the effects of chronic exposure to ultrafine (UF) particles. In addition, few studies have estimated the effects of the constituents of either PM2.5 or UF particles.

METHODS: We used a statewide cohort of over 100,000 women from the California Teachers Study who were followed from 2001 through 2007. Exposure data at the residential level were provided by a chemical transport model that computed pollutant concentrations from over 900 sources in California. Besides particle mass, monthly concentrations of 11 species and 8 sources or primary particles were generated at 4 km grids. We used a Cox proportional hazards model to estimate the association between the pollutants and all-cause, cardiovascular, ischemic heart disease (IHD) and respiratory mortality.

RESULTS: We observed statistically significant (p < 0.05) associations of IHD with PM2.5 mass, nitrate elemental carbon (EC), copper (Cu), and secondary organics and the sources gas- and diesel-fueled vehicles, meat cooking, and high sulfur fuel combustion. The hazard ratio estimate of 1.19 (95% CI: 1.08, 1.31) for IHD in association with a 10-µg/m(3) increase in PM2.5 is consistent with findings from the American Cancer Society cohort. We also observed significant positive associations between IHD and several UF components including EC, Cu, metals, and mobile sources.

CONCLUSIONS: Using an emissions-based model with a 4 km spatial scale, we observed significant positive associations between IHD mortality and both fine and ultrafine particle species and sources. Our results suggest that the exposure model effectively measured local exposures and facilitated the examination of the relative toxicity of particle species.

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: 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  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  Fine particulate matter <2.5 μm (PM2.5) has been associated with human health issues; however, findings regarding the influence of PM2.5 on respiratory disease remain inconsistent. The short-term, population-based association between the respiratory clinic visits of children and PM2.5 exposure levels were investigated by considering both the spatiotemporal distributions of ambient pollution and clinic visit data. We applied a spatiotemporal structured additive regression model to examine the concentration-response (C-R) association between children's respiratory clinic visits and PM2.5 concentrations. This analysis was separately performed on three respiratory disease categories that were selected from the Taiwanese National Health Insurance database, which includes 41 districts in the Taipei area of Taiwan from 2005 to 2007. The findings reveal a non-linear C-R pattern of PM2.5, particularly in acute respiratory infections. However, a PM2.5 increase at relatively lower levels can elevate the same-day respiratory health risks of both preschool children (<6 years old) and schoolchildren (6-14 years old). In preschool children, same-day health risks rise when concentrations increase from 0.76 to 7.44 μg/m(3), and in schoolchildren, same-day health risks rise when concentrations increase from 0.76 to 7.52 μg/m(3). Changes in PM2.5 levels generally exhibited no significant association with same-day respiratory risks, except in instances where PM2.5 levels are extremely high, and these occurrences do exhibit a significant positive influence on respiratory health that is especially notable in schoolchildren. A significant high relative rate of respiratory clinic visits are concentrated in highly populated areas. We highlight the non-linearity of the respiratory health effects of PM2.5 on children to investigate this population-based association. The C-R relationship in this study can provide a highly valuable alternative for assessing the effects of ambient air pollution on human health.Journal of Exposure Science and Environmental Epidemiology advance online publication, 8 April 2015; doi:10.1038/jes.2015.21.

Abstract  OBJECTIVES: To study the effect of long term exposure to airborne pollutants on the incidence of acute coronary events in 11 cohorts participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE).

DESIGN: Prospective cohort studies and meta-analysis of the results.

SETTING: Cohorts in Finland, Sweden, Denmark, Germany, and Italy.

PARTICIPANTS: 100 166 people were enrolled from 1997 to 2007 and followed for an average of 11.5 years. Participants were free from previous coronary events at baseline.

MAIN OUTCOME MEASURES: Modelled concentrations of particulate matter <2.5 μm (PM2.5), 2.5-10 μm (PMcoarse), and <10 μm (PM10) in aerodynamic diameter, soot (PM2.5 absorbance), nitrogen oxides, and traffic exposure at the home address based on measurements of air pollution conducted in 2008-12. Cohort specific hazard ratios for incidence of acute coronary events (myocardial infarction and unstable angina) per fixed increments of the pollutants with adjustment for sociodemographic and lifestyle risk factors, and pooled random effects meta-analytic hazard ratios.

RESULTS: 5157 participants experienced incident events. A 5 μg/m(3) increase in estimated annual mean PM2.5 was associated with a 13% increased risk of coronary events (hazard ratio 1.13, 95% confidence interval 0.98 to 1.30), and a 10 μg/m(3) increase in estimated annual mean PM10 was associated with a 12% increased risk of coronary events (1.12, 1.01 to 1.25) with no evidence of heterogeneity between cohorts. Positive associations were detected below the current annual European limit value of 25 μg/m(3) for PM2.5 (1.18, 1.01 to 1.39, for 5 μg/m(3) increase in PM2.5) and below 40 μg/m(3) for PM10 (1.12, 1.00 to 1.27, for 10 μg/m(3) increase in PM10). Positive but non-significant associations were found with other pollutants.

CONCLUSIONS: Long term exposure to particulate matter is associated with incidence of coronary events, and this association persists at levels of exposure below the current European limit values.

Abstract  PURPOSE: Although exposure to polycyclic aromatic hydrocarbons (PAHs) is common in both environmental and occupational settings, few studies have compared PAH exposure among people with different professions. The purpose of this study was to investigate the variations in recent PAH exposure among different occupational groups over time using national representative samples.

METHOD: The study population consisted of 4162 participants from the 2001 to 2008 National Health and Nutrition Examination Survey, who had both urinary PAH metabolites and occupational information. Four corresponding monohydroxy-PAH urine metabolites: naphthalene (NAP), fluorene (FLUO), phenanthrene (PHEN), and pyrene (PYR) among seven broad occupational groups were analyzed using weighted linear regression models, adjusting for creatinine levels, sociodemographic factors, smoking status, and sampling season.

RESULTS: The overall geometric mean concentrations of NAP, FLUO, PHEN, and PYR were 6927, 477, 335, and 87 ng/L, respectively. All four PAH metabolites were elevated in the "extractive, construction, and repair (ECR)" group, with 21-42 % higher concentrations than those in the reference group of "management." Similar trends were seen in the "operators, fabricators, and laborers (OFL)" group for FLUO, PHEN, and PYR. In addition, both "service" and "support" groups had elevated FLUO. Significant (p < 0.001) upward temporal trends were seen in NAP and PYR, with an approximately 6-17 % annual increase, and FLUO and PHEN remained relatively stable. Race and socioeconomic status show independent effects on PAH exposure.

CONCLUSIONS: Heterogeneous distributions of urinary PAH metabolites among people with different job categories exist at the population level. The upward temporal trends in NAP and PYR warrant reduction in PAH exposure, especially among those with OFL and ECR occupations.

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  One of the largest rail yard facilities in the Southeastern US, the Inman and Tilford yards, is located in the northwestern section of Atlanta, Georgia alongside other industries, schools, businesses, and dwellings. It is a significant source of fine particulate (PM2.5) and black carbon (BC) (Galvis, Bergin, & Russell, 2013). We calculate 2011 PM2.5 and BC emissions from the rail yards and primary industrial and on-road mobile sources in the area and determine their impact on local air quality using Gaussian dispersion modeling. We determine the change in PM2.5 and BC concentrations that could be accomplished by upgrading traditional switcher locomotives used in these rail yards to a lower emitting technology and evaluate the health benefits for comparison with upgrade costs. Emissions from the rail yards were estimated using reported fuel consumption data (GAEPD, 2012b) and emission factors previously measured in the rail yards (Galvis et al., 2013). Model evaluation against 2011 monitoring data found agreement between measured and simulated concentrations. Model outputs indicate that the line-haul and switcher activities are responsible for increments in annual average concentrations of approximately 0.5±0.03μg/m(3) (39%) and 0.7±0.04μg/m(3) (56%) of BC, and for 1.0±0.1μg/m(3) (7%) and 1.6±0.2μg/m(3) (14%) of PM2.5 at two monitoring sites located north and south of the rail yards respectively. Upgrading the switcher locomotives at the yards with a lower emitting technology in this case "mother slug" units could decrease PM2.5 and BC emissions by about 9 and 3t/year respectively. This will lower annual average PM2.5 concentrations between 0.3±0.1μg/m(3) and 0.6±0.1μg/m(3) and BC concentrations between 0.1±0.02μg/m(3) and 0.2±0.03μg/m(3) at monitoring sites north and south of the rail yards respectively, and would facilitate PM2.5 NAAQS attainment in the area. We estimate that health benefits of approximately 20 million dollars per year could be gained.

Abstract  Exposure to particulate air pollution and socioeconomic risk factors are shown to be independently associated with adverse pregnancy outcomes; however, their confounding relationship is an epidemiological challenge that requires understanding of their shared etiologic pathways affecting fetal-placental development. The purpose of this paper is to explore the etiological mechanisms associated with exposure to particulate air pollution in contributing to adverse pregnancy outcomes and how these mechanisms intersect with those related to socioeconomic status. Here we review the role of oxidative stress, inflammation and endocrine modification in the pathoetiology of deficient deep placentation and detail how the physical and social environments can act alone and collectively to mediate the established pathology linked to a spectrum of adverse pregnancy outcomes. We review the experimental and epidemiological literature showing that diet/nutrition, smoking, and psychosocial stress share similar pathways with that of particulate air pollution exposure to potentially exasperate the negative effects of either insult alone. Therefore, socially patterned risk factors often treated as nuisance parameters should be explored as potential effect modifiers that may operate at multiple levels of social geography. The degree to which deleterious exposures can be ameliorated or exacerbated via community-level social and environmental characteristics needs further exploration.

Abstract  BACKGROUND: Studies on the association between prenatal exposure to fine particulate matter with ≤ 2.5 micrometers in aerodynamic diameter (PM2.5) and term low birth weight (LBW) have resulted in inconsistent findings. Most studies were conducted in snapshots of small geographic areas and no national study exists. OBJECTIVES: We investigated geographic variation in the associations between ambient PM2.5 during pregnancy and term LBW in the contiguous United States (US). METHODS: 3,389,450 term singleton births in 2002 (37 - 44 weeks gestational age and birth weight of 1,000g - 5,500g) were linked to daily PM2.5 via imputed birth days. We generated average daily PM2.5 during the entire pregnancy and each trimester. Multilevel logistic regression models with county-level random effects were used to evaluate the associations between term LBW and PM2.5 during pregnancy. RESULTS: Without adjusting for covariates, the odds of term LBW increased 2% (OR=1.02; 95% CI: 1.00, 1.03) for every 5 µg/m3 increase in PM2.5 exposure during the second trimester only, which remained unchanged after adjusting for county-level poverty (OR=1.02; 95% CI: 1.01, 1.04). The odds did change to null after adjusting for individual-level predictors (OR=1.00; 95% CI: 0.99, 1.02). Multilevel analyses, stratified by census division, revealed significant positive associations of term LBW and PM2.5 exposure (during the entire pregnancy or a specific trimester) in three census divisions: Middle Atlantic, East North Central, and West North Central, and significant negative association in the Mountain division. CONCLUSIONS: Our study provided additional evidence on the associations between PM2.5 exposure during pregnancy and term LBW from a national perspective. The magnitude and direction of the estimated associations between PM2.5 exposure and term LBW varied by geographic locations in the US.

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  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  Background: We and others have shown that increases in particulate air pollutant (PM) concentrations in the previous hours and days have been associated with increased risks of myocardial infarction, but little is known about the relationships between air pollution and specific subsets of myocardial infarction, such as ST-elevation myocardial infarction (STEMI) and non ST-elevation myocardial infarction (NSTEMI). Methods: Using data from acute coronary syndrome patients with STEMI (n = 338) and NSTEMI (n = 339) and case-crossover methods, we estimated the risk of STEMI and NSTEMI associated with increased ambient fine particle (<2.5 um) concentrations, ultrafine particle (10-100 nm) number concentrations, and accumulation mode particle (100-500 nm) number concentrations in the previous few hours and days. Results: We found a significant 18% increase in the risk of STEMI associated with each 7.1 mu g/m(3) increase in PM2.5 concentration in the previous hour prior to acute coronary syndrome onset, with smaller, non-significantly increased risks associated with increased fine particle concentrations in the previous 3, 12, and 24 hours. We found no pattern with NSTEMI. Estimates of the risk of STEMI associated with interquartile range increases in ultrafine particle and accumulation mode particle number concentrations in the previous 1 to 96 hours were all greater than 1.0, but not statistically significant. Patients with pre-existing hypertension had a significantly greater risk of STEMI associated with increased fine particle concentration in the previous hour than patients without hypertension. Conclusions: Increased fine particle concentrations in the hour prior to acute coronary syndrome onset were associated with an increased risk of STEMI, but not NSTEMI. Patients with pre-existing hypertension and other cardiovascular disease appeared particularly susceptible. Further investigation into mechanisms by which PM can preferentially trigger STEMI over NSTEMI within this rapid time scale is needed.

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  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  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  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  BACKGROUND: Population-based studies have estimated health risks of short-term exposure to fine particles using mass of PM(2.5) (particulate matter
OBJECTIVE: In this study we investigated the association between hospital admission for cardiovascular disease (CVD) and respiratory disease and the chemical components of PM(2.5) in the United States.

METHODS: We used a national database comprising daily data for 2000-2006 on emergency hospital admissions for cardiovascular and respiratory outcomes, ambient levels of major PM(2.5) chemical components [sulfate, nitrate, silicon, elemental carbon (EC), organic carbon matter (OCM), and sodium and ammonium ions], and weather. Using Bayesian hierarchical statistical models, we estimated the associations between daily levels of PM(2.5) components and risk of hospital admissions in 119 U.S. urban communities for 12 million Medicare enrollees (>or= 65 years of age).

RESULTS: In multiple-pollutant models that adjust for the levels of other pollutants, an interquartile range (IQR) increase in EC was associated with a 0.80% [95% posterior interval (PI), 0.34-1.27%] increase in risk of same-day cardiovascular admissions, and an IQR increase in OCM was associated with a 1.01% (95% PI, 0.04-1.98%) increase in risk of respiratory admissions on the same day. Other components were not associated with cardiovascular or respiratory hospital admissions in multiple-pollutant models.

CONCLUSIONS: Ambient levels of EC and OCM, which are generated primarily from vehicle emissions, diesel, and wood burning, were associated with the largest risks of emergency hospitalization across the major chemical constituents of PM(2.5).