PM2.5 Constituents and Related Air Quality Variables As Predictors of Survival in a Cohort of U.S. Military Veterans

Air quality data on trace metals, other constituents of PM_2.5, and criteria air pollutants were used to examine relationships with long-term mortality in a cohort of male U.S. military veterans, along with data on vehicular traffic density (annual vehicle-miles traveled per unit of land area). The analysis used county-level environmental data for the period 1997–2002 and cohort mortality for 1997–2001. The proportional hazards model included individual data on age, race, smoking, body mass index, height, blood pressure, and selected interactions; contextual variables also controlled for climate, education, and income. In single-pollutant models, traffic density appears to be the most important predictor of survival, but potential contributions are also seen for NO₂, NO₃^?, elemental carbon, nickel, and vanadium. The effects of the other main constituents of PM_2.5, of crustal particles, and of peak levels of CO, O₃, or SO₂ appear to be less important. Traffic density is also consistently the most important environmental predictor in multiple-pollutant models, with combined relative risks up to about 1.2. However, from these findings it is not possible to discern which aspects of traffic (pollution, noise, stress) may be the most relevant to public health or whether an area-based predictor such as traffic density may have an inherent advantage over localized measures of ambient air quality. It is also possible that traffic density could be a marker for unmeasured pollutants or for geographic gradients per se. Pending resolution of these issues, including replication in other cohorts, it will be difficult to formulate additional cost-effective pollution control strategies that are likely to benefit public health.     

The relationship between traffic-related air pollutants and cardiac autonomic function in a panel of healthy adults: a further analysis with existing data

Context: Epidemiological studies have linked particulate matter (PM) and carbon monoxide (CO) exposures with alterations in cardiac autonomic function as measured by heart rate variability (HRV) in populations. Recently, we reported association of several HRV indices with marked changes in particulate air pollution around the Beijing 2008 Olympic Games in a panel of healthy adults.

Objective: We further investigated the cardiac effects of traffic-related air pollutants over wide exposure ranges with expanded data set in this panel of healthy adults.

Methods: We obtained real-time data on nine taxi drivers’ in-car exposures to PM ≤2.5?µm in aerodynamic diameter (PM_2.5) and CO and on multiple HRV indices during a separate daily work shift in four study periods with dramatically changing air pollution levels around the Beijing 2008 Olympic Games. Mixed effect models and a loess smoother method were used to investigate the associations of exposures with HRV indices.

Results: Results showed overall negative associations of traffic-related air pollutants with HRV indices across periods, as well as differences in period-specific and individual associations. After stratifying the individuals into two different response groups (positive/negative), cardiac effects of air pollutants became stronger within each group. Exposure–response modeling identified changed curvilinear relationships between air pollution exposures and HRV indices with threshold effects.

Discussion and conclusion: Our results support the association of exposure to traffic-related air pollution with altered cardiac autonomic function in young healthy adults free of cardiovascular compromises. These results suggest a complicated mechanism that traffic-related air pollutants influence the cardiovascular system of healthy adults.     

Cardiovascular disease and air pollutants: evaluating and improving epidemiological data implicating traffic exposure

Evidence suggests that traffic-related pollutants play a role in the observed associations between air pollution and adverse cardiovascular health effects. The contribution of traffic to individual exposures is difficult to quantify in traditional epidemiological studies, however, and researchers have employed various approaches in attempt to isolate its effects. Many investigators have employed ambient measurements such as nitrogen oxides, carbon monoxide, or black carbon as surrogates for traffic in studying associations with health outcomes. Source-apportionment techniques also have been used in a few studies to identify associations with the mixture of pollutants from specific origins, including traffic. In other studies, estimates of traffic near a person's home have predicted cardiovascular endpoints, and local traffic levels have modified the effect of regional air pollution. More recently, studies have linked changes in cardiovascular health to time spent in traffic. In this article, we review the epidemiological evidence regarding the impact of traffic-related pollution on cardiovascular diseases and examine the different techniques used to examine this important research question. We conclude with a discussion of the future directions being used in ongoing epidemiological studies to identify the cardiovascular health impacts of traffic.     

Air pollution-related peak expiratory flow rates among asthmatic children in Chiang Mai,Thailand

The severity of air pollution in northern Thailand has long been recognized; in spite of that there have been no epidemiological studies regarding the associations between the air pollution and health effects in the area. The authors followed a cohort of 31 asthmatic children (4–11 years of age) residing in Muang district, Chiang Mai, Thailand, from 29 August 2005 to 30 June 2006, for 306 days. The daily air pollutants, including particulate matter with aerodynamic diameter?<?2.5?μm, particulate matter with aerodynamic diameter?<?10?μm, carbon monoxide, ozone (O₃), nitrogen dioxide, and sulfur dioxide (SO₂), and the meteorological parameters, including pressure, temperature, relative humidity, rain quantity, and sunshine duration, were recorded. The peak expiratory flow rates (PEFRs) were fitted with pollutants and meteorological covariates using general linear mixed models to account for random effects and autocorrelation. The authors found that there were inverse associations of SO₂ and evening PEFR, with a coefficient of -2.12 (95% confidence interval (CI)?=?-3.22 to -0.28); of SO₂ and daily percent deviation of PEFR, with a coefficient of -0.73 (95% CI?=?-1.33 to -0.12); and of O₃ combining with SO₂ and daily average PEFR, with a coefficient of -0.16 (95% CI?=?-0.31 to -0.00) and -1.60 (95% CI?=?-3.10 to -0.11), respectively. The associations of O₃ and SO₂ with PEFR were found even when SO₂ concentrations never exceeded the standard level.     

Air Pollution and Hospital Admissions for Congestive Heart Failure in a Tropical City: Kaohsiung,Taiwan

This study was undertaken to determine whether there was an association between air pollutant levels and hospital admissions for congestive heart failure (CHF) in Kaohsiung, Taiwan. Hospital admissions for CHF and ambient air pollution data for Kaohsiung were obtained for the period 1996–2004. The relative risk of hospital admission was estimated using a case-crossover approach, controlling for weather variables, day of the week, seasonality, and long-term time trends. In the single-pollutant models, on warm days (> 25°C) statistically significant positive associations were found in all pollutants except sulfur dioxide (SO₂). On cool days (< 25°C), all pollutants were significantly associated with CHF admissions. For the two-pollutant model, CO and O₃ were significant in combination with each of the other four pollutants on warm days. On cool days, NO₂ remained statistically significant in all the two-pollutant models. This study provides evidence that higher levels of ambient air pollutants increase the risk of hospital admissions for CHF and that the effects of air pollutants on hospital admissions for CHF were temperature dependent.     

Air Pollution and Hospital Admissions for Chronic Obstructive Pulmonary Disease in a Tropical City: Kaohsiung,Taiwan

This study was undertaken to determine whether there is an association between air pollutants levels and hospital admissions for chronic obstructive pulmonary disease (COPD) in Kaohsiung, Taiwan. Hospital admissions for COPD and ambient air pollution data for Kaohsiung were obtained for the period from 1996 to 2003. The odds ratio of hospital admission was estimated using a case-crossover approach, controlling for weather variables, day of the week, seasonality, and long-term time trends. In the single-pollutant models, on warm days (≥25°C) statistically significant positive associations were found in all pollutants except sulphur dioxide (SO₂). On cool days (< 25°C), all pollutants were significantly associated with COPD admissions. For the two-pollutant models, CO and O₃ were significant in combination with each of the other four pollutants on warm days. On cool days, NO₂ remained statistically significant in all the two-pollutant models. This study provides evidence that higher levels of ambient pollutants increase the risk of hospital admissions for COPD.     

Air Pollution and Cardiac Arrhythmias in Patients with Implantable Cardioverter Defibrillators

Epidemiological studies have demonstrated associations between short-term increases in outdoor air pollution concentrations and adverse cardiovascular effects, including cardiac mortality and hospitalizations. One possible mechanism behind this association is that air pollution exposure increases the risk of developing a cardiac arrhythmia. To investigate this hypothesis, dates of implantable cardioverter defibrillator (ICD) discharges were abstracted from patient records in patients attending the two ICD clinics in Vancouver, BC, for the years 1997–2000. Daily outdoor air pollutant concentrations and daily meteorological data from the Vancouver region were obtained for the same 4-yr period. Generalized estimating equations were used to assess the association between short-term increases in air pollutant concentrations and ICD discharges while controlling for temporal trends, meteorology, and serial correlation in the data. Air pollution concentrations in the Vancouver region were relatively low from 1997 to 2000, as expected. In the 50 patients who resided within the Vancouver region and who experienced at least 1 ICD discharge during the period of follow-up, no significant associations between increased air pollution concentrations and increased ICD discharges were present. When the patient sample was restricted to the 16 patients who had at least 6 months of follow-up and experienced a rate of at least 2 days with ICD discharges per year, there was a statistically significant association between increased sulfur dioxide (SO₂) concentration and ICD discharge 2 days after the SO₂ increase. When stratified by season, no associations between increased air pollutant concentrations and increased risk of ICD discharge were observed in the summer, although for several pollutants, concentration increases were associated with a decrease in ICD discharges. In the winter, increased SO₂ concentrations again were seen to be associated with increased risk of ICD discharge, at both 2 and 3 days following increases in SO₂ concentrations. These findings provide no compelling evidence that short-term increases in relatively low concentrations of outdoor air pollutants have an adverse effect on individuals at risk of cardiac arrhythmias. The findings regarding SO₂ are difficult to interpret. They may be chance findings. Alternatively, given the very low concentrations of SO₂ that were present in Vancouver, SO₂ may have been serving as a surrogate measure of other environmental or meteorological factors.     

Do pollution time-series studies contain uncontrolled or residual confounding by risk factors for acute health events?

Acute health effects from air pollution are based largely on weak associations identified in time-series studies comparing daily air pollution levels to daily mortality. Much of this mortality is due to cardiovascular disease. Time-series studies have many potential limitations, but are not thought to be confounded by traditional cardiovascular risk factors (e.g., smoking status or hypertension) because these chronic risk factors are not obviously associated with daily pollution levels. However, acute psychobehavioral variants of these risk factors (e.g., smoking patterns and episodes of stress on any given day) are plausible confounders for the associations observed in time-series studies, given that time-series studies attempt to predict acute rather than chronic health outcomes. There is a fairly compelling literature on the strong link between cardiovascular events and daily "triggers" such as stress. Stress-related triggers are plausibly associated with daily pollution levels through surrogate stressors such as ambient temperature, daily workload, local traffic congestion, or other correlates of air pollution. For example, variables such as traffic congestion and industrial activity increase both stress-related health events and air pollution, suggesting the potential for classical confounding. Support for this argument is illustrated through examples of the well-demonstrated relationship between emotional stress and heart attack/stroke.     

Pollution profiles at different kindergarten sites in Leipzig,Germany

Between Jan. and Dec. 1994, the outdoor air quality of the city of Leipzig, Germany, was examined at 13 kindergartens. SO₂, CO, NO_X, O₃, total suspended particles, sedimentation dust and volatile organic compounds were measured. Although each monitoring site appears to have its own individual pollutant profile, two general pollution profiles could be identified using principal component analysis. These profiles are largely attributable to two dominant emission sources, domestic heating and traffic. Indicator components were identified for both pollution profiles. Benzene was found to be the indicator component for traffic and SO₂ for domestic heating. The predominating types of pollution are reflected in the prevalences of respiratory diseases among 311 children investigated based on parent-completed questionnaires. High traffic pollution was found to be associated with an increased occurrence of asthma and allergies and domestic heating with bronchitis. ©1999 John Wiley & Sons, Inc. Environ Toxicol 14: 321–327, 1999     

Air Pollution and Hospital Admissions for Pneumonia in a Subtropical City: Taipei,Taiwan

This study was undertaken to determine whether there was an association between air pollutant levels and hospital admissions for pneumonia in Taipei, Taiwan. Hospital admissions for pneumonia and ambient air pollution data for Taipei were obtained for the period from 1996–2004. The relative risk of hospital admission was estimated using a case-crossover approach, controlling for weather variables, day of the week, seasonality, and long-term time trends. In the single pollutant models, on warm days (>23°C) statistically significant positive associations were found in all pollutants. On cool days (<23°C), all pollutants were significantly associated with pneumonia admissions except SO₂. For the two-pollutant model, O₃ and NO₂ were significant in combination with each of the other 4 pollutants on warm days. On cool days, PM_{1 0}, CO, and O₃ remained statistically significant in all the two-pollutant models. This study provides evidence that higher levels of ambient air pollutants increase the risk of hospital admissions for pneumonia.     

The effects of ambient particulate matter on human adipose tissue

ABSTRACT

The effects of particulate matter (PM) air pollution on adipose tissue have mainly been studied in animal models. The aim of this study was to examine the potential associations between PM exposure and 25 cellular markers in human omental (OM) and subcutaneous (SC) adipose tissue. The PM exposure assessments for both PM_2.5 (PM <2.5 μm in diameter) and PM₁₀ (<10 μm) were based upon a novel hybrid satellite-based spatio-temporally resolved model. We calculated the PM exposure above the background threshold for 1 week (acute phase), 3 and 6 months (intermediate phase), and 1 year (chronic phase) prior to tissue harvesting and tested the associations with adipose cell metabolic effects using multiple linear regressions and heat maps strategy. Chemokine levels were found to increase after acute and intermediate exposure duration to PM₁₀. The levels of stress signaling biomarkers in the SC and OM tissues rose after acute exposure to PM₁₀ and PM_2.5. Macrophage and leucocyte counts were associated with severity of PM exposure in all three duration groups. Adipocyte diameter decreased in all exposure periods. Our results provide evidence for significant contribution of air pollutants exposure to adipose tissue inflammation as well as for pathophysiological mechanisms of metabolic dysregulation that may be involved in the observed responses.     

Air pollution and short‐term clinical outcomes of patients with acute myocardial infarction

Ambient air pollution is well‐known to be a serious risk factor for cardiovascular diseases, stroke, and death. However, the association between air pollutants (AP ) exposure and short‐term clinical outcomes in acute myocardial infarction (AMI ) patients (pts) has not been elucidated well. In the present study, 37 880 AMI pts were enrolled from October 2005 to December 2013 in a nationwide large‐scale, prospective, multicentre Korea AMI registry (KAMIR registry; http://www.kamir.or.kr ). We obtained data on AP (e.g., NO ₂, SO ₂, CO , O₃ and PM ₁₀) from the Korean National Institute of Environmental Research (NIER ; http://www.nier.go.kr ). Clinical endpoints included death, recurrent myocardial infarction (Re‐MI ), any revascularization and composite of all‐cause death and Re‐MI . Exposure to AP is defined as the average exposure to AP within 24 hours before AMI admission. We observed that a 0.01 part per million (ppm) increase in NO ₂ concentration, 0.001 ppm increase in SO ₂ concentration, and 0.1 ppm increase in CO concentration each increased the risk of total death by 9.7% (95% CI , 6.2%‐13.4%), 1.9% (95% CI , 0.3%‐3.6%), and 2.1% (95% CI , 0.5%‐3.9%), respectively. Exceptionally, O₃ decreased the risk of total death by 0.6% (95% CI ?0.2% to ?1.0%) per 0.01 ppm increase. PM ₁₀ was not related to any cardiovascular events. AP were each stratified into five quintiles according to ranges of AP levels. After adjusting analysis for risk variables, only high quintiles (Q4, Q5) of NO ₂ were positively associated with total death, cardiac death and MI , while SO ₂, CO , O₃ and PM ₁₀ were shown to be not related to any cardiovascular events at all levels. In AMI patients, each AP and its concentration has shown a different effect to short‐term mortality and cardiovascular events.     

Longitudinal relationships between lung cancer mortality rates,smoking, and ambient air quality: a comprehensive review and analysis

Abstract

Lung cancer mortality (LCM) has been associated with smoking and air pollution. This article draws on smoking relationships to clarify air pollution relationships. We analyzed cohort and population-based smoking studies and identified effects of latency and cumulative exposures. We found cogent relationships through longitudinal rather than cross-sectional analysis, thus involving historical data. We also considered passive smoking, occupational exposures, radon, and established carcinogens. We found stable nonsmoking LCM rates during periods of improving ambient air quality. We considered 59 cross-sectional studies of lung cancer and air pollution and found similar statistically significant relative risks for PM_2.5, PM₁₀, EC, NO₂, SO₂, SO^2?₄, and O₃, and minimal risks for benzo(alpha)pyrene and trace metals. Most air pollution studies did not consider latency, exposure duration, or temporal trends; none included estimates of smoking risks implied by their models. We conclude that while LCM studies of smoking, radon, and occupational exposures appropriately considered latency and cumulative exposures; ambient air quality studies have not. Lung cancer has a long memory and exposure histories are required. Effects of cumulative exposures after pollution abatement include substantially reduced risk estimates, delayed health benefits, inability to show accountability for the abatement. However, associations of lung cancer with ambient air pollution cannot be ruled out, especially for historic periods when much higher exposures persisted. Given the major reductions in air quality and smoking habits that have been realized since the Clean Air Act, new studies of LCM and air pollution, including smoking histories and exposure data decades before diagnosis, are needed.

• Highlights

• Lifetime cigarette consumption is a good predictor of lung cancer risk.

• The latent period for lung cancer ranges from about 10 to 30 y.

• Lung cancer risks for nonsmokers have been stable during the period when ambient air quality improved substantially.

• Risks of established airborne carcinogens may have been important in the past but not under current conditions.

• Radon can be important.

• Air pollution-lung cancer risks should be evaluated jointly with smoking risks but are sensitive to their accuracy.

• When cumulative exposures to conventional air pollutants are considered rather than concurrent, the applicable risk estimates may decrease by an order of magnitude and abatement benefits will not be readily apparent.

• Most of the recent cross-sectional studies of lung cancer and regulated air pollutants did not consider latency, duration of exposure, or established carcinogens and their findings have been misinterpreted.

• Effects of smoking on LCM are now well established as are the spatial distributions of ambient air pollution; however, linkages among the three parameters remain uncertain.

     

Air Pollution and Postneonatal Mortality in a Tropical City: Kaohsiung,Taiwan

With growing evidence of the association between daily mortality and air pollution in adults, it is important to investigate whether infants are also susceptible to the adverse health effects of ambient air pollutants. The purpose of this study is to examine the relationship between air pollution and postneonatal mortality in Kaohsiung, Taiwan, a large industrial city with a tropical climate, during the period 1994–2000, using a case-crossover analysis. Case–crossover analysis provides an alternative to Poisson time-series regression for studying the short-term adverse health effects of air pollution. The air pollutants examined included particulate matter (PM₁₀), sulfur dioxide (SO₂), ozone (O₃), nitrogen dioxide (NO₂), and carbon monoxide (CO). The risk of postneonatal deaths was estimated to increase by 4.0% per 67 μg/m³ (the interquartile range in daily ambient concentration of PM₁₀) for PM₁₀, 1.8% per 17.84 ppb for NO₂, 5.1% per 0.31 ppm for CO, and 4.6% per 19.20 ppb for O₃. Although positive, none of these associations achieved statistical significance. The established link between air pollution levels and infant mortality may not be as strong in cities with tropical climates, although other factors such as differences in pollutant mix or the underlying health of the postneonates may explain the lack of a strong association in this study. Further studies of this type in cities with varying climates and cultures are needed.     

Association between gaseous air pollution and hospital admissions for hypertension in Taipei,Taiwan

Air pollution exposure has been reported to influence blood pressure. However, only a few epidemiological studies demonstrated association between ambient air pollution exposure and acute hypertensive events. The aim of this study was to examine the association between gaseous air pollutants exposure and hospital admissions for hypertension in Taipei, Taiwan. Data on hospital admissions for hypertension and ambient air pollution in Taipei were obtained for the 2009–2013 period. An odds ratio (OR) for number of hospital admissions for hypertension associated with each interquartile range increase in each gaseous air pollutant was calculated using a case-crossover approach, after controlling for weather variables, day of the week, seasonality, and long-term time trends. In the single-pollutant model, significant correlation was observed between number of hospital admissions for hypertension and ozone (O₃) levels both on warm (>23°C) and cool (<23°C) days, with OR of 1.2 (95% confidence interval [CI] = 1.03–1.4) and 1.2 (95% CI = 1.02–1.42), respectively. No significant associations were found between levels of other gaseous pollutants and risk of hospital admissions for hypertension. In the two-pollutant model, O₃ levels remained significant after inclusion of particulate matter 10 μm or less in diameter (PM₁₀), sulfur dioxide (SO₂), or carbon monoxide (CO) on warm days. On cool days, O₃ levels remained significant after inclusion of air pollutants other than SO₂. These findings indicated that O₃ exposure may trigger a rise in blood pressure to a level that results in higher number of hospital admissions.     

Current data on atmospheric pollutions

Atmospheric pollutions (AP) are very important for human health and ecological equilibrium. They may be natural or anthropogenic and in this later case they can appear outdoor or indoor. Urban air pollution is the most known form of AP. Its main sources are industries, individual and collective heating and now mainly automobile traffic in most cities. Classical AP indicators are SO2, particles, NOx, CO and Pb measured in networks. Important factors of AP are amounts of pollutants emitted and local climatic and meteorological characteristics. Health effects of AP peaks and of AP background levels are not well known. But generally, mean AP levels of SO2 and particles decreased in the last years in most towns as the consequence of collective actions on the three main sources of AP and on fuels, emission and immission levels; but more is wanted about motor-cars. Progress are necessary for limitation of three major ecological risks: "acid-rain" (SO2 and NOx derivatives, ozone,...) which participates in lake and forest attacks; "green house" effects whose air CO2 concentration increase is the main responsible, and stratospheric ozone depletion mainly due to freons (CFC); the consequences of these two last phenomena are not well known but ecological and health risk exist. Besides, indoor air pollution (IAP) is very important because we live more than 20 h a day indoor. IAP may be occupational (a lot of chemical or biological agents) or not. In the later case air pollutants are very various: CO, NOx and particles from heating or cooking, formaldehyde from wood glue, plywood or urea-formol foams, radon and derivatives in some granitic countries, odd jobs products, cosmetics, aero-allergens of chemical or biological origins, microbes,... Environmental tobacco smoke (ETS) is also an important pollutant complex. Risks of IAP are real or potential: acute risk is obvious for CO, aero-allergens, formaldehyde, NOx,...); irritations are produced by ETS, formaldehyde, solvants,...; long term or potential risks are of concern for asbest, radon,... A complex and bad known pathology is described in a lot of modern buildings as the "Sick Building Syndrom". Indoor air quality is very dependant of the quality of ventilation and possible air treatment. It may be considered in all urban epidemiological studies about air pollution.     

Association between fine particulate air pollution and hospital admissions for chest pain in a subtropical city: Taipei,Taiwan

This study determined the association between fine particles (PM_2.5) levels and hospital admissions for chest pain (CP) in Taipei, Taiwan. Hospital admissions for CP and ambient air pollution data for Taipei were obtained for the period 2009–2013. The relative risk of hospital admissions was estimated using a case-crossover approach, after controlling for weather variables, day of the week, seasonality, and long-term time trends. For single-pollutant models (without adjustment for other pollutants), increased frequency of CP admissions was significantly associated with PM_2.5 levels on warm days (>23°C), with an interquartile range rise correlated with a 15% (95% confidence interval = 11–31%) elevation in number of CP admissions. In two-pollutant models, PM_2.5 remained significant after inclusion of each of the other four pollutants: sulfur dioxide (SO₂), nitrogen dioxide (NO₂), carbon monoxide (CO), and ozone (O₃) on warm days. Generally, no marked associations were observed between PM_2.5 levels and risk of CP admissions on cool days in both single- and two-pollutant models. This study provides evidence that higher PM_2.5 concentrations enhance the risk of hospital admissions for CP on warm days.     

Influence of Relatively Low Level of Particulate Air Pollution on Hospitalization for COPD in Elderly People

To assess the association between relatively low levels of size-fractioned particulate matter (PM) and hospitalization for chronic obstructive pulmonary disease (COPD), we conducted a time-series analysis among elderly people 65 yr of age or more living in Vancouver between June 1995 and March 1999. Measures of thoracic PM (PM₁₀), fine PM (PM_2.5), coarse PM (PM_10?2.5), and coefficient of haze (COH) were examined over periods varying from 1 to 7 days prior to hospital admissions. Generalized additive models (GAMs; general linear models, GLMs) were used, and temporal trends and seasonal and subseasonal cycles in COPD hospitalizations were removed by using GLM with parametric natural cubic splines. The relative risks were calculated based on an incremental exposure corresponding to the interquartile range of these measures, and were adjusted for daily weather conditions and gaseous pollutants. PM measures had a positive effect on COPD hospitalization, especially 0 to 2 days prior to the admissions, before copollutants were accounted for. For 3-day average levels of exposure the relative risk estimates were 1.13 (95% confidence interval: 1.05–1.21) for PM₁₀, 1.08 (1.02–1.15) for PM_2.5, 1.09 (1.03–1.16) for PM_10?2.5, and 1.05 (1.01–1.09) for COH. The associations were no longer significant when NO₂ was included in the models. We concluded that the particle-related measures were significantly associated with COPD hospitalization in the Vancouver area, where the level of air pollution is relatively low, but the effects were not independent of other air pollutants.     

Inferring frail life expectancies in Chicago from daily fluctuations in elderly mortality

Abstract

Susceptible sub-populations with existing disease have exhibited stronger relationships between air quality and mortality in time-series studies, but their associated life expectancies have largely been overlooked. Murray and Nelson developed a new time-series model that estimated a small unobserved (frail) sub-population and their resulting life expectancies in Philadelphia, including environment relationships. As a further example in a different geographic area, we used this model with 1987–2000 daily mortality data in Chicago and found a stable frail population at risk of ～900 persons with a mean life expectancy of ～11 days; fewer than two daily deaths were associated with air pollution. We considered daily concentrations of CO, NO₂, O₃, PM₁₀ and SO₂, and found PM₁₀ and O₃ to have stronger associations with frail mortality. Our estimates of life expectancy and air pollution and temperature relationships are similar to those found in other studies that used different methods. Temperature was more important than air pollution during the 1995 heat wave, when mortality risks increased dramatically after 2?d exposure and life expectancies decreased to 3–5?d. Modeling this event separately had substantial effects on lagged mortality – air pollution relationships and the population at risk. The premises of the Murray–Nelson model were supported by simultaneously considering an additional subgroup of non-frail individuals; they contributed only ～1% of total elderly deaths. We conclude that frail life expectancies estimated by the Murray–Nelson model are robust, and that under these conditions non-frail persons have little risk of acute mortality, with or without contributions from air pollution.     

PM2.5 constituents and related air quality variables as predictors of survival in a cohort of U.S. military veterans

Air quality data on trace metals, other constituents of PM2.5, and criteria air pollutants were used to examine relationships with long-term mortality in a cohort of male U.S. military veterans, along with data on vehicular traffic density (annual vehicle-miles traveled per unit of land area). The analysis used county-level environmental data for the period 1997-2002 and cohort mortality for 1997-2001. The proportional hazards model included individual data on age, race, smoking, body mass index, height, blood pressure, and selected interactions; contextual variables also controlled for climate, education, and income. In single-pollutant models, traffic density appears to be the most important predictor of survival, but potential contributions are also seen for NO2, NO3-, elemental carbon, nickel, and vanadium. The effects of the other main constituents of PM2.5, of crustal particles, and of peak levels of CO, O3, or SO2 appear to be less important. Traffic density is also consistently the most important environmental predictor in multiple-pollutant models, with combined relative risks up to about 1.2. However, from these findings it is not possible to discern which aspects of traffic (pollution, noise, stress) may be the most relevant to public health or whether an area-based predictor such as traffic density may have an inherent advantage over localized measures of ambient air quality. It is also possible that traffic density could be a marker for unmeasured pollutants or for geographic gradients per se. Pending resolution of these issues, including replication in other cohorts, it will be difficult to formulate additional cost-effective pollution control strategies that are likely to benefit public health.