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BACKGROUND: Exceptional aging, defined as reaching age 85 years, shows geographic inequalities that may depend on local environmental conditions. Links between particulate pollution--a wellrecognized environmental risk factor--and exceptional aging have not been investigated. OBJECTIVES: We conducted a nationwide analysis of ~28 million adults in 3,034 United States counties to determine whether local [PM.sub.2.5] levels (particulate matter < 2.5 pm in aerodynamic diameter) affected the probability of becoming 85-to 94-year-olds or centenarians (100- to 104-year-olds) in 2010 for individuals who were 55-64 or 70-74 years old, respectively, in 1980. METHODS: We used population-weighted regression models including county-level [PM.sub.2.5] from hybrid land-use regression and geostatistical interpolation, smoking, obesity, sociodemographic, and age-specific migration variables. RESULTS: On average, 2,295 and 71.4 per 10,000 of the 55- to 64- and 70- to 74-year-olds in 1980, respectively, remained in the 85- to 94- and 100- to 104-year-old population in 2010. An interquartile range (4.19 µg/[m.sup.3]) increase in [PM.sub.2.5] was associated with 93.7 fewer 85- to 94-yearolds (p < 0.001) and 3.5 fewer centenarians (p < 0.05). These associations were nearly linear, were stable to model specification, and were detectable below the annual [PM.sub.2.5] national standard. Exceptional aging was strongly associated with smoking, with an interquartile range (4.77%) increase in population who smoked associated with 181.9 fewer 85- to 94-year-olds (p < 0.001) and 6.4 fewer centenarians (p < 0.001). Exceptional aging was also associated with obesity rates and median income. CONCLUSIONS: Communities with the most exceptional aging have low ambient air pollution and low rates of smoking, poverty, and obesity. Improvements in these determinants may contribute to increasing exceptional aging. http://dx.doi.org/10.1289/EHP197, Introduction Recent declines in mortality have resulted in a worldwide increase in exceptional aging, defined as reaching age 85 years or older [National Institute on Aging (NIA) 2013]. Persons ≥ [...]

INTRODUCTION Herein is the discussion of the 2006 A & WMA Critical Review (1,2) on 'Health Effects of Fine Particulate Air Pollution: Lines that Connect.' In the review, Drs. C. [...]

ABSTRACT Efforts to understand and mitigate the health effects of particulate matter (PM) air pollution have a rich and interesting history. This review focuses on six substantial lines of research [...]

Intermittent operation of a steel mill in a mountain valley in central Utah provides a unique opportunity to measure the external health costs of air pollution. A nearby valley provides a control. This paper analyzes data on hospital admissions and daily deaths for the two valleys, using negative binomial regression models of daily hospital admissions and deaths. Hospital admissions for respiratory diseases increase significantly when the mill is in operation. Mortality also increases during mill operation. Estimated excess hospitalization costs are about 2 million dollars per year, and the increased cost of mortality exceeds 40 million dollars per year., I. INTRODUCTION This study estimates some of the external health costs associated with the operation of an integrated steel mill in Utah Valley. The mill is the largest source of [...]

BACKGROUND: Estimating the burden of disease attributable to long-term exposure to fine particulate matter ([PM.sub.2.5]) in ambient air requires knowledge of both the shape and magnitude of the relative risk (RR) function. However, adequate direct evidence to identify the shape of the mortality RR functions at the high ambient concentrations observed in many places in the world is lacking. OBJECTIVE: We developed RR functions over the entire global exposure range for causes of mortality in adults: ischemic heart disease (IHD), cerebrovascular disease (stroke), chronic obstructive pulmonary disease (COPD), and lung cancer (LC). We also developed RR functions for the incidence of acute lower respiratory infection (ALRI) that can be used to estimate mortality and lost-years of healthy life in children < 5 years of age. METHODS: We fit an integrated exposure--response (IER) model by integrating available RR information from studies of ambient air pollution (AAP), second hand tobacco smoke, household solid cooking fuel, and active smoking (AS). AS exposures were converted to estimated annual [PM.sub.2.5] exposure equivalents using inhaled doses of particle mass. We derived population attributable fractions (PAFs) for every country based on estimated worldwide ambient [PM.sub.2.5] concentrations. RESULTS: The IER model was a superior predictor of RR compared with seven other forms previously used in burden assessments. The percent PAF attributable to AAP exposure varied among countries from 2 to 41 for IHD, 1 to 43 for stroke, < 1 to 21 for COPD, < 1 to 25 for LC, and < 1 to 38 for ALRI. CONCLUSIONS: We developed a fine particulate mass--based RR model that covered the global range of exposure by integrating RR information from different combustion types that generate emissions of particulate matter. The model can be updated as new RR information becomes available. CITATION: Burnett RT, Pope CA III, Ezzati M, Olives C, Lim SS, Mehta S, Shin HH, Singh G, Hubbell B, Brauer M, Anderson HR, Smith KR, Balmes JR, Bruce NG, Kan H, Laden F, Pruss-Ustun A, Turner MC, Gapstur SM, Diver WR, Cohen A. 2014. An integrated risk function for estimating the global burden of disease attributable to ambient fine particulate matter exposure. Environ Health Perspect 122:397-403; http://dx.doi.org/10.1289/ehp.1307049, Introduction Long-term exposure to ambient fine particulate matter ([less than or equal to] 2.5 µg/[m.sup.3] in aerodynamic diameter; [PM.sub.2.5]) is associated with increased mortality from nonaccidental and cause-specific diseases (Brook [...]

An editorial is presented on adults with Chronic Obstructive Pulmonary Disease being vulnerable to air pollution and cardiovascular risk. Topics include mortality associations being observed in cohorts of patients receiving a cardiac transplant and survivors of myocardial infarction (MI); and allowing for model adjustments for age, sex, race/ethnicity, smoking, body mass index, and baseline comorbidities.

BACKGROUND: Evidence indicates that air pollution contributes to cardiopulmonary mortality. There is ongoing debate regarding the size and shape of the pollution-mortality exposure-response relationship. There are also growing appeals for estimates of pollution-mortality relationships that use public data and are based on large, representative study cohorts. OBJECTIVES: Our goal was to evaluate fine particulate matter air pollution (PM2:5) and mortality using a large cohort that is representative of the U.S. population and is based on public data. Additional objectives included exploring model sensitivity, evaluating relative effects across selected subgroups, and assessing the shape of the PM2:5-mortality relationship. METHODS: National Health Interview Surveys (1986-2014), with mortality linkage through 2015, were used to create a cohort of 1,599,329 U.S. adults and a subcohort with information on smoking and body mass index (BMI) of 635,539 adults. Data were linked with modeled ambient PM2:5 at the census-tract level. Cox proportional hazards models were used to estimate PM2:5-mortality hazard ratios for all-cause and specific causes of death while controlling for individual risk factors and regional and urban versus rural differences. Sensitivity and subgroup analyses were conducted and the shape of the PM2:5-mortality relationship was explored. RESULTS: Estimated mortality hazard ratios, per 10 lg=m³ long-term exposure to PM2:5, were 1.12 (95% CI: 1.08, 1.15) for all-cause mortality, 1.23 (95% CI: 1.17, 1.29) for cardiopulmonary mortality, and 1.12 (95% CI: 1.00, 1.26) for lung cancer mortality. In general, PM2:5-mortality associations were consistently positive for all-cause and cardiopulmonary mortality across key modeling choices and across subgroups of sex, age, race-ethnicity, income, education levels, and geographic regions. DISCUSSION: This large, nationwide, representative cohort of U.S. adults provides robust evidence that long-term PM2:5 exposure contributes to cardiopulmonary mortality risk. The ubiquitous and involuntary nature of exposures and the broadly observed effects across subpopulations underscore the public health importance of breathing clean air. [ABSTRACT FROM AUTHOR]

Exposure to ambient fine particulate matter (PM2.5) is a major global health concern. Quantitative estimates of attributable mortality are based on disease-specific hazard ratio models that incorporate risk information from multiple PM2.5 sources (outdoor and indoor air pollution from use of solid fuels and secondhand and active smoking), requiring assumptions about equivalent exposure and toxicity. We relax these contentious assumptions by constructing a PM2.5-mortality hazard ratio function based only on cohort studies of outdoor air pollution that covers the global exposure range. We modeled the shape of the association between PM2.5 and nonaccidental mortality using data from 41 cohorts from 16 countries-- the Global Exposure Mortality Model (GEMM). We then constructed GEMMs for five specific causes of death examined by the global burden of disease (GBD). The GEMM predicts 8.9 million [95% confidence interval (CI): 7.5-10.3] deaths in 2015, a figure 30% larger than that predicted by the sum of deaths among the five specific causes (6.9; 95% CI: 4.9-8.5) and 120% larger than the risk function used in the GBD (4.0; 95% CI: 3.3-4.8). Differences between the GEMM and GBD risk functions are larger for a 20% reduction in concentrations, with the GEMM predicting 220% higher excess deaths. These results suggest that PM2.5 exposure may be related to additional causes of death than the five considered by the GBD and that incorporation of risk information from other, nonoutdoor, particle sources leads to underestimation of disease burden, especially at higher concentrations. [ABSTRACT FROM AUTHOR]

BACKGROUND: The International Agency for Research on Cancer classified both outdoor air pollution and airborne particulate matter as carcinogenic to humans (Group 1) for lung cancer. There may be associations with cancer at other sites; however, the epidemiological evidence is limited. OBJECTIVE: The aim of this study was to clarify whether ambient air pollution is associated with specific types of cancer other than lung cancer by examining associations of ambient air pollution with nonlung cancer death in the Cancer Prevention Study II (CPS-II). METHODS: Analysis included 623,048 CPS-II participants who were followed for 22 y (1982-2004). Modeled estimates of particulate matter with aerodynamic diameter <2:5 μm (PM2.5) (1999-2004), nitrogen dioxide (NO2) (2006), and ozone (O3) (2002-2004) concentrations were linked to the participant residence at enrollment. Cox proportional hazards models were used to estimate associations per each fifth percentile-mean increment with cancer mortality at 29 anatomic sites, adjusted for individual and ecological covariates. RESULTS: We observed 43,320 nonlung cancer deaths. PM2.5 was significantly positively associated with death from cancers of the kidney {adjusted hazard ratio (HR) per 4:4 μg=m3 =1:14 [95% confidence interval (CI): 1.03, 1.27]} and bladder [HR=1:13 (95% CI: 1.03, 1.23)]. NO2 was positively associated with colorectal cancer mortality [HR per 6:5 ppb=1:06 (95% CI: 1.02, 1.10). The results were similar in two-pollutant models including PM2:5 and NO2 and in three-pollutant models with O3. We observed no statistically significant positive associations with death from other types of cancer based on results from adjusted models. CONCLUSIONS: The results from this large prospective study suggest that ambient air pollution was not associated with death from most nonlung cancers, but associations with kidney, bladder, and colorectal cancer death warrant further investigation. [ABSTRACT FROM AUTHOR]

Estimates of excess mortality associated with exposure to ambient concentrations of fine particulate matter have been obtained from either a single cohort study or pooling information from a small number of studies. However, standard frequentist methods of pooling are known to underestimate statistical uncertainty in the true risk distribution when the number of studies pooled is small. Alternatively, Bayesian pooling methods using noninformative priors yield unrealistically large amounts of uncertainty in this case. We present a new hybrid frequentist-bayesian framework for meta-analysis that incorporates features of both frequentist and Bayesian approaches, yielding estimated uncertainty distributions that are more useful for burden estimation. We also present an example of mortality risk due to long-term exposure to ambient fine particulate matter obtained from a small number of cohort studies conducted in the United States and Europe. We compare our new risk uncertainty distribution to that obtained by the integrated exposure-response (IER) model used in the Global Burden of Disease 2010 project for which risk was modeled over the entire global concentration range. We suggest a method to incorporate our new risk uncertainty distribution based on the relatively low concentrations observed in the United States and western Europe into the IER model, thus extending risk estimation to the global concentration range. [ABSTRACT FROM AUTHOR]

Background: Income, air pollution, obesity, and smoking are primary factors associated with human health and longevity in population-based studies. These four factors may have countervailing impacts on longevity. This analysis investigates longevity trade-offs between air pollution and income, and explores how relative effects of income and air pollution on human longevity are potentially influenced by accounting for smoking and obesity.Methods: County-level data from 2,996 U.S. counties were analyzed in a cross-sectional analysis to investigate relationships between longevity and the four factors of interest: air pollution (mean 1999-2008 PM2.5), median income, smoking, and obesity. Two longevity measures were used: life expectancy (LE) and an exceptional aging (EA) index. Linear regression, generalized additive regression models, and bivariate thin-plate smoothing splines were used to estimate the benefits of living in counties with higher incomes or lower PM2.5. Models were estimated with and without controls for smoking, obesity, and other factors.Results: Models which account for smoking and obesity result in substantially smaller estimates of the effects of income and pollution on longevity. Linear regression models without these two variables estimate that a $1,000 increase in median income (1 μg/m(3) decrease in PM2.5) corresponds to a 27.39 (33.68) increase in EA and a 0.14 (0.12) increase in LE, whereas models that control for smoking and obesity estimate only a 12.32 (20.22) increase in EA and a 0.07 (0.05) increase in LE. Nonlinear models and thin-plate smoothing splines also illustrate that, at higher levels of income, the relative benefits of the income-pollution tradeoff changed-the benefit of higher incomes diminished relative to the benefit of lower air pollution exposure.Conclusions: Higher incomes and lower levels of air pollution both correspond with increased human longevity. Adjusting for smoking and obesity reduces estimates of the benefits of higher income and lower air pollution exposure. This adjustment also alters the tradeoff between income and pollution: increases in income become less beneficial relative to a fixed reduction in air pollution-especially at higher levels of income. [ABSTRACT FROM AUTHOR]

BACKGROUND: Fine particulate matter (PM2.5) air pollution exposure has been identified as a global health threat. However, the types and sources of particles most responsible are not yet known. OBJECTIVES: We sought to identify the causal characteristics and sources of air pollution underlying past associations between long-term PM2.5 exposure and ischemic heart disease (IHD) mortality, as established in the American Cancer Society's Cancer Prevention Study-II cohort. METHODS: Individual risk factor data were evaluated for 445,860 adults in 100 U.S. metropolitan areas followed from 1982 through 2004 for vital status and cause of death. Using Cox proportional hazard models, we estimated IHD mortality hazard ratios (HRs) for PM2.5, trace constituents, and pollution source-associated PM2.5, as derived from air monitoring at central stations throughout the nation during 2000-2005. RESULTS: Associations with IHD mortality varied by PM2.5 mass constituent and source. A coal combustion PM2.5 IHD HR = 1.05 (95% CI: 1.02, 1.08) per microgram/cubic meter, versus an IHD HR = 1.01 (95% CI: 1.00, 1.02) per microgram/cubic meter PM2.5 mass, indicated a risk roughly five times higher for coal combustion PM2.5 than for PM2.5 mass in general, on a per microgram/cubic meter PM2.5 basis. Diesel traffic-related elemental carbon (EC) soot was also associated with IHD mortality (HR = 1.03; 95% CI: 1.00, 1.06 per 0.26-µg/m³ EC increase). However, PM2.5 from both wind-blown soil and biomass combustion was not associated with IHD mortality. CONCLUSIONS: Long-term PM2.5 exposures from fossil fuel combustion, especially coal burning but also from diesel traffic, were associated with increases in IHD mortality in this nationwide population. Results suggest that PM2.5-mortality associations can vary greatly by source, and that the largest IHD health benefits per microgram/cubic meter from PM2.5 air pollution control may be achieved via reductions of fossil fuel combustion exposures, especially from coal-burning sources. [ABSTRACT FROM AUTHOR]

BACKGROUND: Few studies examining the associations between long-term exposure to ambient air pollution and mortality have considered multiple pollutants when assessing changes in exposure due to residential mobility during follow-up. OBJECTIVE: We investigated associations between cause-specific mortality and ambient concentrations of fine particulate matter (≤ 2.5 µm; PM2.5), ozone (O3), and nitrogen dioxide (NO2) in a national cohort of about 2.5 million Canadians. METHODS: We assigned estimates of annual concentrations of these pollutants to the residential postal codes of subjects for each year during 16 years of follow-up. Historical tax data allowed us to track subjects' residential postal code annually. We estimated hazard ratios (HRs) for each pollutant separately and adjusted for the other pollutants. We also estimated the product of the three HRs as a measure of the cumulative association with mortality for several causes of death for an increment of the mean minus the 5th percentile of each pollutant: 5.0 µg/m³ for PM2.5, 9.5 ppb for O3, and 8.1 ppb for NO2. RESULTS: PM2.5, O3, and NO2 were associated with nonaccidental and cause-specific mortality in single-pollutant models. Exposure to PM2.5 alone was not sufficient to fully characterize the toxicity of the atmospheric mix or to fully explain the risk of mortality associated with exposure to ambient pollution. Assuming additive associations, the estimated HR for nonaccidental mortality corresponding to a change in exposure from the mean to the 5th percentile for all three pollutants together was 1.075 (95% CI: 1.067, 1.084). Accounting for residential mobility had only a limited impact on the association between mortality and PM2.5 and O3, but increased associations with NO2. CONCLUSIONS: In this large, national-level cohort, we found positive associations between several common causes of death and exposure to PM2.5, O3, and NO2. [ABSTRACT FROM AUTHOR]

Background: Few cohort studies have evaluated the risk of mortality associated with long-term exposure to fine particulate matter [≤ 2.5 µm in aerodynamic diameter (PM2.5)]. This is the first national-level cohort study to investigate these risks in Canada. Objective: We investigated the association between long-term exposure to ambient PM2.5 and cardiovascular mortality in nonimmigrant Canadian adults. Methods: We assigned estimates of exposure to ambient PM2.5 derived from satellite observations to a cohort of 2.1 million Canadian adults who in 1991 were among the 20% of the population mandated to provide detailed census data. We identified deaths occurring between 1991 and 2001 through record linkage. We calculated hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for available individual-level and contextual covariates using both standard Cox proportional survival models and nested, spatial random-effects survival models. Results: Using standard Cox models, we calculated HRs of 1.15 (95% CI: 1.13, 1.16) from nonaccidental causes and 1.31 (95% CI: 1.27, 1.35) from ischemic heart disease for each 10-µg/m3 increase in concentrations of PM2.5. Using spatial random-effects models controlling for the same variables, we calculated HRs of 1.10 (95% CI: 1.05, 1.15) and 1.30 (95% CI: 1.18, 1.43), respectively. We found similar associations between nonaccidental mortality and PM2.5 based on satellite-derived estimates and ground-based measurements in a subanalysis of subjects in 11 cities. Conclusions: In this large national cohort of nonimmigrant Canadians, mortality was associated with long-term exposure to PM2.5. Associations were observed with exposures to PM2.5 at concentrations that were predominantly lower (mean, 8.7 µg/m3; interquartile range, 6.2 µg/m3) than those reported previously. [ABSTRACT FROM AUTHOR]

Background: Lung cancer and cardiovascular disease (CVD) mortality risks increase with smoking, secondhand smoke (SHS), and exposure to fine particulate matter < 2.5 μm in diameter (PM2.5) from ambient air pollution. Recent research indicates that the exposure-response relationship for CVD is nonlinear, with a steep increase in risk at low exposures and flattening out at higher exposures. Comparable estimates of the exposure-response relationship for lung cancer are required for disease burden estimates and related public health policy assessments.Objectives: We compared exposure-response relationships of PM2.5 with lung cancer and cardiovascular mortality and considered the implications of the observed differences for efforts to estimate the disease burden of PM2.5.Methods: Prospective cohort data for 1.2 million adults were collected by the American Cancer Society as part of the Cancer Prevention Study II. We estimated relative risks (RRs) for increments of cigarette smoking, adjusting for various individual risk factors. RRs were plotted against estimated daily dose of PM2.5 from smoking along with comparison estimates for ambient air pollution and SHS. Results: For lung cancer mortality, excess risk rose nearly linearly, reaching maximum RRs > 40 among long-term heavy smokers. Excess risks for CVD mortality increased steeply at low exposure levels and leveled off at higher exposures, reaching RRs of approximately 2-3 for cigarette smoking. Conclusions: The exposure-response relationship associated with PM2.5 is qualitatively different for lung cancer versus cardiovascular mortality. At low exposure levels, cardiovascular deaths are projected to account for most of the burden of disease, whereas at high levels of PM2.5, lung cancer becomes proportionately more important. [ABSTRACT FROM AUTHOR]

Exposure to fine particulate air pollution has been implicated as a risk factor for cardiopulmonary disease and mortality. Proposed biological pathways imply that particle- induced pulmonary and systemic inflammation play a role in activating the vascular endothelium and altering vascular function. Potential effects of fine particulate pollution on vascular function are explored using controlled chamber exposure and uncontrolled ambient exposure. Research subjects included four panels with a total of 26 healthy nonsmoking young adults. On two study visits, at least 7 days apart, subjects spent 3 hr in a controlled-exposure chamber exposed to 150-200g/m⊃ of fine particles generated from coal or wood combustion and 3 hr in a clean room, with exposure and nonexposure periods alternated between visits. Baseline, postexposure, and post-clean room reactive hyperemia-peripheral arterial tonometry (RH-PAT) was conducted. A microvascular responsiveness index, defined as the log of the RH-PAT ratio, was calculated. There was no contemporaneous vascular response to the few hours of controlled exposure. Declines in vascular response were associated with elevated ambient exposures for the previous 2 days, especially for female subjects. Cumulative exposure to real-life fine particulate pollution may affect vascular function. More research is needed to determine the roles of age and gender, the effect of pollution sources, the importance of cumulative exposure over a few days versus a few hours, and the lag time between exposure and response. [ABSTRACT FROM AUTHOR]

The article presents the American Cancer Society Cancer Prevention Study-II conducted in the U.S. in 1982 which examined the link between residential radon and lung cancer mortality. The Cox proportional hazards regression model used is described, which also assessed other risk factors including cigarette smoking and ambient sulfate concentrations. Results show a positive trend between radon concentrations and lung cancer mortality. Efforts should be directed towards reducing radon concentrations in homes to the lowest possible level.

The article focuses on a study which examined whether exposure fine PM affects the endothelial progenitor cell (EPC) populations, inflammation, and coagulation. The EPC populations were quantified by flow cytometry in young adult humans exposed along the Wasatch Mountain Front in Utah. The study found no correlation between PM exposure and circulating EPC levels. It concludes that exposure to PM induces reversible vascular injury.

In September 2006, the US Environmental Protection Agency and the US Centers for Disease Control (CDC) co-organized a symposium on “Air Pollution Exposure and Health.” The main objective of this symposium was to identify opportunities for improving the use of exposure and health information in future studies of air pollution health effects. This paper deals with the health information needs of such studies. We begin with a selected review of different types of health data and how they were used in previous epidemiologic studies of health effects of ambient particulate matter (PM). We then examine the current and emerging information needs of the environmental health community, dealing with PM and other air pollutants of health concern. We conclude that the past use of routinely collected health data proved to be essential for activities to protect public health, including the identification and evaluation of health hazards by air pollution research, setting standards for criteria pollutants, surveillance of health outcomes to identify incidence trends, and the more recent CDC environmental public health tracking program. Unfortunately, access to vital statistics records that have informed such pivotal research has recently been curtailed sharply, threatening the continuation of the type of research necessary to support future standard setting and research on emerging exposure and health problems (e.g. asthma, multiple sclerosis, diabetes, and others), as well as our ability to evaluate the efficacy of regulatory and other prevention activities. A comprehensive devoted effort, perhaps new legislation, will be needed to address the standardization, centralization, and sharing of data sets, as well as to harmonize the interpretation of confidentiality and privacy protections across jurisdictions. These actions, combined with assuring researchers and public health practitioners appropriate access to data for evaluation of environmental risks, will be essential for the achievement of our environmental health protection goals.Journal of Exposure Science and Environmental Epidemiology (2009) 19, 45–58; doi:10.1038/jes.2008.41; published online 10 September 2008 [ABSTRACT FROM AUTHOR]

This article evaluates the dynamic exposure-response relationship between particulate matter air pollution (PM) and mortality risk by integrating epidemiological evidence from studies that use different time scales of exposure. The evidence suggests that short-term exposure studies are observing more than just harvesting or mortality displacement. There is little evidence of short-term compensatory reduction in deaths, and estimated PM effects are generally larger for intermediate and longer term time scales of exposure. Although proximity in time matters, with most recent exposure having the largest health impact, there is evidence that the short-term exposure studies capture only a small amount of the overall health effects of long-term repeated exposure to PM. The overall epidemiological evidence suggests that adverse health effects are dependent on both exposure concentrations and length of exposure, and that long-term exposures have larger, more persistent cumulative effects than short-term exposures. [ABSTRACT FROM AUTHOR]

Epidemiologic studies report associations between particulate air pollution and cardiopulmonary morbidity and mortality. Although the underlying pathophysiologic mechanisms remain unclear, it has been hypothesized that altered autonomic function and pulmonary/systemic inflammation may play a role. In this study we explored the effects of air pollution on autonomic function measured by changes in heart rate variability (HRV) and blood markers of inflammation in a panel of 88 elderly subjects from three communities along the Wasatch Front in Utah. Subjects participated in multiple sessions of 24-hr ambulatory electrocardiographic monitoring and blood tests. Regression analysis was used to evaluate associations between fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM2.5)] and HRV, C-reactive protein (CRP), blood cell counts, and whole blood viscosity. A 100-μg/m³ increase in PM2.5 was associated with approximately a 35 (SE = 8)-msec decline in standard deviation of all normal R-R intervals (SDNN, a measure of overall HRV); a 42 (SE = 1 1)-msec decline in square root of the mean of the squared differences between adjacent normal R-R intervals (r-MSSD, an estimate of short-term components of HRV); and a 0.81 (SE = O.17)-mg/dL increase in CRP. The PM2.5-HRV associations were reasonably consistent and statistically robust, but the CRP association dropped to 0.19 (SE = 0.10) after excluding the most influential subject. PM2.5 was not significantly associated with white or red blood cell counts, platelets, or whole-blood viscosity. Most short-term variability in temporal deviations of HRV and CRP was not explained by PM2.5 however, the small statistically significant associations that were observed suggest that exposure to may be one of multiple factors that influence HRV and CRP. [ABSTRACT FROM AUTHOR]

Discusses the epidemiologic research needs for particulate air pollution. Concerns over a series of reports of daily time-series analysis; Variation of effects of particles across locations; Magnitude of life shortening associated with particle exposure; Determinants of the toxicity of particles.

Comments on the Health Effects Institute (HEI) Reanalysis Project, a direct response to letters received from the U.S. Environmental Protection Agency (EPA) stating that EPA would encourage reasonable accommodations within the scientific and governmental community. Contributions of the reanalysis project; Basic concerns about the reanalysis.

Cohort study designs are often used to assess the association between community-based ambient air pollution concentrations and health outcomes, such as mortality, development and prevalence of disease, and pulmonary function. Typically, a large number of subjects are enrolled in the study in each of a small number of communities. Fixed-site monitors are used to determine long-term exposure to ambient pollution. The association between community average pollution levels and health is determined after controlling for risk factors of the health outcome measured at the individual level (i.e., smoking). We present a new spatial regression model linking spatial variation in ambient air pollution to health. Health outcomes can be measured as continuous variables (pulmonary function), binary variables (prevalence of disease), or time-to-event data (survival or development of disease). The model incorporates risk factors measured at the individual level, such as smoking, and at the community level, such as air pollution. We demonstrate that the spatial autocorrelation in community health outcomes, an indication of not fully characterizing potentially confounding risk factors to the air pollution--health association, can be accounted for through the inclusion of location in the deterministic component of the model assessing the effects of air pollution on health or through a distance-decay spatial autocorrelation function in the stochastic component of the model, or both. We present a statistical approach that can be implemented for very large cohort studies. Our methods are illustrated with an analysis of the American Cancer Society cohort to determine whether the prevalence of heart disease is associated with concentrations of sulfate particles. From a statistical point of view, it appears that a location surface in the deterministic component of the model was preferred to a distance-decay autocorrelation structure in the model's stochastic component. [ABSTRACT FROM AUTHOR]

Examines the effects of exposure to environmental tobacco smoke (ETS) on the cardiovascular system. Indication of an altered cardiac autonomic control; Association of heart rate variability with ETS exposure; Deviation of normal-to-normal heart beat intervals.