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C Arden Pope

Publications and source records attributed to C Arden Pope.

7 recordsLinked to original sources
PubMed2004

Ambient particulate air pollution, heart rate variability, and blood markers of inflammation in a panel of elderly subjects.

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 less than or equal to 2.5 microm (PM2.5)] and HRV, C-reactive protein (CRP), blood cell counts, and whole blood viscosity. A 100- microg/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 = 11)-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 = 0.17)-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 PM2.5 may be one of multiple factors that influence HRV and CRP.

Aged↗
PubMed2003

Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

BACKGROUND: Epidemiologic studies have linked long-term exposure to fine particulate matter air pollution (PM) to broad cause-of-death mortality. Associations with specific cardiopulmonary diseases might be useful in exploring potential mechanistic pathways linking exposure and mortality. METHODS AND RESULTS: General pathophysiological pathways linking long-term PM exposure with mortality and expected patterns of PM mortality with specific causes of death were proposed a priori. Vital status, risk factor, and cause-of-death data, collected by the American Cancer Society as part of the Cancer Prevention II study, were linked with air pollution data from United States metropolitan areas. Cox Proportional Hazard regression models were used to estimate PM-mortality associations with specific causes of death. Long-term PM exposures were most strongly associated with mortality attributable to ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. For these cardiovascular causes of death, a 10-microg/m3 elevation in fine PM was associated with 8% to 18% increases in mortality risk, with comparable or larger risks being observed for smokers relative to nonsmokers. Mortality attributable to respiratory disease had relatively weak associations. CONCLUSIONS: Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function. Although smoking is a much larger risk factor for cardiovascular disease mortality, exposure to fine PM imposes additional effects that seem to be at least additive to if not synergistic with smoking.

Adult↗
PubMed2002

Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution.

CONTEXT: Associations have been found between day-to-day particulate air pollution and increased risk of various adverse health outcomes, including cardiopulmonary mortality. However, studies of health effects of long-term particulate air pollution have been less conclusive. OBJECTIVE: To assess the relationship between long-term exposure to fine particulate air pollution and all-cause, lung cancer, and cardiopulmonary mortality. DESIGN, SETTING, AND PARTICIPANTS: Vital status and cause of death data were collected by the American Cancer Society as part of the Cancer Prevention II study, an ongoing prospective mortality study, which enrolled approximately 1.2 million adults in 1982. Participants completed a questionnaire detailing individual risk factor data (age, sex, race, weight, height, smoking history, education, marital status, diet, alcohol consumption, and occupational exposures). The risk factor data for approximately 500 000 adults were linked with air pollution data for metropolitan areas throughout the United States and combined with vital status and cause of death data through December 31, 1998. MAIN OUTCOME MEASURE: All-cause, lung cancer, and cardiopulmonary mortality. RESULTS: Fine particulate and sulfur oxide--related pollution were associated with all-cause, lung cancer, and cardiopulmonary mortality. Each 10-microg/m(3) elevation in fine particulate air pollution was associated with approximately a 4%, 6%, and 8% increased risk of all-cause, cardiopulmonary, and lung cancer mortality, respectively. Measures of coarse particle fraction and total suspended particles were not consistently associated with mortality. CONCLUSION: Long-term exposure to combustion-related fine particulate air pollution is an important environmental risk factor for cardiopulmonary and lung cancer mortality.

Adult↗
PubMedDate not supplied

Spatial regression models for large-cohort studies linking community air pollution and health.

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.

Air Pollution↗