Particulate air pollution, C-reactive protein, and cardiac risk.
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Air Pollution↗
Biomedical subjects
C A Pope
Publications and source records attributed to C A Pope.
Acute exposure to environmental tobacco smoke and heart rate variability.
Environmental tobacco smoke (ETS) has been associated with cardiovascular mortality. Pathophysiologic pathways leading from ETS exposure to cardiopulmonary disease are still being explored. Reduced cardiac autonomic function, as measured by heart rate variability (HRV), has been associated with cardiac vulnerability and may represent an important pathophysiologic mechanism linking ETS and risk of cardiac mortality. In this study we evaluated acute ETS exposure in a commercial airport with changes in HRV in 16 adult nonsmokers. We conducted ambulatory electrocardiographic (ECG) monitoring for 8-hr periods while participants alternated 2 hr in nonsmoking and smoking areas. Nicotine and respirable suspended particle concentrations and participants' blood oxygen saturation were also monitored. We calculated time and frequency domain measures of HRV for periods in and out of the smoking area, and we evaluated associations with ETS using comparative statistics and regression modeling. ETS exposure was negatively associated with all measures of HRV. During exposure periods, we observed an average decrement of approximately 12% in the standard deviation of all normal-to-normal heart beat intervals (an estimate of overall HRV). ETS exposures were not associated with mean heart rate or blood oxygen saturation. Altered cardiac autonomic function, assessed by decrements in HRV, is associated with acute exposure to ETS and may be part of the pathophysiologic mechanisms linking ETS exposure and increased cardiac vulnerability.
Adult↗
The spatial association between community air pollution and mortality: a new method of analyzing correlated geographic cohort data.
We present a new statistical model for linking spatial variation in ambient air pollution to mortality. The model incorporates risk factors measured at the individual level, such as smoking, and at the spatial level, such as air pollution. We demonstrate that the spatial autocorrelation in community mortality rates, an indication of not fully characterizing potentially confounding risk factors to the air pollution-mortality association, can be accounted for through the inclusion of location in the model assessing the effects of air pollution on mortality. Our methods are illustrated with an analysis of the American Cancer Society cohort to determine whether all cause mortality is associated with concentrations of sulfate particles. The relative risk associated with a 4.2 microg/m(3) interquartile range of sulfate distribution for all causes of death was 1.051 (95% confidence interval 1.036-1.066) based on the Cox proportional hazards survival model, assuming subjects were statistically independent. Inclusion of community-based random effects yielded a relative risk of 1.055 (1.033, 1.077), which represented a doubling in the residual variance compared to that estimated by the Cox model. Residuals from the random-effects model displayed strong evidence of spatial autocorrelation (p = 0.0052). Further inclusion of a location surface reduced the sulfate relative risk and the evidence for autocorrelation as the complexity of the location surface increased, with a range in relative risks of 1.055-1.035. We conclude that these data display both extravariation and spatial autocorrelation, characteristics not captured by the Cox survival model. Failure to account for extravariation and spatial autocorrelation can lead to an understatement of the uncertainty of the air pollution association with mortality.
Adolescent↗
Particulate matter-mortality exposure-response relations and threshold.
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Air Pollutants↗
What do epidemiologic findings tell us about health effects of environmental aerosols?
In the last 10 years there has been an abundance of new epidemiological studies on health effects of particulate air pollution. The overall evidence suggests that fine particulate pollution can be an important risk factor for cardiopulmonary disease. Long-term, repeated exposure to fine particulate air pollution may increase the risk of chronic respiratory disease and the risk of cardiopulmonary mortality. Short-term exposures exacerbate existing cardiovascular and pulmonary disease and increase the risk of becoming symptomatic, requiring medical attention, or even dying. This paper outlines the results of the basic epidemiologic studies and briefly reviews and discusses recent studies that have looked at specific physiologic health endpoints in addition to lung function. A few recent, mostly exploratory pilot studies, have observed particulate pollution associations with blood plasma viscosity, heart rate, heart rate variability, and indicators of bone marrow stimulation. A systemic response to particulate-related pulmonary inflammation remains somewhat speculative. The epidemiologic evidence, nevertheless, seems consistent with the hypothesis that particle-induced pulmonary inflammation, cytokine release, and altered cardiac autonomic function may be part of the pathophysiological mechanisms or pathways linking particulate pollution with cardiopulmonary disease.
Aerosols↗
Dissociative experience in hypothetically psychosis-prone college students.
The relationship between dissociative experiences and psychosis proneness was investigated in a sample of 523 college undergraduates. Participants were administered the Dissociative Experiences Scale (DES), the Perceptual Aberration Scale, the Magical Ideation Scale, the Social Anhedonia Scale, and the Physical Anhedonia Scale. As hypothesized, the Perceptual Aberration and Magical Ideation Scales were positively correlated with the DES. The Social Anhedonia Scale had a modest correlation with the DES, but this relationship was largely mediated by the Perceptual Aberration and Magical Ideation Scales. The Physical Anhedonia Scale was uncorrelated with the DES. Exploratory factor analysis of the psychosis-proneness scales and the DES subscales resulted in a three-factor solution: dissociative experiences, positive schizotypy, and negative schizotypy. The DES depersonalization subscale loaded on both the dissociation and positive schizotypy factors.
Adult↗
Epidemiology of fine particulate air pollution and human health: biologic mechanisms and who's at risk?
This article briefly summarizes the epidemiology of the health effects of fine particulate air pollution, provides an early, somewhat speculative, discussion of the contribution of epidemiology to evaluating biologic mechanisms, and evaluates who's at risk or is susceptible to adverse health effects. Based on preliminary epidemiologic evidence, it is speculated that a systemic response to fine particle-induced pulmonary inflammation, including cytokine release and altered cardiac autonomic function, may be part of the pathophysiologic mechanisms or pathways linking particulate pollution with cardiopulmonary disease. The elderly, infants, and persons with chronic cardiopulmonary disease, influenza, or asthma are most susceptible to mortality and serious morbidity effects from short-term acutely elevated exposures. Others are susceptible to less serious health effects such as transient increases in respiratory symptoms, decreased lung function, or other physiologic changes. Chronic exposure studies suggest relatively broad susceptibility to cumulative effects of long-term repeated exposure to fine particulate pollution, resulting in substantive estimates of population average loss of life expectancy in highly polluted environments. Additional knowledge is needed about the specific pollutants or mix of pollutants responsible for the adverse health effects and the biologic mechanisms involved.
Air Pollution↗
Heart rate variability associated with particulate air pollution.
BACKGROUND: Epidemiologic studies have linked fine particulate air pollution with cardiopulmonary mortality, yet underlying biologic mechanisms remain unknown. Changes in heart rate variability (HRV) may reflect changes in cardiac autonomic function and risk of sudden cardiac death. This study evaluated changes in mean heart rate and HRV in human beings associated with changes in exposure to particulate air pollution. METHODS: Repeated ambulatory electrocardiographic monitoring was conducted on 7 subjects for a total of 29 person-days before, during, and after episodes of elevated pollution. Mean HR, the standard deviation of normal-to-normal (NN) intervals (SDNN), the standard deviation of the averages of NN intervals in all 5-minute segments of the recording (SDANN), and the square root of the mean of squared differences between adjacent NN intervals (r-MSSD) were calculated for 24-hour and 6-hour time segments. Associations of HRV with particulate pollution levels were evaluated with fixed-effects regression models. RESULTS: After controlling for differences across patients, elevated particulate levels were associated with (1) increased mean HR, (2) decreased SDNN, a measure of overall HRV, (3) decreased SDANN, a measure that corresponds to ultralow frequency variability, and (4) increased r-MSSD, a measure that corresponds to high-frequency variability. The associations between HRV and particulates were small but persisted even after controlling for mean HR. CONCLUSIONS: This study suggests that changes in cardiac autonomic function reflected by changes in mean HR and HRV may be part of the pathophysiologic mechanisms or pathways linking cardiovascular mortality and particulate air pollution.
Adult↗
Air pollution and respiratory illness of children in São Paulo, Brazil.
This investigation reports the association between air pollution and paediatric respiratory emergency visits in São Paulo, Brazil, the largest city in South America. Daily records of emergency visits were obtained from the Children's Institute of the University of São Paulo for the period from May 1991 to April 1993. Visits were classified as respiratory and non-respiratory causes. Respiratory visits were further divided into three categories: upper respiratory illness, lower respiratory illness and wheezing. Daily records of SO2, CO, particulate matter (PM10), O3 and NO2 concentrations were obtained from the State Air Pollution Controlling Agency of São Paulo. Associations between respiratory emergency visits and air pollution were assessed by simple comparative statistics, simple correlation analysis and by estimating a variety of regression models. Significant associations between the increase of respiratory emergency visits and air pollution were observed. The most robust associations were observed with PM10, and to a lesser extent with O3. These associations were stable across different model specifications and several controlling variables. A significant increase in the counts of respiratory emergency visits--more than 20%--was observed on the most polluted days, indicating that air pollution is a substantial paediatric health concern in São Paulo.
Adolescent↗
Mortality and air pollution: associations persist with continued advances in research methodology.
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Air Pollution↗
Particulate air pollution and daily mortality on Utah's Wasatch Front.
Reviews of daily time-series mortality studies from many cities throughout the world suggest that daily mortality counts are associated with short-term changes in particulate matter (PM) air pollution. One U.S. city, however, with conspicuously weak PM-mortality associations was Salt Lake City, Utah; however, relatively robust PM-mortality associations have been observed in a neighboring metropolitan area (Provo/Orem, Utah). The present study explored this apparent discrepancy by collecting, comparing, and analyzing mortality, pollution, and weather data for all three metropolitan areas on Utah's Wasatch Front region of the Wasatch Mountain Range (Ogden, Salt Lake City, and Provo/Orem) for approximately 10 years (1985-1995). Generalized additive Poisson regression models were used to estimate PM-mortality associations while controlling for seasonality, temperature, humidity, and barometric pressure. Salt Lake City experienced substantially more episodes of high PM that were dominated by windblown dust. When the data were screened to exclude obvious windblown dust episodes and when PM data from multiple monitors were used to construct an estimate of mean exposure for the area, comparable PM-mortality effects were estimated. After screening and by using constructed mean PM [less than/equal to] 10 microm in aerodynamic diameter (PM10) data, the estimated percent change in mortality associated with a 10-mg/m3 increase in PM10 (and 95% confidence intervals) for the three Wasatch Front metropolitan areas equaled approximately 1. 6% (0.3-2.9), 0.8% (0.3-1.3), and 1.0% (0.2-1.8) for the Ogden, Salt Lake City, and Provo/Orem areas, respectively. We conclude that stagnant air pollution episodes with higher concentrations of primary and secondary combustion-source particles were more associated with elevated mortality than windblown dust episodes with relatively higher concentrations of coarse crustal-derived particles.
Air Pollution↗
Daily changes in oxygen saturation and pulse rate associated with particulate air pollution and barometric pressure.
Epidemiologic studies have linked fine particulate air pollution with increases in morbidity and mortality rates from cardiopulmonary complications. Although the underlying biologic mechanisms responsible for this increase remain largely unknown, potential pathways include transient declines in blood oxygenation and changes in pulse rate following exposures to particulate air pollution episodes. This study evaluated potential associations between daily measures of respirable particulate matter (PM) with pulse rate and oxygen saturation of the blood. Pulse rate and oxygen saturation (Spo2) using pulse oximetry were measured daily in 90 elderly subjects living near air pollution monitors during the winter of 1995-96 in Utah Valley. We also evaluated potential associations of oxygen saturation and pulse rate with barometric pressure. Small but statistically significant positive associations between day-to-day changes in Spo2 and barometric pressure were observed. Pulse rate was inversely associated with barometric pressure. Exposure to particulate pollution was not significantly associated with Spo2 except in male participants 80 years of age or older. Increased daily pulse rate, as well as the odds of having a pulse rate 5 or 10 beats per minute (bpm) above normal (normal is defined as the individual's mean pulse rate throughout the study period), were significantly associated with exposure to particulate pollution on the previous 1 to 5 days. The medical or biologic relevance of these increases in pulse rate following exposure to particulate air pollution requires further study.
Aged↗
Particulate and ozone pollutant effects on the respiratory function of children in southwest Mexico City.
We assessed the contributions of particulate matter with aerodynamic diameters < or =10 and < or =2.5 microm (PM2.5 and PM10) and ozone (O3) to peak expiratory flow (PEF) and respiratory symptoms in 40 schoolchildren 8-11 years of age for 59 days during three periods in 1991 at a school in southwest Mexico City. We measured peak expiratory flow in the morning on the children's arrival at school and in the afternoon before their departure from school. Separately for morning and afternoon, we normalized each child's daily measurement of peak flow by subtracting his or her mean peak flow from the daily measurement. Child-specific deviations were averaged to obtain a morning and afternoon mean deviation (APEF) for each day. Mean 24-hour O3 level was 52 parts per billion (ppb; maximum 103 ppb); mean 24-hour PM2.5 and PM10 were 30 microg/m3 (maximum 69 microg/m3) and 49 microg/m3 (maximum 87 microg/m3), respectively. We adjusted moving average and polynomial distributed lag multiple regression analyses of APEF vs pollution for minimum daily temperature, trend, and season. We examined effects of PM2.5, PM10, and O3, on deltaPEF separately and in joint models. The models indicated a role for both particles and O3 in the reduction of peak expiratory flow, with shorter lags between exposure and reduction in peak expiratory flow for O3 than for particle exposure (0-4 vs 4-7 days). The joint effect of 7 days of exposure to the interquartile range of PM2.5 (17 microg/m3) and O3 (25 ppb) predicted a 7.1% (95% confidence interval = 11.0-3.9) reduction in morning peak expiratory flow. Pollutant exposure also predicted higher rates of phlegm; colinearity between pollutants limited the potential to distinguish the relative contribution of individual pollutants. In an area with chronically high ambient O3 levels, school children responded with reduced lung function to both O3 and particulate exposures within the previous 1 to 2 weeks.
Air Pollution↗
Respiratory changes due to long-term exposure to urban levels of air pollution: a histopathologic study in humans.
STUDY OBJECTIVES: To evaluate the potential associations between long-term exposure to air pollution and histopathologic evidence of damage to the lungs in humans. DESIGN: Lung tissue samples were collected during necropsies of individuals who died due to violent causes, selected on the basis of their exposure background. PATIENTS: The exposed group was composed of individuals who lived in Guarulhos, an area with high mean levels of inhalable particles. The control group was composed of individuals who lived in two cities with economies based on agricultural activities: Ribeirão Preto and Ourinhos. INTERVENTIONS: Information about cigarette smoking and occupational exposure was obtained from family members. MEASUREMENTS AND RESULTS: Morphometric evaluation of the main bronchus was conducted to determine the volume ratio of submucosal glands. Histopathologic alterations of the bronchioli were evaluated by scoring the presence of inflammatory reaction, wall thickening, and secretory hyperplasia. The number of spots of carbon deposition was counted along the regions of lymphatic drainage (visceral pleura and axial connective tissue around bronchi and blood vessels). Statistical analysis was done by means of regression models controlled for age, smoking, and occupational exposure. Lungs collected from the high pollution area presented evidence of more histopathologic damage in comparison to those from the clean environments. These effects were observed even after controlling for individual differences in age, sex, and cigarette smoking levels. CONCLUSIONS: These results suggest that long-term exposure to air pollution may contribute to the pathogenesis of airway disease, and that urban levels of air pollution have adverse effects on the respiratory tract.
Adult↗
Continuous intrathecal meperidine via an implantable infusion pump for chronic, nonmalignant pain.
OBJECTIVE: To report a continuous infusion of intrathecal meperidine via an implanted infusion pump for nonmalignant, chronic pain. CASE SUMMARY: A 69-year-old white woman had chronic, nonmalignant low-back pain and bilateral leg pain. Multiple drug therapies and other interventional techniques had failed. The patient achieved significant pain relief by a continuous infusion of intrathecal meperidine via an implanted infusion pump. DISCUSSION: To our knowledge, this is the first report of meperidine administered intrathecally by continuous infusion. Continuous infusion of intrathecal and epidural opiates by implanted infusion pumps is becoming more widely recognized as an alternative treatment for patients with chronic, benign pain. Epidural and intrathecal meperidine is an effective analgesic for short-term surgical procedures. Data reporting effective relief and safety with continuous intrathecal meperidine remain limited. CONCLUSIONS: Continuous intrathecal meperidine via an implantable infusion pump may be an effective alternative in the treatment of chronic pain.
Aged↗
Adverse health effects of air pollutants in a nonsmoking population.
Utah Valley has provided an interesting and unique opportunity to evaluate the health effects of respirable particulate air pollution (PM10). Residents of this valley are predominantly nonsmoking members of the Church of Jesus Christ of Latter-day Saints (Mormons). The area has moderately high average PM10 levels with periods of highly elevated PM10 concentrations due to local emissions being trapped in a stagnant air mass near the valley floor during low-level temperature inversion episodes. Due to a labor dispute, there was intermittent operation of the single largest pollution source, an old integrated steel mill. Levels of other common pollutants including sulfur dioxide, ozone, and acidic aerosol are relatively low. Studies specific to Utah Valley have observed that elevated PM10 concentrations are associated with: (1) decreased lung function; (2) increased incidence of respiratory symptoms; (3) increased school absenteeism; (4) increased respiratory hospital admissions; and (5) increased mortality, especially respiratory and cardiovascular mortality.
Air Pollutants↗
Air pollution and daily mortality in three Swiss urban areas.
Particulate air pollution, in association with other common urban air pollutants, has been associated with various measured health endpoints, including the incidence and duration of respiratory symptoms, lung function, absence from work or school due to respiratory illness, hospitalization for respiratory disease, and cardiopulmonary disease mortality. In this study, the association between daily mortality and air pollution was assessed in Zurich, Basle, and Geneva (Switzerland) for the time period 1984 through 1989. Various regression modeling techniques were used to estimate the effect of air pollution on mortality, to control for time trends, seasonal factors, and weather variables, and to assess the sensitivity of the results. A positive, statistically significant association between daily mortality counts and measures of ambient air pollution in all three cities was observed. Mortality was associated with total suspended particulate pollution, sulfur dioxide, and nitrogen dioxide. The strongest association was with a 3-day moving average (including the concurrent day and the preceding 2 days) of these pollutants. The estimated mortality-air pollution effects were not highly sensitive to regression modeling techniques used to control for seasonality, long-term trends, and weather variables.
Aged↗
Time series for the analysis of pulmonary health data.
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Humans↗