Juvenile idiopathic arthritis and exposure to fine particulate air pollution.

OBJECTIVES: Inhalation of fine particulate matter, including particles with an aerodynamic diameter less than or equal to a 2.5-microm cut point (PM2.5), has been associated with systemic inflammation and the clinical presentation of various cardiopulmonary heath events. The urban area along Utah's Wasatch Mountains has high PM2.5 concentrations during periods of stagnant air conditions. Short-term inhalation exposures may trigger inflammatory events presenting as symptom onset in new patients with juvenile idiopathic arthritis (JIA). This study evaluated potential associations between JIA symptom onset and temporal changes in regional air pollution measured by stagnant air conditions and PM2.5 concentrations. METHODS: A case-crossover design was used to analyze associations of regional ambient PM2.5 concentrations with onset date of 338 JIA cases living on Utah's Wasatch Front. Patients were drawn from the Intermountain States Database of Childhood Rheumatic Diseases (1993-2006). Time trends, seasonality, month, and weekday were controlled for by matching. Selected exposure windows of PM2.5 and stagnant air days were used in the model to determine the effect of short term cumulative exposure on JIA symptom onset. RESULTS: Increased concentrations of PM2.5 and stagnant air conditions in the preceding 14 days were associated with significantly elevated risk of JIA onset in preschool aged children (RR=1.60, 95% CI 1.00-2.54) but not older children. Elevated risk was larger in males and in systemic onset JIA. CONCLUSION: Exposure to stagnant polluted air may be an environmental risk factor for JIA in young children, potentially triggered by pollution-induced pulmonary mediated inflammation.

The challenge of tetradic relationships in medically interpreted pediatric primary care visits: A descriptive study of communication practices.

OBJECTIVE: To examine spoken interactions between pediatricians and community-based interpreters speaking with adolescents and parents with Limited English proficiency (LEP) in primary care to identify the challenges of interpreting in a four-person or tetradic visit, its sources of co-constructed errors, and specific practices for educational intervention. METHODS: As part of a larger study of vaccine decision-making at six clinical sites in two states, this descriptive study used discourse analysis to examine 20 routine primary care visits in a Latino Clinic in interactions between adolescents, parents, community-based interpreters, and pediatricians. Specific patterns of communication practices were identified that contributed to inaccuracies in medical interpretation RESULTS: Practices needing improvement were tallied for simple frequencies and included: omissions; false fluency; substitutions; editorializing; added clarification, information, or questions; medical terminology; extra explanation to mother; and, cultural additions. Of these speaking practices, omissions were the most common (123 out of 292 total) and the most affected by pediatricians. CONCLUSION: The dynamics of both pediatricians and interpreters contributed to identification of areas for improvement, with more adolescent participation in bilingual than monolingual visits. PRACTICE IMPLICATIONS: These observations provide opportunities for mapping a communication skills training intervention based on observations for future testing of an evidence-based curriculum.

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.

Passive cigarette smoke, coal heating, and respiratory symptoms of nonsmoking women in China.

In this study we evaluated data from a sample of 973 never-smoking women, ages 20-40, who worked in three similar textile mills in Anhui Province, China. We compared prevalence rates of respiratory symptoms across homes with and without coal heating and homes with different numbers of smokers. Multiple logistic regression models that controlled for age, job title, and mill of employment were also estimated. Respiratory symptoms were associated with combined exposure to passive cigarette smoke and coal heating. Effects of passive cigarette smoke and coal heating on respiratory symptoms appeared to be nearly additive, suggesting a dose-response relationship between respiratory symptoms and home indoor air pollution from these two sources. The prevalence of chest illness, cough, phlegm, and shortness of breath (but not wheeze) was significantly elevated for women living in homes with both smokers and coal heating.

Lung cancer and air pollution.

Epidemiologic studies over the last 40 years suggest rather consistently that general ambient air pollution, chiefly due to the incomplete combustion of fossil fuels, may be responsible for increased rates of lung cancer. This evidence derives from studies of lung cancer trends, studies of occupational groups, comparisons of urban and rural populations, and case-control and cohort studies using diverse exposure metrics. Recent prospective cohort studies observed 30 to 50% increases in lung cancer rates associated with exposure to respirable particles. While these data reflect the effects of exposures in past decades, and despite some progress in reducing air pollution, large numbers of people in the United States continue to be exposed to pollutant mixtures containing known or suspected carcinogens. It is not known how many people in the United States are exposed to levels of fine respirable particles that have been associated with lung cancer in recent epidemiologic studies. These observations suggest that the most widely cited estimates of the proportional contribution of air pollution to lung cancer occurrence in the United States based largely on the results of animal studies, may be too low. It is important that better epidemiologic research be conducted to allow improved estimates of lung cancer risk from air pollution among the general population. The development and application of new epidemiologic methods, particularly the improved characterization of population-wide exposure to mixtures of air pollutants and the improved design of ecologic studies, could improve our ability to measure accurately the magnitude of excess cancer associated with air pollution.

Synoptic weather modeling and estimates of the exposure-response relationship between daily mortality and particulate air pollution.

This study estimated the association between particulate air pollution and daily mortality in Utah Valley using the synoptic climatological approach to control for potential weather effects. This approach was compared with alternative weather modeling approaches. Although seasonality explained a significant amount of variability in mortality, other weather variables explained only a very small amount of additional variability in mortality. The synoptic climatological approach performed as well or slightly better than alternative approaches to controlling for weather. However, the estimated effect of particulate pollution on mortality was mostly unchanged or slightly larger when synoptic categories were used to control for weather. Furthermore, the shape of the estimated dose-response relationship was similar when alternative approaches to controlling for weather were used. The associations between particulate pollution and daily mortality were not significantly different from a linear exposure-response relationship that extends throughout the full observed range of 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.

Health effects of particulate air pollution: time for reassessment?

Numerous studies have observed health effects of particulate air pollution. Compared to early studies that focused on severe air pollution episodes, recent studies are more relevant to understanding health effects of pollution at levels common to contemporary cities in the developed world. We review recent epidemiologic studies that evaluated health effects of particulate air pollution and conclude that respirable particulate air pollution is likely an important contributing factor to respiratory disease. Observed health effects include increased respiratory symptoms, decreased lung function, increased hospitalizations and other health care visits for respiratory and cardiovascular disease, increased respiratory morbidity as measured by absenteeism from work or school or other restrictions in activity, and increased cardiopulmonary disease mortality. These health effects are observed at levels common to many U.S. cities including levels below current U.S. National Ambient Air Quality Standards for particulate air pollution.

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.

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.

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.

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.

Particulate pollution and health: a review of the Utah valley experience.

Utah Valley has provided an interesting and unique opportunity to evaluate the health effects of respirable particulate pollution (PM10) for several reasons. (1) It has moderately high average PM10 levels, and during low-level temperature inversion episodes, local emissions may become trapped in a stagnant air mass near the valley floor, resulting in highly elevated PM10 concentrations. (2) The valley experienced the intermittent operation of the local integrated steel mill, the largest single particulate pollution source. (3) Valley residents have very low smoking rates. (4) Levels of sulfur dioxide, ozone, and aerosol strong acidity are relatively low. Several studies specific to Utah Valley have evaluated associations between various indicators of health and PM10 pollution. Each of these individual studies has limitations imposed by data and analytic constraints. Taken together, however, they suggest a coherence or cascade of associations across various health end points for a specific location and population. Apparent health effects of elevated PM10 pollution observed in Utah Valley include: 1) decreased lung function; 2) increased incidence of respiratory symptoms; 3) increased school absenteeism; 4) increased respiratory hospital admissions; 5) increased mortality, especially respiratory and cardiovascular mortality; and 6) possibly increased lung cancer. This paper reviews these Utah Valley studies and evaluates the possibility that the overall health associations observed are due primarily to methodological bias or confounding by inadequate controls for risk factors such as smoking, weather, season, infectious agents, and socioeconomic distress.

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.

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.

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.

Respiratory hospital admissions associated with PM10 pollution in Utah, Salt Lake, and Cache Valleys.

This study assessed the association between respiratory hospital admissions and PM10 pollution in Utah, Salt Lake, and Cache valleys during April 1985 through March 1989. Utah and Salt Lake valleys had high levels of PM10 pollution that violated both the annual and 24-h standards issued by the Environmental Protection Agency (EPA). Much lower PM10 levels occurred in the Cache Valley. Utah Valley experienced the intermittent operation of its primary source of PM10 pollution: an integrated steel mill. Bronchitis and asthma admissions for preschool-age children were approximately twice as frequent in Utah Valley when the steel mill was operating versus when it was not. Similar differences were not observed in Salt Lake or Cache valleys. Even though Cache Valley had higher smoking rates and lower temperatures in winter than did Utah Valley, per capita bronchitis and asthma admissions for all ages were approximately twice as high in Utah Valley. During the period when the steel mill was closed, differences in per capita admissions between Utah and Cache valleys narrowed considerably. Regression analysis also demonstrated a statistical association between respiratory hospital admissions and PM10 pollution. The results suggest that PM10 pollution plays a role in the incidence and severity of respiratory disease.

Daily mortality and PM10 pollution in Utah Valley.

The association between daily mortality and respirable particulate pollution (PM10) in Utah County was assessed from April 1985 through December 1989. Poisson regression analysis was used to regress daily death counts on PM10 pollution levels, controlling for variability in the weather. A significant positive association between nonaccidental mortality and PM10 pollution was observed. The strongest association was with 5-d moving average PM10 levels, including the concurrent day and the preceding 4 d. An increase in 5-d moving average PM10 levels, equal to 100 micrograms/m3, was associated with an estimated increase in deaths per day equal to 16%. The association with mortality and PM10 was largest for respiratory disease deaths, next largest for cardiovascular deaths, and smallest for all other deaths. Mean PM10 concentrations during the study period equaled 47 micrograms/m3. The maximum 24-h and 5-d moving average PM10 levels equaled 365 and 297 micrograms/m3, respectively. Relatively low levels of sulfur dioxide, aerosol acidity, and ozone suggested an independent association between mortality and PM10. The relative risk of death increased monotonically with PM10, and the relationship was observed at PM10 levels that were well below the current National Ambient Air Quality Standard of 150 micrograms/m3.

Differences in lung function among school children in communities in Israel.

Differences in lung functions of school-age children who lived near two electrical power plants in the Ashkelon district of Israel were studied. Lung-function tests were performed, and the American Thoracic Society questionnaire was administered in three study periods during the following years: (1) 1990, (2) 1994, and (3) 1997. Measurements of air pollutants (i.e., sulfur dioxide, nitric oxides, ozone) were also taken during the aforementioned study periods. Statistical analysis included an estimation of a series of fixed-effects regression models. A total of 2,455, 1,613, and 4,346 observations were included in the analyses for study years 1990, 1994, and 1997, respectively. The authors controlled for age, sex, height, weight, parents' education and smoking status, and being born out of Israel, and, consequently, substantial differences in lung function across the different communities and study periods were demonstrated in the study area. No robust association with air pollution was demonstrated. The cause of these differences in the respiratory health of children remains unknown.

Air pollution and mortality in elderly people: a time-series study in Sao Paulo, Brazil.

The relationship between daily mortality of elderly (65+ y) persons and air pollution in the metropolitan area of Sao Paulo, Brazil, for the period May 1990 to April 1991 was evaluated by time series regression, controlling for season, weather, and other factors. Mortality was associated with respirable particles (PM10), nitrogen oxides (NOx), sulfur dioxide (SO2), and carbon monoxide (CO). The association with PM10 was most statistically significant, robust, and independent of other air pollutants. An increase in PM10 equal to 100 micrograms/m3 was associated with an increase in overall mortality equal to approximately 13%. This association was consistent across various model specifications and estimation techniques. The dose-response relationship between mortality and respirable particulate pollution was almost linear, with no evidence of a "safe" threshold level. The results were similar to those observed in London and several U.S. cities. The results were also supportive of recent animal studies that have observed adverse health outcomes in experimental animals exposed to air pollution in Sao Paulo.