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.

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.

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.

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.

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.

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.

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.

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 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.

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.

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.

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.

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.

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.

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.

Ambient air pollution as a risk factor for lung cancer.

Epidemiologic studies over the last 40 years have observed that general ambient air pollution, chiefly due to the by-products of the incomplete combustion of fossil fuels, is associated with small relative increases in lung cancer. The 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 30-50% increases in the risk of lung cancer in relation to approximately a doubling of respirable particle exposure. 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 US continue to be exposed to pollutant mixtures containing known or suspected carcinogens. These observations suggest that the most widely cited estimates of the proportional contribution of air pollution to lung cancer occurrence in the US, based largely on the results of animal experimentation, may be too low. It is important that better epidemiologic research be conducted to allow improved estimates of lung cancer risk from air pollution in 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 related to air pollution.