Abstract  BACKGROUND: The mechanism behind the triggering effect of fine particulate matter (PM) air pollution on cardiovascular events remains elusive. We postulated that elevated levels of PM would be associated with increased blood levels of inflammatory and thrombotic markers in elderly individuals. We also hypothesized that elevated PM would increase levels of cytokines in individuals with heart disease. METHODS: We measured these blood markers in 47 elderly individuals with (23) and without (16 COPD and 8 healthy) cardiovascular disease (CVD) on 2 or 3 mornings over a 5 or 10-day period between February 2000 and March 2002. Blood measures were paired with residence level outdoor PM measured by nephelometry. Analyses determined the within-individual effect of 24-hour averaged outdoor PM on blood measures. RESULTS: Analyses found no statistically significant effect of a same day 10 ug/m3 increase in fine PM on log transformed levels of CRP 1.21 fold-rise [95% CI: 0.86, 1.70], fibrinogen 1.02 fold-rise [95% CI: 0.98, 1.06], or D-dimer 1.02 fold-rise [95% CI: 0.88, 1.17] in individuals with CVD. One-day lagged analyses in the CVD subgroup found similar null results. These same models found no change in these blood markers at the same-day or 1-day lag in the group without CVD. In 21 individuals with CVD, a 10 mug/m3 increase in same-day PM was associated with a 1.3 fold-rise [95% CI: 1.1, 1.7] in the level of monocyte chemoattractant protein-1. CONCLUSION: We did not find consistent effects of low ambient levels of PM on blood measures of inflammation or thrombosis in elderly individuals.

Abstract  AIM: The aim of this study was to evaluate the frequency of carbon monoxide diffusing capacity (DLCO) impairment and microalbuminuria in patients with active ulcerative colitis (UC) and to assess whether these nonexpensive and noninvasive tests correlate with intestinal inflammation.

METHODS: A prospective observational study was set up at the Fiorenzuola Hospital and performed during a 4-year period. We enrolled 30 consecutive subjects with clinical and histological diagnosis of active UC and 20 healthy subjects matched for age and sex. After full colonscopic assessment with multiple mucosal biopsies, the clinical disease activity of each patient was quantified. A global spirometry and 24-h urine collection at rest to measure microalbuminuria were performed. Each biopsy specimen was assessed blindly by a histopathologist, who assigned a score according to the severity of enterocyte damage, cryptitis and acute and chronic inflammation of the lamina propria.

RESULTS: A latent pulmonary involvement with a reduction in DLCO was present in 20 patients (67%). A subclinical renal involvement with microalbuminuria was detected in 19 subjects (63%). The mean DLCO was 78.2+/-15.2 in Group 1 vs 94.7+/-13.1 in Group 2 (P<0.001). Microalbuminuria was 103.6+/-90.8 in Group 1 vs 57+/-31.7 in the control group (P=0.062). DLCO reduction correlated significantly with intestinal histopathological grading in Group 1 (r = -0.742, P< 0.001), although there was no correlation between microalbuminuria and histological grading (r = -0.273, P= 0.143).

CONCLUSION: Our data confirm that latent pulmonary involvement (DLCO impairment) and microalbuminuria are frequent in UC. The DLCO may provide a useful noninvasive indicator of colonic inflammation in subjects with UC and concomitant subclinical lung involvement.

Abstract  Objective. To assess whether severe gastroesophageal reflux (GER) is associated with abnormalities in lung function including measures of lung volume and gas diffusion.

Methods: Data from 147 patients with obesity (body mass index [BMI] range, 31.7 to 70 kg/m(2)) who presented for obesity surgery was analyzed retrospectively. A questionnaire was completed preoperatively that included a history of GER, frequency and severity of symptoms, investigations, and medications used. A history of lung disease, sleep-disordered breathing, and smoking also was obtained. A physician who was blinded to lung function graded GER severity prospectively by the results of pH monitoring and/or gastroscopy, and medication use. Spirometry, lung volumes, and gas transfer were measured preoperatively.

Results: Patients with severe GER had reduced levels of the diffusing capacity of the lung for carbon monoxide (DLCO) [21.1 mL/min/mm Hg; 95% confidence interval (CI), 18.9 to 23.2], as measured by CO transfer, compared with those patients without GER (26.3 mL/min/mm Hg; 95% CI, 24.4 to 28.2; p = 0.001). This remained significant after adjusting for age, gender, BMI, and smoking history. Gas transfer corrected for lung volume also was reduced in the group with severe GER (4.6 mL/min/mm Hg per L; 95% CI, 4.3 to 4.9) compared to the group without GER (5.3 mL/min/mm Hg per L; 95% CI, 5.1 to 5.5; p = 0.001). There was no significant difference in other measures of lung function.

Conclusions: Severe GER is associated with an impairment of gas exchange. This may be due to microaspiration of gastric acid or fluid into the airways.

Abstract  The report provides the Oversight Review Board`s (ORB`s) conclusions on the performance of the National Acid Precipitation Assessment Program (NAPAP) as requested by the Joint Chairs Council, and suggests lessons to be drawn from the NAPAP experience which may be of use in other similar endeavors.The ORB concludes that, taken as a whole, NAPAP was a successful enterprise which furthered effective decision making with respect to acid precipitation and other air quality matters, which improved scientific and technical understanding of underlying processes, and which provided an innovative institutional departure for addressing other problems at the intersection of science, technology and policy.

Abstract  Biomass burning represents an important source of atmospheric aerosols and greenhouse gases, yet little is known about its interannual variability or the underlying mechanisms regulating this variability at continental to global scales. Here we investigated fire emissions during the 8 year period from 1997 to 2004 using satellite data and the CASA biogeochemical model. Burned area from 2001–2004 was derived using newly available active fire and 500 m. burned area datasets from MODIS following the approach described by Giglio et al. (2006). ATSR and VIRS satellite data were used to extend the burned area time series back in time through 1997. In our analysis we estimated fuel loads, including organic soil layer and peatland fuels, and the net flux from terrestrial ecosystems as the balance between net primary production (NPP), heterotrophic respiration (Rh), and biomass burning, using time varying inputs of precipitation (PPT), temperature, solar radiation, and satellite-derived fractional absorbed photosynthetically active radiation (fAPAR). For the 1997–2004 period, we found that on average approximately 58 Pg C year−1 was fixed by plants as NPP, and approximately 95% of this was returned back to the atmosphere via Rh. Another 4%, or 2.5 Pg C year−1 was emitted by biomass burning; the remainder consisted of losses from fuel wood collection and subsequent burning. At a global scale, burned area and total fire emissions were largely decoupled from year to year. Total carbon emissions tracked burning in forested areas (including deforestation fires in the tropics), whereas burned area was largely controlled by savanna fires that responded to different environmental and human factors. Biomass burning emissions showed large interannual variability with a range of more than 1 Pg C year−1, with a maximum in 1998 (3.2 Pg C year−1) and a minimum in 2000 (2.0 Pg C year−1).

Abstract  Air pollution's mortality effects may differ by subpopulation; however, few studies have investigated this issue in Asia. We investigated susceptibility to air pollutants on total, cardiovascular, and respiratory mortality in Seoul, Korea for the period 2000-2007. We applied time-stratified case-crossover analysis, which allows direct modeling of interaction terms, to estimate susceptibility based on sex, age, education, marital status, and occupation. An interquartile range increase in pollution was associated with odds ratios of 0.94 (95% confidence interval, 0.25-1.62), 2.27 (1.03-3.53), 1.94 (0.80-3.09), and 2.21 (1.00-3.43) for total mortality and 1.95 (0.64-3.27), 4.82 (2.18-7.54), 3.64 (1.46-5.87), and 4.32 (1.77-6.92) for cardiovascular mortality for PM(10), nitrogen dioxide (NO(2)), sulfur dioxide (SO(2)), and carbon monoxide (CO), respectively. Ozone effect estimates were positive, but not statistically significant. Results indicate that some populations are more susceptible than others. For total or cardiovascular mortality, associations were higher for males, those 65-74 years, and those with no education or manual occupation for some pollutants. For example, the odds ratio for SO(2) and cardiovascular mortality was 1.19 (1.03-1.37) times higher for those with manual occupations than professional occupations. Our findings provide evidence that some populations are more susceptible to the effects of air pollution than others, which has implications for public policy and risk assessment for susceptible subpopulations.Journal of Exposure Science and Environmental Epidemiology advance online publication, 7 March 2012;  doi:10.1038/jes.2012.6.

Abstract  CONTEXT: Short-term exposure to high levels of air pollution may trigger myocardial infarction (MI), but this association remains unclear.

OBJECTIVE: To assess and quantify the association between short-term exposure to major air pollutants (ozone, carbon monoxide, nitrogen dioxide, sulfur dioxide, and particulate matter ≤10 μm [PM(10)] and ≤2.5 μm [PM(2.5)] in diameter) on MI risk.

DATA SOURCES: EMBASE, Ovid MEDLINE in-process and other nonindexed citations, and Ovid MEDLINE (between 1948 and November 28, 2011), and EBM Reviews-Cochrane Central Register of Controlled Trials and EBM Reviews-Cochrane Database of Systematic Reviews (between 2005 and November 28, 2011) were searched for a combination of keywords related to the type of exposure (air pollution, ozone, carbon monoxide, nitrogen dioxide, sulfur dioxide, PM(10), and PM(2.5)) and to the type of outcome (MI, heart attack, acute coronary syndrome).

STUDY SELECTION: Two independent reviewers selected studies of any study design and in any language, using original data and investigating the association between short-term exposure (for up to 7 days) to 1 or more air pollutants and subsequent MI risk. Selection was performed from abstracts and titles and pursued by reviewing the full text of potentially eligible studies.

DATA EXTRACTION: Descriptive and quantitative information was extracted from each selected study. Using a random effects model, relative risks (RRs) and 95% CIs were calculated for each increment of 10 μg/m(3) in pollutant concentration, with the exception of carbon monoxide, for which an increase of 1 mg/m(3) was considered.

DATA SYNTHESIS: After a detailed screening of 117 studies, 34 studies were identified. All the main air pollutants, with the exception of ozone, were significantly associated with an increase in MI risk (carbon monoxide: 1.048; 95% CI, 1.026-1.070; nitrogen dioxide: 1.011; 95% CI, 1.006-1.016; sulfur dioxide: 1.010; 95% CI, 1.003-1.017; PM(10): 1.006; 95% CI, 1.002-1.009; and PM(2.5): 1.025; 95% CI, 1.015-1.036). For ozone, the RR was 1.003 (95% CI, 0.997-1.010; P = .36). Subgroup analyses provided results comparable with those of the overall analyses. Population attributable fractions ranged between 0.6% and 4.5%, depending on the air pollutant.

CONCLUSION: All the main air pollutants, with the exception of ozone, were significantly associated with a near-term increase in MI risk.

Abstract  Cardiovascular morbidity has been associated with particulate matter (PM) air pollution, although the relation between pollutants and sudden death from cardiac arrest has not been established. This study examined associations between out-of-hospital cardiac arrests and fine PM (of aerodynamic diameter < /=2.5 mum, or PM(2.5)), ozone, nitrogen dioxide, sulfur dioxide, and carbon monoxide in New York City. The authors analyzed 8,216 out-of-hospital cardiac arrests of primary cardiac etiology during the years 2002-2006. Time-series and case-crossover analyses were conducted, controlling for season, day-of-week, same-day, and delayed/apparent temperature. An increased risk of cardiac arrest in time-series (relative risk (RR) = 1.06, 95% confidence interval (CI): 1.02, 1.10) and case-crossover (RR = 1.04, 95% CI: 0.99, 1.08) analysis for a PM(2.5) increase of 10 mug/m(3) in the average of 0- and 1-day lags was found. The association was significant in the warm season (RR = 1.09, 95% CI: 1.03, 1.15) but not the cold season (RR = 1.01, 95% CI: 0.95, 1.07). Associations of cardiac arrest with other pollutants were weaker. These findings, consistent with studies implicating acute cardiovascular effects of PM, support a link between PM(2.5) and out-of-hospital cardiac arrests. Since few individuals survive an arrest, air pollution control may help prevent future cardiovascular mortality.

Abstract  BACKGROUND: Growing evidence indicates that ambient air pollution is associated with exacerbation of chronic diseases like chronic pulmonary disease. A prospective panel study was conducted to investigate short-term changes of blood markers of inflammation and coagulation in response to daily changes in air pollution in Erfurt, Germany. 12 clinical visits were scheduled and blood parameters were measured in 38 male patients with chronic pulmonary disease during winter 2001/2002. Additive mixed models with random patient intercept were applied, adjusting for trend, weekday, and meteorological parameters. Hourly data on ultrafine particles (UFP, 0.01-0.1 mum), accumulation mode particles (ACP, 0.1-1.0 mum), PM10 (particulate matter <10 mum in diameter), elemental (EC) and organic carbon (OC), gaseous pollutants (nitrogen monoxide [NO], nitrogen dioxide [NO2], carbon monoxide [CO], and sulphur dioxide [SO2]) were collected at a central monitoring site and meteorological data were received from an official network. For each person and visit the individual 24-hour average of pollutants immediately preceding the blood withdrawal (lag 0) up to day 5 (lag1-4) and 5-day running means were calculated. RESULTS: Increased levels of fibrinogen were observed for an increase in one interquartile range of UFP, PM10, EC, OC, CO, and NO revealing the strongest effect for lag 3. E-selectin increased in association with ACP and PM10 with a delay of one day. The ACP effect was also seen with the 5-day-mean. The pattern found for D-dimer was inconsistent. Prothrombin fragment 1+2 decreased with lag 4 consistently for all particulate pollutants. Von Willebrand factor antigen (vWF) showed a consistent decrease in association with almost all air pollutants with all lags except for lag 0. No associations were found for C-reactive protein, soluble intercellular adhesion molecule 1, serum amyloid A and factor VII. CONCLUSION: These results suggest that elevated concentrations of air pollution are associated with changes in some blood markers of inflammation and coagulation in patients with chronic pulmonary disease. The clinical implications of these findings need further investigation.

Abstract  Exhaled nitric oxide (eNO) levels are increased in untreated or unstable asthma and measurements can be made easily. Our aim was to assess the usefulness of eNO for diagnosing and predicting loss of control (LOC) in asthma following steroid withdrawal. Comparisons were made against sputum eosinophils and airway hyperresponsiveness (AHR) to hypertonic saline (4.5%). Seventy-eight patients with mild/moderate asthma had their inhaled steroid therapy withdrawn until LOC occurred or for a maximum of 6 wk. Sixty (77.9%) developed LOC. There were highly significant correlations between the changes in eNO and symptoms (p < 0.0001), FEV(1) (p < 0.002), sputum eosinophils (p < 0.0002), and saline PD(15) (p < 0.0002), and there were significant differences between LOC and no LOC groups. Both single measurements and changes of eNO (10 ppb, 15 ppb, or an increase of > 60% over baseline) had positive predictive values that ranged from 80 to 90% for predicting and diagnosing LOC. These values were similar to those obtained using sputum eosinophils and saline PD(15) measurements. We conclude that eNO measurements are as useful as induced sputum analysis and AHR in assessing airway inflammation, with the advantage that they are easy to perform.

Abstract  California Air Resources Board. #Seventeen men with stable-angina pectoris who resided at or near sea level performed cardiopulmonary exercise stress tests after they were exposed to either carbon monoxide (3.9%), carboxyhemoglobin, or clean air. Investigators conducted the tests at sea level, and they simulated 2.1-km altitudes (i.e., reduced arterial oxygen saturation by approximately 4%) in a randomized double-blind experiment in which each subject acted as his or her own control. The duration of symptom-limited exercise, heart rate, indicators of cardiac ischemia and arrhythmia, blood pressure, and respiratory gas exchange were measured. Analyses of variance showed that both independent variables-altitude and carbon monoxide-significantly (p

Abstract  We investigated the relationship between air pollution and incidence of cardiac arrhythmia in a study of patients with implantable cardioverter defibrillators (ICDs). Thirty-four patients (ages 15-85 yr, 80% male) with ICDs residing in the Vancouver, Canada, area were included in the analyses, representing all patients attending the 2 ICD clinics in the study region who had recorded at least 1 ICD discharge during the 14 February to 31 December 2000 study period. Air pollutant (PM2.5, PM10, SO42 -, elemental carbon [EC], organic carbon [OC], O3, SO2, NO2, and CO) concentrations on days for which ICD discharges were observed ("case days") were compared to concentrations on control days in case-crossover analyses. Control days were selected symmetrically, 7 days before and after each case day. ICD discharges occurring within 72 h of 1 another were grouped and considered as 1 discharge event. Temperature, relative humidity, barometric pressure, rainfall, and wind speed were included simultaneously as covariates. Sensitivity analyses examined the effect of grouping ICD discharges, of including meteorological variables, and of excluding discharges that were considered inappropriate by a cardiologist. As in previous studies, mean concentrations and interquartile ranges of air pollutants in Vancouver were low (e.g., PM2.5 mean = 8.2 ug/m3). Although in general there were no statistically significant results, there were trends that might indicate associations between pollutants and ICD discharges. Odds ratios (OR) were consistently higher in summer than in winter (e.g., lag 0 per interquartile range increase in EC: 1.09 [0.86-1.37] vs. 0.61 [0.31-1.18]) and, in general, the highest ORs were observed for same-day effects. The one major exception was the observation of high ORs for ozone in winter (e.g., lag 1: 2.27 [0.67-7.66]). While an OR of 1.55 (0.51-4.70) was observed in summer at lag 0 for PM10, no indications of positive associations were observed for PM2.5 or SO42 -. For indicators of local combustion-source pollution, EC, OC, CO, and SO2, ORs were elevated at all lags (0-3 days) in summer. In summary, this study provides little evidence that specific components of PM affect risk of cardiac arrhythmias, although power limited the ability of the study to detect small effects.

Abstract  In this review an attempt is made to integrate our knowledge about sensory receptors lining the respiratory tract and the reflex reactions evoked following their stimulation by inhaled chemicals. The nature of the chemicals capable of eliciting sensory irritation and the mechanisms proposed for their interactions with nerve endings are reviewed. Methods proposed for evaluation of the effects of airborne chemicals in animals are reviewed and their usefulness for predicting the reactions to be expected in humans is evaluated. The application of these methods in industrial hygiene also discussecl. Articles reviewed Include mainly those concerned with acute exposures and the effects of the chemicals following stimulation of nervous structures in the respiratory tract. Other actions of inhaled chemicals such as their effect on ciliary motion, mucous secreting cells, etc. are excluded. Airborne chemicals can also impinge on the cornea and skin. Their action on nerve endings in these structures is compared with their action on nerve endings in the upper respiratory tract in an attempt to integrate the results obtained for chemicals capable of stimulating the "common chemical sense" receptor.

Abstract  We recently reported an association between daily fluctuations in ambient air pollution and daily mortality in the Netherlands. To adjust for long-term time trends and seasonal variation, we used generalized additive models (GAMs*). The use of GAM has been questioned because of inappropriate convergence criteria and underestimation of standard errors. We performed a reanalysis of the data to test whether the conclusions were sensitive to the convergence criteria in S-Plus and replacement of the GAM model by a natural spline (ns) function, which is assumed to give correct standard errors. Air pollution effect estimates were in general very similar between the two GAMs (default and strict convergence criteria) and natural spline models. Standard errors of the natural spline model were between 10% and 25% higher. The specification of stricter convergence criteria and the use of natural splines instead of GAM did not change any of the conclusions drawn in the two original papers.

Abstract  Epidemiological studies have shown that air pollution is associated with increased cardiovascular mortality. Although the pathophysiological mechanisms behind this association have remained largely unknown, it has been suggested that changes in cardiac autonomic function may play a role. In this study, we investigated the association between acute carbon monoxide (CO) exposure and cardiac autonomic function as measured by heart rate variability (HRV) in subjects with stable coronary artery disease. Twenty-four hour ambulatory electrocardiographic recording with simultaneous continuous personal CO concentration monitoring was performed in six male patients with angiographically verified coronary artery disease three times with 1-week intervals. Time domain measures of HRV were calculated for 5-min segments before and during the CO exposure periods. For further analysis CO exposures were divided into low (2.7 p.p.m.) CO exposure periods. The mean of maximum CO levels during 61 CO exposure periods was 4.6 p.p.m. (SD 5.0 p.p.m.). High CO exposure was associated with an increase in the square root of the mean of the sum of the squares of differences between adjacent RR intervals (r-MSSD) (P = 0.034). Heart rate remained unchanged during the CO exposure. In conclusion, acute CO exposure which represented most likely exposure derived from traffic seems to modify cardiac autonomic control in patients with stable coronary artery disease.

Abstract  Background: Exhaled carbon monoxide has been reported to increase in inflammatory pulmonary diseases and to be correlated with blood carboxyhaemoglobin (Hb-CO) concentration. A study was undertaken to determine whether arterial blood Hb-CO increases in patients with inflammatory pulmonary diseases. Methods: The Hb-CO concentration in arterial blood was measured with a spectrophotometer in 34 normal control subjects, 24 patients with bronchial asthma, 52 patients with pneumonia, and 21 patients with idiopathic pulmonary fibrosis (IPF). Results: The mean (SE) Hb-CO concentrations in patients with bronchial asthma during exacerbations (n=24, 1.05 (0.05)%), with pneumonia at the onset of illness (n=52, 1.08 (0.06)%), and with IPF (n=21, 1.03 (0.09)%) were significantly higher than those in control subjects (n=34, 0.60 (0.07)%) (mean difference 0.45% (95% confidence interval (CI) 0.23 to 0.67), p<0.01 in patients with bronchial asthma, mean difference 0.48% (95% CI 0.35 to 0.60), p<0.0001 in patients with pneumonia, and mean difference 0.43% (95% CI 0.26 to 0.61) p<0.001 in patients with IPF). In 20 patients with bronchial asthma the Hb-CO concentration decreased after 3 weeks of treatment with oral glucocorticoids (p<0.001). In 20 patients with pneumonia the Hb-CO concentration had decreased after 3 weeks when patients showed evidence of clinical improvement (p<0.001). The values of C-reactive protein (CRP), an acute phase protein, correlated with Hb-CO concentrations in patients with pneumonia (r=0.74, p<0.0001) and in those with IPF (r=0.46, p<0.01). In patients with bronchial asthma changes in Hb-CO concentrations were significantly correlated with those in forced expiratory volume in 1 second (FEV1) after 3 weeks (r=0.67, p<0.01). Exhaled carbon monoxide (CO) concentrations were correlated with Hb-CO concentrations (n=33, r=0.80, p<0.0001). Conclusions: Hb-CO concentrations are increased in inflammatory pulmonary diseases including bronchial asthma, pneumonia, and IPF. Measurement of arterial Hb-CO may be a useful means of monitoring pulmonary inflammation.

Abstract  An extensive survey has been designed to provide detailed information on carbon monoxide (CO) concentration in the main transport modes and along heavy traffic routes in the Athens urban area. Specifically the study identifies the main factors affecting CO exposure during commuting. Several portable, electrochemical CO monitors (Solomat's MPM4100), were used to record the in-vehicle CO concentrations every 15 s. Measurements were performed during rush hour periods. Field monitoring was conducted in summer 1998 and winter 1998û1999. Exposure estimates were compared to WHO guidelines. The findings showed that the mean CO level over trips of 30 min was 21.4 ppm for private car against 10.4, 9.6, 4 and 11.5 ppm for bus, trolley, electric train and pedestrians, respectively. Transport mode, route, monitoring period and season had a significant influence on the measured CO concentrations. The study points out the importance of microenvironmental monitoring, instead of using fixed-site data in assessing commuter's CO exposure.

Abstract  The association between particulate air pollution and asthma medication use and symptoms was assessed in a panel study of 53 adult asthmatics in Erfurt, Germany in winter 1996/1997. Number concentrations of ultrafine particles, 0.01-0.1 microm in diameter (NC0.01-0.1), mean 17,300.cm-3, and mass concentrations of fine particles 0.01-2.5 microm in diameter (MC0.01-2.5), mean 30.3 microg.m-3, were measured concurrently. They were not highly correlated (r=0.45). The associations between ambient particle concentrations and the prevalence of inhaled 'beta'2-agonist, corticosteroid use and asthma symptoms, were analysed separately with logistic regression models, adjusting for trend, temperature, weekend, holidays, and first order autocorrelation of the error. Cumulative exposures over 14 days of ultrafine and fine particles were associated with corticosteroid use. 'Beta'2-agonist use was associated with 5-day mean NC0.01-0.1 and MC0.01-2.5. The prevalence of asthma symptoms was associated with ambient particle concentrations. The results suggest that reported asthma medication use and symptoms increase in association with particulate air pollution and gaseous pollutants such as nitrogen dioxide.

Abstract  Background: A number of emergency department studies have corroborated findings from mortality and hospital admission studies regarding an association of ambient air pollution and respiratory outcomes. More refined assessment has been limited by study size and available air quality data. Methods: Measurements of 5 pollutants (particulate matter [PM10], ozone, nitrogen dioxide [NO2], carbon monoxide [CO], and sulfur dioxide [SO2]) were available for the entire study period (1 January 1993 to 31 August 2000); detailed measurements of particulate matter were available for 25 months. We obtained data on 4 million emergency department visits from 31 hospitals in Atlanta. Visits for asthma, chronic obstructive pulmonary disease, upper respiratory infection, and pneumonia were assessed in relation to air pollutants using Poisson generalized estimating equations. Results: In single-pollutant models examining 3-day moving averages of pollutants (lags 0, 1, and 2): standard deviation increases of ozone, NO2, CO, and PM10 were associated with 1–3% increases in URI visits; a 2 μg/m3 increase of PM2.5 organic carbon was associated with a 3% increase in pneumonia visits; and standard deviation increases of NO2 and CO were associated with 2–3% increases in chronic obstructive pulmonary disease visits. Positive associations persisted beyond 3 days for several of the outcomes, and over a week for asthma. Conclusions: The results of this study contribute to the evidence of an association of several correlated gaseous and particulate pollutants, including ozone, NO2, CO, PM, and organic carbon, with specific respiratory conditions.

Abstract  Ontario Heart and Stroke Foundation; Upjohn Company of Canada.

Abstract  Motor vehicle emissions usually constitute the most significant source of ultrafine particles (diameter <0.1 um) in an urban environment. Zhu et al. (J. Air Waste Manage. Assoc., 2002, accepted for publication) conducted systematic measurements of the concentration and size distribution of ultrafine particles in the vicinity of a highway dominated by gasoline vehicle. The present study compares these previous measurements with those made on Interstate 710 freeway in Los Angeles. The 710 freeway was selected because more than 25% of the vehicles are heavy-duty diesel trucks. Particle number concentration and size distribution in the size range from 6 to 220 nm were measured by a condensation particle counter and a scanning mobility particle sizer, respectively. Measurements were taken at 17, 20, 30, 90, 150, and 300 m downwind and 200 m upwind from the center of the freeway. At each sampling location, concentrations of carbon monoxide (CO) and black carbon (BC) were also measured by a Dasibi CO monitor and an Aethalometer, respectively. The range of average concentration of CO, BC and total particle number concentration at 17 m was 1.9-2.6 ppm, 20.3-24.8 ug/m3, 1.8 x 10E5 - 3.5 x 10E5/cm3, respectively. Relative concentration of CO, BC and particle number decreased exponentially and tracked each other well as one moves away from the freeway. Both atmospheric dispersion and coagulation appears to contribute to the rapid decrease in particle number concentration and change in particle size distribution with increasing distance from the freeway. Average traffic flow during the sampling periods was 12,180 vehicles/h with more than 25% of vehicles being heavy-duty diesel trucks. Ultrafine particle number concentration measured at 300 m downwind from the freeway was indistinguishable from upwind background concentration. These data may be used to estimate exposure to ultrafine particles in the vicinity of major highways.

Abstract  The use of meta-analysis in environmental epidemiology can enhance the value of epidemiologic data in debates about environmental health risks. Meta-analysis may be particularly useful to formally examine sources of heterogeneity, to clarify the relationship between environmental exposures and health effects, and to generate information beyond that provided by individual studies or a narrative review. However, meta-analysis may not be useful when the relationship between exposure and disease is obvious, when there are only a few studies of the key health outcomes, or when there is substantial confounding or other biases which cannot be adjusted for in the analysis. Recent increases in the use of meta-analysis in environmental epidemiology have highlighted the need for guidelines for the application of the technique. Guidelines, in the form of desirable and undesirable attributes, are presented in this paper for various components of a meta- analysis including study identification and selection; data extraction and analysis; and interpretation, presentation, and communication of results. Also discussed are the appropriateness of the use of meta-analysis in environmental health studies and when meta-analysis should or should not be used.

Abstract  The case-crossover design was proposed for the study of a transient effect of an intermittent exposure on the subsequent occurrence of a rare acute-onset disease. This design can be an alternative to Poisson time series regression for studying the health effects of fine particulate matter air pollution. Characteristics of time-series of particulate matter, including long-term time trends, seasonal trends, and short-term autocorrelations, require that referent selection in the case-crossover design be considered carefully and adapted to minimize bias. We performed simulations to evaluate the bias associated with various referent selection strategies for a proposed case-crossover study of associations between particulate matter and primary cardiac arrest. Some a priori reasonable strategies were associated with a relative bias as large as 10%, but for most strategies the relative bias was less than 2% with confidence interval coverage within 1% of the nominal level. We show that referent selection for case-crossover designs raises the same issues as selection of smoothing method for time series analyses. In addition, conditional logistic regression analysis is not strictly valid for some case-crossover designs, introducing further bias.