Abstract  #BACKGROUND: A number of studies have shown that both temperature and air pollution are associated with health outcomes. In assessing air pollution effects, temperature is usually considered a confounder. However, only a few recent studies considered air pollution as confounders while assessing temperature effects. Few studies are available on whether or not air pollution modifies the temperature-disease relationship. METHODS: In this study, we used three parallel Poisson generalized additive models to examine whether particulate matter < 10 mum in aerodynamic diameter (PM10) modified the effects of minimum temperature on cardiorespiratory morbidity and mortality in Brisbane, Australia. RESULTS: Results show that PM10 statistically significantly modified the effects of temperature on respiratory and cardiovascular hospital admissions, all nonexternal-cause mortality, and cardiovascular mortality at different lags. The enhanced adverse temperature effects were found at higher levels of PM10, but no clear evidence emerged for interactive effects on respiratory and cardiovascular emergency visits. Three parallel models produced similar results, which strengthened the validity of findings. CONCLUSION: We conclude that it is important to evaluate the modification role of air pollution in the assessment of temperature-related health impacts.

Abstract  Objective: It is still unknown whether specific components in fine particles are associated with heart rate variability (HRV) reduction. Methods: We recruited 46 patients with or at risk for cardiovascular diseases to measure 24-hour HRV by ambulatory electrocardiographic monitoring. Fixed-site air-monitoring stations were used to represent participants' exposures to particles with aerodynamic diameters less than 10 ?m (PM10) and 2.5 ?m (PM2.5), and particulate components of sulfate, nitrate, organic carbon (OC) and elemental carbon, and gaseous pollutants. Results: We found that HRV reduction was associated with sulfate, OC, and PM2. 5 but not with the other five pollutants in single-pollutant models. Sulfate was found to remain in significant association with HRV reduction adjusting for OC and PM2.5 in three-pollutant models. Conclusions: Exposures to sulfate and OC in PM2.5were associated with HRV reduction in patients with or at risk for cardiovascular diseases.

Abstract  The National Children's Study is considering a wide spectrum of airborne pollutants that are hypothesized to potentially influence pregnancy outcomes, neurodevelopment, asthma, atopy, immune development, obesity, and pubertal development. In this article we summarize six applicable exposure assessment lessons learned from the Centers for Children's Environmental Health and Disease Prevention Research that may enhance the National Children's Study: a) Selecting individual study subjects with a wide range of pollution exposure profiles maximizes spatial-scale exposure contrasts for key pollutants of study interest. b) In studies with large sample sizes, long duration, and diverse outcomes and exposures, exposure assessment efforts should rely on modeling to provide estimates for the entire cohort, supported by subject-derived questionnaire data. c) Assessment of some exposures of interest requires individual measurements of exposures using snapshots of personal and microenvironmental exposures over short periods and/or in selected microenvironments. d) Understanding issues of spatial-temporal correlations of air pollutants, the surrogacy of specific pollutants for components of the complex mixture, and the exposure misclassification inherent in exposure estimates is critical in analysis and interpretation. e) "Usual" temporal, spatial, and physical patterns of activity can be used as modifiers of the exposure/outcome relationships. f) Biomarkers of exposure are useful for evaluation of specific exposures that have multiple routes of exposure. If these lessons are applied, the National Children's Study offers a unique opportunity to assess the adverse effects of air pollution on interrelated health outcomes during the critical early life period.

Abstract  We report on the first application of a novel fast on-road sensing method for measurement of particulate emissions of individual passing passenger cars. The study was motivated by the shift of interest from gases to particles in connection with strong adverse health effects. The results correspond very much to findings by Beaton et al. (Science, May 19,1995) for gaseous hydrocarbon and CO emissions: A small percentage of "superpolluters" (here 5%) account for a high percentage (here 43%) of the pollution (here elemental carbon). We estimate that up to 50% of the particulate emissions of vehicles could be avoided on the basis of the present legislation, if on-road monitoring would be applied to enforce maintenance. Our fast sensing method for particles is based on photoelectron emission from the emitted airborne soot particles in combination with a CO2 sensor delivering a reference.

Abstract  Several studies have documented potential health effects due to agricultural burning smoke. However, there is a paucity of literature characterizing community residents exposure to agricultural burning smoke. This study assesses personal exposures to particulate matter (PM) with aerodynamic diameters <2.5 mu m (PM sub(2.5)) from agriculture burning smoke (E sub(b)) for 33 asthmatic adults in Pullman, WA. PM sub(2.5) concentrations were measured on 16 subjects, inside of all but four residences, outside of 6 residences, and at a central site. The mean+/-standard deviation of personal exposure to PM sub(2.5) was 13.8+/-11.1 mu g m super(-3), which was on average 8.0 mu g m super(-3) higher during the agricultural burning episodes (19.0+/-11.8 mu g m super(-3)) than non-episodes (11.0+/-9.7 mu g m super(-3)). The levoglucosan (LG, a unique marker for biomass burning PM) on personal filter samples also was higher during the episodes than non-episodes (0.026+/-0.030 vs. 0.010+/-0.012 mu g m super(-3)). We applied the random component superposition model on central-site and home indoor PM measurements, and estimated a central-site infiltration factor between 0.21 and 2.05 for residences with good modeling performance. We combined the source apportionment and total exposure modeling results to estimate individual E sub(b), which ranged from 1.2 to 6.7 mu g m super(-3) and correlated with personal LG with an r of 0.51. The sensitivity analysis of applying the infiltration efficiency estimated from the recursive model showed that the E sub(b) (range: 1.3-4.3 mu g m super(-3)) obtained from this approach have a higher correlation with personal LG (r=0.75). Nevertheless, the small sample size of personal LG measurements prevents a comparative and conclusive assessment of the model performance. We found a significant between-subject variation between episodes and non-episodes in both the E sub(b) estimates and subjects activity patterns. This suggests that the LG measurements at the central site may not always represent individual exposures to agricultural burning smoke. We recommend collecting more microenvironmental samples to model the E sub(b) and more personal samples to validate the E sub(b) estimates.

Abstract  Background: Automobile exhaust is a major source of air pollution in urban areas. To study health effects of traffic exhaust fumes epidemiologists need specific tools in order to achieve a precise assessment of human exposure to traffic air pollution (TAP) and avoid misclassification. The aim of this review is to study the different ways of assessing human exposure to TAP in epidemiological studies dealing with short-term or long-term health effects of TAP. Methods: After presenting the different designs and goals of the studies mentioned above, this review focuses on methods of assessing exposure to TAP and their different associated health endpoints. Results: To assess exposure to TAP, most published studies have used more or less complex exposure indices. Several teams have used residence location and its proximity to traffic, traffic counts, or a combination of both. More recently, some authors have developed mathematical dispersion models and statistical regression models. Discussion: Our analysis shows that reliable and validated tools would be needed to assess accurately human exposure to TAP. This can only be achieved with statistical regression models and mathematical dispersion models. Although such methods may be difficult to implement, their use can be facilitated by adding a geographic information system.

Abstract  BACKGROUND: Outdoor air pollution and lead exposure can disturb cardiac autonomic function, but the effects of both these exposures together have not been studied. METHODS: We examined whether higher cumulative lead exposures, as measured by bone lead, modified cross-sectional associations between air pollution and heart rate variability among 384 elderly men from the Normative Aging Study. We used linear regression, controlling for clinical, demographic, and environmental covariates. RESULTS: We found graded, significant reductions in both high-frequency and low-frequency powers of heart rate variability in relation to ozone and sulfate across the quartiles of tibia lead. Interquartile range increases in ozone and sulfate were associated respectively, with 38% decrease (95% confidence interval = -54.6% to -14.9%) and 22% decrease (-40.4% to 1.6%) in high frequency, and 38% decrease (-51.9% to -20.4%) and 12% decrease (-28.6% to 9.3%) in low frequency, in the highest quartile of tibia lead after controlling for potential confounders. We observed similar but weaker effect modification by tibia lead adjusted for education and cumulative traffic (residuals of the regression of tibia lead on education and cumulative traffic). Patella lead modified only the ozone effect on heart rate variability. CONCLUSIONS: People with long-term exposure to higher levels of lead may be more sensitive to cardiac autonomic dysfunction on high air pollution days. Efforts to understand how environmental exposures affect the health of an aging population should consider both current levels of pollution and history of lead exposure as susceptibility factors.

Abstract  #In Asia, limited literature has been published on the association between daily mortality and ambient air pollution. We examined the associations of daily cause-specific mortality with daily mean concentrations of particulate matter (PM) with a mass median aerodynamic diameter less than 10 mu m (PM10) in Wuhan, China using 4 years of data (2001-2004). There are approximately 4.5 million residents in Wuhan who live in the city core area of 201 km(2) where air pollution levels are higher and pollution ranges are wider than the majority of cities in the published literature. We use quasi-likelihood estimation within the context of the generalized additive models (GAMs) (natural spline (NS) models in R) to model the natural logarithm of the expected daily death counts as a function of the predictor variables. We found consistent PM10 effects on mortality with the strongest effects on lag 0 day. Every 10 mu g/m3 increase in PM10 daily concentration at tag 0 day was significantly associated with an increase in non-accidental (0.36%; 95% CI 0.19-0.53%), cardiovascular (0.51%; 95% CI 0.28-0.75%), stroke (0.44%; 95% CI 0.16-0.72%), cardiac (0.49%; 95% CI 0.08-0.89%), respiratory (0.71%; 95% CI 0.20-1.23%), and cardiopulmonary (0.46%; 95% CI 0.23-0.69%). In general, these effects were stronger among the elderly (>= 65 years or >= 45 years) than among the young. The exploration of exposure-response relationships between PM10 and cause-specific mortality suggests the appropriateness of assuming linear relationships, where the PM10 concentration in Wuhan ranged from 24.8 to 477.8 mu g/m(3). We conclude that there is consistent evidence of acute effects of PM10 on cardiopulmonary mortality. A linear no threshold exposure-response relationship is suggested between PM10 and the studied cause-specific mortality.

Abstract  BACKGROUND: Fine particulate matter has been linked to allergies by experimental and epidemiological data having used aggregated data or concentrations provided by fixed-site monitoring stations, which may have led to misclassification of individual exposure to air pollution. METHODS: A semi-individual design was employed to relate individual data on asthma and allergy of 5338 school children (10.4 +/- 0.7 years) attending 108 randomly chosen schools in 6 French cities to the concentrations of PM2.5 (fine particles with aerodynamic diameter 2.5 microm) assessed in proximity of their homes. Children underwent a medical visit including skin prick test (SPT) to common allergens, exercise-induced bronchial (EIB) reactivity and skin examination for flexural dermatitis. Their parents filled in a standardised health questionnaire. RESULTS: After adjustment for confounders and NO2 as a potential modifier, the odds of suffering from EIB and flexural dermatitis at the period of the survey, past year atopic asthma and SPT positivity to indoor allergens were significantly increased in residential settings with PM2.5 concentrations exceeding 10 microg/m3 (WHO air quality limit values). The relationships were strengthened in long-term residents (current address for at least 8 years). CONCLUSIONS: Findings support the hypothesis that changes in allergy prevalence observed in recent decades might be partly related to interactions between traffic-related air pollution and allergens. Further longitudinal investigations are needed to corroborate such results.

Abstract  The effect of exposure to irritant air pollutants on the development of allergic airway disease is poorly understood. This study examines the effects of the lower respiratory tract irritant, NO2, on the outcome of ovalbumin (OVA)-induced allergic airway disease. Male and female C57Bl/6 mice were sensitized by weekly intraperitoneal (ip) OVA injections for 3 wk followed by daily 1-h OVA aerosol inhalation challenge for 3 or 10 d. Initially, mice were exposed daily for 3 d to air or 0.7 or 5 ppm NO2 for 2 h following each OVA aerosol challenge. OVA exposure resulted in pronounced lower airway inflammation, as evidenced by a significant increase in bronchoalveolar lavage (BAL) total cellularity and eosinophil levels. BAL eosinophil levels were significantly lower in OVA-NO2 compared to OVA-air animals. The reduction was similar at both NO2 exposure concentrations. In a subsequent study, sensitized animals were exposed for 3 or 10 d to aerosolized OVA followed by air or 0.7 ppm NO2. BAL eosinophils were again reduced at 3 d by OVA-NO2 exposure compared to OVA-air mice. At 10 d the eosinophilia was virtually abolished. This reduction in OVA-induced cellular inflammation by NO2 was confirmed by histopathological analysis. Contrary to expectations, exposure to NO2 during the aerosol challenge to OVA dramatically diminished the outcome of allergic disease in lungs as measured by airway cellular inflammation.

Abstract  Background: Many studies have shown a consistent association between ambient air pollution and an increase in death due to cardiovascular causes. An increase in blood pressure is a common risk factor for a variety of cardiovascular diseases. However, the association between air pollution and blood pressure has not been evaluated extensively. Methods: In this cross-sectional study, we measured blood pressure in 10 459 subjects who had a health examination from 2001 to 2003, and calculated individual’s exposure to ambient levels of air pollutants. To evaluate the relationship between exposure to air pollutants and blood pressure with respect to season, we performed a multiple regression analysis, separately, according to season, controlling for individual characteristics and meteorological variables. Results: In the warm-weather season (July–September), particulate air pollutant of <10 μm (PM10) and nitrogen dioxide (NO2) concentrations were significantly associated with measures of blood pressure. During cold weather (October–December), blood pressure was significantly associated with sulphur dioxide (SO2) and ozone (O3) concentrations. The significant association between PM10 or NO2 and blood pressure disappeared during the cold-weather season. Conclusion: We found a seasonal variation for the association between ambient air-pollutant concentrations and blood pressure.

Abstract  OBJECTIVE: Recent studies indicate that the U.S. Environmental Protection Agency (EPA) ozone standards may not protect sensitive individuals. In this study we examined respiratory effects of ozone in infants who may be vulnerable, particularly if they are children of asthmatic mothers. DESIGN: Women delivering babies at one of five hospitals in southwestern Virginia between 1994 and 1996 were invited to participate in a cohort study; 780 women enrolled. Ambient air quality data (ozone and particulate matter) were collected at a central monitoring site. PARTICIPANTS: This analysis is of 691 infants followed for approximately 83 days between 10 June and 31 August 1995 and/or 1996; they contributed a total of 52,421 infant-days of follow-up. Mothers were interviewed at enrollment and approximately biweekly to report infants daily symptoms. Repeated measures logistic regression models were run separately for wheeze, difficulty breathing, and cough. Ozone metrics included 24-hr average, peak 1-hr, and maximum 8-hr average. Analyses were repeated for the 61 infants whose mothers had asthma. RESULTS: For every interquartile-range increase in same-day 24-hr average ozone, likelihood of wheeze increased 37% [95% confidence interval (CI), 2-84%]. Among infants of asthmatic mothers, same-day 24-hr average ozone increased likelihood of wheeze 59% (95% CI, 1-154%) and of difficulty breathing 83% (95% CI, 42-136%). Maximum 8-hr ozone and peak 1-hr ozone were associated with difficulty breathing, but not wheeze, in infants of asthmatic mothers. Ozone was not associated with cough. CONCLUSIONS: At levels of ozone exposure near or below current U.S. EPA standards, infants are at increased risk of respiratory symptoms, particularly infants whose mothers have physician-diagnosed asthma.

Abstract  A fuel-based method for estimating heavy-duty diesel truck emissions is described. In this method, emission factors are normalized to fuel consumption; vehicle activity is measured by the amount of diesel fuel consumed. For the San Francisco Bay Area during summer 1996, on-road heavy-duty diesel trucks were estimated at the upper bound to emit 110 x 10(3) kg/day of nitrogen oxides (NOx) and 3.7 x 10(3) kg/day of fine black carbon (BC) particles. These upper bound values were 2.3 and 4.5 times, respectively, the corresponding predictions of Californias motor vehicle emission inventory model, MVEI 7G. Significant decreases in diesel truck activity and emissions, 70-80% below typical weekday levels, were observed in the Bay Area on weekends. Reductions in diesel NOx and BC particle emissions on weekends may contribute to higher ambient ozone concentrations and higher organic carbon (OC) to BC ratios observed on weekends. Heavy-duty truck traffic peaks on weekdays during the middle of the day and falls off before the afternoon rush hour. Therefore, the diurnal pattern of heavy-duty truck travel may contribute to increases in ambient OC/BC ratios observed during late afternoon hours.

Abstract  Air pollutant exposure may induce deterioration of respiratory health. Concentrations of air particles, ozone, nitrogen dioxide, sulfur dioxide, and sulfate are among the players involved in the initiation and/or exacerbation of lung diseases. We have previously documented that the pollutant sodium sulfite (Na2SO3) is a human neutrophil agonist. To date, there is no evidence in the literature that Na2SO3 can activate epithelial lung cells. In the present study, we found that Na2SO3 (0.01û10 mM) induces tyrosine phosphorylation events and interleukin-8 production in human epithelial lung A549 cells. In addition, we found that Na2SO3 did not promote A549 cell apoptosis as assessed by the degradation of the cytoskeletal gelsolin protein and by FITC-annexin-V binding. Human neutrophil adhesion to Na2SO3-induced A549 cells was increased when compared with untreated A549 cells. As assessed by flow cytometry, cell surface expression of intercellular adhesion molecule (ICAM)-1, ICAM-3, and vascular cell adhesion molecule-1 (VCAM-1) on A549 cells was not affected by Na2SO3. We conclude that Na2SO3 can activate A549 cells. In addition, we conclude that neutrophil adhesion to Na2SO3-induced A549 cells is increased via an ICAM-1-, ICAM-3-, and VCAM-1-independent mechanism.

Abstract  NOx emissions from commercial aircraft consist primarily of NO2 at low power.

Abstract  This paper explores the range of CALINE4's PM2.5 modeling capabilities by comparing previously collected PM2.5 data with CALINE4 predicted values. Two sampling sites, a suburban site located at an intersection in Sacramento, CA, and an urban site located in London, were used. Predicted concentrations are graphed against observed concentrations and evaluated against the criterion that 75% of the points fall within the factor-of-two prediction envelope. For the suburban site, data estimated by CALINE4 produced results that fell within the acceptable factor-of-two percentage envelope. A reverse dispersion test was also conducted for the suburban site using observed and calculated emission factors, and although it showed correlations between the observed values and CALINE4 predicted values, it could not conclusively prove that the model is accurate at predicting PM2.5 concentrations. Although the results suggest that CALINE4 PM2.5 predictions may be reasonably close to observed values, the number of observations used to verify the model was small and consequently, findings from the suburban site should be considered exploratory. For the urban site, a much larger data set was evaluated; however, the CALINE4 results for this site did not fall 75% within the factor-of-two envelope. Several factors, including street canyon effects, likely contributed to an inaccuracy of the emission factors used in CALINE4, and therefore, to the overall CALINE4 predictions. In summary, CALINE4 does not appear to perform well in densely populated areas and differences in topography may be a decisive factor in determining when CALINE4 may be applicable to modeling PM2.5. For critical transportation projects requiring PM2.5 analysis, use of CALINE4 may not be optimal because of its inability to produce reasonable estimates for highly trafficked areas. Additional data sets for CALINE4 analysis, particularly in urban environments, are required to fully understand CALINE4's PM2.5 modeling capabilities. (C) 2007 Elsevier Ltd. All rights reserved.

Abstract  In this paper, the CALINE4 software package, designed for calculation of concentrations of carbon monoxide near a busy road, is adapted for the analysis of aerosols of fine and ultra-fine particles, generated by vehicles on the road. A scaling procedure of the CALINE4 package is developed and justified. A new efficient method of determination of the average emission factor for fine particle emission from the average fleet (one average vehicle) on a given road is also developed. This method is based on measurements of the average particle number concentration at just one point near the road.

An example of a specific road in the Brisbane area, Australia, is considered. The average emission factor for vehicles on this road is calculated to be similar to4.5 x 10(14) particle/vehicle/mile. The obtained scaling coefficient is shown to be correct, and the procedure is directly applicable for the analysis of an arbitrary road with different types of vehicles and their average speed.

Good agreement between the experimental results and the predicted theoretical dependencies of concentration on distance from the road clearly confirms the applicability of the CALINE4 package for the analysis of propagation of fine particle aerosols from a busy road. Statistical analysis of the experimental and theoretical results demonstrates that the concentration of fine and ultra-fine particles approximately reduces as a power law in distance from the road. (C) 2002 Elsevier Science Ltd. All rights reserved.

Abstract  The lungs of 8 male beagle dogs were examined morphologically and morphometrically after exposure for 13 mo to a respirable sulfur( IV) aerosol at a mass concentration of 1.53 mg m-3 (16.5 h/ day) , and to an acidic sulfate aerosol carrying 15.2 mumol m-3 hydrogen ions into the lungs (6 h/day). An additional eight dogs served as unexposed controls. Standard morphometric analyses of both the surface epithelia of the conducting airways and the alveolar region were performed. These analyses showed no difference between the exposure group and control group. However, there was a tendency to an increase in the volume density of bronchial glands in the exposure group. Five of eight exposed animals showed thickened ridges (knob-like structures) at the entrance to alveoli in the alveolar duct and alveolar sac. Transmission electron microscopy revealed that the thickening was mainly due to type II cell proliferation. As the previous experiment using sulfite aerosol only showed no alterations in the proximal alveolar regions, the changes observed may be considered as effects of acidic sulfate aerosol alone or in combination with sulfite. These findings suggest that sulfur aerosols have the potential to induce epithelial alterations in the proximal alveolar region, which is a primary target for air pollutants.

Abstract  The airway epithelial lining serves as an efficient barrier against penetration of exogenous particles and macromolecules. Disruption of this barrier following O3 exposure represents a state of compromised epithelial defenses leading to increased transmucosal permeability. Although the barrier disruption following an acute exposure is transient in nature, the brief period of disruption caused by O3 an oxidant air pollutant, provides an opportunity for facilitated entry of a potentially toxic particulate copollutant(s) across the airway epithelia. The subsequent deposition and retention of the copollutant(s) in the subepithelial compartment for prolonged periods adds the risk of injury due to chronic exposure following an acute episode. Toxicological studies from several laboratories have demonstrated alterations in epithelial permeability, suggestive of barrier disruption, in animals and humans exposed to O3. Inflammatory cells represent another important component of pulmonary defenses, but upon activation these cells can both induce and sustain injury. The recruitment of these cells into the lung following O3 exposure presents a risk of tissue damage through the release of toxic mediators by activated inflammatory cells. Several studies have reported concomitant changes in permeability and recruitment of the inflammatory cells in the lung following O3 exposure. In these studies, an inflammatory response, as detected by an increase in the number of polymorphonuclear leukocytes in the bronchoalveolar lavage (BAL) or in lung parenchyma, was accompanied by either an increased tracer transport across the airway mucosa or an elevation in the levels of total protein and/or albumin in the BAL. The magnitude of response and the time at which the permeability changes and inflammatory response peaked varied with O3 concentration, exposure duration, and the mode of analysis. The responsiveness to O3 also appeared to vary with the animal species, and increased under certain conditions such as physical activity and pregnancy. Some of the effects seen after an acute exposure to O3 were modified upon repeated exposures. The responses following repeated exposures included attenuation, persistence, or elevation of permeability and inflammation. Mechanistic studies implicate chemotactic factors, cellular mediators, and cell-surface-associated molecules in the induction of inflammation and lung injury. In discussing these studies, this review serves to introduce the mucosal barrier functions in the lung, evaluates inflammatory and permeability consequences of O3 addresses mechanisms of inflammatory reactions, and offers alternate viewpoints.

Abstract  The effect of indoor exposure to nitrogen dioxide, ammonia, particulate matter and parental tobacco smoke on respiratory health was studied over a period of six months in all second graders born and living in two area of continental Croatia 8-10 yr of age. The study group was divided into two sections corresponding to area of residence (industrial/rural). Information on respiratory symptoms was collected from a self-administered questionnaire completed by the parents of the children. The mean values of concentrations of indoor air pollution that had been recorded in 24-h samples of air collected at schools were mostly below threshold limit for ambient pollution. In addition, information on parental smoking, the density of habitation and the type of fuel used for heating and/or cooking in the home was obtained by a questionnaire. In the investigated period the prevalence of respiratory illness was 22% in the children exposed to lower indoor air pollution acid 25% in those exposed to higher indoor air pollution. Exposure to parental smoking was also associated with more respiratory symptoms (28 : 19%). The results indicate that the measured air pollutants only had a slight effect on the respiratory health of preadolescent children. However, the effect of exposure to parental smoking was more pronounced. (C) 1999 Elsevier Science Ltd. All rights reserved.

Abstract  1 In previous studies a rat inhalation model was developed to investigate the treatment of acute nitrogen dioxide (NO2) intoxication.

2 Biochemical parameters, which may be important for the evaluation of lung injury and repair, were reviewed and compared with the histology.

3 After exposure to high NO2 concentrations (75 ppm, 125 ppm or 175 for 10 min) 1 the lung injury observed by light microscope was most pronounced after 24 h and became worse with increasing concentration.

4 The most sensitive indicators for lung injury in the broncho-alveolar lavage fluid (BAL) were protein and albumin concentrations, angiotensin converting enzyme activity, beta-glucuronidase activity and the presence of neutrophil leucocytes. The changes observed in these variables were dose-dependent. Following exposure to 175 ppm the protein and albumin concentrations and the angiotensin converting enzyme activity showed a 100-fold increase, while the beta-glucuronidase activity showed a 10-fold increase.

5 Glucose-6-phosphate dehydrogenase and glutathione peroxidase in the supernatant of lung homogenate and gamma-glutamyl transferase activity in BAL are likely to be the most practical parameters for monitoring the phase of repair because their activities were maximal at the moment histological changes were reduced in intensity. 6 Repair was almost complete 7 d following exposure.

Abstract  Porjekt Umwelt und Gesundheit of the State of Baden-Wurtemberg, Karlsruhe, Germany. #The aim of this study was to investigate the cellular and biochemical events associated with repeated exposures to ozone. Twenty-three healthy subjects underwent single exposures to 200 ppb ozone and to filtered air (FA), as well as repeated exposures to 200 ppb ozone on 4 consecutive days, each for 4 h of intermittent exercise. Bronchoalveolar lavage was performed and mucosal biopsies were taken 20 h after the single or the last of the repeated exposures. As compared with FA, the single exposure to ozone caused a decrease in FEV1 , an increase in the percentages of neu-trophils and lymphocytes, the concentrations of total protein, IL-6, IL-8, reduced glutathione, urate, and ortho-tyrosine in BAL fluid (BALF), but no changes in the cellular composition of biopsy. After the repeated exposure, the effect on lung function was abolished and differential cell counts in BALF were not significantly different from those after FA. However, the concentrations of total protein, IL-6, IL-8, reduced glutathione, and ortho-tyrosine were still increased. IL-10 could only be detected in BALF after repeated ozone exposures. Furthermore, macroscopic scores for bronchitis, erythema, and hypervulnerability of airway mucosa were in-creased, as well as numbers of neutrophils in bronchial mucosal biopsies. Our data demonstrate that airway inflammation persists after repeated ozone exposure, despite attenuation of some in-flammatory markers in BALF and adaptation of lung function.

Abstract  Personal exposures to nitrogen dioxide (NO2) were monitored for 176 randomly selected inhabitants (25-55 years old) of Helsinki Metropolitan area as a part of the EXPOLIS (Air Pollution Exposure Distributions Within Adult Urban Populations in Europe) study between October 1996 and December 1997. NO2 measurements were 48-h averages collected by Palmes passive sampler tubes. Differences in personal exposures to NO2 were analyzed between sub-populations stratified by microenvironment, behavioral, socioeconomic and demographic factors. Factors significantly associated with differences in exposures to NO2 were home and work location, housing characteristics, traffic volume near home, season and keeping windows open at home. Exposure to environmental tobacco smoke (ETS) and use of gas stove were also associated with increased personal exposures, although only few participants had a gas stove in Helsinki, and other gas appliances are non-existent. Single adults had higher average exposures to NO2 than married or cohabiting participants, suggesting differences in living conditions between these two groups. Increased education was associated with decreased exposures to NO2 and employed men were more exposed than unemployed men. Increased exposures to NO2 were not associated with age or occupational status in Helsinki. Thus, behavioral and sociodemographic factors may have significant impact on personal exposures to NO2 and should be considered in addition to environmental determinants in any monitoring program.

Abstract  #BACKGROUND: Nitrogen dioxide (NO2) or home gas appliance use has been inconsistently associated with adverse respiratory outcomes in childhood. OBJECTIVES: (i) To examine the contribution of home gas appliance type and personal NO2 exposure. (ii) To examine the relationship between NO2 exposure and child lung function and respiratory history. (iii) To assess whether these relationships vary by house dust mite sensitization status. METHODS: A cross-sectional survey of 344 children (71% of the eligible group) with a mean age of 9.1 years from four randomly selected schools in the Australian Capital Territory from July to September 1999. Study measurements included a parental questionnaire, NO2 exposure by passive gas samplers, skin prick testing for 10 aeroallergens and lung function at rest and after cold air challenge. RESULTS: Total NO2 exposure was low with a mean concentration of 10.1 ppb. No associations were found between NO2 exposure or gas appliance use and asthma, wheeze or baseline lung function. Personal NO2 exposure was associated with a reduction in forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) after cold air challenge (adjusted difference - 0.12% (- 0.23% to - 0.01%) per 1 ppb increase). After exclusion of children who had home heating changed because of asthma, gas heater use was also significantly associated with a reduction in this measure (adjusted difference - 2.0% (- 3.7% to - 0.2%)). There was some evidence that these reductions were greater among the non-mite-sensitized children. CONCLUSIONS: The effect of low-level NO2 exposure on these respiratory outcomes was not marked. The possible effect of low-level NO2 exposure on non-specific bronchial reactivity requires confirmation. Future studies on NO2 and respiratory health should include measures of house dust mite sensitization and bronchial hyper-responsiveness.

Abstract  The size, composition, and concentration of particulate matter (PM) vary with location and time. Several monitoring/sampling programs are operated in California to characterize PM less than 2.5 and 10 mm in aerodynamic diameter (PM25 and PM10). This paper presents a broad summary of the spatial and temporal variations observed in ambient PM2.5 and PM10 concentrations in California. Many areas that have high PM10 concentrations also have relatively high PM2.5 concentrations, and data indicate that a significant portion of the PM10 air quality problem is caused by PM2.5. To develop effective plans for attaining the ambient PM standards, improved understanding of these unique problems is needed. Since 1989, pollution control efforts-whether specifically targeted for particulate matter or indirectly via controls on gaseous emissions-have caused annual average PM2.5 and PM10 concentrations to decline at most sites in California.