Abstract  Nitrogen dioxide exposure-induced mucosal pathology of the guinea pig nose was studied. Guinea pigs were exposed to 3 ppm or 9 ppm of nitrogen dioxide for 6 h a day, 6 times weekly for 2 weeks, and sacrificed 24 h after the final exposure. Exposure to 3 ppm of nitrogen dioxide resulted in decreased ciliary activity and slight eosinophil accumulation on the epithelium and submucosal layer. More serious pathologies were observed in the nose of guinea pigs exposed to 9 ppm of nitrogen dioxide, including a more prominent eosinophil influx to the epithelium and epithelial injury due to activation of eosinophils. Epithelial damage induced by nitrogen dioxide could lead to hyperresponsiveness and may result in a prolonged allergic inflammation. Our study suggests that environmental nitrogen dioxide may contribute to hyperresponsiveness and thus be involved in the increased morbidity of allergic rhinitis.

Abstract  To determine if nitrogen dioxide (NO2), a gaseous free radical, modifies the protective antioxidant pool present in respiratory tract lining fluids, a random, double-blind study utilizing flexible fiberoptic bronchoscopy with bronchial and bronchoalveolar lavage was performed. Healthy, nonsmoking, asymptomatic subjects were exposed to filtered air and 2 ppm NO2 for 4 h on separate occasions. To examine the kinetics of the NO2-induced antioxidant reactions, 44 subjects were randomly assigned to one of three groups. Bronchoscopy was performed 1.5 h (group 1), 6 h (group 2) or 24 h (group 3) after each exposure. Reduced glutathione (GSH), uric acid, and ascorbic acid concentrations were determined in both bronchial and bronchoalveolar lavage fluid fractions. In addition, bronchoalveolar lavage fluid was screened for malondialdehyde as a marker of lipid peroxidation. Exposure to NO2 resulted in a rapid (1.5 h) loss of uric acid from the bronchial region, however by 6 h after exposure it had increased significantly above control uric acid concentration in this region. At 24 h after exposure, uric acid concentration had returned to the control level. A similar response of uric acid to NO2 was seen in the bronchoalveolar region. Ascorbic acid was also decreased in bronchial and bronchoalveolar lavage fluids 1.5 h after exposure to NO2, but returned to control values by 6 h. In marked contrast, significant increases in GSH concentration were seen at 1.5 and 6 h in bronchial lavage fluid after exposure to NO2, which subsequently returned to control levels by 24 h. No change in bronchoalveolar lavage fluid GSH concentration or malondialdehyde content was seen after NO2 exposure. These data support the view that antioxidants present in lung fluids react with, and hence modulate the impact of, NO2 on the lung.

Abstract  In order to investigate the relationship between indoor and outdoor elemental concentrations and to characterize the infiltration behavior of elemental PM2.5constituents, we conducted an analysis of indoor and outdoor PM2.5elemental data collected during a comprehensive particle characterization study of nine nonsmoking homes in Boston, MA. Using data from nighttime periods when little or no particle-generating activity occurred, analyses focused on six elements that were consistently detected in both indoor and outdoor samples and that spanned a range of particle sizes: sulfur, nickel, zinc, iron, potassium, and silicon. Results showed that outdoor levels of all the elements were highly correlated with their corresponding indoor levels. Correlations remained high for different air exchange rate conditions, building characteristics, and seasons, suggesting that variability in ambient elemental infiltration into residences may not be a large source of variability affecting personal-ambient correlations for these elements. Elemental infiltration factors showed strong relationships with air exchange rate and season and were suggestive of an effect of particle size, which was likely obscured by remaining indoor source impacts. Analyses of this small dataset provided an indication that several elements--in particular nickel--could potentially serve as accurate tracers for infiltration of total PM2.5mass- and size-resolved particles into residential buildings. Similar to previously reported findings for sulfur, these elemental tracers showed the poorest performance for smaller and larger particle sizes.

Abstract  The Global Ozone Monitoring Experiment (GOME) is a new instrument aboard the European Space Agency's (ESA) Second European Remote Sensing Satellite (ERS-2), which was launched in April 1995. The main scientific objective of the GOME mission is to determine the global distribution of ozone and several other trace gases, which play an important role in the ozone chemistry of the earth's stratosphere and troposphere. GOME:measures the sunlight scattered from the earth's atmosphere and/or reflected by the surface in nadir viewing mode in the spectral region 240-790 nm at a moderate spectral resolution of between 0.2 and 0.4 nm. Using the maximum 960-km across-track swath width, the spatial resolution of a GOME ground pixel is 40 X 320 km(2) for the majority of the orbit and global coverage is achieved in three days after 43 orbits. Operational data products of GOME as generated by DLR-DFD, the German Data Processing and Archiving Facility (D-PAF) for GOME, comprise absolute radiometrically calibrated earthshine radiance and solar irradiance spectra (level 1 products) and global distributions of total column amounts of ozone and NO2, (level 2 products), which are derived using the DOAS aroach (Differential Optical Absorption Spectroscopy). (Under certain conditions and some restrictions, the operational data products are publically available from the European Space Agency via the ERS Helpdesk.) In addition to the operational data products, GOME has delivered important information about other minor trace gases such as OClO, volcanic SO2, H2CO from biomass burning, and tropospheric BrO. Using an iterative optimal estimation retrieval scheme, ozone vertical profiles can be derived from the inversion of the UV/VIS spectra. This paper reports on the GOME instrument, its operation mode, and the retrieval techniques, the latter with particular emphasis on DOAS (total column retrieval) and advanced optimal estimation (ozone profile retrieval). Observation of ozone depletion in the recent polar spring seasons in both hemispheres are presented. OClO observed by GOME under twilight conditions provides valuable information on the chlorine activation inside the polar vortex, which is believed to be responsible for the rapid catalytic destruction of ozone. Episodes of enhanced BrO in the Arctic, most likely contained in the marine boundary layer, were observed in early and late spring. Excess tropospheric nitrogen dioxide and ozone have been observed during the recent Indonesian fire in fall 1997. Formaldehyde could also clearly be identified by GOME and is known to be a by-product resulting from biomass burning.

Abstract  The aim of this study was to investigate the relation between two toxic volatile organic compounds, 1,3-butadiene and benzene, and a commonly used indicator of vehicle exhaust fumes, NO(2). This was to see if NO(2) can be used to indicate personal exposure to carcinogenic substances or at least estimate ambient levels measured at a stationary point. During the winter of 2001, 40 randomly selected persons living in the City of Umea (in the north of Sweden) were recruited to the study. Personal measurements of 1,3-butadiene, benzene and NO(2) were performed for one week, and were repeated for 20 of the 40 participants. Additional information was gathered using a diary kept by each participant. During the same time period weekly stationary measurements were performed at one urban background station and one street station in the city centre. The results from the personal measurements showed a negligible association of NO(2) with 1,3-butadiene (r= 0.06) as well as with benzene (r= 0.10), while the correlation coefficient between 1,3-butadiene and benzene was high and significant (r= 0.67). In contrast to the personal measurements, the stationary measurements showed strong relations between 1,3-butadiene, benzene and NO(2) both within and in-between the street and urban background station. This study supports NO(2) as a potential indicator for 1,3-butadiene and benzene levels in streets or urban background air, while the weak relations found for the personal measurements do not support the use of NO(2) as an indicator for personal 1,3-butadiene and benzene exposure.

Abstract  Epidemiological studies have found negative associations between human health and particulate matter in urban air. In most studies outdoor monitoring of urban background has been used to assess exposure. In a field study, personal exposure as well as bedroom, front door and background concentrations of PM(2.5), black smoke (BS), and nitrogen dioxide (NO(2)) were measured during 2-day periods in 30 subjects (20-33 years old) living and studying in central parts of Copenhagen. The measurements were repeated in the four seasons. Information on indoor exposure sources such as environmental tobacco smoke (ETS) and burning of candles was collected by questionnaires. The personal exposure, the bedroom concentration and the front door concentration was set as outcome variable in separate models and analysed by mixed effect model regression methodology, regarding subject levels as a random factor. Seasons were defined as a dichotomised grouping of outdoor temperature (above and below 8 degrees C). For NO(2) there was a significant association between personal exposure and both the bedroom, the front door and the background concentrations, whereas for PM(2.5) and BS only the bedroom and the front door concentrations, and not the background concentration, were significantly associated to the personal exposure. The bedroom concentration was the strongest predictor of all three pollution measurements. The association between the bedroom and front door concentrations was significant for all three measurements, and the association between the front door and the background concentrations was significant for PM(2.5) and NO(2), but not for BS, indicating greater spatial variation for BS than for PM(2.5) and NO(2). For NO(2), the relationship between the personal exposure and the front door concentration was dependent upon the "season", with a stronger association in the warm season compared with the cold season, and for PM(2.5) and BS the same tendency was seen. Time exposed to burning of candles was a significant predictor of personal PM(2.5), BS and NO(2) exposure, and time exposed to ETS only associated with personal PM(2.5) exposure. These findings imply that the personal exposure to PM(2.5), BS and NO(2) depends on many factors besides the outdoor levels, and that information on, for example, time of season or outdoor temperature and residence exposure, could improve the accuracy of the personal exposure estimation.

Abstract  A three-dimensional cloud-scale chemical transport model has been used to simulate trace gas transport, lightning NO production, and photochemical ozone production in the 12 July 1996 storm observed during the Stratosphere-Troposphere Experiment: Radiation, Aerosols and Ozone (STERAO-A) field experiment. The model is driven by meteorological fields from a nonhydrostatic cloud-resolving model (see Stenchikov et al., 2005). An assumption that both cloud-to-ground and intracloud flashes produce 460 moles NO/flash on average yielded the best comparison with the profile of NO observed in the storm anvil. Scenarios in which the NO production of an intracloud flash was 75 to 100% of the production of a cloud-to-ground flash best matched the column NOx mass computed from observations. Additional ozone production attributable to lightning NO within the storm cloud during the lifetime of the storm was very small (∼2 ppbv). However, simulations of the photochemistry over the 24 hours following the storm show that an additional 10 ppbv of ozone production can be attributed to lightning NO production in the upper troposphere. Convective transport of HOx precursors led to the generation of a HOx plume, which substantially aided the downstream ozone production. Soluble species mixing ratios in the simulated cloud were all within a factor of two of observations.

Abstract  #Occupational and nonoccupational personal nitrogen dioxide (NO2) exposures were measured using passive samplers for 31 taxi drivers in Asan and Chunan, Korea. Exposures were also estimated using a microenvironmental time-weighted average model based on indoor, outdoor and inside the taxi area measurements. Mean NO2 indoor and outdoor concentrations inside and outside the taxi drivers' houses were 24.7+/-10.7 and 23.3+/-8.3 ppb, respectively, with a mean indoor to outdoor NO2 ratio of 1.1. Mean personal NO2 exposure of taxi drivers was 30.3+/-9.7 ppb. Personal NO2 exposures for drivers were more strongly correlated with interior vehicle NO2 levels (r = 0.89) rather than indoor residential NO2 levels (r = 0.74) or outdoor NO2 levels (r = 0.71). The main source of NO2 exposure for taxi drivers was considered to be occupational driving. Interestingly, the NO2 exposures for drivers' using LPG-fueled vehicles (26.3+/-1.3 ppb) were significantly lower than those (38.1+/-1.3 ppb) using diesel-fueled vehicle (P <0.01). Since drivers spent most of their time inside their vehicle and indoors at home, a microenvironmental model was used to estimate the personal NO2 exposure with indoor and outdoor NO2 levels of the residence, and interior vehicle NO2 levels (P <0.001). Some subpopulations, such as professional drivers, might be exposed to high NO2 levels because they drive diesel-using vehicles outdoors in Korea.

Abstract  #The ExTra index, produced by the French Scientific Center for Building Physics, evaluates ambient concentrations of transport-related pollutants in front of the work and living places of urban dwellers. This study contributes to the validation of the ExTra index by carrying out measurements in four French cities. It compares nitrogen oxide concentrations (NOx) measured over 6 weeks with passive samplers, and NOx calculated concentrations using the ExTra index. The study takes into account traffic density, topographical parameters (building height, road, and pavement width), weather conditions (wind direction and strength), and background pollution levels. The model was tested at 100 street canyons sites. There were highly significant correlations (0.90 in Grenoble, 0.95 in Nice, 0.89 in Paris, and 0.89 in Toulouse) and good intraclass correlation coefficients (0.75 in Grenoble, 0.91 in Nice, 0.89 in Paris, and 0.86 in Toulouse) between the two series of values. These results suggest that if the ExTra index were to be applied to all the different residences and workplaces of a subject throughout his (her) life, it could be a useful epidemiological tool for studying the long-term health effects of transport-related emissions and for reconstructing individual exposure to such pollution in order to avoid misclassification.

Abstract  The aim of the study was to evaluate the predictions derived from the Danish Operational Street Pollution Model (OSPM) when the input data are obtained by simple methods that could be used in large-scale epidemiological studies. The model calculations were thus compared with passive sampler measurements of nitrogen dioxide and benzene at 103 street locations in Copenhagen, Denmark, and at 101 locations in rural areas. Data on traffic and street configuration were collected by means of a simple registration scheme in which forms were filled out by local municipal authorities. Meteorological data were derived from routine measurements at Copenhagen airport, and data on background air pollution were based on a simple empirical model. Differences in air pollution levels between rural areas and Copenhagen and differences in nitrogen dioxide concentrations at various locations in Copenhagen were well reproduced by the OSPM. The correlation coefficients (r) between the measured and the predicted half-year average concentrations of nitrogen dioxide in Copenhagen were between 0.75 and 0.80 for various degrees of precision of the input data for the model. The results indicate that the OSPM used with the presented methods for generation of input data might be useful in assessing long-term exposure to air pollutants in epidemiological studies.

Abstract  Nitrogen dioxide (NO2) is often present in inhaled air and may be generated in vivo from nitric oxide. Exposure of human blood plasma to NO2. caused rapid losses of ascorbic acid, uric acid and protein thiol groups, as well as lipid peroxidation and depletions of alpha-tocopherol, bilirubin and ubiquinol-10. No increase in protein carbonyls was detected. Supplementation of plasma with ascorbate decreased the rates of lipid peroxidation, alpha-tocopherol depletion and loss of uric acid. Uric acid supplementation decreased rates of lipid peroxidation but not the loss of alpha-tocopherol. We conclude that ascorbic acid, protein -SH groups, uric acid and alpha-tocopherol may be important agents protecting against NO2. in vivo. If these antioxidants are depleted, peroxidation of lipids occurs and might contribute to the toxicity of NO2.

Abstract  Background: Sulfur dioxide (SO2) is one of the major air pollutants. It is known to aggravate asthma symptoms in human beings, but few studies have focused on the effects of SO2 upon the development of bronchial asthma in animal models. Objective: This study was undertaken to evaluate the role of SO2 upon the development of ovalbumin (OA)-induced asthmatic reactions in guinea pigs. Methods: Guinea pigs were divided into four groups: (1) OA- and SO2-exposed group (n = 12), (2) SO2-exposed group (n = 12), (3) OA-exposed group (n = 11), and (4) saline-exposed group (n = 7). Guinea pigs of the first and second groups were exposed to 0.1 ppm SO2 for 5 hours a day on 5 consecutive days. Guinea pigs in the first and third groups inhaled 0.1% OA aerosols for 45 minutes a day on days 3, 4, and 5. One week after the sensitization procedure, all the guinea pigs underwent bronchial challenge with 1.0% OA aerosols, using unrestricted whole-body plethysmography. Bronchoalveolar lavage and histopathologic examination were performed 24 hours after the bronchial challenge. Results: Increases in enhanced pause (Penh), as an index of airway obstruction, after the bronchial challenge was significantly higher in OA- and SO2-exposed group (group 1) than the other groups (P < .05, respectively). Eosinophil counts in bronchoalveolar lavage fluids were also significantly higher in group 1 than in the other groups (P < .05, respectively). Histopathologic findings of bronchial and lung tissue in the group 1 showed an infiltration of inflammatory cells, bronchiolar epithelial damage, and mucus and cell plug in the lumen, but no significant abnormalities were observed in the other groups. Conclusions: These results indicate that repeated exposure to low levels of sulfur dioxide may enhance the development of ovalbumin-induced asthmatic reactions in guinea pigs.

Abstract  #The short-term effects of nitrogen dioxide (NO2) on total, cardiovascular and respiratory mortality in 30 European cities participating in the Air Pollution on Health: a European Approach (APHEA)-2 project were investigated. The association was examined using hierarchical models implemented in two stages. In the first stage, data from each city were analysed separately, whereas in the second stage, the city-specific air pollution estimates were regressed on city-specific covariates to obtain overall estimates and to explore sources of possible heterogeneity. A significant association of NO2 with total, cardiovascular and respiratory mortality was found, with stronger effects on cause-specific mortality. There was evidence of confounding in respiratory mortality with black smoke and sulphur dioxide. The effect of NO2 on total and cardiovascular mortality was observed mainly in western and southern European cities, and was larger when smoking prevalence was lower and household gas consumption was higher. The effect of NO2 on respiratory mortality was higher in cities with a larger proportion of elderly persons in the population and higher levels of particulate matter with a 50% cut-off aerodynamic diameter of 10 microm. The results of this large study are consistent with an independent effect of nitrogen dioxide on mortality, but the role of nitrogen dioxide as a surrogate of other unmeasured pollutants cannot be completely ruled out.

Abstract  Objectives: NO2 is a major urban air pollutant. Previously reported associations between ambient NO2 and children’s respiratory health have been inconsistent, and independent effects of correlated pollutants hard to assess. The authors examined effects of NO2 on a spectrum of 11 respiratory symptoms, controlling for PM10 and SO2, using a large pooled dataset. Methods: Cross sectional studies were conducted in Russia, Austria, Italy, Switzerland, and the Netherlands, during 1993–99, contributing in total 23 955 children. Study-specific odds ratios for associations with ambient NO2 are estimated using logistic regressions with area-level random effects. Heterogeneity between study-specific results, and mean estimates (allowing for heterogeneity) are calculated. Results: Long term average NO2 concentrations were unrelated to prevalences of bronchitis or asthma. Associations were found for sensitivity to inhaled allergens and allergy to pets, with mean odds ratios around 1.14 per 10 μg/m3 NO2. SO2 had little confounding effect, but an initial association between NO2 and morning cough was reduced after controlling for PM10. Associations with reported allergy were not reduced by adjustment for the other pollutants. Odds ratios for allergic symptoms tended to be higher for the 9–12 year old children compared with the 6–8 year old children. Conclusions: Evidence for associations between NO2 and respiratory symptoms was robust only for inhalation allergies. NO2 most likely is acting as an indicator of traffic related air pollutants, though its direct effect cannot be ruled out. This remains important, as policies to reduce traffic related air pollution will not result in rapid reductions.

Abstract  Nitrogen dioxide levels were measured in 80 homes in the Latrobe Valley, Victoria, Australia, using passive samplers. Some 148 children between 7 and 14 yr of age were recruited as study participants, 53 of whom had asthma. Health outcomes for the children were studied using a respiratory questionnaire, skin prick tests, and peak flow measurements. Nitrogen dioxide concentrations were low, with an indoor median of 11.6 microgram/m3 (6.0 ppb), and a maximum of 246 microgram/m3 (128 ppb). Respiratory symptoms were more common in children exposed to a gas stove (odds ratio 2.3 [95% CI 1. 0-5.2], adjusted for parental allergy, parental asthma, and sex). Nitrogen dioxide exposure was a marginal risk factor for respiratory symptoms, with a dose-response association present (p = 0.09). Gas stove exposure was a significant risk factor for respiratory symptoms even after adjusting for nitrogen dioxide levels (odds ratio 2.2 [1.0-4.8]), suggesting an additional risk apart from the average nitrogen dioxide exposure associated with gas stove use. Atopic children tended to have a greater risk of respiratory symptoms compared with nonatopic children with exposure to gas stoves or nitrogen dioxide, but the difference was not significant.

Abstract  A personalized, miniaturized air sampling system was evaluated to estimate the daily exposure of pediatric asthmatics to nitrogen dioxide (NO2). The lightweight device (170 g) uses a sampling pump connected to a solid sorbent tube containing triethanolamine (TEA)-impregnated molecular sieve. The pump is powered by a 9 V battery and samples air over a 24 h period at a collection rate of 0.100 L/min. After exposure, the solid sorbent is removed from the tubes for spectrophotometric analysis (Griess Assay). The lower detection limit of the overall method for NO2 is 11 microg/m3. The linearity, precision and accuracy of the sampler was evaluated. Different NO2 concentrations generated in the laboratory (range: 50 to 340 microg/m3) were simultaneously measured by the TEA tube samplers and colocated continuous chemiluminescent NO(x) analyzers (reference method). The coefficient of determination for the laboratory test derived from ordinary linear regression (OLR) was r2 = 0.99 (y(OLR) = 0.94 x -4.58) and the precision 3.6%. Further, ambient NO2 concentrations in the field (range: 10-120 microg/m3) were verified with continuous chemiluminescent monitors next to the active samplers. Re-weighted least squares analysis (RLS) based on the least median squares procedure (LMS) resulted in a correlation of r2 = 0.68 for a field comparison in Riverside, CA (y(RLS) = 1.01 x -0.94) and r2 = 0.92 in Los Angeles, CA (y(RLS) = 1.31 x -7.12). The precision of the TEA tube devices was 7.4% (at 20-60 microg/m3 NO2) under outdoor conditions. Data show that the performance of this small active sampling system was satisfactory for measuring environmental concentrations of NO2 under laboratory and field conditions. It is useful for personal monitoring of NO2 in environmental epidemiology studies where daily measurements are desired.

Abstract  Background: Acute myocardial infarction (AMI) is the leading cause of death attributed to cardiovascular diseases. An association between traffic-related air pollution and AMI has been suggested, but the evidence is still limited. Objectives: to evaluate in a multi-centre study association between hospitalisation for first AMI and daily levels of traffic-related air pollution. Methods: We collected data on first AMI hospitalisations in 5 European cities. AMI registers were available in Augsburg and Barcelona; hospital discharge registers (HDRs) were used in Helsinki, Rome and Stockholm. NO2, CO and PM10 (particles <10 mu m) were measured at central monitoring sites. Particle number concentration (PNC), a proxy for ultrafine particles (<0.1 mu m), was measured for a year in each centre, and then modelled retrospectively for the whole study period. We used generalized additive models for statistical analyses. Age and 28-day fatality and season were considered as potential effect modifiers in the 3 HDR centres. Results: Nearly 27 000 cases of first AMI were recorded. There was a suggestion of an association of the same day CO and PNC levels with AMI: RR=1.005 (95% confidence interval: 1.000-1.010) per 0.2 mg/m3 and RR=1.005 (95%CI: 0.996-1.015) per 10000 particles/cm3, respectively. However, associations were only observed in the 3 cities with HDR, where power for city-specific analyses was higher. We observed in these cities the most consistent associations among fatal cases aged <75 years: RR at 1-day lag for CO=1.021 (95%CI: 1.000-1.048) per 0.2 mg/m3, for PNC= 1.058 (95% CI: 1.012-1.107) per 10000 particles/cm3, and for NO2=1.032 (95%CI: 0.998-1.066) per 8 mu g/m3. Effects of air pollution were more pronounced during the warm than the cold season. Conclusions: We found support for the hypothesis that exposure to traffic-related air pollution increases the risk of AMI. Most consistent associations were observed among fatal cases aged <75 years and in the warm season.

Abstract  BACKGROUND: Living close to major roads or highways has been suggested to almost double the risk of dying from cardiopulmonary causes. We assessed whether long-term exposure to air pollution originating from motorized traffic and industrial sources is associated with total and cause-specific mortality in a cohort of women living in North Rhine-Westphalia, Germany. METHODS: The study was a follow-up of a series of cross-sectional studies carried out during the 1980s and 1990s on the health of women (age 50-59 years). Approximately 4800 women were followed up for vital status and migration. Exposure to air pollution was defined by distance to major roads calculated from Geographic Information System data and by 1- and 5-year average nitrogen dioxide (NO2) and particle (PM10) concentrations calculated from air monitoring station data. We analyzed associations between exposure and mortality using Cox's proportional hazards models adjusting for confounders. Relative risks (RRs) refer to an interquartile range increase in exposure (16 microg/m for NO2; 7 microg/m for PM10). RESULTS: During the follow-up period, 8% of the women died, 3% from cardiopulmonary causes. Cardiopulmonary mortality was associated with living within a 50-meter radius of a major road (adjusted RR = 1.70; 95% confidence interval = 1.02-2.81), with NO2 (1.57; 1.23-2.00 for 1-year average), and with PM10 (1.34; 1.06-1.71 for 1-year average). Exposure to NO2 was also associated with all-cause mortality (1.17; 1.02-1.34). No association was seen with noncardiopulmonary nonlung cancer mortality. CONCLUSIONS: Living close to major roads and chronic exposure to NO2 and PM10 may be associated with an increased mortality due to cardiopulmonary causes.

Abstract  BACKGROUND: The human health effects of exposure to indoor nitrogen dioxide (NO2) are unclear, and few studies have examined the effects of short-term peak levels of exposure. METHODS: The association between indoor exposure to NO2 and respiratory illness was examined in 388 children aged 6-11 years. The NO2 levels were monitored during winter in 41 classrooms, from four schools with unflued gas heating and four schools with electric heating. Each classroom was monitored daily with 6-hour passive diffusion badge monitors over nine alternate weeks, and with hourly monitors over two of those weeks. Children living in homes with unflued gas appliances were also monitored daily over four evenings during times of gas use. RESULTS: Exposure to NO2 at hourly peak levels of the order of > or = 80 ppb, compared with background levels of 20 ppb, was associated with a significant increase in sore throat, colds and absences from school. An increase in cough with phlegm was marginally significant. Significant dose-response relationships were demonstrated for these four measures with increasing levels of NO2 exposure. CONCLUSIONS: Short-term peak levels of exposure are important to consider in relation to adverse respiratory effects associated with NO2 exposure.

Abstract  In the past few years many studies on air pollution and health based on time series have been carried out. Yet, this approach does not assess exposure to air pollution at an individual level but it is based on ambient concentrations measured by air quality monitoring networks. Questions on the estimates of exposure to pollutants have been raised, in particular the fact that background measuring stations only have been considered in the set up of pollution indicators. To assess the impact of exposure indicator characteristics on the results of time series analysis, two series (black smoke and sulfur dioxide, respectively) of exposure indicators to urban air pollution were set up taking into account a growing part of proximity measures (industrial sources) available in the studied urban area (Le Havre, France). For each pollutant, indicators distributions were almost similar, especially for black smoke. Whatever the pollutant, the most obvious heterogeneity could be observed between the 100% background indicator and the indicator including the arithmetic mean for all the stations (50% background stations and 50% proximity stations). Then the sensitivity of the associations between mortality and air pollution to these indicators was studied. These indicators did not show statistically significant differences in the estimated excess risk. Yet, confidence intervals were more statistically significant as the contribution of proximity stations was more substantial, in particular for SO2. To conclude, the use of proximity measurements did not influence dramatically on the mean estimates of the association between air pollution and mortality indicators in Le Havre. Therefore it does not seem relevant to include the data provided by the proximity stations in the urban exposure indicators within the context of the epidemiology monitoring system.

Abstract  Although progress has been made in the last few decades at reducing ambient concentrations of air pollutants, scientific evidence suggests that there remains a risk to human health from exposure to these pollutants at current levels in Canada. Much of the motivation for air pollution reduction efforts is to protect population health. This article presents a method of monitoring changes in air pollution-related health outcomes over time in conjunction with temporal changes in ambient pollution concentrations. The progress measure is a function of temporal changes in location-specific ambient concentrations and the potentially time-dependent association between those concentrations and daily deaths. The progress measure can be determined for a single location or at a national level. The measure can also be extended to include several pollutants. The progress measure is illustrated with an example of how changes in nitrogen dioxide levels in 12 Canadian cities from 1981 to 1999 have translated into changes in the percent of nonaccidental mortality burden attributable to this pollutant over time.

Abstract  #In 1995, daily mortality in a district of Chongqing, China, was analyzed from January through December for associations with daily ambient sulfur dioxide and fine particles (airborne particles with diameters less than or equal to 2.5 microm; PM2.5. The mean concentration of PM2.5 was 147 microg/m3 (maximum, 666 microg/m3), and that of SO2 was 213 microg/m3 (maximum, 571 microg/m3). On average, 9.6 persons died each day. We used a generalized additive model using robust Poisson regression to estimate the associations of mean daily SO2 and PM2.5 with daily mortality (on the same day and at lags up to 5 days) adjusted for trend, season, temperature, humidity, and day of the week. The relative risk of mortality associated with a 100 microg/m3 increase in mean daily SO2 was highest on the second lag day [1.04; 95% confidence interval (CI), 1.00-1.09] and the third lag day (1.04; 95% CI, 0.99-1.08). The associations between daily mortality and mean daily PM2.5 were negative and statistically insignificant on all days. The relative risk of respiratory mortality on the second day after a 100 microg/m3 increase in mean daily SO2 was 1.11 (95% CI, 1.02-1.22), and that for cardiovascular mortality was 1.10 (95% CI, 1.02-1.20). The relative risk of cardiovascular mortality on the third day after a 100 microg/m3 increase in mean daily SO2 was 1.20 (95% CI, 1.11-1.30). The relative risks of mortality due to cancer and other causes were insignificant on both days. The estimated effects of mean daily SO2 on cardiovascular and respiratory mortality risk remained after controlling for PM2.5.

Abstract  Background Airborne particulate matter (PM) is an important factor associated with the enhanced prevalence of respiratory allergy. The PM adjuvant activity on allergic sensitization is a possible mechanism of action involved, and the induction of airway inflammation is suggested to be of importance in PM-induced adjuvant activity. Objective Because differently sized PM have different toxic potentials, we studied the role of particle size in the induction of airway inflammation and allergic sensitization. This was done using fine (0.250 and 0.260 μm) and ultrafine (0.029 and 0.014 μm) titanium dioxide (TiO2) and carbon black particles (CBP) with known differences in airway toxicity. Methods Mice were intranasally exposed to ovalbumin (OVA) alone or in combination with one of the different particles. The induction of airway inflammation and the immune adjuvant activity were studied in the lungs and lung-draining peribronchial lymph nodes (PBLN) at day 8. OVA-specific antibodies were measured at day 21, and the development of allergic airway inflammation was studied after OVA challenges (day 28). Results When administered at the same total particle mass (200 μg), exposure to ultrafine TiO2 and CBP-induced airway inflammation, and had immune adjuvant activity. The latter was shown by increasing both the PBLN cell numbers and the production of OVA-specific T-helper type 2 (Th2) cytokines (IL-4, IL-5, IL-10 and IL-13). Whereas OVA-specific IgE and IgG1 levels in serum were only increased in animals exposed to the ultrafine TiO2, allergic airway inflammation could be detected in both ultrafine TiO2-and CBP-treated groups after challenges with OVA. Conclusion Our data show that only the ultrafine particles, with a small diameter and a large total surface area/mass, cause airway inflammation and have immune adjuvant activity in the current model supporting the hypothesis that particle toxicity is site-dependent and related to adjuvant activity.

Abstract  In Asia, limited studies have been published on the association between daily mortality and gaseous pollutants of nitrogen dioxide (NO2), ozone (O3), and sulfur dioxide (SO2). Our previous studies in Wuhan, China, demonstrated long-term air pollution effects. However, no study has been conducted to determine mortality effects of air pollution in this region. This study was to determine the acute mortality effects of the gaseous pollutants in Wuhan, a city with 7.5 million permanent residents during the period from 2000 to 2004. There are approximately 4.5 million residents in Wuhan who live in the city's core area of 201 km2, where air pollution levels are highest, and pollution ranges are wider than the majority of the cities in the published literature. We used the generalized additive model to analyze pollution, mortality, and covariate data. We found consistent NO2 effects on mortality with the strongest effects on the same day. Every 10-microg/m3 increase in NO2 daily concentration on the same day was associated with an increase in nonaccidental (1.43%; 95% confidence interval [CI]: 0.87-1.99%), cardiovascular (1.65%; 95% CI: 0.87-2.45%), stroke (1.49%; 95% CI: 0.56-2.43%), cardiac (1.77%; 95% CI: 0.44-3.12%), respiratory (2.23%; 95% CI: 0.52-3.96%), and cardiopulmonary mortality (1.60%; 95% CI: 0.85-2.35%). These effects were stronger among the elderly than among the young. Formal examination of exposure-response curves suggests no-threshold linear relationships between daily mortality and NO2, where the NO2 concentrations ranged from 19.2 to 127.4 microg/m3. SO2 and O3 were not associated with daily mortality. The exposure-response relationships demonstrated heterogeneity, with some curves showing nonlinear relationships for SO2 and O3. We conclude that there is consistent evidence of acute effects of NO2 on mortality and suggest that a no-threshold linear relationship exists between NO2 and mortality.

Abstract  The widely used source apportionment model, positive matrix factorization (PMF2), has been applied to various air pollution data. Recently, U.S. Environmental Protection Agency (EPA) developed EPA positive matrix factorization (PMF), a version of PMF that will be freely distributed by EPA. The objectives of this study were to conduct source apportionment studies for particulate matter less than 2.5 mu m in aerodynamic diameter (PM2.5) speciation data using PMF2 and EPA PMF (version 1.1) and to compare identified sources between the two models. In the present study, ambient PM2.5 compositional datasets of 24-hr integrated samples collected at EPA Speciation Trends Network monitoring sites in Chicago, IL, and Portland, OR, were analyzed. Both PMF2 and EPA PMF extracted eight sources for the Chicago data and 10 sources for the Portland data. The model-resolved source profiles were similar between two models for both datasets. However, in several sources, the average contributions did not agree well and the time series contributions were not highly correlated. The differences between PMF2 and EPA PMF solutions were caused by the different least-square algorithm and the different nonnegativity constraints. Most of the average source contributions resolved by both models were within 5-95% uncertainty provided by EPA PMF, indicating that the sources resolved by both models were reproducible.