Home outdoor NO2 and new onset of self-reported asthma in adults

BACKGROUND: Few studies have investigated new onset of asthma in adults in relation to air pollution. The aim of this study is to investigate the association between modeled background levels of traffic-related air pollution at the subjects' home addresses and self-reported asthma incidence in a European adult population. METHODS: Adults from the European Respiratory Health Survey were included (n = 4185 from 17 cities). Subjects' home addresses were geocoded and linked to outdoor nitrogen dioxide (NO2) estimates, as a marker of local traffic-related pollution. We obtained this information from the 1-km background NO2 surface modeled in APMoSPHERE (Air Pollution Modelling for Support to Policy on Health and Environmental Risk in Europe). Asthma incidence was defined as reporting asthma in the follow-up (1999 to 2001) but not in the baseline (1991 to 1993). RESULTS: A positive association was found between NO2 and asthma incidence (odds ratio 1.43; 95% confidence interval = 1.02 to 2.01) per 10 microg/m. Results were homogeneous among centers (P value for heterogeneity = 0.59). CONCLUSIONS: We found an association between a marker of traffic-related air pollution and asthma incidence in European adults.     

Childhood asthma and exposure to traffic and nitrogen dioxide

BACKGROUND: Evidence for a causal relationship between traffic-related air pollution and asthma has not been consistent across studies, and comparisons among studies have been difficult because of the use of different indicators of exposure. METHODS: We examined the association between traffic-related pollution and childhood asthma in 208 children from 10 southern California communities using multiple indicators of exposure. Study subjects were randomly selected from participants in the Children's Health Study. Outdoor nitrogen dioxide (NO2) was measured in summer and winter outside the home of each child. We also determined residential distance to the nearest freeway, traffic volumes on roadways within 150 meters, and model-based estimates of pollution from nearby roadways. RESULTS: Lifetime history of doctor-diagnosed asthma was associated with outdoor NO2; the odds ratio (OR) was 1.83 (95% confidence interval=1.04-3.22) per increase of 1 interquartile range (IQR=5.7 ppb) in exposure. We also observed increased asthma associated with closer residential distance to a freeway (1.89 per IQR; 1.19-3.02) and with model-based estimates of outdoor pollution from a freeway (2.22 per IQR; 1.36-3.63). These 2 indicators of freeway exposure and measured NO2 concentrations were also associated with wheezing and use of asthma medication. Asthma was not associated with traffic volumes on roadways within 150 meters of homes or with model-based estimates of pollution from nonfreeway roads. CONCLUSIONS: These results indicate that respiratory health in children is adversely affected by local exposures to outdoor NO2 or other freeway-related pollutants.     

Traffic-related outdoor air pollution and respiratory symptoms in children: the impact of adjustment for exposure measurement error

BACKGROUND: Outdoor concentrations of soot and nitrogen dioxide (NO2) outside of schools have been associated with children's respiratory and eye symptoms. We assessed how adjustments for measurement error affect these associations. METHODS: Concentrations of air pollutants outside children's schools were validated by personal measurements of exposure to traffic-related air pollution. We estimated prevalence ratios of 4 health outcomes (current wheeze, conjunctivitis, phlegm, and elevated total serum immunoglobulin E) using school outdoor measurements, and then adjusted for measurement error using the personal exposure data and applying a regression calibration method. The analysis adjusting for measurement error was carried out using a main study/external validation design. RESULTS: Adjusting for measurement error produced effect estimates related to soot and NO2 that were 2 to 3 times higher than in the original study. The adjusted prevalence ratio for current phlegm was 5.3 (95% confidence interval = 1.2-23) for a 9.3 microg/m3 increase in soot, and 3.8 (1.0-14), for a 17.6 microg/m3 increase in NO2, compared with the original results of 2.2 (1.3-3.9) and 1.8 (1.1-2.8), respectively. Corrections were of similar magnitude for the prevalence of current wheeze, current conjunctivitis, and total elevated total immunoglobulin E. CONCLUSIONS: The estimated effects of outdoor air pollution on respiratory and other health effects in children may be substantially attenuated when based on exposure measurements outside schools instead of personal exposure.     

Synergistic effects of traffic-related air pollution and exposure to violence on urban asthma etiology

BACKGROUND: Disproportionate life stress and consequent physiologic alteration (i.e., immune dysregulation) has been proposed as a major pathway linking socioeconomic position, environmental exposures, and health disparities. Asthma, for example, disproportionately affects lower-income urban communities, where air pollution and social stressors may be elevated. OBJECTIVES: We aimed to examine the role of exposure to violence (ETV), as a chronic stressor, in altering susceptibility to traffic-related air pollution in asthma etiology. METHODS: We developed geographic information systems (GIS)-based models to retrospectively estimate residential exposures to traffic-related pollution for 413 children in a community-based pregnancy cohort, recruited in East Boston, Massachusetts, between 1987 and 1993, using monthly nitrogen dioxide measurements for 13 sites over 18 years. We merged pollution estimates with questionnaire data on lifetime ETV and examined the effects of both on childhood asthma etiology. RESULTS: Correcting for potential confounders, we found an elevated risk of asthma with a 1-SD (4.3 ppb) increase in NO(2) exposure solely among children with above-median ETV [odds ratio (OR) = 1.63; 95% confidence interval (CI), 1.14-2.33)]. Among children always living in the same community, with lesser exposure measurement error, this association was magnified (OR = 2.40; 95% CI, 1.48-3.88). Of multiple exposure periods, year-of-diagnosis NO(2) was most predictive of asthma outcomes. CONCLUSIONS: We found an association between traffic-related air pollution and asthma solely among urban children exposed to violence. Future studies should consider socially patterned susceptibility, common spatial distributions of social and physical environmental factors, and potential synergies among these. Prospective assessment of physical and social exposures may help determine causal pathways and critical exposure periods.     

Traffic-related air pollution and otitis media

BACKGROUND: Otitis media is one of the most common infections in young children. Although exposure to environmental tobacco smoke is a known risk factor associated with otitis media, little information is available regarding the potential association with air pollution. OBJECTIVE: We set out to study the relationship between exposure to traffic-related air pollution and otitis media in two birth cohorts. METHODS: Individual estimates of outdoor concentrations of traffic-related air pollutants-nitrogen dioxide, fine particles [particulate matter with aerodynamic diameters 相似文献   

Does traffic exhaust contribute to the development of asthma and allergic sensitization in children: findings from recent cohort studies

The aim of this review was to assess the evidence from recent prospective studies that long-term traffic pollution could contribute to the development of asthma-like symptoms and allergic sensitization in children. We have reviewed cohort studies published since 2002 and found in PubMed in Oct 2008. In all, 13 papers based on data from 9 cohorts have evaluated the relationship between traffic exposure and respiratory health. All surveys reported associations with at least some of the studied respiratory symptoms. The outcome varied, however, according to the age of the child. Nevertheless, the consistency in the results indicates that traffic exhaust contributes to the development of respiratory symptoms in healthy children. Potential effects of traffic exhaust on the development of allergic sensitization were only assessed in the four European birth cohorts. Long-term exposure to outdoor air pollutants had no association with sensitization in ten-year-old schoolchildren in Norway. In contrast, German, Dutch and Swedish preschool children had an increased risk of sensitization related to traffic exhaust despite fairly similar levels of outdoor air pollution as in Norway. Traffic-related effects on sensitization could be restricted to individuals with a specific genetic polymorphism. Assessment of gene-environment interactions on sensitization has so far only been carried out in a subgroup of the Swedish birth cohort. Further genetic association studies are required and may identify individuals vulnerable to adverse effects from traffic-related pollutants. Future studies should also evaluate effects of traffic exhaust on the development and long term outcome of different phenotypes of asthma and wheezing symptoms.     

Association between air pollution and daily consultations with general practitioners for allergic rhinitis in London, United Kingdom

Few published studies have looked at the health effects of air pollution in the primary care setting, and most have concentrated on lower rather than upper respiratory diseases. The authors investigated the association of daily consultations with general practitioners for allergic rhinitis with air pollution in London, United Kingdom. Generalized additive models were used to regress time series of daily numbers of patients consulting for allergic rhinitis against 1992--1994 measures of air pollution, after control for possible confounders and adjustment for overdispersion and serial correlation. In children, a 10th--90th percentile increase in sulfur dioxide (SO(2)) levels 4 days prior to consultation (13-31 microg/m(3)) was associated with a 24.5% increase in consultations (95% confidence interval: 14.6, 35.2; p < 0.00001); a 10th--90th percentile increase in averaged ozone (O(3)) concentrations on the day of consultation and the preceding 3 days (6--29 parts per billion) was associated with a 37.6% rise (95% confidence interval: 23.3, 53.5; p < 0.00001). For adults, smaller effect sizes were observed for SO(2) and O(3). The association with SO(2) remained highly significant in the presence of other pollutants. This study suggests that air pollution worsens allergic rhinitis symptoms, leading to substantial increases in consultations. SO(2) and O(3) seem particularly responsible, and both seem to contribute independently.     

Traffic-related air pollution and respiratory symptoms in children living along trunk roads in Chiba Prefecture,Japan

Automobile exhaust is considered to be a potential risk factor for respiratory diseases. To investigate the effects of traffic-related air pollution on respiratory symptoms among children who lived near trunk roads, we conducted a cohort study on 2,506 schoolchildren in eight different communities in Japan. Over that four-year period, the prevalence of asthma was higher among girls who lived less than 50 m from trunk roads (roadside areas) than among girls in the other areas studied. Testing for trends showed that the prevalence of asthma among girls increased significantly with increases in the concentration of air pollution in each area. Among boys, the prevalence of asthma did not differ in relation to the distance from roads, although the rate was higher in urban areas than in rural areas. The incidence of asthma during the follow-up period significantly increased among boys living in roadside areas relative to rural areas (odds ratio = 3.75; 95% confidence interval: 1.00-14.06). Among girls, the incidence of asthma also increased (odds ratio = 4.06; 95% confidence interval:0.91-18.10), although the risk was not significant. These findings suggest that traffic-related air pollution may be of particular importance in the development of asthma among children living near major trunk roads with heavy traffic.     

Effect of residential proximity to traffic on respiratory disorders in school children in upper Silesian Industrial Zone, Poland

Objective

A number of studies show an association between traffic-related air pollution and adverse respiratory health effects in children. However, most evidence relates to the regions with low or moderate levels of ambient air pollution. The study was undertaken to assess the impact of traffic-related air pollution on respiratory health status in children living in the area of high levels of industrial and municipal ambient air pollution.

Materials and Methods

Analyses involved data obtained from cross-sectional study on respiratory health in children (N = 5733), conducted between 2003–2004 in Bytom, one of the largest cities of Silesian Metropolis (Poland). Exposure to traffic-related air pollution was assessed by means of geographic information system and expressed as several measures of potential exposure to traffic-related air pollution, involving residential distance to major road and traffic density in the residential area. Logistic regression was used to examine association between reported respiratory health and traffic measures.

Results

Statistically significant association was found between doctor-diagnosed asthma and residential proximity to traffic. Results of multivariate logistic regression (logOR; 95%CI) confirmed the effect of living in an area of a city with high-traffic-density on childhood asthma: 1.60 (1.07–2.39). Similar effects were found in case of allergic rhinitis and rhinitis symptoms, but the observed associations were not statistically significant.

Conclusion

The study findings suggest that even in an area with poor regional ambient air quality, adverse respiratory health outcomes are more frequent in children living in a proximity to the high vehicle traffic flow.     

Exposure to motor vehicle traffic and allergic sensitization. The Swiss Study on Air Pollution and Lung Diseases in Adults (SAPALDIA) Team

We examined the association between the presence of an allergic sensitization and seasonal allergic diseases or symptoms and the exposure to road traffic in Basel, Switzerland. Traffic counts at the domiciles of subjects ranged from 24 to 32,504 cars per 24 hours, with a median of 1,624. To investigate the relation of road traffic and allergies, we matched the data of the traffic inventory of Basel with those of the 820 participants of the SAPALDIA study (Swiss Study on Air Pollution and Lung Diseases in Adults), ages 18-60 years, who had completed a detailed respiratory health questionnaire and had undergone allergy testing (skin prick tests and serologic examinations). We observed a positive association with a sensitization to pollen that was most pronounced among persons with a duration of residence of at least 10 years. The odds ratios (adjusted for educational level, smoking behavior, number of siblings, age, sex, and family history of atopy) for cars, contrasting four exposure categories with the lowest quartile as referent category, were 1.99 [95% confidence interval (CI) = 0.91-4.38], 2.47 (95% CI = 1.06-5.73), and 2.83 (95% CI = 1.26-6.31). These results suggest that living on busy roads is associated with a higher risk for a sensitization to pollen and could possibly be interpreted as an indication for interactions between pollen and air pollutants. We did not, however, find a similar relation between motor vehicle traffic and hay fever or seasonal allergic symptoms, and we saw no trend that increasing traffic exposure was associated with a rise in sensitization rates to indoor allergens.     

Traffic-related air pollution and childhood respiratory symptoms, function and allergies

BACKGROUND: Urban air pollution can trigger asthma symptoms in children, but there is conflicting evidence on effects of long-term exposure on lung function, onset of airway disease and allergic sensitization. METHODS: The spatial distribution of nitrogen oxides from traffic (traffic-NOx) and inhalable particulate matter from traffic (traffic-PM10) in the study area was assessed with emission databases and dispersion modeling. Estimated levels were used to assign first-year exposure levels for children in a prospective birth cohort (n = 4089), by linking to geocoded home addresses. Parents in 4 Swedish municipalities provided questionnaire data on symptoms and exposures when the children were 2 months and 1, 2, and 4-year-old. At 4 years, 73% of the children underwent clinical examination including peak expiratory flow and specific IgE measurements. RESULTS: Exposure to air pollution from traffic during the first year of life was associated with an excess risk of persistent wheezing (odds ratio [OR] for 44 microg/m3 [5th-95th percentile] difference in traffic-NOx = 1.60; 95% confidence interval [CI] = 1.09-2.36). Similar results were found for sensitization (measured as specific IgE) to inhalant allergens, especially pollen (OR for traffic-NOx = 1.67; 95% CI = 1.10-2.53), at the age of 4 years. Traffic-related air pollution exposure during the first year of life was also associated with lower lung function at 4 years of age. Results were similar using traffic-NOx and traffic-PM10 as indicators. CONCLUSIONS: Exposure to moderate levels of locally emitted air pollution from traffic early in life appears to influence the development of airway disease and sensitization in preschool children.     

Interactions between glutathione S-transferase P1, tumor necrosis factor, and traffic-related air pollution for development of childhood allergic disease

BACKGROUND: Air pollutants may induce airway inflammation and sensitization due to generation of reactive oxygen species. The genetic background to these mechanisms could be important effect modifiers. OBJECTIVE: Our goal was to assess interactions between exposure to air pollution and single nucleotide polymorphisms (SNPs) in the beta2-adrenergic receptor (ADRB2), glutathione S-transferase P1 (GSTP1), and tumor necrosis factor (TNF) genes for development of childhood allergic disease. METHODS: In a birth cohort originally of 4,089 children, we assessed air pollution from local traffic using nitrogen oxides (traffic NO(x)) as an indicator based on emission databases and dispersion modeling and estimated individual exposure through geocoding of home addresses. We measured peak expiratory flow rates and specific IgE for inhalant and food allergens at 4 years of age, and selected children with asthma symptoms up to 4 years of age (n = 542) and controls (n = 542) for genotyping. RESULTS: Interaction effects on allergic sensitization were indicated between several GSTP1 SNPs and traffic NO(x) exposure during the first year of life (p(nominal) < 0.001-0.06). Children with Ile105Val/Val105Val genotypes were at increased risk of sensitization to any allergen when exposed to elevated levels of traffic NO(x) (for a difference between the 5th and 95th percentile of exposure: odds ratio = 2.4; 95% confidence interval, 1.0-5.3). In children with TNF-308 GA/AA genotypes, the GSTP1-NO(x) interaction effect was even more pronounced. We observed no conclusive interaction effects for ADRB2. CONCLUSION: The effect of air pollution from traffic on childhood allergy appears to be modified by GSTP1 and TNF variants, supporting a role of genes controlling the antioxidative system and inflammatory response in allergy.     

Urban background particulate matter and allergic sensitization in adults of ECRHS II

BACKGROUND: Epidemiological studies have shown weak or inconsistent associations between ambient air pollutants and allergic sensitization. The aim of this study was to evaluate whether regional urban air pollution may partly explain the large variation in the prevalence of allergic sensitization across cities of the European Community Respiratory Health Survey (ECRHS) II. METHODS: ECRHS is a cross-sectional survey initiated in 29 countries across Europe in the 1990s (ECRHS I) with a follow-up conducted 10 years later (ECRHS II). Subject characteristics were measured by questionnaires and blood tests conducted for the measurement of specific immunoglobulin E. Fine particle mass (PM(2.5), <2.5 microm) and sulphur on PM(2.5) were measured in 21 centres and annual averages of urban regional background air pollution were calculated. Results were scaled by an interquartile range increase in ambient PM(2.5) (6.03 microg/m(3)) and sulphur (1336 ng/m(3)). Generalized estimating equations were applied to compute population average effect estimates with adjustment for age, gender, smoking habit, education and number of siblings. RESULTS: A notable variation in pollution level and prevalence of allergic sensitization was observed. Moreover, exposure to urban regional background air pollution was not associated with allergic sensitization; adjusted odds ratios and 95% confidence interval were 1.02 (0.95-1.09) for PM(2.5) and 1.08 (0.86-1.31) for sulphur. These statistically non-significant associations were sensitive to model specification. CONCLUSIONS: The study suggests that regional air pollution measured at fixed sites is not associated with allergic sensitization among adults in ECRHS II.     

Association between indoor and outdoor air pollution and adolescent asthma from 1995 to 1996 in Taiwan

The study aim was to estimate the contribution of indoor and outdoor air pollution to the 1-year prevalence of adolescent asthma after personal susceptibility and other potential risk factors were taken into account. A large-scaled cross-sectional study was conducted among 165,173 high school students aged 11 to 16 years in the different communities of Kaohsiung and Pintong in Taiwan, from October 1995 to June 1996. Each student and his/her parents participating in the study completed a video and a written International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire about symptoms of wheezing and allergies, passive smoking, and demographic variables. After adjustment for potential confounders, adolescents exposed to cigarette smoking (odds ratio = 1.29, 95% confidence interval (CI), 1.17-1.42) and environmental tobacco smoke (odds ratio = 1.08, 95% CI, 1.05-1.12) were found to suffer from asthma at an increased frequency. We observed a statistically significant association between outdoor air pollution and asthma, after controlling for potential confound variables. Total suspended particulate, nitrogen dioxide, carbon monoxide, ozone, and airborne dust particles all displayed an independent association with asthma, respectively. There were no selection biases in this community-based study, which provides evidence that passive smoking and long-term, high average outdoor air pollution are independent risk factors of asthma.     

Exposure to urban nitrogen dioxide pollution and the risk of myocardial infarction

OBJECTIVES: This study attempted to determine whether long-term exposure to nitrogen dioxide (NO2), an indicator of motor vehicle exhaust, increases the risk of myocardial infarction (MI). METHODS: A population-based case-control study was conducted among men aged 25-64 years and residing in Kaunas, Lithuania. The study included all cases of first-time myocardial infarction in 1997-2000. Interviews with patients treated in hospitals elicited information on smoking and other risk factors, including residential histories. A high response rate (77.4%) resulted in 448 cases and 1777 controls. Nitrogen dioxide (NO2) was selected for analysis as an indicator of traffic-related air pollution. The annual air pollution levels were estimated for the residential districts; thereafter the data were linked to the home addresses of the cases and controls. RESULTS: After adjustment for age, education, smoking, blood pressure, body mass index, marital status, and psychological stress, the risk of myocardial infarction was higher for the men exposed to medium [odds ratio (OR) 1.43, 95% confidence interval (95% CI) 1.04-1.96] and high (OR 1.43, 95% CI 1.07-1.92) NO2 levels. The data suggested a stronger association among 55- to 64-year-old men. The risk of myocardial infarction increased by 17% among the 25- to 64-year-old men (OR 1.17, 95% CI 1.01-1.35) and by 34% among those aged 55-64 years (OR 1.34, 95% CI 1.08-1.67) from the first to the third tertile of NO2 exposure. CONCLUSIONS: The results indicate that urban NO2 pollution may increase the risk of myocardial infarction and that vehicle emissions may be of particular importance.     

Traffic-related air pollution in relation to incidence and prognosis of coronary heart disease

BACKGROUND: Long-term air pollution exposure is associated with increased mortality, but the association with incidence of fatal and nonfatal coronary heart disease is less certain. Moreover, it is unknown how chronic exposure to air pollution affects prognosis among survivors of a first coronary event. This study evaluated the association between long-term traffic-related air pollution exposure and incidence of nonfatal and fatal coronary events, as well as subsequent hospital readmission and mortality among myocardial infarction survivors. METHODS: The study population comprised all residents of Rome aged 35-84 years during the period 1998-2000. Residential nitrogen dioxide (NO2) exposure as a marker of traffic pollution was assessed by a land-use regression model in 1995-1996 (R = 0.69). A total of 11,167 incident coronary events were observed (4654 fatal, including 3598 out-of-hospital coronary deaths, and 6513 nonfatal). The cohort of 6513 survivors was followed 4.0-7.5 years for readmission or mortality, starting 28 days from the date of first event. Relative risks per 10 mug/m of NO2 exposure, adjusted for age, sex, and socioeconomic status, were calculated by Poisson regression (population-based incidence) and Cox regression (cohort analysis). RESULTS: The relative risk for incidence in coronary events per 10 mug/m of NO2 was 1.03 (95% confidence interval = 1.00-1.07). Stronger associations were found for fatal cases (1.07; 1.02-1.12) and out-of-hospital deaths (1.08; 1.02-1.13). Using NO2 exposure at the time of the first event, there was no association of air pollution exposure with either subsequent hospital readmission or mortality among survivors of the first coronary event. CONCLUSIONS: Long-term air pollution exposure increases the risk of coronary heart disease, particularly fatal events. Hospital readmission or subsequent mortality among survivors was not associated with traffic air pollution.     

Urban air pollution and lung cancer in Stockholm

We conducted a population-based case-control study among men 40-75 years of age encompassing all cases of lung cancer 1985-1990 among stable residents of Stockholm County 1950-1990. Questionnaires to subjects or next-of-kin (primarily wives or children) elicited information regarding smoking and other risk factors, including occupational and residential histories. A high response rate (>85%) resulted in 1,042 cases and 2,364 controls. We created retrospective emission databases for NOx/NO2 and SO2 as indicators of air pollution from road traffic and heating, respectively. We estimated local annual source-specific air pollution levels using validated dispersion models and we linked these levels to residential addresses using Geographical Information System (GIS) techniques. Average traffic-related NO2 exposure over 30 years was associated with a relative risk (RR) of 1.2 (95% confidence interval 0.8-1.6) for the top decile of exposure, adjusted for tobacco smoking, socioeconomic status, residential radon, and occupational exposures. The data suggested a considerable latency period; the RR for the top decile of average traffic-related NO2 exposure 20 years previously was 1.4 (1.0-2.0). Little association was observed for SO2. Occupational exposure to asbestos, diesel exhaust, and other combustion products also increased the risk of lung cancer. Our results indicate that urban air pollution increases lung cancer risk and that vehicle emissions may be particularly important.     

Residential outdoor air pollution and lung function in schoolchildren

BACKGROUND: Long-term exposure to outdoor air pollution has typically been estimated on the aggregate level, and more individual measures of exposure are needed. We investigated the associations with lung function of residential outdoor air pollution in early life, total lifetime, and days before lung function test. METHODS: In 2001-2002, spirometry was performed in 2307 9- and 10-year-old children who had lived in Oslo, Norway, since birth. Outdoor air pollution exposure for each child was assessed by the EPISODE dispersion model, calculating hourly concentrations of nitrogen dioxide (NO2), particulate matter (PM) with aerodynamic diameter less than 10 microm (PM10) and 2.5 microm (PM2.5). We applied linear regression analysis stratified by sex. RESULTS: Early and lifetime exposures to outdoor air pollution were associated with reduced peak expiratory flow and reduced forced expiratory flow at 25% and 50% of forced vital capacity, especially in girls. One interquartile increase of lifetime exposure to NO2, PM10, and PM2.5 was associated with change in adjusted peak respiratory flow of, respectively, -79 mL/s (95% confidence interval = -128 to -31), -66 mL/s (-110 to -23), and -58 mL/s (-94 to -21). We also found short-term effects of NO2 that became stronger with increasing time lags, but no short-term effects of PM. When we included short- and long-term NO2 exposures simultaneously, only the long-term effect remained. We found no effect on forced volumes. Adjusting for a contextual socioeconomic factor diminished the associations. CONCLUSIONS: Short- and long-term residential exposures to traffic-related pollutants in Oslo were associated with reduced peak expiratory flow and forced expiratory flow at 25% and 50% in 9- to 10-year-old children, especially in girls, with weaker associations after adjusting for a contextual socioeconomic factor.     

Outdoor air concentrations of nitrogen dioxide and sulfur dioxide and prevalence of wheezing in school children

We report analysis of data on outdoor air pollution and respiratory symptoms in children collected in the Czech part of the international Small Area Variations in Air pollution and Health (SAVIAH) Project, a methodological study designed to test the use of geographical information systems (GIS) in studies of environmental exposures and health at small area level. We collected the following data in two districts of Prague: (1) individual data on 3,680 children (response rate 88%) by questionnaires; (2) census-based socio-demographic data for small geographical units; (3) concentrations of nitrogen dioxide (NO2) and sulfur dioxide (SO2) measured by passive samplers in three 2-week surveys at 80 and 50 locations, respectively. We integrated all data into a geographical information system. Modeling of NO2 and SO2 allowed estimation of exposure to outdoor NO2 and SO2 at school and at home for each child. We examined the associations between air pollution and prevalence of wheezing or whistling in the chest in the last 12 months by logistic regression at individual level, weighted least squares regression at small area (ecological) level and multilevel modeling. The results varied by the level of analysis and method of exposure estimation. In multilevel analyses using individual data, odds ratios per 10 microg/m3 increase in concentrations were 1.16 (95% CI = 0.95-1.42) for NO2, and 1.08 (95% CI = 0.97-1.21) for SO2. While mapping of spatial distribution of NO2 and SO2 in the study area appeared valid, the interpolation from outdoor to personal exposures requires consideration.     

The relationship between diabetes mellitus and traffic-related air pollution

OBJECTIVE: Air pollution is associated with an increased risk for cardiovascular events. Many of the biological pathways involved could also promote diabetes mellitus (DM). We therefore investigated the association between DM prevalence and exposure to traffic-related air pollution (nitrogen dioxide [NO 2]). METHODS: Study participants were patients who attended two respiratory clinics in Hamilton (n = 5228) and Toronto (n = 2406). The diagnosis of DM was ascertained by linkage to administrative databases of the Ontario universal Health Insurance Plan for patients aged 40 years and above. Geographic Information systems methodology was used to assign individual estimates of NO2 based on a network of samplers in each city. Logistic regression was used to estimate the relations between NO2 exposures and the odds of DM diagnosis. RESULTS: After adjusting for age, body mass index, and neighborhood income there were positive effects in women on the odds ratio for DM for each 1 ppb NO2 exposure in Toronto (OR 1.055, 95% CI: 0.99 to 1.11) and Hamilton (OR 1.029, 95% CI: 0.98 to 1.08). In a meta-analytic model including both cities, there was a significant effect in women (OR = 1.04; 95% CI: 1.00 to 1.08). Across the inter-quartile range (approximately 4 ppb NO2) there was nearly a 17% increase in the odds of DM for women. There were no positive associations among men. CONCLUSIONS: Exposure to NO2, a marker of traffic-related air pollutants, was associated with DM prevalence among women. Exposure estimate errors in men may explain the apparent gender difference. These results suggest that common air pollutants are associated with DM and warrant more investigation to determine if this is a cause-and-effect relationship.