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Association between traffic-related air pollution and asthma in preschool children in a national Japanese nested case-control study.

ABSTRACT: There has been little study on the effect of traffic-related air pollution on the incidence and persistence of asthma in preschool children. We evaluated the association of exposure to traffic-related air pollution with the incidence/persistence of asthma during the first 3 years of life using a population-based study.A baseline survey was conducted in 1½-year-old children (n=63,266). A follow-up survey at 3 years of age (n=43,343) identified new-onset asthma cases (n=853) and persistence of asthma (n=214). In the prevalence/persistence study, the outdoor concentrations of nitrogen oxides (NOx) and elemental carbon (EC) at home during the first 1½ years of life were estimated by a dispersion model. In the nested case-control study, which regarded incidence of asthma as cases, the personal exposure levels were estimated by dispersion model including time-activity pattern.There was no statistically significant association between the incidence of asthma between age 1½ and 3 years and personal exposure levels to NOx nor EC. However, the persistence of asthmatic symptoms (between 1½ and 3 ears) was significantly associated with outdoor concentrations of NOx. ORs for the persistence of asthmatic symptoms were 6.02 (95% CI 1.51 to 23.92) for the comparison between the upper 5th and lower 25th centiles of NOx.While no statistically significant association was observed for the incidence of asthma, the persistence of asthmatic symptoms in preschool children was significantly associated with traffic-related air pollution. This supports its importance as a risk factor in childhood airway disease.

SUBMITTER: Hasunuma H

PROVIDER: S-EPMC4769392 | biostudies-other | 2016 Feb

REPOSITORIES: biostudies-other

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Association of traffic air pollution and rhinitis quality of life in Peruvian children with asthma.

Project description:BackgroundAir pollution exposure may contribute to rhinoconjunctivitis morbidity in children with underlying airways disease. Prior studies have not assessed rhinoconjunctivitis-related quality of life (QOL) in children with asthma chronically exposed to air pollution.MethodsChildren ages 9-19 years with asthma from peri-urban Peru, self-reporting rhinoconjunctivitis symptoms (n = 484), were administered the Rhinoconjunctivitis QOL Questionnaire (RQLQ) at repeated intervals over one year, with scores dichotomized into bothered (>0) and not bothered (= 0). Individual weekly exposures to particulate matter<2.5?m (PM2.5) and its black carbon (BC) component were estimated by inverse distance weighted methods. Generalized estimating equations, adjusting for covariates, estimated associations of PM2.5 and BC with QOL.ResultsParticipants were on average 13 years old, 55% female, and majority were atopic (77%). Mean (SD) PM2.5 and BC concentrations were 21(3.2) ?g/m3 and 4.4(1.5) ?g/m3, respectively. In adjusted multi-pollutant models, each 10?g/m3 increase in PM2.5 was associated with increased odds of worse rhinoconjunctivitis QOL (OR;[95% CI]: 1.83;[1.33,2.52]). A 10% increase in the BC proportion was associated with higher rhinitis burden (OR;[95% CI]: 1.80;[1.22,2.66]), while increases in the non-BC component of PM did not significantly impact rhinoconjunctivitis QOL. Associations were similar regardless of atopy.ConclusionHigher PM2.5 and BC exposure is associated with worse rhinitis QOL among asthmatic children.

| S-EPMC5862476 | biostudies-literature

Association between Traffic Related Air Pollution and the Development of Asthma Phenotypes in Children: A Systematic Review.

Project description:Introduction:Traffic related air pollution (TRAP) has long been associated with the onset of childhood asthma. The relationship between TRAP exposure and the development of childhood asthma phenotypes is less understood. To better understand this relationship, we performed a systematic review of the literature studying childhood TRAP exposure and the development of childhood asthma and wheezing phenotypes (transient, persistent, and late-onset asthma/wheezing phenotypes). Methods:A literature search was performed in PubMed, Embase, and Scopus databases for current literature, returning 1706 unique articles. After screening and selection, 7 articles were included in the final review. Due to the low number of articles, no meta-analysis was performed. Results:TRAP exposure appears to be associated with both transient and persistent asthma/wheezing phenotypes. However, there was little evidence to suggest a relationship between TRAP exposure and late-onset asthma/wheezing. The differing results may be in part due to the heterogeneity in study methods and asthma/wheezing phenotype definitions, in addition to other factors such as genetics. Conclusion:TRAP exposure may be associated with transient and persistent asthma/wheezing phenotypes in children. The low number of studies and differing results suggest that further studies are warranted.

| S-EPMC6304508 | biostudies-other

Project description:BACKGROUND: Traffic-related air pollution is related with asthma, and this association may be modified by genetic factors. OBJECTIVES: We investigated the role of genetic polymorphisms potentially modifying the association between home outdoor levels of modeled nitrogen dioxide and asthma. METHODS: Adults from 13 cities of the second European Community Respiratory Health Survey (ECRHS II) were included (n = 2,920), for whom both DNA and outdoor NO(2) estimates were available. Home addresses were geocoded and linked to modeled outdoor NO(2) estimates, as a marker of local traffic-related pollution. We examined asthma prevalence and evaluated polymorphisms in genes involved in oxidative stress pathways [gluthatione S-transferases M1 (GSTM1), T1 (GSTT1), and P1 (GSTP1) and NAD(P)H:quinine oxidoreductase (NQO1)], inflammatory response [tumor necrosis factor alpha (TNFA)], immunologic response [Toll-like receptor 4 (TLR4)], and airway reactivity [adrenergic receptor beta2 (ADRB2)]. RESULTS: The association between modeled NO(2) and asthma prevalence was significant for carriers of the most common genotypes of NQO1 rs2917666 [odds ratio (OR) = 1.54; 95% confidence interval (CI), 1.10-2.24], TNFA rs2844484 (OR = 2.02; 95% CI, 1.30-3.27). For new-onset asthma, the effect of NO(2) was significant for the most common genotype of NQO1 rs2917666 (OR = 1.52; 95% CI, 1.09-2.16). A significant interaction was found between NQO1 rs2917666 and NO(2) for asthma prevalence (p = 0.02) and new-onset asthma (p = 0.04). CONCLUSIONS: Genetic polymorphisms in the NQO1 gene are related to asthma susceptibility among persons exposed to local traffic-related air pollution. This points to the importance of antioxidant pathways in the protection against the effects of air pollution on asthma.

| S-EPMC2799467 | biostudies-literature

Do Variants in GSTs Modify the Association between Traffic Air Pollution and Asthma in Adolescence?

Project description:Polymorphisms in genes involved in the oxidative stress response may partially explain the documented heterogeneous associations between traffic-related air pollution (TRAP) exposure and asthma and allergies in children. We investigated whether the GSTT1, GSTM1 and GSTP1 gene polymorphisms modified the associations between TRAP exposure during the first year of life and asthma, wheeze and hay fever in adolescence. We used a birth cohort of 620 high risk infants from the Melbourne Atopy Cohort Study. TRAP exposure during the first year of life was defined as the cumulative length of major roads within 150 m of each participant's residence during the first year of life. Wheeze, asthma and hay fever were measured at ages 12 (n = 370) and 18 (n = 434) years. The associations and interactions with glutathione S-transferases (GST s) were investigated using regression models. Overall, there was no relationship between TRAP exposure during the first year of life and current asthma, wheeze and hay fever at ages 12 or 18 years. However, in GSTT1 null carriers, every 100 m increase in cumulative lengths of major road exposure during the first year of life was associated with a 2.31-fold increased risk of wheeze and a 2.15-fold increased risk of asthma at 12 years. TRAP is associated with some respiratory outcomes in carriers of genetic polymorphisms in oxidative stress metabolism genes.

| S-EPMC4848941 | biostudies-literature

Project description: Not available

| S-EPMC7328327 | biostudies-literature

Association between Exposure to Traffic-Related Air Pollution and Prevalence of Allergic Diseases in Children, Seoul, Korea.

Project description:Although there has been suggestive evidence of the association between TRAP and ADs, findings remained inconsistent possibly due to limited population. We investigated the association between TRAP and ADs in a large population of children with rich spatial coverage and expanded age span in Seoul, Korea. TRAP exposures were estimated by categorized proximity to the nearest major road (≤150, 150-300, 300-500, and >500 m) and density of major roads within 300 meters from children's residences. We estimated the association between two TRAP exposures and three ADs using generalized mixed model after adjusting for individual characteristics. We also investigated whether the association varied by household and regional socioeconomic status. We found associations of atopic eczema with road density [OR = 1.08; 95% CI = 1.01-1.15] and road proximity [1.15, 1.01-1.32; 1.17, 1.03-1.34; and 1.16, 1.01-1.34 for ≤150, 150-300, and 300-500 m, resp., compared to >500 m]. There was no association with asthma and allergic rhinitis. Effect estimates were generally the highest in the low socioeconomic region. Children living in areas surrounded by large and busy roads were likely to be at greater risks for atopic eczema, with increased vulnerability when living in deprived areas.

| S-EPMC5615949 | biostudies-literature

Exposure to Traffic-Related Air Pollution and Serum Inflammatory Cytokines in Children.

Project description:Long-term exposure to ambient air pollution can lead to adverse health effects in children; however, underlying biological mechanisms are not fully understood.We evaluated the effect of air pollution exposure during different time periods on mRNA expression as well as circulating levels of inflammatory cytokines in children.We measured a panel of 10 inflammatory markers in peripheral blood samples from 670 8-y-old children in the Barn/Child, Allergy, Milieu, Stockholm, Epidemiology (BAMSE) birth cohort. Outdoor concentrations of nitrogen dioxide (NO2) and particulate matter (PM) with aerodynamic diameter <10 ?m (PM10) from road traffic were estimated for residential, daycare, and school addresses using dispersion modeling. Time-weighted average exposures during infancy and at biosampling were linked to serum cytokine levels using linear regression analysis. Furthermore, gene expression data from 16-year-olds in BAMSE (n=238) were used to evaluate links between air pollution exposure and expression of genes coding for the studied inflammatory markers.A 10??g/m3 increase of NO2 exposure during infancy was associated with a 13.6% (95% confidence interval (CI): 0.8; 28.1%) increase in interleukin-6 (IL-6) levels, as well as with a 27.8% (95% CI: 4.6, 56.2%) increase in IL-10 levels, the latter limited to children with asthma. However, no clear associations were observed for current exposure. Results were similar using PM10, which showed a high correlation with NO2. The functional analysis identified several differentially expressed genes in response to air pollution exposure during infancy, including IL10, IL13, and TNF;.Our results indicate alterations in systemic inflammatory markers in 8-y-old children in relation to early-life exposure to traffic-related air pollution. https://doi.org/10.1289/EHP460.

| S-EPMC5714301 | biostudies-literature

Project description:Mechanisms for the adverse respiratory effects of traffic-related air pollution (TRAP) have yet to be established. We evaluated the acute effects of TRAP exposure on proximal and distal airway inflammation by relating indoor nitric oxide (NO), a marker of TRAP exposure in the indoor microenvironment, to airway and alveolar sources of exhaled nitric oxide (FeNO).FeNO was collected online at four flow rates in 1635 schoolchildren (aged 12-15 years) in southern California (USA) breathing NO-free air. Indoor NO was sampled hourly and linearly interpolated to the time of the FeNO test. Estimated parameters quantifying airway wall diffusivity (DawNO) and flux (J'awNO) and alveolar concentration (CANO) sources of FeNO were related to exposure using linear regression to adjust for potential confounders.We found that TRAP exposure indoors was associated with elevated alveolar NO. A 10 ppb higher indoor NO concentration at the time of the FeNO test was associated with 0.10 ppb higher average CANO (95% CI 0.04-0.16) (equivalent to a 7.1% increase from the mean), 4.0% higher J'awNO (95% CI -2.8-11.3) and 0.2% lower DawNO (95% CI -4.8-4.6).These findings are consistent with an airway response to TRAP exposure that was most marked in the distal airways.

| S-EPMC5402887 | biostudies-literature

Project description:BackgroundBiologically plausible mechanisms link traffic-related air pollution to metabolic disorders and potentially to obesity. Here we sought to determine whether traffic density and traffic-related air pollution were positively associated with growth in body mass index (BMI?=?kg/m2) in children aged 5-11 years.MethodsParticipants were drawn from a prospective cohort of children who lived in 13 communities across Southern California (N?=?4550). Children were enrolled while attending kindergarten and first grade and followed for 4 years, with height and weight measured annually. Dispersion models were used to estimate exposure to traffic-related air pollution. Multilevel models were used to estimate and test traffic density and traffic pollution related to BMI growth. Data were collected between 2002-2010 and analyzed in 2011-12.ResultsTraffic pollution was positively associated with growth in BMI and was robust to adjustment for many confounders. The effect size in the adjusted model indicated about a 13.6% increase in annual BMI growth when comparing the lowest to the highest tenth percentile of air pollution exposure, which resulted in an increase of nearly 0.4 BMI units on attained BMI at age 10. Traffic density also had a positive association with BMI growth, but this effect was less robust in multivariate models.ConclusionsTraffic pollution was positively associated with growth in BMI in children aged 5-11 years. Traffic pollution may be controlled via emission restrictions; changes in land use that promote jobs-housing balance and use of public transit and hence reduce vehicle miles traveled; promotion of zero emissions vehicles; transit and car-sharing programs; or by limiting high pollution traffic, such as diesel trucks, from residential areas or places where children play outdoors, such as schools and parks. These measures may have beneficial effects in terms of reduced obesity formation in children.

| S-EPMC4106205 | biostudies-literature

National cohort and meteorological data based nested case-control study on the association between air pollution exposure and thyroid cancer.

Project description:The objective of this study was to evaluate the influence of exposure to meteorological conditions, including air pollution, on thyroid cancer. A nested case-control study was conducted utilizing 4632 patients with thyroid cancer and 18,528 control subjects who were matched at a 1:4 ratio by age group, sex, income, and region of residence. Korean National Health Insurance Service-Health Screening Cohort data from 2002 to 2015 were used. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated for thyroid cancer correlated with meteorological and air pollution exposure over a moving average of 3 years before the index dates. For all participants, the adjusted ORs associated with relative humidity (1.01, 95% CI 1.00-1.03, P value = 0.023), ambient atmospheric pressure (1.02, 95% CI 1.01-1.03, P value < 0.001), and sunshine duration (1.17, 95% CI 1.04-1.31, P value = 0.007) indicated correlations with the occurrence of thyroid cancer; however, these results were inconsistent in the subgroup analyses. Overall, exposure to nitrogen dioxide (NO2) (1.33, 95% CI 1.24-1.43, P value < 0.001) and particulate matter (PM10) (0.64, 95% CI 0.60-0.69, P value < 0.001) were related to thyroid cancer. These relationships persisted in the subgroup analyses. In conclusion, thyroid cancer occurrence was positively associated with NO2 exposure and negatively associated with PM10 exposure.

| S-EPMC8566463 | biostudies-literature

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