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

ABSTRACT: 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.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.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.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.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.

SUBMITTER: Melen E

PROVIDER: S-EPMC2516580 | biostudies-literature | 2008 Aug

REPOSITORIES: biostudies-literature

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

Melén Erik E Nyberg Fredrik F Lindgren Cecilia M CM Berglind Niklas N Zucchelli Marco M Nordling Emma E Hallberg Jenny J Svartengren Magnus M Morgenstern Ralf R Kere Juha J Bellander Tom T Wickman Magnus M Pershagen Göran G

Environmental health perspectives 20080801 8

<h4>Background</h4>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.<h4>Objective</h4>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 disea ...[more]

PMID: 18709160

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Project description:BackgroundStudies of potential adverse effects of traffic related air pollution (TRAP) on allergic disease have had mixed findings. Nutritional studies to examine whether fish oil supplementation may protect against development of allergic disease through their anti-inflammatory actions have also had mixed findings. Extremely few studies to date have considered whether air pollution and dietary factors such as fish oil intake may interact, which was the rationale for this study.MethodsWe conducted a secondary analysis of the Childhood Asthma Prevention Study (CAPS) birth cohort, where children were randomised to fish oil supplementation or placebo from early life to age 5 years. We examined interactions between supplementation and TRAP (using weighted road density at place of residence as our measure of traffic related air pollution exposure) with allergic disease and lung function outcomes at age 5 and 8 years.ResultsOutcome information was available on approximately 400 children (~ 70% of the original birth cohort). Statistically significant interactions between fish oil supplementation and TRAP were seen for house dust mite (HDM), inhalant and all-allergen skin prick tests (SPTs) and for HDM-specific interleukin-5 response at age 5. Adjusting for relevant confounders, relative risks (RRs) for positive HDM SPT were RR 1.74 (95% CI 1.22-2.48) per 100 m local road or 33.3 m of motorway within 50 m of the home for those randomised to the control group and 1.03 (0.76-1.41) for those randomised to receive the fish oil supplement. The risk differential was highest in an analysis restricted to those who did not change address between ages 5 and 8 years. In this sub-group, supplementation also protected against the effect of traffic exposure on pre-bronchodilator FEV1/FVC ratio.ConclusionsResults suggest that fish oil supplementation may protect against pro-allergic sensitisation effects of TRAP exposure. Strengths of this analysis are that supplementation was randomised and independent of TRAP exposure, however, findings need to be confirmed in a larger experimental study with the interaction investigated as a primary hypothesis, potentially also exploring epigenetic mechanisms. More generally, studies of adverse health effects of air pollution may benefit from considering potential effect modification by diet and other factors.Trial registrationAustralia New Zealand Clinical Trial Registry. www.anzctr.org.au Registration: ACTRN12605000042640 , Date: 26th July 2005. Retrospectively registered, trial commenced prior to registry availability.

Project description:BackgroundTraffic-related air pollution exposure may influence brain development and function and thus be related to neurobehavioral problems in children, but little is known about windows of susceptibility.AimsExamine associations of gestational and childhood exposure to traffic-related pollution with executive function and behavior problems in children.MethodsWe studied associations of pre- and postnatal pollution exposures with neurobehavioral outcomes in 1212 children in the Project Viva pre-birth cohort followed to mid-childhood (median age 7.7years). Parents and classroom teachers completed the Behavior Rating Inventory of Executive Function (BRIEF) and the Strengths and Difficulties Questionnaire (SDQ). Using validated spatiotemporal models, we estimated exposure to black carbon (BC) and fine particulate matter (PM2.5) in the third trimester of pregnancy, from birth to 3years, from birth to 6years, and in the year before behavioral ratings. We also measured residential distance to major roadways and near-residence traffic density at birth and in mid-childhood. We estimated associations of BC, PM2.5, and other traffic exposure measures with BRIEF and SDQ scores, adjusted for potential confounders.ResultsHigher childhood BC exposure was associated with higher teacher-rated BRIEF Behavioral Regulation Index (BRI) scores, indicating greater problems: 1.0 points (95% confidence interval (CI): 0.0, 2.1) per interquartile range (IQR) increase in birth-age 6BC, and 1.7 points (95% CI: 0.6, 2.8) for BC in the year prior to behavioral ratings. Mid-childhood residential traffic density was also associated with BRI score (0.6, 95% CI: 0.1, 1.1). Birth-age 3BC was not associated with BRIEF or SDQ scores. Third trimester BC exposure was not associated with teacher-rated BRI scores (-0.2, 95% CI: -1.1, 0.8), and predicted lower scores (fewer problems) on the BRIEF Metacognition Index (-1.2, 95% CI: -2.2, -0.2) and SDQ total difficulties (-0.9, 95% CI: -1.4, -0.4). PM2.5 exposure was associated with teacher-rated BRIEF and SDQ scores in minimally adjusted models but associations attenuated with covariate adjustment. None of the parent-rated outcomes suggested adverse effects of greater pollution exposure at any time point.ConclusionsChildren with higher mid-childhood exposure to BC and greater near-residence traffic density in mid-childhood had greater problems with behavioral regulation as assessed by classroom teachers, but not as assessed by parents. Prenatal and early childhood exposure to traffic-related pollution did not predict greater executive function or behavior problems; third trimester BC was associated with lower scores (representing fewer problems) on measures of metacognition and behavioral problems.

Project description:BACKGROUND:Pediatric allergic diseases are a major public health concern, and previous studies have suggested that exposure to traffic-related air pollution (TRAP) exposure is a risk factor. These studies have typically assessed TRAP exposure using traffic measures, such as distance to major roads, or by modeling air pollutant concentrations; however inconsistent associations with pediatric allergic diseases have often been found. Using road proximity and density, we previously found an association between TRAP and atopic eczema among approximately 15,000 children living in Seoul, Korea, heavily populated and highly polluted city in which traffic is a major emission source. We aimed to conduct a parallel analysis using modeled air pollution concentrations and thus examine the consistency of the association. Specifically, we examined the associations of individual-level annual-average concentrations of NO2, PM10, and PM2.5 with symptoms and diagnoses of three pediatric allergic diseases including asthma, allergic rhinitis, and atopic eczema. METHODS:The study population included 14,614 children from the Seoul Atopy Friendly School Project Survey in Seoul, Korea, in 2010. To assess individual exposures to TRAP among these children, we predicted annual-average concentrations of NO2, PM10, and PM2.5 at the children's home addresses in 2010 using universal kriging and land use regression models along with regulatory air quality monitoring data and geographic characteristics. Then, we estimated odds ratios (ORs) of the three allergic diseases for interquartile increases in air pollution concentrations after adjusting for individual risk factors in mixed effects logistic regression. RESULTS:Symptoms and diagnoses of atopic eczema symptoms showed an association with NO2 (OR?=?1.07, 95% confidence interval?=?1.02-1.13; 1.08, 1.03-1.14) and PM10 (1.06, 1.01-1.12; 1.07, 1.01-1.13). ORs of PM2.5 were positive but not statistically significant (1.01, 0.95-1.07; 1.04, 0.98-1.10). No association was found between asthma and allergic rhinitis, although PM2.5 showed a marginal association with allergic rhinitis. CONCLUSIONS:Our consistent findings regarding the association between TRAP and the prevalence of atopic eczema using traffic measures and surrogate air pollutants suggested the effect of TRAP on children's health. Follow-up studies should elucidate the causal link, to support subsequent policy considerations and minimize adverse health effects in children.

Project description:BackgroundChronic exposure to air pollutants is associated with increased risk of cardiovascular disease (CVD) among adults. However, little is known about how air pollution may affect the development of subclinical atherosclerosis in younger populations. Carotid artery intima-media thickness (CIMT) is a measure of subclinical atherosclerosis that provides insight into early CVD pathogenesis.MethodsIn a pilot study of 70 participants from the Southern California Children's Health Study, we investigated CIMT progression from childhood to adulthood. Using carotid artery ultrasound images obtained at age 10 and follow-up images at age 21-22, we examined associations between childhood ambient and traffic-related air pollutants with changes in CIMT over time and attained adult CIMT using linear mixed-effects models adjusted for potential confounders. Average residential childhood exposures (i.e., birth to time of measurement at 10-11 years) were assigned for regional, ambient pollutants (ozone, nitrogen dioxide, particulate matter, interpolated from regulatory air monitoring data) and traffic-related nitrogen oxides (NOx) by road class (modeled using the CALINE4 line source dispersion model). Traffic density was calculated within a 300-m residential buffer.ResultsFor each 1 standard deviation (SD) increase in childhood traffic-related total NOx exposure, we observed greater yearly rate of change in CIMT from childhood to adulthood (β: 2.17 μm/yr, 95% CI: 0.78-3.56). Increases in annual rate of CIMT change from childhood to adulthood also were observed with freeway NOx exposure (β: 2.24 μm/yr, 95% CI: 0.84-3.63) and traffic density (β: 2.11 μm/yr, 95% CI: 0.79-3.43). Traffic exposures were also related to increases in attained CIMT in early adulthood. No associations of CIMT change or attained level were observed with ambient pollutants.ConclusionsOverall, we observed adverse changes in CIMT over time in relation to childhood traffic-related NOx exposure and traffic density in our study population. While these results must be cautiously interpreted given the limited sample size, the observed associations of traffic measures with CIMT suggest a need for future studies to more fully explore this relationship.

Dataset Information

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

Publications

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

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