Traffic-related Air Pollution, Dust Mite Allergen, and Childhood Asthma in Puerto Ricans.
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ABSTRACT:
SUBMITTER: Stevens EL
PROVIDER: S-EPMC7328327 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundPuerto Rican children share a disproportionate burden of prematurity and asthma in the United States. Little is known about prematurity and childhood asthma in Puerto Rican subjects.ObjectiveWe sought to examine whether prematurity is associated with asthma in Puerto Rican children.MethodsWe performed a case-control study of 678 children aged 6 to 14 years with (n = 351) and without (n = 327) asthma living in San Juan, Puerto Rico. Prematurity was defined by parental report for our primary analysis. In a secondary analysis, we only included children whose parents reported prematurity that required admission to the neonatal intensive care unit. Asthma was defined as physician-diagnosed asthma and wheeze in the prior year. We used logistic regression for analysis. All multivariate models were adjusted for age, sex, household income, atopy (≥1 positive IgE level to common allergens), maternal history of asthma, and early-life exposure to environmental tobacco smoke.ResultsIn a multivariate analysis there was a significant interaction between prematurity and atopy on asthma (P = .006). In an analysis stratified by atopy, prematurity was associated with a nearly 5-fold increased odds of asthma in atopic children (adjusted odds ratio, 4.7; 95% CI, 1.5-14.3; P = .007). In contrast, there was no significant association between prematurity and asthma in nonatopic children. Similar results were obtained in our analysis of prematurity requiring admission to the neonatal intensive care unit and asthma.ConclusionsOur results suggest that atopy modifies the estimated effect of prematurity on asthma in Puerto Rican children. Prematurity might explain, in part, the high prevalence of atopic asthma in this ethnic group.
| S-EPMC3960360 | biostudies-literature
Project description:BackgroundDietary patterns might influence the pathogenesis of asthma in Puerto Ricans, the ethnic group most affected by this disease in the United States.ObjectiveTo examine the association among diet, T-helper cell type 17 cytokines, and asthma in Puerto Rican children.MethodsAs part of a case-control study of 678 Puerto Rican children 6 to 14 years old in San Juan, participants completed a 75-item questionnaire on the child's food consumption in the prior week. Foods were aggregated into 7 groups: fruits, vegetables, grains, protein foods, dairy, fats, and sweets. Logistic regression was used to evaluate consumption frequency of each group, plasma T-helper cell type 17 cytokine levels, and asthma. Based on this analysis, a food score (range -2 [unhealthy diet: high consumption of dairy products and sweets, low consumption of vegetables and grains] to +2 [healthy diet: high consumption of grains and vegetables, low consumption of dairy and sweets]) was created to identify dietary patterns.ResultsHigh consumption of grains was associated with lower odds of asthma (adjusted odds ratio [aOR] 0.52, 95% confidence interval [CI] 0.33-0.82), whereas frequent consumption of dairy products (aOR 1.93, 95% CI 1.32-2.84) or sweets (aOR 1.82, 95% CI 1.08-2.72) was associated with higher odds of asthma. A healthier diet (each 1-point increment in food score) was associated with lower levels of interleukin-17F (β = -1.48 pg/mL, 95% CI -1.78 to -1.20) and with 36% decreased odds of asthma (aOR 0.64, 95% CI 0.53-0.77).ConclusionA healthy diet, with frequent consumption of vegetables and grains and low consumption of dairy products and sweets, was associated with lower levels of interleulin-17F and decreased odds of childhood asthma in Puerto Ricans.
| S-EPMC4721241 | biostudies-literature
Project description:BackgroundThe relative contributions of genetics and environment to asthma in Hispanics or to asthma in children younger than 3 years are not well understood.ObjectiveTo examine the relative contributions of genetics and environment to early-childhood asthma by performing a longitudinal twin study of asthma in Puerto Rican children ≤ 3 years old.Methods678 twin infants from the Puerto Rico Neo-Natal Twin Registry were assessed for asthma at age 1 year, with follow-up data obtained for 624 twins at age 3 years. Zygosity was determined by DNA microsatellite profiling. Structural equation modeling was performed for three phenotypes at ages 1 and 3 years: physician-diagnosed asthma, asthma medication use in the past year, and ≥ 1 hospitalization for asthma in the past year. Models were additionally adjusted for early-life environmental tobacco smoke exposure, sex, and age.ResultsThe prevalences of physician-diagnosed asthma, asthma medication use, and hospitalization for asthma were 11.6%, 10.8%, 4.9% at age 1 year, and 34.1%, 40.1%, and 8.5% at 3 years, respectively. Shared environmental effects contributed to the majority of variance in susceptibility to physician-diagnosed asthma and asthma medication use in the first year of life (84%-86%), while genetic effects drove variance in all phenotypes (45%-65%) at age 3 years. Early-life environmental tobacco smoke, sex, and age contributed to variance in susceptibility.ConclusionOur longitudinal study in Puerto Rican twins demonstrates a changing contribution of shared environmental effects to liability for physician-diagnosed asthma and asthma medication use between ages 1 and 3 years. Early-life environmental tobacco smoke reduction could markedly reduce asthma morbidity in young Puerto Rican children.
| S-EPMC3700929 | biostudies-literature
Project description:BackgroundThere has been no longitudinal study of the relation between concurrent exposure to dust mite allergen and endotoxin in early life and asthma and atopy at school age.ObjectivesTo examine the relation between exposure to dust mite allergen and endotoxin at age 2 to 3 months and asthma, wheeze, and atopy in high-risk children.MethodsBirth cohort study of 440 children with parental history of atopy in the Boston metropolitan area.ResultsIn multivariate analyses, early exposure to high levels of dust mite allergen (> or =10 microg/g) was associated with increased risks of asthma at age 7 years (odds ratio [OR], 3.0; 95% CI, 1.1-7.9) and late-onset wheeze (OR, 5.0; 95% CI, 1.5-16.4). Exposure to endotoxin levels above the lowest quartile at age 2 to 3 months was associated with reduced odds of atopy at school age (OR, 0.5; 95% CI, 0.2-0.9). In contrast with its inverse association with atopy, endotoxin exposure in early life was associated with an increased risk of any wheeze between ages 1 and 7 years that did not change significantly with time (hazard ratio for each quartile increment in endotoxin levels, 1.23; 95% CI, 1.07-1.43).ConclusionAmong children at risk of atopy, early exposure to high levels of dust mite allergen is associated with increased risks of asthma and late-onset wheeze. In these children, endotoxin exposure is associated with a reduced risk of atopy but an increased risk of wheeze.Clinical implicationsEarly endotoxin exposure may be a protective factor against atopy but a risk factor for wheeze in high-risk children.
| S-EPMC3737770 | biostudies-literature
Project description:BackgroundAsthma is a complex disorder influenced by genetics and the environment. Recent findings have linked abnormal DNA methylation in T cells with asthma; however, the potential dysregulation of methylation in airway epithelial cells is unknown. Studies of mouse models of asthma have observed greater levels of 5-hydroxymethylcytosine (5-hmC) and ten-eleven translocation 1 (TET1) expression in lungs. TET proteins are known to catalyze methylation through modification of 5-methylcytosine to 5-hmC.ObjectiveWe sought to examine the association of TET1 methylation with asthma and traffic-related air pollution (TRAP).MethodsTET1 methylation levels from DNA derived from nasal airway epithelial cells collected from 12 African American children with physician-diagnosed asthma and their nonasthmatic siblings were measured by using Illumina 450K arrays. Regions of interest were verified by means of locus-specific pyrosequencing in 35 sibling pairs and replicated in an independent population (n = 186). Exposure to TRAP in participants' early life and at current home addresses was estimated by using a land-use regression model. Methylation studies in saliva, PBMCs, and human bronchial epithelial cells were done to support our findings.ResultsLoss of methylation at a single CpG site in the TET1 promoter (cg23602092) and increased global 5-hmC levels were significantly associated with asthma. In contrast, TRAP exposure at participants' current homes significantly increased methylation at the same site. Patterns were consistent across tissue sample types. 5-Aza-2'-deoxycytidine and diesel exhaust particle exposure in human bronchial epithelial cells was associated with altered TET1 methylation and expression and global 5-hmC levels.ConclusionsOur findings suggest a possible role of TET1 methylation in asthmatic patients and response to TRAP.
| S-EPMC4783231 | biostudies-literature
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
Project description:Background: Current levels of traffic-related air pollution (TRAP) are associated with the development of childhood asthma, although some inconsistencies and heterogeneity remain. An important part of the uncertainty in studies of TRAP-associated asthma originates from uncertainties in the TRAP exposure assessment and assignment methods. In this work, we aim to systematically review the exposure assessment methods used in the epidemiology of TRAP and childhood asthma, highlight recent advances, remaining research gaps and make suggestions for further research. Methods: We systematically reviewed epidemiological studies published up until 8 September 2016 and available in Embase, Ovid MEDLINE (R), and "Transport database". We included studies which examined the association between children's exposure to TRAP metrics and their risk of "asthma" incidence or lifetime prevalence, from birth to the age of 18 years old. Results: We found 42 studies which examined the associations between TRAP and subsequent childhood asthma incidence or lifetime prevalence, published since 1999. Land-use regression modelling was the most commonly used method and nitrogen dioxide (NO₂) was the most commonly used pollutant in the exposure assessments. Most studies estimated TRAP exposure at the residential address and only a few considered the participants' mobility. TRAP exposure was mostly assessed at the birth year and only a few studies considered different and/or multiple exposure time windows. We recommend that further work is needed including e.g., the use of new exposure metrics such as the composition of particulate matter, oxidative potential and ultra-fine particles, improved modelling e.g., by combining different exposure assessment models, including mobility of the participants, and systematically investigating different exposure time windows. Conclusions: Although our previous meta-analysis found statistically significant associations for various TRAP exposures and subsequent childhood asthma, further refinement of the exposure assessment may improve the risk estimates, and shed light on critical exposure time windows, putative agents, underlying mechanisms and drivers of heterogeneity.
| S-EPMC5369148 | biostudies-literature
Project description:BackgroundPuerto Ricans, an admixed population of African, European, and Native American ancestries, have the highest asthma prevalence, morbidity, and mortality rates of any United States' population. Although socioeconomic status (SES) is negatively correlated with asthma incidence in most populations, no such relationship has been identified among Puerto Ricans. We hypothesized that, in this admixed population, the association between SES and asthma may interact with genetic ancestry.MethodsWe analyzed 135 Puerto Rican subjects with asthma and 156 control subjects recruited from six different recruitment centers in Puerto Rico. Individual ancestry for each subject was estimated using 44 ancestry informative markers. SES was assigned using the census tracts' median family income. Analyses of SES were based on the SES of the clinic site from which the subjects were recruited and on a subset of individuals on whom home address-based SES was available.ResultsIn the two (independent) analyses, we found a significant interaction between SES, ancestry, and asthma disease status. At lower SES, European ancestry was associated with increased risk of asthma, whereas African ancestry was associated with decreased risk. The opposite was true for their higher SES counterparts.ConclusionsThe observed interaction may help to explain the unique pattern of risk for asthma in Puerto Ricans and the lack of association with SES observed in previous studies when not accounting for varying proportions of ancestry.
| S-EPMC2648109 | biostudies-literature
Project description:While many studies have evaluated the association between acute childhood leukemia and environmental factors, knowledge is limited. Ambient air pollution has been classified as a Group 1 carcinogen, but studies have not established whether traffic-related air pollution is associated with leukemia. The goal of our study was to determine if children with acute leukemia had higher odds of exposure to traffic-related air pollution at birth compared to controls.We conducted a case-control study using the Oklahoma Central Cancer Registry to identify cases of acute leukemia in children diagnosed before 20 years of age between 1997 and 2012 (n=307). Controls were selected from birth certificates and matched to cases on week of birth (n=1013). Using a novel satellite-based land-use regression model of nitrogen dioxide (NO2) and estimating road density based on the 2010 US Census, we evaluated the association between traffic-related air pollution and childhood leukemia using conditional logistic regression.The odds of exposure to the fourth quartile of NO2 (11.19-19.89ppb) were similar in cases compared to controls after adjustment for maternal education (OR: 1.08, 95% CI: 0.75, 1.55). These estimates were stronger among children with acute myeloid leukemia (AML) than acute lymphoid leukemia, with a positive association observed among urban children with AML (4th quartile odds ratio: 5.25, 95% confidence interval: 1.09, 25.26). While we observed no significant association with road density, male cases had an elevated odds of exposure to roads at 500m from the birth residence compared to controls (OR: 1.39, 95% CI: 0.93, 2.10), which was slightly attenuated at 750m.Although we observed no association overall between NO2 or road density, this was the first study to observe an elevated odds of exposure to NO2 among children with AML compared to controls suggesting further exploration of traffic-related air pollution and AML is warranted.
| S-EPMC4874884 | biostudies-literature
Project description:BACKGROUND: Genetics may partially explain observed heterogeneity in associations between traffic-related air pollution and incident asthma. OBJECTIVE: Our aim was to investigate the impact of gene variants associated with oxidative stress and inflammation on associations between air pollution and incident childhood asthma. METHODS: Traffic-related air pollution, asthma, wheeze, gene variant, and potential confounder data were pooled across six birth cohorts. Parents reported physician-diagnosed asthma and wheeze from birth to 7-8 years of age (confirmed by pediatric allergist in two cohorts). Individual estimates of annual average air pollution [nitrogen dioxide (NO2), particulate matter ? 2.5 ?m (PM2.5), PM2.5 absorbance, ozone] were assigned to each child's birth address using land use regression, atmospheric modeling, and ambient monitoring data. Effect modification by variants in GSTP1 (rs1138272/Ala114Val and rs1695/IIe105Val) and TNF (rs1800629/G-308A) was investigated. RESULTS: Data on asthma, wheeze, potential confounders, at least one SNP of interest, and NO2 were available for 5,115 children. GSTP1 rs1138272 and TNF rs1800629 SNPs were associated with asthma and wheeze, respectively. In relation to air pollution exposure, children with one or more GSTP1 rs1138272 minor allele were at increased risk of current asthma [odds ratio (OR) = 2.59; 95% CI: 1.43, 4.68 per 10 ?g/m3 NO2] and ever asthma (OR = 1.64; 95% CI: 1.06, 2.53) compared with homozygous major allele carriers (OR = 0.95; 95% CI: 0.68, 1.32 for current and OR = 1.20; 95% CI: 0.98, 1.48 for ever asthma; Bonferroni-corrected interaction p = 0.04 and 0.01, respectively). Similarly, for GSTP1 rs1695, associations between NO2 and current and ever asthma had ORs of 1.43 (95% CI: 1.03, 1.98) and 1.36 (95% CI: 1.08, 1.70), respectively, for minor allele carriers compared with ORs of 0.82 (95% CI: 0.52, 1.32) and 1.12 (95% CI: 0.84, 1.49) for homozygous major allele carriers (Bonferroni-corrected interaction p-values 0.48 and 0.09). There were no clear differences by TNF genotype. CONCLUSIONS: Children carrying GSTP1 rs1138272 or rs1695 minor alleles may constitute a susceptible population at increased risk of asthma associated with air pollution.
| S-EPMC3984232 | biostudies-literature