The impact of air pollutants as an adjuvant for allergic sensitization and asthma

Viera, Loida; Chen, Karin; Nel, André E.; Lloret, Maria Garcia

doi:10.1007/s11882-009-0046-x

Cited by 22 publications

(12 citation statements)

References 63 publications

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“…Increased levels of total IgG have been shown when ovalbumin was coupled SO 2 exposure in rats (29). In human populations, increased levels of CD4+ and CD8+ lymphocytes have been documented with increased exposure to PM 2.5 and PM 10 , and increases in total IgG were linked with higher levels of PM 2.5 (30), demonstrating that particulate matter activates immunologic response (31, 32). The increased risk of atopy with closer proximity to major roadways provides mechanistic insights into the increased risk of asthma symptoms.…”

Section: Discussionmentioning

confidence: 99%

Effects of distance from a heavily transited avenue on asthma and atopy in a periurban shantytown in Lima, Peru

Baumann

Robinson

Combe

et al. 2011

Journal of Allergy and Clinical Immunology

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Background Proximity to roadways increases the risk of asthma in developed countries; however, relatively little is known about this relationship in developing countries, where rapid and uncontrolled growth of cities has resulted in urban sprawl and heavy traffic volumes. Objective Determine the effect of distance from a heavily transited avenue on asthma symptoms and quantitative respiratory outcome measures in a peri-urban shanty town in Lima, Peru. Methods We enrolled 725 adolescents aged 13–15 years, administered a survey on asthma symptoms and measured spirometry, response to allergy skin testing and eNO. We calculated distances from the main avenue for all households and measured indoor PM in 100 households. We used multivariable regression to model the risk of asthma symptoms, risk of atopy, eNO and FEV1/FVC as a function of distance. Results Compared against 384 meters, the odds of current asthma symptoms in households living within 100 meters increased by a factor of 2 (p<0.05). The odds of atopy increased by a factor of 1.07 for every 100 meters difference in the distance from the avenue (p=0.03). We found an inverse relationship in pre-bronchodilator FEV1/FVC and distance to the avenue in females (p=0.01) but not in males. We did not find an association between eNO or household PM levels and distance. Conclusion Living in close proximity to a high traffic-density avenue in a peri-urban community in Peru was associated with a greater risk of asthma symptoms and atopy. Regulation of mobile source pollutants in peri-urban areas of developing countries may help reduce the burden of asthma symptoms and atopy.

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Section: Discussionmentioning

confidence: 99%

Effects of distance from a heavily transited avenue on asthma and atopy in a periurban shantytown in Lima, Peru

Baumann

Robinson

Combe

et al. 2011

Journal of Allergy and Clinical Immunology

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“…Higher BPA exposure was shown to lead to a decrease in MAPK1 5 CGI methylation in our study. Lower methylation of MAPK1 5 CGI is associated with increased gene expression, which in turn increases MAPK1 expression at protein levels and triggers the development of allergic inflammation [49][50][51][52][53]. We demonstrated that the methylation of MAPK1 5 CGI is an intervening factor between BPA exposure and asthma.…”

Section: Discussionmentioning

confidence: 75%

Bisphenol a Exposure, DNA Methylation, and Asthma in Children

Yang

Karmaus

Yang³

et al. 2020

IJERPH

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Epidemiological studies have reported the relationship between bisphenol A (BPA) exposure and increased prevalence of asthma, but the mechanisms remain unclear. Here, we investigated whether BPA exposure and DNA methylation related to asthma in children. We collected urinary and blood samples from 228 children (Childhood Environment and Allergic Diseases Study cohort) aged 3 years. Thirty-three candidate genes potentially interacting with BPA exposure were selected from a toxicogenomics database. DNA methylation was measured in 22 blood samples with top-high and bottom-low exposures of BPA. Candidate genes with differential methylation levels were validated by qPCR and promoter associated CpG islands have been investigated. Correlations between the methylation percentage and BPA exposure and asthma were analyzed. According to our findings, MAPK1 showed differential methylation and was further investigated in 228 children. Adjusting for confounders, urinary BPA glucuronide (BPAG) level inversely correlated with MAPK1 promoter methylation (β = −0.539, p = 0.010). For the logistic regression analysis, MAPK1 methylation status was dichotomized into higher methylated and lower methylated groups with cut off continuous variable of median of promoter methylation percentage (50%) while performing the analysis. MAPK1 methylation was lower in children with asthma than in children without asthma (mean ± SD; 69.82 ± 5.88% vs. 79.82 ± 5.56%) (p = 0.001). Mediation analysis suggested that MAPK1 methylation acts as a mediation variable between BPA exposure and asthma. The mechanism of BPA exposure on childhood asthma might, therefore, be through the alteration of MAPK1 methylation. The mechanism of BPA exposure on childhood asthma might, therefore, be through the alteration of MAPK1 methylation.

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“…In children with asthma, exposure to NO 2 has been shown to worsen asthma control based on symptoms and lung function 93-96 . It also has a synergistic effect with allergen exposures to elicit airway inflammation and symptoms in allergen-sensitized individuals 97-100 . Mouse models of asthma have shown prolonged allergen induced airway reactivity and augmentation of eosinophilic airway inflammation in the presence of NO 2 101 .…”

Section: Air Pollutionmentioning

confidence: 99%

Perinatal and early childhood environmental factors influencing allergic asthma immunopathogenesis

Gaffin¹,

Kanchongkittiphon²,

Phipatanakul³

2014

International Immunopharmacology

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Background The prevalence of asthma has increased dramatically over the past several decades. While hereditary factors are highly important, the rapid rise outstrips the pace of genomic variation. Great emphasis has been placed on potential modifiable early life exposures leading to childhood asthma. Methods We reviewed the recent medical literature for important studies discussing the role of the perinatal and early childhood exposures and the inception of childhood asthma. Results and Discussion Early life exposure to allergens (House dust mite (HDM), furred pets, cockroach, rodent and mold)air pollution (nitrogen dioxide (NO2), ozone (O3), volatile organic compounds (VOCs), and particulate matter (PM)) and viral respiratory tract infections (Respiratory syncytial virus (RSV) and human rhinovirus (hRV)) have been implicated in the development of asthma in high risk children. Conversely, exposure to microbial diversity in the perinatal period may diminish the development of atopy and asthma symptoms.

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The impact of air pollutants as an adjuvant for allergic sensitization and asthma

Cited by 22 publications

References 63 publications

Effects of distance from a heavily transited avenue on asthma and atopy in a periurban shantytown in Lima, Peru

Effects of distance from a heavily transited avenue on asthma and atopy in a periurban shantytown in Lima, Peru

Bisphenol a Exposure, DNA Methylation, and Asthma in Children

Perinatal and early childhood environmental factors influencing allergic asthma immunopathogenesis

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