Relation between air pollution and allergic rhinitis in Taiwanese schoolchildren

BACKGROUND: Recent findings suggest that exposure to outdoor air pollutants may increase the risk of allergic rhinitis. The results of these studies are inconsistent, but warrant further attention. The objective of the study was to assess the effect of relation between exposure to urban air pollution and the prevalence allergic rhinitis among school children. METHODS: We conducted a nationwide cross-sectional study of 32,143 Taiwanese school children. We obtained routine air-pollution monitoring data for sulphur dioxide (SO(2)), nitrogen oxides (NOx), ozone (O(3)), carbon monoxide (CO), and particles with an aerodynamic diameter of 10 μm or less (PM(10)). A parent-administered questionnaire provided information on individual characteristics and indoor environments (response rate 92%). Municipal-level exposure was calculated using the mean of the 2000 monthly averages. The effect estimates were presented as odds ratios (ORs) per 10 ppb change for SO(2), NOx, and O(3), 100 ppb change for CO, and 10 μg/m(3 )change for PM(10). RESULTS: In two-stage hierarchical model adjusting for confounding, the prevalence of allergic rhinitis was significantly associated with SO(2 )(adjusted odds ratio (OR) = 1.43, 95% confidence interval (CI): 1.25, 1.64), CO (aOR = 1.05, 95% CI: 1.04, 1.07), and NOx (aOR = 1.11, 95% CI: 1.08, 1.15). Contrary to our hypothesis, the prevalence of allergic rhinitis was weakly or not related to O(3 )(aOR = 1.05, 95% CI: 0.98, 1.12) and PM(10 )(aOR = 1.00, 95% CI: 0.99, 1.02). CONCLUSION: Persistent exposure to NOx, CO, and SO(2 )may increase the prevalence of allergic rhinitis in children

T cell activation, from atopy to asthma: more a paradox than a paradigm

International audienceDuring the last 15 years, it was largely shown that allergic inflammation was orchestrated by activated Th2 lymphocytes, leading to IgE production and eosinophil activation. Indeed, Th2 activation was shown to be necessary to induce allergic sensitization in animal models. In humans, a Th2 skewing was shown in atopic children soon after birth. In asthma, descriptive studies showed that Th2 cells were more numerous in patients than in controls. In addition, during specific allergen stimulation, an increase of Th2 cells was described in most cases. According to this Th2 paradigm, it was proposed that early avoidance of microbial exposure could explain the increase of atopic diseases seen in the last 20 years in developed countries, as the "hygiene hypothesis". Recently, it was proposed that early exposure to lipopolysaccharide (LPS) could be protective against atopic diseases. However, it is well established that exposure to LPS can induce asthma symptoms, both in animals and humans, although it induces a Th1 inflammatory response. In addition, most infections induce asthma exacerbations and Th1 responses. Recently, some studies have showed that some Th1 cells were present in asthmatic patients, which could be related to bronchial hyperreactivity. There is therefore an "infectious paradox" in asthma, which contributes to show that the Th2 paradigm is insufficient to explain the whole inflammatory reaction of this disease. We propose that the Th2paradigm is relevant to atopy and inception of asthma albeit a Th1 activation would account at least in part for bronchial hyperreactivity and asthma symptoms

Protein expression and genetic variability of canine Can f 1 in golden and Labrador retriever service dogs

BACKGROUND: Valued for trainability in diverse tasks, dogs are the primary service animal used to assist individuals with disabilities. Despite their utility, many people in need of service dogs are sensitive to the primary dog allergen, Can f 1, encoded by the Lipocalin 1 gene (LCN1). Several organizations specifically breed service dogs to meet special needs and would like to reduce allergenic potential if possible. In this study, we evaluated the expression of Can f 1 protein and the inherent variability of LCN1 in two breeds used extensively as service dogs. Saliva samples from equal numbers of male and female Labrador retrievers (n = 12), golden retrievers (n = 12), and Labrador-golden crosses (n = 12) were collected 1 h after the morning meal. Can f 1 protein concentrations in the saliva were measured by ELISA, and the LCN1 5′ and 3′ UTRs and exons sequenced. RESULTS: There was no sex effect (p > 0.2) nor time-of-day effect; however, Can f 1 protein levels varied by breed with Labrador retrievers being lower than golden retrievers (3.18 ± 0.51 and 5.35 ± 0.52 μg/ml, respectively, p < 0.0075), and the Labrador-golden crosses having intermediate levels (3.77 ± 0.48 μg/ml). Although several novel SNPs were identified in LCN1, there were no significant breed-specific sequence differences in the gene and no association of LCN1 genotypes with Can f 1 expression. CONCLUSIONS: As service dogs, Labrador retrievers likely have lower allergenic potential and, though there were no DNA sequence differences identified, classical genetic selection on the estimated breeding values associated with salivary Can f 1 expression may further reduce that potential. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s40575-016-0031-3) contains supplementary material, which is available to authorized users