Αρχειοθήκη ιστολογίου

Αλέξανδρος Γ. Σφακιανάκης
ΩτοΡινοΛαρυγγολόγος
Αναπαύσεως 5
Άγιος Νικόλαος Κρήτη 72100
2841026182
6032607174

Τρίτη 16 Οκτωβρίου 2018

Non-atopic eczema in elderly women – Impact of air pollution and genes

Publication date: Available online 16 October 2018

Source: Journal of Allergy and Clinical Immunology

Author(s): Anke Hüls, Michael J. Abramson, Dorothea Sugiri, Kateryna Fuks, Ursula Krämer, Jean Krutmann, Tamara Schikowski

Abstract
Background

Whilst many risk factors have been described for atopic eczema in children, little is known about the eczema phenotype in middle aged or elderly adults.

Objective

To examine the association between air pollution, atopy and eczema in adulthood.

Methods

This analysis was based on 834 women from the Study on the influence of Air pollution on Lung Function, Inflammation and Ageing (SALIA) cohort in Germany. Incident symptoms of eczema after the age of 55 years and prevalent symptoms of eczema ≤12 months before investigation were assessed by questionnaire at second follow-up (2007-2010). Total serum Immunoglobulin E (IgE) was measured at baseline (1985-1994) and in 2007-2010. Exposure to air pollution was assessed using land use regression. Adjusted logistic regression models were applied to estimate the association between air pollution and incident and prevalent symptoms of eczema. Weighted genetic risk scores were used to investigate the impact of atopic eczema related risk alleles on this association.

Results

Exposures to oxides of nitrogen (NO2 and NOx) and particulate matter (PM2.5 and PM10) were significantly associated with increased odds of incident eczema (e.g. with PM2.5 per 4.7μg/m3: OR=1.45, 95%CI: 1.06,1.99). These associations were slightly more pronounced with non-atopic eczema (e.g. with PM2.5 OR=1.65, 95%CI: 1.15, 2.34 for participants without hay fever or elevated IgE levels). Associations with air pollution were stronger in carriers of fewer risk alleles for atopic eczema.

Conclusion

Non-atopic eczema in the elderly is associated with traffic related air pollutants and this phenotype differs from genetically driven atopic eczema.



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