Air pollution, genetics, and allergy: an update : Current Opinion in Allergy and Clinical Immunology (original) (raw)

GENETICS AND EPIDEMIOLOGY: Edited by Catherine Laprise and Emmanuelle Bouzigon

an update

aAir Pollution Exposure Laboratory, Department of Medicine, University of British Columbia

bSchool of Population and Public Health, University of British Columbia, Vancouver, British Columbia, Canada

cInstitute of Environmental Medicine, Centre for Allergy Research, Karolinska Institutet

dAstrid Lindgren Children's Hospital, Karolinska University Hospital, Stockholm, Sweden

Correspondence to Chris Carlsten, 7th floor, The Lung Centre, 2775 Laurel Street, Vancouver, BC, Canada V5Z 1M9. Tel: +1 604 875 4729; fax: +1 604 875 4727; e-mail: [email protected]

Abstract

Purpose of review

Air pollution has been increasingly associated with diverse adverse health outcomes, including airway diseases. Data suggest that gene–environment interactions are important in this context. However, evidence regarding causal effects of exposure and development of allergic conditions specifically remains immature. We review the developments of the past 18 months regarding air pollution, genetics and epigenetics, and allergy.

Recent findings

Conflicting evidence for air pollution as causative in the development of allergic disease persists. However, recent data support the associations between long-term exposure to traffic-related pollutants and newly developed sensitization in children. Studies from India and China demonstrate the global burden of health-related costs attributed to air pollutants and allergic diseases. The effect of exposure seems to be modified by coexposures of allergens as well as genetic variants, particularly those moderating response to oxidative stress. Potential links between exposures and epigenetic (DNA methylation) changes with consequences for disease development are also reinforced.

Summary

Data over the past 18 months support prior literature that air pollutants cause exacerbation, and possibly onset, of allergic disease. Regarding the onset of asthma specifically, the evidence of causality has grown significantly, but it remains difficult to separate allergic from nonallergic asthma. Effect of modification by genetic variants and epigenetic changes warrants further study.