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Review
. 2011 Sep;26(3):262-73.
doi: 10.3904/kjim.2011.26.3.262. Epub 2011 Sep 13.

Impact of air pollution on allergic diseases

Affiliations
Review

Impact of air pollution on allergic diseases

Hajime Takizawa. Korean J Intern Med. 2011 Sep.

Abstract

The incidence of allergic diseases in most industrialized countries has increased. Although the exact mechanisms behind this rapid increase in prevalence remain uncertain, a variety of air pollutants have been attracting attention as one causative factor. Epidemiological and toxicological research suggests a causative relationship between air pollution and the increased incidence of asthma, allergic rhinitis, and other allergic disorders. These include ozone, nitrogen dioxide and, especially particulate matter, produced by traffic-related and industrial activities. Strong epidemiological evidence supports a relationship between air pollution and the exacerbation of asthma and other respiratory diseases. Recent studies have suggested that air pollutants play a role in the development of asthma and allergies. Researchers have elucidated the mechanisms whereby these pollutants induce adverse effects; they appear to affect the balance between antioxidant pathways and airway inflammation. Gene polymorphisms involved in antioxidant pathways can modify responses to air pollution exposure. While the characterization and monitoring of pollutant components currently dictates pollution control policies, it will be necessary to identify susceptible subpopulations to target therapy/prevention of pollution-induced respiratory diseases.

Keywords: Air pollutants; Antioxidant; Asthma; Particulate matter; Vehicle emissions.

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Conflict of interest statement

No potential conflict of interest relevant to this article was reported.

Figures

Figure 1
Figure 1
The transcription factor nuclear factor-like 2 (Nrf-2) plays an important role in cellular defense mechanisms against a variety of oxidant stresses, such as diesel exhaust fumes. ARE, antioxidant response element; EpRE, electrophile response element; Keap1, Kelch-like ECH-associated protein 1.

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