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Abstract

Abstract

The prevalence and incidence of allergic respiratory diseases have increased in Europe during the last decades, as in most industrialized countries in other parts of the world. Persistent exposure to traffic related air pollution and especially particulate matter from motor vehicles has often been discussed as one of the factors responsible for this increase. It has been recently suggested by many epidemiological studies that traffic related air pollution may increase allergic symptoms and illnesses like asthma and allergic rhinitis, although for allergic sensitisation less consistent results have been found. This view seems to be supported by recent human and animal laboratory-based studies which have shown that particulate pollutants, and in particular diesel exhaust particles, can enhance allergic inflammation and induce the development of allergic immune responses. Indeed, recent in-vivo and in-vitro studies strongly suggest that diesel exhaust particles (DEP) induce pro-inflammatory products by activating their transcription. If pollutants are to be controlled in the urban environment in a cost-effective manner, it is important that the molecular targets of DEP-induced responses be elucidated. In particular, bronchial epithelial cells are the key regulators of airway inflammation, and therefore it is crucial to clarify the cellular and molecular mechanisms that are activated by DEP in these cells. Based on the available experimental and epidemiological studies, the World Health Organisation concluded cautiously that traffic related air pollution may increase the risk of allergy development and may exacerbate symptoms in particular in susceptible subgroups, although there are still many open questions.

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/content/papers/10.5339/qproc.2012.mutagens.3.3
2012-03-01
2019-10-17
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http://instance.metastore.ingenta.com/content/papers/10.5339/qproc.2012.mutagens.3.3
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  • Received: 07 May 2012
  • Accepted: 07 May 2012
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