Global increases in allergic respiratory disease: the possible role of diesel exhaust particles.
OBJECTIVE
Reading this article will enable the readers to recognize and evaluate i e potential relationship between allergic respiratory disease and polyaromatic hydrocarbons as air pollutants from industrial and automotive fuel sources. In this article we review the long-term trends in the prevalence of allergic airway diseases (rhinitis and asthma). We then examine the epidemiologic and other research data relating to the role that hydrocarbon fuel emissions may have had on allergic respiratory disease.


METHODS
Published literature on the relationship between specific air pollutants and trends in allergic respiratory disease were reviewed. Reports of research on pollutant effects on allergic antibody (IgE) were also studied. In both cases, the Melvyl-Medline database since 1975 was used for literature searches. Older references were identified from the bibliographies of relevant articles and books and with the help of the rare books collection at UCLA's Louis M. Darling Biomedical library.


RESULTS
Examination of the historical record indicates that allergic rhinitis and allergic asthma have significantly increased in prevalence over the past two centuries. Although the reasons for this increase are not fully elucidated, epidemiologic data suggest that certain pollutants such as those produced from the burning of fossil fuels may have played an important role in the prevalence changes. Also important are studies showing that diesel exhaust, a prototypical fossil fuel, is able to enhance in vitro and in vivo IgE production.


CONCLUSIONS
Increased levels of the compounds resulting from fossil fuel combustion may be partly responsible for the increased prevalence of allergic respiratory disease. If the nature of these compounds and the mechanisms by which they exacerbate allergic disease can be identified, steps can be taken to reduce the production or the impact of these allergy producing compounds.
Peterson
B
B
Hart and Louise Lyon Laboratory, USA.
Saxon
A
A
D006801:Humans; D010316:Particle Size; D012130:Respiratory Hypersensitivity / Q000209:etiology*; D001335:Vehicle Emissions / Q000009:adverse effects*
D001335:Vehicle Emissions