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Hypothesis for Induction and Propagation of Chemical Sensitivity Based on Biopsy Studies

William J. Meggs
Environmental Health Perspectives
Vol. 105, Supplement 2: Chemical Sensitivity (Mar., 1997), pp. 473-478
DOI: 10.2307/3433355
Stable URL: http://www.jstor.org/stable/3433355
Page Count: 6
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Hypothesis for Induction and Propagation of Chemical Sensitivity Based on Biopsy Studies
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Abstract

The reactive airways dysfunction syndrome (RADS), the reactive upper airways dysfunction syndrome (RUDS), the sick building syndrome (SBS), and the multiple chemical sensitivity syndrome (MCS) are overlapping disorders in which there is an intolerance to environmental chemicals. The onset of these illnesses is often associated with an initial acute chemical exposure. To understand the pathophysiology of these conditions, a study of the nasal pathology of individuals experiencing these syndromes was undertaken. Preliminary data indicate that the nasal pathology of these disorders is characterized by defects in tight junctions between cells, desquamation of the respiratory epithelium, glandular hyperplasia, lymphocytic infiltrates, and peripheral nerve fiber proliferation. These findings suggest a model for a relationship between the chronic inflammation seen in these conditions and an individual's sensitivity to chemicals. A positive feedback loop is set up: the inflammatory response to low levels of chemical irritants is enhanced due to the observed changes in the epithelium, and the epithelial changes are propagated by the inflammatory response to the chemicals. This model, combined with the concept of neurogenic switching, has the potential to explain many aspects of RADS, RUDS, SBS, and MCS in a unified way.

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