Nasal Pathology in Patients with Chronic Airway Inflammation
Jule Klotter
A single acute exposure to dust, smoke, or chemicals such as acetic acid, ammonia, chlorine, ethylene oxide, and sulfur dioxide can cause an asthma-like condition known as reactive airways dysfunction syndrome (RADS). Bronchoscopic lung biopsies in patients with RADS show epithelial damage, chronic inflammation with lymphocytic infiltrates, and basement membrane (underlies the epithelium) thickening. Exposure to solvents and pesticides have caused a similar condition called reactive upper airways dysfunction syndrome (RUDS). A report in Clinical Toxicology by William J. Meggs, MD and colleagues at East Carolina University School of Medicine (Greenville, North Carolina) presents findings on the nasal pathology and ultrastructure of the nasal mucosa in 13 patients who developed RUDS after an occupational exposure to chlorine dioxide.
The researchers evaluated the patients five years after the chlorine dioxide exposure. They reviewed the patients’ medical records and test results, had the patients fill out a standardized questionnaire concerning complaints of chemical sensitivities and lifestyle changes, and performed nasal examinations with a nasal telescope, and nasal biopsies. These results were compared to similiar evaluations of three non-symptomatic volunteers. Nasal examination of the patients found abnormalities that included congestion, telangiectasia (dilation of capillaries producing an angioma, a usually benign tumor), paleness, cobblestoning, edema, and thick mucous. Nasal biopsies from the patients showed congestion and edema and mild to severe inflammation.
Nerve fibers were found in the biopsies of several patients; the greatest number of fibers appeared in the patient with severe inflammation. Electron micrographs from patients showed abnormal spaces between epithelial cells, while those from the normal patients did not. Detachment of respiratory epithelial cells from the basement membrane was also evident in some cases. Unlike patients with allergic rhinitis, the patients with RUDS showed an increase in lymphocytes and no increase in eosinophils.
Dr. Meggs and colleagues suggest that chronic airway disease may result from an interaction between the irritant chemical and sensory nerves, producing neurogenic inflammation (accounting for the presence of lymphocytes) as well as damage to the respiratory mucosa. Epithelial damage and the proliferation of nerve fibers may be the cause of sensitivity to low levels of chemical irritants.
“Nasal Pathology and Ultrastructure in Patients with Chronic Airway Inflammation (RADS and RUDS) Following an Irritant Exposure” by William J. Meggs, MD; Tarik Elsheik, MD; W. James Metzger, MD; Marcus Albernaz, MD; Richard M. Bloch, PhD. Clinical Toxicology, 34(4), 383-396 (1996).
COPYRIGHT 2001 The Townsend Letter Group
COPYRIGHT 2001 Gale Group
