Wegener's granulomatosis: role of environmental exposures.
OBJECTIVE
The etiology of Wegener's granulomatosis (WG) remains unknown. The predominant involvement of the airways and the presence of neutrophilic alveolitis at disease onset have led us to postulate that an inhaled agent may trigger the onset of WG. This study is designed to analyze differences in self-reported environmental exposures between patients with WG and various control populations.


METHODS
We conducted a standard interviewer-administered questionnaire case controlled survey of 101 patients with WG, 54 healthy controls, 24 patients with sarcoidosis or idiopathic pulmonary fibrosis, and 45 patients with various inflammatory rheumatologic diseases. We assessed environmental exposures for one year prior to the onset of symptoms or prior to the interview date for healthy controls.


RESULTS
Seasonal differences in the onset of WG were not apparent. More than 75% of the patients in all groups noted remarkable environmental exposure to inhaled substances (fumes or particulate matter), within one year prior to disease onset for WG and other diseases or prior to the interview date for healthy controls. Differences between WG and control groups were apparent in several categories of exposure. Statistically significant differences occurred in regard to a vocational exposure to fumes or particulate materials (WG > healthy controls and rheumatic disease controls), residential exposure to particulate materials from construction (WG > pulmonary disease controls) and occupational exposure to pesticides (WG > healthy, pulmonary and rheumatic disease controls).


CONCLUSIONS
This study confirms the absence of seasonal differences in the onset of WG. It also demonstrates high rates of self-reported environmental exposures to inhaled substances in WG and all control populations. It is possible that more significant differences in the quality, quantity and intensity of exposure to inhaled potential precipitants of WG had occurred between groups, but were not detected by our survey. Alternatively, the absence of substantial differences in patients with WG and controls may reflect the more important role of host susceptibility factors.
Duna
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GF
Cleveland Clinic Foundation, Department of Rheumatic and Immunologic Diseases, Ohio, USA.
Cotch
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MF
Galperin
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Hoffman
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DB
Hoffman
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GS
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000393:Air Pollutants / Q000009:adverse effects*; D016022:Case-Control Studies; D002648:Child; D004198:Disease Susceptibility; D005260:Female; D014890:Granulomatosis with Polyangiitis / Q000453:epidemiology / Q000209:etiology*; D006801:Humans; D019570:Inhalation Exposure / Q000009:adverse effects*; D008297:Male; D008396:Maryland / Q000453:epidemiology; D008875:Middle Aged; D009820:Ohio / Q000453:epidemiology; D011658:Pulmonary Fibrosis / Q000453:epidemiology / Q000209:etiology; D012216:Rheumatic Diseases / Q000453:epidemiology / Q000209:etiology; D017565:Sarcoidosis, Pulmonary / Q000453:epidemiology / Q000209:etiology; D012621:Seasons; D012650:Self Disclosure; D011795:Surveys and Questionnaires
D000393:Air Pollutants