Objective The etiology of Wegener's granulomatosis (WG) remains unknow
n. The predominant involvement of the airways and the presence of neut
rophilic alveolitis at disease onset have led us to postulate that an
inhaled agent may trigger the onset of WG. This study is designed to a
nalyze differences in self-reported environmental exposures between pa
tients with WG and various control populations. Methods We conducted a
standard interviewer-administered questionnaire case controlled surve
y of 101 patients with WG, 54 healthy controls, 24 patients with sarco
idosis or idiopathic pulmonary fibrosis, and 45 patients with various
inflammatory rheumatologic diseases. We assessed environmental exposur
es for one year prior to the onset of symptoms or prior to the intervi
ew date for healthy controls. Results Seasonal differences in the onse
t 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 c
ategories of exposure. Statistically significant differences occurred
in regard to avocational exposure to fumes or particulate materials (W
G > healthy controls and rheumatic disease controls), residential expo
sure to particulate materials from construction (WC > pulmonary diseas
e controls) and occupational exposure to pesticides (WG > healthy, pul
monary and rheumatic disease controls). Conclusion This study confirms
the absence of seasonal differences in the onset of WG. It also demon
strates high rates of self-reported environmental exposures to inhaled
substances in WG and all control populations. It is possible that mor
e significant differences in the quality, quantity and intensity of ex
posure to inhaled potential precipitants of WG had occurred between gr
oups, but were not detected by our survey Alternatively, the absence o
f substantial differences in patients with WG and controls may reflect
the more important role of host susceptibility factors.