Grain fever syndrome induced by inhalation of airborne grain dust.

To study the clinical and physiologic manifestations of the grain fever syndrome and the potentially pathogenic role of complement activation, 12 subjects (six grain workers and six healthy non-grain workers) underwent inhalation provocations with airborne grain dust. The clinical response was characterized by facial warmth, headache, malaise, myalgias, feverish sensation, chilliness, throat and tracheal burning sensation, chest tightness, dyspnea, cough, and expectoration. Fever developed in four grain workers and two controls. Leukocytosis, ranging between 11,700 and 24,300 leukocytes/mm3 with left shift, developed in five grain workers and five controls. There was no evidence of complement activation by the classical or alternate pathway. None of the subjects had serum precipitins to grain dust. The pulmonary response was characterized by a decrease in FEV1, FVC, MMF, Vmax50, and Vmax75, with significant rise in pulmonary resistance and consistent change in dynamic compliance but without changes in static compliance or diffusing capacity. Hence, grain dust inhalation induced diffuse airways obstruction without detectable parenchymal reaction. The airways response to high concentrations of grain dust inhalation were unrelated to the presence of immediate skin hypersensitivity. Although we cannot exclude the etiopathogenetic role of an immunologic reaction to grain dust, our data do not support the hypothesis that the grain fever syndrome is a precipitin-mediated allergic pneumonitis. More likely, the manifestations of grain fever probably reflect the host reaction to grain dust bacterial endotoxins and/or nonallergic mediator release by grain or grain dust constituents.