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A 50-y-old male worker developed an asthmatic reaction after exposure to bichromate in a metal-plating plant. Evaluation included skin tests, bronchial provocation tests, and specific radioallergosorbent tests with metal salts. A 49-y-old worker who suffered from hard metal asthma was the control. These workers were not atopic, and they exhibited similar bronchial hyperresponsiveness in methacholine-PC20 (74 mg/ml versus 81 mg/ml, respectively) and IgE titers (129 IU/ml versus 130 IU/ml). Positive intradermal and patch tests to bichromate were found in the subject. A bronchial provocation test with inhalation of .01 % bichromate produced an immediate decrease in forced vital capacity in 1 s, followed by a rapid recovery within 5 min absent any treatment. There was no reaction to cobalt (1% cobalt chloride) or to nickel (2% nickel sulfate) salts. In the control, a positive bronchial provocation occurred (absent chromium) with cobalt and nickel. Administration of a subcutaneous preparation of 1 mg atropine sulfate or of 1 puff of disodium cromoglycate or beta-stimulant reduced bronchial responsiveness to methacholine-PC20, and no asthmatic reaction occurred following inhalation of 1% bichromate. No blocking of asthmatic reaction occurred after pretreatment with beclomethasone dipropionate inhalation. Administration of propranolol, however, potentiated the acute bronchoconstriction induced by bichromate. The 50-y-old worker had evidence of IgE antibody to chromium-conjugated human serum albumin and to chromium-conjugated exchange resin. His serum selectively bound 51Cr, but antibodies specific to cobalt and nickel were absent. These results, if viewed collectively, suggest that bichromate exposure causes brief reversible bronchospasm via alteration of autonomic balance and increased vagal activation.