Clin Chest Med 1981 May; 2(2):255-272
Occupational asthma is reviewed. The induction of asthmatic reactions in the workplace is considered. Reflex bronchoconstriction may be produced by exposure to irritant or toxic pollutants in the workplace. Inflammatory mediators associated with late onset asthma may be generated by activation of the classical and alternate pathways of serum complement with or without a preceding immune reaction. Major pathophysiologic factors in occupational asthma include: reflex bronchoconstriction, inflammatory bronchoconstriction, activation of complement, direct pharmacologic effects, or immediate hypersensitivity responses induced by allergenic substances. The enhancement of mediator release from mast cells is illustrated. Specific etiologic factors are considered in the context of the pathophysiologic basis of occupational asthma. Occupational causes of reflex bronchoconstriction are outlined. Some causes of inflammatory bronchoconstriction are detailed. Pharmacologic agonists are listed by industry. Organic and inorganic compounds of varying molecular weight that occur as occupational allergens are tabulated. Occupational dusts that cause asthma by mixed mechanisms are examined. Essential components of the occupational asthma model are illustrated. An epidemiological evaluation of occupational asthma is discussed. Processes involved in the clinical determination of occupational asthma are evaluated. Treatment and prevention techniques are presented in terms of pharmacologic and immunologic management procedures, control measures for prevention of asthma, and reduction of disability.
NIOSH-Publication; Respiratory-hypersensitivity; Physiological-response; Employee-exposure; Airborne-dusts; Aerosol-particles; Toxic-vapors; Occupational-exposure; Occupational-respiratory-disease; Immune-reaction
Clinics in Chest Medicine
Internal Medicine University of Cincinnati 231 Bethesda Avenue Cincinnati, Ohio 45267