Aluminum is known to cause occupational asthma very rarely¹⁾. Some investigators^2–4) have reported asthmatic symptoms and the presence of nonspecific bronchial reactivity in potroom workers. Pot fume emissions include gaseous and particulate fluorides, alumina and carbon dusts, sulfur dioxide (SO2), carbon monoxide (CO) and particulate polycyclic organic matter. There are no distinctive respiratory sensitizers. However, workers exposed to aluminum fluoride have been shown to have increased bronchial reactivity and to develop asthma, which improves away from exposure⁵⁾.

Here we report a case of occupational asthma induced by aluminum powder.

More than 200 substances can cause occupational asthma⁸⁾, but metal asthma is a rare phenomenon. Metals that are known to cause asthma are nickel^9–12), platinum¹³⁾, chromium^11,14), cobalt^15,16), vanadium¹⁷⁾ and zinc⁸⁾. In 1985, Simonsson et al⁵⁾. reported two types, of aluminum salt (aluminum fluoride and sulfate) associated with occupational asthma. Kongerud and Soyseth¹⁹⁾ reported that the prevalence of work-related asthmatic symptoms in a cross-sectional study of 337 aluminum potroom workers was 9%. Bronchial hyperresponsiveness was noted in 12% of them. Female gender, past smoking history and airflow limitation were predictors of methacholine responsiveness. Our subject showed a significant bronchoconstriction after the inhalation of aluminum powder and AlCl₃ solution. Follow-up methacholine PC20 was decreased after the bronchoprovocation test. These data suggested that aluminum dust can induce occupational asthma in exposed patient.

Some investigators^11,20) have postulated that low-weight metal (less than 500 daltons of molecular weight) could act as haptens in vivo following conjugation with serum proteins to be antigens, and this has been shown for platinum³⁾, nickel¹⁴⁾, cobalt¹⁶⁾ and chromium¹¹⁾ at least in some exposed workers. Mackay et al²¹⁾. studied serum levels of IgM, IgG, IgA, immune complexes and IgE in 33 asthmatic and 127 non-asthmatic potroom workers. Asthmatic workers differed only by lower mean serum levels of IgM. There has been no report of specific IgE antibody to aluminum. Simonson et al⁵⁾. suggested that aluminum could irritate, the bronchial mucosa, increasing the excitability of irritant receptors and/or c-fibers, lowering the threshold to stimulants which result in the development of airway hyperresponsiveness²²⁾.

Knogerud et al^4,23) reported that subjects exposed for more than 10 years to aluminum are at higher risk for development of work-related dyspnea and wheezing. This effect of cumulative exposure may suggest that pathogenetic mechanisms due to irritants might be acting. They also reported that fluoride exposure and smoking could be related to asthmatic symptoms in potroom workers, whether or not this increased sensitivity is due to chemical irritation with an inflammatory reaction. We do not know whether the hypersensitivity is due to changes in the airway mucosa, the neural structures or the bronchiolar smooth muscles. Particulate materials of Al₂O₃, Fe₂O₃ and Cr₂O₃ can release histamine in vitro from rat peritoneal mast cells²⁴⁾. Such particulates may, thus, also act in an non-antigenic way on mast cells. Moreover, aluminum salts are known to change antigen sensitivity in animals. Indeed, in animal studies, aluminum increases the reactive capacity of mast cells and lung tissue to ovalbumin, an effect which is accompanied by increased levels of IgE or IgG2-antibodies. Such non-specific precipitation of allergy has not been established in humans, however, and Bergstrom et al²⁵⁾. had not noted a general increase of IgE response with aluminum-salt exposure. In our subject, the intradermal skin test as well as the prick test and a patch test with aluminum chloride solution were negative response. Total IgE level by PRIST was 180 IU/ml. These do not support an IgE-mediated sensitization process.

Neutrophilia had been noted in bronchoalveolar lavage fluid in the late asthmatic reaction induced by isocyanate challenge test²⁶⁾. Kay²⁷⁾ reported that peripheral blood mononuclear cells, from patients with severe acute asthma, generated significantly greater amounts of neutrophil chemotactic activity into the culture supernatant after 24 hours, as compared with all control groups which reduced after 1 week of therapy. Various kinds of inflammatory cells produce different types of neutrophil chemotactic factors from those of mast cells²⁸⁾. In our patient, post-challenge neutrophil chemotactic activity was markedly increased in comparison with that of pre-challenge time, which was blunted by sodium cromoglycate pretreatment. In other in vivo study, accumulation and activation of neutrophils, eosinophils and macrophages after allergen bronchial challenge were reduced by sodium cromoglycate²⁹⁾. These data suggested the possible role of neutrophils in the pathogenesis of aluminum-induced occupational asthma.

It is suggested that aluminum powder might induce bronchoconstriction, which was mediated by non-immunologic mechanism. Possible role of neutrophils in aluminum-induced bronchoconstriction was also suggested.