The Bulletin of the Society of Pharmacological and EnvironmentalPathologists PULMONARY ALUMlNOSlS -*A REVIEW Tee L. Guidotti, M. D. Fellow, Department of Medicine The Johns Hopkins University School of Medicine Baltimore, MD 21205 Although aluminum is not considered a highly toxic sub- stance, it has been associated with a pneumoconiosis under certain circumstances of exposure (1:9). As a metal powder, the element also has unusual and unexplained properties which modify the course of pulmonary fibrosis in silicosis(l0-16). Our industrial society is using increasing quantities of alumi- num, and chemical research and development are contributing special handling techniques, processing, and methods of dis- persing aluminum-containing compounds. Opportunities for worker, consumer, and even community exposure therefore will increase in number and variety. EXPOSURE AND CLINICAL PRESENTATION The normal lung contains about 2,500 (+,180) pg of alumi- num per gram of wet tissue. Aluminum, titanium, and van- adium behave similarly as relatively insoluble metallic con- tam in an^ of lung, unlike lead which migrates rapidly in its soluble inhaled form(l7). Pulmonary disease resulting from inhalati~n of aluminum powder was first described in 1934 by both Baader in Germany(9) and Filipo in Italy(l), working inde~~ndently. Shaver contributed the series of Canadian alumina abrasive manufacture workers, which led to their occupational pneu- moconiosis being named "Shaver's disease"(3). The contem- porary states of knowledge have been p!esented by extensive reviews between 1938 and 1956(2,20,21,33) and in case reports since(6AW. Pulmonary aluminosis has been shown not to result from exposure to ambient particulate aluminum resulting from grinding operations(22) nor from the manufacture of aluminum powder for paints(23). Rather, reported cases have resulted from bauxite (A1203.3H20) fumes, alumina abrasive manu- facture(3). and the process of repetitively stamping bar metal under lubricant to yield an extremely finely divided powder known, as "pyro"f4,6*9). JPyro is used in the manufacture of munitions, flares, and fireworks. Workers exposed to pyro have developed symptoms in as short a period as three and one-half years(4) to as long as thir- teen and one-half years(8). Several years may pass between cessation of exposure and the onset of symptoms(9). Typically, dyspnea is the presenting complaint. Chronic nonproductive cough is common, occasionally provoking hemoptysis. Pleu- ritic pain may be present, but diffuse substernal distress is more common. Diaphragmatic excursion and chest wall motion are reduced. Breath sounds are harsh, prominent rales. The trachea, the mediastinal structures, and the diaphragm are distorted by traction in advanced cases. Bilateral, fine opaque foci may be scattered throughout both lung fields on the chest film and may aggregate into linear striations. Alter- natively, a diffusely grainy or a reticular pattern may be evi- dent. Pulmonary function studies reveal a predominantly restrictive pattern wiih accompanying obstructive airway dis- ease and .impaired diffusing capacity. Lung bullae.rnay de- velop, and spontaneous, sometimes bilateral and fatal, pneu- 16 mothoraces occur in advanced cases(4.5-9,21). The basic patho- logic process of pulmonary fibrosis is frequently progressive and ultimatelv may be fatal from respiretorvfailure(6). pulmon- ary hypertension and cor p~lmonaIe(4-6~~), and broncho- pneumonia(8). The differential diagnosis includes all causes of interstitial fibrosis, which are myriad. The usual patient's occupational and clinical history often suggests silicosis, asbestosis, complicated coal workers' pneumoconiosis (in previous miners), tuberculosis, usual interstitial pneumonia (idiopathic type), and the related Hamman-Rich syndromeflg). Findings at necropsy include diffuse interstitial fibrosis. Bauxite workers in particular present especjally severe fibrosis with large bands of fibroticscar in rays(19). Bullous emphysema and structural deformation by traction may be severe. Sub- cutaneous injection of aluminum hydroxide into the skin results indiscretegranulomata(24) and local inflammation with an infiltrate of rnonocytes and macroph~es(25), which may reflect the sequence of reaction in the alveolar septa. The alumjnum content of the ashed lung is elevated, and aluminum is also demonstrable intracheobronchiallymph node~(4,6,8#~). A bizarre encephalopathy has been described in a patient following thirteen and a half years of very brief intermittent exposure to pyro. This patient suffered from seizures, aphasia, and rapidly progressive dementia. A t necropsy, mod- erate diffuse cerebral atrophy was seen without the stigmata of Alzheimer's or Pick's diseases. Levels of aluminum 20 times the normal were found in samples of lung and brain@).Alumi- num oxide gel applied directly to the cerebral hemispheks of experimental animals produces severe, recurrent seizures and has been developed as a model of motor epilepsy(8t26). Alumi. num-induced dementia in cats is similar behjlviorly to human presenile dementia, and patients with Alzheimer's disease are known to have elevated cerebral aluminum tevels(27). The neurofibrillary degeneration peculiar to Alzheimer's disease has not been reproduced experimentally with aluminum, however. It is not clear whether aluminum accumulation is a consequence or a contributing factor to the disease. Another patient developed rheumatoid arthritis at a very young age, possibly a convergence with Caplan's syndrome of rheumatoid arthritis and coal workers' pneumoconiosis(28). Similar associations have been reported in other pneumoconio- Experimental inhalation of a glycol complex of aluminum- chloride-hydroxide in development for use in antiperspirant sprays has been associated with granulomas in the lungs of hamsters repeatedly exposed t o 50 mg/m3 of the compound. These lesions were observed to be localized to the transi- tional region from terminal to respiratory bronchiole. Marked but reversible alveolar septa1 thickening and interstitial macro- phage infiltration were noted acutely following three expo- sures to 150 mg/m3 of the compound(43).Additional studies with slightly different chemical systems are in progress. (Robert T. Drew, personal communication, 1974.) By impli- cation, these products could represent a substantial source of community consumer exposure to inhaled aluminum. seS(29). PROBLEMS IN PATHOPHYSIOLOGY The recommended maximum allowable con cent ratio^ of alumina (A12031 in the workplace is 50 x 106 partictes/ft3, a standard informally applied to aluminum metal as well(3o). Aluminum paint powder is only composed 11%of particles in
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