SPECIFIC ENTITIES - DISEASES WITH KFiOWIi ETIOLOGIES -



Pneumoconioses are lung diseases produced by the inhalation of inorganic dust. These dusts may be fibrous minerals, such as asbestos, or nonfi-brous minerals, like silica or metals. The clinical spectrum varies widely according to the nature of the inhaled substance and the type of response it evokes in the lung. Some substances such as as­bestos lead to progressive fibrosis, while others such as iron dust produce little or no reaction even when deposited in large amounts. The com­mon organic dusts are listed in and are divided according to their structure and fi-brogenic potential.

Among the fibrous minerals, asbestos is the most important health hazard , The pulmonary fibrosis (asbestosis) is dose-depen­dent, while diseases in the pleural space do not seem to be related to the intensity of exposure. In addition to pulmonary fibrosis and benign pleural disease, there is a five-fold increase in the rate of bronchogenic carcinoma among nonsmoking as­bestos workers when compared to a nonsmoking control population. Among smoking asbestos workers the risk is 60- to 90-fold. Malignant mes­otheliomas of the pleura and peritoneum are also associated with asbestos exposure but bear no ap­parent relationship to smoking. There is a pro­longed latency period between the exposure and the development of the tumors, usually at least 20 years and sometimes as long as 30 to 40 years.

Deposition of coal dust around the first- and second-order respiratory bronchioles causes coal workers’ pneumoconiosis or “black lung.” This may be accompanied by minimal inflammation but is insufficiently severe to cause symptoms or measurable physiological derangement in most workers. Simple pneumoconiosis consisting of a fine, diffuse reticulonodular pattern seen on chest roentgenogram and a productive cough develop in 5 per cent of coal workers. Physiological im­pairment when present is slight. In a smaller num­ber of miners, perhaps 0.4 per cent, nodular den­sities of 1 cm or .greater may be present on chest x-ray, representing dense collagenous nodules (complicated coal workers’ pneumoconiosis). Un­like the simple form, this can eventually result in progressive massive fibrosis and restrictive lung disease.

The pulmonary response to a more fibrogenic dust, such as silica, is dramatically magnified. Sil­ica exposure occurs in most mining operations,sandblasting, pottery working, brick making, and foundries. In most cases, silicosis develops after at least 20 years of exposure, although it can de­velop in 5 years or less with intense exposure to a high concentration of dust. Roentgenographic gradation of disease ranges from small diffuse nodules with minimal hilar node enlargement to large nodules, predominantly in the upper lobes, that vary from about 1 cm to conglomerate masses occupying most of a lobe (progressive massive fi­brosis). Eggshell calcification of the hilar nodes is characteristic. The chest x-ray findings do not cor­relate well with the symptomatology and physi­ological impairment in silicosis. The course of the disease may be modified by other factors such as coexisting smoke or superinfection with myco­bacterial disease, either M. tuberculosis, M. intra-cellulare, or M. kansasii. The more acute the sil­icosis, the more likely it will be complicated by tuberculosis.

No specific treatment exists for any pneumo­coniosis, and only removal from the offending en­vironment may modify the eventual progression to respiratory failure. A careful and repeated search for mycobacterial disease is mandatory in silicosis, especially with sudden worsening of the condition. Cessation of smoking, aggressive treat­ment of routine bacterial infections, and the use of oxygen to treat complicating cor pulmonale may improve function and prolong life.