Occupational Interstitial Lung Diseases

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Asbestos-related pleural disease

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Asbestos-related pleural disease can occur in the absence of interstitial fibrosis. Pleural abnormalities include: pleural plaques, diffuse pleural thickening, pleural effusions, and rounded atelectasis. Pleural plaques are the radiographic hallmarks of asbestos exposure. They are circumscribed areas of fibrous thickening of the parietal pleura, and they are usually bilateral. Pleural plaques may calcify, but they do not usually cause symptoms or restriction of lung function. They have a latency of at least 20 years. Pleural effusions are the only manifestations of asbestos exposure seen with a latency of less than 10 years. They tend to resolve spontaneously and may recur. Diffuse pleural thickening is thought to represent residual scarring from pleural effusions. Diffuse pleural thickening affects the visceral pleura, is less common than pleural plaques, rarely calcifies, and may cause a restrictive defect of pulmonary function and dyspnea on exertion. Rounded atelectasis is a peripheral atelectasis resulting from formation of scar tissue in pleura and adjacent lung.

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Asbestosis

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The diagnosis of asbestosis depends on a history of exposure to asbestos dust, a latency of at least 10 years, and evidence of diffuse fibrosis and pleural plaques by chest x-ray or CT scan. The likelihood of the diagnosis is increased by the presence of a restrictive pattern on pulmonary function testing. The risk of developing asbestosis is directly related to the cumulative dose. Bibasilar rales is the typical physical finding in patients with asbestosis. Dyspnea on exertion is the primary symptom. Asbestos insulators, shipyard workers, and other workers heavily exposed to asbestos in the past have an increased risk for asbestosis, lung cancer, and malignant mesothelioma. High-resolution computerized tomography (HRCT) is more sensitive than conventional radiography in detecting asbestosis. Findings by HRCT include interstitial lines, subpleural curvilinear lines, parenchymal bands, and honeycombing. Normal and abnormal values exist for sputum and lung lavage samples (asbestos bodies) and lung tissue (asbestos bodies and fiber counts). [Harber, p. 93-96, 297-310] Medical surveillance is required if exposed above the PEL >30 days per year or if must wear negative pressure respirator when working with asbestos. [Rosenstock, p. 1266] Of 706 retired workers with an average age of 65 years and a history of occupational asbestos exposure, the mean duration of asbestos exposure was 25 years with a mean cumulative-exposure index (CEI) of 140 fibers/ml x years. The study found a fibrosis threshold of 25 fibers/ml x years in that only 2 cases of HRCT asbestosis were found in 112 workers under this threshold. No cases of HRCT asbestosis were found in the 52 workers below the threshold and with no signs or symptoms of asbestosis. [Paris C, et al. Factors associated with early-stage pulmonary fibrosis as determined by high-resolution computed tomography among persons occupationally exposed to asbestos.

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Chronic beryllium disease

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In addition to dyspnea, cough, fatigue, anorexia, and weight loss, symptoms of CBD may include fever, arthralgias, and chest pain. The typical chest x-ray findings in CBD are small nodular opacities throughout the lung fields, and mediastinal lymphadenopathy is present in about 1/3 of cases. Conglomerate masses and pleural reactions are seen in advanced cases. In addition to the above, the CT detects septal lines and areas of ground-glass attenuation. Pulmonary function studies show obstruction or mixed obstruction/restriction with restriction predominating in more advanced disease. Over 1/2 of workers who have an abnormal BeLPT develop chronic beryllium disease.

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Coal workers' pneumoconiosis

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Simple coal workers' pneumoconiosis (CWP) is defined by the presence of small lung opacities that develop after at least ten years of exposure to coal dust. The disease is rarely seen in miners who have spent less than 20 years underground. Workers are often asymptomatic with normal pulmonary function studies. Chest x-ray findings resemble those of simple silicosis. Studies of miners with simple CWP have not shown increased mortality rates.

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Hard metal disease

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Hard metal disease is a "giant cell interstitial pneumonitis" that affects a small minority of workers who manufacture or use high-speed tungsten carbide saw tips, drill tips, or discs. These tools are used to polish diamonds and to cut hard materials such as metals, hardwoods, and cement. The workers are exposed to fume or dust from the cobalt used as a binder in the cemented tungsten carbide metal. The usual symptoms are dyspnea on exertion, cough, and fatigue. The chest x-ray may show infiltrates, and the pulmonary function test may reveal a restrictive defect. The same workers are at risk for cobalt-induced asthma.

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Hypersensitivity pneumonitis

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Acute presentation: flu-like illness with cough;
Subacute: recurrent "pneumonia";
Chronic: exertional dyspnea, productive cough, and weight loss;
Most patients have abnormal imaging studies (chest x-ray or high-resolution CT). Crepitant rales are heard in some cases. Pulmonary function testing shows a restrictive defect in early disease and a restrictive, obstructive or mixed defect in late disease. Precipitating antibodies are neither sensitive nor specific, and their presence is no longer considered a hallmark of HP. Some patients have decreased diffusion capacity and arterial hypoxemia. If the diagnosis is in doubt, bronchoalveolar lavage (BAL) typically shows lymphocytosis. Surgical lung biopsy may be indicated if bronchoscopy is nondiagnostic. The disease latency varies from a few weeks to years after first exposure. Symptoms appear or worsen within a few hours of antigen exposure to bioaerosols of microbial or animal antigens or rarely to a few reactive chemicals. Complete recovery usually occurs if exposure is terminated early. Otherwise, the disease may progress to interstitial fibrosis.

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Pneumoconioses, benign

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The most common benign pneumoconioses are siderosis (iron), stannosis (tin), and baritosis (barium). Chest x-rays of workers with benign pneumoconioses show small opacities caused by lung retention of one of these radiopaque metals. Workers are asymptomatic and have normal pulmonary function studies. The x-ray changes gradually resolve after the workers are removed from exposure. Tin and barium miners may also be exposed to silica. [Rom, p. 526, 537; Rosenstock, p. 410] Other metals with high radiodensity that can potentially produce benign pneumoconioses are titanium, vanadium, zirconium, antimony, hafnium, and the rare earth metals.

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Pneumoconioses, other

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Occupational mineral dust exposures can be broadly categorized as strongly fibrogenic dusts (silica, asbestos, and coal) and other mineral dusts (emery, graphite, gypsum, marble, mica, perlite, plaster of Paris, Portland cement, silicon, silicon carbide, soapstone, and talc) that may also be associated with adverse lung effects. The authors of a 1990 review concluded that (1) there is little evidence that occupational exposure to pure kaolin, talc, mica, or vermiculite carries any important risk for health; (2) long and heavy exposure to kaolin and mica may result in low-grade radiographic changes, but clinically important pneumoconioses in work forces exposed to these phyllosilicates are likely to be the result of contamination by silica or asbestos fiber. It is suspected that this lung airway defense system can be overcome by several different mechanisms: by the physical characteristics of the particle that prevent phagocytosis or cell movement, as seen in asbestosis; by direct cytotoxicity, as in the case of silica dust or cytoxic metals and compounds; or by simply overloading the clearance capacity of the system, which is most likely the mechanism of injury from normally non-fibrogenic 'nuisance' dusts.

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Silicosis, complicated

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Complicated silicosis refers to the development of progressive massive fibrosis (PMF) in which pulmonary nodules (typically 2-6 mm in diameter) coalesce into larger conglomerations. PMF has been observed to develop in a small percentage of patients with simple chronic silicosis and a large percentage of patients with accelerated silicosis. Accelerated silicosis is similar to simple silicosis, but the disease develops after a heavier exposure over a shorter time period. The latency is 2 to 5 years for accelerated silicosis, versus greater than 10 years for simple silicosis. Accelerated silicosis follows a course of increasing dyspnea.