SILICOSIS

S. K. HALDER

INTRODUCTION

Silicosis is a fibrotic disease of the lung caused by the inhalation of crystalline silica. Despite extensive knowledge about the cause of this pneumoconiosis (respiratory exposure to silica-containing dusts), this serious and potentially fatal occupational lung disease is tragically still seen even today, in the last part of the century in the United State and throughout the world. Silica, or silicon dioxide, is the predominant component of the earth’s crust. The three important crystalline form of silica are quartz, tridymite, and cristobalite. These forms are also called free silica to distinguish them from the silicates. The silica content¹ in different rock formations, such as sandstone, granite, and slate, varies from 20% to nearly 100%. Occupational exposure to silica particles of respirable size (0.5 to 5 micrometer) is associated with mining, quarrying, drilling and tunneling operation. Silica exposure is also a potential hazard to sandblasters, stonecutters and pottery, foundry, ground silica and refractory workers. The national or worldwide prevalence of silicosis is unknown but more than 2 million workers in the United State alone are employed in trades at risk for the development of silicosis; in the developing world, cumulative estimates exceed 1 million cases of the disease.

Dry Drilling in Sandstone

Silica exposure in the agate & quartz grinding industries, India, (Courtesy Dr. H.N.Saiyed)

The precise pathogenic mechanism for the development of silicosis remains uncertain. Abundant evidence implicates the interaction between pulmonary alveolar macrophages and silica particles deposited in the lung. It is proposed that surface properties of the silica particle activate macrophage. These cells then release chemotactic factors and inflammatory mediators that result in a further cellular response by polymorphonuclear leukocytes, lymphocytes and additional macrophages. Fibroblast-stimulating factors are released that promote hyalinization and collagen deposition. The resulting pathologic silicotic lesion is the hyaline nodule, which contains a central acellular zone with extra cellular silica surrounded by whorls of collagen and fibroblasts and an active zone composed of macrophages, fibroblasts, plasma cells and additional extra cellular silica. Impaired macrophage function also plays a role in susceptibility to infectious organisms such as Mycobacterium tuberculosis and Nocardia asteroids.

Silicotic Nodule (Courtesy Dr. Jack Parker)

There is mounting evidence that freshly fractured silica may be more toxic than aged silica, perhaps related to reactive radical groups on the cleavage planes of freshly fractured silica. This may offer a pathogenic explanation for the observation of cases of advanced disease in both sandblasters and rock drillers where exposure to recently fractured silica is particularly intense.

FORMS OF DISEASE: CLINICAL PICTURE

Chronic silicosis is often asymptomatic and presents as a radiographic abnormality with small (<10mm), rounded opacities predominantly in the upper lobes. A history of 15 years or more since onset of exposure is common. Results of pulmonary function testing may be normal or may show mild restriction. Less commonly, mild obstruction to airflow or reduced diffusing capacity may be present. Chronic nodular silicosis not frequently progresses to more advanced disease or progressive massive fibrosis.

Complicated silicosis, also called progressive massive fibrosis, is more likely to present with exertional dyspnoea. Progressive massive fibrosis is characterized by nodular opacities greater than 1 cm on the chest radiograph and commonly involves reduced carbon monoxide diffusing capacity, reduced arterial oxygen tension at rest or with exercise and marked combined obstruction and restriction on spirometry or lung volume component.Distortion of the bronchial tree may also lead to airways obstruction and productive cough. Recurrent bacterial infection not unlike that seen in bronchiectesis may occur. Weight loss and cavitation of the large opacities should prompt concern for tuberculosis or other mycobacterial infection.

Chronic Silicosis

Pneumothrox may be a life-threatening complication, because the fibrotic lung may be difficult to re-expand. Hypoxemic respiratory failure with cor pulmonale is a common terminal event.

PMF

Accelerated silicosis may appears after more intense exposures of shorter (5 to 10 years) duration. Symptoms, radiographic findings and physiologic measurements are similar to those seen in the complicated form. Deterioration in lung function is more rapid and some countries, as many as 25% of patients with accelerated disease may develop mycobacterial infection. Autoimmune diseases, including scleroderma and rheumatoid arthritis are seen with silicosis, often of the accelerated type. The progression of radiographic abnormalities and functional impairment can be rapid when autoimmune disease is associated with silicosis. Acute silicosis may develop within 6 months to 2 years of massive silica exposure. Dramatic dyspnoea, weakness, and weight loss are often presenting symptoms. The radiographic findings of diffuse alveolar filling differ from those in the more chronic forms of silicosis. Histologic findings similar to pulmonary alveolar proteinosis have been described and extrapulmonary (renal & hepatic) abnormalities are reported. Rapid progression to severe hypoxemic ventilatory failure is the usual course. The potential for mycobacterial infection in acute silicosis requires constant vigilance.

Calcified Nodules

PREVENTION

There is no specific therapy for silicosis. Prevention remains the cornerstone of eliminating this occupational lung disease. The education of workers and employers regarding the hazards of silica dust exposure and measures to control exposure is important. Improved ventilation and local exhaust, process enclosure, wet technique, personal protection including the proper selection of respirators and where possible, industrial substitution of agents less hazardous than silica, reduce exposure. Silicosis is a reportable disease. Medical examination of coworkers may also identify additional cases of early or at times, advance disease. If silicosis is recognized in a worker, limited future significant exposure is advisable. Unfortunately, the disease may progress even without further silica exposure.

TREATMENT

When prevention has been unsuccessful and silicosis developed, therapy is directed largely at complications of the disease. Therapeutic measures are similar to those commonly used in the management of airway obstruction, infection, pneumothorax, hypoxemia and respiratory failure complicating other pulmonary disease. Historically, the inhalation of aerosolized aluminum has been unsuccessful as a specific therapy for silicosis. Polyvinyl pyridine N-oxide, a polymer that has protected laboratory animals, is not available for use in humans. Laboratory work with tetrandrine has shown in vivo reduction in fibrosis and collagen synthesis in silica-exposed animal treated with this drug. However, strong evidence of human efficacy is currently lacking and this drug is not available in the United States.

Tuberculosis is a common and serious complication, especially in complicated, accelerated and acute silicosis. Patients with silicosis who have a significant tuberculine skin reaction but no clinical, bacteriological or radiographic evidence of active disease should be treated with isoniazid (INH) or rifampin as a preventive therapy. These anti-microbial should be given for a minimum of 6 months to 1 year. Some physicians recommend life-long preventive therapy for tuberculine skin test-positive patients with silicosis. Silicotic patients receiving glucocorticoids should also be considered for INH or rifampin preventive therapy.

The diagnosis of active tuberculosis infection in patients with silicosis can be difficult. Clinical symptoms of weight loss, fever, sweats and malaise should prompt radiographic evaluation and sputum acid fast bacilli strain and cultures. Radiographic changes, including enlargement or cavitations of progressive massive fibrosis lesions or nodular opacities, are of particular concerns. Bacteriological studies on expectorated sputum may not always be reliable in silicotuberculosis. Fiberoptic bronchoscopy to obtain additional specimens for culture and study may often be helpful in establishing a diagnosis of active disease.

Proven active tuberculosis and clinically suspected disease should be treated with appropriate antimicrobials, now commonly including three or four drugs such as INH, rifampin, pyrazinamide and ethambutol for a minimum of 6 to 9 months. Because of the difficulties intreating tuberculosis in the setting of silicosis, many authorities have recommended more prolonged courses. Antituberculous therapy, of course, should always be guided by laboratory studies of sensitivity, especially with the increasing recognition of multi drug-resistant organisms. Initiation of therapy before bacteriological confirmation is prudent in silicotic patients with clinical signs compatible with active tuberculosis. Careful long-term follow-up with chest radiograph, bacteriologic culcure and monitoring of clinical symptoms is imperative in view of numerous reports of recurrent pulmonary tuberculosis in silicotic patients after the completion of conventional therapeutic courses of antimicrobials.

Acute silicosis may rapidly progress to respiratory failure. When this disease resembles pulmonary alveolar proteinosis and severe hypoxemia is present, aggressive therapy has included selective whole-lung lavage with the patient under G.A. in an attempt to improve gas exchange and remove alveolar debris. Although it is appealing in concept, the efficacy of whole-lung lavage remains to be established. Glucocorticoids therapy has also been used for acute silicosis; however, it is still of unproven benefit. Prednisone has been used at doses of 40 to 60 mg. per day for 1 to 2 months and if accompanied by evidence of clinical improvement, has been tapered to 15 to 20 mg per day and continued for 6 months to 1 year. Early, rigorous initial evaluation for tuberculosis and other mycobacterial infection cannot be overemphasized. INH or rifampin should be given while steroids are administered. Empirical therapy with three or four A.T.D. pending results of cultures for 6 weeks may be appropriate in the life-threatening acute form of disease.

Some young patients with end-stage silicosis may be considered candidates for lung or heart-lung transplantation by centers experienced with this procedure. Early referral and evaluation for this intervention may be offered to selected patients. The discussion of an aggressive and high technology therapeutic intervention such as whole-lung lavage and transplantation serves to dramatically underscore the serious and potentially fatal nature of silicosis as well as emphasize the crucial role for primary prevention.

REFERENCES

1. Parker, John E., Silicosis in Rakel RE: Conn’s Current Therapy, Philadelphia, W.B.Saunders,
1998.

2. Guidelines for the use of the ILO International Classification of Radiographs of Pneumoconiosis,
Rev. ed. Geneva, ILO.

3. Carl Zenz, Occupational Medicine, 3^rd ed., Missouri, Mosby, St. Louis, 1994.

4. Parkes, W.R., Occupational Lung Disorders, 3^rd ed., Oxford, Jordan Hill, Butterworth-Heinemann
Ltd., 1995.

Dr. S.K. Halder

Dy. Director (Medical)

Regional Labour Institute, Kolkata, DGFASLI

DGFASLI AT A GLANCE

The Directorate General Factory Advice Service & Labour Institutes (DGFASLI) is an attached office of the Ministry of Labour & Employment Government of India. DGFASLI organization was set up in 1945 under the Ministry of Labour, Government of India to serve as a technical arm to assist the Ministry in formulating national policies on occupational safety and health in factories and docks and to advise State Governments and factories on matters concerning safety, health, efficiency and well-being of the persons at workplace. It also enforces safety and health statutes in major ports of the country.

The Directorate General Factory Advice Service & Labour Institutes (DGFASLI) comprises:

· Headquarters situated in Mumbai

· Central Labour Institute in Mumbai

· Regional Labour Institutes in Kolkata, Chennai,

Faridabad* and Kanpur

Vision of DGFASLI: DGFASLI envisions emerging as an organization of excellence in creating knowledge, formulating policies, standards and practices to ensure safe and healthy workplaces for all in factories and ports.

Mission of DGFASLI: The mission of DGFASLI is to render its expertise in occupational safety and health for evolving safe and healthy workplaces in factories and ports through a process of partnership, guidance, regulatory activities in specific sector and information sharing.

DGFASLI organization comprises of its Headquarters situated in Mumbai, Central Labour Institute (CLI) in Mumbai, four Regional Labour Institutes (RLI) in Chennai, Faridabad, Kanpur & Kolkata and eleven Inspectorate of Dock Safety (IDS) offices located in Mumbai, Jawaharlal Nehru Port, Kandla, Mormugao, New Mangalore, Chennai, Tuticorin, Cochin, Visakhapatnam, Kolkata, and Paradip. DGFASLI organization consists of a multidisciplinary team of around 129 officers (engineers, physicians, industrial hygienists, physiologists, ergonomists, industrial psychologists, commercial artists etc.) and 81 technical staff members. Various specialty divisions/cells under DGFASLI office and Central Labour Institutes in Mumbai include a) Factory Advice Service, b) Dock Safety, c) Construction Safety, d) Awards, e) Statistics, f) Industrial Safety, g) Industrial Hygiene, h) Industrial Medicine, i) Industrial Physiology & Ergonomics, j) Staff Training, Productivity & Small Scale, k) Industrial Psychology, I) Major Hazards Chemical Safety, m) Management Information Services; n) Environmental Engineering and 0) Communication Division. The Regional Labour Institutes are a scaled-down version of the Central Labour Institute and cater to the needs of their respective regions through its specialty divisions like Industrial Safety, Industrial Hygiene and Medical. The organization is poised to grow further, and meet the increased demands on it. In a developing country with a large number of industries having diverse and complex nature, the task of protecting safety and health of workers is an uphill task. Armed with the technology, good will of the industrial society and the strength of the dedicated staff, the organization is well prepared to meet the challenges of tomorrow. It is committed to the goal of making the workplace safer.

Visit us at: www.dgfasli.nic.in