Hospital: Report by phone, fax, or mail
Lab: Report by phone, fax, or mail
Physician/Health care providers: Report by phone, fax, or mail
Medical Examiners: Report by phone, fax, or mail
Poison Control Centers: Report by phone, fax, or mail
Occupational Nurses: Report by phone, fax, or mail
Local Public Health Agency (LPHA): No follow-up required, unless outbreak occurrence
Report to the IDPH Division of Environmental Health:
Iowa Department of Public Health
Division of Environmental Health
Lucas State Office Building
321 E. 12th Street
Des Moines, Iowa 50319-0075
Phone (Mon-Fri 8 am - 4:30 pm): 800-972-2026
24-hour Disease Reporting Hotline: (For use outside of EH office hours) 800-362-2736
A. Clinical Description
Silicosis is an irreversible but preventable disease, and is the illness most closely associated with occupational exposure to silica dust. Overexposure to dust that contains microscopic particles of crystalline silica can cause scar tissue to form in the lungs, which reduces the lungs ability to extract oxygen from the air we breathe. Occupational exposures to respirable crystalline silica are associated with the development of silicosis, lung cancer, pulmonary tuberculosis, and airways diseases. These exposures may also be related to the development of autoimmune disorders, chronic renal disease, and other adverse health effects.
The symptoms of silicosis are a cough, with or without sputum, chest tightness, and shortness of breath, particularly on exertion. Pure silica dust can lead to widespread scarring of the lungs and can be extremely disabling. Additional information is provided under the prognosis section of this document.
B. Sources of Exposure
Silicosis results from exposure to free crystalline silica. Silica is the second most common mineral in the earth’s crust and is a major component of sand, rock and mineral ores. Virtually any process that involves movement of earth or disturbance of silica-containing products such as masonry and concrete may expose a worker to silica. Silica dust is often found in heavy construction involving concrete or masonry, mines, foundries, blasting operations, and in stone, clay, and glass manufacturing. Sand mining, hauling, and use in some hydraulic fracturing (fracking) operations have been identified as potential silica health hazard risks. Typical sand found at the beach does not pose a silicosis threat.
C. Population at Risk
At least 1.7 million U.S. workers are exposed to respirable crystalline silica in a variety of industries and occupations, including construction, sandblasting, and mining. Almost 60,000 workers are expected to suffer from some degree of silicosis. In addition, an undetermined portion of the greater than 3 million U.S. agricultural workers may be exposed to dust containing a significant percentage of respirable crystalline silica.
Every year, 200 to 300 workers in the United States die with silicosis. Between 1979 and 1995, 2,594 U.S. deaths were attributed to silicosis. The construction industry has one of the highest rates of deaths due to the disease.
Workers in the following occupations are at risk for developing silicosis:
- Highway and bridge construction and repair
- Building construction, demolition, and repair
- Abrasive blasting
- Masonry work
- Concrete finishing
- Drywall finishing
- Rock drilling
- Sand and gravel screening
- Rock crushing (for road base)
More than 100,000 workers in the United States encounter high-risk, silica exposures through sandblasting, rock drilling and mining. Workers who remove paint and rust from buildings, bridges, tanks and other surfaces; clean foundry castings; work with stone or clay; etch or frost glass; and work in construction are at risk of overexposure to crystalline silica. Coal miners are at risk of mixed silicosis and coal workers' pneumoconiosis. Examples of the industries and activities that pose the greatest potential risk for worker exposure:
- Construction (sandblasting, rock drilling, masonry work, jack hammering, tunneling)
- Hydraulic fracturing (fracking) and support operations (sand/silica transportation delivery)
- Mining (cutting or drilling through sandstone and granite)
- Foundry work (grinding, moldings, shakeout, core room)
- Ceramics, clay, and pottery
- Stone cutting (sawing, abrasive blasting, chipping, grinding)
- Glass manufacturing
- Shipyards (abrasive blasting)
- Railroad (setting and laying track)
- Manufacturing and use of abrasives
- Manufacturing of soaps and detergents
Surveillance of exposed workers with respiratory questionnaires, spirometry, and chest x-rays is recommended. Frequency of surveillance depends to some degree on the expected intensity of the exposure. As part of its National Emphasis Program on Silica, OSHA recommends that employers medically monitor all workers who may be exposed to silica dust levels at or above one-half the PEL. Recommended medical tests include:
- A medical exam that focuses on the respiratory system and includes a work and medical history.
- A chest X-ray, evaluated by a qualified professional as described in Directive CPL 03-00-007.
OSHA recommends that these tests be repeated every three years if the employee has less than 15 years of silica exposure, every two years if the employee has 15 to 20 years of exposure, and every year if the employee has 20 or more years of exposure.
D. Diagnosis, Treatment, and Prognosis
Diagnosis of the disease is based on a combination of occupational history of silica exposure, chest CT or chest x-ray, and possible tissue biopsy for confirmation. Additional testing may be needed to distinguish silicosis from other disorders, and for determining the level of impairment to lung function.
Silicosis is usually recognized on the basis of chest x-ray or CT appearance in patients with a history of exposure. CT is more sensitive than x-ray. In most cases, chest CT is preferable because it is more sensitive for detecting silicosis as well as the transition from simple to conglomerate silicosis. Chest CT also can better distinguish asbestosis from silicosis, although this differentiation can usually be made on the basis of chest x-ray and exposure history. If the patient worked in coal mines, silicosis may be present along with coal workers’ pneumoconiosis. Patients who have never worked in coal mines, but have worked as sandblasters or in other silica-dust areas have characteristic findings on their chest x-rays of widespread scarring in the upper parts of the lungs.
If diagnosis or screening is being done for a worker covered by the Coal Workers' X-Ray Surveillance Program as mandated by the Federal Mine Safety and Health Act of 1977, regulations mandate that all physicians who participate in the examination and/or classify chest radiographs under the Act must utilize the ILO System and Standard Films. This may also apply for asbestos-exposed workers covered by U.S. Department of Labor regulations, or for other medical screening, surveillance, research, or compensation programs. B Reader approval is granted to physicians with a valid U.S. state medical license who demonstrate proficiency in the classification of chest radiographs for the pneumoconioses using the International Labour Office (ILO) Classification System. Additional information about the B Reader program can be found at www.cdc.gov/niosh/topics/chestradiography/breader-info.html.
Tuberculin skin testing, sputum culture and cytology, PET scan, and bronchoscopy all may assist in distinguishing silicosis from disseminated TB or cancer.
Pulmonary function tests and measures of gas exchange (diffusing capacity for carbon monoxide (DLco], ABG) are not diagnostic but help monitor progression. Early chronic silicosis may manifest with reduced lung volumes that are at the lower end of the predicted range and with normal functional residual capacity and residual volume. In conglomerate silicosis, pulmonary function tests reveal decreased lung volumes, decreased DLco, and airway obstruction. ABGs show hypoxemia usually without CO2 retention. Measurement of gas exchange during exercise, using pulse oximetry or preferably indwelling arterial catheter, is one of the most sensitive measures of pulmonary impairment.
Antinuclear antibodies and elevated rheumatoid factor are detectable in some patients and are suggestive but not diagnostic of a coexisting connective tissue disorder (e.g., scleroderma, rheumatoid arthritis).
The National Institute of Occupational Safety and Health (NIOSH) and the Occupational Safety and Health Administration (OSHA) released new guidance and educational documents in 2011 for spirometry screening tests: OSHA-NIOSH Info Sheet: Maximize Your Spirometry Screening and Surveillance Resources: www.cdc.gov/niosh/docs/2011-133/pdfs/2011-133.pdf and OSHA-NIOSH Worker Info: Protect Yourself – Spirometry Breathing Test: www.cdc.gov/niosh/docs/2011-132/pdfs/2011-132.pdf.
Although early treatment is generally supportive care, additional treatment options may be used to aid patient comfort and improve quality of life.
Patients with airway obstruction may be treated empirically with bronchodilators and inhaled corticosteroids. Patients should be monitored and treated for hypoxemia to forestall pulmonary hypertension. Pulmonary rehabilitation may help patients carry out activities of daily living. Workers who develop silicosis should be removed from further exposure when possible.
Occasionally whole lung lavage and oral corticosteroids are used. Whole lung lavage may be useful in some cases of acute silicosis. Whole lung lavage can reduce the total mineral dust load in the lungs of patients with chronic silicosis. Some studies have shown short-term reduction in symptoms after lavage, but controlled trials have not been done. Anecdotal evidence supports the use of oral corticosteroids in acute and accelerated silicosis. Lung transplantation is a last-resort.
Management of tuberculosis is the same as for other patients with tuberculosis except that longer courses of drug therapy are usually recommended because relapse is more common in patients with silicotuberculosis.
Silicosis is an irreversible, progressive disease, especially if further ongoing exposure to respirable crystalline silica is not eliminated.
Chronic silicosis is the most common form of the disorder and generally develops only after exposure over decades. Chronic silicosis is often asymptomatic, but many patients eventually develop dyspnea on exertion that progresses to dyspnea at rest. Productive cough, when present, may be due to silicosis, coexisting chronic occupational (industrial) bronchitis, or smoking. Breath sounds diminish as the disorder progresses, and pulmonary consolidation, pulmonary hypertension, and respiratory failure with or without right ventricular failure may develop in advanced disease.
Acute silicosis and the rarer accelerated silicosis are caused by intense silica dust exposure over short periods (several months or years). Acute silicosis patients experience rapid progression of dyspnea, weight loss, and fatigue with diffuse bilateral crackles. Respiratory failure often develops within 2 yr. Patients with accelerated silicosis experience the same symptoms as those with chronic silicosis, but symptoms develop over a shorter period.
Conglomerate (complicated) silicosis is the advanced form of chronic or accelerated silicosis and is characterized by widespread masses of fibrosis, typically in the upper lung zones. Conglomerate silicosis causes severe, chronic respiratory symptoms.
Patients with silicosis are at risk for other disorders:
- Lung cancer
- Progressive systemic sclerosis (scleroderma)
- Rheumatoid arthritis
All patients with silicosis are at about a 30-fold increased risk of pulmonary tuberculosis or nontubercular mycobacterial disease and are more likely to develop both pulmonary and extrapulmonary manifestations. Increased risk may be from impaired macrophage function and an increased risk of activation of latent infection. People exposed to silica but without silicosis have 3 times the risk of developing tuberculosis compared with the nonexposed general population.
Other complications include spontaneous pneumothorax, broncholithiasis, and tracheobronchial obstruction. Emphysema is a common finding in areas immediately peripheral to conglomerate nodules and in areas of progressive massive fibrosis.
E. Prevention of Exposure
The limited value of treatment for conditions associated with silica exposure lends urgency to their prevention.
The most effective preventive interventions occur at an industrial rather than clinical level and include dust suppression, process isolation, ventilation, and use of non–silica-containing abrasives. Respiratory masks provide imperfect protection and, although helpful, are not adequate solutions.
Other preventive measures include smoking cessation and pneumococcal and influenza vaccination.
Physicians must be alert to the risk of TB and nontuberculous mycobacterial infections in silica-exposed patients, especially miners. People exposed to silica should have annual tuberculin testing. Those with a positive skin test should have sputum culture for TB. In some cases, CT and bronchoscopy may be needed to confirm TB. Patients with a positive tuberculin test and negative TB cultures should be given isoniazid chemoprophylaxis in keeping with standard guidelines for tuberculin reactors – ask for consultation by IDPH as needed.
Worker and employer education should include information emphasizing the role of primary prevention, which includes engineering controls, personal protective equipment and methods to avoid home contamination with work place dusts. Materials have been developed by a number of national programs, including NIOSH, MSHA, and OSHA – see references.