New Jersey Department of Health and Senior Services (NJDHSS), Public Health Services Branch, Division of Epidemiology, Environmental and Occupational Health, Occupational Health Service, Occupational Health Surveillance Program
Construction, demolition, and renovation workers are At risk of developing silicosis. Construction Materials Containing Crystalline Silica: - Many abrasives used for blasting - Brick, refractory brick - Concrete, concrete block, cement, mortar - Granite, sandstone, quartzite, slate - Gunite -Mineral deposits - Rock and stone - Sand, fill dirt, top soil - Asphalt containing rock or stone. Many construction, demolition, and renovation occupations are at risk, including: . abrasive blasters . masonry workers -- bricklayers, stone masons . laborers . operating engineers . painters and plasterers . plumbers . truck drivers Other occupations that do not work directly with construction materials or tasks involving silica may be exposed as bystanders if they are in the construction, demolition, or renovation area when crystalline silica containing materials are being used. Definition and Clinical Features Silicosis is a diffuse, nodular, interstitial pulmonary fibrosis caused by a tissue reaction to inhaled crystalline silica dust. It can take the acute form under conditions of intense exposure but usually takes the chronic form, requiring several to many years to develop. People who have silicosis have increased susceptibility to infections such as tuberculosis, complicating the patient.s prognosis. There is also increasing evidence that crystalline silica causes cancer and that individuals with silicosis are at increased risk of developing lung cancer. Except in its acute form, silicosis begins with few, if any, symptoms. When clinical symptoms of silicosis are present, they could include cough and shortness of breath of increasing severity. On physical examination, breath sounds may be normal or distant and, with increased severity, there may be signs of right heart failure. Evidence of pathological response to silica exposure exists well before symptoms occur. Chronic reactions, occurring after 10 or more years from first exposure, involve nodular lesions, (bilateral, multiple, rounded opacities) often more prominent in the upper lobes. In this simple stage of silicosis, nodules are usually small (1 cm or less). There may be little effect on pulmonary function at this stage. Complicated silicosis or progressive massive fibrosis (PMF) also usually develops in the upper lobes but the nodules go on to consolidate and exceed 1 cm and encompass blood vessels and airways. Lung function may be severely compromised, often with a mixed restrictive/obstructive pattern, but either pure restriction or obstruction may be seen. Acute reactions may appear within a few weeks to two years after the onset of massive exposure. The distinguishing feature of acute silicosis is intraalveolar deposits, similar to those seen with alveolar proteinosis. In contrast to the nodular fibrosis seen in the chronic form, diffuse interstitial fibrosis is not found. Silicosis developing in less than 10 years, the accelerated form, has been described most often in sandblasters. In these cases, diffuse fibrosis is likely to develop and may be located throughout all lobes of the lung.