Silicosis and Coal Workers' Pneumoconiosis

Mineral or organic dust inhalation can result in slowly progressive pulmonary fibrosis. Common causes include coal dust and silica exposure. Less common exposures include talc, kaolin, and mica. Chest radiographs may reveal small rounded opacities that may eventually coalesce into massive fibrosis (Figure 3). Not infrequently, workers may have no respiratory symptoms such as cough or shortness of breath but have significant abnormal findings on chest radiograph.

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Figure 3. Silicosis. Courtesy of Dr. Ami N. Rubinowitz.

Workers in foundries, tunneling, sandstone grinding, sandblasting, concrete breaking, granite carving, and china manufacturing are exposed to silica. In 1995, the WHO, in conjunction with the International Labour Organization (ILO), launched the International Programme on the Global Elimination of Silicosis. In China, more than 500 000 cases of silicosis and 24 000 deaths were recorded between 1991 and 1995.

While acute silicosis has been reported after intense short-term exposure, more commonly chronic exposure by inhalation of quartz or other forms of silica dioxide may lead to a proliferation of small and large rounded opacities and, in some cases, massive pulmonary fibrosis. Lung biopsies combined with energy-dispersive, X-ray analysis may confirm diagnosis but are not generally necessary if given a suggestive history. Two significant complications of silicosis include an increased risk for both lung cancer and active tuberculosis. Pulmonary function tests may reveal reduced lung volumes (restrictive ventilatory defects) associated with a decreased diffusion capacity – that is, a decrease in the ability to absorb and excrete gases. Treatment options for silicosis are limited but may include oral steroids.

Occupational Pneumoconioses

The occupational pneumoconioses are diffuse parenchymal lung diseases caused by airborne exposure to inorganic materials such as asbestos, silica, and coal dust. In 1998 and 1999, asbestosis passed coal workers’ pneumoconiosis (coal miner’s lung) as the leading cause of death from occupational pneumoconiosis in the United States. Men accounted for 98% of these deaths. The rise in deaths caused by asbestosis is illustrated in Figure 18-10 (NIOSH, 2004b). Other occupational lung diseases are linked to heavy metal dust or fumes in specific syndromes such as berylliosis (beryllium) and stannosis (tin). Byssinosis, or brown-lung disease, occurs most often among workers in yarn, thread, and fabric mills from exposure to cotton dust.

Patients with occupational pneumoconioses may first develop symptoms of cough and dyspnea, with signs of small-airway disease or overt airway obstruction on pulmonary function testing. As the disease progresses, patients may also develop spirometric evidence of restrictive lung disease as well as chest x-ray changes. Removing the patient from the exposure or workplace is the most important step for preventing progression of disease. These pneumoconioses respond poorly to corticosteroids. Smoking significantly worsens the progression of occupational pneumoconiosis (Wang and Christiani, 2000).

Unintentional Tattoos

Tattoos may occur accidentally if pigmented foreign material is introduced under the skin as, for example, occurs with coal miners who may have extensive deposits of coal dust in the skin of the hands and face. Dental work may cause amalgam tattooing of the gums. The most commonly observed non-intentional tattooing in the morgue is that of gunshot residue from close contact discharge of a firearm. Such tattooing was much more extensive with earlier black powder firearms, but can still be useful in helping to determine the range and direction of a shot (Hartwig et al., 2009; Swift, 2004).

Pneumoconioses