Surface coalminers are generally thought to be at minimal risk of developing pneumoconiosis. Biopsy-proved silicoproteinosis was found in a 34-year-old surface coalmine driller, and two of nine other drill crew members who worked for the same company had chest radiographic findings compatible with simple silicosis. Reanalysis of data from a previous United States Public Health Service survey of surface coalminers, after exclusion of those with underground mining experience, showed that 38% of the cases of pneumoconiosis occurred in drill crew members, a group comprising only 11% of the study population. On the basis of these data surface coalmine drillers appear to have an increased risk of developing occupational lung disease.The development of silicosis among underground coalminers has been well documented, particularly among roof bolters and transportation workers. We report a case of acute silicosis in a surface coalmine drill operator. An important feature is the occurrence of rapidly fatal silicosis in a miner with no underground experience who had not worked in enclosed spaces.The recognition of acute silicosis in the index case prompted a medical survey of nine other current and former drill crew workers who worked for the same company. Two of these nine had simple silicosis. In addition, we reanalysed data from a previous survey of the respiratory health of surface coalminers,l which concluded, "current surface mining techniques are not likely to lead to the development of pneumoconiosis." We found that drill crew workers have a disproportionately high risk of developing pneumoconiosis. Case reportA 34-year-old white man was admitted to hospital in April 1979 with a six-month history of progressive dyspnoea, dry cough, weight loss of 13 kg, and Raynaud's phenomenon. He had operated a rotary drill using a dry drilling technique at a surface coal mine for the preceding five years. Previously he had been in good health and a routine examination and chest radiograph in February 1977 both gave normal results.Physical examination showed an afebrile, slender man, breathing 30 times per minute at rest. His blood pressure was 110/84 mm Hg and his pulse rate was 88 beats per minute and regular. There were coarse crackles at both lung bases, healed ulceration on several fingertips, and sclerodactyly.The haemoglobin concentration, packed cell volume, white blood cell count and differential, and serum electrolyte concentrations were normal. The blood urea concentration was 7-7 mmoIIl (20 mg/ 100 ml) and the serum creatinine concentration 130 ,umol/I (1.5 mg/100 ml). Urine analysis showed microscopic haematuria, grade 2 + proteinuria, and occasional hyaline casts. The serum albumin concentration was 21 g/l, and the C3 component of complement was 1-66 g/l (normal 0-88-1*77 g/l). Cryoglobulins, antinuclear antibodies, and rheumatoid factor were not detected but circulating immune complexes2 were present. An intermediate tuberculin (PPD) skin test produced no reaction, but a mumps skin test gave a positive resp...
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