Abstract
To the Editor: We read with interest the recent article by McCunney, Morfeld, and Payne entitled What Component of Coal Causes Coal Workers' Pneumoconiosis (CWP)?1 The intent of the article was to identify the specific substance(s) in the underground coal mining environment that are directly responsible for causing CWP. In addressing this question, the authors use a substantial portion of their work to point out that exposure to silica does not likely contribute to CWP. The authors are not wrong in their assessment of the role of silica in the development of CWP when it occurs at low levels. Epidemiologic studies dating back to the early 1970s showed through modeling of quantitative exposure data that mixed coal mining dust was the primary factor relating to CWP development, whereas silica's role was much smaller.2–4 Anthracite workers in many parts of the world have long been known to suffer high rates of CWP, although anthracite usually contains very low levels of silica. We believe that by downplaying silica in their desire to seek a more precise explanation for the cause of CWP, the authors have potentially done coal miners a great disservice. There is an important distinction that the authors fail to highlight in their report—silica may not be a major factor in the development of the clinical condition known as CWP, but silica does cause another form of pneumoconiosis among coal workers—silicosis. Silica remains a major risk factor for coal miners. This was amply demonstrated by the rapid development of pneumoconiosis among Scottish coal miners who had been engaged in cutting through a fault composed of sandstone rock.5 Weight for weight, silica is considerably more toxic than coal dust, and failure to control silica dust using a standard intended for coal dust can easily lead to massive overexposure to silica. In this, the approach to enforcing a silica standard in underground coal mines in the United States has been criticized as inadequate.6–9 As easily accessible coal seams are being depleted, attention is being paid increasingly to thin seams or to seams with rock intrusions that might not have been considered economically feasible to mine in the past. Mining these seams often requires cutting the adjacent rock, the roof, the floor, and intrusions, leading to exposures rich in silica dust.10 It is, therefore, critically important that the role of silica not be discounted when evaluating pneumoconiosis risk among coal miners. As surface and underground thin seam mining becomes more prominent the likelihood of increased silica exposure among miners, and the development of pneumoconiosis associated with those exposures becomes increasingly important. Situations where there is a risk of silica exposure must be identified, and silica dust levels controlled to the regulated level or lower. Only in this way will the potential future tragedy of an epidemic of silicosis in coal miners be averted. A. Scott Laney, PhD Michael D. Attfield, PhD Surveillance Branch, Division of Respiratory Disease Studies National Institute for Occupational Safety and Health Centers for Disease Control and Prevention Morgantown, WVa
Published Version
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