786
LETTERS to the EDITOR Coal dust and
compensation
SiR,—Your Feb 10 editorial (p 322) criticises the Industrial Injuries Advisory Council (IIAC), implying that it was remiss and ignored the obvious. It sounds as if your editorialist had submitted evidence to the IIAC and was peeved that his or her recommendations were not accepted. Many others feel that the IIAC report was fair and balanced. Your editorial claims that epidemiological evidence led to the widely held belief "that simple pneumoconiosis does not give rise to perceptible disability", and implies that this belief is mistaken. However, increasing severity of simple coalworkers’ pneumoconiosis (CWP), as recognised by the presence of small rounded opacities, is not associated with a decrease in forced expiratory volume in 1 s (FEV 1) or other evidence of significant impairment of lung function. The radiographic category "simple CWP" correlates well with the dust content of the lung.1-3 The lungs of coalminers have more emphysema than do the lungs of non-miners, and the extent of the emphysema is related to radiographic category and retained dust.3 Thus miners with simple CWP have more dust, more emphysema, and more coal in their lungs-yet their FEV is not significantly different from that in miners without X-ray evidence of CWP, unless one chooses to include irregular opacities as a manifestation of CWP. Longitudinal studies have indeed shown a loss of lung function associated with coal dust which is present after allowing for smoking.4A correction factor for smoking for all miners in a particular cohort can be derived but the correction cannot be applied to subgroups of that cohort. Airways obstruction occurs in only 13-14% of smokers whereas bronchitis affects about 50% of non-smoking coalminers who have worked for 20 or more years.6,7 To compare a disabling decrement in FEV1 in a minority of smoking miners with a smaller decrement in a greater proportion of non-smoking miners obscures the truth.’ You cite a paper in which 199 men were selected on the basis that they showed an exceptionally severe inverse relation between dust exposure and FEV l’ This study postulated that some miners were especially susceptible to dust but how does one exclude the possibility that they were not unusually susceptible to cigarette smoke? Only 11 were non-smokers. Since the 199 men were drawn from over 4000, it is difficult to see how one can apply a correction factor for smoking to this small group. The fallacies of applying multiple regression analysis to apportioning the contributions of age, dust, cigarette smoking, and other factors has been pointed out by Oldham.9 Your editorial implies that irregular opacities are part-and-parcel of CWP but all of the studies cited indicate that the strongest influence on irregular opacities is smoking, and all but one were done on men referred to pneumoconiosis medical panels or to a chest clinic. Despite the fact that the smoking histories were retrospective and may have been underestimated, irregular opacities were closely related to present or past cigarette smoking. It is suggested that such opacities were associated with defects in lung function and centracinar emphysema. 10 This is hardly surprising when in this study of 46 patients referred for lung-function testing all but 2 were smokers. Your editorial does not refer to a study in an unselected group of working coalminers where the only exclusion criterion was progressive massive fibrosis.11 Smoking histories were prospective, and this paper showed that while dust did induce small irregular opacities, the changes in lung function in non-smokers
consisted of a slight increase in residual volume with no detectable obstruction. In the smoking miners with irregular opacities total lung capacity and residual volume were increased significantly, and FEV, and forced vital capacity were significantly reduced. Irregular opacities may be seen in workers exposed to silica, bauxite, asbestos (in the absence of asbestosis), and man-made mineral fibres12-15 as frequently as in coalmines. You ask us to accept that irregular opacities in a coalminer denote emphysema. Are we to make the same assumption when irregular opacities are seen in those exposed to silica? Silica exposure is not associated with the development of emphysema. 16 Moreover, such opacities have been observed in female smokers not exposed to dust.l’ They are associated with age and obesity and can be mimicked by poor radiographic technique and by exposure to many dusts. The most important factor in their aetiology seems to be smoking, dust exposure and age playing smaller parts. Multiple regression does not always sort out the relative contributions.9 Perhaps the IIAC took this into account. There is much to be said for awarding equal compensation for equal disability, whatever the cause. However, were your recommendations to be accepted, coalminers with emphysema would have an advantage over non-coalminers with the same condition, many of whom happen to be employed in other dusty trades, not to mention those who work in a non-dusty environment. Chest Diseases Unit,
University Hospital, London, Ontario N6A 5A5, Canada
W. K. C. MORGAN
1. Rivers
D, Wise ME, King EJ, Nagelschmidt G. Dust content, radiology, and pathology m simple pneumoconiosis of coal workers. Br J Ind Med 1960; 17: 87-108.
2. Fernie
JM, Ruckley VA. Coalworkers pneumoconiosis: correlation between opacity profusion and number and type of dust lesions with special reference to opacity type. Br J Ind Med 1987; 44: 273-87. 3. Ruckley VA, Gauld SJ, Chapman JS, et al. Emphysema and dust exposure in a group of coal workers. Am Rev Respir Dis 1984; 129: 528-32. 4. Love RG, Miller BG. Longitudinal study of lung function in coalminers. Thorax 1982, 37: 103-07.
Longitudinal decline in FEV in coalworkers in United States coalmines. Thorax 1985; 40: 132-37. 6. Kibelstis JA, Morgan EJ, Reger RB, et al. Prevalence of bronchitis and airways obstruction in American bituminous coal miners. Am Rev Respir Dis 1973; 107: 886-93. 7. Morgan WKC. Dust, disability and death. Am Rev Respir Dis 1986; 133: 639-41. 8. Hurley JF, Soutar CA. Can exposure to coal mine dust cause severe impairment of lung function? Br J Ind Med 1986; 43: 150-57. 9. Oldman PD. Decline of FEV, Thorax 1987; 42: 161-64. 10. Cockcroft A, Wagner JC, Seal RME, et al. Irregular opacities in coalworkers’ pneumoconiosis correlation with pulmonary function and pathology. Ann Occ Hyg 1982; 26: 767-87. 11. Amandus HE, Lapp NL, Jacobsen G, Reger RB. Significance of small irregular opacities in radiographs of coal miners in the USA. Br J Ind Med 1974; 33: 13-17. 12. Theriault GP, Peters JM, Johnson WM. Pulmonary function and roentgenographic changes in granite dust exposure. Arch Environ Hlth 1974; 28: 23-27. 13. Hnizdo E, Sluis-Cremer GK. Effect of tobacco smoke on the presence of asbestosis at postmortem and on the reading of irregular opacities on the roentgenograms m asbestos exposed workers. Am Rev Respir Dis 1988; 138: 1207-12. 14. Townsend MC, Sussman NB, Enterline PR, et al. Radiographic abnormalities in relation to total dust exposure at a Bauxite Refinery and Alumina-based Chemical products plant. Am Rev Respir Dis 1988; 138: 90-95. 15. Weill H, Hughes JM, Hammad YY, et al. Respiratory health m workers exposed to manmade vitreous fibres. Am Rev Respir Dis 1983; 128: 104-12. 16. Ruckley VA, Chapman JS, Lollings PL, et al. Autopsy studies of coalminers lungs: Final report on CEC contract 7246-15/8/001. Edinburgh Institute of Occupational 5. Attfield MD.
Medicine, 1981: 67-68 AD, Kotzen LM, Fischer MJ. The chest roentograph in smoking females Am Rev Respir Dis 1973; 107: 133-36.
17. Carilli
LETTERS to the EDITOR Coal dust and
compensation
SiR,—Your Feb 10 editorial (p 322) criticises the Industrial Injuries Advisory Council (IIAC), implying that it was remiss and ignored the obvious. It sounds as if your editorialist had submitted evidence to the IIAC and was peeved that his or her recommendations were not accepted. Many others feel that the IIAC report was fair and balanced. Your editorial claims that epidemiological evidence led to the widely held belief "that simple pneumoconiosis does not give rise to perceptible disability", and implies that this belief is mistaken. However, increasing severity of simple coalworkers’ pneumoconiosis (CWP), as recognised by the presence of small rounded opacities, is not associated with a decrease in forced expiratory volume in 1 s (FEV 1) or other evidence of significant impairment of lung function. The radiographic category "simple CWP" correlates well with the dust content of the lung.1-3 The lungs of coalminers have more emphysema than do the lungs of non-miners, and the extent of the emphysema is related to radiographic category and retained dust.3 Thus miners with simple CWP have more dust, more emphysema, and more coal in their lungs-yet their FEV is not significantly different from that in miners without X-ray evidence of CWP, unless one chooses to include irregular opacities as a manifestation of CWP. Longitudinal studies have indeed shown a loss of lung function associated with coal dust which is present after allowing for smoking.4A correction factor for smoking for all miners in a particular cohort can be derived but the correction cannot be applied to subgroups of that cohort. Airways obstruction occurs in only 13-14% of smokers whereas bronchitis affects about 50% of non-smoking coalminers who have worked for 20 or more years.6,7 To compare a disabling decrement in FEV1 in a minority of smoking miners with a smaller decrement in a greater proportion of non-smoking miners obscures the truth.’ You cite a paper in which 199 men were selected on the basis that they showed an exceptionally severe inverse relation between dust exposure and FEV l’ This study postulated that some miners were especially susceptible to dust but how does one exclude the possibility that they were not unusually susceptible to cigarette smoke? Only 11 were non-smokers. Since the 199 men were drawn from over 4000, it is difficult to see how one can apply a correction factor for smoking to this small group. The fallacies of applying multiple regression analysis to apportioning the contributions of age, dust, cigarette smoking, and other factors has been pointed out by Oldham.9 Your editorial implies that irregular opacities are part-and-parcel of CWP but all of the studies cited indicate that the strongest influence on irregular opacities is smoking, and all but one were done on men referred to pneumoconiosis medical panels or to a chest clinic. Despite the fact that the smoking histories were retrospective and may have been underestimated, irregular opacities were closely related to present or past cigarette smoking. It is suggested that such opacities were associated with defects in lung function and centracinar emphysema. 10 This is hardly surprising when in this study of 46 patients referred for lung-function testing all but 2 were smokers. Your editorial does not refer to a study in an unselected group of working coalminers where the only exclusion criterion was progressive massive fibrosis.11 Smoking histories were prospective, and this paper showed that while dust did induce small irregular opacities, the changes in lung function in non-smokers
consisted of a slight increase in residual volume with no detectable obstruction. In the smoking miners with irregular opacities total lung capacity and residual volume were increased significantly, and FEV, and forced vital capacity were significantly reduced. Irregular opacities may be seen in workers exposed to silica, bauxite, asbestos (in the absence of asbestosis), and man-made mineral fibres12-15 as frequently as in coalmines. You ask us to accept that irregular opacities in a coalminer denote emphysema. Are we to make the same assumption when irregular opacities are seen in those exposed to silica? Silica exposure is not associated with the development of emphysema. 16 Moreover, such opacities have been observed in female smokers not exposed to dust.l’ They are associated with age and obesity and can be mimicked by poor radiographic technique and by exposure to many dusts. The most important factor in their aetiology seems to be smoking, dust exposure and age playing smaller parts. Multiple regression does not always sort out the relative contributions.9 Perhaps the IIAC took this into account. There is much to be said for awarding equal compensation for equal disability, whatever the cause. However, were your recommendations to be accepted, coalminers with emphysema would have an advantage over non-coalminers with the same condition, many of whom happen to be employed in other dusty trades, not to mention those who work in a non-dusty environment. Chest Diseases Unit,
University Hospital, London, Ontario N6A 5A5, Canada
W. K. C. MORGAN
1. Rivers
D, Wise ME, King EJ, Nagelschmidt G. Dust content, radiology, and pathology m simple pneumoconiosis of coal workers. Br J Ind Med 1960; 17: 87-108.
2. Fernie
JM, Ruckley VA. Coalworkers pneumoconiosis: correlation between opacity profusion and number and type of dust lesions with special reference to opacity type. Br J Ind Med 1987; 44: 273-87. 3. Ruckley VA, Gauld SJ, Chapman JS, et al. Emphysema and dust exposure in a group of coal workers. Am Rev Respir Dis 1984; 129: 528-32. 4. Love RG, Miller BG. Longitudinal study of lung function in coalminers. Thorax 1982, 37: 103-07.
Longitudinal decline in FEV in coalworkers in United States coalmines. Thorax 1985; 40: 132-37. 6. Kibelstis JA, Morgan EJ, Reger RB, et al. Prevalence of bronchitis and airways obstruction in American bituminous coal miners. Am Rev Respir Dis 1973; 107: 886-93. 7. Morgan WKC. Dust, disability and death. Am Rev Respir Dis 1986; 133: 639-41. 8. Hurley JF, Soutar CA. Can exposure to coal mine dust cause severe impairment of lung function? Br J Ind Med 1986; 43: 150-57. 9. Oldman PD. Decline of FEV, Thorax 1987; 42: 161-64. 10. Cockcroft A, Wagner JC, Seal RME, et al. Irregular opacities in coalworkers’ pneumoconiosis correlation with pulmonary function and pathology. Ann Occ Hyg 1982; 26: 767-87. 11. Amandus HE, Lapp NL, Jacobsen G, Reger RB. Significance of small irregular opacities in radiographs of coal miners in the USA. Br J Ind Med 1974; 33: 13-17. 12. Theriault GP, Peters JM, Johnson WM. Pulmonary function and roentgenographic changes in granite dust exposure. Arch Environ Hlth 1974; 28: 23-27. 13. Hnizdo E, Sluis-Cremer GK. Effect of tobacco smoke on the presence of asbestosis at postmortem and on the reading of irregular opacities on the roentgenograms m asbestos exposed workers. Am Rev Respir Dis 1988; 138: 1207-12. 14. Townsend MC, Sussman NB, Enterline PR, et al. Radiographic abnormalities in relation to total dust exposure at a Bauxite Refinery and Alumina-based Chemical products plant. Am Rev Respir Dis 1988; 138: 90-95. 15. Weill H, Hughes JM, Hammad YY, et al. Respiratory health m workers exposed to manmade vitreous fibres. Am Rev Respir Dis 1983; 128: 104-12. 16. Ruckley VA, Chapman JS, Lollings PL, et al. Autopsy studies of coalminers lungs: Final report on CEC contract 7246-15/8/001. Edinburgh Institute of Occupational 5. Attfield MD.
Medicine, 1981: 67-68 AD, Kotzen LM, Fischer MJ. The chest roentograph in smoking females Am Rev Respir Dis 1973; 107: 133-36.
17. Carilli
