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Professors Coggon and Newman Taylor1 correctly state that it is my opinion that the adverse effects of cigarette smoking vary markedly with only around 15–20% of smokers being affected, while the effects of coal mine dust are distributed much more evenly. They find my arguments unconvincing because Fletcher and coworkers’ “seminal longitudinal study into the natural history of COPD found that the presence of chronic bronchitis had no independent influence on the decline of the FEV1.”2
I yield to none in my admiration for the work of Fletcher and his coworkers, but it needs to be pointed out that the men they selected were “aged 30 to 59 years since younger men were thought unlikely to have developed airflow obstruction by this age”. In this connection their assumption was incorrect. While non-smoking men aged 23–35 show either an extended plateau or a period of slow continued growth, at about the age of 35 they start to lose FEV1 due to ageing. In contrast, male smokers show a plateau or a minimal increase between the ages of 23 and 30 but a decline in the FEV1 at the start of the third decade, with the rate being slightly greater than that for non-smokers over the age of 35. In addition, the increase in the FEV1 between the ages of 20 and 30 in smokers is substantially less than that noted in non-smokers.3-5 The second or rapid progressive decline in the FEV1 of smokers occurs later, around the age of 40–45 years. The early decline in young persons appears completely reversible and cannot be attributed to emphysema. Moreover, it is known that many young smokers have what is termed a “smoker’s cough” with the production of sputum. In this connection Coggon and Newman Taylor quote two papers, both of which claim to show the early onset of a reduction in the FEV1 in coal miners—that is to say, in the first 10 years.6 7None of these early changes would have been apparent in the studies of Fletcher and colleagues.
Clearly some thought must be given to explaining the early decline in the FEV1 that occurs in the 20–30 age group, be they non-miners who smoke or miners exposed to either dust or cigarette smoke, or both. Emphysema cannot account for this reduction and some other mechanism must be sought. It will not do to torture the data until they confess so that some other statistical explanation becomes apparent. Perhaps Coggon and Newman Taylor would also explain why older smokers with established chronic airflow limitation show a mean improvement of around 50 ml in the FEV1 after they stop smoking.8 Presumably the emphysema does not improve but we know that their smoker’s cough and sputum usually do—that is, their bronchitis disappears.
authors’ reply We remain unconvinced that bronchitis can explain other than at most a small part of the loss of FEV1 associated with exposure to coal mine dust. If bronchitis had a major influence on airflow, we would have expected it to be apparent in Fletcher’s study.1-1 Professor Morgan refers to an early decline in FEV1 in young smokers that is reversible and therefore cannot be attributable to emphysema, and also to a mean improvement in FEV1 of 50 ml among older smokers with established chronic airflow obstruction who stop smoking. However, he does not indicate that these effects are restricted to, or even more prominent in, subjects with symptoms of bronchitis. Moreover, the improvement of 50 ml is small in comparison with the deficits of FEV1 associated with coal mine dust, which average more than 225 ml in miners with heavy cumulative exposure.1-2These deficits persist after cessation of exposure and are of similar magnitude in miners with and without symptoms of bronchitis.1-2
For these reasons and the others set out in our review, we stand by our conclusion that there is strong evidence that coal mine dust can have a critical influence on health in an important number of people.
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