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.