In a recent commentary Kilburn [1981] concluded that "Critical analysis not only provides no support for this thesis (that cigarette smoke causes pulmonary fibrosis) but provides adequate reasons to bury the suggestion. " Kilburn's analysis was both erroneous and superficial.
In 1963 Auerbach et al reported a dose-response relationship between cigarette smoking and pulmonary fibrosis, which increased with age in autopsy specimens of human lungs carefully studied in a "blind" fashion. The fibrosis was very advanced in some cases and therefore probably detectable by X-ray: 39% in 61 men aged 65 and over who had smoked two or more packs per day. This relationship was confirmed roentgenographically by Boucot et al [ 19641 and by Weiss [ 1967, 19691. It was also demonstrated in smoking beagles by Hammond et a1 [1970]. The X-ray studies were corroborated by Carilli et al [1973]. In addition, Theriault et al [1974] found the frequency of small irregular opacities in granite workers to be related to cigarette smoking, and Amandus et al [1976] described similar findings in coal workers. Thus, the evidence that cigarette smoking can cause pulmonary fibrosis is considerable.
Kilburn's criticisms are unjustified for a number of reasons. First, he made errors in two references: (1) the work of Carilli et al [1973] was described in the text and attributed in the references to an unrelated paper on coal workers, and (2) his references for the beagle studies deal only with emphysema, whereas the correct reference for pulmonary fibrosis in smoking beagles is Hammond et a1 [1970].
Second, Kilburn is wrong in the methodologic problems he perceived in my radiologic studies. Those of us who are extensively experienced in reading 70-mm photofluorograms of the chest became aware many years ago that small faint lesions sometimes were more easily recognized in the miniature films than in 14 x 17-in. films. The fact that I disagreed with myself 25% of the time in repeated "blind" reading of roentgenograms is only another example of the well-known intraobserver error of the same degree described in so many studies since World War I1 that references need not be cited. The fact that the ILO criteria were not used in my papers on smoking and pulmonary fibrosis is irrelevant because I was not studying pneumoconiosis and because my studies were designed to test the hypothesis that an X-ray abnormality consistent with pulmonary fibrosis was related to cigarette smoking, not to test the ILO criteria. The readings of the X-rays were done without knowledge of smoking habits, so the findings were unbiased, regardless of their pathological significance. That the roentgenographic abnormalities represented pulmonary fibrosis was supported by Auerbach's autopsy and beagle studies. While it would have been desirable to have pathologic confirmation of the radiologic findings 0 1984 Alan R. Liss, Inc.