Mesothelioma Disease and Lung Cancer as it Relates to Cigarette Smoke and Asbestos Exposure

Mesothelioma Disease and Lung Cancer as it Relates to Cigarette Smoke and Asbestos Exposure

One interesting study concerning the impact of cigarette smoking when combined with asbestos exposure is called, “The Interaction of Asbestos and Smoking in Lung Cancer” by F. D. K. Liddell – Oxford Journals Medicine – The Annals of Occupational HygieneVolume 45, Issue5Pp. 341-356. Here is an excerpt: “Abstract – Both cigarette smoke and inhaled asbestos fibres can cause lung cancer, but the assessment of how these agents act in combination is a matter of great difficulty. In non-smokers, the condition is so rare that, in any cohort of asbestos workers, the standardised mortality ratio (SMR, that is the ratio of the numbers of deaths observed and expected) is quite imprecise. The SMR for smokers, with which it has to be compared, is also subject to sampling error, making the interaction even more unstable. This accounts for much of the variation that has bedevilled evaluation. The debate has been concentrated on two hypotheses: additive (asbestos and cigarette smoke act independently) and multiplicative (asbestos produces an effect proportional to the effect of smoking). The very few data available until 1977 failed to fit the former and fitted the latter only poorly. They would have fitted better a hypothesis of greater synergism, but the only one proposed was too convoluted. So the multiplicative model appeared the only alternative, and was deemed ‘accepted’. The ratio of lung cancer SMRs for non-smokers and smokers was generalised into the relative asbestos effect, RAE, with all the advantages of a parametric statistic (Berry et al., 1985, British Journal of Industrial Medicine 42, 12). On the multiplicative hypothesis, RAE=1, while RAE>1 indicates less synergism. The RAEs for the three most recent of the six results then available were >1; for one, P<0.005. From the six results combined, it was concluded that ‘overall non-smokers have a relative risk of lung cancer due to asbestos that is 1.8 times that of smokers’. Some admitted uncertainty about the figure 1.8 was seized upon and even the thrust of the conclusion has been very largely disregarded. So too has the RAE and all its benefits. As a result, all later reviewers have been led into error, much of it serious: in particular, they have failed to appreciate how much of the variation arises from the inevitable imprecision of all RAEs. This failure led reviewers in 1994 to discard, quite without justification, those interactions which were less than multiplicative and came from cohort studies. Although case-referent studies seemed to support the multiplicative hypothesis, the information from them is essentially unreliable. Thus it cannot weaken the conclusions from the cohort studies, that the multiplicative hypothesis is untenable and that the relative risk of lung cancer from asbestos exposure is about twice as high in non-smokers as in smokers; the best estimate of RAE is 2.04, with 95% confidence interval 1.28–3.25. This finding is not only of high statistical significance but of great social and scientific importance.”

Another interesting study is called, “Pulmonary toxicology of silica, coal and asbestos.” By A G Heppleston – Environ Health Perspect. 1984 April; 55: 111–127.   Here is an excerpt: “Abstract – Mineral particles are customarily inhaled as mixtures, though one component may predominate and determine the response. Although the lesions often possess a characteristic structure, according to the main type of particle deposited, morphology affords little indication of pathogenesis. Being a major element in the evolution of dust lesions, macrophage behavior has been examined extensively in vitro after treatment with mineral particles, attention being directed to membrane and biochemical changes; however, no clear lead to the origin of the lesions has emerged. Pulmonary fibrosis, as one of the ultimate consequences of dust accumulation, required a direct in vitro approach in which the products of the macrophage-particle interaction were utilized to provoke collagen formation by fibroblasts in a two-phase system. By this means, silica and asbestos stimulated connective tissue formation and application of the technique to coal dusts appears promising. Coal workers may develop a peculiar type of emphysema in relation to lesions whose fibrous content is comparatively small. Type II alveolar epithelium is also stimulated by inhaled particles and lipid accumulation follows. Alveolar lipidosis interferes with the fibrotic response by preventing contact between macrophage and particles. This phenomenon may account in part for anomalies, apparent in coal workers, between epidemiological findings and dust composition. Carcinogenesis is a well-recognized feature of asbestos exposure, but, as with fibrosis, risk prediction on the basis of in vitro tests of cytotoxicity is premature and may not be valid.”

Another interesting study is called, “Lung structure as a risk factor in adverse pulmonary responses to asbestos exposure. A case-referent study in Quebec chrysotile miners and millers.” Becklake MR, Toyota B, Stewart M, Hanson R, Hanley J. – Am Rev Respir Dis. 1983 Sep;128(3):385-8.  Here is an excerpt: “Abstract – To investigate the hypothesis that lung structure may predispose to the development of asbestos-related pulmonary fibrosis, we carried out a case-referent study using data gathered in a cross-sectional study of Quebec chrysotile asbestos miners and millers. Tracheal and thoracic measurements were derived from the routine chest radiographs of 44 men with established radiologic fibrosis and compared with similar measurements for 88 men matched for age and cumulative exposure in the same industry who had not developed pulmonary fibrosis. Intrathoracic tracheal lengths were, on the average, shorter, and transthoracic diameters narrower in cases compared with those in referents. In addition, cases were shorter than the referents, suggesting that height might be an indirect measure of the structural characteristics relevant to the response to inhaled asbestos particles. Our findings are thus consistent with the hypothesis outlined, and they suggest a line of investigation that might be useful in relation to other inhaled pollutants.”

We all owe a debt of gratitude to these fine researchers for their important work.  If you found any of these excerpts helpful, please read the studies in their entirety.

Monty Wrobleski is the author of this article, for more information please click on the following links


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