Asbestos and smoking

The methods of attribution between asbestos and smoking are obviously more complex and depend on assumptions concerning the interactions between the two agents. Although the field of risk attribution is an old one, its uses for liability are new and fraught with difficulties, some of which are evident from the description above. 

Berry G, Newhouse ML, Antonis P. 1985. Combined effect of asbestos and smoking on mortality from lung cancer and mesothelioma in factory workers. Br J Ind Med 42 12-18. 

Dave SK, Ghodasara NB, Mohanrao N, et al. 1997. The relation of expostrre to asbestos and smoking habit with pulmonary function tests and chest radiograph. Indian J Public Health 41 16-24. 

Erren TC, Jacobsen M, Piekarski C. 1999. Synergy between asbestos and smoking on lung cancer risks. Epidemiology 10(4) 405-411. 

Vainio H, Boffetta P. 1994. Mechanisms of the combined effect of asbestos and smoking in the etiology of lung cancer. Scand J Work Environ Health 20 235-242. 

The debate on the interaction of asbestos and smoking in lung cancer 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). 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 (Liddell 2001). The absolute risks are, of course, substantially less in non-smokers than in smokers. 

Environmental tobacco smoke (ETS) is the diluted mixture of pollutants caused by smoking of tobacco and emitted into the indoor air by a smoker. Constituents of ETS include submicron-size particles composed of a large number of chemicals, plus a large number of gaseous pollutants. Fibers in indoor air include those of asbestos, and man-made mineral fibers such as fiberglass, and glass wool. 

Think how many carcinogens are household names asbestos, cigarette smoke (a mixture of several thousand chemical compounds), DES, dioxin, saccharin, arsenic, PCBs, radon, EDB, Alar. Hundreds more of these substances, some very obscure, are known to the scientific and medical community, and many of these are scattered throughout the land at thousands of hazardous waste sites similar to Love Canal. People are exposed to these dreadful substances through the air they breathe, the water they drink and bathe in, and the foods they eat. Chemicals can also produce many other types of health damage, some very serious, such as birth defects and damage to our nervous and immune systems. 

Selikoff IJ, Hammond EC, ChurgJ Asbestos exposure, smoking and neoplasia. JAMA 204 106-112, 1968... 

A 1-year follow-up of 103 miners and millers of talc ore free from asbestos and silica showed an association between exposure and small opacities on chest radiographs the annual loss in FEVi and FVC was greater than expected and could not be wholly attributed to cigarette smoking." However, effects on pulmonary function in nonsmokers was not associated with lifetime or current talc exposure."... 

Churg, and B. T. Mossman. Asbestos and cigarette smoke cause increased DNA strand breaks and necrosis in bronchiolar epithelial cells in vivo. Free Radic Biol Med 2000 28(8) 1295-1299. 

Wood well treated with current commercial fire-retardant impregnation treatments will have flame-spread ratings of 25 or less. Many treated wood products have obtained a special marking or designation "FR-S" from UL (36) for having a flame-spread, fuel-contributed, and smoke-developed classification of not over 25 and no evidence of significant progressive combustion in an extended 30-minute ASTM E84 (34) test procedure. The fuel-contributed and smoke-developed classifications are also calculated relative to performance of red oak and asbestos-cement board. 

Another area where further research may be useful is the synergistic interaction between asbestos and other risk factors for lung cancer, especially smoking. Particularly helpful may be further studies on the mechanism of such interactions, since this could help improve current means of predicting the consequences of exposures to substances such as cigarette smoke. 

Blanc P. 1991. Cigarette smoking, asbestos, and parenchymal opacities revisited. Ann NY Acad Sci 133-141. 

Hurbankova M, Kaiglova A. 1993. The changes of some immunological parameters in subjects exposed to asbestos in dependence on age, duration of exposure, radiological findings, and smoking habits. Zentralbl Hyg Umweltmed 195(l) 55-65. 

Jackson JH, Schraufstatter lU, Hyslop PA, et al. 1987. Role of oxidants in DNA damage Hydroxyl radical mediates the synergistic DNA damaging effects of asbestos and cigarette smoke. J Clin Invest 80 1090-1095. 

Kilbum KH, Warshaw RH. 1994. Airways obstmction from asbestos exposure Effects of asbestosis and smoking. Chest 106 1061-1070. 

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