Cigarette smoke, cellular

Subsequent studies have confirmed that the reason for this discrepancy is that the rat is able to rapidly metabolise P-carotene to retinol in the intestine, through the action of intestinal dioxygenase. In contrast humans absorb P-carotene systemically such that plasma levels of P-carotene increase to levels not found in the rodent. A more appropriate animal model is the ferret, which shows a similar metabolism to humans. High levels of plasma P-carotene in the ferret induce the cellular transcription factors c-fos and c-jun, and squamous metaplasia is seen in the lung with or without exposure to cigarette smoke (SCF, 2000). Even after the investment of all these resources it has not been possible for the EU Scientific Committee on Food to set an ADI. 

Increasing evidence indicates that diet/nutrition plays an important role in modulating the action and/or metabolism of a number of chemicals, drugs and environmental pollutants. Nutrients are essential for all fundamental cellular processes. The nutritional status of the affected subject may, therefore, influence cellular susceptibility to the effect of xenobiotics, including those from cigarette smoke. While the precise role of vitamin E in cellular metabolism is not yet clear, the vitamin may protect essential cellular components from the adverse effects of xenobiotics either via a free radical scavenging mechanism or as a component of the cell membrane (10-11). Administration of vitamin E has been shown to lessen the toxicity of a variety of compounds (12-16). 

The studies reported herein deal primarily with the influence of dietary vitamin E on cellular susceptibility of rats to cigarette smoke. 

Schwartz DA, Galvin JR, Merchant RK, et al. 1992. Influence of cigarette smoking on bronchoalveolar lavage cellularity in asbestos-induced lung disease. Am Rev Respir Dis 145(2) 400-405. 

Cardiovascular Effects. PAHs are contained in cigarette smoke, and smoking is a well-established risk factor in the development of atherosclerosis. Arterial smooth muscle cell proliferation, collagen synthesis, lipid accumulation, and cellular necrosis are all involved in the pathogenesis of the atherosclerotic plaque. In v//ro studies conducted using bovine, rabbit, and human smooth muscle cells from arteries demonstrated that benzopyrene affects some of the aforementioned processes. 

Coal Tar Products. Elevated red and white cell counts in urine were noted in 6-8% (29-34 of 452) of the employees examined in an industrial health survey in nine coal tar plants in which coal tar creosote and coal tar were the main treatments used (TOMA 1981). Some of these cell count elevations were attributed to urinary tract infections resulting from inadequate personal hygiene, and not to industrial exposure to toxic chemicals. However, some of the workers with elevated red and white cell counts in urine had cellular and granular casts and traces of protein, suggesting abnormal renal function. These individuals were referred to their physicians for diagnosis. No determination of exposure was made at the nine coal tar plants (TOMA 1981). Moreover, no clear relationship could be established because exposure routes in addition to inhalation (e.g., oral and dermal) were likely. Also, the ability to relate renal effects to coal tar creosote and coal tar exposure was further confounded by the possibility that the subjects were also exposed to other chemicals and cigarette smoke. Additional limitations of the study included seasonal and geographical variation in plant locations, past employment history, voluntary participation in the study that could have biased it in favor of healthy workers, lack of statistical analyses, lack of adequate controls, and use of only current employees. 

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