The worldwide epidemiology of Creutzfeldt-Jakob disease (CJD) is presented from an analysis of 1,435 patients. In the United States, the average annual mortality rate is at least 0.26 deaths per million. Temporal-spatial clustering of cases was not found in the United States, but reports from other countries indicate that such clustering does occur. Fifteen percent of the cases were of the familial type, suggesting a genetic susceptibility to infection. Iatrogenic transmission by corneal transplantation and neurosurgical operations has occurred, and the possibility is raised that previous surgery or preexisting neurological operations has occurred, and the possibility is raised that previous surgery or preexisting neurological disease may be associated with an increased risk of developing CJD. It remains to be determined whether the virus of CJD is maintained only by patient-to-patient transmission, has a zoonotic reservoir such as scrapie, or causes widespread latent infection of man that is occasionally activated.

This study examined the effect of cigarette smoking on the fluidity of the rat alveolar macrophage plasma membrane. Rats were subjected to 8 wk of an in vivo smoke exposure protocol, after which their alveolar macrophages were harvested. Fluidity was assessed by measuring steady-state anisotropy of isolated plasma membranes as well as of lipid vesicles made from total lipid extracts of these plasma membranes. The smoke-exposed animals showed a significant decrease in fluidity in both intact plasma membranes (p less than 0.0001) and in their lipid vesicle preparations (p less than 0.0001). To assess the time course of these changes, lipid vesicles were prepared from total cellular lipid extracts of macrophages from paired rats, control and smoke-exposed, at 1 through 4 wk after initiation of exposure. Significant decreases in fluidity were observed as early as 2 wk after smoking was begun (p less than 0.001). To assess the reversibility of these changes, paired rats were exposed for 8 wk, then withdrawn for 8, 12, and 18 wk, after which fluidity was evaluated in lipid vesicles prepared from total cellular lipids. Even after 18 wk of smoking cessation, significant decreases in fluidity persisted (p less than 0.01). We conclude that cigarette smoking causes a decrease in plasma membrane fluidity of rat alveolar macrophages. This is due at least in part to a change in the lipid portion of the membrane. These alterations occur after a very brief period of smoke exposure and persist long after cessation of smoking.

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It has been suggested that low-yield cigarettes (LYC) may be less hazardous and that smokers of these cigarettes are exposed to less tar, nicotine, and carbon monoxide. Recent studies have challenged this and question the analysis techniques for measuring yields of these cigarettes. Because published LYC contents may not reflect tissue toxicity and because compensatory puffing behaviors may alter smoke delivery to end-organ tissues, we studied the effect of smoke from a typical LYC on phagolysosome fusion and phagocytosis in alveolar macrophages of rats that chronically inhaled the smoke generated by an intermittently puffing apparatus. Alveolar macrophages were obtained by lung lavage and established in monolayers. Phagolysosome fusion and phagocytosis were assessed using the acridine orange fluorochrome assay. After 8 wk of exposure, there was no difference in phagolysosome fusion between controls and smokers. Carboxyhemoglobin levels in controls versus smokers were 1.36 +/- 0.09% versus 2.13 +/- 0.32% (mean +/- SE) (p = 0.06). A group of animals was similarly exposed, but the side pores of the cigarette filters were sealed with tape to simulate the compensatory behaviors often used by LYC smokers of occluding filter pores with their lips or fingertips. This significantly increased smoke exposure, and the carboxyhemoglobin level of the smokers increased to 7.0 +/- 1.4% (versus controls, p less than or equal to 0.01). Cells from these rats showed alterations in phagocytosis and in phagolysosome fusion compared with alveolar macrophages of control rats. These data suggest that the tobacco in LYC may have toxic effects similar to those of high-yield cigarettes and that LYC are likely to be less hazardous only if smoked in a fashion similar to that of a smoke-generating apparatus.