Inhalation of sidestream cigarette smoke accelerates development of arteriosclerotic plaques.

Abstract

Thus, relatively brief exposures to sidestream smoke early in life are sufficient to enhance arteriosclerotic plaque development.

The tar fraction of cigarette smoke does not promote arteriosclerotic plaque development.

“…There were 73 segments with plaque in the DMSO group and 74 each in the DMBA and TAR groups. As reported previously (9)(10)(11)16,19) plaque sizes were log-normally distributed, i.e., mean plaque sizes exceeded median values in all three groups (data not shown).…”

“…As in our previous studies, only males were used. Cockerels were distributed randomly into three groups of 10 The crude tar was resuspended in acetone, aliquoted, and frozen until use. The acetone was evaporated before the tar was solubiized in dimethylsulfoxide (DMSO, Fisher, Valley Forge, PA).…”

“…Two recent studies from our laboratory provided direct experimental support for this contention. Results from studies using the cockerel model of arteriosclerotic plaque development (8,9) revealed that inhalation exposure to ETS at levels equal to or even below those that can be encountered by people in smoke-filled environments is sufficient to promote arteriosclerosis (10,11). Atherosclerosis studies in cholesterol-fed, smoke-exposed rabbits confirm these findings (12).…”

Tobacco Industry Efforts Undermining Evidence Linking Secondhand Smoke With Cardiovascular Disease

“…More recent industry-funded publications 68,75 report an increased risk of CVD associated with SHS but claim that the magnitude of the risk is far below the generally accepted 30% increase. 7,8 When early tobacco industry-funded work demonstrated that SHS increased atherosclerosis, 39,45,46 the industry criticized the findings for using smoke concentrations larger than that in the real world and withdrew funding. RJR focused on attacking the biological plausibility of the association between SHS and CVD by conducting indirect platelet aggregation studies, exposure chamber experiments, and literature reviews.…”

“…38 Penn published his results in Circulation in October 1993, stating that sidestream cigarette smoke inhalation from 5 cigarettes per day (total suspended particulate [TSP], 7.5 to 8.5 mg/m 3 ) for 16 weeks accelerated the development of atherosclerosis. 39 Although the tobacco industry had funded and approved the protocol, the unfavorable results (from the industry's perspective) led Chris Coggins, an inhalational toxicologist at RJ Reynolds (RJR), to write a letter to Circulation, 40 criticizing the Penn study for using TSP levels that were 300 times higher than average measurements between smoking and nonsmoking homes (as measured by an industry consultant's 41 study 42 ); Penn responded 43 that exposure levels were only 20 times higher than measurements in public places and only double if measuring carbon monoxide. The CIAR internal progress report expected Penn to perform his next study at a lower "relevant, typical ETS level found indoors (Ϸ1 order of magnitude lower TSP than the original study)" and anticipated sidestream smoke exposures of 1200 and 600 g/m 3 TSP.…”