05 November 2012
The smoke from prototype modified cigarettes would appear to be less harmful to cardiovascular cells than that from conventional cigarettes. Tests in the lab using cells from the human cardiovascular system (in-vitro tests) showed that the ability of wounded cells to repair themselves is inhibited by cigarette smoke, but that this inhibition is significantly reduced in the presence of smoke from experimental reduced toxicant cigarettes.
This suggests that reducing smoke toxicant levels may alleviate certain biological responses in cells to cigarette smoke that may be linked to the development of cardiovascular disease.
“We are very encouraged by these results, as it is the first time we have been able to demonstrate an effect on biological response to the smoke from modified cigarettes,” says Dr Ian Fearon, a senior scientist at British American Tobacco.
The cells, called endothelial cells, line blood vessels and are known to control vascular function and health. Damage to these cells is a critical initiating step in the development of atherosclerosis, which involves thickening of the blood vessel wall, obstructs blood flow and is the underlying cause of cardiovascular or blood vessel disease. Normal healthy endothelial cells have the ability to move to repair and re-establish endothelial integrity.
Scientists at British American Tobacco report the use of an endothelial damage repair (scratch wound) assay to compare the effects of smoke from a conventional cigarette with that of a modified prototype on endothelial migration. The study is published in the International Journal of Toxicology . The test involves scratching layers of endothelial cells and monitoring the migration of cells across the wound over a period of 20 hours. Visual imaging is then used to investigate the effects of smoke on the ability of the cells to close the wound gap.
Under control conditions, endothelial cells travel across the wound and cause a reduction in wound width, which after 20 hours is about 41 per cent of the original wound width.
When the endothelial cells are exposed to increasing concentrations of cigarette smoke particulate matter (PM), the wound width is significantly increased after the allotted time.
However, when the wound was exposed to modified cigarette smoke, the affect of the smoke on cell migration was significantly reduced. Exposure at 48μg/ml (PM) for example resulted in a wound width of ~58 per cent after 20 hours, compared to ~74 per cent at 20 hours after exposure to conventional cigarette smoke PM at the same concentration.
Cigarette smoke is well known to induce oxidative stress (due to an overabundance of damaging reactive oxygen species). If oxidative stress is responsible for the migration response of these cells, than the addition of antioxidants should inhibit the effects of smoke. But it did not.
The exact mechanism of this effect has, therefore, yet to be determined. Nonetheless, this is the first time that scientists have been able to demonstrate that modifying cigarette toxicants levels can cause a difference in a biological response in this way.
“Although we do not yet know what this might mean in terms of disease risk, it is encouraging that we have seen a modification of a cardiovascular disease-related response in an in vitro model by modifying smoke toxicant levels,” said Dr Chris Proctor, Chief Scientific Officer at British American Tobacco.
Learn more by reading the article "Modification of Smoke Toxicant Yields Alters the Effects of Cigarette Smoke Extracts on Endothelial Migration: An In Vitro Study Using a Cardiovascular Disease Model" in International Journal of Toxicology, A SAGE journal, which will be available free for a limited time.
Notes to Editors