Reports have shown that secondhand smoke can have a significant negative impact on health. Next to active smoking and alcohol abuse, secondhand smoke is the third leading cause of poor health and premature death in the developing world. There are multiple mechanisms by which secondhand smoke has a negative effect on coronary risk factors. Inflammation markers have been shown to be related to the development of atherosclerotic disease. However, no studies have shown the effect of secondhand smoke on inflammation markers. Panagiotakos and colleagues evaluated the effect of secondhand smoke on inflammatory markers related to cardiovascular disease in persons without any clinical evidence of cardiovascular or atherosclerotic disease.

The study was a survey evaluation of a randomly selected adult population with no clinical evidence of cardiovascular or atherosclerotic disease. The survey included information about exposure to secondhand smoke at home and in the workplace. Exposure was divided into three subgroups: no exposure, occasional exposure, and regular exposure. Blood pressure, height, and weight were measured. Blood samples were drawn for measurement of high-sensitivity C-reactive protein, fibrinogen, total and low-density lipoprotein (LDL) cholesterol, homocysteine, and blood glucose levels. Dietary and physical activity information was obtained from the participants.

There were 1,128 men and 1,154 women participating in the study. Thirty-eight percent of the men and 33 percent of the women who never smoked reported current exposure to secondhand smoke. When compared with persons who were not currently exposed to secondhand smoke, those with regular exposure had significantly higher white blood cell counts and C-reactive protein levels. In addition, the regularly exposed group had significantly higher homocysteine, fibrinogen, and oxidized LDL cholesterol levels compared with those who had no exposure. After adjusting for age, sex, physical activity, body mass index, and food consumption, persons with regular exposure to secondhand smoke had significantly higher levels of all of the inflammatory markers.

The authors conclude that exposure to secondhand smoke leads to inflammation and oxidation. This finding suggests that the impact of secondhand smoke on inflammation may be another pathophysiologic mechanism for the development of atherosclerosis. They add that more effort should be made to reduce involuntary exposure to secondhand smoke.