Cigarette smoking is the leading preventable cause of death (one in five deaths) in the United States. It is also highly prevalent in China, and globally. Sadly, 90% of all lung cancer deaths can be attributed to smoking. It also causes 80% of chronic obstructive pulmonary disease (COPD) deaths. It is also a risk factor for heart disease and stroke.
Linked to heart disease, cigarette smoking has been implicated in the development and progression of atherosclerosis; a condition characterized by the build up of plaque inside of an artery causing narrowing. A consensus on exactly how this occurs has not been reached. Smoking may mediate thickening of the carotid intima-media (artery wall).
A new study led by Tai Hing Lam of Guangzhou No.12 Hospital, China, investigated possible inflammatory mediators of smoking induced artery wall thickening in the Guangzhou biobank cohort. They published their results in the journal Medicine.
The study confirmed that smokers had thicker carotid intima-media than non-smokers. They found statistical evidence to suggest that this may be mediated by leukocytes, granulocytes, high sensitivity-C reactive protein, and fibrinogen. There was no evidence of lymphocyte involvement.
Although the authors did not test the hypothesis, they noted that cytokines such as interleukin-6 increase fibrinogen transcription, and that a possible source of these cytokines is the recruitment of macrophages to the lungs due to smoking induced damage.
Limitations of the study include that techniques such as Mendelian randomization were not applied so, as the authors acknowledge, although plausible, the markers of inflammation may not be causal for carotid intima-media thickness. The inflammatory markers were only measured once, which may not provide an accurate description of their inflammatory state. The cohort of 1752 people is also relatively small.
“In conclusion, our study showed that the effects of cigarette smoking on carotid intima-media thickness were partly mediated by leukocyte, high sensitivity C-reactive protein, and fibrinogen. Of the inflammatory factors, leukocyte appeared to mediate much of the effect of smoking-induced atherosclerosis, and the mediating role was mainly driven by granulocyte rather than lymphocyte,” stated the authors.