Cigarette Smoking Associated With Changes in Inflammation Markers
In a study reported in the Journal of the National Cancer Institute, Shiels et al found significant changes in levels of inflammatory/immune markers in current cigarette smokers vs nonsmokers. There was a significant relationship between time since quitting and return to nonsmoker levels for several markers.
The study involved multiplex immune assay measurement of 78 inflammation, immune, and metabolic markers in 1,819 Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) participants aged 55 to 74 years from three nested case-control studies. Smoking status was never for 548 participants, former for 857, and current for 414.
Current Smokers
After correction for multiple testing, current smoking was associated with changes in 10 inflammation markers representing several components of the immune/inflammation response, including chemotaxis of T-cells ([C-C motif] ligand CCL 17/thymus and activation-regulated chemokine [CCL17/TARC]), recruitment of eosinophils and allergic inflammation (CCL11/EOTAXIN), chemotaxis and T-cell activation (interleukin [IL]-16), increased inflammation (IL-1β and C-reactive protein), anti-inflammatory response (IL-1Ra), T-cell and natural killer cell regulation (IL-15), regulators of cell growth and differentiation (soluble IL-6 receptor), hematopoiesis (stem cell factor), and angiogenesis (soluble vascular endothelial growth factor receptor 3 [VEGFR3]).
Levels IL-15, IL-1RA, IL-1β, IL-16, soluble IL-6 receptor, stem cell factor, and soluble VEGFR3 were significantly lower (all P < .01) among current smokers vs never-smokers, with odds ratios (ORs) ranging from 0.44 to 0.27. Levels of CCL17/TARC, CCL11/EOTAXIN, and C-reactive protein were significantly higher, with ORs ranging from 2.54 to 4.08 (all P < .01).
Changes by Time Since Quitting
There were no associations between levels of markers and number of cigarettes smoked per day among current smokers; there were significant associations (P < .05 for trends) for lower levels of stem cell factor and soluble IL-6 receptor with duration of smoking among current smokers. There were trends for return to never smoker levels for IL-15 (P = .01), IL-1RA (P = .004), IL-1β (P = .003), CCL17/TARC (P < .001), CCL11/EOTAXIN (P < .001), and C-reactive protein (P = .02) with increasing number of years since quitting among former smokers.
The investigators concluded: “Smoking is associated with a broad range of alterations in systemic immune and inflammation marker levels among older, long-term smokers. Smoking cessation may result in marker levels reverting back to those of never smokers over time.”
Meredith S. Shiels, PhD, MHS, of the National Cancer Institute, is the corresponding author for the Journal of the National Cancer Institute article.
The study was supported by the National Cancer Institute.
The content in this post has not been reviewed by the American Society of Clinical Oncology, Inc. (ASCO®) and does not necessarily reflect the ideas and opinions of ASCO®.
