This Article Full Text Free Full Text (PDF) Free Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Add to My Personal Article Archive Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Yanbaeva, D. G. Articles by Wouters, E. F. M. Search for Related Content PubMed PubMed Citation Articles by Yanbaeva, D. G. Articles by Wouters, E. F. M.

Systemic Effects of Smoking^*

^* From the Department of Respiratory Medicine (Drs. Yanbaeva, Dentener, Wesseling, and Wouters), University Hospital Maastricht/Maastricht University, Maastricht, the Netherlands; and CIRO Horn (Dr. Creutzberg), Haelen, the Netherlands.

Correspondence to: Emiel F. M. Wouters, MD, PhD, FCCP, Department of Respiratory Medicine, University Hospital Maastricht/Maastricht University, PO Box 580, 6202 AZ Maastricht, the Netherlands; e-mail: e.wouters{at}lung.azm.nl

Abstract

Smoking is one of the major lifestyle factors influencing the health of human beings. Life-long cigarette smokers have a higher prevalence of common diseases such as atherosclerosis and COPD with significant systemic impact. The present review evaluates current knowledge concerning possible pathways through which cigarette smoking can affect human health, with special focus on extrapulmonary effects. Long-term smoke exposure can result in systemic oxidants-antioxidants imbalance as reflected by increased products of lipid peroxidation and depleted levels of antioxidants like vitamins A and C in plasma of smokers. A low-grade systemic inflammatory response is evident in smokers as confirmed by numerous population-based studies: elevated levels of C-reactive protein (CRP), fibrinogen, and interleukin-6, as well as increased counts of WBC have been reported. Furthermore, rheologic, coagulation and endothelial function markers like hematocrit, blood and/or plasma viscosity, fibrin d-dimer, circulating adhesion molecules (intracellular adhesion molecule-1, selectins), tissue plasminogen activator antigen, and plasminogen activator inhibitor type I are altered in chronic cigarette smokers. Although most of smoking-induced changes are reversible after quitting, some inflammatory mediators like CRP are still significantly raised in ex-smokers up to 10 to 20 years after quitting, suggesting ongoing low-grade inflammatory response persisting in former smokers. New longitudinal epidemiologic and genetic studies are required to evaluate the role of smoking itself and possible gene/environment interplay in initiation and development of smoking-induced common diseases affecting humans.

Key Words: endothelial dysfunction • hemostasis • smoking • systemic inflammation • systemic oxidative stress

This article has been cited by other articles:

				P. N. Mitrou, V. Kipnis, A. C. M. Thiebaut, J. Reedy, A. F. Subar, E. Wirfalt, A. Flood, T. Mouw, A. R. Hollenbeck, M. F. Leitzmann, et al. Mediterranean Dietary Pattern and Prediction of All-Cause Mortality in a US Population: Results From the NIH-AARP Diet and Health Study Arch Intern Med, December 10, 2007; 167(22): 2461 - 2468. [Abstract] [Full Text] [PDF]