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This Month in Anesthesiology  |   June 2001
Smoking Cessation and Its Effects on Alveolar Macrophage Function.
Article Information
This Month in Anesthesiology
This Month in Anesthesiology   |   June 2001
Smoking Cessation and Its Effects on Alveolar Macrophage Function.
Anesthesiology 6 2001, Vol.94, 5A. doi:
Anesthesiology 6 2001, Vol.94, 5A. doi:
Smoking Cessation and Its Effects on Alveolar Macrophage Function. Kotani et al. (page 999)
How long after smoking cessation does recovery of alveolar macrophage function occur? To evaluate the effects of nonsmoking duration on both antimicrobial and inflammatory function of alveolar macrophages during anesthesia and surgery, Kotani et al.  recruited 71 patients scheduled to undergo general anesthesia for more than 4 h. Of these patients, 15 had never smoked, 15 currently smoked, and 41 were former smokers. The former smokers were further divided into one of three groups determined by how long they had been smoke-free: 2 months (n = 13), 3–5 months (n = 13), or 6–12 months (n = 15).
Immediately after induction of anesthesia (with propofol, fentanyl, and vecuronium), alveolar immune cells were harvested by bronchoalveolar lavage. Cells were also harvested 2 and 4 h after induction and at the end of surgery. To assess alveolar macrophage function, the authors evaluated opsonized and nonopsonized phagocytosis, microbicidal activity, macrophage aggregation, neutrophil influx to the distal airway, and gene expression for proinflammatory cytokines and tumor necrosis factor α (TNF-α). The concentrations and total numbers of alveolar cells were 4–5 times greater in smoking than in nonsmoking patients at each measurement interval. Starting at 4 h after induction of anesthesia, the decreases in antimicrobial functions were 1.5–3 times greater in current and former smokers with 2 months’ abstinence than in patients who had never smoked. Also at 4 h after induction, the increase in expression of all cytokines (except interleukin 8) was 2–5 times less in current and former smokers than in the nonsmoking group.
The authors found that the concentration and total number of alveolar macrophages normalized in patients who had been smoke-free for 6 months and that intraoperative increases in gene expression for antiinflammatory cytokines were reduced far more in smokers than in nonsmoking patients. Additionally, phagocytosis and bactericidal activity, key elements of pulmonary defense, were markedly impaired in current smokers and those who had quit smoking only 2 months before surgery. Although cytokine expression does not necessarily correlate with cytokine production, these results suggest that former smokers may have a limited ability to mount an effective pulmonary immune defense for at least 6 months after smoking cessation.