Effect of smoking and abstention on oxidative burst and reactivity of neutrophils and monocytes

Smoking is associated with surgical wound infections, impaired wound healing, and tissue-destructive disorders. The mechanisms are largely unknown, but changes in the function and activity of inflammatory cells may be involved.

Seventy healthy volunteers (54 smokers and 16 never smokers) were included. The smokers were studied while they smoked and after 20 days of abstinence. After the first 10 days of abstinence, they were randomized to double-blind treatment with transdermal nicotine patch 25 mg per day or placebo. Venous blood neutrophils and monocytes were sampled and isolated. In 22 randomly selected smokers and in all never smokers, the oxidative burst and chemotaxis were determined by a chemiluminescence response assay and a modified Boyden chamber technique, respectively. Stimulants were opsonized zymosan, formyl-Met-Leu-Phe, and zymosan-activated serum.

The neutrophil and monocyte oxidative burst was 50% and 68% lower, respectively, in smokers compared to never smokers (P < .05). Neutrophil chemotaxis was 93% higher in smokers (P < .05). Monocyte chemotaxis was lower in smokers compared to never smokers (P < .05). After 20 days of abstinence, neutrophil oxidative burst increased to the level of never smokers (P < .05); monocyte oxidative burst increased by 50% (P < .05). Chemotaxis was only marginally affected. The changes induced by abstinence were less pronounced in the transdermal nicotine patch group compared to the placebo group.

Smoking attenuates the oxidative burst of inflammatory cells and increases chemotaxis. Three weeks of abstinence normalize the oxidative burst, but affect chemotaxis only marginally.