The response of human bone marrow to chronic cigarette smoking

Chronic cigarette smoking in humans causes leukocytosis, Animal studies sho w that chronic smoking shortens the transit time of polymorphonuclear leuko cytes (PMNLs) through the bone marrow. The present study examines the respo nse of human bone marrow to chronic cigarette smoking. Three characteristics of peripheral blood PMNLs that indicate active bone m arrow release (band cell counts, surface L-selectin expression and myeloper oxidase (MPO) content), were measured in 38 healthy chronic smokers (23+/-5 pack-yrs) and 15 age-and sex-matched nonsmoking controls. The total white cell (6.8+/-0.3x10(9) versus 5.3+/-0.2x10(9) cells L-1 p<0. 0001) and PMNL (4.2+/-0.18x10(9) versus 3.2+/-0.1x10(9) cells.L-1, p<0.003) counts were higher in smokers as were the percentage (4.8+/-0.6 versus 1.1 +/-0.2, p<0.0001) and total number (0.21+/-0.04x10(9) versus 0.03+/-0.001x1 0(9) cells.L-1, p<0.01) of band cells. Flow cytometry showed that the mean fluorescence intensity (MFI) of L-selectin (3.2+/-0.2 versus 2.6+/-0.1, p<0 .05) on PMNLs was higher in smokers. There was no difference in the baselin e or N-formyl-methionyl-leucyl-phenylalanine-stimulated expression of CD63 or CD18/CD11b (surface markers of PMNL, activation) between smokers and con trols, The MPO content of PMNLs was higher in smokers (3.4+/-0.3 versus 1.7 +/-0.2 MFI, p<0.05), Smokers with a low (<75% of the predicted value) diffu sing capacity of the lung for carbon monoxide had higher PMNL MPO levels th an smokers with a diffusing capacity of >75% pred (p<0.05). In conclusion, chronic smoking causes phenotypic changes in circulating pol ymorphonuclear leukocytes that are characteristic of chronic stimulation of the bone marrow and it is speculated that the increased number of immature polymorphonuclear leukocytes contributes to the chronic lung inflammation associated with cigarette smoking.