Leukocytosis and Tobacco Use: An Observational Study of Asymptomatic Leukocytosis
Abstract
Abstract
Objective: This study aimed to characterize the white blood cell differential of tobacco smoking-induced leukocytosis and describe the longitudinal impact of smoking cessation on this peripheral blood abnormality.
Methods: Medical records of patients undergoing evaluation by hematologists for persistent leukocytosis were reviewed. Patients in whom leukocytosis was determined to be secondary to tobacco use after exclusion of other causes were identified. Demographic and laboratory data were collected at time of diagnosis. Patients were longitudinally followed and information regarding smoking cessation and follow up white blood cell values were recorded.
Results: Forty patients were determined to have smoking-induced leukocytosis. The median age was 49.5 years (range: 28-75 years), 24 patients were female, and the mean BMI was 31.5 kg/m2. The mean white blood cell count was 13.3 × 109/L (range: 9.8 to 20.9 × 109/L). 39 patients had absolute neutrophilia (98%), 21 lymphocytosis (53%), 20 monocytosis (50%), and 19 basophilia (48%). During follow up, eleven patients either quit (n=9) or reduced (n=2) tobacco use. Reduction in tobacco smoking led to a significant decrease in mean white blood cell count (13.2 × 109/L vs 11.1 × 109/L, p=0.02). The median time to decrease in white blood cell count following reduction in tobacco use was 8 weeks (range: 2 to 49 weeks).
Conclusions: Tobacco-induced leukocytosis was characterized by a mild elevation in total white blood cell count and was most commonly associated with neutrophilia, lymphocytosis, monocytosis, and basophilia. Cessation of smoking led to improvement in leukocytosis. Tobacco history should be elicited from all patients presenting with leukocytosis to limit unnecessary diagnostic testing, and counseling regarding smoking cessation should be offered.
Keywords: Leukocytosis; Neutrophilia; Tobacco Use.
RPR Commentary
Cigarette smoking can cause a mild reversible leukocytosis. James W. Mold, MD, MPH