Smoking, white blood cell counts, and TNF system activity in Japanese male subjects with normal glucose tolerance
1 Health Care and Promotion Center, Yodogawa Christian Hospital, 2-9-26, Awaji, Higashiyodogawa-ku, Osaka, 533-0032, Japan
2 Division of Clinical Nutrition and Internal Medicine, Okayama Prefectural University, 111, Kuboki, Soja-city, Okayama, 719-1197, Japan
3 Division of Diabetes and Endocrinology, Kyoto Preventive Medical Center, 28, Nishinokyo, Samaryocho, Nakagyo-ku, Kyoto, 604-8091, Japan
4 Department of Pharmacy, Saiseikai-Nakatsu Hospital, 2-10-39, Shibata, Kita-ku, Osaka, 530-0012, Japan
5 Department of Oral Health, Kobe Tokiwa Junior College, 2-6-2, Otani-cho, Nagata-ku, Kobe, 653-0838, Japan
6 Department of Dental Science for Health Promotion, Hiroshima University Graduate School of Biomedical Sciences, 1-2-3, Kasumi, Minami-ku, Hiroshima, 734-8551, Japan
7 Division of Diabetes, Clinical Nutrition and Endocrinology, Kansai Electric Power Hospital, 2-1-7, Fukushima, Fukushima-ku, Osaka, 553-0003, Japan
8 Department of Internal Medicine, Kyoto Postal Services Agency Hospital, 109,Nishirokkakucho, Rokkaku-street, Shinmachi, Nakagyo-ku, Kyoto, 604-8798, Japan
9 Kyoto Institute of Health Science, Karasumaoike-Higashi, Nakagyo-ku, Kyoto, 604-0845, Japan
10 Division of Endocrinology and Metabolism, Jichi Medical University, 3311-1, Yakushiji, Shimono-city, Tochigi, 329-0498, Japan
Tobacco Induced Diseases 2011, 9:12 doi:10.1186/1617-9625-9-12Published: 25 November 2011
Cigarette smokers have increased white blood cell (WBC) counts and the activation of tumor necrosis factor (TNF). The effect of smoking on WBC counts and TNF system activity, however, has not been separately investigated yet.
Subjects and Methods
One hundred and forty-two Japanese male subjects with normal glucose tolerance were recruited. They were stratified into two groups based on the questionnaire for smoking: one with current smokers (n = 48) and the other with current non-smokers (n = 94). Whereas no significant differences were observed in age, BMI, high molecular weight (HMW) adiponectin, and TNF-α between the two groups, current smokers had significantly higher soluble TNF receptor 1 (sTNF-R1) (1203 ± 30 vs. 1116 ± 21 pg/ml, p = 0.010) and increased WBC counts (7165 ± 242 vs. 5590 ± 163/μl, p < 0.001) and lower HDL cholesterol (55 ± 2 vs. 60 ± 1 mg/dl, p = 0.031) as compared to current non-smokers. Next, we classified 48 current smokers into two subpopulations: one with heavy smoking (Brinkman index ≥ 600) and the other with light smoking (Brinkman index < 600).
Whereas no significant difference was observed in age, BMI, HMW adiponectin, WBC counts and TNF-α, sTNF-R1 and sTNF-R2 were significantly higher in heavy smoking group (1307 ± 44 vs. 1099 ± 30 pg/ml, p < 0.001; 2166 ± 86 vs. 827 ± 62 pg/ml, p = 0.005) than in light smoking group, whose sTNF-R1 and sTNF-R2 were similar to non-smokers (sTNF-R1: 1116 ± 15 pg/ml, p = 0.718, sTNF-R2; 1901 ± 32 pg/ml, p = 0.437). In contrast, WBC counts were significantly increased in heavy (7500 ± 324/μl, p < 0.001) or light (6829 ± 352/μl, p = 0.001) smoking group as compared to non-smokers (5590 ± 178/μl). There was no significant difference in WBC counts between heavy and light smoking group (p = 0.158).
We can hypothesize that light smoking is associated with an increase in WBC counts, while heavy smoking is responsible for TNF activation in Japanese male subjects with normal glucose tolerance.