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Effect of smoking on exhaled nitric oxide and flow-independent nitric oxide exchange parameters

Depts of ¹ Medical Cell Biology, Integrative Physiology, ³ Medical Sciences, Respiratory Medicine and Allergology, and, ⁴ Medical Sciences, Occupational and Environmental Medicine, and, ² Asthma and Allergy Research Centre, Uppsala University, Uppsala, and, ⁵ Dept of Caring Sciences and Sociology, Section of Medical Science, University of Gävle, Gävle, Sweden, and ⁶ Dept of Engineering Physics and Mathematics, Helsinki University of Technology, Helsinki, Finland.

CORRESPONDENCE: A. Malinovschi, Uppsala University, Dept of Medical Cell Biology, Integrative Physiology, Box 571, SE-751 23 Uppsala, Sweden. Fax: 46 184714938. E-mail: Andrei.Malinovschi{at}medcellbiol.uu.se

Keywords: Exhaled nitric oxide, extended nitric oxide analysis, oral tobacco, smoking

Received: September 29, 2005
Accepted April 9, 2006

It is a well-known fact that smoking is associated with a reduction in exhaled nitric oxide (NO) levels. There is, however, limited knowledge relating to the smoking-induced changes in production or exchange of NO in different compartments of the airways.

This study comprised 221 adult subjects from the European Community Respiratory Health Survey II, who were investigated in terms of their exhaled NO, lung function, immunoglobulin E sensitisation and smoking habits. The following parameters were determined using extended NO analysis: airway tissue nitric oxide concentration (C_aw,NO), airway transfer factor (or diffusing capacity) for nitric oxide (D_aw,NO), alveolar nitric oxide concentration (C_A,NO) and fractional exhaled nitric oxide concentration at a flow rate of 50 mL·s^-1 (F_eNO,0.05). Maximum total airway nitric oxide flux (J'_aw,NO) was calculated from D_aw,NO(C_aw,NO–C_A,NO).

Current smokers (n = 35) exhibited lower (geometric mean) F_eNO,0.05 (14.0 versus 22.8 ppb), C_aw,NO (79.0 ;versus 126 ppb) and J'_aw,NO (688 versus 1,153 pL·s^-1) than never-smokers (n = 111). Ex-smokers (n = 75) were characterised by lower F_eNO,0.05 (17.7 versus 22.8 ppb) and J_aw,NO (858 versus 1,153 pL·s^-1) than never-smokers. These relationships were maintained after adjusting for potential confounders (sex, age, height, immunoglobulin E sensitisation and forced expiratory volume in one second), and, in this analysis, a negative association was found between current smoking and C_A,NO. Snus (oral moist snuff) consumption (n = 21) in ex-smokers was associated with an increase in D_aw,NO and a reduction in C_aw,NO, after adjusting for potential confounders. Passive smoking was associated with a higher C_A,NO.

Using extended nitric oxide analysis, it was possible to attribute the reduction in exhaled nitric oxide levels seen in ex- and current smokers to a lower total airway nitric oxide flux in ex-smokers and reduced airway and alveolar nitric oxide concentrations in current smokers. The association between snus (oral tobacco) use and reduced nitric oxide concentrations in the airways and increased nitric oxide transfer from the airways warrants further studies.

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