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. 2012;7(4):e35725.
doi: 10.1371/journal.pone.0035725. Epub 2012 Apr 26.

Bronchial responsiveness is related to increased exhaled NO (FE(NO)) in non-smokers and decreased FE(NO) in smokers

Andrei Malinovschi  1 , Christer Janson, Marieann Högman, Giovanni Rolla, Kjell Torén, Dan Norbäck, Anna-Carin Olin
Affiliations

Bronchial responsiveness is related to increased exhaled NO (FE(NO)) in non-smokers and decreased FE(NO) in smokers

Andrei Malinovschi et al. PLoS One. 2012.

Abstract

Rationale: Both atopy and smoking are known to be associated with increased bronchial responsiveness. Fraction of nitric oxide (NO) in the exhaled air (FE(NO)), a marker of airways inflammation, is decreased by smoking and increased by atopy. NO has also a physiological bronchodilating and bronchoprotective role.

Objectives: To investigate how the relation between FE(NO) and bronchial responsiveness is modulated by atopy and smoking habits.

Methods: Exhaled NO measurements and methacholine challenge were performed in 468 subjects from the random sample of three European Community Respiratory Health Survey II centers: Turin (Italy), Gothenburg and Uppsala (both Sweden). Atopy status was defined by using specific IgE measurements while smoking status was questionnaire-assessed.

Main results: Increased bronchial responsiveness was associated with increased FE(NO) levels in non-smokers (p = 0.02) and decreased FE(NO) levels in current smokers (p = 0.03). The negative association between bronchial responsiveness and FE(NO) was seen only in the group smoking less <10 cigarettes/day (p = 0.008). Increased bronchial responsiveness was associated with increased FE(NO) in atopic subjects (p = 0.04) while no significant association was found in non-atopic participants. The reported interaction between FE(NO) and smoking and atopy, respectively were maintained after adjusting for possible confounders (p-values<0.05).

Conclusions: The present study highlights the interactions of the relationship between FE(NO) and bronchial responsiveness with smoking and atopy, suggesting different mechanisms behind atopy- and smoking-related increases of bronchial responsiveness.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. Number of subjects in each FENO quartile (FENO Q1–Q4) for non-smoking non-atopics, non-smoking atopics, smoking non-atopics and smoking atopics, respectively.
Figure 2
Figure 2. Methacholine challenge dose-response slope for all subjects divided upon their FENO quartiles values and smoking status.
Data is presented as mean values ± standard error of the mean and a regression line (p-value in the brackets) is drawn for non- and current smokers, respectively.
Figure 3
Figure 3. Effect size* (95%CI) for the association between slope and FENO (log-transformed) in non-, light (<10 cigarettes/day) and heavy smokers (≥10 cigarettes/day).
* The effect size is the regression coefficient obtained by linear regression models with slope as outcome and log-transformed FENO as dependent variable where the estimates of the three centres were combined by meta-analysis.
Figure 4
Figure 4. Methacholine challenge dose-response slope for all subjects divided upon their FENO quartiles values and atopy status.
Data is presented as mean values ± standard error of the mean and a regression line (p-value in the brackets) is drawn for non-atopics and atopics, respectively.
See this image and copyright information in PMC

References

    1. Sont JK, Willems LN, Bel EH, van Krieken JH, Vandenbroucke JP, et al. Clinical control and histopathologic outcome of asthma when using airway hyperresponsiveness as an additional guide to long-term treatment. The AMPUL Study Group. Am J Respir Crit Care Med. 1999;159:1043–1051. - PubMed
    1. Smith AD, Cowan JO, Filsell S, McLachlan C, Monti-Sheehan G, et al. Diagnosing asthma: comparisons between exhaled nitric oxide measurements and conventional tests. AmJRespirCrit Care Med. 2004;169:473–478. - PubMed
    1. Smith AD, Cowan JO, Brassett KP, Herbison GP, Taylor DR. Use of exhaled nitric oxide measurements to guide treatment in chronic asthma. N Engl J Med. 2005;352:2163–2173. - PubMed
    1. Taylor DR, Pijnenburg MW, Smith AD, De Jongste JC. Exhaled nitric oxide measurements: clinical application and interpretation. Thorax. 2006;61:817–827. - PMC - PubMed
    1. Ricciardolo FL, Sterk PJ, Gaston B, Folkerts G. Nitric oxide in health and disease of the respiratory system. Physiol Rev. 2004;84:731–765. - PubMed

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