Smoking is associated with an age-related decline in exhaled nitric oxide

¹ Dept of Medicine, Division of Rheumatology and Immunology; and Division of Pulmonary, Allergy and Critical Care Medicine
² Dept of paediatrics, Division of Allergy and Immunology, Duke University Medical Center, Durham, NC
³ Dept of Medicine, Division of Rheumatology and Immunology

^* To whom correspondence should be addressed. E-mail: marc.levesque{at}duke.edu.

	Abstract

Age-related declines in lung function (FEV₁) are accelerated in smokers. Smoking is associated with decreased FeNO. We determined the impact of age on FeNO in otherwise healthy smokers and non-smokers.

We measured FeNO and serum cotinine levels in 994 healthy subjects between ages 18–40. We used ATS questionnaire data on smoking habits to validate serum cotinine levels as a surrogate marker for categorization of smokers and non-smokers in our cohort.

Serum cotinine levels were a good discriminator of smokers (N=99) and non-smokers (N=895). FeNO levels were significantly lower in otherwise healthy smokers compared with non-smokers (p<0.0001). There was an inverse correlation of serum cotinine levels with FeNO (p=0.0003). We found no correlation of age with FeNO in non-smokers but did find an inverse correlation of FeNO with age in smokers (p=0.0001). FeNO was significantly lower in older (ages 21–40) smokers compared to older non-smokers (p<0.0001), but was not lower in younger (ages 18–20) smokers compared to younger non-smokers.

Smoking was associated with decreased FeNO. The greatest smoking-related declines in FeNO occurred in older subjects. This suggests that smoking is associated with age-related declines in FeNO and justifies future mechanistic studies that address the impact of FeNO decline on lung function.