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Differential effect of cigarette smoke exposure on exhaled nitric oxide and blood eosinophils in healthy and asthmatic individuals

Jacinto, Tiago (author)
Inst & Hosp CUF, Dept Allergy, Oporto, Portugal.;Univ Porto, Fac Med, CINTESIS Ctr Hlth Technol & Serv Res, Oporto, Portugal.;Porto Hlth Sch, Dept Cardiovasc & Resp Sci, Oporto, Portugal.
Malinovschi, Andrei, 1978- (author)
Uppsala universitet,Klinisk fysiologi
Janson, Christer (author)
Uppsala universitet,Lung- allergi- och sömnforskning
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Fonseca, Joao (author)
Inst & Hosp CUF, Dept Allergy, Oporto, Portugal.;Univ Porto, Fac Med, CINTESIS Ctr Hlth Technol & Serv Res, Oporto, Portugal.;Univ Porto, Fac Med, MEDCIDS Dept Community Med Informat & Hlth Sci, Oporto, Portugal.
Alving, Kjell, 1959- (author)
Uppsala universitet,Pediatrisk inflammationsforskning
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Inst & Hosp CUF, Dept Allergy, Oporto, Portugal;Univ Porto, Fac Med, CINTESIS Ctr Hlth Technol & Serv Res, Oporto, Portugal.;Porto Hlth Sch, Dept Cardiovasc & Resp Sci, Oporto, Portugal. Klinisk fysiologi (creator_code:org_t)
2017-08-21
2017
English.
In: Journal of Breath Research. - : IOP Publishing. - 1752-7155 .- 1752-7163. ; 11:3
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Background:Tobacco smoking affects both the fraction of exhaled nitric oxide (FeNO) and blood eosinophil (B-Eos) count, two clinically useful biomarkers in respiratory disease that represent local and systemic type-2 inflammation, respectively.Objective:We aimed to study the influence of objectively measured smoke exposure on FeNO and B-Eos in a large population of subjects with and without asthma.Methods:We utilized the US National Health and Nutrition Examination Surveys 2007-2012 and included 10 669 subjects aged 6-80 years: 9869 controls and 800 asthmatics. Controls were defined as having no respiratory disease, no hay fever in the past year, and B-Eos count ≤0.3 × 109 l−1. Asthma was defined as self-reported current asthma and at least one episode of wheezing or an asthma attack in the past year, but no emphysema or chronic bronchitis. Tobacco use was collected via questionnaires and serum cotinine was measured with mass spectrometry.Results:Increasing cotinine levels were associated with a progressive reduction in FeNO in both controls and asthmatics. FeNO remained significantly higher in asthmatics than controls except in the highest cotinine decile, equivalent to an average reported consumption of 13 cigarettes/day. B-Eos count increased with cotinine in controls, but was unchanging in asthmatics. Interestingly, B-Eos count was significantly higher in presently non-exposed (cotinine below detection limit) former smokers than never smokers.Conclusion:Smoke exposure decreases FeNO and increases B-Eos count. These effects should be considered in the development of normalized values and their interpretation in clinical practice. The persistence of elevated B-Eos in former smokers warrants further studies.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine (hsv//eng)

Keyword

exhaled nitric oxide
blood eosinophils
smoking
asthma
inflammation

Publication and Content Type

ref (subject category)
art (subject category)

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