Fractional exhaled nitric oxide concentration is increased in asbestosis and pleural plaques

Our plain-English summary of Fractional exhaled nitric oxide concentration is increased in asbestosis and pleural plaques, by A. Sandrini, A.R. Johnson, P.S. Thomas, et al (Respirology, 2006).

The study

• Authors: A. Sandrini, A.R. Johnson, P.S. Thomas, D.H. Yates
• Journal: Respirology
• Published: 2006;11(3):325-9
• Cited by: 28 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Objective And Background: Asbestos exposure induces generation of reactive oxygen and nitrogen species. Nitric oxide is involved in asbestos-related lung toxicity in vitro and can be measured non-invasively in humans in exhaled breath. The authors hypothesized that fractional exhaled nitric oxide concentration (FENO) would be increased in subjects with asbestos-related lung disorders.

Methods: FENO was measured in 56 subjects with asbestos-related disorders (asbestosis: 12; pleural plaques: 32; asbestos-related diffuse pleural thickening: 12) and in 35 normal subjects. The authors also measured exhaled carbon monoxide, another marker of lung inflammation.

Results: Median (25-75 percentile) FENO was increased in subjects with asbestosis (7.9 (6.6-15.7) p.p.b.; P=0.001) and pleural plaques (6.3 (5.3-9) p.p.b.; P=0.03) compared with normal controls (4.6 (3.5-6) p.p.b.). Subjects with DPT had a median FENO of 5.6 p.p.b., similar to controls. No significant differences in exhaled carbon monoxide were observed between controls (1.0+/-0.3 p.p.m.) and subjects with asbestosis (1.3+/-0.3 p.p.m.), pleural plaques (1.2+/-0.3 p.p.m.) or diffuse pleural thickening (1.1+/-0.3 p.p.m.).

Conclusions: FENO is raised in asbestosis consistent with lung inflammation, and also in pleural plaques.

In plain English

This short communication from Sydney, Australia, measured nitric oxide in exhaled breath (FENO), which the authors describe as a marker of lung inflammation. The study included 91 men: 12 with asbestosis, 32 with pleural plaques, 12 with asbestos-related diffuse pleural thickening (DPT) and 35 normal controls. Smokers and people with other lung diseases or other factors known to affect FENO were excluded. Ex-smokers were included. Median FENO was 7.9 parts per billion in the asbestosis group (P = 0.001) and 6.3 in the pleural plaques group, compared with 4.6 in controls. For the plaques group, the article's results section gives P = 0.006 but its abstract gives P = 0.03. FENO in the DPT group (5.6) did not differ from controls. Exhaled carbon monoxide, another marker, showed no significant differences between controls and any of the three disease groups. The authors concluded that FENO is raised in asbestosis, consistent with lung inflammation, and also in pleural plaques. The authors noted that the plaques result could be a chance finding, that the DPT group was small, and that an effect of past smoking could not be altogether excluded.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Cross-sectional comparison of patient groups with normal controls (published as a short communication)
• Who was studied: 91 male subjects attending St Vincent's Hospital and the Dust Diseases Board in Sydney, Australia: 35 normal controls, 12 with asbestosis, 32 with pleural plaques and 12 with diffuse pleural thickening. 54 were ex-smokers and 37 never smokers. Study dates are not given.
• Exposure: Subjects were grouped by diagnosed asbestos-related disorder (asbestosis, pleural plaques, asbestos-related diffuse pleural thickening). The article gives no information on fiber types, jobs or exposure amounts.
• Main results:
  • Median FENO was higher in the asbestosis group: 7.9 parts per billion (25 to 75 percentile 6.6 to 15.7), P = 0.001, compared with normal controls
  • Median FENO was higher in the pleural plaques group: 6.3 parts per billion (5.3 to 9.0), P = 0.006, than in normal controls at 4.6 parts per billion (3.5 to 6.0). The abstract gives P = 0.03 for this comparison.
  • FENO in the diffuse pleural thickening group (median 5.6 parts per billion, 3.1 to 9.1) did not differ from controls (P = 0.77)
  • Exhaled carbon monoxide showed no significant differences between controls (1.0 plus or minus 0.3 parts per million) and the asbestosis (1.3 plus or minus 0.3), pleural plaques (1.2 plus or minus 0.3) or diffuse pleural thickening (1.1 plus or minus 0.3) groups
  • FENO was not correlated with lung function measures, except for per cent predicted total lung capacity in the asbestosis group (r = minus 0.66; P = 0.04)
  • The asbestosis and diffuse pleural thickening groups had a restrictive deficit on lung function. Lung function in the pleural plaques group did not differ from controls.
• The authors' conclusion: The authors concluded that FENO is raised in asbestosis, consistent with lung inflammation, and also in pleural plaques. They suggested that FENO could potentially prove of value in assessing asbestos-related disorders.
• Limitations the authors state:
  • FENO and exhaled carbon monoxide were not compared with other, more invasive markers of lung inflammation (lavage, biopsy or induced sputum)
  • Extended exhaled nitric oxide measurements, which might separate alveolar from bronchial inflammation, were not performed
  • The raised FENO in the pleural plaques group could be a false-positive (type I) error
  • The diffuse pleural thickening group was small, so its result could be a false-negative (type II) error
  • Ex-smokers were included in all groups, and an effect of past smoking cannot be altogether excluded
  • Whether FENO detects inflammation before lung function changes would require prospective longitudinal studies

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis, Pleural plaques and thickening.

Medical terms in this study, explained in our Lexicon: Pleural Plaques, Asbestos Exposure, Diffuse Pleural Thickening, Inflammation.

Related studies

• Increased alveolar nitric oxide concentration and high levels of leukotriene B(4) and 8-isoprostane in exhaled breath condensate in patients with asbestosis — H. Lehtonen, P. Oksa, et al. (2007)
• The role of nitric oxide in pleural disease — O.S. Kotsiou, K.I. Gourgoulianis, et al. (2021)
• Comparison of feasibility and estimates of central and peripheral nitric oxide parameters by different mathematical models — T. Karvonen, H. Kankaanranta, et al. (2017)
• Nitric oxide (NO) synthase activity in the lung and NO synthesis in alveolar macrophages of rats increased on exposure to asbestos — H. Iguchi, S. Kojo, et al. (1996)
• Chronic infections and inflammatory processes as cancer risk factors: possible role of nitric oxide in carcinogenesis — H. Ohshima, H. Bartsch (1994)
• Participation of nitric oxide and iron in the oxidation of DNA in asbestos-treated human lung epithelial cells — C.C. Chao, S.H. Park, et al. (1996)

Browse more research in Respirology, or return to medical research.