Pulmonary inflammation in asbestos-exposed subjects with borderline parenchymal changes on HRCT

Our plain-English summary of Pulmonary inflammation in asbestos-exposed subjects with borderline parenchymal changes on HRCT, by L. Lehtimäki, P. Oksa, R. Järvenpää, et al (Respiratory Medicine, 2010).

The study

• Authors: L. Lehtimäki, P. Oksa, R. Järvenpää, T. Vierikko, R. Nieminen, H. Kankaanranta, J. Uitti, E. Moilanen
• Journal: Respiratory Medicine
• Published: 2010;104(7):1042-9
• Cited by: 27 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Many asbestos-exposed subjects have minor parenchymal changes on high resolution computed tomography (HRCT) that do not fulfil the diagnostic criteria for pulmonary fibrosis and asbestosis. We investigated if these borderline parenchymal changes in asbestos-exposed subjects are related to pulmonary inflammatory activity. Exhaled nitric oxide was measured, exhaled breath condensate collected and HRCT scanned in 104 subjects with moderate to high occupational asbestos exposure. Forty-one healthy unexposed subjects served as a comparison group. After excluding other pulmonary diseases, 35 asbestos-exposed subjects had normal parenchymal findings and 31 subjects had borderline parenchymal changes on HRCT. Lung function was poorer in the latter group, but there was no difference in the degree of asbestos exposure between these groups. As compared with the unexposed comparison group, asbestos-exposed subjects with borderline parenchymal changes had increased alveolar NO concentration (3.0 + or - 0.2 vs. 2.3 + or - 0.1 ppb, p = 0.008) and increased levels of leukotriene B(4) (12.2 + or - 1.1 vs. 3.3 + or - 0.8 pg/ml, p < 0.001) and 8-isoprostane (9.4 + or - 0.7 vs. 7.3 + or - 0.6 pg/ml, p = 0.021) in breath condensate. Asbestos-exposed subjects with normal parenchymal findings had only increased breath condensate levels of leukotriene B(4) (11.4 + or - 0.9, p < 0.001). Borderline parenchymal changes on HRCT in asbestos-exposed subjects are associated with increased markers of pulmonary inflammation. Such borderline parenchymal changes are likely a mild or early form of the same pathological process that leads to asbestosis.

Copyright 2010 Elsevier Ltd. All rights reserved.

In plain English

Researchers in Finland studied signs of lung inflammation in men with moderate or heavy occupational asbestos exposure (at least 20 fiber years). The article does not say which fiber types these men were exposed to. Of 104 exposed men recruited in Tampere, 33 were excluded for other lung conditions and 5 with asbestosis were not analyzed. Of the rest, 35 had normal lung tissue on high resolution CT and 31 had borderline changes too minor to count as asbestosis. All were compared with 41 healthy unexposed men. Asbestos exposure was similar in both exposed groups, but the borderline group had poorer lung function and more extensive pleural plaques. The borderline group had higher alveolar nitric oxide (3.0 vs 2.3 ppb in unexposed men), breath leukotriene B4 and 8-isoprostane, and blood IL-6 and MPO. In exposed men with normal lung tissue, only leukotriene B4 was raised, and bronchial nitric oxide output was slightly lower than in unexposed men. The authors concluded that borderline changes are likely a mild or early form of the process leading to asbestosis. They noted that exposure was estimated from retrospective interviews.

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 inflammation markers in exhaled breath, breath condensate and blood between asbestos-exposed men grouped by HRCT findings and an unexposed comparison group
• Who was studied: 104 men with moderate or heavy occupational asbestos exposure, recruited at the Clinic of Occupational Medicine, Tampere University Hospital, Finland. 33 were excluded under the exclusion criteria and 5 with asbestosis were excluded from the analysis. That left 35 with normal parenchymal findings and 31 with borderline parenchymal changes on HRCT, compared with 41 healthy unexposed men. All participants were never-smokers or had quit at least 5 years earlier. Study dates are not given.
• Exposure: Moderate or heavy occupational asbestos exposure, estimated by occupational physicians as at least 20 fiber years. The fiber types and specific jobs of this study's participants are not reported.
• Main results:
  • Asbestos exposure did not differ between the normal and borderline HRCT groups. The borderline group, on average, had poorer lung function and more extensive pleural plaques.
  • In the borderline group, alveolar NO concentration was increased (mean 3.0 ppb, vs 2.3 ppb in the unexposed comparison group and 2.2 ppb in exposed men with normal findings). Breath condensate LTB4 and 8-isoprostane were also increased, as were serum IL-6 and MPO.
  • Breath condensate LTB4 was increased in both exposed groups compared with unexposed men: 11.4 pg/ml in the normal-findings group, about 12 pg/ml in the borderline group and 3.3 pg/ml in unexposed men. Among exposed men with normal parenchymal findings, this was the only marker raised. Pleural calcifications were still seen in 24 of 35 men (69%) in that group.
  • Breath condensate 8-isoprostane was increased in the borderline group (about 9.4 to 9.5 pg/ml vs 7.3 pg/ml in unexposed men) but not in the normal-findings group.
  • Exposed men with normal parenchymal findings had slightly lower bronchial NO flux than unexposed men (0.7 vs 1.0 nl/s).
  • The asbestos exposure index did not correlate with any inflammatory marker, or with the degree of parenchymal or pleural changes on HRCT.
• The authors' conclusion: The authors concluded that borderline parenchymal changes on HRCT in asbestos-exposed subjects are associated with pulmonary inflammation. In their view, these changes are likely a mild or early form of the same pathological process that leads to asbestosis.
• Limitations the authors state:
  • Asbestos exposure was assessed by retrospective interview, which may make the exposure indices inaccurate.
  • Subjects with asbestosis were excluded. The authors suggest that a correlation between alveolar NO and lung function might have been found had they been included.
  • The lower bronchial NO flux in exposed subjects might reflect their higher proportion of ex-smokers.
  • A follow-up study is needed to assess whether the markers can predict who will develop asbestosis.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis.

Medical terms in this study, explained in our Lexicon: Inflammation, High-Resolution CT (HRCT), Pulmonary Fibrosis, Asbestos Exposure.

Related studies

• Glycoprotein YKL-40 Levels in Plasma Are Associated with Fibrotic Changes on HRCT in Asbestos-Exposed Subjects — T. Väänänen, L. Lehtimäki, et al. (2017)
• 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)
• Adipokine adipsin is associated with the degree of lung fibrosis in asbestos-exposed workers — S. Leivo-Korpela, L. Lehtimäki, et al. (2012)
• Comparison of feasibility and estimates of central and peripheral nitric oxide parameters by different mathematical models — T. Karvonen, H. Kankaanranta, et al. (2017)
• Clinical and HRCT screening of heavily asbestos-exposed workers — T. Vierikko, R. Järvenpää, et al. (2010)
• Fractional exhaled nitric oxide concentration is increased in asbestosis and pleural plaques — A. Sandrini, A.R. Johnson, et al. (2006)

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