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Bioanalytical techniques for detecting biomarkers of response to human asbestos exposure

Our plain-English summary of Bioanalytical techniques for detecting biomarkers of response to human asbestos exposure, by C. Mesaros, A.J. Worth, N.W. Snyder, et al (Bioanalysis, 2015).

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The study

  • Authors: C. Mesaros, A.J. Worth, N.W. Snyder, M. Christofidou-Solomidou, A. Vachani, S.M. Albelda, I.A. Blair
  • Journal: Bioanalysis
  • Published: 2015;7(9):1157-73
  • Type of article: Review
  • Cited by: 11 articles, as counted by NIH iCite
  • Read it: PubMed · Publisher · Free full text

Abstract

Asbestos exposure is known to cause lung cancer and mesothelioma and its health and economic impacts have been well documented. The exceptionally long latency periods of most asbestos-related diseases have hampered preventative and precautionary steps thus far. We aimed to summarize the state of knowledge on biomarkers of response to asbestos exposure. Asbestos is not present in human biological fluids; rather it is inhaled and trapped in lung tissue. Biomarkers of response, which reflect a change in biologic function in response to asbestos exposure, are analyzed. Several classes of molecules have been studied and evaluated for their potential utility as biomarkers of asbestos exposure. These studies range from small molecule oxidative stress biomarkers to proteins involved in immune responses.

In plain English

This article was a review, not a new study. The authors summarized published research on 'biomarkers of response': changes in body chemistry that might show a person was exposed to asbestos. Such markers are needed because asbestos fibers stay trapped in lung tissue rather than appearing in blood or urine. The review focused mainly on comparisons of asbestos-exposed people with unexposed people. The studies it covered measured markers of oxidative damage to DNA and fats, and proteins such as SMRP (mesothelin), osteopontin, fibulin-3, fibronectin, HMGB1, interleukins 6 and 8, and RANTES. Most proteins were measured in blood, but fibronectin was measured in fluid washed from the lungs. Results were mixed. German studies of 636 exposed workers and 214 controls reported DNA-damage levels 1.7 to 2.0 times those of controls, but the authors cautioned that the laboratory methods did not prevent artificial DNA oxidation. A Japanese study found higher levels of a urinary DNA-damage marker that were not statistically significant. Another study of 1894 exposed workers and 102 controls found no significant difference in osteopontin. The authors concluded that current markers are not specific for asbestos exposure but are a starting point for a combined panel of markers.

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: Narrative review of published studies on biomarkers of biological response to asbestos exposure
  • Who was studied: Published studies, mainly comparing asbestos-exposed groups (workers in Germany, Japan, China, Italy, the Czech Republic, Australia, the USA, and residents near naturally occurring asbestos in Turkey) with nonexposed controls
  • Exposure: Asbestos exposure, mostly occupational, assessed indirectly through biological response markers rather than fiber measurement; one reviewed Chinese study involved mainly chrysotile, and one Turkish study involved naturally occurring surface asbestos
  • Main results:
    • In the reviewed German studies by Marczynski et al. (636 exposed workers, 214 unexposed controls), the DNA-damage marker 8-oxo-dGuo in white blood cells was 1.7 to 2.0 times control levels in all 3 years. The review authors said these data must be treated with caution because artificial oxidation was not prevented.
    • In a reviewed Japanese study (48 asbestos-exposed construction workers, 41 unexposed controls), urinary 8-oxo-dGuo was higher in the exposed group, but the difference was not statistically significant.
    • In a reviewed Chinese study of workers exposed mainly to chrysotile (10 exposed, 19 controls), 8-oxo-dGuo levels in blood cell DNA showed no significant difference between groups.
    • In a reviewed Italian study, white blood cell 8-oxo-dGuo poorly separated asbestos-exposed subjects from healthy controls (AUC 0.775).
    • In a reviewed study of exhaled breath (92 former asbestos workers, 46 controls), the oxidative-stress marker 8-iso-PGF2-alpha averaged 69.5 pg/ml in exposed subjects and 47.0 pg/ml in controls (p = 0.0001). There was no correlation with years of fiber exposure.
    • Findings for SMRP (mesothelin) were mixed. A reviewed Australian study (40 exposed, 28 controls) found no significant difference between exposed people and controls, while other reviewed studies found higher levels in exposed people.
    • Osteopontin findings were mixed. A Turkish study (123 exposed to naturally occurring asbestos, 120 controls) found a significant difference (p less than 0.05), but the marker was not useful for predicting malignant transformation.
    • A reviewed study (1894 exposed workers, 102 unexposed controls) found no significant difference in osteopontin between the groups.
    • In reviewed human studies, fibronectin was measured in bronchoalveolar lavage fluid. It was elevated in asbestos-exposed people with ARDs and increased in occupationally exposed men with restricted lung function.
    • In two reviewed studies of factory workers, serum IL-6 and IL-8 were significantly higher in the asbestos-exposed group than in both sets of controls.
  • The authors' conclusion: The authors concluded that current biomarkers of effect, including oxidative stress markers and immune-response proteins, are not specific for asbestos exposure. They saw them as a starting point for a specific and sensitive biomarker panel, possibly aided by more rigorous LC-MS and untargeted methods.
  • Limitations the authors state:
    • The authors noted that oxidative stress markers can be confounded by cigarette smoking.
    • The authors noted that several reviewed 8-oxo-dGuo studies did not take precautions against artificial DNA oxidation, so their reported levels should be treated with caution.

Topics

Medical terms in this study, explained in our Lexicon: Biomarker, Asbestos Exposure, Lung Cancer, Mesothelioma, Latency, Oxidative Stress.

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How to cite it

Cite the study

C. Mesaros, A.J. Worth, N.W. Snyder, M. Christofidou-Solomidou, A. Vachani, S.M. Albelda, et al. Bioanalytical techniques for detecting biomarkers of response to human asbestos exposure. Bioanalysis 2015;7(9):1157-73. doi:10.4155/bio.15.53. PMID: 26039812.

Cite our summary

“Bioanalytical techniques for detecting biomarkers of response to human asbestos exposure.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/bioanalytical-techniques-for-detecting-biomarkers-of-response-to.

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