8-Hydroxy-2'-deoxyguanosine as a marker of oxidative DNA damage related to occupational and environmental exposures

Our plain-English summary of 8-Hydroxy-2'-deoxyguanosine as a marker of oxidative DNA damage related to occupational and environmental exposures, by A. Pilger, H.W. Rüdiger (International Archives of Occupational and Environmental Health, 2006).

The study

• Authors: A. Pilger, H.W. Rüdiger
• Journal: International Archives of Occupational and Environmental Health
• Published: 2006;80(1):1-15
• Type of article: Review
• Cited by: 258 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Oxidative DNA damage is considered to play an important role in pathophysiological processes, ageing and cancer. So far major interest has been on measuring 8-hydroxy-2'-deoxyguanosine (8-OHdG), the preferred methods relying on HPLC or GC-mass spectrometry. The high biological relevance of 8-OHdG is due to its ability to induce G-->T transversions, which are among the most frequent somatic mutations found in human cancers. Effects of workplace exposures on the level of white blood cell 8-OHdG or urinary 8-OHdG have been reported with controversial results. Exposures examined include asbestos, azo-dyes, benzene, fine particulate matter (PM(2.5)), glassworks, polycyclic aromatic hydrocarbons (PAHs), rubber manufacturing, silica, metals, styrene, toluene and xylenes. The available data indicate that there is still a lack of well established dose-response relations between occupational or environmental exposures and the induction of 8-OHdG. Smoking has been most consistently identified as a confounder for 8-OHdG, but various occupational studies did not reveal higher levels of 8-OHdG in smokers. Despite the conflicting results, the reported studies show promise for 8-OHdG as a biomarker of oxidative stress associated with chemical exposure. However, there are critical aspects related to the analytical challenge, artifactual production of 8-OHdG, inter- and intra-individual variation, confounding factors and inter-laboratory differences, implying that further work is needed to reach a consensus on the background level of 8-OHdG.

In plain English

This article was a review, not a new study. The authors reviewed methods for measuring 8-hydroxy-2'-deoxyguanosine (8-OHdG), a marker of oxidative damage to DNA. They also reviewed published studies of 8-OHdG in the white blood cells or urine of people with occupational and environmental exposures, including smoking, benzene, styrene, asbestos, silica, chromium, cobalt, fine particulate matter and polycyclic aromatic hydrocarbons. On asbestos, the review described findings from other research groups. Tagesson and colleagues (1993) reported significantly higher urinary 8-OHdG in 30 asbestos-exposed workers than in 41 controls. Hanaoka and colleagues (1993) found no significant difference between asbestosis patients and unexposed controls. Takahashi and colleagues (1997) reported positive correlations with grades of asbestosis and with cumulative asbestos exposure. Marczynski and colleagues (2000) reported a 1.7- to 2-fold increase in a study of 496 asbestos-exposed workers. The authors concluded that results remained variable, that well established dose-response relations from human exposure were lacking, and that more work was needed to agree on the normal background level of 8-OHdG. They noted that results depend strongly on the measurement method.

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 measurement methods and of published human biomonitoring studies (plus some laboratory studies) of 8-OHdG
• Who was studied: Published occupational and environmental exposure studies of 8-OHdG in human white blood cells, lymphocytes, lung tissue or urine, summarized in a table. The article does not describe how studies were searched for or selected, or how many were included in total.
• Exposure: Several exposures were covered: smoking, benzene, toluene, xylenes, styrene, asbestos, azo-dyes, rubber manufacturing, glassworks, silica/quartz and coal dust, chromium, cobalt, arsenic, fine particulate matter (PM2.5) and polycyclic aromatic hydrocarbons. For asbestos, the review does not name specific fiber types for the worker studies.
• Main results:
  • In a laboratory study cited by the review (Kasai and Nishimura 1984), various types of asbestos fibers induced 8-OHdG when incubated with DNA in the presence of hydrogen peroxide.
  • Tagesson et al. (1993), as reported by the review: urinary excretion of 8-OHdG was significantly higher in 30 asbestos-exposed workers than in 41 controls.
  • Hanaoka et al. (1993), as reported by the review: there was no significant difference in blood cell 8-OHdG between asbestosis patients (7 in the table) and controls without asbestos exposure (6). Those authors concluded that 8-OHdG is not a sensitive marker for past low-level asbestos exposure.
  • Takahashi et al. (1997), as reported by the review: leukocyte 8-OHdG correlated positively with increasing grades of asbestosis and with cumulative asbestos exposure.
  • Marczynski et al. (2000a), as reported by the review: in a study of 496 asbestos-exposed workers, the data pointed to a 1.7- to 2-fold increase in white blood cell 8-OHdG due to asbestos exposure.
  • Marczynski et al. (2000b) found no correlation between 8-OHdG and factors such as duration of asbestos exposure, cumulative fibrous dust dose, asbestos-related diseases, age or smoking. The review authors wrote that this supports the view that inhaled asbestos caused the difference between asbestos workers and controls.
  • On smoking, the review stated that there is substantial evidence that smokers have higher 8-OHdG levels than non-smokers, although not all studies confirmed this.
• The authors' conclusion: The authors concluded that studies of 8-OHdG and occupational or environmental exposures still give variable results, that well established dose-response relations from human exposure are lacking, and that further work is needed to reach a consensus on the background level of 8-OHdG.
• Limitations the authors state:
  • Measuring 8-OHdG remains partly an analytical challenge, and results strongly depend on the method used.
  • 8-OHdG is not specific to any one exposure, and many confounding factors can affect it.
  • Laboratories differ, and quality-control projects are still far from agreeing on the normal level of oxidative damage in DNA.
  • No significant correlation between urinary 8-OHdG and 8-OHdG in DNA had yet been demonstrated.

Topics

Medical terms in this study, explained in our Lexicon: Environmental Exposure, 8-OHdG, Somatic Mutation, Dose-response relationship, Biomarker, Oxidative Stress, Confounding.

Related studies

• 8-hydroxy-2' -deoxyguanosine (8-OHdG): A critical biomarker of oxidative stress and carcinogenesis — A. Valavanidis, T. Vlachogianni, et al. (2009)
• Detection of 8-oxo-2'-deoxyguanosine, a marker of oxidative DNA damage, in culture medium from human mesothelial cells exposed to crocidolite asbestos — Q. Chen, J. Marsh, et al. (1996)
• Association between 8-hydroxy-2'-deoxyguanosine levels in DNA of workers highly exposed to asbestos and their clinical data, occupational and non-occupational confounding factors, and cancer — B. Marczynski, T. Kraus, et al. (2000)
• Determination of carcinogenic potential of mineral fibers by 8-hydroxydeoxyguanosine as a marker of oxidative DNA damage in mammalian cells — N. Murata-Kamiya, T. Tsutsui, et al. (1997)
• Role of nitrative and oxidative DNA damage in inflammation-related carcinogenesis — M. Murata, R. Thanan, et al. (2012)
• Patterns of 8-hydroxydeoxyguanosine formation in DNA and indications of oxidative stress in rat and human pleural mesothelial cells after exposure to crocidolite asbestos — H. Fung, Y.W. Kow, et al. (1997)

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