Chemical interaction: enhancement and inhibition of clastogenicity

Our plain-English summary of Chemical interaction: enhancement and inhibition of clastogenicity, by W.A. Anwar (Environmental Health Perspectives, 1993).

The study

• Author: W.A. Anwar
• Journal: Environmental Health Perspectives
• Published: 1993;101 Suppl 3(Suppl 3):203-6
• Cited by: 2 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Most environmental exposures involve concurrent or sequential exposure to multiple chemicals in air, water, and food. Interactive effects in carcinogenesis have been described for certain combinations of agents. They are described in terms of enhancement or inhibition of carcinogenesis. Enhancement effects have been documented for cigarette smoking in combination with exposure to asbestos, radon, alcohol, or other exposures. A variety of inhibitors of carcinogenesis have also been described. They are classified into agents preventing formation of carcinogens; blocking agents; and suppressing agents. Assessment of risk from exposure to multiple agents can be derived either from epidemiological studies in relation to actual exposure or from laboratory studies after controlled exposure to different agents. Prediction of how toxic components of mixtures will interact should be based on an understanding of the mechanisms of such interactions. Compounds may interact chemically, yielding new toxic components or causing a change in the biological availability of the existing components or metabolites. In humans, great individual variability in response is to be expected because of genetic heterogeneity or acquired host susceptibility factors. Interaction is thus a key component in the risk assessment process. In this paper, the definition of interaction and the theoretical basis for different types of interaction in cancer causation are reviewed. Epidemiological and experimental studies showing interactive effects of two chemical carcinogens are also presented.

In plain English

This paper was a review, not a new study. The author, from Ain Shams University in Cairo, reviewed how two or more chemicals can act together to increase (enhance) or decrease (inhibit) chromosome damage and cancer development. On asbestos, the author cited earlier studies by Selikoff, Hammond and colleagues. As the article prints those figures, asbestos workers who smoked were at an 8-fold greater risk of lung cancer than nonexposed smokers and at a 92-fold greater risk than nonsmoking asbestos workers. The article also stated that chronic asbestos exposure slightly increased bronchogenic carcinoma risk in nonsmokers. The author also described a laboratory study by Reiss and colleagues. In it, rat liver cells exposed to chrysotile asbestos together with benzo[a]pyrene showed more mutation than the two agents' separate effects added together. Those authors discussed possible explanations, including that the fibers may adsorb benzo[a]pyrene and help it enter cells. The review also summarized the author's own earlier work, such as chromosome damage in Cairo traffic policemen that was increased further by smoking. The author concluded that interactions among agents should be considered when estimating risk.

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 epidemiological and experimental studies on interaction between agents in chromosome damage and cancer, including summaries of the author's laboratory's earlier published work
• Who was studied: no new study population; the review drew on published human epidemiological studies, studies of exposed workers, and animal and cell-culture experiments
• Exposure: multiple agents in combination. Asbestos-related content: cigarette smoking combined with asbestos exposure (cited epidemiology), and chrysotile asbestos combined with benzo[a]pyrene in rat liver epithelial cells (cited laboratory study). Other combinations included arsenic, benzene with praziquantel, metals, and dietary inhibitors.
• Main results:
  • Cited earlier studies (references 4 and 5, Selikoff and Hammond): asbestos workers who smoke were at an 8-fold greater risk than nonexposed smokers and a 92-fold greater risk than nonsmoking asbestos workers. Chronic asbestos exposure slightly increased bronchogenic carcinoma risk in nonsmokers.
  • Stated in the same passage: chronic exposure to asbestos slightly increases the risk of bronchogenic carcinoma in nonsmokers.
  • Cited laboratory study (Reiss et al.): chrysotile asbestos plus benzo[a]pyrene was more mutagenic in rat liver epithelial cells than the additive effect of the two. Those authors discussed possible mechanisms, including fibers adsorbing benzo[a]pyrene or affecting cell membranes.
  • Author's laboratory's earlier study: chromosome damage was higher in Cairo traffic policemen than in controls and was enhanced further by smoking.
  • Author's laboratory's earlier mouse study: praziquantel was not clastogenic on its own but enhanced the clastogenic activity of benzene.
• The authors' conclusion: The author concluded that potential interaction among different agents should be considered when estimating risk.

Topics

Medical terms in this study, explained in our Lexicon: Environmental Exposure, Carcinogenesis, Causation.

Related studies

• Environmental toxicants--induced epigenetic alterations and their reversers — M. Kim, M. Bae, et al. (2012)
• Diallylsulfide attenuates asbestos-induced genotoxicity — M. Lohani, S. Yadav, et al. (2003)
• Enhancement of benzo[a]pyrene mutagenicity by chrysotile asbestos in rat liver epithelial cells — B. Reiss, C. Tong, et al. (1983)
• Metal interactions in carcinogenesis: enhancement, inhibition — G.F. Nordberg, O. Andersen (1981)
• Validity of the Lymphocyte Cytokinesis-Block Micronucleus Assay (L-CBMN) as biomarker for human exposure to chemicals with different modes of action: A synthesis of systematic reviews — M. Kirsch-Volders, M. Fenech, et al. (2018)
• Genotoxicity of chemical and physical agents in cultured human tissues and cells — A. Weston, S.M. Plummer, et al. (1986)

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