Quantifying health effects from the combined action of low-level radiation and other environmental agents: can new approaches solve the enigma?

Our plain-English summary of Quantifying health effects from the combined action of low-level radiation and other environmental agents: can new approaches solve the enigma?, by W. Burkart, G.L. Finch, T. Jung (The Science of the Total Environment, 1997).

The study

• Authors: W. Burkart, G.L. Finch, T. Jung
• Journal: The Science of the Total Environment
• Published: 1997;205(1):51-70
• Type of article: Review
• Cited by: 10 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Efforts to assess the quantify deleterious effects from toxicants are directed mainly towards single agents, whereas real world environmental and occupational exposures to natural and anthropogenic agents quite often entail the concomitant presence of several toxicants. These combined exposures may lead to health risks that differ from those expected from simple addition of the individual risks. For example, combined exposures to physical and chemical agents such as radon and smoking or asbestos and smoking produce over-additive effects at exposure levels typical for earlier workplaces. In tumour therapy, the modulation of radiation effects by cytotoxic drugs is widely used to enhance the therapeutic gain. Whether interactions occurring at high exposure levels are important at the low exposure levels set for the public and for modern workplaces is difficult to answer. A scientifically sound extrapolation from these high to low-dose levels should be based on dose-effect relationships of the relevant agents alone and in combination. In general this information is not available. The existing data base on combined effects is rudimentary, mainly descriptive and rarely covers exposure ranges large enough to make direct inferences to present day low-dose exposure situations. In view of the multitude of possible interactions between the large number of potentially harmful agents in the human environment, descriptive approaches will have to be supplemented by the use of mechanistic models for critical health endpoints such as cancer. To generalise and predict the outcome of combined exposures, agents will have to be grouped depending on their physical or chemical mode of action on the molecular and cellular level. Such a grouping must be guided by specific mechanistic studies designed to examine the underlying hypothesis regarding how various classes of agents interact.

In plain English

This article was a review and discussion paper, not a new study. The authors, from radiation-protection and inhalation-toxicology institutes in Germany and the United States, considered how ionising radiation and other environmental agents might act together on health, especially cancer. They asked whether combined effects seen at high exposures can be applied to the low exposures of the public and modern workplaces. They discussed what additivity, synergism and antagonism mean and summarised examples from molecular, cell, animal and human research by others. On asbestos, they cited earlier work (Selikoff and colleagues, 1979) on the strong dependence of asbestos-related lung cancer risk on smoking in exposed workers. They listed a cell-culture example in which alpha radiation and asbestos acted synergistically on cell transformation in hamster cells. They also noted that converting asbestos exposure into local or averaged doses was not feasible. The authors concluded that theory did not rule out very strong synergistic effects even at low exposure levels, but that there was little experimental and no sound epidemiological evidence on this for the human environment. They also wrote that classifying interactions into groups by mechanism should be promoted.

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: Review and conceptual discussion of published findings on combined effects of ionising radiation and other agents; no new data were collected
• Exposure: Ionising radiation combined with other physical, chemical and biological agents. Asbestos, tobacco smoke, radon daughters, metals and drugs are discussed as examples.
• Main results:
  • Citing earlier work by others (Selikoff et al., 1979), the authors described the strong dependence of asbestos-related lung cancer risk on smoking status in exposed workers as an early example of an important interaction.
  • In a table of cell-culture examples drawn from other studies, alpha radiation in hamster cell culture was listed as acting synergistically with asbestos, with cell transformation as the endpoint.
  • The authors stated that for asbestos, chromosome segregation may be impaired close to single fibres. They said such responses cannot be converted into local or averaged doses.
  • The authors judged that high-exposure studies can indicate possibly critical interactions. As a basis for risk assessment or for deriving risk coefficients at low exposures, however, they called the outlook bleak.
• The authors' conclusion: The authors concluded that theory does not rule out very strong synergistic effects even at low exposure levels, but that little experimental and no sound epidemiological evidence on this exists for the human environment. They wrote that classifying interactions into groups by mechanism may help predict health effects from complex exposures and should be promoted.
• Limitations the authors state:
  • The authors stated that the available data on combined effects are not comprehensive and are mostly descriptive rather than mechanistic.
  • The authors stated that most existing findings come from high exposure levels, so conclusions for today's occupational or environmental exposures are difficult to draw.

Topics

Medical terms in this study, explained in our Lexicon: Occupational Exposure.

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Browse more research in The Science of the Total Environment, or return to medical research.