Executive Summary


This report, prepared by the National Research Council’s Committee on the Biological Effects of Ionizing Radiation (BEIR), is the seventh in a series that addresses the health effects of exposure of human populations to low-dose, low-LET (linear energy transfer) ionizing radiation. The current report focuses on new information available since the 1990 BEIR V report on low-dose, low-LET health effects.

Ionizing radiation arises from both natural and man-made sources and at very high doses can produce damaging effects in tissues that can be evident within days after exposure. At the low-dose exposures that are the focus of this report, so-called late effects, such as cancer, are produced many years after the initial exposure. In this report, the committee has defined low doses as those in the range of near 0 up to about 100 milligray (mGy) of low-LET radiation, with emphasis on the lowest doses for which meaningful effects have been found. Additionally, effects that may occur as a result of chronic exposures over months to a lifetime at dose rates below 0.1 mGy/min, irrespective of total dose, are thought to be most relevant. Medium doses are defined as doses in excess of 100 mGy up to 1 Gy, and high doses encompass doses of 1 Gy or more, including the very high total doses used in radiotherapy (of the order of 20 to 60 Gy).

Well-demonstrated late effects of radiation exposure include the induction of cancer and some degenerative diseases (e.g., cataracts). Also, the induction of mutations in the DNA of germ cells that, when transmitted, have the potential to cause adverse health effects in offspring has been demonstrated in animal studies.


There is an intimate relationship between responses to DNA damage, the appearance of gene or chromosomal mutations, and multistage cancer development. Molecular and cytogenetic studies of radiation-associated animal cancers and more limited human data are consistent with the induction of a multistage process of cancer development. This process does not appear to differ from that which applies to spontaneous cancer or to cancers associated with exposure to other carcinogens.

Animal data support the view that low-dose radiation acts principally on the early stages of tumorigenesis (initiation). High-dose effects on later stages (promotion or progression) are also likely. Although data are limited, the loss of specific genes whose absence might result in animal tumor initiation has been demonstrated in irradiated animals and cells.

Adaptation, low-dose hypersensitivity, bystander effect, hormesis, and genomic instability are based mainly on phenomenological data with little mechanistic information. The data suggest enhancement or reduction in radiation effects and in some cases appear to be restricted to special experimental circumstances.

Radiation-Induced Cancer: Mechanisms, Quantitative Experimental Studies, and the Role of Molecular Genetics

A critical conclusion about mechanisms of radiation tumorigenesis is that the data reviewed greatly strengthen the view that there are intimate links between the dose-dependent induction of DNA damage in cells, the appearance of gene or chromosomal mutations through DNA damage misrepair, and the development of cancer. Although less well established, the available data point toward a single-cell (monoclonal) origin of induced tumors. These data also provide some evidence on candidate radiation-associated mutations in tumors. These mutations include loss-of-function DNA deletions, some of which have been shown to be multigene deletions. Certain point mutations and gene amplifications have also been characterized in radiation-associated tumors, but their origins and status are uncertain.

One mechanistic caveat explored was that novel forms of cellular damage response, collectively termed induced genomic instability, might contribute significantly to radiation

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