average, assuming a sex and age distribution similar to that of the entire U.S. population, the BEIR VII lifetime risk model predicts that approximately 1 person in 100 would be expected to develop cancer (solid cancer or leukemia) from a dose of 0.1 Sv above background, while approximately 42 of the 100 individuals would be expected to develop solid cancer or leukemia from other causes. Lower doses would produce proportionally lower risks. For example, the committee predicts that approximately one individual per thousand would develop cancer from an exposure to 0.01 Sv. As another example, approximately one individual per hundred would be expected to develop cancer from a lifetime (70-year) exposure to low-LET, natural background radiation (excluding radon and other high-LET radiation). Because of limitations in the data used to develop risk models, risk estimates are uncertain, and estimates that are a factor of two or three larger or smaller cannot be excluded.

Health Effects Other Than Cancer

In addition to cancer, radiation exposure has been demonstrated to increase the risk of other diseases, particularly cardiovascular disease, in persons exposed to high therapeutic doses and also in A-bomb survivors exposed to more modest doses. However, there is no direct evidence of increased risk of noncancer diseases at low doses, and data are inadequate to quantify this risk if it exists. Radiation exposure has also been shown to increase risks of some benign tumors, but data are inadequate to quantify this risk.

Estimating Risks to Children of Parents Exposed to Ionizing Radiation

Naturally occurring genetic (i.e., hereditary) diseases contribute substantially to illness and death in human populations. These diseases arise as a result of alterations (mutations) occurring in the genetic material (DNA) contained in the germ cells (sperm and ova) and are heritable (i.e., can be transmitted to offspring and subsequent generations). Among the diseases are those that show simple predictable patterns of inheritance (which are rare), such as cystic fibrosis, and those with complex patterns (which are common), such as diabetes mellitus. Diseases in the latter group originate from interactions among multiple genetic and environmental factors.

Early in the twentieth century, it was demonstrated that ionizing radiation could induce mutations in the germ cells of fruit flies. These findings were subsequently extended to a number of other organisms including mice, establishing the fact that radiation is a mutagen (an agent that can cause mutations in body cells); human beings are unlikely to be exceptions. Thus began the concern that exposure of human populations to ionizing radiation would cause an increase in the frequency of genetic diseases. This concern moved to center stage in the aftermath of the detonation of atomic weapons over Hiroshima and Nagasaki in World War II. Extensive research programs to examine the adverse genetic effects of radiation in the children of A-bomb survivors were soon launched. Other studies focusing on mammals that could be bred in the laboratory—primarily the mouse—were also initiated in different research centers around the world.

The aim of the early human genetic studies carried out in Japan was to obtain a direct measure of adverse effects in the children of A-bomb survivors. The indicators that were used included adverse pregnancy outcomes (i.e., stillbirths, early neonatal deaths, congenital abnormalities); deaths among live-born infants over a follow-up period of about 26 years; growth and development of the children; chromosomal abnormalities; and specific types of mutations. Specific genetic diseases were not used as indicators of risk, because not enough was known about them when the studies began.

The initial goal of the mouse experiments was to examine the effects of different doses, types, and modes of delivery of radiation on mutation frequencies and the extent to which the germ cell stages in the two sexes might differ in their responses to radiation-induced mutations. As it turned out, however, the continuing scarcity of data on radiation-induced mutations in humans and the compelling need for quantitative estimates of genetic risk to formulate adequate measures for radiological protection necessitated the use of mouse data for indirect prediction of genetic risks in humans.

As in previous BEIR reports, a method termed the “doubling dose method,” is used to predict the risk of inducible genetic diseases in the children of people exposed to radiation using naturally occurring genetic diseases as a framework. The doubling dose (DD) is defined as the amount of radiation that is required to produce as many mutations as those occurring spontaneously in one generation. The doubling dose is expressed as a ratio of mutation rates. It is calculated as a ratio of the average spontaneous and induced mutation rates in a set of genes. A large DD indicates small relative mutation risk, and a small doubling dose indicates a large relative mutation risk. The DD used in the present report is 1 Sv (1 Gy)18 and derives from human data on spontaneous mutation rates of disease-causing genes and mouse data on induced mutation rates.19 Therefore, if three mutations occur spontaneously in 1 million people in one generation, six mutations will occur per generation if 1 million people are each exposed to 1 Sv of ionizing radiation, and three of these six mutations would be attributed to the radiation exposure.

More than four decades have elapsed since the genetic studies in Japan were initiated. In 1990, the final results of

18  

For the purposes of this report, when low-LET radiation is considered, 1 Gy is equivalent to 1 Sv.

19  

UNSCEAR. 2001. Hereditary Effects of Radiation. Report to the General Assembly. New York: United Nations.



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