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Immediate effects are explained by the effects of radiation on cells and the sensitivity of rapidly reproducing cells to radiation. The first clue that a person has been exposed to radiation is a change in blood count, which is not surprising since blood cells are the most rapidly reproducing cells in the body. At higher doses, nausea and hair loss are observed, which may be due to interference with cell reproduction. Cells in the lining of the digestive system also rapidly reproduce, and their destruction causes nausea. When the growth of hair cells slows, the hair follicles become thin and break off. High doses cause significant cell death in all systems, but the lowest doses that cause fatalities do so by weakening the immune system through the loss of white blood cells.
The two known long-term effects of radiation are cancer and genetic defects. Both are directly attributable to the interference of radiation with cell reproduction. For high doses of radiation, the risk of cancer is reasonably well known from studies of exposed groups. Hiroshima and Nagasaki survivors and a smaller number of people exposed by their occupation, such as radium dial painters, have been fully documented. Chernobyl victims will be studied for many decades, with some data already available. For example, a significant increase in childhood thyroid cancer has been observed. The risk of a radiation-induced cancer for low and moderate doses is generally assumed to be proportional to the risk known for high doses. Under this assumption, any dose of radiation, no matter how small, involves a risk to human health. This is called the linear hypothesis and it may be prudent, but it is controversial. There is some evidence that, unlike the immediate effects of radiation, the long-term effects are cumulative and there is little self-repair. This is analogous to the risk of skin cancer from UV exposure, which is known to be cumulative.
There is a latency period for the onset of radiation-induced cancer of about 2 years for leukemia and 15 years for most other forms. The person is at risk for at least 30 years after the latency period. Omitting many details, the overall risk of a radiation-induced cancer death per year per rem of exposure is about 10 in a million, which can be written as .
If a person receives a dose of 1 rem, his risk each year of dying from radiation-induced cancer is 10 in a million and that risk continues for about 30 years. The lifetime risk is thus 300 in a million, or 0.03 percent. Since about 20 percent of all worldwide deaths are from cancer, the increase due to a 1 rem exposure is impossible to detect demographically. But 100 rem (1 Sv), which was the dose received by the average Hiroshima and Nagasaki survivor, causes a 3 percent risk, which can be observed in the presence of a 20 percent normal or natural incidence rate.
The incidence of genetic defects induced by radiation is about one-third that of cancer deaths, but is much more poorly known. The lifetime risk of a genetic defect due to a 1 rem exposure is about 100 in a million or , but the normal incidence is 60,000 in a million. Evidence of such a small increase, tragic as it is, is nearly impossible to obtain. For example, there is no evidence of increased genetic defects among the offspring of Hiroshima and Nagasaki survivors. Animal studies do not seem to correlate well with effects on humans and are not very helpful. For both cancer and genetic defects, the approach to safety has been to use the linear hypothesis, which is likely to be an overestimate of the risks of low doses. Certain researchers even claim that low doses are beneficial . Hormesis is a term used to describe generally favorable biological responses to low exposures of toxins or radiation. Such low levels may help certain repair mechanisms to develop or enable cells to adapt to the effects of the low exposures. Positive effects may occur at low doses that could be a problem at high doses.
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