 Chernobyl.
Leukemia The incidence of leukemia among patients treated with RAI for Graves’ disease has not exceeded that calculated from a control group . This problem was also studied by the consortium of 26 hospitals . The incidence of leukemia in this group was slightly lower than in a control group treated surgically, but slightly higher in the latter surgical group than in the general population.
In the group of RAI-treated patients, there has been no evidence of genetic damage, although, as will shortly be seen, this problem cannot be disregarded. In the United States, about 100 x 106 children will be born to a population of over 200 x 106 persons. Approximately 4% of these children will have some recognizable defect at birth. Of these, about one-half will be genetically determined or ultimately mutational, and represent the the effects of the baseline mutation rate in the human species. These mutations are attributed in part to naturally occurring radiation. All penetrating radiation, from whatever sources, produces mutations. The effects may vary with rate of application, age of the subject, and no doubt many other factors, and are partially cumulative. Nearly all of these mutations behave as recessive genetic factors; perhaps 1% are dominant. Almost all are minor changes, and those produced by experimental radiation are the same as those produced by natural radiation. Whether or not mutations are bad is in essence a philosophic question. Most of us would agree that the cumulative effect of mutations over past eras brought the human race to its present stage of development. However, most mutations, at least those that are observable, are detrimental to individual human adaptation to the present environment. In terms of the human population as a whole, detrimental mutant genes must be eliminated by the death of the carrier. We can agree that an increase in mutation rate is not desirable. It is hardly worth considering the pros and cons of the already considerable spontaneous mutation rate.
In mice, the occurrence of visible genetic mutations in any population group is probably doubled by acute exposure of each member of the group over many generations to about 30 – 40 rads, and by chronic exposure to 100 – 200 rads . This radiation dosage is referred to as the doubling dose. Ten percent of this increase might be expressed in the first-generation offspring of radiated parents, the remainder gradually appearing over succeeding generations. The change in mutation rate in Drosophila is in proportion to the dosage in the range above 5 rads. Data from studies of mice indicate that at low exposures (from 0.8 down to 0.0007 rads/min), the dose causing a doubling in the spontaneous rate of identifiable mutations is 110 rads . Linearity, although surmised, has not been demonstrated at lower doses. At present, residents of the United States receive about 300 mrad/year, or 9 rad before age 30, the median parental age. Roughly half of this dose is from natural sources and half from medical and, to a lesser extent, industrial exposure. The National Research Council has recommended a maximum exposure rate for the general population of less than 10 rad above background before age 30. (The present level may therefore approach this limit.) The radiation received by the thyroid and gonads during 131-I therapy of thyrotoxicosis can be estimated from the following formula: Total beta radiation dose = 73.8 x concentration of 131-I in the tissue (µCi/g) x average beta ray energy (0.19 meV) x effective isotope half-life For illustration, we can assume a gland weight of 50 g, an uptake of 50% at 24 hours, a peak level of circulating protein-bound iodide (PB 131-I) of 1% dose/liter, an administered dose of 10 mCi, a thyroidal iodide biologic half-life of 6 days, and a gamma dose of about 10% of that from beta rays. On this basis, the thyroid receives almost 8200 rads, or roughly 1,600 rads/mCi retained. The gonadal dose, being about one-half the body dose, would approximate 4 rads, or roughly 0.4 rads/mCi administered.
If the radiation dat