ecessive gene derived from the normal complement carried by all persons.
Assuming that only one parent received radiation from 131-I therapy amounting to 2% of the doubling dose, the risk of apparent birth defects in the patient’s children might increase from the present 4.0% to 4.008%. 0.02 (present genetic defect rate) x 0.04 (fraction of the doubling dose) x 0.1 (fraction of defects appearing in the first generation) = 0.00008, or an increase from 4.0% to 4.008%. Similar estimates can be derived by considering the number of visible mutations derived from experimental radiation in lower species.[ 92, 93] 6 x 10-8 (mutations produced per genetic locus per rad of exposure) x 104 (an estimate of the number of genetic loci in humans) x 2 (gonadal radiation in rads as estimated above) x 0.1 (fraction of mutations appearing in the first generation) = 0.00012 or 0.012% On this basis, the increase in the birth defect rate would be from 4.0% to 4.012%.
One important observation stemming from these calculations is that large numbers of children born to irradiated parents must be surveyed if evidence of genetic damage is ever to be found. Reports of “no problems” among 30 to 100 such children are essentially irrelevant when one is seeking an increase in the defect rate of about 4.0% to about 4.008%. These statistics are presented in an attempt to give some quantitation to the genetic risk involved in 131-I therapy, and should not be interpreted as in any sense exact or final. The point we wish to stress is that radiation delivered to future parents probably will result in an increased incidence of genetic damage, but an increase so slight that it is difficult to measure. Nonetheless, the use of 131-I for large numbers of women who subsequently become pregnant will inevitably introduce change in the gene pool. In considering the significance of these risks, one must remember that the radiation exposure to the gonads from the usual therapeutic dose of 131-I may be only one or two times that produced during a procedure such as a barium enema [ 94, 95] and similar to the 10 rads received from a CAT scan. These examinations are ordered by most physicians without fear of radiation effect ( Table 11-8).
When assessing the risks of 131-I therapy, one must, of course, consider the risks of any alternative choice of procedure. Surgery carries a small but finite mortality, as well as a risk of permanent hypoparathyroidism, hypothyroidism, and vocal cord paralysis. Some of these risks are especially high in children, the group in which radiation damage is most feared. Some physicians have held that 131-I therapy should not be given to patients who intend subsequently to have children. In fact, there is at present no evidence to support this contention, as discussed above. Chapman  studied 110 women treated with 131-I who subsequently became pregnant and were delivered of 150 children. There was no evidence of any increase in congenital defects or of accidents of pregnancy. Sarkar et al  also found no evidence of excess abnormalities among children who received 131-I therapy for cancer. Other studies have confirmed the apparent lack of risk[ 42, 43]. It should be noted that no increase in congenital abnormalities has been detected among the offspring of persons who received much larger radiation doses during atomic bomb explosions . Often the patient wishes to know about the possibility of carcinogenesis or genetic damage. These questions must be fully but delicately handled. It is not logical to treat a patient of childbearing age with 131-I and have the patient subsequently live in great fear of bearing children. These problems and considerations must be faced each time a patient is considered for RAI therapy.
Pregnancy and 131-I
Pregnancy is an absolute contraindication to 131-I therapy. The fetus is exposed to considerable radiation from transplacental migration of 131-I, as well as from the isotope in the maternal circulatory and excretory systems. In addition, the fetal thyroid collects 131-I after the 12th week of gestation and may be 