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In spite of the abundance of information on the general subject of effects of radiocontamination in man, the mechanism of intrauterine irradiation and subsequent effects on both mother and fetus, remain poorly known. Adult results cannot be extrapolated to fetus, nor can animal experiments allow conclusions applied to humans; thalidomide accidents are a tragic illustration of this statement. Indeed, animal experimentation and clinical use in adults were unanimous in showing a complete lack of toxicity, to the extent that thalidomide was hailed as the most innocuous soporific ever made for man or animal(1). Most of the previous claims made for this drug still remain valid even today, after more than 5,000 cases of phocomelia, but for the case when it was given to women until the 45th day of pregnancy. Studies with microorganisms have suggested that the spatial structure of thalidomide has some similarity to that of vitamin B1(2); this might lead to a competitive inhibition and subsequent vitamin B, deficiency, if the vitamin is replaced in larger amounts by the drug. When the deficiency occurs during the organogenetic period of the embryo, it impairs the development of limb buds for a short, but critical period sufficient for the production of a permanent damage in fetus. This is by no means the final word in the understanding of thalidomide mechanism in fetus, but it underscores the importance of a thorough knowledge of physiology of pregnancy, when an apparently harmless drug has to be given. There was some speculation that the high incidence of phocomelic embryopathies was related to a simultaneous increase of fallout and subsequent placental transfer, of the radiocontaminant. This argument has a powerful emotional impact, but it cannot be supported by any objective evidence. Indeed,

Placental Transfer of Fission Products and Effects on Fetal Development