Tumour development following internal exposures to radionuclides during the perinatal period.
Exposure to radiation from internally deposited radionuclides during the prenatal and/or neonatal periods bears a distinct oncogenic potential. The fundamental mechanisms of perinatal radionuclide carcinogenesis seem to be generally similar to those that pertain to external radiation exposures and other carcinogenic agents, but unique interactions may be superimposed. Specific dose-effect relationships differ among radionuclides; in many studies, there have been dose-related increases in the incidence of tumours or decreases in age at tumour appearance following prenatal or neonatal radiation exposure. Tumour incidences may be decreased, especially at high dose levels; these are usually attributable to cell death, inhibited development of target tissues or to endocrine malfunction. Age-related differences in predominant tumour types and/or sites of tumour development are often detected, and are explainable by the existence of nuclide-specific target organs or tissues, dosimetric factors and developmental considerations.
Sikov
M R
MR
Biology and Chemistry Department, Pacific Northwest Laboratory, Richland, Washington.
D000818:Animals; D000831:Animals, Newborn; D002250:Carbon Radioisotopes / Q000633:toxicity; D005260:Female; D007457:Iodine Radioisotopes / Q000633:toxicity; D009381:Neoplasms, Radiation-Induced; D010761:Phosphorus Radioisotopes / Q000633:toxicity; D011005:Plutonium / Q000633:toxicity; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011868:Radioisotopes / Q000633:toxicity*; D013326:Strontium Radioisotopes / Q000633:toxicity; D014316:Tritium / Q000633:toxicity
D002250:Carbon Radioisotopes; D007457:Iodine Radioisotopes; D010761:Phosphorus Radioisotopes; D011868:Radioisotopes; D013326:Strontium Radioisotopes; D014316:Tritium; D011005:Plutonium