The accident at Chernobyl and outcome of pregnancy in Finland.
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OBJECTIVE: To evaluate the outcome of pregnancy in Finnish women after the accident at the Chernobyl nuclear power plant on 26 April 1986. DESIGN: Geographic and temporal cohort study. SETTING: Finland divided into three zones according to amount of radioactive fallout. SUBJECTS: All children who were exposed to radiation during their fetal development. Children born before any effects of the accident could be postulated--that is, between 1 January 1984 and 30 June 1986--served as controls. INTERVENTIONS: Children were divided into three temporal groups: controls, children who were expected to be born in August to December 1986, and children who were expected to be born in February to December 1987. They were also divided, separately, into three groups according to the three geographic zones. END POINT: Incidence of congenital malformations, preterm births, and perinatal deaths. MEASUREMENTS AND MAIN RESULTS: There were no significant differences in the incidence of malformations or perinatal deaths among the three temporal and three geographic groups. A significant increase in preterm births occurred among children who were exposed to radiation during the first trimester whose mothers lived in zones 2 and 3, where the external dose rate and estimated surface activity of caesium-137 were highest. CONCLUSIONS: The results suggest that the amount of radioactive fallout that Finnish people were exposed to after the accident at Chernobyl was not high enough to cause fetal damage in children born at term. The higher incidence of premature births among malformed children in the most heavily polluted areas, however, remains unexplained. (+info)
Effects of neonatal ovarian X-irradiation in the Chinese hamster. II. Absence of chromosomal and developmental damages in surviving oocytes irradiated at the pachytene and resting dictyate stages.
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Ovaries of Chinese hamsters were irradiated with 1 Gy of X-rays on day 0, 4, 8 and 14 after birth, and the late effects on pachytene and resting dictyate oocytes, which had been proven to be radioresistant and to survive acute oocyte-killing, were studied in the progeny of the irradiated females. Thirty hours after mating, fertilized ova were collected and female pronuclear chromosomes were karyotyped. On day 18.5 of gestation, the number of corpora lutea and implantation sites were counted and the live and dead fetuses were examined phenotypically. There was no increase of chromosome aberrations in female pronuclei of one-cell embryos of the irradiated groups. There was no significant difference in the incidences of pre- and postimplantation deaths and of congenital malformations between the irradiated groups and the non-irradiated controls. These findings indicated clearly that oocytes at the pachytene and resting dictyate stages which had survived the acute oocyte-killing effects of X-rays were also free from late deleterious effects on genetic and developmental abilities. The radiosensitivity of oocytes of the Chinese hamster was compared with that of the mouse with respect to chromosome aberrations, lethal mutations and congenital anomalies, and the difference between both species was discussed. (+info)
Teratogenic effect of californium-252 irradiation in rats.
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The teratogenicity of californium-252 (Cf-252) irradiation which generates approximately 70% 2.3 MeV fast neutron and 30% gamma rays was evaluated. A single whole body exposure of Cf-252 at various doses was given to pregnant rats on day 8 or 9 of pregnancy, followed by microscopic autopsy of the fetuses at the terminal stage of pregnancy to search for external and internal malformations. For comparison, pregnant rats were irradiated with various doses of cobalt-60 (Co-60) standard gamma rays at the same dose rate (1 rad/min.). The doses were 20-120 rad of Cf-252 and 80-220 rad of Co-60. Using frequency of radiation induced malformations observed on day 8 of pregnancy as an index, relative biological effectiveness (RBE) of 2.3-2.7 was obtained from the straight line obtained by modifying by the least squares method the frequency curves of malformed fetuses in total implants and in surviving fetuses. The types of malformations induced by Cf-252 and Co-60 irradiation were alike. Using fetal LD50 as an index, 2.4 was obtained as RBE when irradiated on day 8 of pregnancy and 3.1 as that when irradiated on day 9. The results showed that Cf-252 had stronger a teratogenic effect than Co-60 gamma rays. (+info)
Prevention of avoidable mutational disease: memorandum from a WHO meeting.
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About 1% of children are born with a serious disorder which is the direct result of a mutational event in a parent or a more distant ancestor. These disorders, of which several thousand are known, mainly afflict the blood, bone, brain, ear, eye or muscle and the changes are usually irrevocable by the time of diagnosis. Another 1% of individuals will develop a serious genetic disease some time after birth. In addition to these direct consequences of a mutant event, far higher proportions will suffer from the indirect effects of one or several mutations.In view of their chronic and severe nature most of these disorders impose a burden disproportionate to their frequency, and it is sound public health policy to avoid the birth of babies known to have the established mutations and prevent further cases in the immediate or distant future by minimizing the exposure of people at risk to known mutagens. The advantages in permitting certain mutagenic exposures must be assessed against the later costs.Owing to the natural mutation rate and the vast backlog of previous mutations, the prospects of prevention are limited to preventing an increase, rather than to achieving any substantial decrease. This Memorandum describes progress in the ability to dissect and interpret the mutational process, to identify populations at risk, and to evaluate the consequences of the various types of mutational event and emphasizes that the current approach to prevention of mutational disease must involve improving our ability to study populations that appear to be at increased risk. (+info)
The estimation of risks from the induction of recessive mutations after exposure to ionising radiation.
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Since recent assessments of genetic risks from radiation have concentrated on harmful dominant effects, a quantitative assessment of risks from recessives is needed. Presumably, harmful recessives can arise at all loci coding for essential proteins (perhaps 10 000), but mutation to dominant alleles is likely to be a property of relatively few loci. While many recessives doubtless remain to be discovered, those known at present tend to have earlier and more severe effects than dominants. Induced recessive mutations can cause harm by partnership with a defective allele already established in the population; partnership with another recessive mutation induced at the same locus; the formation of homozygous descendants, that is, identity by descent; and heterozygous effects. Calculations based on a combination of data from observations on human populations and from mouse experiments suggest that an extra genetically significant dose of 1 cGy (centiGray, equivalent to 1 rad) X or gamma irradiation received by each parent in a stable population with a million liveborn offspring would induce up to 1200 extra recessive mutations. From partnership effects, about one extra case of recessive disease would be expected in the following 10 generations. Homozygosity resulting from identity by descent could not normally occur until the fourth generation after exposure but, on certain assumptions, about ten extra cases of recessive disease would be expected from this cause by the tenth generation. In the same period, about 250 recessive alleles would be eliminated in heterozygotes (that is, Muller's 'genetic deaths') given 2.5% heterozygous disadvantage. These deleterious heterozygous effects should not be combined with those of dominants, as has been done in some previous risk estimates. It is considered unlikely that many radiation induced recessives would show heterozygous advantage. Certain dominants (combined frequently at least 10(-3)) should be excluded from calculations of mutational risk because they are unlikely to be maintained by mutation. (+info)
Testing for nondisjunction in the mouse.
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Tests for nondisjunction have been carried out in male and female mice. Ten-day fetal progeny of control and treated adults have been karyotyped to establish spontaneous and induced levels of aneuploidy. In males, the effects of 100 rad x-rays on type A spermatogonia and early primary spermatocytes, and the effects of Mitomycin C (2 mg/kg) on early primary spermatocytes, have been tested. The results show insensitivity of primary spermatocytes to both agents, but a 3.5-fold increase in nondisjunction following spermatogonial irradiation. In females, comparisons have been made between young controls, young x-rayed (5 rad), aged controls and aged x-rayed (5 rad) animals. The "ageing effect" on nondisjunction is observed, but too few fetuses have been analyzed to reach conclusions regarding enhancement of nondisjunction levels by low doses of x-rays. (+info)