Summary Detailed data were provided by the Oxford Survey of Childhood Cancer OSCC on deaths from childhood cancer in Britain after irradiation of the fetus during diagnostic radiology of the mother. In each age group at death, 0-5, 6-9 and 10-15 years, excess cancer deaths decreased suddenly for births in and after 1958. A major factor was concerted action initiated in 1956 to reduce radiation exposure of fetal gonads for fear of genetic hazards. Dose reduction was achieved during 1957 and early 1958 by reducing the rising rate of obstetric radiography and by virtually abandoning pelvimetry as that had been understood. In the 1970s the rate of X-raying increased again and so did cancer risk but not significantly.Direct evidence that diagnostic X-rays can cause childhood cancer is the similar excess rate per X-ray in twins and singleton births when X-raying rate is 5-6 times higher in twins. In the past a dose-response for cancer in OSCC data based on number of films per X-ray examination was taken to be evidence for causation but dose per film varies with kind of X-ray examination. Fixed values for dose per film were mistakenly assumed by UNSCEAR (1972) and used by it and others when deriving risk co-efficients. In updated OSCC data cancer risk is independent of film number.The odds ratio for childhood cancer deaths after X-raying in birth years 1958-61 (1.23 with 95% confidence intervals CI 1.04-1.48) and the mean fetal whole body dose from obstetric radiography in 1958 (0.6 cGy) can each be derived from nationwide surveys in Britain. The corresponding risk coefficient for irradiation in the third trimester for childhood cancer deaths at ages 0-15 years = 4-5 x 10-4 per cGy fetal whole body dose (95% CI 0.8-9.5 x 10-4 per cGy). It is the same for cancer incidence and mortality.A lower risk in bomb survivors exposed in utero is not incompatible since its CI are wide. There is no dependable evidence that radiosensitivity is greater in early pregnancy. A significantly raised cancer rate after diagnostic X-raying supports the hypothesis that carcinogenesis by ionising radiation has no threshold.

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SUMMARY Low birthweight infants aged 4-41 days were given from birth one of three experimental milk formulae varying widely in content of calcium and phosphate. Ca and P in feed, urine, and faeces were measured between carmine markers corresponding to a metabolic period of 48 hours. Calcium enriched in 46Ca to provide a marker for the dietary Ca was added to one feed and 46Ca measured in urine and faeces. True absorption of Ca and endogenous excretion into the bowel could then be inferred. True absorption of Ca was proportional to Ca intake and independent of P intake. Endogenous faecal excretion seemed to be independent of both Ca and P intakes, and varied widely between different infants in the range 4-150 mg/day. Urine Ca was low and retention was essentially the difference between true absorption and endogenous faecal excretion. Retention of Ca tended to be much greater on a high Ca intake, but the variability in retention between infants on a given intake was large, paralleling the variability in endogenous faecal excretion.The variability in plasma Ca concentrations in newborn infants may in part be a consequence of wide individual variability in endogenous faecal excretion. The 46Ca marker technique provides a means of investigating the factors determining this variability.

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A re-analysis of published data from the Oxford Childhood Cancer Survey shows that the frequency of leukaemia and of solid cancers in childhood is greater following antenatal x-radiography, not only in singleton births but also in monozygotic and dizygotic twins. The radiography rate was 10% in singletons and 55% in twins. A similar excess of leukaemia and of solid cancers in the x-rayed with such different rates of radiography is strong evidence for irradiation as the cause. The low observed frequency of malignant disease in Japanese bomb survivors exposed in utero may not be in serious conflict with this conclusion, as has been supposed.

Cancer is naturally very common, and practical questions about the possibility of radiation-induced harm are often questions about what in other contexts would be called background noise. Central to the question of whether small radiation exposures are carcinogenic is the effect of antenatal radiography. A comparison of singleton and twin births with radiography rates of 10 and 55 per cent respectively showed that radiography must be the main cause of the elevated frequency of malignant disease. In Japanese bomb survivors, most radiation-induced cancer has been found in those irradiated in adult life, less in those irradiated in childhood and adolescence, and least for exposure in utero. Specific biological differences between different kinds of malignant disease in their induction by ionizing radiation are becoming increasingly evident. When dose-response relationships for observed cancer frequencies are to be used as evidence about dose-response relationships for cancer induction, it will always be necessary to allow for the concomitant cell sterilization. When this is done, there is little support for linearity as the method of extrapolation when making predictions about possible effects of low doses but the absence of threshold seems scientifically inescapable. In cellular terms, radiation induction of cancer must be a very rare phenomenon, so rare compared with cell sterilization or mutation induction, that the general corpus of radiobiological understanding may be inapplicable.

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