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GENETIC AND SOMATIC EFFECTS FOLLOWING INTERNAL EXPOSURE TO MAN MADE RADIOACTIVE SUBSTANCES
Abstract for presentation to Children's Genotox Network meeting Copenhagen
Chris Busby PhD
University of Liverpool and Green Audit: Aberystwyth November 2003
Abstract I am suggesting that the major cause of the increase in childhood cancer which has occurred this century is increased internal exposure to the child, the foetus and germ cells from internal radioactive isotopes. These are both novel man-made substances like Strontium-90 or Plutonium-239 or natural substances in increased concentrations and new forms e.g. Uranium particles. I review evidence that supports this claim and explain how the radiological risk model of the International Commission on Radiological Protection (ICRP) is unsafe because it fails to distinguish between external and internal radiation. The ICRP linear no threshold model involves the physics-based assumption of isotropic exposure. The units of dose are energy per unit volume: all cells are assumed to have equal chance of receiving equivalent damage. This is unsafe when dealing with certain internal exposures where local tissue/ organelles/ cell structures receive high ionization density and other tissues no damage at all. Comparisons of cancer and genetic damage in the A-Bomb lifespan studies (which form the basis of risk estimates) make no allowance for internal doses. Nevertheless the apparently unexposed control groups living in the contaminated bombed cities exhibited significant cancer and leukaemia increases relative to the Japanese national rates and also sex ratio and chromosome aberration effects. The base for radiation protection is both theoretically and epidemiologically flawed and must be dismissed. Evidence for a significant enhancement of risk from internal exposures is presented in a brief historical review. This begins with the 1959-63 atmospheric weapons test exposures to Strontium-90 in milk which increased infant mortality, particularly from congenital heart developmental defects. These had been shown to occur in mice and rats exposed to Sr-90 by Luning et al, 1963 and Smirnova and Lyaginskaya, 1969. Although the Darby et al. (1993) Nordic leukaemia fallout study was to show little effect, the study used a combined dataset spliced at the peak fallout exposure point. Danish childhood (0-4) leukaemia series from 1943 to 1982 (Clemmensen) show a significant 30% increase in childhood leukaemia 0-4 over this period in line with England and Wales childhood leukemia examined by Bentham and Haynes. In addition both the Clemmensen and Olsen (Darby et al.) raw data exhibit an increase in infant leukaemia following the weapons fallout peaks. Childhood leukaemia became associated with radiation exposure after the discovery of the Sellafield cluster and subsequent nuclear site leukemias (Dounreay, La Hague, Aldermaston, Krummel). Authoritative dismissal of causality in these cases was based on the flawed reasoning of the ICRP/ Hiroshima external model. Children near nuclear sites were exposed to internal man-made radiation, and particularly hot and warm sub micron particles translocated to the lymphatics following sea to land transfer or resuspension and inhalation. The mis-match between ICRP predicted and observed child leukaemia rates in the nuclear site clusters is between 300 and 2000-fold. For this reason, the reports of infant leukaemia in the in utero cohort after Chernobyl from five countries (Gibson et al., Michelis et al., Petridou et al., Mangano, Busby and Scott Cato 2000) is of critical interest. We have calculated the expected yield in the in utero cohort for Wales and Scotland based on well characterised exposures and show that the mis-match between ICRP calculation and observation is also between 100 and 500-fold but in this case radiation can be the only cause. A similar level of error for radiological genetic damage (700-fold) is suggested recently by findings of Dubrova et al (2000) and by Weinberg et al (2002) in objective measurements of minisatellite mutation rates in the offspring of Chernobyl liquidators and by certain other findings in the Chernobyl affected territories (Bandashevsky 2001). Error factors of this magnitude point to the likely existence of increased levels of childhood cancer near nuclear pollution sites, for example the Irish Sea coasts. I complete my argument by presenting some data from the shores of the Irish Sea based on Wales Cancer Registry small area data for 1974-1990.
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