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K H Chadwick

Publications and source records attributed to K H Chadwick.

At least 19 recordsLinked to original sources
PubMed2001

Bone cancer risk.

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Bone Neoplasms↗
PubMed2000

Analysis of thyroid cancer data from the Ukraine after 'Chernobyl' using a two-mutation carcinogenesis model.

The thyroid cancer data of children in the northern regions of the Ukraine after the reactor accident at Chernobyl were combined with thyroid dose measurements in the same regions and analysed using a two-mutation carcinogenesis model. The best fit was obtained for radiation acting as an initiating agent, i.e. on the first mutation of the model. The observed relatively high increase of thyroid cancer incidence after 1990 in children exposed to radiation released after the reactor accident could be ascribed to the high thyroid doses and the relatively low background thyroid cancer incidence in children. The maximum annual incidence is predicted to occur fairly soon after the reactor accident, i.e. about 10 years. For adults, the predicted relative increase of annual thyroid cancers is much lower than for children younger than 20 years. The modelling results are used to derive risk estimates for radiation-induced thyroid cancer. These risk estimates are dependent on age at exposure, follow-up time and the background thyroid cancer incidence. The calculated excess absolute risk for a population of all ages is about one-third of that currently used by ICRP, but for children the calculated absolute risks are about a factor of 3 higher than derived in other epidemiological studies. The model results indicate that the excess absolute radiation risk per unit dose for children is about the same as or a little lower than that for adults.

Adolescent↗
PubMed1998

Radiation induced chromosome aberrations: some biophysical considerations.

The implications of recent results using FISH chromosome painting and soft X-ray exposures for the mechanisms of chromosome aberration formation are discussed. It is concluded that the evidence in favour of exchange aberrations arising from one radiation induced chromosome break has increased to the point where a 'change in paradigm' from the older breakage-reunion hypothesis needs to be taken seriously into account. A potential role for recombinational repair of DNA double strand breaks, as known in yeast, in the formation of aberrations in mammalian cells is presented and the relationship between DNA repair studies and radiation cytology is emphasized.

Animals↗
PubMed1998

Health consequences of Chernobyl and other radiation accidents. Report on the European Union Cluster Contractors' workshop (San Miniato, Italy, 17-22 June 1997).

The Radiation Protection Research Unit of the European Commission has been supporting collaborative research projects on the radiological consequences of the Chernobyl accident since 1991. However, in the Fourth Framework Programme of the Commission which started in 1996, the collaboration with scientists in the former Soviet Union has been placed on a different footing, and the programme has been expanded to include other regions, especially in Russia and Kazakhstan, where previous nuclear incidents have led to the exposure of workers and the local populations and to widespread radioactive contamination. There are 15 projects on health-related studies in the newly started programme, and in order to improve the collaboration between the different scientists working in these projects a Cluster Contractors' Meeting was organised in San Miniato, Italy, in June 1997 with the participation of some 50 scientists from the European Union (EU) and the Newly Independent States (NIS). This report summarizes the different topics, including molecular biology and treatment of childhood thyroid cancer, various epidemiological studies and dose reconstruction, which were discussed at the meeting and which form the major projects in the new collaborative programme.

Chromosome Aberrations↗
PubMed1997

Multistage carcinogenesis modeling and the initiation event.

Carcinogenesis is generally considered to be a multistage process classified under "initiation," "promotion," and "progression," and it is therefore of interest to know how radiation might affect them. Models which are currently being used with some success to analyze a variety of data are based on the two-mutation with clonal expansion model developed by Moolgavkar and Knudson [J Natl Cancer Inst 66:1037-1052, 1981]. These models imply that the "initiation" event would be a mutation but also imply that "progression" also involves mutation and that both these events could be influenced by radiation. The models offer the possibility of calculating the incidence of cancer over lifetime and can simultaneously provide the age and dose dependence of cancer. The models have implications for radiation protection and imply that radiation risk is related to spontaneous cancer incidence and that spontaneously induced "initiation" may also be associated with radiation-induced cancer.

Age Factors↗
PubMed1994

On the linearity of the dose-effect relationship of DNA double strand breaks.

Most radiation biologists believe that DNA double-strand breaks are induced linearly with radiation dose for all types of radiation. Since 1985, with the advent of elution and gel electrophoresis techniques which permit the measurement of DNA double-strand breaks induced in mammalian cells at doses having radiobiological relevance, the true nature of the dose-effect relationship has been brought into some doubt. Many investigators measured curvilinear dose-effect relationships and a few found good correlations between the induction of the DNA double-strand breaks and cell survival. We approach the problem pragmatically by assuming that the induction of DNA double-strand breaks by 125I Auger electron emitters incorporated into the DNA of the cells is a linear function of the number of 125I decays, and by comparing the dose-effect relationship for sparsely ionizing radiation against this standard. The conclusion drawn in that the curvilinear dose-effect relationships and the correlations with survival are real. The problem of why the dose-effect relationship is curvilinear when microdosimetric considerations predict that even for sparsely ionizing radiation energy deposition in and close to the Watson-Crick double helix should give a linear dose-effect relationship remains.

DNA↗
PubMed1989

The molecular basis of stochastic and nonstochastic effects.

Stochastic effects have been defined as those for which the probability increases with dose, without a threshold. Nonstochastic effects are those for which incidence and severity depends on dose, but for which there is a threshold dose. These definitions suggest that the two types of effects are not related. In this paper it will be shown that at least some of the nonstochastic effects are the consequence of accumulated stochastic effects and that both types of effect can be related to a common cellular damage. It is proposed that, at the cellular level, effects such as mutation induction and cell reproductive death are related to DNA double-strand breaks caused by radiation. Further, we propose that stochastic effects depend on a mutational event induced in a critical cell of a target organ. Nonstochastic effects are considered to arise because the function of a substantial proportion of critical cells is impaired. In some cases the predominant effect is comparable to cell reproductive death. Animal mortality, for instance, may occur because a substantial proportion of bone marrow cells is killed. Using this concept, mathematical formulas can be derived for the various effects. Modification of the irradiation conditions (e.g., low dose rate or density ionizing radiation) leads to changes in the initial molecular lesions and, consequently, to changes in the dose effect relationships of stochastic and nonstochastic effects. Experimental support will be discussed, using animal mortality as an endpoint. The implications of this approach will be discussed with emphasis on its application to radiological protection.

Animals↗
PubMed1986

Dosimetry concepts and measurements in food irradiation processing.

The associations between the dosimetry concepts, Minimum absorbed dose (D min), maximum absorbed dose (D max), and average dose and median dose are investigated for the case of a large cobalt-60 plaque source irradiating homogeneous bulk product in a two-pass, two-sided irradiation. It is assumed that to a first approximation the intensity of radiation decreases exponentially with the depth, t, in the product. A series of mathematical relationships is derived for the average dose, the maximum and minimum dose, the median dose [defined as (D max/D min)/2], and the uniformity ratio (defined as U.R. = (D max/D min). The relationships are derived in terms of a constant D0 (the dose on the surface of the product in the pass close to the source) and the relaxation length (mu t) of the radiation in the product. Since the uniformity ratio and other dose parameters can be calculated for certain chosen values of mu t, the individual values of mu (the energy absorption coefficient) and t do not need to be known. By dividing the dose range from D min to D max into 10 equal fractions, the amount of product irradiated to each of the fractions is calculated, and it is shown that, independent of the value of U.R., about a third of the product receives a dose in the first fraction above D min. It is also shown that for a given median dose, the average dose decreases as U.R. increases. The calculated dose relationships are confirmed by measurements in homogeneous dummy product, using the lyoluminescence of glutamine to measure dose. The implications of these results for the regulation of the food irradiation process and for the design of irradiation facilities are discussed.

Cobalt Radioisotopes↗
PubMed1986

The combined effect of DBE and X-rays on the induction of somatic mutations in Tradescantia.

The induction of somatic mutations in the stamen hair cells of Tradescantia KU 9 has been used to investigate the effects of combined exposure to 1,2-dibromoethane (DBE) and X-rays. At low radiation doses a synergistic interaction has been found between the two agents for both DBE exposure followed by acute X-rays and chronic simultaneous exposures. The synergism is discussed in terms of an interaction of single strand lesions in the DNA. It is concluded that although this type of interaction should not be too important for radiological protection, it could be of significance in evaluating the effects of chemicals at low exposure rates.

Dose-Response Relationship, Drug↗