Biomedical subjects
Publications and source records attributed to J Lafuma.
Lung cancer can be induced in rats, by radon daughter products, after exposure as low as 25 WLM (80 mJ.h.m-3) protracted over 4 to 6 months with a dose rate of 100 to 150 WL (2 to 3 mJ.m-3). The incidence of lung cancer is not increased and is equal to that of controls when the same cumulated dose is protracted over 18 months at 2 WL (0.042 mJ.m-3).
The probability that rats develop tumours following a 3 Gy exposure to gamma rays from cobalt 60 was observed to depend on age at exposure. Lifetime excess of neoplasia decreased by a factor of about 10 in 9-month-old rats as compared to animals irradiated in utero. The 3-month age group developed slightly fewer tumours than the group irradiated in utero, and tumour location was different. The higher incidence of tumours observed in the foetal group was mainly due to the high sensitivities of central nervous system and gonads during organogenesis.
For a dose of 3 Gy delivered by cobalt 60 gamma rays on rats, a reduction of the dose rate by a factor of 60 decreased the carcinogenic effectiveness by a factor of about 5. This decreased effect was essentially observed for carcinomas.
The effectiveness of radon-daughter inhalation and irradiation with fission neutrons and gamma rays in the induction of lung carcinomas in Sprague-Dawley rats at low doses is compared. Earlier reports which compared radon-daughter inhalations and neutron irradiations over a wider range of doses were based on dosimetry for the radon-daughter inhalations which has recently been found to be faulty. In the present analysis, low-dose experiments were designed to derive revised equivalence ratios between radon-daughter exposures, and fission neutron or gamma irradiations. The equivalence is approximately 15 working level months (WLM) of radon daughters to 10 mGy of neutrons (the earlier value was 30 WLM to 10 mGy). The relative biological effectiveness (RBE) of neutrons is 50 or more at a gamma-ray dose of 1 Gy. In these experiments with low doses and exposures, the lifetime incidences can be estimated from the raw incidences, while the derivation of the time dependence of the prevalence is essential for the estimation of RBE values and equivalence ratios.
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Measurement of sister chromatid exchanges (SCEs) frequency of inbred Rat or nu/nu Mice bone marrow cells, following tumour grafts, have been developed. Increase of SCEs was observed in hosts which present or not metases and with reduced survival rates after malignant tumour grafts. These results suggest a remote control of tumoral tissue by a diffused matter effect.
The translocation of fibrous dusts through the respiratory system is discussed on the basis of human and experimental data obtained with the transmission electron microscope. Comparison of the characteristics (numerical and mass concentrations, sizes, types) of asbestos fibers retained in different locations of the respiratory system in humans exposed to asbestos has shown that there is no relationship between the numerical concentrations in lung parenchyma and those in parietal pleura. Moreover, almost al fibers encountered in the pleura were ultimate, short fibrils of chrysotile. The animal data are from rats injected intrapleurally with different types of fibers (chrysotile, crocidolite and glass fibers) and sacrificed at different times. There was a progressive increase in the number and mass of fibers translocated into lung parenchyma from the pleural cavity that was particularly obvious after 90 days. After this time, the mean length of fibers, especially chrysotile, increased, indicating that more long fibers are retained in alveolar tissue than short fibers.
Haemolytic activities and effects on alveolar macrophages (AM) of various fibres were studied. UICC asbestos fibres and attapulgites either untreated or acid-leached were used. Amphiboles and commercial attapulgites were both cytotoxic on AM, but attapulgites and chrysotile were only haemolytic. Chrysotile fibres induced a release of B galactosidase; when acid treated these fibres were cytotoxic and less haemolytic. Acid treated amphiboles were more haemolytic than untreated.
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The inducibility of pulmonary microsomal enzymes and the biological effects of chronic induction by 5-6 benzoflavone and methylcholanthrene were compared in normal and precancerous rats. Two important points were shown out: a dose of 6000 WLM resulted in a permanent modification of the pulmonary microsomal enzymatic pool and 5-6 benzoflavon was a strong co-factor of radiation induced carcinogenesis. This synergistic action was demonstrated by a much shorter latency, moreover neo-formed tissue and epidermoid cancers with a particular morphology were observed. In all the cases cancers appeared within 100 days following the beginning of the chemical treatment.
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A colloidal suspension of radioactive cerium chloride was inoculated into the hind legs of Sprague Dawley rats. Bone and soft-tissue tumours were induced at the site of inoculation in 77% of the animals. All bone tumours were osteogenic osteosarcomas. Soft tissue tumours were mostly malignant and were of various histological types, predominantly fibrosarcomas, haemangiopericytomas, angiosarcomas and rhabdomyosarcomas. A kinetic study showed that the doubling time (DT) of tumours was closely correlated with the anatomical site of tumour development: bone tumours had a DT of 17.4 +/- 4.3 days and malignant tumours which developed in soft tissues had a DT ranging from 7.4 to 8.4 days with the exception of two haemangiosarcomas which had a long DT of 17 +/- 0.6 days. Pulmonary metastases were frequent for osteosarcomas and tumours of vascular origin. This model of induction of bone and soft-tissue tumours in rats by injection of a colloidal suspension of radioactive cerium chloride offers the possibility of more comprehensive physiopathological and kinetic studies of these tumours and may constitute a good model for their human counterparts.
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