Chromosomal analysis in vinyl chloride exposed workers: Comparison of the standard technique with the sister-chromatid exchange technique

Anderson, Diana; Richardson, C.R.; Purchase, I. F. H.; Evans, H. J.; O'riordan, M. L.

doi:10.1016/0027-5107(81)90078-6

Cited by 44 publications

(6 citation statements)

References 19 publications

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“…In later follow-up studies it was evident that the aberration frequencies had declined with time and that the measures taken to severely limit VCM levels in the workplace had been successful. In our studies (Anderson et al, 1981) we showed that although the aberra tion frequency declined in the 18 to 24 months following original exposure, the levels were still high in some of the more highly exposed workers. In contrast, the incidence of sister chromatid exchanges (SCE's) in these individuals did not differ significantly from control levels.…”

Section: The Response Of Populations Exposed To Chemical Mutagensmentioning

confidence: 67%

Chromosomal mutations in human populations

Evans¹

1982

Cytogenet Genome Res

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Chromosomal mutations in human populations are of two forms: those which arise in germ cells, or their precursors, and result in constitutional chromosomal anomalies in offspring—and contribute to a substantial proportion of congenital abnormality and heritable diseases in man; and those that arise in somatic cells and which may result in cell killing, loss or diminution of cell function, or contribute to the processes involved in neoplastic transformation. The incidence of somatic chromosome mutations (aberrations) can be readily ascertained from studies on peripheral blood lymphocytes. Data on their prevalence in cells from “normal” populations are presented. The incidence of aberrations is increased in people exposed to mutagens so that changes in aberration frequency provide a means for monitoring population exposure. This is illustrated by studies on populations exposed to ionising radiations and to various chemical mutagens including cigarette smoke. An alternative approach to the cytogenetical assessment of chromosome damage is described, in which the incidence of lymphocytes resistant to cell killing by 8-azaguanine is utilised. The frequencies of such resistant cells are shown to increase with increasing age of the individual, and it is further demonstrated that their incidence is increased, in a dose-dependent fashion, when cells are exposed in vitro to X-rays or chemical mutagens.

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Section: The Response Of Populations Exposed To Chemical Mutagensmentioning

confidence: 67%

Chromosomal mutations in human populations

Evans¹

1982

Cytogenet Genome Res

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“…Recent studies of the lymphocytes from medically or occupationally exposed human subjects or experimentally exposed laboratory rodents indicate that the levels of genetic lesions capable of inducing SCEs or CAs decline more or less rapidly to control or slightly higher than control levels [Lambert et al, 1978;Anderson et al, 1981;Stetka and Wolff, 1976;Stetka et al, 1978;Kligerman et al, 19811. Consequently, the efficacy of peripheral lymphocytes as a target cell to monitor genotoxic exposure of natural fish populations may well depend on the extent to which small increases in SCE or CA frequencies can be resolved in lymphocyte cultures.…”

Section: Discussionmentioning

confidence: 99%

In vitro induction of sister chromatid exchanges and chromosomal aberrations in peripheral lymphocytes of the oyster toadfish and american eel

1986

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A series of experiments was conducted to characterize the proliferation of oyster toadfish lymphocytes in medium containing 5-bromodeoxyuridine (BrdUrd) and to determine the effectiveness of cytogenetic endpoints for assessing the genotoxic effects of in vitro exposure of toadfish and eel lymphocytes to known mammalian clastogens. Although the rate of proliferation of toadfish lymphocytes was low compared to that of mammalian lymphocytes, the effects of increasing BrdUrd concentrations were similar, in that proliferation exhibited a concentration-dependent inhibition for concentrations above 10 microM BrdUrd, and sister chromatid exchange (SCE) frequencies exhibited a concentration-dependent increase for concentrations above 100 microM BrdUrd. Mitomycin C (MMC) and ethylene dibromide (EDB) induced concentration-dependent increases in chromatid-type exchange and SCE frequencies with least effective concentrations (control SCE frequency divided by the slope of the least-squares line) for SCE induction by MMC (6.8 X 10(-9) M) and EDB (2.6 X 10(-4) M) that were comparable to or slightly lower than those that have been obtained with mammalian in vitro systems. In vitro exposure of toadfish lymphocytes to dimethoate (DIM) induced a concentration-dependent increase in SCE frequency with a least effective concentration of 2.8 X 10(-3) M that was much higher than that observed with mammalian in vitro systems. In vitro exposure of American eel lymphocytes to MMC also induced a concentration-dependent increase in the frequency of chromosomal aberrations and SCEs with a least effective concentration for SCE induction of 2.0 X 10(-9) M. These results indicate that cytogenetic endpoints can be effectively scored with cultured lymphocytes from these and perhaps other fish species with comparable karyotypes that contain an average of at least 0.07 pg DNA/chromosome.

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“…Today thousands of workers employed in this industry are exposed to its influence. Exposure to this gas causes multisystem disorders including acroosteolysis, thrombocytopenia, portal fibrosis, hepatic and pulmonary dysfunction, immune complex disorder, primarily angiosarcoma of the liver, lung cancer, brain tumors, and malignant melanoma [Creech and Johnson, 1974;Tabershaw and Gaffey, 1974;Waxweiler et al, 1976;Buffler et al, 1979;Doll, 1988;Ward, 19761 together with increased frequencies of SCE, chromosome aberrations, and micronuclei [Ducatman, 1975;Anderson, 1981;Sinues et al, 1991;FuEiC et al, 1990al. It has been suggested by several investigators that chromosome breakpoints caused by radiation and some chemical agents cluster on certain parts of chromosomes [Funes-Cravioto et al, 1974;Casperson et al, 1972;Holmberg and Jonasson, FuEiC et al 1973;Bauchinger and Gotz, 1979;Kano and Little, 19861. This phenomenon could be connected with increasing evidences that some nonrandom chromosome changes are involved in certain cancers [Yunis and Soreng, 1984;Sandberg, 1991;Mitelman et al, 1978;Barrios et al, 19881.…”

Section: Introductionmentioning

confidence: 99%

Relationship between locations of chromosome breaks induced by vinyl chloride monomer and lymphocytosis

Fučić

Hitrec

Garaj‐Vrhovac

et al. 1995

American J Industrial Med

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The distribution of vinyl chloride monomer (VCM)-induced chromosome breaks was studied in cultured lymphocytes of subjects occupationally exposed to this gas. In the examined subjects, the mean group value of chromosome aberrations is 6.5% and for sister chromatid exchange (SCE) frequencies, the mean value per cell is 7.9. These values are significantly higher than in the control population. Occupational exposure to VCM caused lymphocytosis together with disturbances of mitogenic activity in lymphocytes stimulated by phytohaemagglutinin. The results of G-banding showed that sites of chromosome breakpoints caused by VCM can be related to the lymphatic tissue disorders.

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Chromosomal analysis in vinyl chloride exposed workers: Comparison of the standard technique with the sister-chromatid exchange technique

Cited by 44 publications

References 19 publications

Chromosomal mutations in human populations

Chromosomal mutations in human populations

In vitro induction of sister chromatid exchanges and chromosomal aberrations in peripheral lymphocytes of the oyster toadfish and american eel

Relationship between locations of chromosome breaks induced by vinyl chloride monomer and lymphocytosis

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