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espectively. The list of longest held jobs for the afflicted individualsincluded PVC loader, dryer operator, and maintenance worker for primaryliver cancer-A and primary liver cancer-non-A. It was concluded that vinylchloride may have a broader carcinogenicity spectrum on the liver thanknown before and that exposure lower than that occurring in autoclavecleaning can cause primary liver cancers. [Pirastu R et al; AmericanJournal of Industrial Medicine 17 (2): 155-61 (1990)]**PEER REVIEWED**Cytogenetic analysis of peripheral blood lymphocytes was used to examine43 workers, average age 34.4 years, having an average of 11.2 yr exposureto vinyl chloride monomer and 22 referent subjects, average age 40.3 yr,not exposed to vinyl chloride monomer or other known mutagenic agents. Atleast 100 metaphases with 46 centromeres were analyzed per person for thepresence of chromosomal aberrations, specifically, chromatid breaks,chromosome breaks, chromatid exchanges, and gaps. All aberration typeswere increased in the exposed group as compared to the referent group,with the differences highly significant for chromatid breaks, percentageof aberrant cells, and breaks per cell. In both groups of subjects, therewas no difference between smokers and nonsmokers in respect to percentageof aberrant cells; however, there was a highly significant difference inthis percentage between nonsmokers in the two groups, as well as asignificant difference between smokers in the two groups. It was concludedthat the main reason for the increased aberration frequencies is theexposure to vinyl chloride monomer. [Hrivnak L et al; Mutation Research240 (2) 83-85 (1990)]**PEER REVIEWED**A group of 67 workers occupationally exposed for an average of 15 years tovinyl chloride monomer were examined for the presence of chromosomeaberrations and their distribution along the chromosomal length. Theprocedure made use of lymphocyte cultures from blood samples. Measurementsof 2000 cells per person were scored for chromatid and bichromatidchromosomal breaks. The estimation of the number and locations of breaksinvolved the division of each chromosome into five and six segments. Atotal of 626 breaks were counted in chromosomes A1, A2, and A3, andchromosome group-B, group-C, and group-D. The distribution of breaks alongthe chromosome arms of the lymphocytes of the vinyl chloride monomerexposed workers was not identical to the expected random distribution ofbreaks in the lymphocytes of an unexposed normal population. Astatistically larger number of breaks compared with that expected wasobserved on the first and second segment of chromosome A1, the fifth andsixth segment of chromosome A2, and the third, fourth, and fifth segmentof chromosomes in group-B and group-C. However, a statistically smallernumber of breaks was observed on the first segment of chromosome A2, thefirst and third segment of chromosome A3, the first and second segment ofchromosomes from group-B and group-C, and the first and fourth segment ofchromosome from group-D. The results indicated the existence of chromosomelocations highly sensitive and highly resistant to the actions of vinylchloride monomer. [Fucic A et al; Mutation Research 243 (2) 95-9(1990)]**PEER REVIEWED**An investigation was made of 13 workers at a vinyl chloride monomerpolymerization facility in Singapore, who showed persistent abnormalitiesin liver function tests. All subjects were males aged 19 to 55 years attime of first exposure. All began employment between 1971 and 1982, whenenvironmental monomer levels ranged from 1 to 21 ppm. After 1983,environmental levels were controlled to a geometric mean of 1.5ppm.Exposure duration was 1 to 13 years, with a mean of 5.1 years. Only one