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El policloruro de vinilo (PVC) es el polímero que ocupa el tercer puesto en el mercado de producción de plásticos a nivel mundial. Como consecuencia de la exposición crónica, los operarios pueden desarrollar cambios óseos degenerativos, Raynaud, trastornos circulatorios en extremidades, trombocitopenia y lesiones cutáneas semejantes a esclerodermia; esto se conoce como “enfermedad por cloruro de vinilo”. Presentamos un paciente masculino de 24 años de edad que presenta fenómeno de Raynaud, cefaleas, malestar en manos y pies, sensación de frío, fatiga y pérdida de apetito asociado a exposición a policloruro de vinilo. El estudio de la microcirculación cutánea periungueal por videocapilaroscopía muestra alteraciones estructurales y funcionales características. Se recomienda un seguimiento multidisciplinario estricto de los trabajadores expuestos a PVC.

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To study whether exposure to low levels of vinyl chloride monomer (VCM) causes increased risk for cancer morbidity and death from ischemic heart disease, a cohort study was performed among 2,031 male workers at a polyvinyl chloride (PVC) processing plant who had been employed for at least 3 months during the period 1945-1980. An almost significantly increased total mortality (SMR = 116, 95% CI 99-136) was found. Deaths caused by violence or intoxication were significantly increased (SMR = 153, 95% CI 109-213), but not deaths from ischemic heart disease (SMR = 100, 95% CI 73-135). A significant increase in total cancer morbidity was observed (SMR = 128, 95% CI 101-161). Respiratory cancers were significantly increased (SMR = 213, 95% CI 127-346). Furthermore, six brain tumors (vs. 2.6 expected) were observed. This increase, however, was not significant (SMR = 229, 95% CI 84-498). No liver hemangiosarcoma was observed. Applying a latency period of greater than or equal to 10 years from start of employment did not change the risk patterns. There were no significant exposure-response associations between exposure estimates for VCM, asbestos, and plasticizers and cancer morbidity.

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Microcirculatory disorders of the extremities may have an occupational origin, which it is desirable to specify. Exposure to vinyl monochloride results in a chemical nuisance which also proved to be carcinogenic in man. Strict preventive measures are therefore enforced in the industry and angioneurotic disorders should no longer be observed. Use of vibrating tools results in a microvascular response to a physical nuisance which is difficult to prevent completely. In both cases the physiopathology is not well-known, but compensation is possible as occupational diseases. Repeated trauma of the ulnar artery, and/or its superficial palmar branch are, on the contrary, the main explanation for hypothenar hammer syndrome, which is easily prevented by mere adjustment of the work position and occupational movements: the conditions for medico-legal compensation for this particular syndrome, which is still not listed among occupational diseases, will be in effect in the very near future.

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We have previously reported a genetic susceptibility to a scleroderma-like disorder in a group of workers exposed to polyvinyl chloride and this susceptibility could be mapped to the major histocompatibility complex area of the 6th chromosome. To date no genetic studies have been reported comparing affected with unaffected workers. We report such data and discuss it in the light of our previous findings in vinyl chloride exposed patients and in patients with classical scleroderma. Our results suggest that susceptibility to this disorder is increased in the presence of HLA-DR5 or of a gene in linkage disequilibrium with it and an antigen associated with the haplotype A1 B8, while DR3 favours progression of the disease.

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In view of divergent opinions concerning MAC value for vinyl acetate, a study on acute and chronic inhalatory toxic effect of this compound on animals was carried out. The scope of the study included determination of CL50 value after Litchfield and Wilcoxon and 10-month exposure of animals to vinyl acetate at concentrations 10, 100 and 500 mg/m3, 5 days weekly, 5 hours daily. During 10-month experiment the animals were observed and body weight controlled. In addition, periodically some hematological examinations and biochemical of blood serum as well as histopathological examinations of inner organs were carried on. Post-mortally the weight of inner organs was determined. CL50 value determined on rats has amounted to 4100 ppm. In the study on chronic effect, the prevalence and the degree of intensity of the changes of the used by us indicators was the least in the group of animals exposed to vinyl acetate at concentration of 10 mg/m3. These changes were transient not involved reticulopenia and animals' body weight decrease. Histopathological examinations revealed some inflammatory changes in respiratory system both in control and exposed animals. Only planoepithelial metaplasia of bronchi was found exclusively in animals exposed to vinyl acetate at all concentrations used. The changes within liver were found only in animals exposed to vinyl acetate at concentration of 100 and 500 mg/m3. These changes involved fatty degeneration of hepatic parenchyma, proliferation and extension of smooth endoplasmatic reticulum and the changes within the biliary canaliculi. Taking the above results into account it seems that the lowest of the recommended in the world MAC value--10 mg/m3 may be accepted as the upper limit of the maximum admissible concentration for vinyl acetate.

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Most previous studies proposing serum bile acids as indicators of hepatic function have been performed in hospitalized patients in whom overt symptomatic liver disease was present. The ability of fasting levels of serum bile acids to identify mild, clinically inapparent chemical liver injury in an occupational setting was compared with that of indocyanine green clearance and routine biochemical liver tests in 67 asymptomatic chemical workers in whom liver biopsies had been performed for medical indications. Histologically, 15 were found to have chemical liver injury, 27 had nonchemical liver disease, and 25 were normal. Two serum bile acids, cholylglycine and conjugates of cholic acid, were determined by radioimmunoassay, using 466 "normal" males from the same worker cohort as a reference range. The geometric mean concentrations of cholylglycine in patients with chemical liver injury, patients with nonchemical liver disease, and normal subjects were 47.9, 19.1, and 20.0 micrograms/dl, respectively (p = 0.036 by analysis of variance). Conjugates of cholic acid showed similar differences (p = 0.027), as did indocyanine green clearance with mean half-life of 4.2, 3.2, and 3.3 minutes in the three biopsy subgroups, respectively (p = 0.043). Such differences were not observed for biochemical liver tests. The fasting level of serum bile acids provided high specificity but lower sensitivity in the detection of all types of liver disease. However, serum bile acids and indocyanine green clearance provided a higher specificity and sensitivity for chemical liver injury than for nonchemical liver disease. An index of average exposure to vinyl chloride was significantly greater in the subgroup with chemical liver injury than in the other two groups, further supporting the association of chemical type injury with impaired anion uptake. These data identify the fasting level of serum bile acids as a clinically usable indicator of early chemical injury in chemically exposed asymptomatic worker populations with liver dysfunction. Further investigation is needed in other occupational hepatotoxic environments to determine if this association is limited to vinyl monomer type injury.

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Discussion is limited to an analysis of texts directly concerned with safety, hygiene and the industrial physician. After a review of features related to poisoning with the vinyl chloride monomer, the problems of vibration-induced angioneurotic disorders are outlined. Medical prevention and technique and then compensation for these occupational nuisances are then described.

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Focal hepatocellular hyperplasia and focal mixed (hepatocytes and sinusoidal cells) hyperplasia are early histological alterations indicative of vinyl monomer exposure. To evaluate their uses in screening chemical workers, 93 liver biopsy specimens from 78 persons were examined in double-blind duplicative fashion. Forty-eight specimens were from exposed chemical workers, 35 of them having liver biopsy(ies) for hepatic test abnormalities and 13 for nonliver -related reasons. A comparison group consisted of 30 nonchemical workers who had undergone liver biopsy for nonliver related reasons. Twenty-three of the exposed workers (48%) had hepatic lesions consistent with exposure: 17 (35%) of these had focal hepatocytic hyperplasia, while 6 (13%) had focal mixed hyperplasia or more advanced lesions. Only five of the comparison group had like findings: four (13%) had focal hepatocytic hyperplasia; one had focal mixed hyperplasia and sinusoidal dilatation. This individual had persistent hepatic test abnormalities with the focal mixed hyperplasia and a sinusoidal dilatation, and on subsequent biopsy, angiosarcoma (and a history of using hair spray containing vinyl chloride propellant ). Ten individuals had 25 multiple biopsies also read double-blindly; 10 had two or more readings of the same biopsy. Duplicate 21 of 23 (91%) and multiple 27 of 28 (96%) biopsy interpretations in the same individual were identical. Only 6% of either duplicate and/or multiple readings disagreed. Both focal hepatocellular and mixed hyperplasia were always associated with abnormalities in hepatic test results of which indocyanine green clearance was the most sensitive and gamma-glutamyl transpeptidase the least specific.(ABSTRACT TRUNCATED AT 250 WORDS)

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