Several reported studies on the effects of polyvinyl chloride (PVC) dust in animals and man have been conflicting. The present study of the ventilatory function of 509 male workers exposed to PVC dust was made in 1977. Altogether 104 men exposed to PVC dust only, 112 men exposed to non-chlorinated solvents only, and 293 men exposed to a mixture of both completed the MRC questionnaire on respiratory function and performed simple spirometric tests (forced expiratory volume in one second and forced vital capacity). No differences were found between the three groups after allowance was made for age, height, and smoking. When exposure and smoking effects were considered separately, the latter was shown to be the dominant cause of reduced lung function. In this study work with PVC dust has not produced deleterious effects on ventilatory function.Polyvinyl chloride (PVC), a large tonnage raw material of fundamental importance to the plastics industry, is a white powder that was until recently considered to be inert. The basic material is formed from its monomer, the gas vinyl chloride (VCM). Although VCM and PVC have been synthesised for over 30 years, it is only in the past 10 years that the sinister nature of VCM has become apparent. VCM has been found to produce a wide spectrum of clinical conditions, the most important being angiosarcoma of the liver in workers exposed to high concentrations of the gas in PVC production plants. This was discovered in 1974 and because a small quantity of the gas is carried forward with the PVC powder to its containers, and thus to the formulating industries the effects, if any, of the PVC powder came into question. The chance of finding effects similar to those associated with VCM is considered remote, since the concentrations are greatly reduced. The possibility of pulmonary changes being caused by inhalation of the dust however, has led to experimental and clinical research.The cytotoxicity of various polymer dusts, including PVC, to suspensions of rat alveolar and peritoneal macrophages in culture' indicated that PVC caused deaths of cells similar in amount to kaolin, magnesium trisilicate, and polyethylene. These materials produced less than 2 % fibrogenicity compared with over 10 % for asbestos.On such evidence PVC had been considered inert and therefore incapable of producing lung changes.
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