Vinyl chloride, occupational exposure

The hazards of chemicals are commonly detected in the workplace first, because exposure levels there are higher than in the general environment. In addition, the exposed population is well known, which allows early detection of the association between deleterious health effects and the exposure. The toxic effects of some chemicals, such as mercury compounds and soot, have been known already for centuries. Already at the end of the eighteenth century, small boys who were employed to climb up the inside of chimneys to clean them suffered from a cancer of the scrotum due to exposure to soot. This was the first occupational cancer ever identified. In the viscose industry, exposure to carbon disulfide was already known to cause psychoses among exposed workers during the nineteenth century. As late as the 1970s, vinyl chloride was found to induce angiosarcoma of the liver, a tumor that was practically unknown in ocher instances. ... 

Toxicology. Occupational exposure to vinyl chloride is associated with an increased incidence of angiosarcoma of the liver and other malignant tumors, acroosteolysis, Raynaud syndrome, scleroderma, thromhocytopenia, circulatory dismrbances, and impaired liver function. Very high concentrations cause central nervous system (CNS) depression. 

Di(2-ethylhexyl) phthalate is a liquid of low volatility, widely used as a plasticizer in flexible poly(vinyl chloride) products at concentrations of up to 40%, as well as in a number of other minor applications. Occupational exposure occurs mainly by inhalation as an aerosol during its manufacture and its use as a plasticizer in poly(vinyl chloride) product manufacturing plants, at concentrations usually below 1 mg/m. ... 

Fig. 6.4 Distribution of death from angiosarcomas of the liver in relation to time after onset of exposure, in persons exposed occupationally to vinyl chloride and persons injected intravenously with Thorotrast (thorium dioxide) (reproduced from Spirtas et al., 1983).

One case has been reported of liver angiosarcoma (pathologically confirmed) in a worker exposed to polychloroprene who had no known occupational exposure to vinyl chloride (lARC, 1987b) or medical exposure to thorotrast (Infante, 1977). [It is unclear whether and how much this worker was exposed to chloroprene monomer.]... 

Current occupational exposure to 1,2-dichloroethane in North America occurs predominantly during the manufacture of other chemicals, such as vinyl chloride, where 1,2-dichloroethane is used as an intermediate. In a 1982 National Occupational Exposure Survey by the United States National Institute for Occupational Safety and Health (NIOSH), 28% of employees working with adhesives and solvents were exposed to 1,2-dichloroethane, while between 5 and 9% of workers were exposed to the substance in the medicinals and botanicals, biological products, petroleum refining and organic chemicals industries, and in museums and art galleries (United States Department of Labor, 1989). 

Anon, Recommended Standard for Occupational Exposure to Vinyl Chloride , PB-246691, NIOSH, Rockville (1975) [The report recommends, in part, that ... Despite the fact that animal experiments have shown no liver tumors... 

I have chosen to deal with vinyl chloride in my discussion of exposure in the workplace as it serves to demonstrate the problems that may arise from exposure to novel chemicals, how these can be prevented, and how crucial a knowledge of toxicology is to occupational health and the safe use of chemicals. 

The need for improved sampling and analytical techniques for monitoring employee exposure extends to substances other than the trace metals. The "no detectable limit philosophy for occupational exposure to carcinogens dates back to the 1974 situation with vinyl chloride in which NIOSH recommended that airborne concentrations be reduced "to levels not detectable by the recommended method (1 ppm) (16). Very low maximum permissible exposure levels are likely to be recommended in the future for substances which are determined to be potential human carcinogens. 

Recommended Standard for Occupational Exposure to Vinyl Chloride, ... 

The NIOSH thresholds for carcinogens were not designed to be protective of 100% of the population. NIOSH usually recommends that occupational exposures to carcinogens be limited to the lowest feasible concentration. This perhaps is the reason that the NIOSH exposure limit for vinyl chloride is the lowest reliably detectable concentration and the OSHA exposure limit is 1 ppm. 

The main route of occupational exposure to vinyl chloride is by inhalation that can occur in plastics manufacturing plants. Inhalation exposure to the general public is generally quite limited and probably restricted to accidental releases from hazardous waste sites and landfills. Vinyl chloride has been detected in surface and well waters, sediment and soil samples near manufacturing facilities. Some dietary exposure can occur from leaching from certain PVC materials into packaged foodstuffs. 

Chronic inhalation or oral exposure to low levels of vinyl chloride may cause liver damage in humans. Some individuals occupationally exposed to high levels of vinyl chloride develop a specific syndrome termed vinyl chloride disease . This is characterized by dizziness, numbness, earache, headache, blurred vision, fatigue, nausea, shortness of breath, Raynaud s phenomenon, loss of weight, changes in bone structure at the ends of the fingers, joint, and muscle pain, and scleroderma-type changes in the skin. 

Several unsubstantiated case reports have reported reduced male sexual performance upon occupational exposure to vinyl chloride. There have been mixed epidemiological results with respect to teratogenic effects in human exposure. 

The Occupational Safety and Health Administration (OSHA) has set the permissible exposure level (PEL) of vinyl chloride (VC) at 1.0 part per million (ppm) as a maximiun time-weighted average (TWA) for an 8-h workday. The PEL was set at 1.0 ppm because vinyl chloride is a suspected carcinogen. Thus, if vinyl chloride escapes into the air, the concentration of vinyl chloride must be maintained at or below 1.0 ppm. The major source of VC escape into the workplace air in typical process conditions is fugitive emissions from pipe connections such as valves, flanges, and pump seals. 

A fairly strong and consistent association between exposure, primarily in occupational settings, to solvents (e.g. trichloroethylene) and scleroderma has been reported in numerous epidemiological studies (see chapter 8). Scleroderma-like diseases can also be induced by other chemical compounds, such as drugs (D Cruz, 2000) and silica ( Erasmus syndrome ). Workers exposed to vinyl chloride monomers exhibit clinical features that resemble systemic sclerosis, such as fibrotic skin lesions, pulmonary fibrosis, and skin capillary abnormalities. However, vinyl chloride disease also harbours several features that are clearly distinct from systemic sclerosis. After exposure is discontinued, skin lesions, capillary abnormalities, and acroosteolytic lesions revert to nearly normal (Haustein Ziegler, 1985). 

Micu D, Mihailescu E, Vilau C, et al. 1985. The value of some cytoenzymochemical investigations of the leukocytes and platelets in estimating the effects of occupational exposure to benzene, vinyl chloride and carbon disulfide. Rev Roum Med Intern 23 115-120. 

---