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Vinyl chloride, inhaled

Acute inhalation exposure of rats to 200,000 ppm VF for 30 minutes or more produced weak anaesthesia and no deaths (90). In rats VF is only slightly metabolized at a rate of one-fifth that of vinyl chloride (91—95). An extensive program of toxicity testing of vinyl fluoride is ia progress (96,97). [Pg.381]

Because routine inhalation of dust of any kind should be avoided, reduction of exposure to poly(vinyl chloride) dust may be accompHshed through the utilization of care when dumping bags, sweeping, mixing, or performing other tasks that can create dust. The use of an approved dust respirator is recommended where adequate ventilation may be unavailable. [Pg.508]

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. ... [Pg.121]

Caution must be observed in such an interpolation, however, and all the relevant data must be used. In at least one case—vinyl chloride-careless use of the procedure could have underestimated the risk, Le., in rats exposed to inhaled vinyl chloride monomer, the dose-inddence curve was observed to satiuate at the dose at which 20% of rats had angiosarcomas (Maltoni, 1977). Hence, if experimental points at lower doses had not been available, a simple interpolation between the zero dose incidence and the inddence at the maximum dose would have underestimated the computed risk at low doses, as illustrated in Fig uie 8.3. [Pg.115]

Fig. 8.3 Incidence of liver angiosorcouia in rats versus concentration of vinyl chloride monomer in air inhaled for 4 hours/day, 5 days/week. The line connecting the origin to the highest measured point obviously gives too low a computed risk at the lower dose levels. Also, shown are int polations indicating the number of cases per ppm inhaled (fixun Maltoni, 1977). Fig. 8.3 Incidence of liver angiosorcouia in rats versus concentration of vinyl chloride monomer in air inhaled for 4 hours/day, 5 days/week. The line connecting the origin to the highest measured point obviously gives too low a computed risk at the lower dose levels. Also, shown are int polations indicating the number of cases per ppm inhaled (fixun Maltoni, 1977).
Vinyl Chloride Yes (500ppm, intermittent) 20 Cardiovascular 500 (rat LD50) None detected Inhalation 2 3... [Pg.275]

Vinyl Ethylene Vinylidene Chloride Vinyl Pyridine isomers No — Same as Vinyl Chloride 8160 (rat LDS0) 1000 Inhalation 1 3 3... [Pg.275]

Inhalation of vapor in high concentrations may produce dizziness and narcosis. The liquid irritates the eyes and may irritate the skin by its defatting action it is assumed to be harmful if taken by mouth. In view of the recent observation that vinyl chloride can cause liver cancer, it must be assumed that vinyl bromide may behave similarly. Prevent inhalation of vapor. Prevent contact with skin and eyes.1 TLV-TWA 0.5 ppm (2.2 mg/m3).3... [Pg.649]

Inhalation of vapor in high concentrations produces dizziness and narcosis. The liquid may irritate and burn the skin, the latter due to its freezing action. As a result of observations made in the U.S. (1974), exposure to vinyl chloride monomer (VCM) in the workplace has been shown to cause a rare liver cancer, angiosarcoma. This may not manifest itself until more than 20 years after initial exposure. Prevent inhalation of gas. Prevent contact with liquid.4 TLV-TWA 1 ppm.5 Listed as known human carcinogen.6... [Pg.652]

The adverse effects of tetrachloroethylene are similar to those of carbon tetrachloride (CQ4), but less severe. Tetrachloroethylene is hepatotoxic and neurotoxic, but gastrointestinal disturbance is the only common adverse effect when it is used carefully. There is some risk of addiction to the inhaled vapor inhalation can result in vascular reactions, loss of consciousness, pulmonary edema, and fatal hepatic and renal damage. Alcohol and fatty foods increase absorption and hepatic toxicity. Exposure to tetrachloroethylene has been known to lead to vinyl chloride disease. Allergic reactions have not been reported. [Pg.3329]

While various types of lung cancer have been noted in humans, all known human pulmonary carcinogens are taken into the body by inhalation. It is equally important that inhaled chemicals can cause neoplasms at sites elsewhere in the body. For example, exposure to vinyl chloride, butadiene, acrylonitrile, and ethylene oxide by inhalation may produce a significant increase in cancer incidence in other organs (liver, brain, and blood) as well as in the... [Pg.2275]

As expected, based on very strong similarity with vinyl chloride in terms of kinetics and dynamics, vinyl bromide provided a truncated, but up to metabolic saturation, perfect dose response in terms of liver angiosarcoma in both male and female rats inhaling 0, 10, 50, 250, and 1250 ppm (44, 219, 1093, and 5875 mg m ) vinyl bromide. Increased tumor incidences were also observed in squamous cell carcinomas of the Zymbal gland and neoplastic nodules and hepatocellular carcinomas. [Pg.2827]

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. [Pg.2829]

Vinyl chloride is readily absorbed via all routes of exposure and rapidly distributed throughout the body. Following oral administration in male rats, peak blood concentrations are noted in less than 10 min. Approximately 40% of inhaled vinyl chloride is absorbed while as much as 95% is absorbed upon ingestion. Highest concentrations are found in the liver and kidneys. [Pg.2829]

Storage of vinyl chloride is limited by the rapid metabolism and subsequent excretion. Vinyl chloride is biotransformed by cytochrome P450-mixed function oxidase systems (CYP 2E1), with the two primary metabolites being chloroethylene oxide and chloroacetaldehyde. These materials are further converted to chloroethanol and monochloroacetic acid. Metabolites are primarily excreted in urine. When rats were exposed to vinyl chloride at 100 ppm for 5 h, 70% of the absorbed dose was excreted as urinary metabolites within 24 h. The half-life for urinary excretion in rats was 4h. With an increase in dose via either inhalation or ingestion, the proportion exhaled increased and urinary and fecal elimination decreased. [Pg.2829]

Vinyl chloride appears to have a low toxicity when administered by inhalation, with LC50 values... [Pg.2829]

Chronic animal studies report increased mortality and weight loss, as well as effects on the liver, kidney, and CNS at levels as low as 1.3 mg kg day Animal studies have shown increased testicular damage as well as decreased male fertility in rats exposed to low levels of vinyl chloride for 12 months. In addition, some animal studies have shown decreased fetal weights and increased terata at maternally toxic inhalation exposure levels of vinyl chloride. Animal studies have also reported that inhaled vinyl chloride increases the incidence of angiosarcoma of the liver. [Pg.2830]

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. [Pg.2830]

Epidemiological studies conducted on humans exposed to inhaled vinyl chloride have shown increases in angiosarcoma of the liver. Hepatocellular carcinoma of the liver as well as some brain tumors... [Pg.2830]

Methylene chloride, vinyl chloride, and toluene will be present in liquid form in the trench. All would also be expected to be present in the vapor state, with vinyl chloride being the most volatile due to its high Henry s law constant. The principal dangers to site remediation workers, therefore, would be from inhalation of vapors and skin absorption of contacted liquids. Pentachlorophenol and PCBs will be present in solid and semisolid forms. Minimal vapors of these compounds would be expected. The principal dangers would be from inhalation of dusts and fumes, ingestion of solids, and skin absorption due to solids contact. In the absence of engineering controls and work practices, the necessary worker PPE would include, at a minimum, respirators and chemical protective clothing. [Pg.750]

Vinyl chloride 1986/1996 Likely to be Carcinogenic to Humans Sufficient 0 Inhalation, oral (likely dermal) Liver cancer, specifically angiosarcoma Y... [Pg.413]


See other pages where Vinyl chloride, inhaled is mentioned: [Pg.100]    [Pg.100]    [Pg.508]    [Pg.403]    [Pg.62]    [Pg.173]    [Pg.360]    [Pg.731]    [Pg.732]    [Pg.188]    [Pg.103]    [Pg.275]    [Pg.276]    [Pg.925]    [Pg.36]    [Pg.508]    [Pg.304]    [Pg.1425]    [Pg.103]    [Pg.119]    [Pg.1867]    [Pg.2251]    [Pg.2253]    [Pg.2273]    [Pg.2776]    [Pg.2830]    [Pg.505]    [Pg.72]   
See also in sourсe #XX -- [ Pg.249 , Pg.250 ]




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