Document 6REa67XGMQeLkQ8L9wYX9BVX3

HEALTH & ENVIRONMENT INTERNATIONAL, LTD. RECEIVED OCT 0 2 1991 TA PATNESKY 0 OMPREHENSIVE He*TM AND Environmental M ONOGRAPH ON VINYL CHLORIDE 75-01-4 BOR 006688 111 CHESTNUT AVENUE WILMINGTON, DE 19809 (302) 764-8810 PLEASE NOTE: No part of this publication may be reproduced or transmitted in any form, or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the copyright owner. (Copyright BC11990, All Rights Reserved) ****************************************************** The information reported in this monograph has been obtained from many databases. Health and Environment International, Ltd. (H&EI) is not responsible for errors in fact or interpretation contained in these original databases, nor for any damage of any kind that results from any errors or omissions in the monograph. The information is extensively referenced and original publications should be examined before action oriented decisions are made. While the monographs are intended to be comprehensive, there is no guarantee that no relevant important information has been overlooked. If a user detects any errors or significant omissions, H&EI should be advised so that corrections can be made in subsequent editions. HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. BOR 006689 CONTENTS IDENTIFICATION ................................................................................................................. 1 MANUFACTURING INFORMATION ..................................................................................... 3 USE AND CONSUMPTION INFORMATION ...................................................................... 6 CHEMICAL AND PHYSICAL PROPERTIES ................................................................... 7 PHARMACOKINETICS ABSORPTION, DISTRIBUTION AND EXCRETION .................................... METABOLISM AND METABOLITES ................................................................... BIOLOGICAL HALF-LIFE .................................................................................. MECHANISM OF ACTION ..................................................................................... INTERACTIONS ....................................................................................................... 10 10 11 11 11 TOXICOLOGY TOXIC HAZARD RATING ..................................................................................... HUMAN TOXICITY EXCERPTS .......................................................................... HUMAN REPRODUCTION AND DEVELOPMENT EXCERPTS ........................ HUMAN ENVIRONMENTAL EXPOSURE .............................................................. ANIMAL TOXICITY EXCERPTS ........................................................................ HUMAN STANDARDS AND RECOMMENDATIONS ............................................ 13 13 18 19 20 23 ENVIRONMENTAL FATE AND EXPOSURE EXCERPTS ENVIRONMENTAL FATE AND EXPOSURE SUMMARY .................................. ENVIRONMENTAL FATE ....................................................................................... ENVIRONMENTAL TRANSPORT .......................................................................... ENVIRONMENTAL CONCENTRATIONS .............................................................. ENVIRONMENTAL TRANSFORMATIONS ........................................................... 25 26 27 28 30 REGULATIONS AND COMPLIANCE STANDARDS WATER STANDARDS ............................................................................................... ATMOSPHERIC STANDARDS ................................................................................ CERCLA REQUIREMENTS ..................................................................................... RCRA REQUIREMENTS .......................................................................................... FI FRA REQUIREMENTS ....................................................................................... FDA REQUIREMENTS ............................................................................................ 32 32 33 33 33 33 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. CODE OF FEDERAL REGULATIONS PROTECTION OF ENVIRONMENT ...................................................................... FOOD AND DRUGS .................................................................................................. LABOR ......................................................................................................................... COMMERCIAL PRACTICES .................................................................................. SHIPPING ................................................................................................................. TRANSPORTATION .................................................................................................. NAVIGATION AND NAVIGABLE WATERS ...................................................... MINERAL RESOURCES .......................................................................................... COMMERCE AND FOREIGN TRADE ................................................................... NATIONAL DEFENSE ............................................................................................ 35 37 38 38 38 39 39 40 40 40 MONITORING AND ANALYSIS INFORMATION ........................................................... 41 SAFE HANDLING AND DISPOSAL INFORMATION .................................................... 43 ADDITIONAL INFORMATION TSCA TEST SUBMISSIONS ................................................................................ 52 SPECIAL REPORTS ............................................................................................... 53 BIBLIOGRAPHY ...................................................................................................................... 55 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. BOR 006691 IDENTIFICATION COMMON NAME Vinyl chloride CAS REGISTRY NUMBER 75-01-4 CHEMICAL STRUCTURE Update: July 17, 1990 Cl CHEMICAL NAME Ethene, ehloro- MOLECULAR FORMULA C2-H3-C1 NIOSH/RTECS NUMBER NIOSH/KU962SOOO OHM-TADS NUMBER 7216947 SHIPPING NAME/NUMBER - DOT/UN/NA/IMCO ON 1086; Vinyl chloride IMO 2.1; Vinyl chloride HEALTH AND ENVIRONMENT INTERNATIONAL, LTD BOR 006692 Page 1 STANDARD TRANSPORTATION COMMODITY CODE 49 057 92; Vinyl chloride EPA HAZARDOUS HASTE NUMBER 0043; A toxic waste when a discarded commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or manufacturing chemical intermediate. SYNONYMS Chlorethene Chlorethylene Chloroethene Chloroethylene Chlorure de vinyle (French) Cloruro di vinile (Italian) Ethylene monochloride Ethylene, chloro Monochloroethene Monochloroethylene VC VCM Vinile (cloruro di) (Italian) Vinyl C monomer Vinyl chloride monomer Vinylchlorid (German) Vinyle(chlorure de) (French) Winylu chlorek (Polish) Ethene, chloro Trovidur Monovinyl chloride (MVC) HEALTH AND ENVIRONMENT INTERNATIONAL, LTD BOR 006693 Page 2 MANUFACTURING INFORMATION METHODS OF MANUFACTURING Cracking of ethylene dichloride obtained via oxychlorination or direct chlorination of ethylene; vapor-phase reaction of acetylene and hydrogen chloride in the presence of mercuric chloride [98] From ethylene dichloride and alcoholic potassium: Regnault, Ann 14, 22 (1835); by halogenation of ethylene: Miller, Jenks, US patent 2,896,000 (1959 to National Distillers and Chemical Corp.) Comprehensive Monograph on Toxicity of Vinyl Chloride: Ann NY Acad Sci 246, 1 (1975). [123] IMPURITIES Commercial grade contains 1-2 percent impurities: water, non-volatile residues, acetaldehyde, hydrogen chloride, hydrogen peroxide, and methyl chloride. [61] Specifications for a typical commercial product call for maxima in mg/kg by weight of the following impurities: unBaturated hydrocarbons - 10; acetaldehyde - 2; dichloro compounds - 16; water - 15; hydrogen chloride - 2; nonvolatiles - 200; iron - 0.4. Phenol at levels of 25-50 mg/kg by weight is used as a stabilizer to prevent polymerization [57] The impurities of vinyl chloride are as follows: acetic aldehyde 5 ppm, butane 8 ppm, 1,3-butadiene 10 ppm, chlorophene 10 ppm, diacetylene 4 ppm, vinyl acetylene 10 ppm, propine 3 ppm, methylchloride 100 ppm. [51] FORMULATIONS AND PREPARATIONS Grade: Technical, pure 99.9 percent [91] Vinyl chloride monomer is available commercially in cylinders or in bulk and is generally supplied as a liquid under pressure. [57] Liquefied gas, polymer grade [69] MANUFACTURERS Borden Chemicals and Plastics, Headquarters, Hwy 73, Geismar, LA 70734, (504) 387-5101; Production site: Geismar, LA 70734 [98] Dow Chemical USA, Headquarters, 2020 Dow Center, Midland, MI 48640, (317) 636-1000; Production sites: Oyster Creek, TX 77541; Plaquemine, LA 70764 [98] Formosa Plastics Corporation USA, Headquarters, 66 Hanover Rd, Florham Park, NJ 07932 (201) 966-0025; Production sites: Baton Rouge, LA 70821; Point Comfort, TX 77978 [98] Georgia Gulf Corporation, Headquarters, 400 Perimeter Center Terrace, suite 595, PO Box 105197, Atlanta, GA 30348 (404) 395-4500; Production site: Plaquemine, LA 70764 [98] BOR 006694 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD Page 3  The BF Goodrich Company, Headquarters, 3925 Embassy Parkway, Akron, OH 44313, (216) 374-2000; BF Goodrich Chemical Group, 6100 Oak Tree Blvd, Cleveland, OH 44131, (216) 447-6000; Production sites: Calvert City, KY 42029; La Porte, TX 77571 (Independence Plant) [98] PPG Industries, Inc, Chemicals Group, Headquarters, One PPG Place, Pittsburgh, PA 15272 (412) 434-3131; Production site: Lake Charles, LA 70601 [98] Occidental Petroleum Corporation, Headquarters, 10889 Wilshire Boulevard, Suite 1500, Los Angeles, CA 90024, (213) 879-1700; Subsidiary: Occidental Chemical Corporation, 5005 LBJ Freeway, Dallas, TX 75244, (214) 404-3800; PVC Resins and Fabricated Products, Arroand Hammer Blvd, Pottstown, PA 19464, (215) 327-6400; Production site: Deer Park, TX 77536 [98] Vista Chemical Company, Headquarters, 15990 N Barker's Landing Road, Houston, TX 77029, (713) 531-3200; Production site: Lake Charles, LA 70669 [98] OTHER MANUFACTURING INFORMATION Because it has been confirmed that vinyl chloride monomer is a human and animal carcinogen, sale of propellants and all aerosols containing it was banned in 1974 (USEPA, 1974; USA Consumer Product Safety Commission, 1974). [83] Sometimes stabilized by adding hydroquinone, butyl catechol, or phenol. [72] The most important vinyl monomer; 19th highest-volume chemical produced in the US (1985) [91] Dichloroethane used for pyrolysis to vinyl chloride must be of purity greater than 99.5 weight-percent because the cracking process is exceedingly susceptible to inhibitors. It must also be dry to prevent corrosion. [66] HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. BOR 006695 Page 4 U.S. PRODUCTION (1977) 2.72X10+12 grams [98] (1982) 2.22X10+12 grams [98] (1985) 4.30X10+12 grams [103] (1986) 8.41X10+9 pounds [102] (1987) 8.40X10+9 pounds [104] U.S. IMPORTS (1977) 6.05X10+5 grams [98] (1982) 2.30X10+10 grams [98] (1985) 5.89X10+10 grams [15] (1986) 2.06X10+8 pounds [17] U.S. EXPORTS (1978) 4.08X10+11 grams [98] (1983) 3.11X10+11 grams [98] (1985) 4.61X10+11 grams [16] (1987) 8.43X10+8 pounds [14] HEALTH AND ENVIRONMENT INTERNATIONAL, LTD BOR 006696 Page 5 USE AND CONSUMPTION INFORMATION MAJOR OSES In plastic industry; in organic syntheses [123] Monomer for poly(vinyl chloride) homopolymer [98] Comonomer, e.g., with vinyl acetate or vinylidene chloride [98] Chemical intermediate for methyl chloroform and 1,1,1-trichloroethane [98] Chemical intermediate for other organic chemicals-e.g., chloroacetaldehyde [98] Monomer and comonomer for fibers, e.g., vinyon and saran fibers [98] Oxidation inhibitor in ethylene oxide production [98] Refrigerant and extraction solvent (former use) [98] Vinyl chloride is used in the manufacture of numerous products in building and construction, automotive industry, electrical wire insulation and cables, piping, industrial and household equipment, medical supplies, and is depended upon heavily by the rubber, paper, and glass industries. [108] Adhesives for plastics [91] Vinyl chloride was formerly a component of aerosol propellants. Vinyl chloride and vinyl acetate copolymers are used extensively to produce vinyl asbestos floor tiles. [30] Limited quantities of chloroethene were used in the United States as an aerosol propellant and as an ingredient of drug and cosmetic products. (Former use) [111] CONSUMPTION PATTERNS Monomer for poly(vinyl chloride) resins, 85 percent; exports, 13.5 percent; miscellaneous (mostly copolymer use), 1.5 percent (1982) [98] Ninty five percent for polyvinyl chloride homopolymer and copolymer resin; 4 percent for synthesis of methyl chloroform; 1 percent for miscellaneous applications (1972) [98] Ninty one percent for polyvinyl chloride [65] CHEMICAL PROFILE; Vinyl Chloride. Polyvinyl chloride, 91 percent; exports, 7 percent; other, including chlorinated solvents, 2 percent. [64] CHEMICAL PROFILE: Vinyl chloride. Demand: 1988: 9.1 billion pounds; 1989: 9.2 billion pounds; 1993 (projected): 11.0 billion pounds. (Includes exports, but not imports, which totaled 227 million pounds last year.) [64] HEALTH AND ENVIRONMENT INTERNATIONAL LTD BOR 006697 Page 6 CHEMICAL AND PHYSICAL PROPERTIES COLOR AMD FORM Colorless gas or liquid [90] ODOR Ethereal odor [91] Sweet odor [6] BOILING POINT -13.37 degrees C [123] MELTING POINT -153.8 degrees C [123] MOLECULAR WEIGHT 62.50 [98] CRITICAL TEMPERATURE AND PRESSURE 424.61 degrees K; 151.5 degrees C; 304.6 degrees F/5,755 kPa; 57.55 bar; 834.7 psia; 56.8 atmospheres [10] DENSITY AND SPECIFIC GRAVITY 0.9106 at 20 degrees C/4 degrees c [59] HEAT OF VAPORIZATION 20.9 kJ/mole at -13.4 degrees C [36] OCTANOL/WATER PARTITION COEFFICIENT Log Kow= 0.6 (calculated) [18] HEALTH AND ENVIRONMENT INTERNATIONAL, LTD BOR 006698 Page 7 SOLUBILITIES Soluble in alcohol, ether, carbon tetrachloride, benzene [123] Soluble in hydrocarbons, oil, chlorinated solvents, and most common organic solvents. [45] Water solubility of 2,700 mg/liter [89] SPECTRAL PROPERTIES Index of refraction: 1.3700 at 20 degrees C/d [122] IR: 10973 (Sadtler Research Laboratories IR Grating Collection) [121] MASS: 42 (Atlas of Mass Spectral Data, John Wiley and Sons, New York) [121] SURFACE TENSION 23.1 dyn/cm at -20 degrees C [10] VAPOR DENSITY 2.15 [90] VAPOR PRESSURE 2660 mm Hg at 25 degrees C [59] VISCOSITY Viscosity, gas at 101.325 kPa at 20 degrees C is 0.01072 cP; viscosity, liquid at -20 degrees C is 0.280 cP [10] FLASH POINT -78 degrees C (open cup) [23] AUTOIGNITION TEMPERATURE 882 degrees F [90] OTHER CHEMICAL AND PHYSICAL PROPERTIES Undergoes rapid photochemical oxidation. [41] 1 mg/cubic meter= 0.39 ppm; 1 ppm= 2.60 mg/cubic meter [115] HEALTH AND ENVIRONMENT INTERNATIONAL, LTD BOR 006699 Page 8 CORROSIVITY Vinyl chloride is not corrosive when dry but in presence of moisture it corrodes iron and steel. [72] HAZARDOUS REACTIONS REACTIVITIES RED INCOMPATIBILITIES Can react vigorously with oxidizing materials. [90] It loses hydrogen chloride (HC1) on treatment with strong alkalis at high temperatures. [59] DECOMPOSITION Very dangerous; when heated to decomposition, it emits highly toxic fumes of phosgene [90] Vinyl chloride is decomposed into gaseous hydrochloric acid, carbon monoxide, and carbon dioxide. [61] POLYMERIZATION Polymerization occurs if heated in sunlight or presence of air; reaction is exothermic. [37] Polymerized in presence of catalyst [123] Prolonged exposure of cylinders or tank cars to heat or fire may cause the material to polymerize with possible container rupture. [6] Tends to self-polymerize explosively if peroxidation occurs, and several industrial explosions have been recorded. [11] May polymerize violently under fire condition or loss or removal of inhibitor. [61] HEALTH AND ENVIRONMENT INTERNATIONAL, LTD BOR 006700 Page 9 PHARMACOKINETICS ABSORPTION/ DISTRIBUTION AND EXCRETION Following exposure of male rats by inhalation to 10 ppm (14)C vinyl chloride for 6 hours, urinary (14)C activity and expired vinyl chloride comprised 68 and 2 percent, respectively, of the recovered radioactivity; after exposure to 1,000 ppm (14)c vinyl chloride, the proportion of radioactivity in the urine was lower and that expired as vinyl chloride higher, representing 56 and 12 percent, respectively [59] Male Sprague-Dawley rats were given single oral doBes (gavage) of (14)C vinyl chloride at 0.05, 1.0 or 100 mg/kg; routes and rates of eliminaton of (14)C activity were followed for 72 hours. Of the samples examined (liver, skin, plasma, muscle, lung, fat, and carcass), liver retained the greatest percentage of administered radioactivity at all doses. [118] Experiments with volunteers showed that 42 percent of an inhaled dose of vinyl chloride was retained in the lung. This value was independent of the concentration of vinyl chloride in the air. Elimination of vinyl chloride through the lung was negligible since its concentration in expired air decreased immediately after cessation of exposure. [68] Oral doses of 0.05-1.0 mg/kg were given rats. Pulmonary excretion was monophasic at these doses, and urinary metabolites were N-acetyl-S-(2hydroxyethyl)cysteine and thiodiglycolic acid. At 100 mg/kg, pulmonary excretion was biphasic and a greater percentage was expired as vinyl chloride--67 percent, compared with 1 or 2 percent at the lower dose. [83] The metabolic elimination of vinyl chloride in Rhesus monkeys following inhalation exposure is a dose-dependent, saturable process. Below 200300 ppm elimination is first-order. [13] It is easily absorbed by the human organism through the respiratory system from where it passes into the blood circuit and from there to the various organs and tissues. It is also absorbed through the digestive system as a contaminant of food and beverages, and through the skin. [61] Gastrointestinal absorption of vinyl chloride in rats occurs rapidly following ingestion of aqueous or vegetable oil treatment solutions. Quantitatively, absorption of 98.7 percent from the gut occurred at an oral dose of 450 mg/kg. [124] METABOLISM AND METABOLITES After inhalation of (14)C-vinyl chloride by rats, three urinary metabolites have been detected: n-acetyl-S-(2-hydroxyethyl)cysteine, thiodiglycolic acid, and an unidentified substance. [83] N-acetyl-S-(2-chloroethyl)cysteine or N-acetyl-S-(2-hydroxyethyl)cysteine may be isolated from rat body fluids depending on the method of protective esterification used. [46] BOR 006701 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 10  Rats were subjected to an airborne concentration of (14)C-vinyl chloride ranging from 200-1,200 ppm in a closed system, the rate of decrease of vinyl chloride levels in the chamber atmosphere was measured. Saturation of the vinyl chloride-metabolizing enzymes of the rat was achieved at 250 ppm. [9] Data indicate a dose-dependent fate of vinyl chloride after inhalation or oral administration in rats. The primary mechanism of detoxification of vinyl chloride or its reactive metabolites involves conjugation with hepatic glutathione. Glutathione conjugates subject to hydrolysis yielding cysteine conjugates. [83] The principal center of the metabolic process is the liver, where the monomer undergoes a number of oxidative processes, being catalyzed partly by alcohol dehydrogenase, and partly by a catalase. [61] Data suggest that the alcohol dehydrogenase pathway is the major route of metabolism below 50 ppm, while the microsomal oxidase pathway is the major route at higher concentrations. [47] A strong correlation was found between vinyl chloride (VC) concentration at working places and the increased excretion of thiodiglycolic acid of 18 exposed workers. The values obtained were in the range of 0.14-7.00 ppm. The excretion of thiodigylcolic acid, measured by GC-HS analysis, amounted to 0.3-4.0 mg/liter. [80] BIOLOGICAL HALF-LIFE The pattern of pulmonary elimination of 10 and 1,000 ppm vinyl chloride was described by apparently similar first-order kinetics, with half-lives of 20.4 and 22.4 minutes respectively. The half lives for the initial phase of excretion of (14)C radioactivity in urine were 4.6 and 4.1 hours, respectively. [59] MECHANISM OF ACTION Precarcinogen vinyl chloride converted to alkylating intermediate responsible for introduction of 2-oxyethyl group onto nucleophilic sites in DNA and proteins of mice. [44] INTERACTIONS Sprague-Dawley male rats received either 5 percent ethanol in drinking water or drinking water only for 4 weeks prior to beginning inhalation of 600 ppm vinyl chloride for 4 hours/day on 5 days/week for 12 months. After 60 weeks from the first vinyl chloride exposure, liver tumors were found in 75 percent of the vinyl chloride-ethanol rats and in 38 percent of the vinyl chloride-only group (Radlike et al, 1977). [59] Vinyl chloride exerts a protective effect on hepatotoxicity when administered with vinylidene chloride. [62] The metabolism of vinyl chloride was inhibited by administering a single dose of 320 mg/kg pyrazole one hour prior to inhalation of vinyl chloride gas. [48] BOR 006702 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 11  Vinyl chloride and ethylene are acutely hepatotoxic in rats pretreated with polychlorinated biphenyl. Trichloropropane oxide significantly increases vinyl chloride toxicity in fasted but not in fed rats. Diethylmaleate significantly lowered hepatic glutathione during exposure, but did not increase hepatotoxicity of either vinyl chloride or ethylene. In polychlorinated biphenyl-treated rats, hepatic glutathione and hepatic epoxide hydrase influence the acute hepatotoxicity of vinyl chloride. [24] Combining 1 mg/cubic meter vinyl chloride with 1 mg phenol/cubic meter antagonized the effects on the nervous system of rats in a 7-month continuous inhalation study. The mixture did not affect the learning ability which wbb impaired by 1 mg/cubic meter of either compound separately. Vinyl chloride alone extended the blood clotting time. [21] HEALTH AND ENVIRONMENT INTERNATIONAL, LTD BR 006703 Page 12 TOXICOLOGY TOXIC HAZARD RATING IAPC Classification of carcinogenicity: 1) evidence in humans: sufficient; 2) evidence in animals: sufficient; Overall summary evaluation of carcinogenic risk to humanB is group 1: The chemical is carcinogenic to humans. [58] HUMAN TOXICITY EXCERPTS Vinyl chloride does not exert clearly perceptible acute effects below 1,000 ppm. At that dose humans exhibit slight anesthesia, drowsiness, slight visual disturbances, faltering gait, numbness, and tingling of extremities. [72] There was significant increase in chromosomal abnormalities in cultured peripheral lymphocytes from 57 male workers when compared with controls. Greatest statistical increases occurred in autoclave operators. [87] The health status of 13 workers employed for 1.75-18 years in a polyvinyl chloride factory was studied. Eight of them had scleroderma-like skin changes characterized histologically by thickening and rarefraction of the elastic fibers. In seven patients, thickening of terminal finger phalanges resembling clubbing was noted; 11 patients had circulatory disturbances of the extremities (four had Raynaud's syndrome) and six patients had band-like osteolyses of terminal finger phalanges. Thrombocytopenia was observed in all patients, splenomegaly in 12 patients, and malfunction of the liver in 11 patients. Long term exposure to vapors may cause occupational acroosteolysis. [71] An unusual distribution in the cell type of brain cancer was noted in vinyl chloride exposed workers, of 10 brain cancer deaths identified, nine had a histologic diagnosis of glioblastoma multiforme. The other case did not have histological confirmation. [119] A population of 10,173 men employed in 37 plants, were identified as having worked for at least one year in jobs involving probable exposure to vinyl chloride monomer (VCM). Of the 9,677 men whose vital status was determined, 707 were known to have died. For 699, death certificates were obtained. The only type of malignancy found in significant excess was malignant neoplasms of the brain and other parts of the nervous system. There were slight but inconclusive upward trends for malignancies of the respiratory tract, digestive tract, and central nervous system associated with reported levels of maximum exposure to vinyl chloride. [25] Hepatic angiosarcoma in man was first associated with exposure to vinyl chloride in Louisville, Kentucky, where it was identified in 10 persons from a single vinyl chloride polymerization plant. Clinical manifestations were nonspecific hepatic injury with mildly abnormal liver test results. Carcinoembryonic antigen and alpha-fetoprotein were undetectable. A definite diagnosis was made only by open liver biopsy. Average survival from diagnosis is about 12 months. Overt liver failure usually occurs only as a preterminal event and was the major cause of death. [28] BOR 006704 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 13  The livers from five vinyl chloride workers showed angioformative and hepatocellular growth disturbance in varying proportions: angiosarcoma in four cases, liver cell hyperplasia in all cases, hyperplastic nodules in three cases, and hepatocellular carcinoma in two cases- [39] The results of angiography of the hand in workers in the vinyl chloride industry were described. Among 93 patients, there were 19 on whom angiograms of the hand were performed because of Raynaud-like changes, pain, or other pathological findings. All patients examined by angiography showed abnormalities of the vessels in the hands and fingers of varying severity. Vascular occlusions (17 patients), stenoses (9 patients), and thread-like narrowing of the digital arteries (6 patients) with the development of a collateral circulation were prominent findings There was elongation and tortuosity of the digital arteries (14 patients) which were regarded as crisoid aneurysms. [67] Of a group of 155 males and 45 females employed for 1 to 25 years (mean 14 years) in a facility producing vinyl chloride, 58 (29 percent) were free of complaints and nervous disturbances. An astheno-autonomic syndrome was found in 54 (27 percent) and in 88 (44 percent) in combination with positive neurological findings, i.e. pyramidal syndrome in 52, cerebellar disturbances in 38, trigeminal neuropathy in 24, and extrapyramidal symptoms in 3, pyramidal + cerebellar in 12, trigeminal + pyramidal in 7, trigeminal + cerebellar in 5. Headaches (48 percent), nervousness (26 percent), Decrease in physical strength (16 percent), loss of memory (14 percent), sleeping disturbances and somnolence were the most frequent complaints. Scleroderma-like skin changes were found in 10 subjects, but only six of them had any neurological disturbances. Frequency of the arterial hypertension were the same in both groups, whereas acroparesthesias, Raynaud's syndrome, and increased gamma guanidine triphosphate serum activity were significantly more frequent in workers with neurological disturbances. 62 percent of the neurologically positive group and only 24 percent of the negative group reported euphoric or narcotic states after exposure. This probably indicates episodic exposures to high concentrations of vinyl chloride. This difference points to a possibility that neurological disturbances may be related to short exposures to peak concentrations. The neurological injury may be both a direct neurotoxic effect of vinyl chloride and secondary to vascular disorders. [70] The nervous system and bioelectric functioning of the brain (EEG) were evaluated in 114 workers aged 20-62, employed in significant exposed to vinyl chloride for 1-28 years on average 7.5 + or - 4.0 years. Clinical symptoms of the nervous system occurred in the form of peripheralvegetative syndrome with accompanying vasomotor disturbances of Raynaud syndrome type. EEG yielded 39 (34.2 percent) correct and 75 (65.8 percent) incorrect records. Among incorrect records most frequent (32.5 percent) were low-voltage and flat records; those with fast spindled activity and frequent changes typical for reduced wakefulness. The nature of clinical symptoms and EEG disturbances may point to the contribution of the hypothalmus in the pathomechanism of changes in those chronically exposed to vinyl chloride. [93] The mortality in a cohort of 451 workers exposed to vinyl chloride monomer (VCM) for more than 5 years was compared with that of 870 workers from the same company not exposed to vinyl chloride. The relative risk for digestive cancer was significantly higher than 1 (6.25, confidence interval 2.69-14.52) in the exposed group. The standardized mortality ratio (SMR) for digestive cancer was also higher (standardized mortality HEALTH AND ENVIRONMENT INTERNATIONAL, LTD Page 14 BQR 006705 ratio 259.26 p < 0.01) than that of the general population. No other cancer was in excess. Since the exposed workers are known to have had a cigarette Bmoking experience similar to that of those who were not exposed, it is concluded that the association between lung cancer and VCM exposure is rather small. [97] The incidence of birth defects in infants born to residents of Shawinigan, Canada, in 1966-1979 were significantly higher than in three comparison communities. Since there has been a vinyl chloride polymerization plant in this town, since 1943 from which ten cases of liver angiosarcoma have been identified, this study explored the possible association between exposure to vinyl chloride monomer in ambient air and the occurrence of birth defects in the community. The excess of birth defects fluctuated seasonally in a way that corresponded to changes in vinyl chloride monomer (VCM) concentrations in the environment. There was no excess of still births in Shawinigan. The excess in birth defects involved most organ systems, and variation in birth-defect rates among school districts could not be accounted for by estimates of VCM in the atmosphere. The occupational and residential histories of parents who gave birth to malformed infants were compared with those of normal infants. The two groups did not differ in occupational exposure or closeness to the vinyl chloride polymerization plant. [96] Results of massive and apparently repeated exposures greater than 10,00020,000 ppm volume/volume: euphoria followed by state of inebriation similar to that of alcohol intoxication, epigastric pain, anorexia, allergic dermatitis, and scleroderma [2] An excess of central nervous system defects, deformities of the upper alimentary and genital tracts, and clubfoot were observed in stillborn and live children in three Ohio cities in which vinyl chloride polymerization plants are located. [59] A mortality study of 8,384 men with at least 1 year exposure before Dec 31, 1972, demonstrated that cancers of digestive system (primarily angiosarcoma), respiratory system, brain, and cancers of unknown site, as well as lymphomas occurred more often than expected in the study population with greatest estimated exposure. [2] Skin Changes: In a small number of cases, the angioneurotic disorders may be associated with scleroderma on the back of the hand at the metacarpal and phalangeal joints and on the inside of the forearms. [61] Pathologic porphyrinuria, especially secondary coproporphyrinuria with transition to subclinical chronic hepatic porphyria, is a consistent pathobiochemical parameter for the recognition of vinyl chloride hepatic lesions. Erythrocyte uroporphyrinogen decarboxylase activity studied in six eases with initial chronic hepatic porphyria was normal, suggesting that vinyl chloride affects this enzyme only in the liver. [31] Nine retrospective mortality studies of workers exposed to vinyl chloride were reviewed to determine whether differences in their hypothesis testing results might be due to differences in statistical power. Where possible, the power of each study was calculated for cancer of the lung, brain and liver. When power was taken into consideration, the results for liver and brain cancer were consistent with an etiologic role for vinyl chloride. For lung cancer, the data were not consistent with an etiologic role, in that two studies with very high power yielded negative results. [7] A case of angiosarcoma of the penis associated with two hepatic angiomata in a 61-year old man is presented. The patient had worked in a polyvinyl chloride factory as an accountant for 10 years. The relationship of this HEALTH AND ENVIRONMENT INTERNATIONAL, LTD Page i BOR 006706 low vinyl chloride exposure to the development of the vascular lesions is discussed with a review of the experimental and epidemiologic data on this subject. [42] This study briefly reviews suspected causes of malignant melanoma. Industrial chemicals that have been suggested include arsenic, polychlorinated biphenyls, alcohol and alpha-chloroacetophenone. Recent studies of an increased incidence at plants producing polyvinyl chloride and asbestos products are reported. The question of the mechanism of action is discussed: inhaled vinyl chloride monomer migrates to the subcutaneous layers of the skin after a short time. Transcutaneous penetration of asbestos fibers is a possibility. [52] The carcinogenicity of vinyl chloride (VC) and polyvinyl chloride is reviewed with specific attention to the gaps in knowledge for risk estimation and epidemiological presentation of the available data. Although experimental studies have demonstrated the carcinogenicity and mutagenicity of vinyl chloride/polyvinyl chloride in general, the epidemiologic studies available for review do not include an assessment of carcinogenic risk among humans exposed to these chemicals. This conclusion is based on the observation that the majority of cohort studies reviewed, lacked sufficient statistical power because of small sample sizes. Further, in epidemiological studies, individuals were not followed over an adequate period of time during which cancer could become clinically manifest. [63] Epidemiological evidence of an occupational risk of brain cancer has been reported in four industries where chemical exposures are likely, most recently in a series of prospective studies in the petrochemical industry. However, only in the case of vinyl chloride exposure has an occupational central nervous system carcinogen been identified. This report reviews the convergence of epidemiological and laboratory evidence that established the occupational carcinogenicity of vinyl chloride, and discusses in detail the current evidence for an occupational risk of brain tumors in the petrochemical industry. [79] There are three mechanisms by which exposure of the male to toxic substances may cause poor reproductive performance or congenital malformations in his offspring; a direct effect on pituitary- hypothalamic function or male sex hormones; a direct effect on the sperm itself; abnormalities in seminal fluid with secondary abnormalities due to dissolved toxins. Experimental studies with seven drugs and five groups of toxic chemicals are reviewed. Clinical studies reviewed relate to lead, vinyl chloride, the insecticide carbaryl, the pesticides chlordecone and dibromochloropropane, radiation, fathers with epilepsy, and male and female anesthesiologists. [86] Occupational influences on male fertility and sexuality are reviewed. The potential risks of physical factors (trauma, temperature, radiation, microwaves), of chemical factors (metalB, mineral oils, hormones (oral contraceptives and estrogen) pesticides and herbicides, neurotoxins, vinyl chloride and analogs, carbon disulfide, of physiopathological factors (infectious diseases occupationally acquired, low-back syndrome) and of psychological factors (stress, alcoholism) are discussed. The methodological aspects in monitoring the fertility and sexuality of male workers are considered. Physicians practicing occupational medicine are cautioned to be aware of these potential risks regarding gonadal function. Occupational hygienic measures are the first step in preventing environmental pollution hazards. [95] BOR 006707 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD Page 16  In 1974, vinyl chloride (VC) was first reported in the open scientific literature to induce angiosarcoma of the liver both in humans and in animals. Additional research has now demonstrated the carcinogenicity of VC to other organs and at lower concentrations. The target organs for vc now clearly include the liver, brain and the lung, and probably the lymphohematopoietic system. The evidence for a carcinogenic risk has been extended to jobs associated with poly (vinyl chloride) exposure. Cases of liver angiosarcoma have been reported among individuals employed in polyvinyl chloride (PVC) fabrication facilities and an epidemiological study has demonstrated a significant association between exposure to PVC dust and the risk of lung cancer mortality. Cases of angiosarcoma of the liver also have been reported among individuals living in near proximity to vinyl chloride-polyvinyl chloride plants. An association between PVC dust and pneumoconiosis also has been demonstrated. On the basiB of findings, prudent control of PVC dust in the industrial setting is indicated. [116] A standardized mortality ratio of 1.49 for respiratory system cancer (42 observed deaths versus 28.2 expected, p < 0.01) was observed among a cohort of 4,806 males employed at a synthetic chemicals plant since its startup in 1942. Upon review of pathologic material, the excess was found to be limited to adenocarcinoma and large cell undifferentiated lung cancer. Many of the workers had been exposed to vinyl chloride, as well as to chlorinated solvents, polyvinyl chloride (PVC) dust, acrylates and acrylonitrile. To evaluate the association between lung cancer and occupational chemical exposures, detailed work histories for each cohort member were combined with exposure ratings for each of 19 chemicals for each job for each calendar year since 1942. A serially additive expected dose model was then constructed which compared the doses of the chemicals observed for the lung cancer cases to the doses expected based on subcohorts without lung cancer individually matched to the cases. PVC dust appeared to be the most likely etiologic agent (p* 0.037). Time trends of PVC dust exposure indicated a potential latent period of 5-16 years before death. [120] A method generally used for chromosomal analysis is presented, and the main morphological abnormalities that may appear spontaneously are summarized. In a survey of 109 persons not exposed to chemicals, abnormalities, mainly of the "gap" or "break" type, were present in 76.1 percent of the cases. A brief review of the literature, giving results of studies of workers exposed to benzene, vinyl chloride monomer, and some metals, showed that these substances induce increased chromosome changes. [94] If spilled on skin rapid evaporation can cause local frostbite. [123] A retrospective mortality study of 454 male workers exposed to chloroethene during its production and polymerization to polyvinyl chloride was conducted. The cohort consisted of men working for at least one year during 1950-1969 and the group was followed during 1953-1979. A total of 23 cancer deaths were observed (20.2 expected) with 1 case of liver angiosarcoma, 5 lung cancers (2.8 expected), 3 colon cancers (1.4 expected), 2 thyroid cancers (0.16 expected) and 4 malignant melanomas of the skin (0.8 expected) "The increased incidence of cancer is accounted for almost entirely by the high exposure group." The high level of malignant melanoma among this group of workers is unique and warrants further attention. [50] BOR 006708 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 17  In view of extreme rarity of angiosarcoma of liver in the general population, observation of 16 caseB in workers exposed to vinyl chloride monomer during polymerization process is evidence of causal relationship. [57] Vinyl chloride is an asphyxiant at high concentrations. [35] It appears that metabolism of vinyl chloride is necessary before many of its toxic effects occur. [23] The Carcinogen Assessment Group (CAG), Office of Health and Environmental Assessment in EPA'S Research and Development Office, has prepared a list of chemical substances for which substantial or strong evidence exists showing that exposure to these chemicals, under certain conditions, causes cancer in humans, or can cause cancer in animal species which in turn, makes them potentially carcinogenic in humans. Substances are placed on the CAG list only if they have been demonstrated to induce malignant tumors in one or more animal species or to induce benign tumors that are generally recognized as early stages of malignancies, and/or if positive epidemiologic studies indicated they were carcinogenic. Vinyl chloride is on that list. [106] Russian studies examined sexual function and hormone levels in men and sexual function and gynecological health in women occupationally exposed to vinyl chloride and in unexposed control groups. An exposure and duration related decline in sexual function was reported in exposed men and women. Ovarian dysfunction, benign uterine growths, and prolapsed genital organs were reported in 77 percent of exposed women. [75] Vinyl chloride causes hepatic damage by interfering with essential metabolic pathways, which leads to cytotoxic (necrosis or steatosis) and/or cholestatic (biliary stasis) injury patterns. [33] To date, 48 cases of hepatic angiosarcoma have been diagnosed in industrial workers around world. All authenticated cases were found in workers engaged in cloBed-in plantB handling very large quantities of liquefied vinyl chloride under pressure. Exposure concentrations were high, probably ranging from 1,000 ppm to several thousand ppm. [83] In 48 workers exposed to 140-1,200 mg/cubic meter vinyl chloride monomer (VCM) during production of polyvinyl chloride in a Russian factory, some workers were reported to have had signs of irritation of respiratory tract and hepatitis. Twenty-three workers were found to have an increased hemoglobin level. [57] Investigators studied 168 workers involved in the polymerization of vinyl chloride monomer, in whom they reported narcotic symptoms, asthenic nervous symptoms, Raynaud's syndrome and liver enlargement. Incidence of Raynaud's syndrome was 6 percent and that of liver enlargement 30 percent. [57] HUMAN REPRODUCTION AND DEVELOPMENT EXCERPT8 Vinyl chloride (chloroethylene) is widely used in the plastics industry to synthesize polyvinyl chloride monopolymer and other copolymer plastics [143]. In the past, it has been used as an anesthetic gas, an aerosol propellant, and a refrigerant. These uses have been abandoned because vinyl chloride is now considered to be a carcinogen in humans and in animals [144] and there is concern that it may produce genetic damage in reproductive tissue. Dominant lethal effects are not seen in rodents [145,146], however, suggesting that vinyl chloride does n*t induce measureable genetic damage in gametes. BOR 006709 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. r-age la  Vinyl chloride was not teratogenic when tested in rats, mice, or rabbits [147-149]. In humans, there have been epidemiologic reports associating vinyl chloride exposure of parents with an increased incidence of adverse pregnancy outcome. For example, one study [150] found pregnancy wastage to occur at a higher rate in the wives of 95 male vinyl chloride workers after employment compared to before employment. Pregnancy wastage also occurred with greater frequency in the wives of male vinyl chloride workers compared to the wives of men working with polyvinyl chloride or in the rubber industry. This study has been criticized for inadequacies in controlling confounding variables and for the low rate of responses of the eligible subjects [151,152]. These limitations leave this report as a suggestive, but inconclusive, comment on the possibility that vinyl chloride is a male-mediated developmental toxicant. Studies on community rateB of birth defects have found an association between the presence of vinyl chloride industries and congenital anomalies, especially those involving the central nervous system [153-155]. These reports do not, however, establish a relationship between the vinyl chloride in the community and the defects since a number of other community and personal factors (including the presence of other industries and pollutants) are not controlled. These studies are not, therefore, considered to be adequate evidence of vinyl chloride activity as a human teratogen [156]. In addition, evaluation of the parents of affected children in community studies has not shown a relationship between parental occupation in vinyl chloride industries and birth defects in the offspring [155,157] or between proximity of the home to a vinyl chloride factory and birth defects in the offspring [157]. This supports the contention that high rates of birth defects in some communities are related to factors other than exposure to vinyl chloride. HUMAN ENVIRONMENTAL EXPOSURE POPULATIONS AX SPECIAL RISK Older individuals, females, newborns, and alcohol consumers may be particularly sensitive to the effects of vinyl chloride. [105] Those individuals with liver, renal, cardiac, or pulmonary impairments. [61] PROBABLE ROUTES OP BUSAN EXPOSURE Inhalation is the major route of exposure for nearby residents and workers(1). Exposure is also possible by ingestion of contaminated foods, drinking water and absorption through skin from cosmetics(l). [108] PROBABLE EXPOSURES Potential risk groups include workers in vinyl chloride (VC) production or use facilities and nearby residents, people coming in contact with recently manufactured polyvinyl chloride (PVC) in enclosed quarters (e.g., new cars), consumers of food products packaged in PVC and drinking water from PVC pipes(l). The total worldwide work force in VC HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 19 O H r* vo o o g oa and PVC industries exceeds 70,000(1). NIOSH (NOES Survey 1981-1983) has statistically estimated that 18,368 workers are exposed to vinyl chloride in the USA(2). NIOSH (NOHS Survey 1972-1974) has statistically estimated that 239,375 workers are exposed to vinyl chloride in th USA(3). The NOES survey has not been completed (data as of 5/10/88 included) in that exposure to vinyl chloride in trade name products will still to be included. The large difference between the estimates in the NOES and NOHS surveys probably reflects a reduction in exposure to VC rather than the fact that the trade name exposure data from the NOES survey has not been completely processed. Average exposure of a random person living within a 5-mile radius of a plant is 17 ppb(4). The estimated number of persons at risk is 4.6 million(4). (130] BODY BORDENS A strong correlation was found between vinyl chloride (VC) concentration at working places and the increased excretion of thiodiglycolic acid of 18 exposed workers. The value obtained were in the range of 0.14-7.00 ppm. The excretion of thiodigylcolic acid, measured by GC-MS analysis, amounted to 0.3-4.0 mg/liter. [80] ANIMAL TOXICITY EXCERPTS Twenty-six male AH/IRE Wistar rats were exposed to 3-percent volume/volume commercial-grade vinyl chloride monomer (99 percent pure) 4 hours/day on 5 days/week for 12 months. Skin tumors developed in submaxillary parotid region;(14 epidermoid carcinomas, 2 mucoepidermoid carcinomas, 1 papilloma);lung tumors developed in seven rats and osteochondromas in five; no tumors in 25 untreated controls. Skin tumors were zymbal gland tumors and lung tumors were metastasis from these. (Viola et al, 1971). [59] Groups of male and female 11 week-old Swiss mice were exposed to concentrations of 50 to 10,000 ppm vinyl chloride in air for 4 hours/day on 5 days/week for 30 weeks. At 81 weeks, 70 percent (of the 10,000 ppm group) had adenomas and/or adenocarcinomas of the lung, 47 percent had mammary adenocarcinomas and 16 percent had angiosarcomas of the liver. In 80 male and 70 female untreated controls, 8 pulmonary tumors and 3 lymphomas were observed (Maltoni, 1977; Maltoni et al, 1974). [59] Vinyl chloride was administered for 7 hours/day on days 6-18 of gestation in mice, rats, and rabbits. It was concluded that although maternal toxicity was observed, vinyl chloride alone did not cause significant embryonal or fetal toxicity and was not teratogenic in any of the species at the concentration tested. [83] Exposure of Salmonella typhimurium strains TA1530, TA1535, and G-46 increased number of HIS+ revertants/plate 16, 12 or 5 times over spontaneous mutation rate. Mutagenic response for the TA1530 strain increased when S-9 liver fractions from humans, rats, or mice were added. [83] Acute effects: Inhalation of vinyl chloride has been shown to produce lung congestion and some hemorrhaging, blood-clotting difficulties, and congestion of liver and kidneys in lab animals. [83] Acute effects: After two hours at 5-percent vinyl chloride, rats showed moderate intoxication; two hours at 15-percent provoked respiratory failure. [1 83]1 BOR 006711 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 20  Degeneration of bone and connective tiBSue occurred in male Wistar rats exposed to concentrations of 30,000 ppm 4 hours/day on 5 days/week for up to 12 months* Degenerative changes were observed in liver (interstitial hepatitis, necrosis, proliferation of Kupfer cells and fibrosis), kidney (tubular nephrosis and interstitial nephritis), brain (neuronal and glial cell degeneration). [57] Continuous exposure of CFY rats to vinyl chloride (4,000 mg/cubic meter in air) during pregnancy caused increases in fetal deaths and embryotoxic effects. [99] Dominant lethal studies of male CD-I mice that had been exposed to 3,000, 10,000, and 30,000 ppm for 5 days showed no mutagenic effect. [4] Sprague-Dawley rats were exposed to 10,000 ppm vinyl chloride in air for 4 hours/day on 5 days/week for 5 weeks, starting at the age of 13 weeks (120 rats per group) or 1 day (43 and 46 rats), animals were observed for 135 weeks. One hepatoma was reported in the older rats in newborn rats, 10 angiosarcomas and 15 hepatomas were found. No liver tumors were reported in 249 controls (Maltoni, 1977b). [59] Forty rabbits were exposed for 4 hours/day on 5 days/week for 12 months to air containing (10,000 ppm) vinyl chloride. Between 9 and 15 months exposure, 12 skin acanthomas and 6 lung adenocarcinomas were seen. No similar tumors occurred in 20 controls after 15 months observation (Caputo et al, 1974). [59] The embryotoxic and teratogenic action of vinyl chloride on 40 pregnant white Wistar rats was examined. The experiments were carried out under the conditions of daily inhalatory poisoning during gestation at mean daily concentration of 6.15 mg/cubic meter. There was a manifestated embryotoxic and teratogenic effect of elevated total embryonal mortality, lowered fetal weights and induction of external and internal anomalies in the development of the fetus. The threshold value of concentration for embryotoxicity and teratogenicity was calculated to be 10 mg/cubic meter. [78] Rats and mice were exposed in an inhalation chamber to single 1-hour concentration of vinyl chloride ranging from 50-50,000 ppm. A second group was given 10 1-hour exposures to 500 ppm or 100 1-hour exposures to 50 ppm of the same chemical. All animals were then observed for the remainder of their lives, generally 18-24 months. Moribound animals were euthanized, and survivors were sacrificed on schedule and their tissues examined for pathological changes. Specifically, the oncogenic study demonstrated dose-related effects for single 1-hour exposure of vinyl chloride monomer (VCM), at high levels, i.e. 5,000 and 50,000 ppm. The concentration increased the incidence of pulmonary adenomas and carcinomas in mice. Repeated exposure of A/J mice at 500 ppm x 10 1-hour exposures also increased the incidence of pulmonary adenomas and carcinomas. Rats exposed to identical concentrations of VCM failed to elicit a tumorigenic response. [49] Wistar rats were exposed to atmospheres containing 0 (control) or 5,000 ppm vinyl chloride monomer, 7 hours/day, 5 days/week, for 52 weeks. 10 rats/sex per group were killed. Growth, mortality, hematology, clinical chemistry, and organ weights were studied. Slight growth retardation throughout the experimental period and high mortality in the second half of the study were observed in vinyl chloride monomer exposed animals. Blood clotting time was shorter in vinyl chloride monomer exposed rats than controls. There were minor increases in potassium content in the blood serum in vinyl chloride monomer exposed animals during the first w half of the test period. Increased blood urea nitrogen levels and J o HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 21 (oA (Q relative kidney weights were evidence that the kidneys were adversely affected by vinyl chloride monomer. After 52 weeks increased weights of heart and spleen, and slight signs of an anemia were noted in vinyl chloride monomer-exposed rats. [40] Rats exposed to vinyl chloride (in air at 2,500 ppm, 4-7 hours/day, 5 days/week) from day 12 of embryonic life for 57 weeks had a 63.1 percent incidence of liver angiosarcoma with a latency period of 49.9 weeks and a 41.4 percent incidence of lung metastasis. The experimental tumors were similar to those of humans with respect to gross pathology, histopathology, and metastatic behavior. [76] The mutagenicity of vinyl chloride was tested in V79 Chinese hamster cells in the presence of a 15,000 grams supernatant from phenobarbitone pretreated rats and mice. Mutations of 8-azoguanine and ouabain resistance were induced in a dose related fashion by exposure to vapor of vinyl chloride in the presence of liver supernatant from phenobarbital-pretreated rats. [32] Zymbal gland carcinomas, nephroblastomas, and angiosarcomas of liver and of other locations were induced in rats following 52 weeks of exposure for 20 hours each week; concentrations; 10,000 ppm 6000 ppm 2500 ppm 500 ppm 50 ppm, with angiosarcomas in 7, 13, 14, 7, 4, and 1 rats, respectively (air controls were negative). [92] Repeated exposures for 7 hours/day, 5 days/week, at 500 ppm, rats increased liver weight and histopathology. At 200 and 100 ppm, rats increased liver weight, but no changes were observed in dogs or guinea pigs. All species tolerated 50 ppm for 6 months. [23] DNA synthesis was depressed in rat liver in vivo by vinyl chloride and two of its presumed metabolites, chloroethylene oxide and chloroacetaldehyde. [59] A review of the data obtained from various studies on carcinogenicity of vinyl chloride (VC) in rodents, particularly on the effect of dose, age, duration of exposure and potential reversibility of lesions, revealed that vinyl chloride induced carcinogenicity in rodents was dose and time related; no recovery occurred in mice even after only 1 month of VC exposures or in rats after 6 month exposures. In addition, younger animals (2 months old) were more susceptible to VC induced carcinogenicity than animals held for 6 or 12 months prior to exposure. Initial 6 or 12 month exposures were adequate to detect the carcinogenic potential of VC. The above information was used as a basis for discussion on design of carcinogenicity studies. Possibility of determining the carcinogenic potential of a compound in a shorter period than the traditional 2-year studies in rodents was discussed in consideration with appropriate doses, species, age and exposure duration. Although this approach may be applicable to a strong carcinogen, it was not considered practicable in case of weak or unknown carcinogens. [8] The carcinogenicity of vinyl chloride for experimental animals when administered transplacentally is reviewed in comparison with known transplacental carcinogens, including those that, like vinyl chloride, are dependent on enzyme mediated metabolic conversion to a reactive intermediate in maternal or fetal tissues. Vinyl chloride is converted by mixed function oxidases to the reactive metabolite chlorooxirane, the carcinogenicity of which is also reviewed. Vinyl chloride is unequivocally a transplacental carcinogen for the rat. No evidence exists, however, to support the hypothesis that exposure of male rats to vinyl chloride or any other carcinogen confers an increased risk of HEALTH AND ENVIRONMENT INTERNATIONAL, LTD Page 22 BOR 006713 tumor development on their progeny. Many structural analogs of vinyl chloride, i.e., substituted ethylenes, are also carcinogenic for adult animals, and can with confidence likewise be predicted to be effective transplacental carcinogens. [88] Inhaled vinyl chloride (VC) was carcinogenic in rats. Four groups of 2month old CKL:CD rats of both sexes were exposed to filtered air (control), SO, 250, or 1,000 ppm VC for 6 hours/day, 5 days/week for 1, 3, 6, or 10 months. Animals were autopsied when moribund; all others were autopsied at 12 months. There were no differences in the survival rate of control, 1-, or 3-month exposure groups; however, the mortality incidence increased in the 6- and 10-month exposure groups in proportion to the VC concentration. Tumors were examined microscopically. The tumor incidence in the 1- and 3-month exposure groups did not differ from controls. The cumulative tumor incidence in rats exposed for 6- and 10months was: liver neoplasms (including neoplastic nodules, hepatocellular carcinoma, and hemangioBarcoma) 1 of 72 (controls), 0 of 66 (50 ppm VC), 17 of 68 (250 ppm VC), and 23 of 72 (1,000 ppm VC); lung tumors (bronchioloalveolar and hemangiosarcoma) 0 of 72 (controls), 0 of 66 (50 ppm VC), 4 of 68 (250 ppm VC), and 11 of 72 (1000 ppm VC); mammary gland tumors (females only; includes fibroadenoma, adenocarcinoma, and carcinoma) 6 of 36 (controls), 15 of 36 (50 ppm VC), 10 of 32 (250 ppm VC), and 5 of 36 (1000 ppm VC); malignant lymphoma 0 of 72 (controls), 0 of 66 (50 ppm VC), 1 of 68 (250 ppm VC), and 4 of 72 (1000 ppm VC). [53] Recent inhalation studies with albino CD-I mice and CD rats confirmed the carcinogenicity of vinyl chloride at concentrations as low as 50 ppm. Liver angiosarcomas as well as other forms of cancer were found in both species. [109] HUMAN STANDARDS AND RECOMMENDATIONS MEDICAL SURVEILLANCE Examination by wide field capillary microscopy of the hands of polyvinyl chloride workers demonstrated capillary abnormalities in a high percentage of exposed men. This non-invasive technique may be useful as a mass screening procedure in the early detection of vinyl chloride induced disease. [77] A preplacement examination should include an employment history, and a personal history; which should also contain information about alcohol and cigarette consumption, previous episodes of hepatitis, exposures to hepatotoxic agents, and hospitalizations. It is also advisable to carry out a number of laboratory examinations and tests: chest radiography, ECG, blood count, determination of SGOT and SGPT, total bilirubin, alkaline phosphatase, gamma-glutamyl transpeptidase, and urinalysis. Periodic medical examinations may be carried out every 12 months (or every 6 months for workers with particularly high exposure). [61] HEALTH AND ENVIRONMENT INTERNATIONAL, LTD BOR 006714 Page 23  PRECAUTIONS FOR "CARCINOGENS": In relation specifically to cancer hazards, there are at present no health monitoring methods that may ensure the early detection of preneoplastic lesions or lesions which may preclude them. Whenever medical surveillance is indicated, in particular when exposure to a carcinogen has occurred, ad hoc decisions should be taken concerning additional tests that might become useful or mandatory. (Chemical Carcinogens) [56] IMMEDIATELY DANGEROUS TO LITE OR HEALTH NIOSM has recommended that vinyl chloride be treated as a potential human carcinogen. [82] ACCEPTABLE DAILY INTAKES The ten-day health advisory for vinyl chloride for a 10 kg child that consumes one liter of water/day is 2.6 mg/day or 0.26 mg/kg/day. [107] OSHA STANDARDS Eight-hour Time-Weighted Average: 1 ppm. No employee may be exposed to concentrations greater than 5 ppm averaged over any period not exceeding 15 minutes. No employee may be exposed to vinyl chloride by direct contact with liquid vinyl chloride. [29 CFR 1910.1017 (7/1/88)] Meets criteria for OSHA medical records rule. [29 CFR 1910.20 (7/1/88)] EIOSB RECOMMENDATIONS Carcinogen; lowest reliably detectable concentration; liver function testing required. [85] ACGIH THRESHOLD LIMIT VALUES Time-Weighted Average (TWA) 5 ppm, 13 mg/cubic meter (1980) [3] Al. Al= Confirmed human carcinogen. (1980) [3] OTHER OCCUPATIONAL PERMISSIBLE LEVELS MAC, USSR: 30 mg/cubic meter [61] HEALTH AND ENVIRONMENT INTERNATIONAL, LTD Bor 006715 Page 24 ENVIRONMENTAL FATE AND EXPOSURE EXCERPTS ENVIRONMENTAL FATE AND EXPOSURE SUMMARY Although vinyl chloride is produced in large quantities, almost all of it is used captively for the production of polyvinyl chloride (PVC) and other polymers. Therefore, its major release to the environment will be as emissions and wastewater at these production and manufacturing facilities. If vinyl chloride is released to soil, it will be subject to rapid volatilization with reported half-lives of 0.2 and 0.5 days for evaporation from soil at 1 and 10 cm incorporation, respectively. Any vinyl chloride which does not evaporate will be expected to be highly to very highly mobile in soil and it may leach to the groundwater. It may be subject to biodegradation under anaerobic conditions such as exists in flooded soil and groundwater. If vinyl chloride is released to water, it will not be expected to hydrolyze, to bioconcentrate in aquatic organisms or to adsorb to sediments. It will be subject to rapid volatilization with an estimated half-life of 0.805 hours for evaporation from a river 1 m deep with a current of 3 m/sec and a wind velocity of 3 m/sec. In waters containing photoBensitizers such as humic acid, photodegradation will occur fairly rapidly. Limited existing data indicate that vinyl chloride is resistant to biodegradation in aerobic systems and therefore, it may not be subject to biodegradation in aerobic soils and natural waters. It will not be expected to hydrolyze in soils or natural waters under normal environmental conditions. If vinyl chloride is released to the atmosphere, it can be expected to exist mainly in the vapor-phase in the ambient atmosphere and to degrade rapidly in air by gas-phase reaction with photochemically produced hydroxyl radicals with an estimated half-life of 1.5 dayB. Products of reaction in the atmosphere include chloroacetaldehyde, hydrogen chloride, chloroethylene epoxide, formaldehyde, formyl chloride, formic acid, and carbon monoxide. In the presence of nitrogen oxides, e.g., photochemical smog situations, the half-life would be reduced to approximately a few hours. Since vinyl chloride is primarily used in limited number of locations, it is unlikely that contamination will be widespread. Major human exposure will be from inhalation of occupational atmospheres and from ingestion of contaminated food and drinking water which has come into contact with polyvinyl chloride packaging material or pipe which has not been treated adequately to remove residual monomer. [98] POLLUTION SOURCES MATURALLT OCCURRING SOURCES Vinyl chloride monomer is not known to occur in nature. [54] BOR 006716 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 25 ARTIFICIAL SOURCES Small quantities of chloroethene can be exposed to food by migration of chloroethene monomer present in polyvinyl chloride food wrapings and containers. [43] Air emission from vinyl chloride production and use as a feedstock in the plastics industry (principally for polyvinyl chloride production) and wastewater from these industries(l). Vinyl chloride is also a product of anaerobic degradation of chlorination solvents such as would be expected to occur in groundwater and landfills(3). Spills(2). [134] ENVIRONMENTAL FATE TERRESTRIAL FATE: If vinyl chloride is released to soil, it will be subject to rapid volatilization based on a reported vapor pressure of 2,600 mm Hg at 25 degrees C(l); half-lives of 0.2 and 0.S days were reported for volatilization from soil at 1 and 10 cm incorporation, respectively(2). Any vinyl chloride which does not evaporate will be expected to be highly mobile in soil and may leach to the groundwater. It may be subject to biodegradation under anaerobic conditions such as exists in flooded soil and groundwater; however, limited existing data indicate that vinyl chloride is resistant to biodegradation in aerobic systems and therefore, it may not be subject to biodegradation in natural waters. It will not be expected to hydrolyze in soils under normal environmental conditions(SRC). [139] AQUATIC FATE: If vinyl chloride is released to water, it will not be expected to hydrolyze, to bioconcentrate in aquatic organisms or to adsorb to sediments. It will be subject to rapid volatilization with an estimated half-life of 0.805 hours for evaporation from a river 1 meter deep with a current of 3 m/sec and a wind velocity of 3 m/sec(l). In waters containing photosensitizers such as humic acid, photodegradation will occur fairly rapidly. Limited existing data indicate that vinyl chloride is resistant to biodegradation in aerobic systems and therefore, it may not be subject to biodegradation in natural waters. [73] ATMOSPHERIC FATE: If vinyl chloride is released to the atmosphere, it can be expected to exist mainly in the vapor-phase in the ambient atmosphere (1) based on a reported vapor pressure of 2,660 mm Hg at 25 degrees C (2). Gas phase vinyl chloride is expected to degrade rapidly in air by reaction with photochemically produced hydroxyl radicals with an estimated half-life of 1.5 days (3). Products of reaction in the atmosphere include chloroacetaldehyde, HC1, chloroethylene epoxide, formaldehyde, formyl chloride, formic acid, and carbon monoxide (4). In the presence of nitrogen oxides, e.g., photochemical smog situations, the half-life would be reduced to a few hours. [129] AQUATIC FATE; The rate of bulk exchange of gaseous vinyl chloride between atmosphere and water is about twice that of oxygen. As a result the loss of vinyl chloride by volatilization from water is probably the most significant process in its distribution. There is little information pertaining specifically to the rate of adsorption onto particulate matter. In a study on the behavior vinyl chloride in water no significant difference in the rate of loss from distilled water, river water, or effluent from a vinyl chloride plant stirred at the same rate BOR 0 0 6 7 1 7 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD Page 26 was found, thus indicating negligible adsorption onto particulate matter. Aquatic Bediments could exhibit long-term storage of low levels if extreme environmental conditions, such as continual high levels of vinyl chloride input were present in water. [19] AQUATIC FATE: In environments such as municipal water chlorination facilities, high concentrations of chloride would exist. Under certain conditions, vinyl chloride may be converted to more highly chlorinated compounds based on the reactivity of carbon-carbon double bonds with chlorine and hypohalous acid. Dissolved vinyl chloride in water will readily escape into the gas phase, but chemical reactions can occur with water impurities which may inhibit its release. Many saltB have the ability to form complexes with vinyl chloride and can increase its solubility. Therefore, the amounts of vinyl chloride in water could be influenced significantly by the presence of salts. [19] ENVIRONMENTAL TRANSPORT BIOCONCENTATION Based on a reported water solubility of 2,700 mg/liter(l), a BCF of 7 was estimated (3). Based on the estimated BCF, vinyl chloride will not be expected to significantly bioconcentrate in aquatic organism. While not reporting actual bioconcentration factors, a lack of appreciable bioconcentration in extractable fractions of fish and aquatic invertebrates was reported in an ecosystem study (2). [140] Some data indicated that vinyl chloride is too readily volatilized to undergo bioaccumulation, except perhaps in the most extreme exposure conditions, studies on five bacterial, three fungal, and two single organism cultures from natural aquatic systems did not show bioaccumulation to be an appreciable process. [19] SOIL ADSORPTION AND SOIL MOBILITY Based on a reported water solubility of 2,700 ppm (1), a Koc of 56 was estimated (2). According to estimated Koc values, vinyl chloride will be expected to be highly mobile in soil (3) and therefore it may leach to the groundwater. [141] VOLATILIZATION FROM RATER AND SOIL Using a reported Henry's Law constant of 0.0560 atm/cubic meter-mole (4), a half-life of 0.805 hours was calculated for evaporation from a river 1 m deep with a current of 3 m/sec and with a wind velocity of 3 m/sec (1). Based on a high reported vapor preBBure of 2,660 mm Hg at 25 degrees C (3), volatilization from soil would be rapid; half-lives of 0.2 and 0.5 days were reported for volatilization from soil at 1 and 10 cm incorporation, respectively (2). [136] HEALTH AND ENVIRONMENT INTERNATIONAL, LTD BOR 006718 Page 27 ENVIRONMENTAL CONCENTRATIONS WATKR aCmCKHTRATIOIfS DRINKING WATER: In the National Organic Monitoring Survey (1976-7) two samples out of 113 contained detectable levels (greater than 0.1 ppb) and these averaged 0.14 ppb (1). The highest value found in USA drinking water is 10 ppb (5,7). Twenty-three percent of 133 USA cities using finished surface water were positive, 0.1 to 9.8 ppb, 0.4 ppb median of positive samples (2). A finished groundwater survey in 25 USA cities resulted in 4.0 percent positive, 9.4 ppb mean (2,6). One contaminated drinking water well contained 50 ppb (3). Drinking water from polyvinyl chloride (PVC) pipes contained 1.4 ppb in a recent installation, while a 9-year old system had 0.03 to 0.06 ppb (4). [128] DRINKING WATER: USA: National Screening Program, 1977-1981, 142 water supplies, 4.9 percent positive, trace to 76 ppb (1); state sampling data, 1,033 supplies sampled, 7.1 percent positive, trace to 380 ppb (1). [26] GROUNDWATER: 4 of 1,060 wells in New Jersey were positive (4) and vinyl chloride (VC) was present in the 10 most polluted wells from 408 New Jersey samples; however, it was not quantified (5). 15.4 percent of 13 US cities sampled were positive - 2.2 to 9.4 ppb, 5.8 ppb median (1,2). In a 9-state survey, 7 percent of the wells tested were positive, with a maximum value of 380 ppb reported (3). After train derailment in Manitoba on Mar 10, 1980, in which large amounts of VC was spilled in the snow, 10 ppm maximum occurred in groundwater which decreased to below 0.02 ppm by 10 weeks after the spill (6). [127] GROUNDWATER: USA 1982 National Ground Water Supply Survey, 466 samples, 1.1 percent positive, 1.1 ppb median, 1.1 ppb maximum (1 ppb quantification limit) (1). [27] SURFACE WATER: 9.8 ppb maximum value found in a 1981, 9-state survey (2,3). It was not detected in winter or summer samples from the Delaware River (4). Vinyl chloride has been detected in 21 out of 606 samples from New Jersey (5) and other USA samples (6). 7.6 percent of 105 USA cities were positive with positive samples ranging from 0.2 to 5.1 ppb, 3.25 ppb median (1). [126] On the basis of various model simulations it appears that vinyl chloride should not remain in the aquatic ecosystem under most natural conditions. The loss of vinyl chloride at constant temperature and pressure is a function of water turbulence and mixing efficiency. [19] The experimental decrease of 16 mg/liter is 96 percent in 2 hours when stirred rapidly at 22 degrees C in an open beaker of distilled water. In contrast, quiescent water under the same conditions yielded a concentration loss over 2 hours of only 25 percent. Assuming that all processes involved are strictly first order, the volatilization loss data above, yields half-lives of 25.8 minutes for the stirred case and 290 minutes for the quiescent case. [19] BOR 006719 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD Page 28 EFFLUENTS CONCENTRATIONS The only industry with appreciable waste water effluents of vinyl chloride is the organic chemicals manufacturing plastic industry where mean levels are 750 ppb (1). Waste water from 12 polyvinyl chloride (PVC) plants in seven USA areas ranged from 0.05 to 20 ppm with typical levels being 2 to 3 ppm (2). Vinyl chloride has been detected in effluents from chemical and latex plants in Long Beach, California (4). It was not detected in effluents from major municipal waste water discharges in Southern California (3). Groundwater from hazardous waste sites, CERCLA Database: 178 sites, 8.7 percent positive (5). [142] SEDIMENT AND SOIL CONCENTRATIONS After a March 10, 1980, train derailment in Canada in which large quantities of vinyl chloride were spilled in the snow, soil samples reached levels as high as 500 ppm between one and two meters below th soil surface (1). [20] ATMOSPHERIC CONCENTRATIONS RURAL: Less than 5 parts/trillion detected in air sample from the rural northwest USA (1,4) less than 10 ppb at the Whiteface Mountain in New York (3). No vinyl chloride was detected in seven air samples taken in the Grand Canyon, AZ, detection limit* 2.8 ppb (2) and less than 10 ppb at the Whiteface Mountain in New York (3). URBAN/SUBURBAN: NJ area, 36 samples, 42 percent positive, trace-3,132 ng/eubic meter (5). Baton Rouge, LA, area, 16 samples, 56 percent positive, trace-1,334 ng/cubic meter (5). [131] URBAN/SUBURBAN: Vinyl chloride has a low frequency of occurrence in studies done in New Jersey (1,3,5,6), with a concentration range of a trace to less than 10 ppb average (1,3-7). Two of eight sites (1 - Staten Island and 7 - New Jersey) were positive : 0.15 and 46 ppb (2); Baltimore, MD: 38.5 ppb average (4). [125] SOURCE DOMINATED AREAS: Houston, TX -Gulf Coast area (18 samples) 3.1-1,250 ppb, maximum in Texas City (6); Niagara Falls, NY, upwind from plant:0 ppb, downwind: 28 ppb and 40 ppb measured in a nearby residential area (3); Delaware City, DE, highway intersection: 790 ppb average (2); Houston, TX, area which is the site of 40 percent of USA production capacity of PVC had a range of 3.1-1250 ppb (4,5) with 33.0 ppm being detected 0.5 km from the center of a vinyl chloride plant (5). Eight highly industrialized USA areas 0 to 0.513 ppb (1). Not detected in 23 samples from the Kin Buc disposal site in New Jersey (1). [137] HEALTH AND ENVIRONMENT INTERNATIONAL, LTD BOR 006720 Page 29  SOURCE DOMINATED: Ambient air near two vinyl chloride (VC) plants in Long Beach, CA: 0.1-3.4 ppm (1). New auto interiors, less than 0.05 percent positive, 0.4 to 1.2 ppm (1), however, less than 10 ppb was measured in another study involving sixteen new or used cars and four new or old mobile homes (1). After a March 10, 1980, train derailment in Canada in which quantities of VC were spilled during a blizzard, levels in excess of 200 ppm were found at ground levels near some freight cars but levels outside of the spill area were less than 0.02 ppm the detection limit (2). Ambient air near waste site: 2-7.3 ppb; one background site: 2-3 ppb (3); air in homes in neighborhood surrounding the landfill: 108 samples from 19 homes, 4 ppb average, 7 ppb maximum; 420 samples from 50 different homes, 4 ppb average, 9.3 ppb maximum(3). [135] FOOD SURVEY VALUES Twenty mg/kg were detected in alcoholic beverages which were packaged in products containing vinyl chloride (1,3). Alcoholic beverages: 0.025 to 1.60 ppm, 0.44 ppm average; edible oils: 0.3 to 3.29 ppm, 2.16 ppm average; vinegars: 0 (red wine) to 8.40 ppm (apple cider): detected but not quantified in butter and margarine when these products were packaged in PVC (polyvinyl chloride) containers (2,3). [133] OTHER BKVIBOHMEHTAL COHCEHTRATIOHS Vinyl chloride monomer has been found in polyvinyl chloride resins but these levels can be reduced by new processing techniques in food grade resins (1). For example, PVC delivered to a fabricator contained 250 ppm vinyl chloride monomer which was reduced to 0.5-20 ppm after fabrication (1). Residual vinyl chloride monomer found in food packing material ranged from 0.043-71 ppb for film and up to 7.9 ppm for plastic bottles (1). It has been found in domestic and foreign cigarettes and little cigars in concentrations of 5.6-27 mg/cigarette(l). [54] ENVIRONMENTAL TRANSFORMATIONS BIODEGRADATION Limited existing data indicate that vinyl chloride is resistant to biodegradation in aerobic systems (1,2). Vinyl chloride was approximately 50 percent and 100 percent degraded in 4 and 11 weeks, respectively, in the presence of Band by methanogenic microorganisms under anaerobic conditions in laboratory scale experiments (3). In the absence of sand 20 percent and 55 percent degradation occurred in 4 and 11 weeks, respectively (3). [132] ABIOTIC DEGRADATION The rate constant for the vapor phase reaction of vinyl chloride with photochemically produced hydroxyl radicals has been determined in laboratory experiments to be 6.60x10-12 cubic cm/molecule-sec at 26 degrees c (1) which corresponds to an atmospheric half-life of 1.5 days at an atmospheric concentration of 8X10+5 hydroxyl radicals per cubic cm . Disappearance of approximately 50 percent of vinyl chloride exposed HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 30 rl (M t" O o O to sunlight outdoors in air occurred in 0.5 and 2 days in September and December, respectively (2). The products of reaction include chloroacetaldehyde, HC1, chloroethylene epoxide, formaldehyde, formyl chloride, formic acid and carbon monoxide (3,4). in the presence of nitrogen oxides, its reactivity is higher with a half-life of 3-7 hours (2,5,6). In water no photodegradation was observed in 90 hours; however, degradation is rapid in the presence of sensitizers such as might be found in humic waters, etc., or free radicals as might be found in polyvinyl choloride (PVC) manufacturing effluent streams (7). Hydrolysis will not be a significant loss process (8). [138] Reacts at an extremely rapid rate with hydroxyl radicals, exhibiting a half-life on the order of a few hours with the subsequent formation of hydrogen chloride or formyl chloride as posible products. Formyl chloride, if formed, iB reported to decompose thermally at ambient temperatures with a half-life of about 20 minutes, yielding carbon monoxide and hydrogen chloride. [19] Atmospheric ozone prevents essentially all sunlight of wavelengths short r than 290 nm from reaching the earth's surface. Vinyl chloride, in the vapor phase, does not absorb light of wavelengths greater than 220 nm, and in water it does not absorb above 218 nm. As a result, direct photolysis would be expected, at best, to be a very slow process due to lack of overlap between vinyl chloride absorption and sunlight radiation spectra. It is, however, possible that light-induced transformations of vinyl chloride could occur through indirect photolysis. Photolysis experiments were conducted in natural water and in distilled water containing photosensitizers that absorb light of wavelengths greater than 300 nm. It was found that vinyl chloride in solution decomposed rapidly when irradiated with ultraviolet light in the presence of acetone, a high energy triplet Bensitizer, or hydrogen peroxide, a free radical source. [19] Atmospheric photodissociation appears to be much less important than photochemical oxidation. Rapid photochemical oxidation is reported to remove the compound from the troposphere with a half-life of a few hours. As a result, neither the chlorine in vinyl chloride nor vinyl chloride itself is likely to diffuse to the stratosphere. Experiments indicate that if reactive radicals are present in natural waters at significant concentrations, they may degrade vinyl chloride. Experimental results show that vinyl chloride will not be significantly degraded by molecular oxygen at temperatures and oxygen concentrations present in natural waters. [19] Hydrolysis over a pH range of 4.3 to 9.4 does not appear to be an important pathway for loss of vinyl chloride from water. The hydrolytic half-life has been estimated to be less than 10 years at 25 degrees C. Since the volatilization rate is much more rapid than the predicted rate of hydrolysis, hydrolysis should not be a significant aquatic fate. [19] HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. BOR 006722 Page 31 REGULATIONS AND COMPLIANCE STANDARDS Regulations and compliance standards are constantly changing. The following standards are the most commonly cited ones. The Section which follows, entitled Code of Federal Regulations, contains all of the Code of Federal Regulations (CFR) on this chemical at the time of printing from all of the Titles in the Code (e.g., 21 CFR, 29 CFR, 40 CFR etc.). WATER STANDARDS Toxic-pollutant-designated pursuant to section 307(a)(1) of the Clean Water Act and is subject to effluent limitations. [40 CFR 401.15 (7/1/88)] The national revised primary drinking water maximum contaminant level for vinyl choride for community water systems is 0.002 mg/liter. [40 CFR 141.61 (7/1/88)] Based on 2 liters of drinking water consumed and the consumption of 6.5 grams of fish and shellfish, and the corresponding risk levels of 1X105, 1X10-6, 1X10-7, the criteria to protect human health is derived at 0.2 ug/liter, 2.0 ug/liter, and 20 ug/liter, respectively. Consumption of fish and shellfish only are: 52.5 ug/liter, 525 ug/liter, and 5,246 ug/liter, respectively. [108] ATMOSPHERIC STANDARDS Emission standards for vinyl chloride and compliance to the following topic areas are considered: (1) Relief valve discharge; (2) Fugitive emission sources; (3) Leakage from pump, compressor, and agitator seals; (4) Manual venting of gaseB; (5) Samples; (6) Leak detection and elimination; and (7) in process wastewater. [40 CFR 61.65 (7/1/88)] Vinyl chloride formulation and purification: The concentration of vinyl chloride in exhaust gases discharged to the atmosphere from any equipment used in vinyl chloride formation and/or purification is not to exceed 10 ppm, except as provided in 40 CFR 61.65(a). [40 CFR 61.63 (7/1/88)) This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, non air quality health and environmental impact and energy requirements. Vinyl chloride is produced, as an intermediate or final product, by process units covered under this subpart. [40 CFR 60.489 (7/1/89)] Vinyl chloride has been designated as a hazardous air pollutant under section 112 of the Clean Air Act. [40 CFR 61.01 (7/1/88)] B0R 006723 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD Page 32 CERCLA REQUIREMENTS Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 1 pound or 0.454 kg. The toll-free number of the NRC iB (800) 424-8802? In the Washington D.C. metropolitan area (202) 426-2675. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b). [54 FR 33419 (8/14/89)) RCRA REQUIREMENTS As stipulated in 40 CFR 261.33, when vinyl chloride, as a commercial chemical product or manufacturing chemical intermediate or an offspecification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to Federal and/or State hazardous waste regulations. Also defined as a hazardous waste is any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5). (40 CFR 261.33 (7/1/88)) FIFRA REQUIREMENTS Cancelled or suspended, all pesticide products containing this compound, whether an active or inert ingredient, for uses in the home, food handling establishments, hospitals or in enclosed areas. [38] FDA REQUIREMENTS FDA banned the use of vinyl chloride as an aerosol propellant. FDA eliminated the use of vinyl chloride in drug products and has alerted food manufacturers to the need for monitoring packaging materials that may contain it. [30] Vinyl chloride is an indirect food additive for use only as a component of adhesives. [21 CFR 175.105 (4/1/88)] Acrylonitrile copolymers and resins listed in this section, containing less than 30 percent acrylonitrile and complying with the requirements of paragraph (b) of this section, may be safely used as follows: Acrylonitrile/butadiene copolymer blended with vinyl chloride-vinyl acetate (optional at level up to 5 percent by weight of the vinyl chloride resin) resin: for use only in contact with oleomargarine. (Aerylonitrile/butadiene copolymer blended with vinyl chloride-vinyl acetate) [21 CFR 181.32 (4/1/88)] Vinyl Chloride is an indirect food additive polymer for use as a basic component of single and repeated use food contact surfaces. Semirigid and rigid acrylic and modified acrylic plastics may be safely used as articles intended for use in contact with food in accordance with prescribed conditions. The acrylic and modified acrylic polymers or BOR 006724 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD Page 33 plastic described in this section also may be safely used as components of articles intended for use in contact with food. At least 50 weightpercent of the polymer content of the acrylic and modified acrylic materials used as finished articles or as components of articles shall consist of polymer units derived from copolymers produced by copolymerizing one or more of the monomers (listed in paragraph (a)(i)) with vinyl chloride. [21 CFR 177.1010 (4/1/88)] Vinyl chloride is an indirect food additive polymer for use as a basic component of single and repeated use food contact surfaces. Cellophane may be safely used for packaging food in accordance with prescribed conditions. Optional substances used in the base sheet and coating may include vinyl acetate-vinyl chloride copolymer resins, vinyl acetatevinyl chloride-maleic acid copolymer resins, and vinylidence chloride copolymerized with vinyl chloride. [21 CFR 177.1200 (4/1/88)] Vinyl chloride is an indirect food additive polymer for use as a basic component of single and repeated use food contact surfaces. Closures with sealing gaskets may be safely used on containers intended for use in producing, manufacturing, packing, processing, preparing, treating, packaging, transporting, or holding food in accordance with prescribed conditions. Substances that may be employed in the manufacture of closure-sealing gaskets include vinyl chloride-vinyl stearate copolymers. [21 CFR 177.1210 (4/1/88)] Vinyl chloride is an indirect food additive polymer for use as a basic component of single and repeated use food contact surfaces. The vinyl chloride-ethylene copolymers indentified in paragraph (a) of thiB section may be safely used as components of articles intended for contact with food under conditions of use D, E, F, or G described in Table 2 of Section 176.170 (c) of this chapter, subject to the provisions of this section. [21 CFR 177.1950 (4/1/88)] Vinyl chloride is an indirect food additive polymer for use as a basic component of single and repeated use food contact surfaces. The vinyl chloride-hexene-1 copolymers identified in paragraph (a) of this section may be safely used as articles or as components of articles intended for use in contact with food, under conditions of use D, E, F, or G described in Table 2 of Section 176.170 (c) of this chapter, subject to the provisions of this section. [21 CFR 177.1960 (4/1/88)] Vinyl chloride is an indirect food additive polymer for use as a basic component of single and repeated use food contact surfaces. The vinyl chloride-lauryl vinyl ether copolymers indentified in paragraph (a) of this section may be used as an article or as a component of an article intended for use in contact with food subject to the provisions of this section. [21 CFR 177.1970 (4/1/88)] Vinyl chloride is an indirect food additive polymer for use as a basic component of single and repeated use food contact surfaces. The vinyl chloride-propylene copolymers identified in paragraph (a) of thiB section may be safely used as components of articles intended for contact with food, subject to the provisions of this section. [21 CFR 177.1980 (4/1/88)] Vinyl chloride polymer is an indirect food additive for use only as a component of adhesives. (Vinyl chloride polymers) [21 CFR 175.105 (4/1/88)] BOR 006725 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 34 CODE OF FEDERAL REGULATIONS The following Federal Regulations - all of those published at the time of printing - identify restrictions, standards and other regulatory actions which have been issued by the Federal Government (e.g., Environmental Protections Agency (EPA) 40 CFR, Food and Drug Administration (FDA) 21 CFR, Department of Transportation (DOT) 46 CFR and 49 CFR, etc.)* The CFR numbers should be consulted for the specific guidance provided for each. PROTECTION OF ENVIRONMENT EFFLUENT GUIDELINES AND STANDARDS 40 CFR 401.15 40 CFR 403 App. B 40 CFR 413.12(1) 40 CFR 423 App. A 40 CFR 433.11(e) GROUND--WATER MONITORING 40 CFR 264 App. IX LAND DISPOSAL RESTRICTIONS 40 CFR 268 App. Ill 40 CFR 268.10 40 CFR 268.43(a) CONTAMINANT LEVELS IN DRINKING 40 CFR 141.24(g)(6) 40 CFR 141.50(a)(2) 40 CFR 141.61(a) STATE STANDARDS 40 CFR 52.741 App. A - Illinois 40 CFR 52.2220 - Tennessee 40 CFR 60.4(b) - Arizona 40 CFR 60.4(b) - California 40 CFR 60.4(b) - Guam 40 CFR 60.4(b) - Nevada 40 CFR 61.04(c) - Colorado 40 CFR 61.04(c) - Montana 40 CFR 61.04(c) - North Dakota 40 CFR 61.04(c) - South Dakota 40 CFR 61.04(c) - Utah 40 CFR 61.04(c) - Wyoming bOR 006726 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 35 MONITORING DRINKING WATER 40 CFR 141 App. C, Fig. 5 40 CFR 141 App. C, Fig. 6 40 CFR 141.32(e)(4) ORGANIC CHEMICAL MANUFACTURING INDUSTRI 40 CFR 60.489(a) SUPERFUND, REPORTABLE QUANTITY 40 CFR 302.4 App. A 40 CFR 302.4 Table TEST PROCEDURES FOR ANALYSIS OF POLLUTANTS 40 CFR 136 App. A, Heth. 1624 , Table 1 40 CFR 136 App. A, Meth. 1624 , Table 2 40 CFR 136 App. A, Heth. 1624 , Table 4 40 CFR 136 App. A, Meth. 1624 , Table 5 40 CFR 136 App. A, Meth. 601 40 CFR 136 App. A, Meth. 601, Table 1 40 CFR 136 App. A, Meth. 601, Table 2 40 CFR 136 App. A, Meth. 601, Table 3 40 CFR 136 App. A, Meth. 624 40 CFR 136 App. A, Meth. 624, Fig. 5 40 CFR 136 App. A, Meth. 624, Table 1 40 CFR 136 App. A, Meth. 624, Table 4 40 CFR 136 App. A, Meth. 624, Table 5 40 CFR 136 App. A, Meth. 624, Table 6 40 CFR 136.3(a) Table 1C HAZARDOUS WASTE IDENTIFICATION AND 40 CFR 261 App. II 40 CFR 261 App. III 40 CFR 261 App. IX 40 CFR 261 App. VII 40 CFR 261 App. VIII 40 CFR 261.24 Table 1 40 CFR 261.32 40 CFR 261.33(f) NATIONAL POLLUTANT DISCHARGE ELIMINATION SYSTEM 40 CFR 122 App. D HEALTH AND ENVIRONMENT INTERNATIONAL, LTD BOR 006727 Page 36 ORGANIC CHEMICAL EFFLUENT LIMITATIONS AND PRETREATMENT STANDARDS 40 CFR 414.25(b)(2) 40 CFR 414.35(b)(2) 40 CFR 414.45(b)(2) 40 CFR 414.55(b)(2) 40 CFR 414.60(c) 40 CFR 414.65(b)(2) 40 CFR 414.75(b)(2) 40 CFR 414.85(b)(2) 40 CFR 414.91(b)(2) 40 CFR 414.101(b)(2) SUPERFUND, EMERGENCY PLANNING 40 CFR 372.65(a) 40 CFR 372.65(b) NATIONAL EMISSION STANDARDS 40 CFR 61 App, B Meth. 40 CFR 61 App. B Meth. 40 CFR 61 App. B Meth. 40 CFR 61.01(a) 40 CFR 61.60 106 107 107A IMPLEMENTATION PLANS 40 CFR 51.166 40 CFR 52.21 DISTILLATION OPERATIONS EMISSIONS 40 CFR 60.667 FOOD AMD DRUGS AEROSOL PRODUCT 21 CFR 310.506 COSMETICS 21 CFR 700.14 POLYMER MODIFIERS 21 CFR 178.3790 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. BOR 006728 Page 37 LABOR AIR CONTAMINANTS 29 CFR 1910.1000 Table Z-l-A INDUSTRIAL TRUCKS IK ATMOSPHERES COHTAIHIMG HAZARDOUS CONCENTRATIONS 29 CFR 1910.178(C)(2) LABORATORI OCCUPATIONAL EXPOSURE 29 CFR 1910.1450 App. A EXPOSURE LIMIT, PERMISSIBLE 29 CFR 1910.19(b) MANUFACTURING AMD HANDLING 29 CFR 1910.1017 COMMERCIAL PRACTICES BANNED SUBSTANCES, INTERSTATE COMMERCE 16 CFR 1500.17(a)(10) SHIPPING COMPATIBILITY OF CARGO ON TANK VESSELS 46 CFR 150 Table I 46 CFR 150 Table II SAFETT STANDARDS FOR BARGES AND VESSELS CARRYING LIQUEFIED BULK SHIPMENTS 46 CFR 154 Table 4 46 CFR 154a Annex A 46 CFR 154.7 46 CFR 154.1710 46 CFR 154.1740 46 CFR 154.1745 46 CFR 154.1750 46 CFR 154.1870(d)(7) SHIP POLLUTION CONTROL 46 CFR 151.50-34 OR 006729 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 38 BULK SHIPMENT, MINIMUM REQUIREMENTS 46 CFR 151.05 FILLING DENSITIES AND CONTAINER DESIGN PRESSURES 46 CFR 151.50-30(6) BULK SHIPMENT 46 CFR 40.15 TRANSPORTATION SUPERFUND, REPORTABLE QUANTITY 49 CFR 172.101 App. BAXARDOOS MATERIALS TABLE 49 CFR 172 App. A 49 CFR 172.101 49 CFR 172.102 CYLINDERS 49 CFR 173.304(a)(2) CARGO TANKS 49 CFR 173.315(a) 49 CFR 173.315(h) TANK CARS 49 CFR 173.314(c) 49 CFR 179.102-11 49 CFR 179.102-6 49 CFR 179.302(a) NAVIGATION AND NAVIGABLE WATERS CARGO OF PARTICULAR HAZARD 33 CFR 126.10(d) DANGEROUS BULK CARGO DEFINITION 33 CFR 160.203(e) HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. bor 6730 Page 39 MINERAL RESOURCES CHEMICAL CARTRIDGE RESPIRATOR 30 CFR 11.150 30 CFR 11.160 30 CFR 11.162-1 30 CFR 11.203 30 CFR 11.204 30 CFR 11.205 RESPIRATORS 30 CFR 11.200 COMMERCE AND FOREIGN TRADE COMMODITY CONTROL LIST 15 CFR 799.2, Supp. 1 NATIONAL DEFENSE AIR POLLUTION STANDARDS 32 CFR 650.88(b)(4) HEALTH AND ENVIRONMENT INTERNATIONAL, LTD BOR 00673J Page 40 MONITORING AND ANALYSIS INFORMATION SAMPLING PROCEDURES Essential characteristics, advantages, and problems associated with personal monitors for selected air pollutants are discussed and compared with fixed station monitoring. Studies on monitoring of carbon monoxide, nitrogen dioxide, respirable particulates, vinyl chloride, formaldehyde, pesticides and polychlorinated biphenyls, polynuclear aromatics, sulfur dioxide, 02one, and radon are reviewed. [117] NIOSH 1007: Analyte: Vinyl chloride; Matrix: air; Sampler: Solid sorbent tube (2 tandem tubes, each with 150 mg activated coconut charcoal); Flow rate: 0.05 liters/min; Vol: minute: 0.7 liters, maximum: 5 liters; Stability: 10 days at 25 degrees C [34] ANALYTICAL LABORATORY METHODS A gas chromatographic method for determining vinyl chloride in foodstuffs and in vinyl chloride polymers and copolymers intended to come into contact with food. Commission of the European Communitites, Off J Eur Communities number C16 8 (1977). [59] NIOSH 1007: Analyte: Vinyl chloride; Matrix: air; Technique: Gas chromatography, FID; Desorption: 1 ml carbon disulfide, 30 minutes; Range; 0.002 to 0.2 mg/sample; Estimated LOD: 0.00004 mg/sample; Precision: not determined; Interferences: none [34] EPA Method 8010: Halogenated Volatile Organics. For the analysis of solid waste, a representative sample (solid or liquid) is collected in a standard 40 ml glass screw-cap VOA vial equipped with a Teflon-faced silicone septum. Sample agitation, as well as contamination of the sample with air, must be avoided. Two vials are filled per sample location, then placed in separate plastic bags for shipment and storage. Samples may be analyzed by direct injection or purge-and-trap using gas chromatography, with detection achieved with a halogen-specific detector. A temperature program is used in the gas chromatograph to separate the organic compounds. Column 1 is an 8 ft by 0.1 inch ID stainless steel or glass column packed with 1 percent SP-1000 on Carbopack-B 60/80 mesh or equivalent. Column 2 is a 6 ft by 0.1 inch ID stainless steel or glass column packed with chemically bonded n-octane on Porasil-C 100/120 mesh (Durapak) or equivalent. Under the prescribed conditions, vinyl chloride has a detection limit of 0.18 ug/liter, an average recovery range of four measurements of 8.2-29.9 ug/liter, and a limit for the standard deviation of 5.7 ug/liter. [113] EPA Method 8240: Gas Chromatography/Mass Spectrometry for Volatile Organics Method 8240 can be used to quantify most volatile organic commpounds that have boiling points below 200 C (vapor pressure iB approximately equal to mm Hg at 25 degrees C) and that are insoluble or slightly soluble in water, including the title compound. Volatile water-soluble compounds can be included in this analytical technique, however, for the more soluble compounds, quantitation limits are approximately ten times higher because of poor purging efficiency. The method is also limited to compounds that elute as sharp peaks from a GC column packed with graphitized carbon lightly coated with a carbowax (6 ft by 0.1 in ID HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 41 m J o o g n glass, packed with 1 percent SP-1000 on Carbopack-B (60/80 mesh) or equivalant). This gas chromatography/mass spectrometry method is based on a purge-and-trap procedure. The practical quantitation limit (PQL) for Method 8240 for an individual compound is approximately 5 ug/kg (wet weight) for wastes and 5 ug/liter for ground water. PQLs will be proportionately higher for sample extracts and samples that require dilution or reduced sample size to avoid saturation of the detector. [113] EPA Method 601: Purgeable Halocarbons: Grab samples of water in municipal and industrial discharges are analyzed by purge and trap gas chromatography with electrolytic conductivity detection. Using this procedure, vinyl chloride has a method detection limit of 0.18 ug/liter and an overall precision of 0.27 times the average recovery + 0.40, over a working range of 8.0 to 500 ug/liter. [40 CFR 136 (7/1/87)] EPA Method 624: Purgeables: Grab samples of water in industrial and municipal discharges must be collected in glass containers and extracted with methylene chloride. Analysis is performed by a purge and trap gas chromatography/mass spectrometry method. Using this procedure, vinyl chloride has an overall precision of 0.65 ug/liter times the average recovery. [40 CFR 136 (7/1/87)] EPA Method 1624: Volatile Organic Compounds by GC/MS: Grab samples in municipal and industrial discharges are collected. If residual chlorine is present, add sodium thiosulfate. Extraction is performed by a purge and trap apparatus. An isotope dilution gas chromatography/mass spectrometry (GS-MS) method for the determination of volatile organic compounds in municipal and industrial discharges is described. Unlabeled vinyl chloride has a minimum level of 10 ug/liter and a mean retention time of 304 sec. This method has an initial precision of 27.9 ug/liter, an accuracy of greater than 0-58.5 ug/liter, and a labeled compound recovery of ns (no specification) - 452 percent. [40 CFR 136 (7/1/87)] CLINICAL LABORATORY METHODS The possibilities of thioether or mercapturic acid assay for detection of human exposure to electrophilic agents or their precursors were reviewed. Thioether assay was based on the ability of many alkylating or covalently binding compounds (a class of chemicals that included the genotoxic compounds) to react with glutathione. Often glutathione conjugates formed in this reaction were excreted in urine as (pre)mercapturic acids or other thioethers. Thioethers can be determined spectrophotometrically after alkaline hydrolysis of urine extracts. In practice the most important value of the assay was its signal function. Whenever a significant increase in the excretion of thioethers was observed, it was likely to be the result of exposure to 1 or more suspect compounds. When unknown electrophiles or a mixture of such compounds were involved, no quantitative conclusions were drawn with regard to internal exposure. When thioether values were found, ranging within the limits of the normal distribution, it could not be concluded that no or negligible exposures occurred. [114] HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. BOR 006733 Page 42 SAFE HANDLING AND DISPOSAL INFORMATION NFPA HAZARD CLASSIFICATION Health: 2. 2 materials hazardous to health, but areas may be entered freely with full-faced mask self-contained breathing apparatus which provides eye protection. [81] Flammability: 4. 4= very flammable gases or very volatile flammable liquids. Shut off flow and keep cooling water streams on exposed tanks or containers. [81] Reactivity: 1. 1 materials which (in themselves) are normally stable but which may become unstable at elevated temperatures and pressures or which may react with release of energy but not violently. Caution must be used with the fire and applying water. [81] FLAMMABLE PROPERTIES FIRE POTERTIAL Dangerous, when exposed to heat or flame. Large fires of this material are practically inextinguishable, spontaneous heating: no. [90] Forms inflammable mixture with air above -78 degrees C. [72] Flammable gas at room temperature [33] FLAMMABLE LIMITS Percent by volume: lower 3.6; upper 33.0 [81] EXPLOSIVE LIMITS AND POTENTIAL Forms explosive mixture with air. [81] Forms explosive vapor when exposed to heat or flame. [90] Lower 4 percent/v; upper 22 percent/v [90] WARNING PROPERTIES ODOR THRESHOLD Although vinyl chloride has an odor at high concentration, it is of no value in preventing excessive exposure. The actual vapor concentration that can be detected has never been adequately determined and varies from one individual to another, from impurities in the sample and probably from duration of exposure. [23] SKIM, ETE AMD RESPIRATORY IRRITATIOMS Primary irritant for skin [72] OR 006734 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD Page 43 FIRE FIGHTING INFORMATION FIRE FIGBTIRG PROCEDURES Stop flow of gas. Use water to keep fire-exposed containers cool and to protect persons affecting shut-off. [81] If fire becomes uncontrollable or container is exposed to direct flame, consider evacuation of one-half mile radius. If material, is leaking (not on fire), downwind evacuation must be considered. [6] TOXIC COKBOSTIOH PRODUCTS On combustion, it degrades mainly to hydrogen chloride, carbon monoxide, carbon dioxide and traces of phosgene [59] OTHER FIRE FIGHTIRG HAZARDS Gas may travel considerable distance to source of ignition and flash back [81] PREVENTIVE MEASURES PROTECTIVE EQUIPMERT AMD CUOTBIRG Wear rubber gloves and shoes, gas-tight goggles, organic vapor canister or self-contained breathing apparatus. [101] Respiratory protection is as follows for the following concentrations of vinyl chloride: Not over 10 ppm: Combination type C supplied-air respirator, demand type, with half facepiece, and auxiliary self- contained breathing air supply, or type c supplied air respirator, demand type, with half facepiece, or any chemical cartridge respirator with an organic vapor cartridge which provides a service life of at least 1 hour for concentrations up to 10 ppm; Not over 25 ppm: A powered air purifying respirator with hood, helmet, full or half facepiece, and a canister which provides a service life of at least 4 hours for concentrations of vinyl chloride up to 25 ppm, or gas mask, front- or back-mounted canister which provides a service life of at least 4 hours for concentrations of vinyl chloride up to 25 ppm; Not over 100 ppm: Combination type C supplied air respirator, demand type, with full facepiece, and auxiliary self-contained air supply, or open circuit self-contained breathing apparatus with full facepiece in demand mode, or type C supplied air respirator, demand type, with full facepiece; Not over 1000 ppm: Combination type supplied air respirator, continuous flow type with full or half facepiece, and auxiliary self-contained air supply; Not over 3600 ppm: Combination type C supplied air respirator, pressure demand type, with full or half facepiece, and auxiliary self- contained air supply; Unknown, or above 3600 ppm: Open circuit, self- contained breathing apparatus, pressure demand type with a full facepiece. [74] PRECAUTIONS FOR "CARCINOGENS": Dispensers of liquid detergent should be available. Safety pipettes should be used for all pipetting. In animal laboratory, personnel should wear protective suits (preferably disposable, one-piec and close-fitting at ankles and wrists), gloves, in ro f 10 O o HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 44 OS O W hair covering and overshoes. In chemical laboratory/ gloves and gowns should always be worn, however, gloveB should not be assumed to provide full protection. Carefully fitted masks or respirators may be necessary when working with particulates or gases, and disposable plastic aprons might provide additional protection. Gowns should be of distinctive color, this is a reminder that they are not to be worn outside the laboratory. (Chemical Carcinogens) [56] Some data suggests vinyl chloride breakthrough times of approximately an hour or more for nitrile rubber. [1] Some data (usually from immersion tests) suggests vinyl chloride breakthrough times greater than one hour are not likely with chlorinated polyethylene. [1] OTHER PREVENTIVE ERASURES Nobody may keep tobacco or food either in his work clothes or at his workplace. Meals should be eaten in appropriate canteens, which should be ventilated separately and isolated from the work premises. The work clothing should be specially designed for this use and left at the end of the shift. [61] If material is not on fire and not involved in a fire: Keep sparks, flames, and other sources of ignition away; keep material out of water sources and sewers; attempt to stop leak without hazard; use water spray to knock down vapors. [6] PRECAUTIONS FOR "CARCINOGENS": Smoking, drinking, eating, storage of food or of food and beverage containers or utensils, and the application of cosmetics should be prohibited in any laboratory. All personnel should remove gloves, if worn, after completion of procedures in which carcinogens have been used. They should wash hands, preferably using dispensers of liquid detergent, and rinse thoroughly. Consideration should be given to appropriate methods for cleaning the skin, depending on nature of the contaminant. No standard procedure can be recommended, but the use of organic solvents should be avoided. Safety pipettes should be used for all pipetting. (Chemical Carcinogens) [56] PRECAUTIONS FOR "CARCINOGENS": In animal laboratory, personnel should remove their outdoor clothes and wear protective suits (preferably disposable, one-piece and close-fitting at ankles and wrists), gloves, hair covering and overshoes. Clothing should be changed daily but discarded immediately if obvious contamination occurs also, workers should shower immediately. In chemical laboratory, gloves and gowns should always be worn, however, gloves should not be assumed to provide full protection. Carefully fitted masks or respirators may be necessary when working with particulates or gases, and disposable plastic aprons might provide additional protection. If gowns are of distinctive color, this is a reminder that they should not be worn outside of lab. (Chemical Carcinogens) [56] PRECAUTIONS FOR "CARCINOGENS": Operations connected with synthesis and purification should be carried out under well-ventilated hood. Analytical procedures should be carried out with care and vapors evolved during procedures should be removed. Expert advice should be obtained before existing fume cupboards are used and when new fume cupboards are installed. It is desirable that there be means for decreasing the rate of air extraction, so that carcinogenic powders can be handled without powder being blown around the hood. Glove boxes should be kept under negative air pressure. Air changes should be adequate, so that HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 45 BOR 006736 concentration of vapors of volatile carcinogens will not occur. (Chemical Carcinogens) [56] PRECAUTIONS FOR "CARCINOGENS": Vertical laminar-flow biological safety cabinets may be used for containment of in vitro procedures provided that the exhaust air flow is sufficient to provide an inward air flow at the face opening of the cabinet, and contaminated air plenums that are under positive pressure are leak-tight. Horizontal laminar-flow hoods or safety cabinets, where filtered air is blown across the working area towards the operator, should never be used Each cabinet or fume cupboard to be used should be tested before work is begun (e.g., with fume bomb) and label fixed to it, giving date of test and average air-flow measured. This test should be repeated periodically and after any structural changes. (Chemical Carcinogens) [56] PRECAUTIONS FOR "CARCINOGENS": Principles that apply to chemical or biochemical labs also apply to microbiological and cell-culture labs. Special consideration should be given to route of administration. The safest method of administering a volatile carcinogen is by injection of a solution. Administration by topical application, gavage, or intratracheal instillation should be performed under the hood. If chemicals will be exhaled, animals should be kept under hood during this period. Inhalation exposure requires special equipment. Unless specifically required, routes of administration other than in the diet should be used. Mixing of carcinogen in diet should be carried out in sealed mixers under fume hood, from which the exhaust is fitted with an efficient particulate filter. Techniques for cleaning mixer and hood should be devised before an experiment is begun. When mixing diets, special protective clothing and, possibly, respirators may be required. (Chemical Carcinogens) [56] PRECAUTIONS FOR "CARCINOGENS": When administered in diet or applied to skin, animals should be kept in cages with solid bottoms and sides and fitted with a filter top. When volatile carcinogens are given, filter tops should not be used. Cages which have been used to house animals that received carcinogens should be decontaminated. Cage-cleaning facilities should be installed in area in which carcinogens are being used, to avoid moving of contaminated cages. It is difficult to ensure that cages are decontaminated, and monitoring methods are necessary. Situations may exist in which the use of disposable cages should be recommended, depending on type and amount of carcinogen and efficiency with which it can be removed. (Chemical Carcinogens) [56] PRECAUTIONS FOR "CARCINOGENS": To eliminate risk that contamination in the lab could build up during the conduct of the experiment, periodic checks should be carried out on lab atmospheres, surfaces, such as walls, floors and benches, and interior of fume hoods and airducts. As well as regular monitoring, checks must be carried out after cleaning-up of spillage. Sensitive methods are required when testing lab atmospheres for chemicals such as nitrosamines. Methods should where possible, be simple and sensitive. (Chemical Carcinogens) [56] PRECAUTIONS FOR "CARCINOGENS": Rooms in which obvious contamination has occurred, such as spillage, should be decontaminated by lab personnel engaged in the experiment. Design of the experiment should avoid contamination of permanent equipment. Procedures should ensure that maintenance workers are not exposed to carcinogens. Particular care should be taken to avoid contamination of drains or ventilation ducts. In cleaning labs, procedures should be used which do not produce aerosols or dispersal of dust, i.e., wet mop or vacuum cleaner equipped with HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 46 BOR 006737 high-efficiency particulate filter on exhaust, which are available commercially, should be used. Sweeping, brushing and use of dry dusters or mops should be prohibited. Grossly contaminated cleaning materials should not be re-used If gowns or towels are contaminated, they should not be sent to laundry, but decontaminated or burnt, to avoid any hazard to laundry personnel. (Chemical Carcinogens) [56] PRECAUTIONS FOR "CARCINOGENS": Doors leading into areaB where carcinogens are used should be marked distinctively with appropriate labels and access limited to persons involved in the experiment. A prominently displayed notice should give the name of the Scientific Investigator or other person who can advise in an emergency and who can inform others (such as firemen) on the handling of carcinogenic substances. (Chemical Carcinogens) [56] Avoid breathing vapors. Keep up wind. Do not handle broken packages unless wearing appropriate personal protective equipment. [6] Contaminated protective clothing should be segregated in such a manner so that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. Quality assurance to ascertain the completeness of the cleaning procedures should be implemented before the decontaminated protective clothing is returned for reuse by the workers. [98] Emergency situation: A written operational plan for emergency situations shall be developed for each facility storing, handling, or otherwise using vinyl chloride as a liquid or compressed gas. Appropriate portions of the plan shall be implemented in the event of an emergency. [29 CFR 1910.1017 (1986)] STORAGE CONDITIONS Protect against physical damage. Outside or detached storage is preferable. Inside storage: cool, well-ventilated, noncombustible location, away from all possible sources of ignition. Separate from oxidizing materials. [81] Containers of vinyl chloride shall be legibly labeled either: VINYL CHLORIDE: EXTREMELY FLAMMABLE LIQUID AND GAS UNDER PRESSURE: CANCER SUSPECT AGENT or with the additional legend CANCER-SUSPECT AGENT applied near the label or placard. [29 CFR 1910.1017 (7/1/88] Storage temperature: under pressure, ambient; at atmospheric pressure, low. Venting: under pressure, safety relief; at atmospheric pressure, pressure-vacuum. [101] PRECAUTIONS FOR "CARCINOGENS": Storage site should be as close as practicable to lab in which carcinogens are to be used, so that only small quantities required for the experiment need to be carried. Carcinogens should be kept in only one section of the cupboard, an explosion-proof refrigerator or freezer (depending on chemicophysical properties ) that bears appropriate label. An inventory should be kept, showing the quantity of carcinogen and date it was acquired. Facilities for dispensing should be contiguous to storage area. (Chemical Carcinogens) [56] Suitable precautions including the use of 20-30 percent aqueous sodium hydroxide solution to destroy the peroxide. [11] BOR 006738 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD Page 47 STABILITY AMD SHELF LIFE May produce peroxides. [23] SHIPMENT METHODS AMD REGULATIONS No person may transport, offer or accept a hazardous material for transportation in commerce unless that material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by the hazardous materials regulations (49 CFR 171-177).) [49 CFR 171.2 (10/1/87)] PRECAUTIONS FOR "CARCINOGENS": Procurement of an unduly large amount should be avoided. To avoid spilling, carcinogens should be transported in securely sealed glass bottles or ampoules, which should themselves be placed inside strong screw-cap or snap-top container that will not open when dropped and will resist attack from the carcinogen. Both bottle and the outside container should be appropriately labelled. National post offices, railway companies, road haulage companies and airlines have regulations governing transport of hazardous materials. These authorities should be consulted before material is shipped. (Chemical Carcinogens) [56] PRECAUTIONS FOR "CARCINOGENS": When no regulations exist, the following procedure must be adopted. The carcinogen should be enclosed in a securely sealed, watertight container (primary container), which should be enclosed in a second, unbreakable, leakproof container that will withstand chemical attack from the carcinogen (secondary container). The space between primary and secondary container should be filled with absorbent material, which would withstand chemical attack from the carcinogen and is sufficient to absorb the entire contents of the primary container in the event of breakage or leakage. Each secondary container should then be enclosed in a strong outer box. The space between the secondary container and the outer box should be filled with an appropriate quantity of shock-absorbent material. Sender should use fastest and most secure form of transport and notify recipient of its departure. If parcel is not received when expected, carrier should be informed so that immediate effort can be made to find it. Traffic schedules should be consulted to avoid arrival on weekend or holiday (Chemical Carcinogens) [56] International Air Shipments: Chemical: Vinyl chloride, inhibited. IMO Class: 2.0. UN 1086. Primary hazard label: Flammable gas. Vinyl chloride, inhibited is forbidden for transport on passenger aircraft. Additional packaging instructions listed in the table must also be followed. (Vinyl chloride, inhibited) [60] International Air Shipments: Vinyl chloride, uninhibited is forbidden for transport on passenger and cargo aircraft. (Vinyl chloride, uninhibited) [60] Domestic Transportation: Chemical: Vinyl chloride. Primary Hazard Class: Flammable gas. A flammable gas is any compressed gas that will burn. UN 1086. Label(s) required: Flammable gas. Acceptable Modes of Transportation: Air, rail, road, and water. [49 CFR 172.101 (10/1/87)] International Water Shipments: Chemical: Vinyl chloride. IMO Class: 2.0,Gases. UN 1086. Packaging Label(s) required: Flammable gas. [55] BOR 006739 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD Page 48 DOT EMERGENCY GUIDELINES Fire or Explosion: Extremely flammable. Hay be ignited by heat, sparks or flames. Vapors may travel to a source of ignition and flash back. Container may explode violently in heat of fire. Vapor explosion hazard indoors, outdoors or in sewers. [29] Health Hazards: If inhaled, may be harmful; contact may cause burns to skin and eyes. Vapors may cause dizziness or suffocation. Contact with liquid may cause frostbite. Fire may produce irritating or poisonous gases. [29] Emergency Action: Keep unnecessary people away; isolate hazard area and deny entry. Stay upwind, out of low areas, and ventilate closed spaces before entering. Self-contained breathing apparatus (SCBA) and structural firefighter's protective clothing will provide limited protection. Isolate for 1/2 mile in all directions if tank car or truck is involved in fire. CALL CHEMTREC AT 1-800-424-9300 AS SOON AS POSSIBLE, especially if there is no local hazardous materials team available. [29] Fire: Let tank car, tank truck or storage tank burn unless leak can be stopped; with smaller tanks or cylinders, extinguish/isolate from other flammables. Small Fires: Dry chemical, C02 or Halon. Large Fires: Water spray, fog or standard foam is recommended. Move container from fire area if you can do it without risk. Stay away from ends of tanks. For massive fire in cargo area, use unmanned hose holder or monitor nozzles; if this is impossible, withdraw from area and let fire burn. Withdraw immediately in case of rising sound from venting safety device or any discoloration of tank due to fire. Cool container with water using unmanned device until well after fire is out. [29] Spill or Leak: Shut off ignition sources; no flares, smoking or flames in hazard area, stop leak if you can do it without risk. Water spray may reduce vapor; but it may not prevent ignition in closed spaces. Isolate area until gas has dispersed. [29] First Aid: Hove victim to fresh air and call emergency medical care; if not breathing, give artificial respiration; if breathing is difficult, give oxygen. In case of frostbite, thaw frosted parts with water. Keep victim quiet and maintain normal body temperature. [29] CLEANUP METHODS Land Spill: Construct barriers to contain spill. Absorb small amounts of spill with natural or synthetic sorbents, shovel into containers with covers. [35] Water Spill: Contain contaminated water with dams or natural barriers. [35] PRECAUTIONS FOR "CARCINOGENS": A high-efficiency particulate arrestor (HEPA) or charcoal filters can be used to minimize the amount of carcinogen in exhausted air ventilated safety cabinets, lab hoods, glove boxes or animal rooms. Filter housing that is designed so that used filters can be transferred into plastic bags without contaminating maintenance staff is available commercially. Filters should be placed in plastic bags immediately after removals The plastic bag should be sealed immediately. The sealed bag should be labelled properly. Waste liquids should be placed or collected in proper containers for disposal. The lid should be secured and the bottles properly labelled. Once filled, HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. Page 49 o rvo o o Pi O 0) bottles should be placed in plastic bag, so that outer surface is not contaminated. The plastic bag should also be Bealed and labelled. Broken glassware should be decontaminated by solvent extraction, by chemical destruction, or in specially designed incinerators. (Chemical Carcinogens) [56] DISPOSAL METHODS At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices. [98] PRECAUTIONS FOR "CARCINOGENS": There is no universal method of disposal that has been proved satisfactory for all carcinogenic compounds and specific methods of chemical destruction published have not been tested on all kinds of carcinogen-containing waste. The summary of available methods and recommendations given must be treated as a guide only. (Chemical Carcinogens) [56] PRECAUTIONS FOR "CARCINOGENS": Total destruction by incineration may be the only feasible method for disposal of contaminated laboratory waste from biological experiments. However, not all incinerators are suitable for this purpose. The most efficient type is probably the gas-fired type, in which a first-stage combustion with a less than stoichiometric air:fuel ratio is followed by a second stage with excess air. Some are designed to accept aqueous and organic-solvent solutions, otherwise it is necessary to absorb solutions onto suitable combustible material, such as sawdust. Alternatively, chemical destruction may be used, especially when small quantities are to be destroyed in laboratory. (Chemical Carcinogens) [56] PRECAUTIONS FOR "CARCINOGENS": HEPA (high-efficiency particulate arrestor) filters can be disposed of by incineration. For spent charcoal filters, the adsorbed material can be stripped off at high temperatures and carcinogenic wastes generated by this treatment conducted to and burned in an incinerator. LIQUID HASTE: Disposal should be carried out by incineration at temperatures that ensure complete combustion. SOLID WASTE: Carcasses of lab animals, cage litter and miscellaneous solid wastes should be disposed of by incineration at temperatures high enough to ensure destruction of chemical carcinogens or their metabolites. (Chemical Carcinogens) [56] PRECAUTIONS FOR "CARCINOGENS": Small quantities of some carcinogens can be destroyed using chemical reactions, but no general rules can be given. As a general technique treatment with sodium dichromate in strong sulfuric acid can be used. The time necessary for destruction is seldom known but 1-2 days is generally considered sufficient when freshly prepared reagent is used. Carcinogens that are easily oxidizable can be destroyed with milder oxidative agents, such aB a saturated solution of potassium permanganate in acetone, which appears to be a suitable agent for destruction of hydrazines or of compounds containing isolated carbon-carbon double bonds. Concentrations or 50 percent aqueous sodium hypochlorite can also be used as an oxidizing agent. (Chemical Carcinogens) [56] BOR 006741 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD Page 50  PRECAUTIONS FOR "CARCINOGENS": Carcinogens that are alkylating, arylating or acylating agents per se can be destroyed by reaction with appropriate nucleophiles, such as water, hydroxyl ions, ammonia, thiols and thiosulfate. The reactivity of various alkylating agents varies greatly and is also influenced by the solubility of the agent in the reaction medium. To facilitate the complete reaction, it is suggested that th agents be dissolved in ethanol or similar solvents. No method should be applied until it has been thoroughly tested for its effectiveness and safety on material to be inactivated. For example, in case of destruction of alkylating agents, it is possible to detect residual compounds by reaction with 4(4-nitrobenzyl)-pyridine. (Chemical Carcinogens) [56] A potential candidate for fluidized bed incineration at a temperature range of 450 to 980 degrees C and residence times of seconds for liquids and gases, and longer for solids. A potential candidate for rotary kiln incineration at a temperature range of 820 to 1,600 degrees C and residence times of seconds for liquids and gases, and hours for solids. [110] Vinyl chloride is a waste chemical stream constituent which may be subjected to ultimate disposal by controlled incineration. Vinyl chloride is a waste chemical stream constituent which may be subjected to ultimate disposal by controlled incineration; preferably after mixing another combustible fuel. Care must be taken to assure complete combustion to prevent the formation of phosgene. An acid scrubber is necessary to remove the halo acids produced. [110] The following wastewater treatment technologies have been investigated for vinyl chloride: Biological treatment. [112] PRECAUTIONS FOR "CARCINOGENS": There is no universal method of disposal that has been proved satisfactory for all carcinogenic compounds and specific methods of chemical destruction published, have not been tested on all kinds of carcinogen-containing waste. The summary of available methods and recommendations given must be treated as a guide only. (Chemical Carcinogens) [56] Incineration, preferably after mixing with another combustible fuel. Care must be exercised to assure complete combustion to prevent the formation of phosgene. An acid scrubber is necessary to remove the halo acids produced. A variety of techniques have been described for vinyl chloride recovery from PVC polyvinyl chloride latexes. Recommendable method: Incineration. Peer-review: Vinyl chloride is a gas at normal temperatures and pressures and incineration may be difficult to arrange. (Peer-review conclusions of an IRPTC expert consultation (May 1985)) [100] HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. BOR 006742 Page 51 ADDITIONAL INFORMATION TSCA TEST SUBMISSIONS The ability of vinyl chloride (VC) to induce morphological transformation in the BALB/3T3 mouse cell line (Cell Transformation Assay) was evaluated. Based on preliminary toxicity determinations (exposure time=l day), VC was tested as a gas in an exposure chamber which contained VC in the medium at concentrations of 0, 4, 20, 100 and 250 ug/ml in the medium (corresponding to a measured concentration in the chamber of 0, 4.1 and 9.0, 69, 506 and 1024 ppm, respectively) with cell survival ranging from 92 percent to 47 percent for treated cells. VC clearly exhibited a statistically significant increase in transformation activity when compared with controls. [5] The effects of vinyl chloride were examined in the mouse hepatocyte primary culture/ONA repair assay. Based on preliminary toxicity tests, vinylchloride was tested at concentrations of 5, 10 and 15 percent and was found to be cytotoxic at the 15 percent concentration. Vinyl chloride was genotoxic at all concentrations tested. [84] The effects of vinyl chloride were examined in the rat hepatocyte primary culture/DNA repair assay. Based on preliminary toxicity tests, vinyl chloride was tested at concentrations of 5, 10 and 15 percent as a gas in a desiccator exposure chamber. The highest concentration was too toxic to be evaluated in the assay. The lower two concentrations were nontoxic but did cause a significant increase in the unscheduled DNA synthesis over untreated controls. [84] Chronic toxicity and oncogenicity were evaluated in groups of male and female Wistar rats (100/sex/group, except highest dose level, 50/sex/group) ingesting vinyl chloride (VC) in the diet at 0, 0.014, 0.13 and 1.3 mg vinyl chloride/kg body weight/day, which was available for 4 hours/day over the lifespan of the animals. There was a significant increase in the incidence of liver nodules suspected of being tumors in both sexes, especially in females, at the highest dose level. An increased incidence of foci of cellular alteration, neoplastic nodules, hepatocellular carcinomas, liver-cell polymorphism and cysts were observed at the highest dose level. Two females and one male developed a hepatic angiosarcoma, while none were observed in the other groups. Females exhibited a significant increase of basophilic foci of cellular alterations in the low and mid-dose levels, and the number of females in the mid-dose group bearing foci of cellular alteration was significantly increased. There were no significant differences between treated groups and controls in the following: body weight, hematology, or glutathione levels of the liver. [22] HEALTH AND ENVIRONMENT INTERNATIONAL, LTD BOR 006743 Page 52 SPECIAL REPORTS USEPA; Ambient Water Quality Criteria Document: Vinyl Chloride (1980) EPA 440/5-80-078. USEPA, Office of Drinking Water; Criteria Document (Draft): Vinyl Chloride (1983). Environment Canada; Tech Info for Problem spills: Vinyl Chloride (Draft) (1981). A review containing over 100 references of sampling and analytical methods for vinyl chloride in workplace atmosphere, ambient air, water, food, cigarette smoke, and polyvinyl chloride. Egan H et al, eds. Environmental Carcinogens Selected Methods of Analysis Volume 2, Vinyl Chloride (IARC Scientific Publications number 22) Lyon (1979). USEPA; Report on the Activities and Findings of the Vinyl Chloride Task Force (1974) EPA 560/4-74-001. Kluwe WM; The nephrotoxicity of low molecular weight halogenated alkane solvents, pesticides and chemical intermediates; Hook JB, ed Target Organ Toxicology Series: Toxicology of the Kidney p.179-226 (1981). Pers T, Pisarzewska E; Methods for the removal of vinyl chloride from waste gases during its synthesis and processing; Chemik 34 (11-12): 241-3 (1981). Machet de la Martini'ere N; Hepatic fibrosis and development of angiosarcoma following exposure to vinyl chloride; Universit'e de PariB V, Facult'e de M'edecine Necker-Enfants-Malades, Paris, France, 163 p. (1982). This medical thesis attempts to determine whether there is a sequential link between hepatic fibrosis and angiosarcoma. Pond SM; West J Med 137 (6): 506-14 (1982). Effects of workplace chemicals on the liver. Makarov IA; Gig Tr Prof Zabol 0 (11): 40-2 (1982). Effect of vinyl chloride on connective tissue is discussed. Malhotra VP, Saroop UK; Toxicity and Vinyl Chloride. Pop Plast 29 (2): 1720 (1984). The occupational hazard and toxicity exposure of vinyl chloride are reviewed including the occupational health hazard from vinyl chloride exposure and toxicity of vinyl chloride monomer. Duverger M et al; Metabolic Activation and Mutagenicity of 4 Vinyl Monomers (Vinyl chloride, Styrene, Acrylonitrile, Butadiene). Toxicol Eur Res 3 (3): 131-40 (1981). A review with 130 references on the metabolic activation and mutagenicity of vinyl chloride, styrene, acrylonitrile, and butadiene. Jedrychowski R, Chmielnicka J; Med Pr 36 (1): 31-41 (1985). Evaluation of the toxicity of vinyl chloride based on metabolism is discussed including review of absorption, distribution, occupational exposure. Wogan GN, Gorelick NJ; Chemical and Biochemical Dosimetry of Exposure to Genotoxic Chemicals. Environ Health Perspect 62: 5-18 (1985). Sharma RP; Immunol Consid Toxicol 1: 79-88 (1981). A review with 17 references on the immunol responses to vinyl chloride and other industrial chemicals. Suzuki T, Himeno S; Saishin Igaku 37 (12): 2355-61 (1982). A review with 47 references on dominant lethal mutations from vinyl chloride. Suzumura M; Rinsho Kensa 28 (11): 1437-40 (1984). A review with 5 references on the toxicity of vinyl chloride. Tamburro CH; Relationship of Vinyl monomers and Liver Cancers: Angiosarcoma and Hepatocellular Carcinoma. Semin Liver Dis 4 (2): 158-69 '1984). BOR 006744 HEALTH AND ENVIRONMENT INTERNATIONAL, LTD Page 53  Kilbey BJ; Environ Sci Res 24 (Comp Chem Mutagen): 857-81 (1981). A review with 75 references on the comparative mutagenicity of aflatoxin B1 and vinyl chloride. Nauman CH, Grant WF; Environ Sci Res 24 (Comp Chem Mutagen): 329-38 (1981). A review with 27 references on the mutagenicity of ethyl methanesulfonate, mitomycin C, and vinyl chloride in the Tradescantia test systems. DHHS/ATSDR; Toxicological Profile for Vinyl Chloride (8/89). USEPA; Health and Environmental Effects Profile for Chloroethene (1985) ECAO-CIN-P155. USEPA; Drinking water Criteria Document for Vinyl Chloride (1986) PB86- 118320. USEPA; Subst Risk Notice, 8EHQ-0680-0345 (1980). HEALTH AND ENVIRONMENT INTERNATIONAL, LTD. 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