CIBs are prepared by the staff of the Division of Standards Development and Technology Transfer, niosh (Robert A. Taft Laboratories, 4676 Columbia Parkway, Cincinnati, Ohio 45226). We welcome suggestions concerning the content, style, and distribution of these documents.
niosh estimates that more than 200,000 workers in the United States are potentially exposed to propylene oxide. Most workers are exposed to propylene oxide during its use as an intermediate in the manufacture of (1) polyols for urethane applications, (2) propylene glycol for polyester resins, and (3) propylene glycol ethers for solvents, coatings, and cleaning compounds. Propylene oxide is also increasingly considered as a substitute for ethylene oxide as a sterilant for medical equipment and a fumigant for foodstuffs.
The potential for propylene oxide to produce cancer in humans has not been determined. However, the results of studies in animals fulfill the criteria in the Occupational Safety and Health Administration (OSHA) Cancer Policy [Title 29 of the Code of Federal Regulations, Section 1990.112] for classifying a substance as a potential occupational carcinogen. niosh therefore recommends that propylene oxide be regarded as a potential occupational carcinogen and that occupational exposure be reduced to the lowest feasible concentration.
niosh recommends that producers and users of propylene oxide disseminate this information to their workers and customers, that professional and trade associations and unions inform their members of the potential hazards of working with propylene oxide, and that appropriate engineering controls work practices be used to minimize the exposure of workers. Readers seeing more led information on the studies cited in this CIB are urged to consult the original publications.
[signature] J. Donald Millar, M.D., D.T.P.H. (Lond.) Assistant Surgeon General Director, National Institute for Occupational Safety and Health Centers for Disease Control |
The National Institute for Occupational Safety and Health (niosh) estimates that approximately 209,000 U.S. workers are occupationally exposed to propylene oxide [niosh 1983]. An industrial hygiene study conducted at a propylene-oxide-producing plant in the United States found time-weighted average (TWA) exposures to propylene oxide ranging from 0.2 to 2.0 ppm. Peak air concentrations ranged from 10 to 3,800 ppm, with the highest exposures occurring during maintenance operations [Flores 1983].
Other data on occupational exposures to propylene oxide have been reported from a large chemical manufacturing facility that produced more than 200 chemical products, including derivatives of propylene oxide. Propylene oxide was detected in only one of seven personal samples collected at one worksite. That sample contained 1.5 ppm and was obtained for an operator in an area where flexible polyols were produced [Oser et al. 1978].
In a similar study, occupational exposure to propylene oxide was evaluated at three production areas of another large chemical manufacturing facility that produced derivatives of propylene oxide. Worker exposures were reported to range from 0.2 to 2.5 ppm in the polymer polyol and oxide adduct production areas. With an analytical limit of 0.01 mg per sample, propylene oxide was not detected in any samples collected in the flexible polyol production area [Oser et al. 1979].
The American Conference of Governmental Industrial Hygienists (ACGIH) threshold limit value (TLV®) for propylene oxide is 20 ppm (50 mg/m3) as an 8-hr TWA [ACGIH 1988]. The ACGIH TLV is based on the acute toxicity of propylene oxide and its "lesser toxicity in relation to ethylene oxide" [ACGIH 1986a].
Chemical and Physical Properties of Propylene Oxide*
Item | Description |
CAS** registry number | 75-56-9 |
RTECS*** accession number | TZ2975000 |
Synonyms | Epoxypropane 1,2-epoxypropane Methyl ethylene oxide Methyloxirane Propene oxide Propylene epoxide 1,2-propylene oxide |
Molecular formula | C3H6O |
Structural formula | |
Molecular weight | 58.08 |
Flash point | -30°C (-22°F) |
Color | Colorless |
Odor | Ether-like, sweet, alcoholic |
Boiling point | 34.2°C (93.6°F) at 760 mm Hg |
Freezing point | -112°C (-169.6°F) |
Vapor pressure | 445 mm Hg at 20°C (68°F) |
Vapor density | (Air = 1) 2.0 |
Specific gravity | 0.826 at 25°C |
Flammability limits | 2.1% to 38.5% by volume in air |
Odor threshold | 200 ppm |
Solubility | 59% by wt in water at 25°C; miscible with acetone, benzene, carbon tetrachloride, ether, and methanol |
Propylene oxide has been shown to be mutagenic in Bacillus subtilis, yeast, and Drosophila melanogaster. Exposure to propylene oxide vapor caused increased sex-linked recessive lethal mutations in two germ-cell stages of D. melanogaster.
Propylene oxide induced DNA damage (single-strand breaks) in rat hepatocytes and chromosomal aberrations (chromatid gaps, chromosomal gaps, breaks, and fragments) in rat liver cells and human lymphocytes. Dominant, lethal mutations were not induced in mice [Bootman et al. 1979] or rats [Hardin et al. 1983]. Mouse sperm-head morphology examinations following propylene oxide exposure did not reveal an increase in abnormal forms [Hardin et al. 1983].
Lynch et al. [1984b] exposed groups of 12 cynomologus monkeys to 0 (filtered air), 100, of 300 ppm of propylene oxide for 7 hr/day, 5 days/week over a 2-year period. Blood was collected during the final month of exposure and used to culture lymphocytes to assay sister chromatid exchanges (SCEs) and chromosomal aberrations. The incidence of SCEs; or chromosomal aberrations was not significantly altered compared with the control group.
Acute Toxicity of Propylene Oxide for
Various Animal Species and Routes of
Administration
Species | Route | Acute toxicity (LD50/LC50) | References |
Rat | Oral | 1,140 mg/kg | Smyth et al. 1941 |
Guinea pig | Oral | 690 mg/kg | Smyth et al. 1941 |
Rat | Inhalation | 9,486 mg/m3 | Jacobson et al. 1956 |
Mouse | Inhalation | 4,126 mg/m3 | Jacobson et al. 1956 |
Rabbit | Dermal | 1.5 ml/kg | Weil et al. 1963 |
Summary of Positive Mutagenic Responses to
Propylene Oxide
Mutation | Organism | References |
Reverse mutation (base-pair substitutions) | Escherichia coli | McMahon et al. 1979 Bootman et al. 1979 Hemminki et al. 1980 Dean et al. 1985 |
Salmonella typhimurium TA1535, TA100 | Wade et al. 1978 Bootman et al. 1979 McMahon et al. 1979 | |
Bacillus subtilis | Phillips et al. 1980 Bootman et al. 1979 | |
Forward mutation | Schizosaccharomyces pombe | Migliore et al. 1982 |
Bacillus subtilis phage ø 105 | Garro and Phillips 1980 | |
Sex-linked recessive lethal mutation | Drosophila melanogaster | Hardin et al. 1983 |
DNA damage (single-strand breaks) | Rat hepatocytes | Sina et al. 1983 |
Chromosome damage | Human lymphocytes Epithelial rat liver | Bootman et al. 1979 Dean and Hodson-Walker 1979 |
The National Toxicology Program (NTP) has completed a bioassay to determine the carcinogenicity of propylene oxide in F344/N rats and B6C3F1 mice [NTP 1985]. Groups of 50 animals of each sex and species were exposed to propylene oxide (greater than 99.9% pure) by inhalation at concentrations of 0 (chamber control), 200, or 400 ppm for 6 hr/day, 5 days/week for a period of 103 weeks. The survival rate of the exposed rats was comparable with that of the controls; however, the survival rate for the mice was lower than that of the controls. Rats and mice exposed at 400 ppm had lower terminal body weights than controls [NTP 1985].
In both rats and mice, the primary tissue affected by inhalation of propylene oxide was the respiratory epithelium of the nasal turbinates. Suppurative inflammation, epithelial hyperplasia, and squamous metaplasia occurred in male and female rats in a concentration-related manner. Papillary adenoma of the nasal turbinate epithelium and underlying submucosal glands were observed in 3/50 female rats and 2/50 male rats exposed at 400 ppm. These tumors were not observed in the control group or in animals exposed at 200 ppm. The NTP Peer Review Panel concluded that under the conditions of these studies there was "some evidence of carcinogenicity" for F344/N rats, as indicated by the increased incidence of papillary adenomas of the nasal turbinates in the male and female rats exposed at the higher concentration (400 ppm) [NTP 1985].
Inflammation of the respiratory epithelium was observed in a concentration-related pattern among male and female mice exposed to propylene oxide. One squamous-cell carcinoma and one papilloma were found in the nasal cavities of male mice exposed at 400 ppm, and two adenocarcinomas were seen in the nasal cavities of female mice exposed at 400 ppm. In addition, nasal cavity hemangiomas were observed in 5/50 male and 3/50 female mice exposed at 400 ppm, and hemangiosarcomas were observed in 5/50 males and 2/50 females. The increased incidences of hemangiomas and hemangiosarcomas in males were statistically significant (p=0.028, Fisher exact tests). Because of the rarity of these vascular tumors in the B6C3F1 strain, the NTP Peer Review Panel concluded that under the conditions of these studies, there was "clear evidence of carcinogenicity" for male and female B6C3F1 mice [NTP 1985].
In a study by Lynch et al. [1984a], groups of 80 male Fischer 344 rats were exposed to propylene oxide (98% pure) at concentrations of 0 (filtered air), 100, and 300 ppm (0, 237, and 711 mg/m3) for 7 hr/day, 5 days/week over a period of 104 weeks. The survival rates for the two exposed groups were lower than those for the controls. Rats exposed to propylene oxide at 100 and 300 ppm had an increased incidence of inflammatory lesions of the respiratory system and a dose-dependent increase of complex epithelial hyperplasia in the nasal cavity. Two rats exposed at 300 ppm developed nasal cavity adenomas. Statistically significant (P<0.05) increases occurred in the incidences of adrenal phaeochromocytomas in the propylene-oxide-exposed rats (25/78 at 100 ppm and 22/80 at 300 ppm compared with 8/78 at 0 ppm). Increases also occurred in the incidences of peritoneal mesotheliomas (8/78 at 100 ppm and 9/80 at 300 ppm compared with 3/78 for the controls). All rat groups were affected by an outbreak of Mycoplasma pulmonis infection, which occurred about 16 months into the study. Both the infection and the propylene oxide exposure affected the survival of rats in this study. Although the proliferative lesions of the nasal mucosa appeared to be treatment-related, the authors could not ascertain how their development was influenced by the intercurrent inflammatory disease [Lynch et al. 1984a].
Reuzel and Kuper [1983] exposed groups of 100 Wistar rats of each sex to propylene oxide at concentrations of 0 (filtered air), 30, 100, or 300 ppm (71, 238. or 713 mg/m3) for 6 hr/day, 5 days/week over a period of 28 months. Ten rats of each sex from each exposure group were killed for examination after 12, 18, or 24 months of exposure. Body weight reduction, increased mortality, hyperplasia of the mucosa, and degeneration of the olfactory epithelium were found in the male and female animals exposed at 300 ppm. Female rats exposed at 300 ppm had a higher incidence (P<0.05, chi-square test) of myocardial degeneration than did the controls (10/69 at 300 ppm compared with 3/69 for the controls). Females exposed at 30 or 100 ppm showed an increased number of fibroadenomas of the mammary glands, but the number of fibroadenoma-bearing animals did not increase compared with controls. However, for females exposed at 300 ppm, a statistically significant increase was reported in the number of rats with two or more fibroadenomas and in the number of fibroadenoma-bearing animals (Table 4). Compared with the controls, female rats exposed to propylene oxide had a statistically significant increase in the incidence of malignant mammary tumors. However, this incidence did not exceed the historical control incidences (0% to 15%) derived from six different long-term studies by the same laboratory on the same strain of rats. The number of females with benign mammary tumors and the mean number of fibroadenomas per fibroadenoma-bearing animal were both higher than the historical control data. No significant increase occurred in the incidence of any specific type of tumor other than mammary tumors in exposed Wistar rats compared with controls. However, the total incidence of all tumors other than mammary tumors was significantly increased (p<0.01) in the females exposed at 300 ppm compared with controls. In the male mid female rats exposed at 300 ppm, the total number of animals bearing malignant tumors other than mammary tumors was significantly higher than in controls (p<0.05 in males and p<0.01 in females, chi-square test) [Reuzel and Kuper 1983]. The authors questioned whether the observed effects on the mammary glands and the increase in total tumor incidence were due to the direct action of propylene oxide or to some indirect mechanism. They concluded that propylene oxide enhances the development of malignant neoplasms through an indirect, non-specific mechanism.
Incidence of Mammary Tumors in Female Wistar Rats Exposed to Propylene Oxide by Inhalation for 28 Months*
Propylene oxide concentration (ppm) | ||||
Item | 0 | 30 | 100 | 300 |
Number of rats with benign mammary tumors | 32/69 | 30/71 | 39/69 | 47/70** |
Mean number of fibroadenomas per fibroadenoma-bearing animal | 1.3 | 2.1 | 2.2 | 2.4*** |
Number of rats with malignant mammary tumors | 3/69 | 6/71 | 5/69 | 8/70 |
Oral Administration
Dunkelberg [1982] administered 15 or 60 mg of propylene oxide (99% pure) per kg of body weight in salad oil by gavage to groups of 50 female Sprague-Dawley rats 2 times/week for 150 weeks. Control groups consisted of 50 untreated female rats and 50 female rats dosed with salad oil. Survival rates for rats treated with propylene oxide were not statistically different from those of the controls. Treated animals developed hyperplasia, hyperkeratosis, or papillomas of the forestomach (incidence rates were 7/50 at the 15-mg/kg dose and 17/50 at the 60-mg/kg dose) [Dunkelberg 1982]. Squamous-cell carcinomas of the forestomach developed in a dose-dependent manner in rats treated with propylene oxide (incidence rates were 0/50 for controls, 2/50 at the 15-mg/kg dose, and 19/50 at the 60-mg/kg dose). The first of these tumors was observed during the 79th week in the high-dose group. One additional animal in the 60-mg/kg group had an adenocarcinorna.
Subcutaneous Administration
Dunkelberg [1981] injected groups of 100 female NMRI mice subcutaneously with 0.1, 0.3, 1.0, or 2.5 mg of 99% pure propylene oxide (in 0.1 ml tricaprylin) once/week for 95 weeks. Control groups consisted of 200 untreated female mice and 200 female mice injected with 0.1 ml tricaprylin (i.e., the vehicle control group). A dose-related increase in cancers (mostly fibrosarcomas) occurred at the injection site. The incidences of sarcomas (fibrosarcomas and pleomorphic sarcomas) at propylene oxide injection sites were 3/100 at 0.1 mg, 2/100 at 0.3 mg, 12/100 at 1.0 mg, and 15/100 at 2.5 mg. Four fibrosarcomas were observed in the vehicle control group, and no sarcomas were observed in the untreated control group [Dunkelberg 1981].
Twenty-three workers aged 25 to 59 were exposed to propylene oxide in a factory producing alkylated starch. Lymphocytes from these workers were examined for a reduced capacity for unscheduled DNA synthesis following the in vitro induction of DNA damage to their lymphocytes [Pero et al. 1982]. Unscheduled DNA synthesis is a step in the enzymatic repair of DNA damage. Estimates of airborne exposure were obtained using both personal and area sampling. Eight-hour TWA exposure concentrations of propylene oxide were calculated for five of the most highly exposed workers over 5 workdays (8-hr shifts). These concentrations ranged from 0.6 to 12 ppm. The control group consisted of 12 workers aged 21 to 46 who were not exposed to propylene oxide. Under the conditions of this experiment, unscheduled DNA synthesis was significantly inhibited (p<0.001, t-test) in the group exposed to propylene oxide.
Exposure to Propylene oxide has been shown to produce cancer and benign tumors in both rats and mice. niosh therefore recommends that propylene oxide be considered a potential occupational carcinogen in conformance with the OSHA Cancer Policy. The excess cancer risk for workers exposed to propylene oxide has not yet been established, but the probability of developing cancer should be decreased by minimizing exposure. As a matter of prudent public health policy, employers should assess the conditions under which workers may be exposed to propylene oxide and take reasonable precautions (such as appropriate engineering and work practice controls) to reduce exposures to the lowest feasible concentrations.
The niosh Occupational Exposure Sampling Strategy Manual [Leidel et al. 1977] provides guidance for developing effective strategies to monitor worker exposures to toxic chemicals. The manual contains information on determining the need for exposure monitoring, the number of samples to be collected, and the appropriate sampling times.
Product Substitution
When feasible, employers should substitute a less hazardous material for propylene oxide. However, extreme care must be used when selecting substitutes. Possible adverse health effects from exposure to the substitute should be evaluated before selection.
Closed Systems and Ventilation
Engineering controls should be the principal method for reducing propylene oxide exposure in the workplace. Achieving and maintaining reduced concentrations of airborne propylene oxide depend on adequate engineering controls such as closed-system operations and ventilation systems that are properly constructed and maintained.
Closed-system operations provide the most effective means for minimizing worker exposures to propylene oxide. Closed systems should be used for producing, storing, transferring, packaging, and processing propylene oxide. For quality control laboratories or laboratories where production samples are prepared for analyses, exhaust ventilation systems should be designed to capture and contain vapors.
One company has developed techniques that allow for the maintenance of a closed system while process and tank car samples of propylene oxide are obtained and analyzed for quality control. These automated techniques have virtually eliminated the need for manual sampling and have reportedly been successful in reducing exposures [Flores 1983]. Guidance for designing local exhaust ventilation systems can be found in Recommended Industrial Ventilation Guidelines [Hagopian and Bastress 1976], Industrial Ventilation--A Manual of Recommended Practice [ACGIH 1986b], and Fundamentals Governing the Design and Operation of Local Exhaust Systems [ANSI 1979].
Worker Isolation
The area in which propylene oxide is produced or used should be restricted to workers who are essential to the process or operation. If feasible, these workers should be isolated from direct contact with propylene oxide by use of automated equipment operated from a closed control booth or room. This room should be maintained at greater air pressure than that surrounding the process equipment so that air flows out rather than in. When workers must enter the general work area to perform process checks, adjustments, maintenance, assembly line tasks, and related operations, they should take special precautions such as the use of personal protective equipment.
Personal Protective Equipment
Chemical Protective Clothing and Equipment.--To minimize skin contact and absorption, workers using propylene oxide should wear appropriate chemical protective clothing (CPC) such as gloves and aprons. CPC made from butyl rubber and Teflon® should provide adequate protection for at least 1 hr [Schwope et al. 1985]. Note, however, that the quality of gloves may vary significantly among glove producers [Mickelsen and Hall 1987]. Product-specific chemical permeation data should therefore be obtained from the glove manufacturer. Splashproof goggles or face shields should be worn if there is any possibility that liquid propylene oxide will contact the eyes. Safety showers and eye wash stations should be located close to operations that involve propylene oxide.
Respiratory Protective Devices.--The use of respirators is the least desirable method of controlling worker exposures and should not be used as the primary control method during routine operations. However, niosh recognizes that respirators may be required to provide protection in certain situations such as implementation of engineering controls, certain short-duration maintenance procedures, and emergencies. niosh maintains that only the most protective respirators should be used for situations involving carcinogens. These respirators include:
Decontamination and Waste Disposal
If propylene oxide contacts the skin, promptly wash the contaminated area with soap or a mild detergent and water.
The following steps should be taken in the event of a propylene oxide spill [Mackison et al. 1981]:
A medical monitoring program should be established for prevention or early detection of the acute, chronic, or carcinogenic effects of propylene oxide. Medical and work histories (including previous exposure to propylene oxide or other toxic agents) should be taken for each worker before job placement and updated periodically. The worker's physician should be given information on the adverse health effects of propylene oxide exposure and an estimate of the worker's potential for exposure. This information should include results of workplace sampling and a description of any protective devices or equipment the worker is required to use. The examining physician should direct particular attention to the skin and to the nasal and respiratory tracts, as these sites are the most likely to be affected by propylene oxide. The occurrence of disease or other work-related health effects requires immediate evaluation of primary preventive measures (e.g., industrial hygiene monitoring, engineering controls. and personal protective equipment). Medical personnel should ensure that workers are informed of the health effects associated with propylene oxide exposure.
ACGIH [1986b]. Industrial ventilation: A manual of recommended practice. 19th ed. Cincinnati, OH: American Conference of Governmental Industrial Hygienists.
ACGIH [1988]. TLV®s : threshold limit values and biological exposure indices for 1988-1989. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, p. 31.
ANSI [1979]. American national standard fundamentals governing the design and operation of local exhaust systems. New York, NY: American National Standards Institute, Inc., ANSI Z9.2-1979.
Bootman J, Lodge DC, Whalley HE [1979]. Mutagenic activity of propylene oxide in bacterial and mammalian systems. Mutat Res 67:101-112.
CFR [1988]. Code of Federal Regulations. Washington, DC: U.S. Government Printing Office, Office of the Federal Register.
Dean BJ, Hodson-Walker G [1979]. An in vitro chromosome assay using cultured rat-liver cells. Mutat Res 64:329-337.
Dean BJ, Brooks TM, Hodson-Walker G, Hutson DH [1985]. Genetic toxicology testing of 41 industrial chemicals. Mutat Res 153:57-77.
Dunkelberg H [1981]. Carcinogenic activity of ethylene oxide and its reaction products, 2-chloroethanol, 2-bromoethyl ethylene glycol, and diethylene glycol. I. Carcinogenicity of ethylene oxide in comparison with 1,2-propylene oxide after subcutaneous administration in mice (in German). Zentralbl Bakteriol Mikrobiol Hyg Abt I Orig B 174:348-404.
Dunkelberg H [1982]. Carcinogenicity of ethylene oxide and 1,2-propylene oxide upon intragastric administration to rats. Br J Cancer 46:924-933.
Flores GH [1983]. Controlling exposure to alkylene oxides. Chem Eng Prog 79:39-43.
54 FR 2.641 [1989]. Occupational Safety and Health Administration: Air contaminants; final rule. To be codified at 29 CFR 1910.
Garro AJ, Phillips RA [1980]. Detection of mutagen-induced lesions in isolated DNA by marker rescue of Bacillus subtilis phage ø 105. Mutat Res 73:1-13.
Hagopian JH, Bastress EK [1976]. Recommended industrial ventilation guidelines. Cincinnati, OH: U.S. Department of Health, Education, and Welfare, Public Health Service, Center for Disease Control, National Institute for Occupational Safety and Health, DHEW (niosh) Publication No. 76-162.
Hardin BD, Schuler RL, McGinnis PM, Niemeier RW, Smith RJ [1983]. Evaluation of propylene oxide for mutagenic activity in three in vivo test systems. Mutat Res 117:337-344.
Hemminki K, Falck K, Vainio H [1980]. Comparison of alkylation fates and mutagenicity of directly acting industrial and laboratory chemicals. Arch Toxicol 46:277-285.
Hine C, Rowe VK, White ER, Darmer KI Jr, Youngblood GT [1981]. Epoxy compounds. In: Patty's Industrial hygiene and toxicology. 3rd ed. Vol. 2A, Chapter 32. New York, NY: Interscience Publishers.
IARC [1976]. IARC monographs on the evaluation of carcinogenic risk of chemicals to man: Cadmium, nickel, some epoxides, miscellaneous industrial chemicals and general considerations on volatile anesthetics. Vol. 11. Lyon, France: World Health Organization, International Agency for Research on Cancer.
IARC [1985]. IARC Monographs on the evaluation of carcinogenic risk of chemicals to humans: Allyl compounds, aldehydes, epoxides, and peroxides. Vol. 36. Lyon, France: World Health Organization, International Agency for Research on Cancer.
Jacobson KH, Hackley EB, Feinsilver RL [1956]. The toxicity of inhaled ethylene oxide and propylene oxide vapors. Arch Indust Health 13:237-244.
Jensen O [1981]. Contact allergy to propylene oxide and isopropyl alcohol in a skin disinfectant swab. Contact Dermatitis 7:148-150.
Kirk RO, Dempsey TS [1982]. Propylene oxide. In: Grayson M. Eckroth D, eds. Kirk-Othmer encyclopedia of chemical technology. Vol. 19. 3rd ed. New York, NY: John Wiley & Sons, Inc., pp 246-74.
Leidel NA, Busch KA, Lynch JR [1977]. Occupational exposure sampling strategy manual. Cincinnati, OH: U.S. Department of Health, Education, and Welfare, Public Health Service, Center for Disease Control, National Institute for Occupational Safety and Health, DHEW (niosh) Publication No. 77-173, NTIS No. PB-274-792/A07.
Lynch DW, Lewis TR, Moorman WJ, Burg JR, Groth DH, Khan A, Ackerman LJ, Cockrell BY [1984a]. Carcinogenic and toxicologic effects of inhaled ethylene oxide and propylene oxide in F344 rats. Toxicol Appl Pharmacol 76:69-84.
Lynch DW, Lewis TR, Moorman WJ, Burg JR, Gulati DK, Kaur P, Sabharwal PS [1984b]. Sister-chromatid exchanges and chromosome aberrations in lymphocytes from monkeys exposed to ethylene oxide and propylene oxide by inhalation. Toxicol Appl Pharmacol 77:85-95.
Mackison FW, Stricoff RS, Partridge LJ, Jr., eds. [1981]. niosh/OSHA occupational health guidelines for chemical hazards. Occupational safety and health guideline for propylene oxide. Cincinnati, OH: U.S. Department of Health and Human Services, Centers for Disease Control, National Institute for Occupational Safety anti Health, DHHS (niosh) Publication No. 81-123.
McLaughlin RS [1946]. Chemical bums of the human cornea. Am J Ophthalmol 29:1355-1362.
McMahon RE, Cline JC, Thompson CZ [1979]. Assay of 855 test chemicals in ten tester strains using a new modification of the Ames test for bacterial mutagens. Cancer Res 39:682-6693.
Mickelsen RL, Hall RC [1987]. A breakthrough time comparison of nitrile and neoprene glove materials produced by different glove manufacturers. Am Ind Hyg Assoc J 48(11):941-947.
Migliore L, Rossi AM, Lopriene N [1982]. Mutagenic action of structurally related alkane oxides on Schizosaccaromyces pombe: The influence, in vitro, of mouse-liver metabolizing system. Mutat Res 102:425-437.
niosh [1983]. National occupational exposure survey, 1981-83: actual observation and trade-named exposure to propylene oxide. Cincinnati, OH: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control, National Institute for Occupational Safety and Health, Division of Surveillance, Hazard Evaluation and Field Studies, Surveillance Branch. Unpublished data base.
niosh [1985]. Manual of analytical methods. 3rd ed. Vol. 2, Method No. 1612. Cincinnati, OH: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control, National Institute for Occupational Safety and Health.
niosh [1987a]. Guide to industrial respiratory protection. Morgantown, WV: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control, National Institute for Occupational Safety and Health, DHHS (niosh) Publication No. 87-116.
niosh [1987b]. niosh certified equipment list. Cincinnati, OH: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control, National Institute for Occupational Safety and Health, DHHS (niosh) Publication No. 88-107.
niosh [1987c]. niosh respirator decision logic. Cincinnati, OH: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control, National Institute for Occupational Safety and Health, DHHS (niosh) Publication No. 87-116.
niosh [1988]. Testimony of the National Institute for Occupational Safety and Health on the Occupational Safety and Health Administration's Proposed Rule on Air Contaminants, 29 CFR Part 1910, Docket No. H-020. Presented at the OSHA informal public hearing, August 1, 1988. niosh policy statements. Cincinnati, OH: U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control, National Institute for Occupational Safety and Health.
NTP [1985]. Toxicology and carcinogenesis studies of propylene oxide in F344/N rats and B6C3F1 mice (inhalation studies). Research Triangle Park, NC: National Toxicology Program, NTP 83-020.
Oser J, Crandall M, Phillips R, Marlow D [1978]. Indepth industrial hygiene report of ethylene oxide exposure at Union Carbide Corporation, Institute, West Virginia. Springfield, VA: National Technical Information Service, NTIS No. PB-82-14786, pp. 14, 15 and 22.
Oser J, Young M, Boyle T, Marlow D [1979]. Indepth industrial hygiene report of ethylene oxide exposure at Union Carbide Corporation, South Charleston, West Virginia. Springfield, VA: National Technical Information Service, NTIS No. PB-82-110024, pp. 6 and 13.
Pero RW, Bryngelsson T, Widegren B, Hogstedt B, Welinder H [1982]. A reduced capacity for unscheduled DNA synthesis in lymphocytes from individuals exposed to propylene oxide and ethylene oxide. Mutat Res 104:193-200.
Pfeiffer EH, Dunkelberg H [1980]. Mutagenicity of ethylene oxide and propylene oxide and of the glycols and halohydrins formed from them during the fumigation of foodstuffs. Food Cosmet Toxicol 18:115-118.
Phillips RA, Zahler SA, Garro AJ [1980]. Detection of mutagen-induced lesions in isolated DNA using a new Bacillus subtilis transformation-based assay. Mutat Res 74:267- 281.
Reuzel PGJ, Kuper CF [1983]. Chronic (28-month) inhalation toxicity/carcinogenicity study of 1,2-propylene oxide in rats; final report. Zeist, The Netherlands: TNO, Division of Nutrition and Food Research, Report No. V82.215/280853.
Rowe VK, Holingsworth RL, Oyen F, McCollister DD, Spencer HC [1956]. Toxicity of propylene oxide determined on experimental animals. Arch Ind Health 13:228-236.
Schwope AD, Costas PP, Jackson JO, Weitzman DJ [1985]. Guidelines for the selection of chemical protective clothing. 3rd ed. Vol. 11. Technical and reference manual. Cincinnati, OH: American Conference of Governmental Industrial Hygienists, Publication No. 0460.
Sina JF, Bean CL, Dysart GR, Taylor VI, Bradley MO [1983]. Evaluation of the alkaline elution/rat hepatocyte assay as a predictor of carcinogenic/mutagenic potential. Mutat Res 113:357-391.
Smyth HF, Seaton J, Fisher L [1941]. The single dose toxicity of some glycols and derivatives. J Ind Hyg Toxicol 23:259- 268.
USITC [1981]. Synthetic organic chemicals, United States Production and Sales 1980. Washington. DC: U.S. International Trade Commission, USITC Publication 1183.
van Ketel WG [1979]. Contact dermatitis from propylene oxide. Contract Dermatitis 5:191-192.
Wade DR, Airy SC, Sinsheimer JE [1978]. Mutagenicity of aliphatic epoxides. Mutat Res 58:217-223.
Weil CS, Condra N, Haun C, Striegel JA [1963]. Experimental carcinogenicity and acute toxicity of representative epoxides. Am Ind Hyg Assoc J 24:305-325.
WHO [1985]. Environmental Health Criteria 56: Propylene oxide. Geneva, Switzerland: World Health Organization.
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