United States
Environmental Protection
Agency
Pollution Prevention
and Toxics
(7407)
February 1995
EPA749-F-95-010a
&EPA OPPT Chemical Fact Sheets
1, 4-Dioxane Fact Sheet:
Support Document (CAS No. 123-9-1)
This summary is based on information retrieved from a systematic search limited to secondary sources (see Appendix
A). These sources include online databases, unpublished EPA information, government publications, review
documents, and standard reference materials. The literature search was done in February of 1995. No attempt has
been made to verify information in these databases and secondary sources.
I. CHEMICAL IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES
The chemical identity and physical/chemical properties of 1,4-dioxane are summarized in Table 1.
Characteristic/Property
Data
Reference
CAS No.
Common Synonyms
Molecular Formula
Chemical Structure
Physical State
Molecular Weight
Melting Point
Boiling Point
Water Solubility
Density
Vapor Density (air = 1)
KOC
Log Kom
Vapor Pressure
Reactivity
Flash Point
Henry's Law Constant
Log Bioconcentration Factor
Odor Threshold
Conversion Factors
123-91-1
1,4-diethylene oxide
C4H802
flammable liquid,
faint pleasant odor
88.10
11.80°C
101.1 "Cat 760 mm Hg
soluble in water
1.0329g/mLat20°C
3.03
1.23
-0.27
30 mm Hg at 20°C
Tends to form explosive peroxides,
especially when anhydrous
5-18°C
4.88 x 10-6atm-m3/mol
-0.44, calculated
9.8mg/m3(2.7ppm)
1 mg/m3 = 0.278 ppm;
1 ppm = 3.6 mg/m3
Budavari et al. 1989
Budavarietal. 1989
Budavari etal. 1989
Budavari etal. 1989
Budavari etal. 1989
Budavari etal. 1989
Budavari etal. 1989
Keith and Walters 1985
Verschueren 1983
Howard 1990
Howard 1990
Verschueren 1983
Budavari etal. 1989
Budavarietal. 1989
Howard 1990
CHEMFATE 1994
Verschueren 1983
Verschueren 1983
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II. PRODUCTION, USE, AND TRENDS
A. Production
In 1992, there were three producers of 1,4-dioxane in the United States: Ferro Corporation, Dow Chemical,
and Stepan Co. Dow Chemical was also an importer of 1,4-dioxane in 1992 (U.S. EPA
1987-92). In 1990, the total U.S. production volume of 1,4-dioxane was between 10,500,000 and 18,300,000 pounds
(U.S. EPA 1995a). No information on the current capacities of individual producers is available.
Table 2 Producers of 1,4-Dioxane and Plant Sites 1992
Company Name
Ferro Corp.
Dow Chemical Corp.
Stepan Chemical Co.
Plant Site
Zachary, LA
Plaquemine, LA
Elwood, IL
Plant Capacity
NA
NA
NA
Source: U.S. EPA 1987-1992
NA: Not available
B.
Uses
In 1985, 90 percent of 1,4-dioxane produced in the U.S. was used as a stabilizer for chlorinated solvents such
as 1,1,1-trichloroethane (HSDB 1995). Although this application continues to be the primary one, it is quickly
being phased out (Ferro Corp. 1995). In the future, the primary use of 1,4-dioxane will be as a solvent for
various applications, primarily in the manufacturing sector. Other solvent applications include those for
cellulose acetate, dyes, fats, greases, lacquers, mineral oil, paints, resins, varnishes, and waxes. 1,4-Dioxane
is also used in paint and varnish strippers, as a wetting agent and dispersing agent in textile processing, dye
baths, stain and printing compositions, and in the preparation of histological slides. Additionally, 1,4-dioxane
is used in cosmetics, deodorants, fumigants, automotive coolant liquid, and scintillation counters (Chemical
Marketing Reporter 1988; Sax and Lewis 1993; Sittig 1991; USITC 1994).
C.
Trends
The total U.S. production volume of 1,4-dioxane for 1982 was estimated at 15 million pounds, up from 12
million pounds reported in 1977. No recent information on production and demand is available.
ENVIRONMENTAL FATE
B.
Environmental Release
Of the total 1.13 million pounds of 1,4-dioxane released into the U.S. environment in 1992, as
reported to the Toxics Release Inventory by certain types of U.S. industries, 680 thousand pounds
were released into the atmosphere, 450 thousand pounds were released into surface waters, and 33
hundred pounds were released onto the land (TRI92 1994). 1,4-Dioxane at a concentration of 1
microgram/L has been detected in drinking water in the U.S., (no specific locations given); the
chemical was detected in 37% of well water samples collected near a solid waste landfill located 60
miles southwest of Wilmington, DE. 1,4-Dioxane at 1 microgram/L was detected in the Chicago
Sanitary and Ship Channel. In 1981, 51% of air samples from three urban New Jersey sites were
positive for 1,4-dioxane with mean concentrations ranging from 0.01-0.02 ppb. Only 20% of samples
from the same sites were positive in 1982 with a geometric mean concentration of 0-0.01 ppb
(Howard 1990).
Transport
The low estimated soil-sorption coefficient (Koc), indicates that 1,4-dioxane should readily leach to
ground water. The estimated Henry's Law constant suggests that volatilization from moist soils will
be slow. Based on its vapor pressure, volatilization from dry soils should be fast. 1,4-Dioxane is not
expected to adsorb significantly to suspended sediments (Howard 1990).
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C. Transformation/Persistence
1. Air — 1,4-Dioxane in the atmosphere is expected to degrade fairly quickly. The half-life of
the reaction of 1,4-dioxane with photochemically produced hydroxyl radicals in the
atmosphere was estimated to be 6.7-9.6 hours. Experimental results of sunlight-irradiated
mixtures of 1,4-dioxane/NO suggest similar half-lives (Howard 1990).
2. Soil — No adsorption data are available, but the low estimated log soil-sorption coefficient
(Koc) suggests that 1,4-dioxane should readily leach to ground water. No data concerning the
volatilization of 1,4-dioxane are available, but the estimated Henry's Law constant suggests
that volatilization from moist soils will be slow; however, based on its vapor pressure,
volatilization from dry soils should be fast. 1,4-dioxane is not expected to biodegrade in soil
(Howard 1990).
3. Water — No hydrolysis data on 1,4-dioxane are available. Because ethers in general have
been classified as generally resistant to hydrolysis, 1,4-dioxane is not expected to hydrolyze
significantly. The estimated Henry's Law constant for 1,4-dioxane and its miscibility in
water suggest that volatilization will be slow. From its estimated Koc, 1,4-dioxane is not
expected to significantly adsorb to suspended sediments. 1,4-Dioxane is not expected to
biodegrade in water (Howard 1990).
4. Biota — Based on its log P, 1,4-Dioxane is not expected to bioconcentrate in fish (Howard
1990).
IV. HEALTH EFFECTS
A. Pharmacokinetics
1. Absorption — No specific information on the absorption of 1,4-dioxane was found in the
secondary sources searched. However, systemic toxicity has been observed following oral,
inhalation and dermal exposure, indicating that absorption occurs by these routes.
2. Distribution — No specific information on the distribution of 1,4-dioxane was found in the
secondary sources searched.
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3. Metabolism — The major urinary metabolite of 1,4-dioxane is p-hydroxyethoxyacetic acid,
as determined in studies with rats and with human volunteers and dioxane plant personnel
(Rowe and Wolf 1982). A second minor urinary metabolite may be diethylene glycol. There
is evidence that high doses of 1,4-dioxane can improve the body's ability to metabolize it.
One study showed that 1000 mg/kg/day, but not 10 mg/kg/day, caused more rapid excretion
of metabolites, and that the 1000 mg/kg/day doses increased the capacity of the rat to
metabolize 1,4-dioxane by 62-fold (Rowe and Wolf 1982).
During an epidemic logic study, urine samples of 5 workers exposed to <32 ppm 1,4-dioxane
for up to 5 years, were analyzed for 1,4-dioxane and hydroxyethoxyacetic acid (Rowe and
Wolf 1982). Essentially all of the dioxane was metabolized to hydroxyethoxy acetic acid,
suggesting that the metabolic pathway was not saturated at that dose (Rowe and Wolf 1982).
4. Excretion — Rowe and Wolf (1981) report that 1,4-dioxane and its metabolites are excreted
in urine, and that unchanged 1,4-dioxane is found in expired air (IARC 1976).
B. Acute Effects
Dioxane has low acute toxicity. The liquid is painful and irritating to the eyes, irritating to the skin
upon prolonged or repeated contact, and can be absorbed through the skin in toxic amounts. Dioxane
vapor has poor warning properties and can be inhaled in amounts that may cause serious systemic
injury, particularly to the liver and kidneys.
1. Humans — Exposure of 12 volunteers to a concentration of 1080 mg/m3 (300 ppm) 1,4-
dioxane in air for 15 minutes produced irritation of the eyes, nose and throat (IARC 1976).
Five deaths due to acute inhalation exposure to 1,4-dioxane have been reported; hemorrhagic
nephritis and liver necrosis were recorded at autopsy (IARC 1976). Other workers in the
same plant suffered from nausea, vomiting, and irritation of the eyes and respiratory
passages (ACGIH 1991).
Death of a worker, probably attributable to one week's inhalation exposure to about 1800
mg/m3 (500 ppm in air, which is roughly equivalent to 257 mg/kg over an 8-hour work day)1
has been reported. In that case, there was also the possibility of skin absorption since the
dioxane was also used as a solvent to remove glue from hands (IARC 1976).
Dioxane vapor has poor warning properties and can be inhaled in amounts that may cause
serious systemic injury, particularly to the liver and kidneys (Rowe and Wolf 1982).
Serious and fatal exposures can be experienced without forewarning; illness sometimes
becomes apparent hours after exposure (Rowe and Wolf 1982).
2. Animals — The oral LD50 in mice, rats, and guinea pigs is 5.7, 5.2, and 3.9 g/kg body
weight, respectively (IARC 1976).
Three-hour inhalation exposures at concentrations of 1000-30,000 ppm to guinea pigs, and 8-
hour exposures at concentrations of 4000-11,000 ppm to rats, mice, guinea pigs, and rabbits,
resulted in irritation of the mucous membranes at the higher doses (Rowe and Wolf 1982).
Deaths during or shortly after exposure were from respiratory failure due to lung edema,
with animals also exhibiting brain edema. Liver and kidney injuries were almost always
apparent upon microscopic examination of animals dying days after exposure, or sacrificed
after apparent recovery. The 4-hour inhalation LC50 for rats is 14,260 ppm (Rowe and Wolf
1982).
The dermal LD50 for rabbits is 7.6 g/kg (Rowe and Wolf 1982).
1 For dose comparison purposes, this has been calculated by multiplying 1800 mg/m3 by 0.143 (the
occupational standard breathing rate, 10 m3 divided by the assumed adult body weight, 70 kg, and assuming
100% absorption) to obtain the dose in mg/kg/day (U.S. EPA 1988).
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C. Subchronic/Chronic Effects
EPA has not published an RfD or RfC for 1,4-dioxane. Epidemiologic studies of workers exposed to
low levels of 1,4-dioxane have not shown adverse effects. Dose-related liver and kidney damage
have been observed in several species of animals exposed by oral, inhalation, and dermal routes.
1. Humans — No evidence of adverse effects attributable to 1,4-dioxane exposure was found in
three epidemiologic studies of dioxane workers. The studies included: (1) 74 workers
exposed 3-41 years to levels up to 14.24 ppm dioxane; (2) 165 employees exposed between
1954-1959 to levels up to 32 ppm dioxane; and (3) 80 workers with exposure levels ranging
from 0.05 - 51 ppm dioxane (Rowe and Wolf 1982).
Dioxane is not considered to be a skin irritant in the workplace, but prolonged and repeated
contact can cause eczema, as can any effective fat solvent (Rowe and Wolf 1982).
2. Animals — Dropsical changes (excessive fluid retention) in the liver were observed in
rabbits and guinea pigs after 10 gavage feedings of 0.1 mL/kg (0.1 g/kg) of 1,4-dioxane.
Some animals died following repeated (5, 16, or 20) feedings of 0.5 mL/kg (0.52 g/kg)
(Rowe and Wolf 1982).
1,4-Dioxane at levels of 0.01-1.0% (9.6-1000 mg/kg/day, males; 19.0-1600 mg/kg/day,
females) was administered in drinking water to rats for 2 years (Rowe and Wolf 1982).
Effects at the high dose included decreased weight gains, high mortality, (only 1 of 60 male
rats survived), and decreased water consumption. Kidney and liver damage were observed.
At the 0.1% level, the rats developed variable degrees of kidney and liver changes. No
adverse effects were observed at the 0.01% level. The authors concluded that toxicity of
dioxane is dose-related (Rowe and Wolf 1982).
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Rats, mice, guinea pigs, and rabbits were exposed by inhalation to 1,4-dioxane in
concentrations ranging from 1000-10,000 ppm for 1.5 hours/day [140-1,400 mg/kg/day for
rats]2 (reported as chronic exposure, but no duration specified, Rowe and Wolf 1982).
Mortality, usually due to lung injury, was high at the higher levels. Marked liver and kidney
injury was seen in all animals surviving repeated exposures. In another experiment, cats,
rabbits and guinea pigs (two each), were exposed to 1350 ppm 1,4-dioxane for 8 hours/day
for 45 days. Typical liver and kidney damage was seen in the one cat sacrificed after
becoming ill, but either slight or no injury was evident in other animals sacrificed after
exposure. A similar group plus 2 mice, was exposed to 2700 ppm, 8 hours/day. Seven of
the 10 animals died after 4-26 exposures, the rest survived 34 exposures. Observed effects
included irritation of the mucous membranes, emaciation, sporadic cramps, narcosis, and
albuminuria. In some cases, blood urea nitrogen doubled in concentration (Rowe and Wolf
1982).
Kidney and liver injury has been observed in rabbits and guinea pigs as a result of repeated
dermal application of dioxane (Rowe and Wolf 1982).
D. Carcinogenicity
EPA classifies 1,4-dioxane as B2, a probable human carcinogen, based on the induction of nasal
cavity and liver carcinomas in multiple strains of rats, liver carcinomas in mice, and gall bladder
carcinomas in guinea pigs. IARC classifies 1,4-dioxane as Group 2B, possible human carcinogen.
1. Humans — Human carcinogenicity data for 1,4-dioxane are inadequate. In three
epidemiologic studies on workers exposed to 1,4-dioxane, no increase was observed in the
number of cancer deaths over that expected (U. S. EPA 1995b).
2. Animals — EPA classifies 1,4-dioxane as B2, a probable human carcinogen (U.S. EPA
1995b). IARC classifies 1,4-dioxane as Group 2B, possible human carcinogen (IARC
1987). 1,4-Dioxane was administered in drinking water to rats (240 to 640 mg/kg/day for
110 weeks) or mice (380 to 830 mg/kg/day for 90 weeks) (U.S. EPA 1995b). Male and
female rats had a statistically elevated incidence of nasal cavity squamous cell carcinomas,
and female rats had a statistically elevated incidence of liver adenomas, both dose-related.
Male and female mice developed a dose-related, statistically significant elevated incidence
of liver carcinomas and liver carcinomas or adenomas (U.S. EPA 1995b).
In other experiments, 1,4-dioxane was administered in drinking water to Sherman rats (0.01-
1% for up to 716 days), and guinea pigs (0.5-2.0% for 23 months) (U.S. EPA 1995b). There
was a significant increase in the incidence of hepatocellular carcinomas, liver cholangiomas,
and nasal cavity carcinomas in high-dose Sherman rats. In guinea pigs, treatment-related
gall bladder carcinomas (2/22) and liver hepatomas (3/22) were seen. Male Sprague-Dawley
rats were treated with 0.75-1.8% dioxane for 13 months. Nasal cavity carcinomas were
observed at all dose levels, and hepatocellular carcinomas were observed at the higher
levels. Liver tumors (7/26) were induced in male Wistar rats administered 1% dioxane in
drinking water for 63 weeks (U.S. EPA 1995b).
1,4-Dioxane at levels of 0.01-1.0% (9.6-1000 mg/kg/day, males; 19.0-1600 mg/kg/day,
females) was administered in drinking water to rats for 2 years (Rowe and Wolf 1982). At
the high dose nasal carcinomas (3/66) and hepatic tumors (10/66) were observed. The
authors concluded that toxicity of dioxane is dose-related and that liver damage precedes
liver tumor development (Rowe and Wolf 1982).
No treatment-related lesions were observed in gross and microscopic examination of major
2 For dose comparison purposes, this has been calculated using the factor 3.6 to convert 1000 ppm to 3600
mg/m3 which is multiplied by 0.040 (the 1.5 hour breathing rate, 0.014 m3 [standard 24 hour breathing rate,
0.223] divided by the assumed adult rat body weight 0.350 kg, and assuming 100% absorption) to obtain the
dose in mg/kg/day (U.S. EPA 1985).
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tissues and organs of Wistar rats exposed to 111 ppm 1,4-dioxane vapor in a two-year
inhalation study (U.S. EPA 1995b).
E. Genotoxicity
No evidence of adverse effects was found in chromosomal analyses performed on 6 members of a
cohort in an epidemiologic study of dioxane workers (Rowe and Wolf 1982).
1,4-Dioxane induced DNA strand breaks in rat hepatocytes in vitro. It did not induce sex-linked
recessive lethal mutations in Drosophila, or aneuploidy in yeast. It induced chromosomal
abnormalities in plants. It was not mutagenic to bacteria (IARC 1976). The chemical was negative
in the mouse lymphoma assay, negative for the induction of chromosomal aberrations in cultured
Chinese hamster ovary (CHO) cells and weakly positive in the CHO sister-chromatid exchange assay
(ACGIH 1991).
F. Developmental/Reproductive Toxicity
There is very little information on the developmental/reproductive toxicity of 1,4-dioxane. There is
evidence of fetal toxicity in one rat study at high doses.
1. Humans — No information was found in the secondary sources searched regarding the
developmental/reproductive toxicity of 1,4-dioxane in humans.
2. Animals — Rats were administered 0.25-1.0 mL/kg/day (0.25-1.0 g/kg/day) dioxane by
gavage on days 6-15 of gestation. At 1.0 mL/kg (1.0 g/kg) reduced fetal weight and reduced
maternal body weight were observed (U.S. EPA 1987).
Rats and mice given 1,1,1-trichloroethane containing 3.5% (32 ppm) dioxane by inhalation
showed no evidence of maternal, embryonic, or fetal toxicity, nor any signs of a teratogenic
response. These studies are inconclusive with respect to 1,4-dioxane because of the nature
of the product tested (Rowe and Wolf 1982).
G. Neurotoxicity
Impaired neurological function has been observed in humans exposed to high levels of 1,4-dioxane by
inhalation, and in animals exposed by the inhalation, oral, or dermal routes. These effects include
incoordination, narcosis, vertigo, behavioral effects, and coma.
1. Humans — Among symptoms observed in cases of fatal industrial 1,4-dioxane inhalation
poisoning (possibly combined with dermal absorption) were drowsiness, vertigo, headache,
and coma (Rowe and Wolf 1982).
2. Animals — Cats exposed by inhalation to 1,4-dioxane in concentrations ranging from 12,000
ppm for 7 hours to 31,000 ppm for 3 hours exhibited loss of equilibrium, increased
salivation, lacrimation, and narcotic effects. Rapidity of symptom development was
concentration-dependent. Activity of all cats decreased gradually after exposure, followed
by their death. Similar narcotic effects have been reported in the rabbit (Rowe and Wolf
1982).
Trained rats were exposed by inhalation to 1500, 3000, or 6000 ppm 1,4-dioxane for 4
hrs/day, 5 days/week for 2 weeks. Apparently dose-related, temporary, and reversible
inhibition effects on behavior (avoidance and escape response) were observed (Rowe and
Wolf 1982).
Symptoms observed in single-dose, oral toxicity studies in several species progress from
weakness, depression, incoordination, and coma to death (Rowe and Wolf 1982).
Unsteadiness and incoordination have been observed in rabbits and guinea pigs administered
a "sufficient amount" of 1,4-dioxane by repeated topical application (Rowe and Wolf 1982),
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V. ENVIRONMENTAL EFFECTS
1,4-Dioxane has low toxicity to aquatic organisms; toxicity values are greater than 100 mg/L. 1,4-Dioxane is
not likely to be acutely toxic to aquatic or terrestrial animals at levels found in the environment. Long-term
exposure to terrestrial animals may increase tumor incidence.
A. Toxicity to Aquatic Organisms
A report describing acute and chronic toxicity of 1,4-dioxane to Pimephales promelas (fathead
minnows) reported acute effects at concentrations of 10,000 mg/L. The highest NOAEL was 6000
mg/L. A 32-day embryo-larval test identified a Maximum Allowable Toxicant Concentration
(MATC) >145 mg/L (U.S. EPA 1989). The 96-hour LC50 value for Lepomis macrochirus (bluegill)
is 10,000 ppm (10,000 mg/L) in fresh water. The 96-hour LC50 value for the fish Mendia beryllina
in synthetic seawater is reported to be 6,777 ppm (6777 mg/L) (Verschueren 1983).
B. Toxicity to Terrestrial Organisms
No information was found in the secondary sources searched regarding the toxicity of 1,4-dioxane to
terrestrial organisms. Based on the oral LD50 of 1,4-dioxane for rats of 5.2 g/kg, the chemical is not
expected to be acutely toxic to terrestrial animals at levels normally found in the environment.
However, long-term exposure from residues in water may increase tumor incidence based on chronic
drinking water studies in rats.
C. Abiotic Effects
No information was found in the secondary sources searched regarding the abiotic effects of 1,4-
dioxane.
VI. EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY
The Clean Air Act Amendments of 1990 list 1,4-dioxane as a hazardous air pollutant. Occupational exposure
to 1,4-dioxane is regulated by the Occupational Safety and Health Administration (OSHA). The OSHA
permissible exposure limit (PEL) is 100 parts per million of air (ppm) as an 8-hour time-weighted average
(TWA) (29 CFR 1910.000). In addition to OSHA, other federal agencies and groups may develop
recommendations to assist in controlling workplace exposure. These agencies and groups (listed in Tables 3
and 4) should be contacted regarding workplace exposures and for additional information on 1,4-dioxane.
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TABLE 3. EPA OFFICES AND CONTACT NUMBERS INFORMATION ON 1.4-
DIOXANE
EPA Office
Statute
Contact Number
Pollution Prevention & Toxics
Air
Solid Waste &
Emergency Response
Water
PPAa
EPCRA(§313/TRI)b
TSCA (§8A)
Clean Air Act (111, 112B)C
RCRA (action level:
water: 3E-3 mg/L
soil: 6E+1 mg/kg)
RCRA U Wasted
CERCLA (RQ: 100 pounds)6
EPCRA (§304/311/312)'
Safe Drinking Water Act
(Health Advisories: 4 mg/L [ch/1d]
0.4 mg/L [ch/10d];
0.7 mg/L [ca risk])9
PARA-4Ch
(800) 535-0202
(919)541-0808
(415)744-2074
(800) 535-0202
(800) 426-4791
PPA: Pollution Prevention Act
b EPCRA: Emergency Planning and Community Right to Know Act of 1986. §313: Toxic Chemicals (TRI
Chemicals).
c CAA: Clean Air Act. §111: Standards of performance for new stationary sources of air pollutants -
Equipment leaks chemical list. §112B: National emissions standards
RCRA: The Resource Conservation and Recovery Act of 1976, (codified as amended at 42 U.S.C.
§6901 et seq. Action levels : health and environmental-based levels used by the EPA as indicators for the
protection of human health and the environment and as triggers for a Corrective Measures Study (U.S.
EPA 1990). RCRA U Waste : Other discarded commercial chemical products.
e CERCLA: Comprehensive Environmental Response, Compensation, and Liability Act of 1980, as
amended. RQ: level of hazardous substance, which, if equaled or exceeded in a spill or release,
necessitates the immediate reporting of that release to the National Response Center [40 CFR Part 302
(1991)].
f
EPCRA: Emergency Planning and Community Right to Know Act of 1986.
9 Drinking Water Health Advisories : estimated for a 10-kg child or a 70-kg adult consuming 2 L of water
per day. (ch/1d) (one-day health advisory fora child): the concentration of a chemical in drinking water
that is not expected to cause any adverse noncarcinogenic effects for up to 5 consecutive days of
exposure, with a margin of safety. (ch/10d) (for a child): the concentration of a chemical in drinking water
that is not expected to cause any adverse noncarcinogenic effects up to 14 consecutive days of exposure,
with a margin of safety, ca. risk: mg/L at 10~4 cancer risk.
' PARA-4C: Pretreatment pollutants.
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TABLE 4. OTHER FEDERAL OFFICES/CONTACT NUMBERS FOR INFORMATION
ON 1,4-DIOXANE
Other Agency/Department/Group Contact Number
Agency of Toxic Substances & Disease Registry (404) 639-6000
American Conference of Governmental Industrial Hygienists (513) 742-2020
(TLV-TWA:25 ppm [90 mg/m3 ] *)a
National Institute for Occupational Safety & Health (800) 356-4674
(1 ppm [3.6 mg/m3] 30 minutes; ca , LF; IDLH: 500 ppm)b
Occupational Safety & Health Administration
(TWA: 100 ppm [360 mg/m3 ] *)c
(Check local phone book for phone number under Department of Labor)
a TLV-TWA: Time-Weighted-Average concentration for a normal 8-hr workday and a 40-hr workweek to
which nearly all workers may be repeatedly exposed without adverse effects (ACGIH 1994-1995). *: air
sampling alone is insufficient to accurately quantitate exposure. Measures to prevent significant cutaneous
absorption may be required.
C: This concentration that should not be exceeded during any part of the working exposure. Ca:
potential human carcinogen. LF: reduce exposure to lowest feasible concentration; when Ca designation
accompanies lowest feasible designation, use of only the most reliable and protective respirators is
recommended. After a limited review, NIOSH concluded that adverse health effects could occur at the
proposed OSHA PELS and NIOSH did not establish a TWA (NIOSH 1994). IDLH: level immediately
dangerous to life and health.
c TWA: Time-Weighted-Average concentrations that must not be exceeded during any 8-hour work shift of
a 40-hour workweek. OSHA standards promulgated pursuant to the Occupational Safety and Health Act,
29 CFR 1910 (OSHA 1993).
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American Conference of Governmental Industrial Hygienists, Inc. Cincinnati, OH, p. 512-514.
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Rahway, NJ, p. 954.
CHEMFATE. 1994.
Chemical Marketing Reporter. 1988. "1,4-dioxane has more sources than expected, says Gelman." 234:17.
Ferro Corporation. 1995. EPA conversation with Ferro Corp. represeentative, May 1, 1995.
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Publishers, Inc., Chelsea, Ml, pp 216-221.
HSDB. 1995. Hazardous Substances Data Bank. MEDLARS Online Information Retrieval System, National
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TRI92. 1994. 1992 Toxics Release Inventory. Public Data Release. Office of Pollution Prevention and
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U.S. EPA . 1985. U.S. Environmental Protection Agency. Reference Values for Risk Assessment.
Environmental Criteria and Assessment Office, U.S. Environmental Protection Agency, Cincinnati, OH, Table
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U.S. EPA. 1987. Reportable Quantity Document for Dioxane. Environmental Criteria and Assessment Office,
Office of Health and Environmental Assessment, U.S. Environmental Protection Agency, Cincinnati, OH. p. 1.
U.S. EPA. 1987-92. Toxics Release Inventory. Public Data Release. Office of Pollution Prevention and
Toxics, U.S. Environmental Protection Agency, Washington, DC.
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U.S. EPA. 1988. U.S. Environmental Protection Agency. Methodology for Evaluating Potential
Carcinogenicity in Support of Reportable Quantity Adjustments Pursuant to CERCLA Section 102.
Carcinogen Assessment Group, Office of Health and Environmental Assessment, U.S. EPA, Washington,
D.C., pp, 21-22. OHEA-C-073.
U.S. EPA. 1990. U.S. Environmental Protection Agency. Examples of cncentrations meeting criteria for
action levels. Fed. Reg. 55:30865-30867.
U.S. EPA. 1995a. Chemical Update Survey (CUS) Database. Office of Pollution Prevention and Toxics, U.S.
Environmental Protection Agency, Washington, DC.
U.S. EPA. 1995b. Integrated Risk Information System (IRIS) Online. Cover sheet for 1,4-Dioxane. Office of
Health and Environmental Assessment, U.S. EPA, Cincinnati, OH. Retrieved 1/95.
U.S. ITC. ( United States International Trade Commission.) 1994. Synthetic Organic Chemicals: United
States Production and Sales, 1992. 76th edition. USITC Publication 2720, February 1994.
Verschueren, K. 1983. Handbook of Environmental Data on Organic Chemicals, 2nd Ed. VanNostrand
Reinhold Co., New York, p. 578-580.
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APPENDIX A. SOURCES SEARCHED FOR FACT SHEET PREPARATION
ACGIH. 1991. American Conference for Governmental Industrial Hygienists, Inc. TLVs®. Documentation of the Threshold Limit
Values and Biological Exposure Indices. ACGIH, Cincinnati, OH.
ACGIH. 1994-1995. American Conference for Governmental Industrial Hygienists, Inc. Threshold Limit Values for Chemical
Substances and Physical Agents and Biological Exposure Indices. ACGIH, Cincinnati, OH.
AQUIRE. 1994. Aquatic Information Retrieval online data base. Chemical Information Systems, Inc., a subsidiary of Fein-Marquart
Assoc.
ATSDR. 1989-1994. Agency for Toxic Substances and Disease Registry. Toxicological Profiles. Chamblee, GA: ATSDR.
Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.). 1989. The Merck Index, 11th ed. Rahway, N.J.: Merck & Co., Inc.
Clayton GD, Clayton FE. 1981-1982. Patty's Industrial Hygiene and Toxicology, 3rd ed., Vol. 2C. New York: John Wiley & Sons.
(Soon to be updated)
Clean Air Act. 1990. As amended. 42 U.S.C. 7412.
GENETOX. 1994. U.S. EPA GENETOX Program, computerized database.
Howard, P.H., Ed. 1989. Handbook of Environmental Fate and Exposure Data. Lewis Publishers, Chelsea, Ml.
HSDB. 1994. Hazardous Substances Data Bank. MEDLARS Online Information Retrieval System, National Library of Medicine.
IARC. 1979-1994. International Agency for Research on Cancer. IARC Monographs on the Evaluation of Carcinogenic Risk of
Chemicals to Man. Lyon: IARC.
IPCS. International Programme on Chemical Safety. Environmental Health Criteria. World Health Organization, Geneva, Switzerland.
NIOSH (National Institute for Occupational Safety and Health). 1992. NIOSH Recommendations for Occupational Safety and Health.
Compendium of Policy Documents and Statements. Cincinnati, OH: NIOSH.
NIOSH. 1994. National Institute for Occupational Safety and Health. Pocket Guide to Chemical Hazards. NIOSH, U.S. Department of
Health and Human Services, Cincinnati, OH
NTP. National Toxicology Program. Toxicology and Carcinogenesis Studies. Tech Rep Ser.
NTP. National Toxicology Program. Management Status Report. Produced from NTP Chemtrack system. Aprils, 1994. National
Toxicology Program, Research Triangle Park, NC.
OSHA. 1993. Occupational Safety and Health Administration. Table Z-2. Limits for Air Contaminants.
RTECS. Registry of Toxic Effects of Chemical Substances. MEDLARS Online Information Retrieval System, National Library of Medicine.
TRI92. 1994. 1992 Toxics Release Inventory. Public Data Release. Office of Pollution Prevention and Toxics (7408), U.S. Environmental
Protection Agency, Washington, D.C.
TSCATS. MEDLARS Online Information Retrieval System, National Library of Medicine.
U.S. Air Force. 1989. The Installation Restoration Toxicology Guide, Vols. 1-5. Wright-Patterson Air Force Base, OH.
U.S. EPA. 1991. U.S. Environmental Protection Agency. Table 302.4 List of Hazardous Substances and Reportable Quantities 40 CFR,
part 302.4:3-271.
U.S. EPA. U.S. Environmental Protection Agency. Appendix A. Examples of Concentrations Meeting Criteria for Action Levels. 40 CFR
Part 264.521 (a)(2)(i-iv). Fed. Reg. 55:30865-30867.
U.S. EPA. Most current. Drinking Water Regulations and Health Advisories. Office of Drinking Water, U.S. Environmental Protection
Agency, Washington, D.C.
U.S. EPA. Most Current. Health Effects Assessment Summary Tables. Cincinnati, OH: Environmental Criteria and Assessment Office,
U.S.EPA.
U.S. EPA reviews such as Health and Environmental Effects Documents, Health and Environmental Effect Profiles, and Health and
Environmental Assessments, HERD Analogue Profiles, ITC Documents.
U.S. EPA. 1994. Integrated Risk Information System (IRIS) Online. Cincinnati, OH: Office of Health and Environmental Assessment.
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