United States
Environmental Protection
Agency
Pollution Prevention
and Toxics
(7407)
December 1994
EPA749-F-95-014a
OPPT Chemical Fact Sheets
(METHYL METHACRYLATE) Fact Sheet: Support
Document (CAS No. 80-62-6)
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These sources include online databases, unpublished EPA information, government publications, review documents, and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. 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 and chemical properties of methyl methacrylate are summarized in Table 1.
TABLE 1. CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL PROPERTIES OF METHYL METHACRYLATE
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)
Vapor Pressure
Reactivity
Flash Point
Henry's Law Constant
Fish Bioconcentration Factor
Odor Threshold
Conversion Factors
80-62-6
MME;2- methyl-2-propenoic acid,
methyl ester; methyl-2-methyl-
propenoate; Diakon
O—CH3
CH3
liquid
100.1
— 48°C
100-101 °C@ 760 mm Hg
15g/L@25°C
0.939 g/mL25'5
3.45
1.80 (calculated)
1.38 (measured)
29.3mm Hg @20°C
flammable; undergoes polymerizatio
readily by light and heat
10°C
3.37 x 10-4 atm-m3/mol
6.6 (log 0.82) (calculated)
0.2 mg/m3 (detection)
1 ppm = 4.09 mg/m3
1 mg/m = 0.244 ppm
U.S. EPA 1985
Keith and Walters 1985
U.S. EPA 1985
U.S. EPA 1985
U.S. EPA 1985
U.S. EPA 1985
Keith and Walters 1985
U.S. EPA 1985
Hansch and Leo 1985
U.S. EPA 1985
U.S. EPA 1985;
Keith and Walters 1985
Keith and Walters 1985
CHEMFATE1994
CHEMFATE1994
Verschueren 1983
U.S. EPA 1985
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II. PRODUCTION, USES, AND TRENDS
A. Production
According to USITC (1994), CYRO Industries, DuPont Company*, and Rohm and Haas Company were the
principal producers of methyl methacrylate in the United States in 1992. In 1992, the U.S. production volume of
methyl methacrylate was estimated to be 1,205 million pounds (547,824 thousand kilograms) (Mannsville 1993;
USITC 1994). The United States imported 10 million pounds and exported 120 million pounds of methyl
methacrylate in 1992 (Mannsville 1993).
In 1993, Mannsville (1993) estimated CYRO Industries', Id's, and Rohm and Haas' combined total capacity of
methyl methacrylate as 1,435 million pounds (see Table 2). Table 2 shows the U.S. producers, plant locations, and
plant capacities of methyl methacrylate in 1993. CYRO Industries has announced plans to expand its Fortier,
Louisiana plant by 25 percent by the second quarter of 1995 (Mannsville 1993). Table 3 shows the domestic
production capacity and production of methyl methacrylate.
TABLE 2. PRODUCERS OF METHYL METHACRYLATE AND THEIR CAPACITIES
Producer Location 1993 Capacity
(Millions of Pounds)
CYRO Industries
ICI Americas Inc*
ICI Americas Inc*
Rohm and Haas
Fortier, LA
Memphis, TN
Beaumont, TX
Deer Park, TX
200
320
125
790
TOTAL 1435
Source: Mannsville 1993.
In 1993, ICI acquired DuPont's Beaumont, Texas and Memphis, Tennessee plants, which manufacture
methyl methacrylate.
TABLE 3. ESTIMATED U.S. PRODUCTION AND CAPACITY OF METHYL METHACRYLATE
(Millions of Pounds)
Year 1990 1991 1992 1993(Projected) 1995(Projected)
Capacity 1310 1310 1435 1435 1485
Production 1182 1102 1084* 1088* N/A
* Preliminary data.
N/A: Not available
Source: Mannsville 1993.
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B. Uses
The principal application of methyl methacrylate is the production of acrylic plastics and resins for sheeting and
molding compounds, which are used in construction, automotive/ transportation, consumer products, and industrial
applications, and in making signs. Methyl methacrylate-butadiene-styrene (MBS) resins are used as impact
modifiers for PVC used in making bottles. MBS resins help increase the capacity of a material to withstand blows
or shocks.
Methyl methacrylate polymers and copolymers are used in waterborne, solvent, and solventless coatings. The
largest surface coating application is exterior latex housepaint that is based on emulsions containing methyl
methactylate. Table 4 provides the estimated 1993 domestic end use pattern for methyl methacrylate. Among the
miscellaneous uses of smaller amounts of methyl methacrylate are those in dental restorations, in adhesive cements,
and surgical (e.g., bone) implants.
TABLE 4. END USE PATTERN OF METHYL METHACRYLATE-1993 ESTIMATE
Derivative
(Typical Standard Industrial Classification (SIC) Code)1 Percent
Cast and Extruded Sheet
(SIC 2821) 30
Molding and Powder Resins
(production, SIC 2821) 20
Protective Coatings
(SIC 2851) 20
Impact Modifiers
(SIC 2821) 12
Emulsion Polymers
(SIC 2851) 9
Miscellaneous 9
(no applicable SIC(s))
Source: Mannsville 1993.
1 The Standard Industrial Classification (SIC) code is the statistical classification standard for all Federal
economic statistics. The code provides a convenient way to reference economic data on industries of interest
to the researcher. SIC codes presented here are not intended to be an exhaustive listing; rather, the codes
listed should provide an indication of where a chemical may be likely to be found in commerce.
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C. Trends
The United States consumption of methyl methacrylate grew at an average annual rate of five percent from 1983
to 1990. Demand for methyl methacrylate declined, however, in the 1990s due to the faltering of the automobile
and construction industries. It is anticipated that demand for traditional rigid methacrylates will grow by one to
two percent more than the GNP in the future. Overall, future demand for the methyl methacrylate monomer should
grow four to five percent in 1994 with longer term growth at three to four percent per year. Demand for acrylic
emulsions in aqueous systems are growing, replacing systems that contain volatile solvents in paints and adhesives.
The markets for methyl methacrylate-butadiene-styrene (MBS) impact modifiers for PVC and twelve-inch video
disks to record movies and music are expected to grow. Solvent-based applications of methylmethacryalte are
declining.
III. ENVIRONMENTAL FATE
A. Environmental Release
Methyl methacrylate is released to ambient air from production facilities, end-product manufacturers and
storage (U.S. EPA 1985). No atmospheric monitoring information was found for methyl methacrylate in
the secondary sources searched; however, the chemical has been detected in the workplace under various
conditions. In a polystyrene production plant, time-weighted-average (TWA) concentrations of 66 and
169 parts per billion (ppb) methyl methacrylate were detected in the workers' breathing zones and the air
of the workplace, respectively; maximum breathing zone and workplace concentrations were 378 and 3300
ppb, respectively. At five US plants manufacturing polymethyl methacrylate, 8-hour TWA levels of
methyl methacrylate were measured at 16 to 360 mg/irf (3.9-87.84 ppm) (U.S. EPA 1985).
Of 204 heavily industrialized sites tested in the Chicago and Illinois River basin area, only one surface
water sample contained methyl methacrylate (concentration of 10 ppb) (U.S. EPA 1985). Methyl
methacrylate (10 ppb) has been detected in one of nine sites monitored in Lake Michigan, in a few US
drinking waters (<1 ppb), and in commercial deionized charcoal-filtered water (U.S. EPA 1985).
In 1992, environmental releases of the chemical, as reported to the Toxic Chemical release inventory by
certain types of US industries, totaled about 2.8 million pounds, including 2.6 million pounds to the
atmosphere, 220 thousand pounds to underground injection sites, 35 thousand pounds to surface water,
and 4 thousand pounds to land (TRI92 1994).
B. Transport
Limited information was found regarding the atmospheric transport of methyl methacrylate. Given the
water solubility of methyl methacrylate, some removal of methyl methacrylate from the atmosphere is
expected to occur through dissolution into rain droplets (U.S. EPA 1985). Adsorption onto aerosols is
not a likely transport process (U.S. EPA 1985).
Based on the Henry's law constant (3.37 x lO^1 atm-m3/mol [CHEMFATE 1994]) and the vapor pressure
of methyl methacrylate, volatilization from aqueous media is expected to be a significant transport
mechanism for the chemical (U.S. EPA 1985). Log Koc (1.80) and log Kow (0.79) values suggest that
sorption of methyl methacrylate onto particulate matter in aquatic media is not a significant removal
mechanism.
No information was found on the transport of methyl methacrylate in soil. Based on the expected behavior
of the chemical in water and air, it is likely to undergo significant evaporation from soil and, in cases where
the evaporation or biodegradation of the chemical is delayed (such as near a spill or a dumpsite where the
concentration may be higher), methyl methacrylate may leach into groundwater (U.S. EPA 1985).
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C. Transformation/Persistence
1. Air — The major removal processes for methyl methacrylate in air are reaction with NOX and
direct photolysis (U.S. EPA 1985). In a smog chamber, the reaction of methyl methacrylate with
NOX proceeded with half-lives of 2.7 days and >3 days when the methyl methacrylate-to-NOx
ratios were 1:2 and 1:20, respectively (U.S. EPA 1985). At the methacrylate-to-NOx ratio of 1:2,
a maximum amount of ozone of 0.73 ppm was formed in 4.4 hours, whereas at the ratio of 1:20,
0.2 ppm were formed in 1.4 hours.
At wavelengths greater than 300 nm, the photolysis of 2 mL methyl methacrylate in 4 mL dioxane
produced 0.43% of the polymer in 1.2 hours. No information was found for the photolysis of
methyl methacrylate in direct or simulated sunlight, but it is likely that ketonic compounds may
accelerate the photoreaction (U.S. EPA 1985).
2. Water — Experiments conducted under biological treatment conditions suggest that the
biodegradation of methyl methacrylate may be significant in the ambient aquatic environment
(U.S. EPA 1985). The chemical: (a) was biodegradable (no quantitative estimates reported) with
acclimatized sewage sludge; (b) exhibited a 47% theoretical oxidation to CO2 in 10 days, using
19-day acclimatized sewage as microbial inoculum; and (c) underwent 100% degradation in -20
hours with activated sludge as the source of microorganisms (U.S. EPA 1985).
Methyl methacrylate may undergo photochemical reaction in aquatic media, particularly in surface
waters (see section III.C. 1); however, information on the photolysis of methyl methacrylate under
environmental conditions was not found in the secondary sources searched.
3. Soil — No information was found on the fate of methyl methacrylate in soil. Based on the
information on the degradation of methyl methacrylate in water, the chemical should undergo
significant biodegradation in soil (U.S. EPA 1985).
4. Biota — The calculated log BCF of 0.82 and the low Kow for methyl methacrylate suggest that
the chemical will not bioconcentrate in aquatic organisms (U.S. EPA 1985).
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IV. HEALTH EFFECTS
A. Pharmacokinetics
Methyl methacrylate is absorbed by the oral route, is metabolized first to methacrylic acid and ultimately
to CO2 via the Krebs cycle; metabolites are excreted mainly in expired air. Metabolites of methyl
methacrylate may also be excreted in small amounts via the urine. Information indicates that methyl
methacrylate does not acumulate in tissues.
1. Absorption — Animal studies demonstrate the rapid and extensive absorption of methyl
methacrylate from the gastrointestinal (GI) tract following gavage (U.S. EPA 1985). 14C-Methyl
methacrylate, administered to rats at doses of 5.7 mg/kg, was expired as 14CO2 at the rate of
-65% in 2 hours. Recovery of radioactivity for 10 days after oral dosing was 4.7% in urine, 2.7%
in feces, 88% as 14CO2, 0.1% unchanged 14C-methyl methacrylate in expired air, and 6.6% in the
carcass. Total recovery was 99.6%. No information was found on the absorption of methyl
methacrylate via the respiratory tract, but systemic toxicity resulting from inhalation of the
chemical indicates that it is absorbed (see sections IV.B and IV.C) by this route.
2. Distribution — Intravenously injected methyl methacrylate is cleared from the blood within
minutes (U.S. EPA 1985). This, along with its metabolism (see section IV.A.3), suggests a low
potential for the localization of methyl methacrylate in the tissues. Ten days after oral or
intravenous dosing of rats with radiolabeled methyl methacrylate, small amounts of radioactivity,
presumably from a radiolabelled metabolite, were detected only in liver and fat tissues (U.S. EPA
1985).
3. Metabolism — The results of animal studies with radiolabeled methyl methacrylate suggest that
the chemical undergoes hydrolysis to methacrylic acid, which is converted into its coenzyme A
ester (U.S. EPA 1985). The coenzyme A ester then enters the tricarboxylic acid cycle and is
oxidized to carbon dioxide in the Krebs cycle. Other metabolites of methyl methacrylate that have
been identified in the urine include methyl malonate, succinate, hydroxyisobutyrate, and 2-formyl
propionate, with small amounts of the mercapturic acid, thioether, and the parent compound
(ACGIH 1991). In addition, glutathione conjugation may play a minor role in the metabolism of
methyl methacrylate (U.S. EPA 1985).
4. Excretion — Rats treated orally with labeled methyl methacrylate excreted -65-88% of the
administered doses as 14CO2 in expired air (U.S. EPA 1985). Methyl methacrylate and its
metabolites have also been detected in the urine (see section IV.A.3).
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B. Acute Effects
Methyl methacrylate is of low acute toxicity to humans. Workers exposed to high concentrations of the
chemical have experienced irritation of the skin, the eyes, and mucous membranes. Methyl methacrylate
is also of low acute toxicity to animals exposed orally, by inhalation, or by percutaneous application.
1. Humans — Methyl methacrylate has been associated with skin, eye, and mucous membrane
irritation (ACGIH 1991). In an occupational study, irritation (unspecified as to type) occurred
when concentrations of methyl methacrylate reached 170 to 250 ppm (695 to 1022 mg/m3);
generally, workers tolerated levels of about 200 ppm without complaint, whereas 2300 ppm was
intolerable (ACGIH 1991). (Note: to give the reader a rough approximation of approximate
dose, the concentration of 170 ppm converts roughly to an intake of 99 mg/kg over an 8-hour
workday2). In contrast, another study reported irritation of the mucous membranes at 125 to 200
ppm and suggested a tolerance level of 12 ppm (ACGIH 1991).
2. Animals — Oral LD50 values for methyl methacrylate are as follows: 7.8 to 9.4 g/kg for rats, 4.7
g/kg for dogs, 5.2 g/kg for mice, 5.9 g/kg for guinea pigs, and 6.6 g/kg for rabbits (U.S. EPA
1985).
Inhalation LC50 values for methyl methacrylate are as follows: 19,000 mg/m3 (4636 ppm) (8
hours) for rats, rabbits, and guinea pigs, 29,045 mg/m3 (7087 ppm) (4 hours) for rats, and 13,100
mg/m3 (3196 ppm) (2 hours) to 164,220 mg/m3 (40,070 ppm) (27 minutes) for mice (U.S. EPA
1985). Non-lethal effects observed in rats exposed by inhalation to methyl methacrylate include
GI irritation, dyspnea, upper respiratory tract irritation, and decreased GI motor activity at levels
between 2000 ppm and 4000 ppm (8 to 18 g/m3) (U.S.EPA 1990).
The percutaneous LD50 is 7.5 g/kg for rabbits (U.S. EPA 1985). Methyl methacrylate is a potent
skin sensitizer in guinea pigs, causing local necrosis and inflammation (ACGIH 1991).
C. Subchronic/Chronic Effects
Workers exposed to methyl methacrylate experienced allergic responses. Methyl methacrylate is a potent
skin sensitizer in laboratory animals. In animals, the main effects of oral and inhalation exposures to
moderate to high doses/concentrations of methyl methacrylate for 3 months to 2 years include local effects
such as stomach ulcers and damage to the olfactory epithelium and lungs. Repeat inhalation exposure to
large amounts of methyl methacrylate also adversely affect the liver, the spleen and bone marrow.
For dose comparison purposes this has been calculated by multiplying 695 mg/m3 by
0.14 (the calculated occupational 8-hour workday breathing rate, 10 m3, divided by
the assumed adult body weight, 70 kg and assuming 100% absorption) to obtain the
dose in mg/kg.
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1. Humans — Allergic responses have been reported following direct contact with methyl
methacrylate (U.S. EPA 1985). Exposure to methyl methacrylate induced hypersensitivity in 10%
of dental technicians studied (total number not available) after 2-14 years of contact (U.S. EPA
1985).
The following effects of methyl methacrylate have been noted in humans exposed under various
conditions (exposure levels and durations not available): alterations of arterial pressure or heart
rate in patients with total hip joint replacement requiring intraosseous application of methyl
methacrylate; allergic sensitization; allergic contact eczema in dentists, dental technicians, and
orthopedic surgeons; sore mouth in patients with dentures; headache and irritation of the eyes and
respiratory tract resulting from exposure to vapors during surgery; effects on circulation, blood
pressure, and bone metabolism; cardiovascular changes due to direct toxic effect of methyl
methacrylate on the myocardium; and effects on renal function (U.S. EPA 1985).
2. Animals — Groups of 25 male and 25 female Wistar rats received drinking water containing 0,
6, 60, or 2000 ppm methyl methacrylate for five months (U.S. EPA 1985). At the start of the 5th
month, the 6 and 60 ppm levels were increased to 7 and 70 ppm and treatment with all doses was
continued for 2 years. Males and females in the high-dose group exhibited a transient weight
depression at weeks 1 to 3 and high-dose females had an increased kidney-to-body weight ratio
compared with controls. There were no differences in mortality among the groups and there were
no treatment-related microscopic abnormalities.
White rats (50/group) given average oral (gavage) doses of 114.6 mg/kg two days/week methyl
methacrylate for 3, 5, or 8 months developed ulcers of the glandular epithelium of the stomach
and irreversible liver lesions that became more severe as the duration of exposure increased (U.S.
EPA 1985). Reversible lesions in the glomeruli were also noted.
Beagle dogs given capsules containing 1437 ppm (TWA; equivalent dietary level) methyl
methacrylate for 2 years exhibited slightly decreased weight gain, but those given < 100 ppm
showed no significant effect (U.S. EPA 1985).
F344/Nrats mdE6C3fl mice (10 males and 10 females/group) inhaled 500, 1000, 2000, 3000,
or 5000 ppm methyl methacrylate 6 hours/day, 5 days/week for 14 weeks (NTP 1986). No deaths
occurred at the two lowest doses, but body weights were reduced. Mortality was dose-related at
the highest doses (100% of the rats and 80% of the mice died at 5000 ppm). Both rats and mice
had a dose-dependent increase in necrosis and sloughing of the olfactory epithelium. In addition,
male rats exposed to 5000 ppm had follicular atrophy of the spleen and bone marrow atrophy.
The mice displayed metaplasia (all exposed) and inflammation in the nasal turbinates, renal
effects (males only) that included cortical necrosis and tubular degeneration with focal
mineralization, and hepatic necrosis.
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Exposure of white rats (50/group) to 12 ppm (49 mg/m3) for 3 months (20 exposures), 5 months
(41 exposures), or 8 months (63 exposures) produced histological changes in the lungs that were
characterized by interstitial infiltrates, thickening of the septa, and marked alveolar desquamation
(no other experimental details were available) (U.S. EPA 1985). Reversible lesions were
observed in the liver and kidney.
Sprague-Dawley rats (25/group) were exposed to methyl methacrylate vapor concentrations of
0 and 116 ppm (475 mg/m3) 8 hours/day, 5 days/week for 3 months or 6 months (U.S. EPA
1985). Compared with the controls, the treated animals had lower lung and spleen weights at 3
months and significantly lower body weights and fat content at 3 and 6 months. Rats exposed for
6 months also had significantly decreased "average small intestinal transit performance" (U.S.
EPA 1985).
Groups of 56 male and 56 female Golden hamsters and groups of 70 male and 70 female Fischer
rats were exposed by inhalation to 25, 100, or 400 ppm (102, 409, or 1638 mg/m3) 6 hours/day,
5 days/week for 78 weeks (hamsters) or 104 weeks (rats). No treatment-related effects were
noted in the hamsters; the rats had a slightly increased incidence of mild rhinitis, but no other
effects (U.S. EPA 1985).
Groups of 50 male F344/N rats and 50 male and 50 female B6C3Fj mice were exposed by
inhalation to methyl methacrylate concentrations of 0, 500, or 1000 ppm, and groups of 50 female
F344/N rats were exposed to concentrations of 0, 250, or 500 ppm for two years (NTP 1986).
Exposure to methyl methacrylate was associated with concentration-related inflammation of the
nasal cavity and degeneration of the olfactory sensory epithelium in exposed male and female rats
and mice; epithelial hyperplasia of the nasal cavity was also observed in exposed mice.
Effects of inhaled methyl methacrylate noted in animal studies of shorter durations include: liver
enzyme changes in mice exposed to 100 ppm for 6.6 days, lung damage in rats exposed to 1000
ppm for 56 hours, liver and kidney degeneration and death in dogs exposed to 1400 ppm for 1.5
hours/day for 8 days (U.S. EPA 1985).
D. Carcinogenicity
Epidemiology studies have suggested a causal relationship between exposure to methyl methacrylate and
an increase in the incidence of cancer of the rectum and colon; however, the studies to date are
inconclusive. There was no evidence for the carcinogenicity of methyl methacrylate administered to
animals for up to two years, orally, by inhalation, and by skin painting. IARC has categorized methyl
methacrylate as a Group 3 (not classifiable as to its carcinogenicity to humans) carcinogen.
1. Humans — Several epidemiological studies have suggested a causal relationship between
exposure to mixtures of ethyl acrylate/methyl methacrylate and increased relative risk of cancer
of the colon and rectum (U.S. EPA 1985); however, when analyses were broken down according
to estimated accumulated "dose" and latency (the number of years between first exposure and
death), a definite causal relationship could not be established.
IARC (1987) has placed methyl methacrylate in Group 3 (not classifiable as to its carcinogenicity
to humans), based on inadequate evidence of carcinogenicity in humans and animals.
2. Animals — Groups of 25 male and 25 female Wistar rats received drinking water containing 0,
6, 60, or 2000 ppm methyl methacrylate for five months (U.S. EPA 1985). At the start of the 5th
month, the 6 and 60 ppm levels were increased to 7 and 70 ppm, and treatment was continued for
2 years. There were no differences in mortality among the groups and there were no treatment-
related microscopic abnormalities.
Groups of 50 male F344/N rats and 50 male and 50 female B6C3Fj mice were exposed by
inhalation to methyl methacrylate concentrations of 0, 500, or 1000 ppm, and groups of 50 female
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F344/N rats were exposed by inhalation to concentrations of 0, 250, or 500 ppm for two years
(NTP 1986). The NTP concluded that there was no evidence for the carcinogenicity of methyl
methacrylate for male and female rats and male and female mice, under the conditions of the
study.
Groups of 56 male and 56 female Golden hamsters and groups of 70 male and 70 female Fischer
rats were exposed by inhalation to 0, 25, 100, or 400 ppm (102, 409, or 1638 mg/m3) 6
hours/day, 5 days/week for 78 (hamsters) or 104 (rats) weeks. There was no increased incidence
of neoplasm in treated animals compared with controls of either species (U.S. EPA 1985).
Skin painting with methyl methacrylate 3 times/week for 4 months did not produce skin tumors
in 10 Wistar rats observed for the remainder of their lifespan (U.S. EPA 1985).
E. Genotoxicity
Genotoxicity data for methyl methacrylate are mixed. The chemical was positive, with S9, in Salmonella
typhimurium (strain TM677) forward mutation assay and produced chromosomal aberrations in rats
exposed to vapor concentrations of 1000 or 9000 ppm (4,094 or 36,846 mg/m3) 6 hours/day for 5 days;
there was no effect at 100 ppm. Methyl methacrylate was positive in hamster fibroblasts in culture
medium containing 0.0065 mg/mL methyl methacrylate (U.S. EPA 1985). Methyl methacrylate was
negative in Salmonella typhimurium strains TA1535, TA1537, TA1538, TA100, and/or TA98 in the
vapor phase, plate incorporation, or liquid incubation assays, with and without metabolic activation; and
was negative in the micronucleus and dominant lethal assays in mice (U.S. EPA 1985).
F. Developmental/Reproductive Toxicity
Limited information suggest that women and men exposed to methyl methacrylate have experienced
decreased sexuality. Complications during pregnancy have been reported as well. Methyl methacrylate
administered (in some cases, at maternally toxic levels) to pregnant rats has induced fetal toxicity. Methyl
methacrylate has caused elevated estrogen secretion in rats.
1. Humans — Women and men (unspecified as to number) chronically exposed to methyl
methacrylate have experienced decreased sexuality; complications during pregnancy were also
reported (U.S. EPA 1985). Doses and durations of exposures were not reported.
2. Animals — Groups of 30 pregnant rats were exposed by inhalation to concentrations of methyl
methacrylate ranging from 102 mg/m3 to 4094 mg/m3 (25 to 1000 ppm) 5 hours/day on days 6
through 15 of gestation (U.S. EPA 1985). No malformations were observed in any group, but
there was an increased incidence of early resorptions in the animals exposed to 4094 mg/m3. The
highest no-adverse effect level reported for the study is 409 mg/m3 (100 ppm). In another study,
pregnant Sprague-Dawley rats were exposed to 110,000 mg/m3 (26,840 ppm) of methyl
methacrylate vapor for 17 or 54 minutes/day on days 6-15 of gestation. There were dose-related
significant decreases in maternal weight gain and food consumption during and after exposure to
methyl methacrylate. The group exposed for 54 minutes/day had significantly increased
incidences (p<0.05) of early fetal death, decreased fetal weight, decreased crown-rump length,
hematomas, and delayed sternebral ossification, compared with two control groups. The group
exposed for 17 minutes/day also had an increased incidence of delayed sternebral ossification
(p<0.05).
Methyl methacrylate did not produce adverse effects in fetuses of 18 dams exposed by inhalation
to 5445 mg/m3 for 2 hours 2 times/day on days 6-15 of gestation (U.S. EPA 1985). Rats
(unspecified as to sex) inhaling 54 mg/m3 methyl methacrylate continuously for 1 to 4 months
exhibited increased estrogen secretion, which apparently increased the follicle-stimulating activity
of the pituitary (U.S. EPA 1985).
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G. Neurotoxicity
Dental technicians and factory workers exposed to methyl methacrylate developed nerve degeneration in
their hands and "nervous disorders", respectively. Repeated exposure to high concentrations of methyl
methacrylate resulted in central nervous system effects in several animal species.
1. Humans — Five of twenty dental technicians who handled methyl methacrylate daily complained
of neurological problems in their hands (U.S. EPA 1985). Measurement of distal sensory
conduction velocities in the technicians revealed mild axonal degeneration in the areas of the hand
with the closest and most frequent methyl methacrylate contact.
Eighteen workers, employed for an average of 12 years in a factory manufacturing polymethyl
methacrylate sheet, were divided into two groups, the first with exposure to <410 mg/m3 and the
second with exposure to >410 mg/m3. Both groups exhibited nervous disorders (no details were
available) (U.S. EPA 1985).
Among the one hundred and fifty two workers exposed to 2 - 200 mg/m3 (0.5-50 ppm) methyl
methacrylate there were several reported adverse effects, including headaches, pain in extremities,
sleep disturbance, loss of memory, and irritability. An unspecified 'most' of these workers had
been employed for > 10 years (U.S EPA 1985).
2. Animals — Rats exposed by inhalation to 400 ppm (1784 mg/m3) of methyl methacrylate for 60
minutes exhibited depressed multiple-unit electrical activity in the lateral hypothalamus and
ventral hippocampus. Exposures of guinea pigs and mice to 10,000 to 11,000 ppm for 0.5 to 3
hours/day for 15 days resulted in CNS depression and death apparently due to respiratory arrest
(ACGIH 1991). Lethal concentrations of methyl methacrylate (3000 and 5000 ppm administered
for 14 weeks) produced cerebellar congestion and hemorrhage into the cerebellar peduncles,
malacia, and gliosis in F344/N rats (NTP 1986).
V. ENVIRONMENTAL EFFECTS
Methyl methacrylate is toxic to fish and Daphnia and inhibited cell multiplication in microorganisms only at high
concentrations. Toxicity values for aquatic organisms are greater than 100 mg/L. Methyl methacrylate is acutely
toxic to terrestrial animals only when present at very high concentrations.
A. Toxicity to Aquatic Organisms
The 24-, 48-, and 96-hour LC50 values in soft water are 421-455, 338-455, and 159-160 mg/L methyl
methacrylate, respectively, for Pimephales promelas (fathead minnow); 368, 358, and 232 mg/L,
respectively, for Lepomis macrochirus (bluegill); and 423, 423, and 277 mg/L, respectively, for
Carassius auratus (goldfish) (U.S. EPA 1985). ForLeuciscus idus (golden orfe), the 48-hour LC0, LC50,
and LC100 for methyl methacrylate were 320, 350, and 380 mg/L; for Daphnia magna (water flea) in the
immobilization assay, the 24-hour EC0, EC50, and EC100 values were 502, 720, and 1042 mg/L (U.S. EPA
1985). The toxicity threshold levels of methyl methacrylate inhibiting cell multiplication were 37 mg/L
(8 days of exposure) for Scenedesmus quadricauda (green algae), 100 mg/L (16 hours) for Pseudomonas
putida (bacteria), and 450 mg/L (72 hours) for Entosiphon sulcatum (protozoa) (U.S. EPA 1985).
B. Toxicity to Terrestrial Organisms
No information was found in the available literature for the toxicity of methyl methacrylate to terrestrial
organisms. The oral LD50 values are greater than 5g/kg for rats and for mice (U.S. EPA 1985). Methyl
methacrylate is acutely toxic to terrestrial animals only at very high concentrations.
C. Abiotic Effects
The ozone-forming potential of methyl methacrylate (see section III.C. 1 and U.S. EPA 1985) indicates that
the chemical may contribute to the formation of photochemical smog.
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VI. EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY
The Clean Air Act Amendments of 1990 list methyl methacrylate as a hazardous air pollutant. Occupational
exposure to methyl methacrylate is regulated by the Occupational Safety and Health Administration. The
permissible exposure limit (PEL) is 100 parts per million parts of air (ppm) as an 8-hour time-weighted average
(TWA) (29 CFR 1910.1000). 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 5 and
6) should be contacted regarding workplace exposures.
TABLE 5. EPA OFFICES AND CONTACT NUMBERS INFORMATION ON METHYL METHACRYLATE
EPA Office Statute Phone Number
Pollution Prevention & Toxics PPAa (202)260-1023
EPCRA(§313/TRI)b (800)535-0202
TSCA (§ 8A, §8D)C (800) 554-1404
Air Clean Air Act (§111, §112B)d (919)541-0888
Solid Waste & RCRA (U Waste)6 (800) 535-0202
Emergency Response CERCLA (RQ, 1000 pounds)f (800)535-0202
Water Clean Water Act (§311 )9 (202) 260-7588
aPPA: Pollution Prevention Act
bEPCRA: Emergency Planning and Community Right to Know Act of 1986
CTSCA: Toxic Substances Control Act
dCAA: Listed as hazardous air pollutant under § 112 of Clean Air Act [42 U.S.C. 7401 et seq.; NAAQS =
National Ambient Air Quality Standards (40 CFR 50.4, 50.6, 50.8, and 50.9-50.12).
eRCRA: The Resource Conservation and Recovery Act of 1976, (codified as amended at 42 U.S.C. §6901
et seq.
fCERCLA: 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).
SCWA: Clean Water Act. Regulates waters of the United States, including surface waters, ground waters,
and wetlands [40 CFR Part 131 (1994)] (U.S. EPA 1994b).
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TABLE 6. OTHER FEDERAL OFFICES/CONTACT NUMBERS FOR INFORMATION ON METHYL
METHACRYLATE
Other Agency/Department/Group Phone Number
American Conference of Governmental Industrial Hygienists (513) 742-2020
(TLV-TWA, 100 ppm; 410 mg/m3)3
Agency of Toxic Substances & Disease Registry (404) 639-6000
(Group 4, priority list 2)
Consumer Product Safety Commission (301) 504-0994
Food & Drug Administration (301) 443-3170
National Institute for Occupational Safety & Health (800) 356-4674
(TWA, 100 ppm; 410 mg/m3; IDLH, 4000 ppm)b
Occupational Safety & Health Administration
(TWA, 100 ppm; 410 mg/m3)c
(Check local phonebook under Department of Labor)
aTLV-TWA: Time-weighted-average concentration for a normal 8-hour workday and a 40-hour workweek to
which nearly all workers may be repeatedly exposed without adverse effects (ACGIH 1993-1994).
bTWA: Time-weighted-average concentrations for up to a 10-hour workday during a 40-hour workweek; IDLH:
immediate danger to life and health (NIOSH 1990, 1992).
c
TWA: Time-weighted-average that must not be exceeded during any 8-hour work shift of a 40-hour
workweek. Standard promulgated pursuant to the Occupational Safety and Health Act, 29 CFR 1910 (OSHA
1993).
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VII. CITED REFERENCES
ACGIH (American Conference of Governmental Industrial Hygienists, Inc). 1991. Methyl methacrylate. In:
Documentation of the Threshold Limit Values and Biological Exposure Indices, 6th ed. ACGIH, Cincinnati,
OH, pp. 1029-1033.
ACGIH. 1993-1994. American Conference of Governmental Industrial Hygienists. Threshold Limit Values
for Chemical Substances and Physical Agents and Biological Exposure Indices. ACGIH, Cincinnati, OH.
CHEMFATE. 1994. Syracuse Research Corporation's Environmental Fate Data Base. Retrieved 11/94.
Hansch and Leo. 1985.
IARC. 1987. International Agency for Research on Cancer. IARC Monographs on the Evaluation of
Carcinogenic Risk of Chemicals to Man. Overall evaluations of carcinogenicity. An updating of Vols. 1 to 42.
IARC, Lyon, p. 66.
Keith LH, Walters DB. 1985. Compendium of Safety Data Sheets for Research and Industrial Chemicals,
Part II. VCH Publishers, Deerfield Beach.
Mannsville Chemical Products Corporation. Methyl methacrylate. Chemical Products Synopsis, November
1993.
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. 1990. National Institute for Occupational Safety and Health. 1990. Pocket Guide to Chemical
Hazards, 1990 and NIOSH Recommendations for Occupational Safety and Health Compendium of Policy
Documents and Statements, 1992.
NTP. 1986. National Toxicology Program. Toxicology and Carcinogenesis Studies of Methyl Methacrylate
(CAS No. 80-62-6) in F344/N Rats and B6C3F., Mice (Inhalation Studies). National Toxicology Program,
Research Triangle Park, NC. NTP TR 314.
OSHA. 1993. Occupational Safety and Health Administration. Air Contaminants. Final rule. 29 CFR 1910.
Fed. Reg. 58:35338-35351.
Ricerca, Inc. 1991. Adsorption and desorption of methyl methacrylate in soils (final report) with cover letter
dated 6/28/91. OPPT, U.S. EPA, Washington, D.C. (Cited in TSCATS 1994)
TRI92. 1994. 1992 Toxics Release Inventory. Public Data Release. Office of Pollution Prevention and
Toxics (7408), U.S. Environmental Protection Agency, Washington, D.C., p. 92.
TSCATS. 1994. MEDLARS Online Information Retrieval System, National Library of Medicine.
U.S. EPA. 1994a. U.S. Environmental Protection Agency. Methyl Methacrylate (90:10): Acute Percutaneous
Absorption Potential (Final Report). OPPT, U.S. EPA, Washington, D.C. (Cited in TSCATS 1994)
U.S. EPA. 1994b. U.S. Environmental Protection Agency. Clean Water Act. 40 CFR Part 131.
U.S. EPA. 1990. U.S. Environmental Protection Agency. Draft Health and Environmental Effects Document
for Methyl Methacrylate. ECAO, U.S. Environmental Protection Agency. ECAO-CIN-G124.
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U.S. EPA. 1985. U.S. Environmental Protection Agency. Health and Environmental Effects Profile for Methyl
Methacrylate. Prepared for Office of Solid Waste and Emergency Response. Environmental Criteria and
Assessment Office, U.S. EPA, Cincinnati, OH. ECAO-CIN-P144.
Verschueren, K. 1983. Handbook of Environmental Data on Organic Chemicals, 2nd ed. Van Nostrand
Reinhold Co., New York, pp. 860-861.
U.S. International Trade Commission. Synthetic Organic Chemicals: United States Production and Sales,
1992, 76th edition. USITC Publication 2720, February 1994.
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APPENDIX A. SOURCES SEARCHED FOR FACT SHEET PREPARATION
ACGIH. Most recent. American Conference for Governmental Industrial Hygienists, Inc. TLVs®. Documentation of the Threshold Limit Values and
Biological Exposure Indices, ... ed. 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)
CHEMFATE. 1994. Syracuse Research Corporation's Environmental Fate Data Base. Retrieved Oct. 1994.
Clean Air Act. 1990. As amended. 42 U.S.C. 7412.
GENETOX. 1994. U.S. EPA GENETOX Program, computerized database.
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. 19.... International Programme on Chemical Safety. Environmental Health Criteria. World Health Organization, Geneva, Switzerland.
Mannsville Chemical Products Corporation. Methyl methacrylate. Chemical Products Synopsis, November 1993.
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.
NTP. 199... National Toxicology Program. Toxicology and Carcinogenesis Studies. Tech Rep Ser.
NTP. 199... 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-1A. Limits for Air Contaminants.
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. 199... 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.
U.S. International Trade Commission. Synthetic Organic Chemicals: United States Production and Sales, 1992, 76th edition. USITC Publication 2720,
February 1994.
A-1
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