N,N-Dimethyl-p-toluidin

log Kow = 2.81

2.61

2.85

0.9366 g/cu cm at 20 °C

Relative density (water = 1): 0.9

Clear colorless liquid

Colorless to brown oil

In water, 455 mg/L

In water, 650 mg/L at 37 °C

Miscible with ethanol, ethyl ether; soluble in carbon tetrachloride

Solubility in water, g/l at 37 °C: 0.65 (very slightly soluble)

76 °C (closed cup)

83 °C

211 °C

215 °C

Danger

H301: Toxic if swallowed [Danger Acute toxicity, oral]

P203, P260, P261, P264, P270, P271, P273, P280, P301+P316, P304+P340, P317, P318, P319, P321, P330, P405, and P501 (click each P-code to see the statement)

This chemical does not meet GHS hazard criteria for 0.2% (1 of 563) of reports.

Danger

H301+H311+H331 (21.7%): Toxic if swallowed, in contact with skin or if inhaled [Danger Acute toxicity, oral; acute toxicity, dermal; acute toxicity, inhalation]

Chemical: Benzenamine, N,N,4-trimethyl-

Hazard Traits - Carcinogenicity

Benzenamine, N,N,4-trimethyl- is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Benzenamine, N,N,4-trimethyl- are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Status: Active Update: 13-04-2023 https://echa.europa.eu/registration-dossier/-/registered-dossier/8746

Dimethyl-p-toluidine: Does not have an individual approval but may be used under an appropriate group standard

Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]:

Combustible. Above 83 °C explosive vapour/air mixtures may be formed.

N,N-DIMETHYL-P-TOLUIDINE neutralizes acids in exothermic reactions to form salts plus water. May be incompatible with isocyanates, halogenated organics, peroxides, phenols (acidic), epoxides, anhydrides, and acid halides. May generate hydrogen, a flammable gas, in combination with strong reducing agents such as hydrides.

Excerpt from ERG Guide 153 [Substances - Toxic and/or Corrosive (Combustible)]:

Use powder, AFFF, foam, carbon dioxide.

Fresh air, rest. Refer for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap. Refer for medical attention .

Rinse with plenty of water (remove contact lenses if easily possible).

Rinse mouth. Give nothing to drink. Refer for medical attention .

Wear self contained breathing apparatus for fire fighting if necessary.

Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Use water spray to cool unopened containers.

Empty containers retain product residue, (liquid and/or vapor), and can be dangerous. Keep container tightly closed.

Keep container tightly closed in a dry and well-ventilated place. Containers which are opened must be carefully resealed and kept upright to prevent leakage.

Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Contain spillage, and then collect with an electrically protected vacuum cleaner or by wet-brushing and place in container for disposal according to local regulations. Keep in suitable, closed containers for disposal.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal and plant life; and conformance with environmental and public health regulations.

Product: This combustible material may be burned in a chemical incinerator equipped with an afterburner and scrubber. Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Contaminated packaging: Dispose of as unused product.

Personal protection: complete protective clothing including self-contained breathing apparatus. Collect leaking and spilled liquid in sealable containers as far as possible. Absorb remaining liquid in sand or inert absorbent. Then store and dispose of according to local regulations.

Camphorquinone (CQ) is widely used as an initiator in modern visible-light (VL) cured resin systems. CQ is also characterized as a potential allergenic compound. To date, there is growing concern that CQ may produce genetic damage by inducing mutation. In this study, CQ in the presence of reducing agent N,N-dimethyl-p-toluidine (DMT) with or without VL irradiation was analyzed for the induction of chromosomal aberrations indicated by micronuclei (MN) induced in CHO cells. /The/ data demonstrated that an increase in the numbers of MN was observed with CQ/DMT with or without VL irradiation (p < 0.05). Significant prolongation of cell cycles was observed by the treatment with CQ/DMT with or without VL irradiation (p < 0.05). In addition, VL irradiated CQ/DMT was found to exhibit significantly genotoxic and cytotoxic effects as compared with CQ/DMT alone (p < 0.05). Furthermore, to determine whether oxidative stress could modulate the MN induced by CQ/DMT with or without VL irradiation in CHO cells, cells were pre-treated with various antioxidants 10 mM N-acetyl-L-cysteine (NAC), 2 mM ascorbic acid, and 2 mM alpha-tocopherol. The pre-treatment with antioxidants could antagonize not only the increased MN cells but also the prolonged cell cycle induced by CQ/DMT with or without VL irradiation in CHO cells (p < 0.05). /These/ findings provide the evidences for the induction of MN by CQ/DMT employing mammalian test system, indicating clastogenic activity of CQ/DMT with or without VL irradiation in vitro. In addition, VL irradiated CQ/DMT exhibits higher genotoxic and cytotoxic effects than CQ/DMT alone. Moreover, NAC, ascorbic acid, and alpha-tocopherol act as the antagonists against the genotoxicity and cytotoxicity of CQ/DMT with or without VL irradiation.

9-Fluorenone (9F), the aromatic photosensitizer, is widely used as an initiator in visible-light (VL) cured resin systems. There is growing concern that 9F may produce genetic damage by inducing mutation. In this study, 9F in the presence or absence of reducing agent N,N-dimethyl-p-toluidine (DMT) with or without VL irradiation was analyzed for the induction of chromosomal aberrations indicated by micronuclei (MN) induced in CHO cells. /The/ data demonstrated that a dose-related increase in the frequency of MN and prolonged cell cycles in 9F with or without DMT in the presence or absence of VL irradiation (p < 0.05). The rank orders with respect to genotoxicity and cytotoxicity were found to be as follows: 9F/DMT +VL > 9F/DMT = 9F + VL > 9F. To determine whether oxidative stress could modulate MN induced by 9F/DMT with or without VL irradiation in CHO cells, cells were pretreated with N-acetyl-L-cysteine (NAC), ascorbic acid, and alpha-tocopherol. The pretreatment with antioxidants could diminish not only the prolonged cell cycle but also the decreased frequency of MN which is induced by 9F with or without DMT in the presence or absence of VL irradiation in CHO cells (p < 0.05). /These/ findings provide the evidences for the induction of MN by 9F in the presence or absence of DMT with or without VL irradiation in CHO cells, indicating clastogenic activity of 9F/DMT in vitro. These antioxidants act as the antagonists against the genotoxicity and cytotoxicity of 9F/DMT. Thus, leaching photoinitiator and reducing agent might be contributing the sources of oxidative stress.

Resin composites are widely used in dentistry, and are polymerized in situ using a blue-light activated, free-radical polymerization mechanism. Blue light (400-500nm) is used to activate camphoroquinone (CQ), which decomposes to form free radicals that are stabilized by dimethyl-p-toludine (DMPT). CQ and DMPT are applied near tooth pulpal tissues and are irradiated during restorative procedures, suggesting that pulpal cells are exposed to free radicals. Because glutathione is a major component of the cellular redox management system, /the study/ tested the hypothesis that blue light irradiation would shift cellular glutathione redox balance of cells exposed to CQ and DMPT. /The study/ also measured NFkappaB activation, a redox-sensitive transcription factor that regulates inflammatory responses and glutathione synthetic enzyme levels. THP1 human monocytes were exposed to sublethal levels of CQ (0.4 mM) or DMPT (1.0 mM), with or without blue light exposure (25 J/sq cm) from a quartz-tungsten-halogen source. The ratio of reduced to oxidized glutathione was measured using as assay based on 5,5'-dithio-bis(2-nitrobenszoic acid). NFkappaB transactivation was measured by transfection of an NFkappaB-containing plasmid linked to a luciferase reporter. Our results showed that blue light, CQ, or DMPT alone had no significant effect on cellular glutathione redox balance, but that the combination of these agents induced a marked oxidative bias, and reduced total glutathione levels up to 50%. On the other hand, light, CQ, and DMPT alone or in combination suppressed NFkappaB transactivation by >70%. Our results suggest that CQ and DMPT pose risks to pulpal tissues with or without blue light irradiation, and that multiple, interacting mechanisms shape the response to these agents.

LC50; Species: Oryzias latipes (Japanese Medaka) length 2 cm, weight 0.2 g; Conditions: freshwater, static, 25 °C; Concentration: 44000 ug/L for 24 hr

LC50; Species: Oryzias latipes (Japanese Medaka) length 2 cm, weight 0.2 g; Conditions: freshwater, static, 25 °C; Concentration: 20000 ug/L for 48 hr

LC50; Species: Pimephales promelas (Fathead minnow); Conditions: flow through; Concentration: 48.9 mg/L for 96 hr (geometric mean of studies)

LC50; Species: Pimephales promelas (Fathead Minnow) age 32 days, length 24.5 mm, weight 0.242 g; Conditions: freshwater, flow through, 24.9 °C, pH 7.4, hardness 40.3 mg/L CaCO3, alkalinity 46.1 mg/L CaCO3, dissolved oxygen 5.0 mg/L; Concentration: 46000 ug/L for 96 hr (95% confidence interval: 42000-50500 ug/L) /99% purity/

For more Ecotoxicity Values (Complete) data for Dimethyl-4-toluidine (6 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 260(SRC), determined from a log Kow of 2.81(2) and a regression-derived equation(3), indicates that dimethyl-4-toluidine is expected to have moderate mobility in soil(SRC). The pKa of dimethyl-4-toluidine is 5.63(4), indicating that this compound will exist partially in the cation form in the environment and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5). Volatilization of the neutral species of dimethyl-4-toluidine from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 7.0X10-5 atm-cu m/mole(SRC), derived from its vapor pressure, 0.178 mm Hg(6), and water solubility, 455 mg/L(7). Dimethyl-4-toluidine is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(6). Biodegradation data in soil were not available(SRC, 2014).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 260(SRC), determined from a log Kow of 2.81(2) and a regression-derived equation(3), indicates that dimethyl-4-toluidine is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(4) based upon an estimated Henry's Law constant of 7.0X10-5 atm-cu m/mole(SRC), derived from its vapor pressure, 0.178 mm Hg(5), and water solubility, 455 mg/L(6). Using this Henry's Law constant and an estimation method(4), volatilization half-lives for a model river and model lake are 1 and 10 days, respectively(SRC). According to a classification scheme(7), an estimated BCF of 33(SRC), from its log Kow(2) and a regression-derived equation(3), suggests the potential for bioconcentration in aquatic organisms is moderate(SRC). Biodegradation data in water were not available(SRC, 2014).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), dimethyl-4-toluidine, which has a vapor pressure of 0.178 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase dimethyl-4-toluidine is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 2 hrs(SRC), calculated from its rate constant of 2.0X10-10 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Dimethyl-4-toluidine does not contain chromophores that absorb at wavelengths >290 nm(4) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

IDENTIFICATION AND USE: Dimethyl-4-toluidine is a clear to yellow liquid with an aromatic odor; insoluble in water. Dimethyl-4-toluidine is an accelerator in the redox initiator-accelerator system used commercially to cure methyl methacrylate monomers. It is a high-production volume chemical with potential for widespread human exposure through its use in dental materials and bone cements. Dimethyl-4-toluidine has been used in the preparation of acrylic denture materials for the past 50 years. It is used as the accelerator for the cement in most of the hip and bone replacements to activate the polymerization reaction. Dimethyl-4-toluidine is found in industrial glues and artificial fingernail preparations and is used as an intermediate in dye and pesticide synthesis. HUMAN EXPOSURE AND TOXICITY: Toxic by skin absorption and inhalation. Short-term exposure effects are mostly hematotoxic (methemoglobinemia causing cyanosis, brain damage and renal insufficiency) and may be delayed. Exposure to high concentrations may lead to death. An acute cyanotic episode due to methemoglobinemia occurred in a 16-month old girl following the ingestion of dimethyl-4-toluidine (6 mg/kg of body weight ) used in the production of artificial fingernails. Administration of methylene blue was effective in the reversal of the methemoglobinemia. In vitro studies suggest that the activity of the compound was probably due to its biochemical transformation to the toxic metabolite p-methylphenylhydroxylamine. There is potential for widespread human exposure to dimethyl-4-toluidine in occupational settings where bone cements, dental prostheses, industrial glues, and artificial fingernails are manufactured or used. Exposure to dimethyl-4-toluidine may be a concern because of the possible release of unreacted chemicals from polymeric composites. "Sniffing" glue is one possible means of exposure to dimethyl-4-toluidine. Contact allergy to dimethyl-4-toluidine was reported in 3 cases among 22 patients with the burning mouth syndrome who wore complete or partial dentures. ANIMAL STUDIES: Under the conditions of the NTP 2-year oral gavage studies, there was clear evidence of carcinogenic activity of dimethyl-4-toluidine in rats based on increased incidences of hepatocellular carcinoma, and hepatocellular adenoma or carcinoma (combined) in male and female rats, and increased incidences of nasal cavity neoplasms (primarily nasal cavity transitional epithelium adenoma) in male rats. There was clear evidence of carcinogenic activity of dimethyl-4-toluidine in mice based on increased incidences of hepatocellular adenoma (multiple), hepatocellular carcinoma, and hepatoblastoma in male and female mice, and increased incidences of alveolar/ bronchiolar neoplasms (primarily adenoma)in female mice. Administration of dimethyl-4-toluidine resulted in increased incidences of nonneoplastic lesions of the liver and nasal cavity in male and female rats and mice; the kidney in male and female rats; the spleen and bone marrow in male and female rats and female mice; the lung in male and female mice; the forestomach in male rats and female mice; the mesenteric lymph node in male rats and female mice; and the olfactory lobe in male and female mice. Dimethyl-4-toluidine also caused hematologic toxicity and increases in methemoglobin levels in male and female rats and mice (as measured at 3 months). Dimethyl-4-toluidine was tested in two independent bacterial gene mutation studies; both studies gave negative results in S. typhimurium or E. coli tester strains, with and without exogenous metabolic activation. No significant increases in the frequencies of micronucleated erythrocytes were observed in peripheral blood of male or female mice treated with dimethyl-4-toluidine by gavage for 3 months. Furthermore, no increases in micronucleated reticulocytes were observed in male mice treated with dimethyl-4-toluidine for 4 days. Results of DNA damage (comet) studies yielded mixed results. No increases in DNA damage (measured as percent tail DNA) were seen in liver cells or blood leukocytes of male mice administered dimethyl-4-toluidine by gavage once daily for 4 days. However, a small but significant increase in DNA damage was seen in liver cells of male rats administered 60 mg/kg dimethyl-4-toluidine once daily for 4 days. It was also tested for structural and numerical chromosome aberrations in hamster V79 cells (micronucleus test, matched with an immunofluorescent staining for kinetochore proteins), and in vivo DNA damage in mouse and rat liver (alkaline DNA elution test). The results essentially indicate that the chemical is a chromosome damaging agent.

Fatigue. Headache. Dizziness. Nausea. Blue lips, fingernails and skin. Convulsions. Unconsciousness.

MAY BE ABSORBED! See Inhalation.

See Inhalation.

EPA has released the first beta version (version 0.5) of the Interactive Chemical Safety for Sustainability (iCSS) Dashboard. The beta version of the iCSS Dashboard provides an interactive tool to explore rapid, automated (or in vitro high-throughput) chemical screening data generated by the Toxicity Forecaster (ToxCast) project and the federal Toxicity Testing in the 21st century (Tox21) collaboration. /The title compound was tested by ToxCast and/or Tox21 assays; Click on the "Chemical Explorer" button on the tool bar to see the data./[USEPA; ICSS Dashboard Application; Available from, as of June 27, 2014: http://actor.epa.gov/dashboard/]

The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical.[Available from, as of June 30, 2014: http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=99-97-8]

The Koc of dimethyl-4-toluidine is estimated as 260(SRC), using a log Kow of 2.81(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that dimethyl-4-toluidine is expected to have moderate mobility in soil. The pKa of dimethyl-4-toluidine is 5.63(4), indicating that this compound will exist partially in the cation form and cations generally adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5). A Kd value of 380 for sorption to monmorillonite has been reported(6).

/HUMAN EXPOSURE STUDIES/ Aseptic loosening is seen in a significant proportion of cemented total hip replacements (THR). In a small subgroup of patients who suffer early loosening polyethylene debris is unlikely to be responsible. ...one case of allergic contact dermatitis to N,N-dimethylparatoluidine (DMT), an accelerator used in bone cement /was recently reported/. /This study/ have therefore investigated this using skin-patch tests to a variety of substances including metals, polyethylene and the separated individual components of Simplex cement. /The study tested/ 70 patients, 15 with aseptic loosening less than two years after THR, 25 with satisfactory long-term cemented fixation, five with infected loosening of cemented THRs and 25 awaiting hip arthroplasty. /The study/ found seven positive reactions to DMT, all of them in patients with the rapid onset of aseptic loosening. Allergy to DMT is recognized in the dental profession in respect of the 'denture sore mouth' syndrome, and could also be an occupational hazard since some industrial glues contain DMT. /These/ results suggest the need for awareness of possible previous dental or occupational exposure of the constituents of bone cement. /The study/ recommend the use of skin-patch testing in high-risk cases.

/HUMAN EXPOSURE STUDIES/ The pathogenesis of the burning mouth syndrome (BMS) is not yet understood. Apart from psychologic factors, several etiologic "somatic" factors have been reported. In 22 patients (19 women, 3 men, mean age 56 years) classified with BMS, clinical and laboratory investigations were performed, with particular emphasis on the role of contact hypersensitivity. Twenty of the 22 patients wore a complete or partial denture. Besides clinical and laboratory investigations patch testing was performed with a standard routine series and a standardized denture-dental (acrylate and metal) series. Folate, iron, pyridoxine deficiency, and Candida infections were found, but correction of the deficiency or treatment of the infection was of no benefit. Contact allergy to allergens used in the production of acrylate-based dentures was observed in six (27%) of the cases (all wore a denture); positive reactions were seen to N,N,-dimethyl-4-toluidine (3 cases), to 4-tolyldiethanolamine (2 cases), to benzoylperoxide (2 cases), and to oligotriacrylate (1 case). In six cases (27%) a possible relevant sensitization was seen to dental metals and in particular to gold chloride (four cases).

/SIGNS AND SYMPTOMS/ Short-term exposure effects: skin absorption; delayed effects; hematotoxic effects (methemoglobinemia causing cyanosis, brain damage and renal insufficiency); exposure to high concentrations may lead to death.

/CASE REPORTS/ An acute cyanotic episode due to methemoglobinemia occurred in a 16-month old girl following the ingestion of N,N-dimethyl-p-toluidine, a commercially available component used in the production of artificial fingernails. The amount of the parent compound ingested was about 6 mg/kg of body weight. Administration of methylene blue was effective in the reversal of the methemoglobinemia. In vitro studies suggest that the activity of the compound was probably due to its biochemical transformation to the toxic metabolite p-methylphenylhydroxylamine. /The study/ expand the list of aromatic amino or nitro compounds and their derivatives capable of producing methemoglobinemia and call attention to the hazard of their ingestion.

For more Human Toxicity Excerpts (Complete) data for Dimethyl-4-toluidine (8 total), please visit the HSDB record page.

Dimethyl-4-toluidine's production and use as a polymerization accelerator in the manufacture of bone cements and dental materials, in industrial glues, and as an intermediate in dye and pesticide synthesis(1) may result in its release to the environment through various waste streams(SRC).

The metabolism of orally administered N,N-dimethyl-p-toluidine (DMPT) in male F344 rats was investigated. The rat urinary metabolite profile was determined by analytical reverse-phase high performance liquid chromatography (HPLC). Four radiolabeled peaks were observed, isolated, and purified by solid-phase extraction (SPE) and preparative HPLC methods. The 4 peaks were identified as p-(N-acetylhydroxyamino)hippuric acid (M1), DMPT N-oxide (M2), N-methyl-p-toluidine (M3), and parent DMPT. Metabolites M1 and M2 were identified by spectrometric and spectroscopic methods, including mass fragmentation pattern identification from both liquid chromatography/mass spectrometry and gas chromatography/mass spectrometry, and from chemical analysis of nuclear magnetic resonance spectra. Structural confirmation of metabolite M2 was accomplished by comparison with a synthetic standard. Peaks M3 and the peak suspected to be DMPT were identified by comparison of their HPLC retention times and mass fragmentation patterns with authentic standards of N-methyl-p-toluidine and DMPT, respectively. DMPT metabolism is similar to that reported for N,N-dimethylaniline.

DMPT is used as a polymerization accelerator in the manufacture of bone cements and dental materials, in industrial glues, and as an intermediate in dye and pesticide synthesis. Thus, there is potential for human exposure to DMPT, an aromatic amine with a structural alert for potential DNA reactivity. The National Toxicology Program (NTP) is evaluating the toxicity and carcinogenicity of DMPT in male and female Fischer 344 rats and B6C3F1 mice. To aid in the design and interpretation of those studies, we have investigated the excretion and tissue distribution of oral and intravenous (IV) doses of radiolabeled DMPT in these strains of rodents. A single low (2.5 mg/kg), mid (25 mg/kg) or high (250 mg/kg) dose of carbon-14 labeled DMPT was administered. Excreta collected for up to 72 hr after dosing and tissues collected at sacrifice were analyzed for total radioactivity. Early studies were terminated at 72 hr. After a low IV dose to male rats ~100% of the dose was excreted and <2% was recovered in tissues at 72 hr. The high oral dose was acutely toxic to male mice. The same oral dose was not overtly toxic to male rats, and by 72 hr 86% of the dose was excreted and 2% remained in tissues. Subsequent studies were terminated at 24 hr to better understand the tissue distribution of radioactivity at earlier time points, which are more relevant to the interpretation of repeated dose toxicity studies. After the high oral dose to male rats ~18% of the dose was recovered in tissues and ~72% was excreted by 24 hr. In contrast, at the low and mid doses most of the radioactivity (~83-100%) was excreted by 24 hr and <5% remained in tissues. In summary, DMPT derived radioactivity was rapidly excreted by rats and mice after a single oral or IV dose and no striking sex differences in DMPT disposition were observed within a species. However, dose dependent differences in toxicity and disposition were observed. These data will be used to aid in the interpretation of safety/toxicity studies of DMPT conducted by the NTP.

DMPT is a high-production-volume chemical used in the manufacture of bone cements and dental materials, is found in industrial glues and artifical fingernail preparations, and is used as an intermediate in dye and pesticide synthesis. Human exposure to DMPT has resulted in methemoglobinemia and allergic responses; suspected from the formation of a toxic metabolite, p methylphenylhydroxylamine, an analog of the aniline metabolite phenylhydroxlyamine (thought to be responsible for methemoglobinemia from aniline exposure). ...results of disposition studies of DMPT in Fisher 344 (F344) rats and B6C3F1 mice after oral administration of [(14)C]DMPT /were previously reported/. The majority of [(14)C]DMPT-derived radioactivity was excreted in urine by 24 hours. /This study/ report on the metabolism of orally administered DMPT. The profile of radiolabeled metabolites was determined by liquid chromatography (HPLC) using a C18 stationary phase and a mobile phase that transitioned from mostly water (polar) to mostly organic (neutral). The same four radiolabeled chromatographic peaks were observed in both rats and mice. Due to the limited volume of mouse urine, further work to elucidate the DMPT metabolite structures was performed with rat urine only. All four peaks have been isolated and preliminary structural elucidation by gas chromatography/mass spectrometry (GC/MS) and comparison to authentic standards confirmed excretion of the parent compound. We have tentatively identified a second peak by GC/MS as N-methyl-p-toluidine. A third peak had different HPLC and GC retention times than DMPT but an identical electron impact mass spectrum. Attempts at preliminary identification of the most polar metabolite have been unsuccessful. Further purification coupled with infrared and nuclear magenetic resonance spectroscopy will be employed along with incubation of isolated metabolites with glucuronidase and sulfatase enzymes (to assess conjugation) to complete structural elucidation/confirmation

Used to accelerate polymerization of ethyl methacrylate; Used in artificial nail application; [Olson, p. 702]

Plastic Composites Manufacturing [Category: Industry]

N,N-Dimethyl-p-toluidine is an accelerator in the redox initiator-accelerator system used commercially to cure methyl methacrylate monomers. Polymerization is rarely complete

N,N-Dimethyl-p-toluidine is a high-production volume chemical with potential for widespread human exposure through its use in dental materials and bone cements

N,N-Dimethyl-p-toluidine has been used in the preparation of acrylic denture materials for the past 50 years. It is used as the accelerator for the cement in most of the hip and bone replacements to activate the polymerization reaction at concentrations ranging from 0.7% to 2.6% . N,N-Dimethyl-p-toluidine is found in industrial glues and artificial fingernail preparations and is used as an intermediate in dye and pesticide synthesis. It has a shorter setting time (11.5 minutes) than some alternative accelerators.

2023: 301,589 lb

Benzenamine, N,N,4-trimethyl- is listed as a High Production Volume (HPV) chemical (65FR81686). Chemicals listed as HPV were produced in or imported into the U.S. in >1 million pounds in 1990 and/or 1994. The HPV list is based on the 1990 Inventory Update Rule. (IUR) (40 CFR part 710 subpart B; 51FR21438).

Production volumes for non-confidential chemicals reported under the Inventory Update Rule.[Table#8190]

Production volume for non-confidential chemicals reported under the 2006 Inventory Update Rule. Chemical: Benzenamine, N,N,4-trimethyl-. Aggregated National Production Volume: 1 to < 10 million pounds.

Non-confidential 2014 Chemical Data Reporting (CDR) information on the production and use of chemicals manufactured or imported into the United States. Chemical: Benzenamine, N,N,4-trimethyl-. National Production Volume: 1,000,000 - 10,000,000 lb/yr.

Miscellaneous Manufacturing

Benzenamine, N,N,4-trimethyl-: ACTIVE

The residual amounts of N,N-dimethyl-p-toluidine in acrylic resins have been reported to be 0.6% after storage in water for up to 15 months. Others have detected up to 0.2% of N,N-dimethyl-p-toluidine in methyl methacrylates after long term implantation...

Acryl resins used in dental practice are blends of poly(methyl methacrylated) particles and methyl methacrylate monomer, or copolymers of methyl methacrylate with styrene or other acrylic monomers. This blend is a slurry of high viscosity that is hardened by the free radical polymerization of the monomeric components. The hardening process is initiated by the decomposition of a small quantity of organic peroxides (1% to 3%; usually benzoyl peroxide) activated by the redox reaction with the tertiary amine. The tertiary amine, most often N,N-dimethyl-p-toluidine, is the ingredient that induces the reaction giving rise to free radicals capable of initiating polymerization of the acrylic monomers. Polymerization is rarely complete.