| GHS-Einstufung | WarningH302: Harmful if swallowed [Warning Acute toxicity, oral]P261, P264, P264+P265, P270, P271, P280, P301+P317, P302+P352, P304+P340, P305+P351+P338, P317, P319, P321, P330, P332+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)This chemical does not meet GHS hazard criteria for < 0.1% (1 of 1874) of reports.H302 (99.9%): Harmful if swallowed [Warning Acute toxicity, oral] |
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| Regulatorische Informationen | Chemical: 2H-Azepin-2-one, hexahydro-Hazard Traits - Ocular ToxicityRespiratory ToxicityCommission Regulation (EC) No 1565/2000 (Repealed by Com. Implementing Reg. (EU) No 872/2012)2H-Azepin-2-one, hexahydro- is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of 2H-Azepin-2-one, hexahydro- 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: 19-04-2023 https://echa.europa.eu/registration-dossier/-/registered-dossier/15939Caprolactam: Does not have an individual approval but may be used under an appropriate group standard |
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| Brandgefahren | Special Hazards of Combustion Products: Toxic oxides of nitrogen (USCG, 1999)Combustible. Gives off irritating or toxic fumes (or gases) in a fire. |
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| Gesundheitsgefahren | Inhalation causes coughing or mild irritation. Contact with hot liquid will burn eyes and skin. (USCG, 1999) |
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| Gefahrenübersicht | Caprolactam is used in the manufacture of synthetic fibers. Acute (short-term) exposure to caprolactam may result in irritation and burning of the eyes, nose, throat, and skin in humans. Headaches, malaise, confusion, and nervous irritation have been observed in workers exposed to caprolactam by inhalation. Chronic (long-term) exposure of workers to caprolactam has been observed to cause peeling of the hands and some eye, nose, and throat irritation, but no other effects on general health. EPA has not classified caprolactam for carcinogenicity.May cause skin sensitizationA skin, eye, and respiratory tract irritantInhalation of high concentrations may cause CNS effects[ICSC] Liver and kidney changes occur in subchronic animal studies using intraperitoneal doses. [ACGIH] |
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| Reaktive Gruppe | Amides and Imides |
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| EG-Einstufung | Symbol: XnR: 20/22-36/37/38S: (2) |
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| Special Reports | DHHS/NTPCarcinogenesis Bioassay of Caprolactam Technical Report Series No. 214 (1981) NIH Publication No. 81-1770 |
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| TSCA-Anforderungen | Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. 2H-Azepin-2-one, hexahydro- is included on this list. |
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| Reactivity Alerts | Polymerizable |
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| OSHA Standards | Vacated 1989 OSHA PEL TWA 1 mg/cu mSTEl 3 mg/cu m is still enforced in some states. /Dust/Vacated 1989 OSHA PEL TWA 5 ppm (20 mg/cu m)STEL 10 ppm (40 mg/cu m) is still enforced in some states. |
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| Reactivity Profile | CAPROLACTAM is hygroscopic. This compound can react with strong oxidizing agents and strong bases. It can also react with chlorinated hydrocarbons and nitro compounds. A potentially explosive reaction occurs with acetic acid + dinitrogen trioxide. (NTP, 1992) |
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| Luftstandards | This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, non air quality health and environmental impact and energy requirements. Caprolactam is produced, as an intermediate or a final product, by process units covered under this subpart.Listed as a hazardous air pollutant (HAP) generally known or suspected to cause serious health problems. The Clean Air Act, as amended in 1990, directs EPA to set standards requiring major sources to sharply reduce routine emissions of toxic pollutants. EPA is required to establish and phase in specific performance based standards for all air emission sources that emit one or more of the listed pollutants. Caprolactam is included on this list. |
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| Brandbekämpfung | Use foam, powder, carbon dioxide, water in large amounts. |
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| Erste-Hilfe-Maßnahmen | Fresh air, rest. Refer for medical attention.Remove contaminated clothes. Rinse skin with plenty of water or shower.Rinse with plenty of water (remove contact lenses if easily possible). Refer for medical attention.Rinse mouth. Refer for medical attention . |
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| Erste Hilfe | EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.(General first aid procedures) |
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| Sichere Lagerung | Separated from strong oxidants. Dry. |
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| Expositionsschutz und Persönliche Schutzausrüstung | 2.0 [mg/m3], inhalable fraction[German Research Foundation (DFG)] |
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| Entsorgungsverfahren | SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.Controlled incineration (oxides of nitrogen are removed from the effluent gas by scrubbers and/or thermal devices). Also caprolactam may be recovered from caprolactam still bottoms or nylon waste. Recommendable method: Incineration.The following wastewater treatment technologies have been investigated for caprolactam: biological treatment. |
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| Verschüttetes entsorgen | Let solidify. Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Wash away remainder with plenty of water. |
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| Preventive Measures | SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.ALL VESSELS & PIPING SHOULD BE REGULARLY CHECKED FOR LEAKS ... EXHAUST VENTILATION SHOULD BE INSTALLED.CONCN OF.../60 MG/CU M SHOULD/ BE AVOIDED, & HENCE WORKSHOPS SHOULD BE EFFECTIVELY VENTILATED.For more Preventive Measures (Complete) data for CAPROLACTAM (7 total), please visit the HSDB record page. |
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| Eye Prevention | Wear face shield or eye protection in combination with breathing protection. |
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| Fire Prevention | NO open flames. |
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| Inhalation Risk | A harmful concentration of airborne particles can be reached quickly when dispersed. |
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| Skin Prevention | Protective gloves. Protective clothing. |
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| Zielorgane | DevelopmentalEyes, skin, respiratory system, central nervous system, cardiovascular system, liver, kidneys |
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| Umweltverhalten | TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 57(SRC), determined from a structure estimation method(2), indicates that caprolactam is expected to have high mobility in soil(SRC). Volatilization of caprolactam from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 5.4X10-11 atm-cu m/mole from its vapor pressure, 1.9X10-3 mm Hg at 25 °C(5), and water solubility, 5.25X10+6 mg/l(6). Caprolactam is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 1.9X10-3 mm Hg at 25 °C(5). Caprolactam is degraded in aquatic environments with a half life of 5 to 15 days, and is expected to be degraded in aerobic soils in a similar timeframe(6).AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 57(SRC), determined from an estimation method(2), indicates that caprolactam is not expected to adsorb to suspended solids or to sediments in water(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 5.4X10-11 atm-cu m/mole(SRC) calculated from its vapor pressure, 1.9X10-3 mm Hg at 25 °C(4), and water solubility, 5.25X10+6 mg/l(5). According to a classification scheme(6), an estimated BCF of 3.1(SRC), from an estimated log Kow of 0.66(7) suggests the potential for bioconcentration in aquatic organisms is low. Biodegradation in aquatic environments is expected to be extensivecomplete degradation of 50-100 ug/ml caprolactam was observed in nutrient-amended or sediment-associated lake water in 21 days(8). Slightly less caprolactam was degraded (36-85%) after 21 days if higher concentrations (1000 to 2000 ug/ml) were used. However, in none of these control cases was any complete degradation (mineralization) of the caprolactam observed. Based on very slow hydrolysis rates of other aliphatic acid amides, hydrolysis is not expected to be an important fate process(5). Experiments conducted with sterile natural waters, however, demonstrated that caprolactam is abiotically degraded. It is not known whether or not the product of this abiotic degradation is the product of hydrolysis, aminocaproic acid(5).ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), caprolactam, which has a vapor pressure of 1.9X10-3 mm Hg at 25 °C(4), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase caprolactam 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 21 hours(SRC), calculated from its rate constant of 18X10-12 cu cm/molecule-sec at 25 °C(3). Caprolactam does not absorb light in the environmental spectrum (>290 nm), indicating there is little potential for direct photolysis. |
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| Unerwünschte Wirkungen | Neurotoxin - Other CNS neurotoxin |
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| Expositionspfade | The substance can be absorbed into the body by inhalation of its aerosol.inhalation, ingestion, skin and/or eye contact |
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| Signs and Symptoms | Cough. Abdominal cramps. Dizziness. Headache. Confusion.Redness.Redness. Pain.Nausea. Vomiting. Abdominal pain. Diarrhoea.irritation skin, eyes, respiratory systemepistaxis (nosebleed)dermatitis, skin sensitizationasthmairritability, confusion, dizziness, headacheabdominal cramps, diarrhea, nausea, vomitingliver, kidney injury |
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| Ongoing Test Status | 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. [http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=105-60-2] |
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| Effluent Concentrations | July 1976, dye manufacturing plant in MA, concn range 36-150 ug/L(1). Qualitatively identified in water samples taken from advance waste treatment plants in Lake Tahoe, CA Oct 1974 and Washington D.C. Sept 1974(2). Present in trace amounts in the waste waters from nylon 6 manufacturing plants in Japan and Russia(3). |
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| ICSC Environmental Data | This substance does enter the environment under normal use. Great care, however, should be taken to avoid any additional release, for example through inappropriate disposal. |
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| EPA IRIS Information | CaprolactamDevelopmental5 x 10 ^-1 mg/kg-day |
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| Medical Surveillance | ... PERSONS SUBJECT TO PROLONGED EXPOSURE TO EPSILON-CAPROLACTAM SHOULD BE MEDICALLY EXAMINED, ESP THEIR RESP, CIRCULATORY & NERVOUS SYSTEMS /SRP: SKIN, GENITOURINARY TRACT/. |
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| Soil Adsorption/Mobility | Using a structure estimation method based on molecular connectivity indices(1), the Koc for caprolactam is estimated to be 57(SRC). According to a classification scheme(2), this estimated Koc value suggests that caprolactam is expected to have high mobility in soil. |
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| TSCA Test Submissions | Acute dermal toxicity was evaluated in groups of 4 male albino New Zealand strain rabbits receiving single occluded applications of undiluted E-caprolactam at dose levels of 0.5, 1.0 and 2.0 gm/kg of body weight. The test material was held in contact with the intact skin for a 24 hour period. Mortality was observed in 1 animal in the 0.5 gm/kg dose group and in all animals in the 2.0 gm/kg dose group (period of observation not reported)the LD50 was calculated to be 1.41 gm/kg of body weight. Clinical observation were not reported. Gross necropsy revealed mottled livers, congested and hemorrhagic lungs and congested kidneys.Caprolactam (CAS # 105-60-2) was evaluated for acute inhalation toxicity in SPF1-Wistar/Chbb rats (10/sex/group) administered single nose-only exposures to the aerosol (MMAD 50% = 2.69 um86.6% capable of alveolar exposure) in air at mean analytical concentrations of 0, 5.25, 8.35, and 10.12 mg/l for 4 hours. During exposures, the animals exhibited eyelid closure, shallow to spasmodic respiration, and mild to marked defense reactionssteppage gait, bloody nasal exudate, spasmodic respiration, bloody lacrimation, squatting, bristling fur, and severe tremor were noted during 14-day post-exposure recovery. No change in bodyweights or bodyweight gains after exposures could be attributed to substance exposure. Mortality was dose-related, occurred before Day 2 following exposures, and was consistent with LD50's of 9.6 and 7.08 mg/l (p < 0.05 based on a probit analysis of D.J. Finney), respectively, for male and female rats. Among study lethalities, gross pathology on necropsy included general circulatory congestion, elevated hyperemia of the lung, and moderate to severe fatty degeneration of the liver. Histologic evaluation revealed fine-droplet fatty degeneration of peripheral acini in the liver and ischemic tubular nephrosis of the renal cortex in a solitary lethality of a 10.12 mg/l exposure.The effect of subchronic dietary treatments on renal function was evaluated in groups of 6 male and 6 female Fischer 344, Sprague-Dawley and Wistar strain rats administered caprolactam at dietary levels of 0. 0.01, 0.05, 0.1, and 0.5%, available ad libitum, for 90 days. Mortality was observed in one Sprague-Dawley male from the 0.01% feeding level. Clinical observations revealed no treatment-related effects. Body weight were significantly lower (p <= 0.05) than controls in: Fischer 344 females at the 0.50% levelin Sprague-Dawley males at the 0.1% and 0.5% levelsin Sprague-Dawley females at the 0.01%, 0.05% and 0.50% levelsin Wistar males at 0.05% and 0.50%and in Wistar females at 0.50%. Serum chemistry analysis revealed significant increases (p <= 0.05) in BUN, serum chloride levels and decreases in BUN, serum creatine levels, serum chloride levels, serum sodium levels, and serum hematocrit levelsthese results, however, appear to be random and not related to the test material. Urinalysis data revealed dose-related increases in urine volume in Fischer 344 males and females at the 3 highest doses. Dose related increases in the kidney/body weight ratio were observed in Sprague-Dawley males at 0.10 and 0.50% and in Wistar males at 0.50%. Gross necropsy revealed no compound-related incipient nephrosis, chronic inflammation, cytomegalic and chromophobic epithelial cells, protenaceous deposits, increased cytoplasmic vacuolization int eh tubules, increased hyalin droplets, and tubular epithelial hyperplasia and basophilia. In a similar study also evaluating the effects of caprolactam, the only compound-related effect was the altering renal function (fractional reabsorption of water) at the highest dose level (0.50%).Caprolactam (CAS # 105-60-2) was evaluated for subchronic oral toxicity specific to the kidney in groups (100/sex/strain) of Fischer 344, Sprague-Dawley, and Wistar rats randomized to nominal dietary exposures (ad libitum) of 0, 0.01, 0.05, 0.10, and 0.50% for a minimum 84 of 90 consecutive days. Dietary exposures were continued as rats of each strain (2 x 6, 2 x 8 and 2 x 6/sex/dose group) participated in Phases I and II of 3 distinct analyses of previously documented or implied renal toxicity: Phase 1 employed non-invasive techniques to establish the locale of renal toxicity, dose-response correlation, and sex and/or strain specificity by (Part A) measurement of biological markers of degenerative effects on the renal early proximal tubule (PT) and PT reabsorptive processes and (Parts B & C) determination of relative sensitivity and expression of toxicity in stressed (dehydrated or extracellular volume expansion) kidneys. Phase II used invasive procedures on anesthetized animals to (Part A) monitor proteinaceous material in Bowman space and/or the proximal tubule, and (Part B) directly measure glomerular filtration, urine clearance or reabsorption of free water and electrolytes, and blood and urine osmolality. Recovery from (Part A) any nephrotoxic effects (functional and/or histological) and, (Part B, per protocol amendment) specifically those effects documented in Phase 1 was examined in Phase III animals allowed 90-day recovery following cessation of 90 days' dietary exposure. Only all-strain lethalities and those strains demonstrating histological renal toxicity in Phase 1 high dose groups were terminated by pathology in Phase II (for light microscopy evaluation of changes in function and structure per protocol amendment) and Phase III (for evidence of recovery from toxic effects). Results of Phase I revealed functional nephrotoxicity in the stressed kidney only, including inhibited natriuresis upon volume expansion and diminished urine concentrating capacity during water deprivation, suggesting a distal tubule target of toxic action. Treated rats showed no gross pathology, but had increased kidney weights and increased incidence of hyalin droplets within renal tubules, more pronounced in males than females, and in Fischer 344 and Sprague-Dawley than in Wistar rats. Additionally, colloidal iron staining of glomeruli did not correlate with either level of exposure or with occurrence of tubular eosinophilic hyalin droplets. In Phase II, kidney weights were also increased and only fractional reabsorption of water in Fischer 344 or Sprague-Dawley high dose rats was altered, again supporting a distal tubule site of nephrotoxic effects in these strains. Based on urine concentrating capacity, the function of kidneys is fully reclaimed during 90-day recovery, which was verified on histological assessment concluding Phase III of study.For more TSCA Test Submissions (Complete) data for CAPROLACTAM (12 total), please visit the HSDB record page. |
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| Alarmwort | Warnung |
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| Gefahrenhinweise | Code Gefahrenhinweise Gefahrenklasse Abteilung Alarmwort Symbol P-Code H315 |
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