1,1,1-Trichloropropanone

This chemical does not meet GHS hazard criteria for 6.7% (3 of 45) of reports.

Warning

H315 (91.1%): Causes skin irritation [Warning Skin corrosion/irritation]

P261, P264, P264+P265, P271, P280, P302+P352, P304+P340, P305+P351+P338, P319, P321, P332+P317, P337+P317, P362+P364, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 45 reports by companies from 6 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure 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, aquatic, and plant life; and conformance with environmental and public health regulations.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 8.7(SRC), determined from a structure estimation method(2), indicates that 1,1,1-trichloroacetone is expected to have very high mobility in soil(SRC). Volatilization of 1,1,1-trichloroacetone from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.2X10-6 atm-cu m/mole(SRC), using a fragment constant estimation method(3). 1,1,1-Trichloroacetone is expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 4.2 mm Hg(SRC), determined from a fragment constant method(4). Biodegradation data were not available(SRC, 2008).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 9(SRC), determined from a structure estimation method(2), indicates that 1,1,1-trichloroacetone is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces may occur(3) based upon an estimated Henry's Law constant of 2.2X10-6 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 21 days and 160 days, respectively(SRC). According to a classification scheme(5), an estimated BCF of 1.4(SRC), from an estimated log Kow of 1.1(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data were not available(SRC, 2008).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 1,1,1-trichloroacetone, which has an estimated vapor pressure of 4.2 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), will exist solely as a vapor in the ambient atmosphere. Vapor-phase 1,1,1-trichloroacetone 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 1,000 days(SRC), calculated from its rate constant of 1.50X10-14 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). 1,1,1-Trichloroacetone does contain chromophores that absorb at wavelengths >290 and therefore it may be susceptible to direct photolysis in sunlight(SRC).

1,1,1-Trichloroacetone was identified but not quantified in a kraft mill during the acid filtrate stage of elemental chlorine-free bleaching (ECF) of softwood pulp(1). 1,1,1-Trichloroacetone was detected in spent chlorination liquor from bleaching sulphite pulp at 0.1 g/ton pulp with a high lignin content and at 1.0 g/ton pulp with a normal lignin content after oxygen treatment(2). Both studies utilized gas chromatography-mass spectrometry in compound identification.

Using a structure estimation method based on molecular connectivity indices(1), the Koc of 1,1,1-trichloroacetone can be estimated to be 8.7(SRC). According to a classification scheme(2), this estimated Koc value suggests that 1,1,1-trichloroacetone is expected to have very high mobility in soil.

An estimated BCF of 1.4 was calculated using an estimated log Kow of 1.1(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Henry's Law constant for 1,1,1-trichloroacetone is estimated as 2.2X10-6 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that 1,1,1-trichloroacetone is expected to volatilize from water surfaces(2). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(2) is estimated as 21 days(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(2) is estimated as 160 days(SRC). 1,1,1-Trichloroacetone's Henry's Law constant indicates that volatilization from moist soil surfaces may exist(SRC). 1,1,1-Trichloroacetone is expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 4.2 mm Hg(SRC), determined from a fragment constant method(3).

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ 1,1,1-Trichloro-2-propanone (1,1,1-TCP) has been identified as a chlorination by-product in finished drinking water supplies. Since little was known of its oral toxicity, exposure studies were conducted with male and female Sprague-Dawley rats (10 males and 10 females/group) exposed by corn oil gavage at 0, 16, 48, 161, or 483 mg/kg for 10 days or 0, 30, 90, or 270 mg/kg for 90 days. Evaluations included mortality, clinical signs, body weight, food consumption, ophthalmology, hematology, clinical chemistry, urinalysis, organ weights, gross pathology, and histopathology. In the 10-day study, severe toxicity was observed at the highest dose level, since most treated animals (8/10 males and 7/10 females) died. Toxicity was also noted at 161 and 48 mg/kg. At 161 mg/kg, 2 males died and an increase in liver weights in both sexes was observed. Acanthosis and hyperkeratosis of the forestomach was present in males and females at 48 mg/kg and above. In the 90-day study, toxicity was significant at 270 mg/kg, with acanthosis and hyperkeratosis of the forestomach evident in most animals and ataxia in about one-half of them. Retinal degeneration, increased serum potassium, and increased blood urea nitrogen were present in females and increased blood calcium in males at that same dose level. Acanthosis and hyperkeratosis were observed in both sexes, and retinal degeneration was prominent in 2 females at 90 mg/kg. It was concluded that 16 mg/kg was the NOAEL (no observed adverse effect level) for the 10-day study while 30 mg/kg was the NOAEL for the 90-day exposure of Sprague-Dawley rats to 1,1,1,-trichloro-2-propanone.

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Several chlorinated acetones have been identified in drinking water and these, as well as a number of chlorinated acroleins, are produced by chlorination of humic acid solutions. Many of these chlorinated compounds and the brominated acrolein analog were positive in the Ames Assay in the laboratory. To determine if carcinogenic activity was associated with these chemicals the following acetone derivatives: monochloro (MCA); 1,1-dichloro (1,1-DCA), 1,3-dichloro (1,3-DCA), 1,1,1-trichloro (1,1,1-TCA), 1,1,3-trichloro (1,1,3-TCA), and substituted acroleins: 2-chloro (CAC), 3,3-dichloro (DCAC), 2,3,3-trichloro (TCAC) and 2-bromo (BAC), were applied topically to SENCAR mice (25, 30, or 40/group) at the following dose levels: 50 mg/kg (MCA and 1,1,3-TCA); 50, 75 and 100 mg/kg (1,3-DCA); 100, 200 and 400 mg/kg (CAC, DCAC, and TCAC); 200 and 300 mg/kg (BAC); and 400, 600, and 800 mg/kg (1,1-DCA, and 1,1,1-TCA). Doses were applied six times over a 2-week period in 0.2 mL ethanol per application. 1,3-DCA was also tested with single doses of 37.5, 75, 150 and 300 mg/kg in 0.2 mL ethanol. Control animals received 0.2 mL ethanol per application as a single dose or multiple doses to match corresponding studies. Two weeks after the final dose, 1.0 ug TPA in 0.2 mL acetone was applied three times weekly for 20 weeks. After 24 weeks the percentage of animals with tumors for dose groups above were: MCA (8); 1,1,3-TCA (10); 1,3-DCA, multiple doses (48, 45, 32); CAC (30, 28, 38); DCAC (3, 0, 0); TCAC (10, 5, 0); BAC (54, 43); 1,1-DCA (0, 5, 0); 1,1,1-TCA (10, 5, 0); 1,3-DCA, single doses (47, 47, 63, 20); controls (12 ... , 9 ... average). These data show that 1,3-DCA, CAC and BAC, when applied topically, initiate tumors in the mouse skin. These chemicals administered orally in a 2% emulphor solution ... did not initiate tumors in the mouse skin. /Chlorinated acetones and acroleins/

/GENOTOXICITY/ 1,1,1- and 1,1,3-trichloroacetones (TCA) result from the disinfection of municipal water supplies with chlorine, and are direct-acting mutagens in the Ames/Salmonella assay. The objective of this study was to further investigate the genotoxicity of these compounds in mammalian cells using an in vitro chromosomal aberration assay in Chinese hamster ovary (CHO) cells and the micronucleus and spermhead abnormality assays in mice. Both compounds induced significant increases in structural chromosomal aberrations in CHO cells in the presence and in the absence of rat S9 metabolic activation (MA). 1,1,3-TCA was more cytotoxic to CHO cells but 1,1,1-TCA resulted in a higher proportion of cells with aberrations. The clastogenic activities of both compounds were reduced in assays conducted with MA. Neither compound resulted in the induction of a significant increase in micronucleated polychromatic erythrocytes from bone marrow of Swiss-Webster mice when administered by oral gavage; nor were effects seen on the incidence of sperm with head-shape abnormalities, testis weight, or epididymal sperm concentration in B6C3F1 mice 21 or 35 days after treatment...

The rate constant for the vapor-phase reaction of 1,1,1-trichloroacetone with photochemically-produced hydroxyl radicals has been estimated as 1.5X10-14 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 1,000 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). 1,1,1-Trichloroacetone contains chromophores that absorb at wavelengths >290 nm(3) and therefore may be susceptible to direct photolysis by sunlight(SRC).

1,1,1-Trichloroacetone is expected to hydrolyze readily in finished water with a pH ranging from 8 to 9 based on a study performed on chlorinated raw, unclarified water samples from the Ohio River(1). It was detected at a concentration <2 ug/L at a pH of 7, a higher concentration at a pH of 5, and was no longer detected at a pH of 9.4(1). 1,1,1-Trichloroacetone decomposed in fortified drinking water solutions at a rate constant of 0.182 hr-1 at 21 °C and assumed half-life of 4 hr, and at 1.393 hr-1 at 30 °C with a half-life of 0.5 hr(2). It decomposed with a rate constant of 0.062 hr-1 at 30 °C in an ultrapure water solution indicating a 11 hr half-life(2). Its degradation product, chloroform, is produced more rapidly in ultrapure water solutions than in fortified drinking water; this indicates that the decomposition of 1,1,1-trichloroacetone may lead to products other than chloroform such as chloral hydrate when decomposed in drinking water(2).

DRINKING WATER: 1,1,1-Trichloroacetone was detected in 5/10 samples of finished water from operating utilities in the United States. Concentrations ranged from 10 to 100 ug/L at one site and less than 10 ug/L at the four remaining sites(1). Utilities were selected on a basis that they were representative of varying water sources, treatments, three-year average levels, and population sizes to which they served(1). 1,1,1-Trichloroacetone was detected at median concentrations of 0.80 ug/L (spring), 0.35 ug/L (summer), 0.60 ug/L (autumn), 0.66 ug/L (winter) in 35 United States drinking waters during quarterly periods in 1988(1). 1,1,1-Trichloroacetone was detected in drinking water at a concentration of 2.2 ug/L as a by-product of hypochlorous acid(2). 1,1,1-Trichloroacetone was detected at a concentration of 1.1 ug/L in tap water sampled after tertiary water treatment in July 1997(3).

DRINKING WATER: Three Canadian water treatment plants using different disinfection processes were monitored monthly over a year-long period at varying points along each plants' distribution system. 1,1,1-Trichloroacetone was detected at mean concentrations of 2.6 ug/L (at facility directly after disinfection) 2.2 ug/L (3 km from plant), 0.7 ug/L (10 km from plant), 0.5 ug/L (18 km from plant) and at a minimum concentration of <0.1 ug/L and maximum concentration of 4.4 ug/L(1). 1,1,1-Trichloroacetone was detected at concentrations of 0.3 ug/L at 91st Ave and 0.1 ug/L 115th Ave in Phoenix, Arizona(2). Water from the Llobegat River in Barcelona was tested at three stages of a treatment process in a water treatment plant from Nov 1997 to Mar 1998. 1,1,1-Trichloroacetone was detected during prechlorination, sand filtration, and ozonization at concentrations of 0.4 ug/L, 0.3 ug/L, and 0.3 ug/L, respectively, using a modified EPA Method 551.1 analysis method(3).

SURFACE WATER: Water samples from the Tres Rios Wetlands in Arizona, which receives tertiary treated sewage effluent from 91st Ave Wastewater Treatment Plant, were collected in July 1997 to examine the fate of disinfection byproducts in wetlands. 1,1,1-Trichloroacetone was detected at concentrations of 0.4 ug/L (Salt River flood plain inlet), 0.7 ug/L (Hayfield site wetland inlet), and 0.6 ug/L (open water research cell 1 inlet)(1).

1,1,1-Trichloroacetone's production as a result of chlorine-treatment of drinking water may result in its release to the environment through various waste streams. Disinfection byproducts are formed when chlorine or other disinfectants, which are used to control contaminants in drinking water, react with naturally occurring organic and inorganic matter present in water. If released to air, an estimated vapor pressure of 4.2 mm Hg at 25 °C indicates 1,1,1-trichloroacetone will exist solely as a vapor in the atmosphere. Vapor-phase 1,1,1-trichloroacetone will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 1,000 days. 1,1,1-Trichloroacetone contains chromophores that absorb at wavelengths >290 nm and therefore may be susceptible to direct photolysis by sunlight. If released to soil, 1,1,1-trichloroacetone is expected to have very high mobility based upon an estimated Koc of 8.7. Volatilization from moist soil surfaces is expected to be an important fate process based upon an estimated Henry's Law constant of 2.2X10-6 atm-cu m/mole. 1,1,1-Trichloroacetone may volatilize from dry soil surfaces based upon its vapor pressure. Biodegradation data were not available. If released into water, 1,1,1-trichloroacetone is not expected to adsorb to suspended solids and sediment based upon the estimated Koc. Volatilization from water surfaces is expected to be an important fate process based upon this compound's estimated Henry's Law constant. Estimated volatilization half-lives for a model river and model lake are 21 and 160 days, respectively. An estimated BCF of 1.4 suggests the potential for bioconcentration in aquatic organisms is low. Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions. Monitoring data indicate that the general population may be exposed to 1,1,1-trichloroacetone via ingestion of chlorinated drinking water. (SRC)

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Ketones and related compounds/

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR as necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Ketones and related compounds/

Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . For contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Administer activated charcoal ... . /Ketones and related compounds/

Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Ketones and related compounds/

... Dermal absorption of two haloketones (1,1-dichloropropanone and 1,1,1-trichloropropanone) and chloroform while bathing, /were examined/ by collecting and analyzing time profiles of expired breath samples of six human subjects during and following a 30-min bath. The disinfection byproduct concentrations in breath increased towards a maximum concentration during bathing. The maximum haloketone breath concentration during dermal exposure ranged from 0.1 to 0.9 ug /cu m, which was approximately two orders of magnitude lower than the maximum chloroform breath concentration during exposure. Based on a one-compartment model, the in vivo permeability of chloroform, 1,1-dichloropropanone, and 1,1,1-trichloropropanone were approximated to be 0.015, 7.5 x 10- 4, and 4.5 x 10- 4 cm /hr, respectively. Thus, haloketones are much less permeable across human skin under normal bathing conditions than is chloroform...