Trichloroacetonitrile

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.

FIREFIGHTING. Protective Equipment: Wear self-contained breathing apparatus and protective clothing to prevent contact with skin and eyes.

EXTINGUISHING MEDIA. Carbon dioxide, dry chemical powder, or appropriate foam.

SMALL SPILLS AND LEAKAGE: If you spill this chemical, FIRST REMOVE ALL SOURCES OF IGNITION. Then, use absorbent paper to pick up all liquid spill material. Your contaminated clothing and absorbent paper should be sealed in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with 60-70% ethanol followed by washing with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

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.

Observe all federal, state, and local environmental regulations.

SRP: When working with strong solutions of acids or bases or other caustic or corrosive materials, always wear a full face mask. When working with caustic or corrosive gases or vapors, a full face mask will not protect the eyes or prevent inhaling the material. A full face respirator is required.

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.

Do not breathe vapor. Do not get in eyes, on skin, on clothing.

Wear self-contained breathing apparatus, rubber boots, and heavy rubber gloves. In case of leak or spill, evacuate area.

For more Preventive Measures (Complete) data for TRICHLOROACETONITRILE (7 total), please visit the HSDB record page.

MINIMUM PROTECTIVE CLOTHING: If Tyvek-type disposable protective clothing is not worn during handling of this chemical, wear disposable Tyvek-type sleeves taped to your gloves.

ENGINEERING CONTROLS. Safety shower and eye bath. Use only in a chemical fume hood.

PERSONAL PROTECTIVE EQUIPMENT. Other: Wear appropriate government approved respirator, chemical-resistant gloves, safety goggles, other protective clothing.

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ When administered by gavage to pregnant Long-Evans rats in a medium-chain triglyceride vehicle, tricaprylin oil (Tricap), at a volume of 10 mL/kg, trichloroacetonitrile (TCAN) induced fetal cardiovascular anomalies at doses as low as 1 mg/kg/d ... . A slight but possibly biologically significant increase over the water control group in adverse pregnancy outcomes (resorptions, reduced fetal weight, and anomalies) was observed in the Tricap control group. This led .. to /reexamination of/ the development effects of TCAN in a second vehicle, corn oil (CO). Five groups of approximately 20 pregnant female rats received TCAN in CO at 15, 35, 55, and 75 mg/kg/d, and in Tricap at 15 mg/kg/d (10 mL/kg dosing volume). Corn oil, Tricap, and water served as vehicle controls. Animals were treated by oral intubation on gestation d 6-18 (vaginal plug = d 0). Five out of 20 dams (75 mg/kg) died during treatment. Adjusted maternal weight gain was lower in females receiving 35 mg/kg TCAN or greater. The mean percent of nonlive implants per litter was elevated at 55 and 75 mg/kg TCAN (CO). ... Fetal weight was reduced at 15 mg/kg TCAN (Tricap) and at > or = 55 mg/kg TCAN (CO). When TCAN was administered in CO, the mean frequency of soft-tissue malformations decreased with significantly fewer septal and great vessel cardiovascular defects observed. /It was hypothesized/ that the volatile haloacetonitrile, TCAN, may interact with the Tricap vehicle in such a way that effects on the developing cardiovascular system are potentiated. The lowest observed adverse effect level for TCAN (CO) was determined to be 35 kg/kg.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 330(SRC), determined from a log Kow of 2.09(2) and a regression-derived equation(3), indicates that trichloroacetonitrile is expected to have moderate mobility in soil(SRC). Volatilization of trichloroacetonitrile from moist soil surfaces is expected to be an important fate process(SRC) given an estimated Henry's Law constant of 1.3X10-6 atm-cu m/mole(SRC), using a fragment constant estimation method(4). Trichloroacetonitrile is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 74.1 mm Hg(5). Trichloroacetonitrile is a by-product of water chlorination and hydrolyzes quickly; therefore, biodegradation is not expected to be an important fate in the environment(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 330(SRC), determined from a log Kow of 2.09(2) and a regression-derived equation(3), indicates that trichloroacetonitrile is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon an estimated Henry's Law constant of 1.3X10-6 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 33 and 240 days, respectively(SRC). According to a classification scheme(5), an estimated BCF of 8(SRC), from its log Kow(2) and a regression-derived equation(6), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Trichloroacetonitrile has a hydrolysis rate constant of 2.0X10-6/sec, 1.5X10-4/sec and 3.9X10-4/sec at pH of 5.4, 7.2 and 8.7, respectively(7), corresponding to half-lives of 4 days, 1.3 hours, and 29 minutes, respectively(SRC). Trichloroacetonitrile is a by-product of water chlorination and hydrolyzes quickly; therefore, biodegradation is not expected to be an important fate in the environment(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), trichloroacetonitrile, which has a vapor pressure of 74.1 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. There is no mechanistic process by which tichloroacetonitrile can be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(2). Trichloroacetonitrile does not contain chromophores that absorb at wavelengths >290 nm(3) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

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=545-06-2][Available from: http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=545-06-2]

The Koc of trichloroacetonitrile is estimated as 330(SRC), using a log Kow of 2.09(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that trichloroacetonitrile is expected to have moderate mobility in soil.

/SIGNS AND SYMPTOMS/ Multiple Routes: Harmful if swallowed, inhaled, or absorbed through skin.

/SIGNS AND SYMPTOMS/ Material is extremely destructive to tissue of the mucous membranes and upper respiratory tract, eyes, and skin. Inhalation may result in spasm, inflammation and edema of the larynx and bronchi, chemical pneumonitis, and pulmonary edema. Symptoms of exposure may include burning sensation, coughing, wheezing, laryngitis, shortness of breath, headache, nausea, and vomiting.

/GENOTOXICITY/ ... The ability of halogenated acetonitriles (HAN) to induce single-strand breaks on the DNA of HeLa S3 cells was investigated using the single-cell gel electrophoresis (SCGE) assay, which could be a good tool with which to evaluate the genotoxicity of chlorinated water. The results were compared to those obtained in the Ames fluctuation test using the Salmonella typhimurium TA100 strain without activation. With the Ames fluctuation test, a mutagenic effect was observed for chloroacetonitrile (MCAN), dichloroacetonitrile (DCAN), and trichloroacetonitrile (TCAN). No mutagenic effect was found with bromoacetonitrile (MBAN) or dibromoacetonitrile (DBAN). In the SCGE assay, all five HANs induced DNA damage in HeLa S3 cells, increasing the mean tail moment significantly. For each compound, a dose-effect relation was observed. ... Brominated acetonitriles were more genotoxic than chlorinated acetonitriles in the SCGE assay, and the genotoxicity increased with the number of halogenated atoms of the compound. This behavior had already been found with other genotoxicity tests.

/GENOTOXICITY/ The haloacetonitriles produced DNA strand breaks in cultured human lymphoblastic (CCRF-CEM) cells. Trichloroacetonitrile (TCAN) was the most potent DNA strand breaker, and bromochloroacetonitrile (BCAN) greater than dibromoacetonitrile (DBAN) greater than dichloroacetonitrile (DCAN) greater than chloroacetonitrile (CAN), which was only marginally active.

/GENOTOXICITY/ Chlorinated and brominated haloacetonitriles (HAN) ... produced DNA strand breaks in cultured human lymphoblastic (CCRF-CEM) cells /treated for 1 hr with up to 3.0 mM dibromoacetonitrile/. /Chlorinated & brominated haloacetonitriles/

Trichloroacetonitrile's production and use as a chemical intermediate(1) may result in its release to the environment through various waste streams. Trichloroacetonitrile formation in small amounts during the chlorination of water(2,3) will result in its release to the environment through various waste streams(SRC). Its former use as an insecticide(4) resulted in its direct release to the environment(SRC).

Trichloroacetonitrile

Group 3: Not classifiable as to its carcinogenicity to humans

Volume 52: (1991) Chlorinated Drinking-water; Chlorination By-products; Some Other Halogenated Compounds; Cobalt and Cobalt Compounds

1999

1998

An estimated BCF of 8 was calculated in fish for trichloroacetonitrile(SRC), using a log Kow of 2.09(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 trichloroacetonitrile is estimated as 1.3X10-6 atm-cu m/mole(SRC) using a fragment constant estimation method(1). This Henry's Law constant indicates that trichloroacetonitrile 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 33 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 240 days(SRC). Trichloroacetonitrile's Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). Trichloroacetonitrile is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 74.1 mm Hg(3).

/LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity/ Trichloroacetonitrile was tested in a limited carcinogenicity study in female SEN mice by skin application, in an initiation/promotion study in female SEN mice by skin application and in a screening assay for lung tumors in female strain A mice by oral administration. No skin tumor was produced after skin application in mice or in the initiation/promotion study, in which trichloroacetonitrile was applied topically as six equal doses over a two-week period, followed by repeated doses of 12-O-tetradecanoylphorbol 13-acetate for 20 weeks. A small, significant increase in the proportion of mice with lung tumors and in the number of tumors per mouse was observed: control, 3/31 and 0.1; treated group (10 mg/kg bw, three times per week, eight weeks), 9/32 and 0.38 (p < 0.05)

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ The developmental toxicity of acetonitrile and 5 halogenated derivatives was examined with an in vivo teratology screen adapted for use in the Long-Evans rat. The screen was extended to an evaluation of growth till postnatal Days 41-42, and weight of several organs at sacrifice. Acetonitrile was without developmental effects even at doses toxic to the dam. Of the halogenated compounds, treatment with trichloroacetonitrile (TCAN) and dichloroacetonitrile (DCAN) resulted in reduced fertility and increased early implantation failure. There was no effect on litter size in females bearing live litters, but pup birth weight was reduced in all litters exposed to halogenated compounds. Perinatal survival of the pups was adversely impacted by DCAN and TCAN. Postnatal growth till Day 4 was reduced by DCAN and bromochloroacetonitrile (BCAN) while growth /until/ Day 42 was consistently affected only by TCAN. Some general observations were made on the usefulness of the criteria used in the screen, and TCAN, the most toxic of the halogenated compounds, was selected for further in-depth evaluation.

/LABORATORY ANIMALS: Developmental or Reproductive Toxicity/ Long-Evans rats were intubated with trichloroacetonitrile (TCAN) (0, 1, 7.5, 15, 35, 55 mg/kg) in a tricaprylin vehicle on gestation days 6-18. The highest dose tested (55 mg/kg) was lethal in 21% of the dams and produced 100% resorptions in two-thirds of the survivors. Only one maternal death was seen at the next-lower dose; however, fetal weight and viability were decreased in a dose-related manner. The percentage of embryolethality was 13.9% at the lowest dose and 78.4% at the high dose, with resorption of entire litters seen at 7.5 mg/kg and above. At all doses, cardiovascular (interventricular septal defect, levocardia, common carotid, and right-sided aortic arch and ductus arteriosus) and urogenital (hypoplastic, missing, misplaced and fused kidneys, and hypoplastic uterine horns) malformations were seen in the offspring. Frequency of these malformations was dose related, ranging from 8% to 35% at the 1.0- and 35-mg/kg doses, respectively. The incidence of total soft tissue malformations was statistically significant at 15 and 35 mg/kg. There were no significant treatment-related changes in the incidence of skeletal malformations. The no-effect dose was established by statistical analysis to be 1.0 mg/kg/day.