Can CBD help with warts, and if so, how?

Common warts are small, coarse skin growths that occur most often on fingers or hands. Grainy to the touch, common warts also often feature a pattern of tiny black dots, which are clotted blood vessels.

Common warts are caused by HPV (human papillomavirus). Some strains of HPV are acquired through sexual contact. 

However, most forms are spread by casual skin contact or through shared objects, such as towels or washcloths. They can also spread to different parts of the body by nail-biting or shaving.

It can take a wart two to six months to develop after the skin has been exposed to the virus. 

An individual’s immune system responds to the HPV virus differently, so not everyone who comes in contact with HPV develops warts. 

Common warts are typically harmless and eventually disappear on their own. Still, most people choose to have them removed because they find them bothersome or embarrassing.

People at higher risk of developing common warts include children and young adults, as their bodies may not have built up a robust immunity to the virus.

Also, at risk are individuals with weakened immune systems, such as those with HIV/AIDS, or people who have had organ transplants (1). 

Why Some People Are Turning to CBD for Warts

No study indicates that CBD directly treats warts. Still, CBD may help those dealing with the symptoms or effects of some types of warts.

CBD for HPV Vaccine Side Effects

The Centers for Disease Control and Prevention (CDC) recommends two doses of HPV vaccine for children aged 11 or 12 to protect them against cancers caused by HPV infections (2). 

Recent changes to the vaccine recommendations mean preventing cancer is easier now than ever before, said Nancy Messonnier, M.D., director of CDC’s National Center for Immunization and Respiratory Diseases (3). 

Meanwhile, researchers have found that the vaccine may also result in adverse effects for some young adults. They also found that CBD hemp oil can help alleviate those side effects.

Results of a small 2017 study published in the Israel Medical Association Journal suggest that CBD can help relieve symptoms and improve life quality in those with adverse effects following HPV vaccination (4). 

Researchers found CBD-rich hemp oil to be a promising treatment for severe somatoform and dysautonomic syndrome following HPV vaccination.

Somatic symptom disorder is often characterized by an extreme focus on physical symptoms, such as pain or fatigue, that causes significant emotional distress and problems functioning (5). 

Dysautonomia is a disorder that involves the autonomic nervous system, which controls involuntary actions, like the heart beating and the widening or narrowing of blood vessels (6). 

The authors of the study hypothesized that supplementing the endocannabinoid system, a complex signaling network in the body, with plant-derived cannabinoids like CBD, could stimulate the system and bring it back to balance.

Still, the researchers urged for randomized controlled trials to fully characterize the safety profile and efficacy of CBD oil for HPV vaccination side effects.

CBD for Cervical Cancer

Of the over a hundred types of HPV, two types cause 70% of cervical cancers and pre-cancerous cervical lesions, says the World Health Organization (WHO) (7).  

Meanwhile, a 2016 study published in BMC Complementary Medicine and Therapies showed that CBD rather than Cannabis sativa crude extracts prevented cell growth at a significant rate and induced apoptosis (cell death) in laboratory-grown, cervical cancer cell lines (8).

The results prove promising for individuals who do not want to use medical cannabis that contains THC and may change the way experts have been treating cervical cancer.

CBD for the Immune System

Individuals with a weakened immune system are most at risk of developing warts (9). 

Meanwhile, CBD may help boost the immune system. Studies have shown that cannabis is immune-modulating, which means it can bring an over- or under-reacting immune system back into balance (10). 

In other studies, CBD was found to play an integral role in managing autoimmune diseases, such as rheumatoid arthritis, multiple sclerosis (MS), HIV/AIDS, and Parkinson’s disease (11). 

Autoimmune diseases are characterized by an immune system overreacting to non-threatening internal events, leading it to attack healthy cells in the body (12).  

CBD for Skin Care

Warts manifest as a skin problem, caused by a virus that usually spreads through breaks in the skin, such as a scrape or a hangnail (13). 

A study published in the journal Trends in Pharmacological Sciences has suggested the existence of a functional endocannabinoid system (ECS) in the skin and implicated it in various biological processes that might form the basis for future clinical studies on skin disorders (14).  

In the said study, the authors noted that the primary physiological function of the ECS in the skin seemed to be the regulation of the well-balanced proliferation, survival, and tolerance of skin cells. 

They said that the disruption of this delicate balance might facilitate the development of multiple skin problems, such as acne, seborrhea (red, itchy rash and white scales), allergic dermatitis, psoriasis (painful, dry, raised, and red skin lesions), and cancer.

CBD also impacts the TRPV-1 and GPR55 receptors (15). Both receptors are found in the skin and play a role in pain signaling and inflammation.

Conclusion

No study indicates that CBD directly treats warts. Still, CBD may help those dealing with the symptoms or effects of some types of warts.

CBD oil from hemp may help with HPV vaccine side effects, destroy cervical cancer cells in the lab, boost the body’s immunity, and remedy common skin conditions caused by the human papillomavirus (HPV).

However, CBD may interact with other pharmaceuticals. Moreover, its long-term side effects are still unknown. 

Thus, before using CBD for wart symptoms or HPV side effects, or before using CBD as an adjunct therapy, consult with a dermatologist experienced in cannabis use for advice.


  1. Mayo Clinic. (2018, May 19). Common Warts. Retrieved from https://www.mayoclinic.org/diseases-conditions/common-warts/symptoms-causes/syc-20371125.
  2. CDC. (2019, April 29). HPV Diseases and Cancers. Retrieved from https://www.cdc.gov/hpv/parents/cancer.html.
  3. CDC. (2017, Aug 24). Most U.S. teens are getting cancer-preventing vaccine. Retrieved from https://www.cdc.gov/media/releases/2017/p0824-cancer-preventing-vaccines.html.
  4. Palmieri B, Laurino C, Vadalà M. Short-Term Efficacy of CBD-Enriched Hemp Oil in Girls with Dysautonomic Syndrome after Human Papillomavirus Vaccination. Isr Med Assoc J. 2017;19(2):79–84.
  5. Mayo Clinic. (2018, May 8). Somatic symptom disorder. Retrieved from https://www.mayoclinic.org/diseases-conditions/somatic-symptom-disorder/symptoms-causes/syc-20377776.
  6. MedlinePlus. (2016, Feb 2). Autonomic Nervous System Disorders. Retrieved from https://medlineplus.gov/autonomicnervoussystemdisorders.html.
  7. WHO. (2019, Jan 24). Human papillomavirus (HPV) and cervical cancer. Retrieved from https://www.who.int/news-room/fact-sheets/detail/human-papillomavirus-(hpv)-and-cervical-cancer
  8. Lukhele ST, Motadi LR. Cannabidiol rather than Cannabis sativa extracts inhibit cell growth and induce apoptosis in cervical cancer cells. BMC Complement Altern Med. 2016;16(1):335. Published 2016 Sep 1. doi:10.1186/s12906-016-1280-0.
  9. Mayo Clinic. (2018, May 19). Common Warts. Retrieved from https://www.mayoclinic.org/diseases-conditions/common-warts/symptoms-causes/syc-20371125.
  10. Russo S. Molecular Mimicry: The Role of Cannabis in Healing Autoimmune Disease. Retrieved from https://www.fundacion-canna.es/en/molecular-mimicry-role-cannabis-healing-autoimmune-disease
  11. Hammell DC, Zhang LP, Ma F, et al. Transdermal cannabidiol reduces inflammation and pain-related behaviours in a rat model of arthritis. Eur J Pain. 2016;20(6):936–948. DOI:10.1002/ejp.818; Rudroff T, Sosnoff J. Cannabidiol to Improve Mobility in People with Multiple Sclerosis. Front Neurol. 2018;9:183. Published 2018 Mar 22. DOI:10.3389/fneur.2018.00183; Hanson R. (2019, June 4). CBD: A Promising Aid for HIV Patients? Retrieved from http://hivatis.org/cbd-a-promising-aid-for-hiv-patients/; Peres FF, Lima AC, Hallak JEC, Crippa JA, Silva RH, Abílio VC. Cannabidiol as a Promising Strategy to Treat and Prevent Movement Disorders?. Front Pharmacol. 2018;9:482. Published 2018 May 11. DOI:10.3389/fphar.2018.00482.
  12. MedlinePlus. (2020, March 12). Autoimmune Diseases. Retrieved from https://medlineplus.gov/autoimmunediseases.html.
  13. Mayo Clinic. (2018, May 19). Common Warts. Retrieved from https://www.mayoclinic.org/diseases-conditions/common-warts/symptoms-causes/syc-20371125.
  14. Bíró T, Tóth BI, Haskó G, Paus R, Pacher P. The endocannabinoid system of the skin in health and disease: novel perspectives and therapeutic opportunities. Trends Pharmacol Sci. 2009;30(8):411–420. doi:10.1016/j.tips.2009.05.004.
  15. Sharir H, Abood ME. Pharmacological characterization of GPR55, a putative cannabinoid receptor. Pharmacol Ther. 2010;126(3):301–313. DOI:10.1016/j.pharmthera.2010.02.004; Costa B, Giagnoni G, Franke C, Trovato AE, Colleoni M. Vanilloid TRPV1 receptor mediates the antihyperalgesic effect of the nonpsychoactive cannabinoid, cannabidiol, in a rat model of acute inflammation. Br J Pharmacol. 2004;143(2):247–250. DOI:10.1038/sj.bjp.0705920.

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SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number:           539

CCOHS Chemical Name:   Trichloroacetic acid solid

Synonyms:

TCA

Trichloracetic acid

Trichloroethanoic acid

Trichloromethanecarboxylic acid

Acide trichloracetique (solide)

Trichloroacetic acid (non-specific name)

Chemical Name French:    Acide trichloroacétique (solide)

CAS Registry Number:      76-03-9

UN/NA Number(s):          1839

RTECS Number(s):           AJ7875000

EU EINECS/ELINCS Number:         200-927-2

Chemical Family: Halogenated aliphatic carboxylic acid / haloalkanoic acid / chlorinated carboxylic acid / chloroacetic acid

Molecular Formula:          C2-H-Cl3-O2

Structural Formula:          CCl3-C(=O)-OH

SECTION 2. DESCRIPTION

Appearance and Odour:

Colourless to slightly yellow crystals with a sharp, pungent odour; deliquescent (absorbs moisture from the air and forms wet solid or solution).(4,23)

Odour Threshold:

0.24 to 0.375 ppm (1.6 to 2.5 mg/m3) (recognition) (23)

Warning Properties:

NOT RELIABLE – odour threshold about the same magnitude as TLV.

Composition/Purity:

Occurs in two crystalline forms (alpha and beta forms), with different melting points. Dichloroacetic acid may be present as an impurity (1.2- 2.5%); other impurities may include sulfuric acid, sulfated ash and/or water.(4) TCA is sold as a solid with different purities and as a 90% aqueous solution. For information on trichloroacetic acid solutions refer to CHEMINFO record 766.

Uses and Occurrences:

The main use is in the production of its sodium salt, which is used as a herbicide; also used as a pickling or etching agent in metal surface finishing; a swelling agent and solvent in the plastics industry; auxiliary in textile finishing; decalcifier and fixative in microscopy; protein precipitating agent in laboratories; additive in mineral lubricating oils; polymerization catalyst; intermediate in the chemical synthesis of esters; medical agent in treating skin disorders, to remove genital warts and as an astringent and antiseptic.(4,13)

SECTION 3. HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW:

Colourless to slightly yellow crystals with a sharp, pungent odour. Deliquescent. Does not burn or support combustion. Can decompose upon heating, forming irritating/toxic phosgene and chlorinated hydrocarbons, such as chloroform, and hydrogen chloride. TOXIC. Fatal if swallowed. CORROSIVE to the eyes and skin.

POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:

Significant inhalation exposure to trichloroacetic acid (TCA) is not likely to occur since TCA readily absorbs moisture from the air forming a heavy, caked solid. If TCA dust becomes airborne, it would cause mild to severe irritation of the nose and throat, due to its corrosivity.

Skin Contact:

Contact with dust or solid may produce redness, swelling, pain and, in severe cases, corrosive skin damage. Permanent scarring may result. The severity of injury increases with the degree and duration of the exposure. Limited animal evidence has only shown mild irritation following contact with TCA. There is no human information available.

Eye Contact:

Contact with dust or solid can cause mild to severe irritation or corrosive injury. The severity of injury increases with the degree and duration of contact. Permanent eye damage or blindness could result.

In two accidents which occurred during the medical treatment of cataract-like eye tissue, TCA (10% or saturated solutions) contacted healthy tissue and caused pain, redness, swelling and serious corrosive injury. One report describes a very slow recovery from this type of injury.(2) Severe irritation has been observed in one animal test.

Ingestion:

TCA is a corrosive material. Ingestion of the solid can probably produce severe burns to the lips, mouth and throat. Other symptoms may include salivation, vomiting of blood, a burning sensation in mouth and throat, diarrhea, and pain. Permanent digestive tract damage could result. In severe cases, shock, severe respiratory effects, and death may result.(3) Ingestion is not a typical route of occupational exposure.

Effects of Long-Term (Chronic) Exposure

SKIN CONTACT: There is no specific information available for TCA, but repeated or prolonged skin contact can probably cause redness, drying and itching (dermatitis).

Carcinogenicity:

There is inadequate evidence for the carcinogenicity of trichloroacetic acid in humans. There is no specific human available. There is limited evidence for the carcinogenicity of trichloroacetic acid in animal studies. Increased liver tumours were seen in two animal studies following oral administration of neutralized TCA.(4,31)

The International Agency for Research on Cancer (IARC) has concluded that this chemical is not classifiable as to its carcinogenicity to humans (Group 3).

The American Conference of Governmental Industrial Hygienists (ACGIH) has designated this chemical as an animal carcinogen (A3).

The US National Toxicology Program (NTP) has not listed this chemical in its report on carcinogens.

Teratogenicity and Embryotoxicity:

There is no specific human or animal information available for TCA. Developmental effects have been observed in rats following oral administration of maternally toxic doses of neutralized TCA.

Reproductive Toxicity:

There is no relevant human or animal information available.

Mutagenicity:

There are no reports of human in vivo studies. TCA, neutralized to avoid the effects of low pH, did not induce chromosomal aberrations in cultured human lymphocytes.(17) TCA was mutagenic when a large dose was injected into mice. However, this positive effect was probably caused by the low pH, rather than a genotoxic effect. Similar effects were not observed following the oral administration of neutralized TCA. Positive and negative results have been observed in bacteria and cultured mammalian cells.

Toxicologically Synergistic Materials:

There is no specific information available for TCA. Neutralized TCA increased the toxicity of chloroform to the kidneys of rats.(5)

Potential for Accumulation:

Probably does not accumulate. Ingestion of 3 mg/kg of sodium trichloroacetate by humans resulted in very slow excretion of unchanged trichloroacetate. About one half of the ingested dose was excreted by 50 hours.(6) Animal evidence indicates that TCA and its metabolites are mostly excreted in the urine (60-70% of administered dose, of which 60% appears to be unchanged TCA). After oral administration, TCA is metabolized in rats and mice to dichloroacetic acid, which in turn gives oxalate and carbon dioxide, or monochloroacetic acid, which is then further metabolized to thiodiacetic acid. The major urinary products, are unchanged TCA, and oxalic and thiodiacetic acids.(4)

SECTION 4. FIRST AID MEASURES

Inhalation:

If symptoms develop, remove source of contamination or have victim move to fresh air. Obtain medical advice.

Skin Contact:

Avoid direct contact with this chemical. Wear chemical protective gloves, if necessary. As quickly as possible, flush contaminated area with lukewarm, gently flowing water for at least 20-30 minutes, by the clock. If irritation persists, repeat flushing. DO NOT INTERRUPT FLUSHING. If necessary, keep emergency vehicle waiting. Under running water, remove contaminated clothing, shoes, and leather goods (e.g., watchbands, belts). Transport victim to an emergency care facility immediately. Completely decontaminate clothing, shoes and leather goods before re-use or discard.

Eye Contact:

Avoid direct contact with this chemical. Wear chemical protective gloves, if necessary. Immediately flush the contaminated eye(s) with lukewarm, gently flowing water for at least 20-30 minutes, by the clock, holding the eyelid(s) open. Neutral saline solution may be used as soon as it is available. DO NOT INTERRUPT FLUSHING. If necessary, keep emergency vehicle waiting. Take care not to rinse contaminated water into the unaffected eye or onto the face. If irritation persists, repeat flushing. Quickly transport victim to an emergency care facility.

Ingestion:

NEVER give anything by mouth if victim is rapidly losing consciousness, or is unconscious or convulsing. Have victim rinse mouth thoroughly with water. DO NOT INDUCE VOMITING. Have victim drink 240 to 300 mL (8 to 10 oz.) of water to dilute material in the stomach. If milk is available, it may be administered AFTER the water has been given. If vomiting occurs naturally, rinse mouth and repeat administration of water. Quickly transport victim to an emergency care facility.

First Aid Comments:

Provide general supportive measures (comfort, warmth, rest). Consult a doctor and/or the nearest Poison Control Centre for all exposures except minor instances of inhalation or skin contact.

All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.

SECTION 5. FIRE FIGHTING MEASURES

Flash Point:

Will not burn (not combustible)

Lower Flammable (Explosive) Limit (LFL/LEL):

Not applicable

Upper Flammable (Explosive) Limit (UFL/UEL):

Not applicable

Autoignition (Ignition) Temperature:

Not applicable

Sensitivity to Mechanical Impact:

Probably not sensitive. Stable material.

Sensitivity to Static Charge:

Information not available

Combustion and Thermal Decomposition Products:

Trichloroacetic acid (TCA) can decompose when heated, to form toxic phosgene and chlorinated hydrocarbons, such as chloroform, and irritating/corrosive hydrogen chloride gas, as well as carbon dioxide and carbon monoxide.(13,21,22) Solutions decompose to form chloroform and carbon dioxide.(13)

Fire Hazard Summary:

TCA does not burn or support combustion. TCA decomposes upon heating, forming toxic phosgene and chlorinated hydrocarbons, such as chloroform, and irritating/corrosive hydrogen chloride. Closed containers may explode in the heat of a fire.

Extinguishing Media:

TCA does not burn or support combustion. Use fire extinguishing media appropriate to the surrounding fire conditions. Extinguishing media which have basic properties (such as dry chemical powder) may react violently with TCA.

Fire Fighting Instructions:

Evacuate area and fight fire from a safe distance or protected location. Approach fire from upwind to avoid toxic decomposition products.

Move containers from fire area if it can be done without risk. Otherwise, use water in flooding quantities as a spray or fog to keep fire-exposed containers cool and absorb heat to help prevent rupture. Water spray may also be used to knock down irritating/toxic combustion products which may be produced in a fire. Apply water from as far a distance as possible.

TCA decomposition products, such as phosgene and hydrogen chloride, are hazardous to health. Do not enter without wearing specialized protective equipment suitable for the situation. Firefighter’s normal protective equipment (Bunker Gear) will not provide adequate protection. A full-body encapsulating chemical resistant suit with positive pressure self-contained breathing apparatus (MSHA/NIOSH approved or equivalent) may be necessary.

NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION

NFPA – Comments:

NFPA has no listing for this chemical in Codes 49 or 325.

SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight:            163.39

Conversion Factor:

1 ppm = 6.67 mg/m3; 1 mg/m3 = 0.150 ppm at 25 deg C (calculated)

Physical State:    Solid

Melting Point:      58 deg C (136.4 deg F) (alpha); 49.6 deg C (121.3 deg F) (beta) (4,24)

Boiling Point:      197.5 deg C (387.5 deg F) (4,24,25)

Relative Density (Specific Gravity): 1.62 at 25 deg C (water = 1) (4,24)

Solubility in Water:          Extremely soluble at 25 deg C (1306 g/100 g) (25)

Solubility in Other Liquids: Extremely soluble in methanol; very soluble in ethanol, diethyl ether, acetone and benzene.(25)

Coefficient of Oil/Water Distribution (Partition Coefficient):     Log P(oct) = 0.10 to 1.96 (calculated) (26)

pH Value:           1.2 (0.1 M solution).

Vapour Density:   5.6 (air = 1) (21)

Vapour Pressure: Low; 0.133 kPa (1 mm Hg) at 51 deg C (23,24)

Saturation Vapour Concentration:   Low; 1300 ppm (0.13%) at 51 deg C (calculated)

Evaporation Rate:            Not available

Critical Temperature:       Not available

Other Physical Properties:

ACIDITY: Strong acid; pKa = 0.70 (Ka = 0.2) at 25 deg C (13,24) (25) NOTE: Trichloroacetic acid is as strong an acid as hydrochloric acid.(25)

SURFACE TENSION: 27.8 mN/m (27.8 dynes/cm) at 80.2 deg C (24)

SECTION 10. STABILITY AND REACTIVITY

Stability:

Normally stable. Decomposes above the boiling point (197.5 deg C). Dilute solutions of trichloroacetic acid (TCA) in water may decompose slowly depending on the temperature, giving off chloroform and carbon dioxide.(4,13,21)

Hazardous Polymerization:

Does not occur.

Incompatibility – Materials to Avoid:

NOTE: Chemical reactions that could result in a hazardous situation (e.g. generation of flammable or toxic chemicals, fire or detonation) are listed here. Many of these reactions can be done safely if specific control measures (e.g. cooling of the reaction) are in place. Although not intended to be complete, an overview of important reactions involving common chemicals is provided to assist in the development of safe work practices.

STRONG OXIDIZING AGENTS (e.g. chromium trioxide, perchlorates, peroxides) – may react violently or explosively. Increased risk of fire.(22)

ORGANIC BASES (e.g. amines) or INORGANIC BASES (e.g. sodium hydroxide) – may react violently producing heat and pressure, forming chloroform and carbon dioxide. Facilitate thermal decomposition of water solutions, forming chloroform.(13,25)

DIMETHYL SULFOXIDE AND COPPER WOOL – mixture reacted violently and explosively.(22,27)

REACTIVE METALS (eg. aluminum, zinc) – highly reactive; may produce flammable and explosive hydrogen gas.

Hazardous Decomposition Products:

Chloroform, carbon dioxide.

Conditions to Avoid:

Heat, generation of dust.

Corrosivity to Metals:

Corrosive to cast iron, stainless steels, copper, brass, bronze, aluminum, zinc and lead.(28)

SECTION 11. TOXICOLOGICAL INFORMATION

LD50 (oral, rat): 400 mg/kg (7)

Eye Irritation:

Application of 3.5 mg trichloroacetic acid for 5 seconds produced severe irritation in rabbits.(9, unconfirmed)

Skin Irritation:

Application of 0.21 mg in a standard Draize test produced mild irritation on rabbit skin.(9, unconfirmed) A single application of trichloroacetic acid to the tail of a rat apparently caused no change, but repeated application produced severe tissue death (necrosis).(3)

Effects of Short-Term (Acute) Exposure:

Ingestion:

Oral administration of 30 or 300 mg/kg/day of neutralized trichloroacetic acid in the drinking water of rats for 7 days resulted in reduced weight and severe toxicity, at the high dose. Oral administration of 24 or 240 mg/kg/day of neutralized trichloroacetic in the drinking water of rats for 14 days caused reduced weight gain only, at the high dose.(10)

Effects of Long-Term (Chronic) Exposure:

Ingestion:

Administration of trichloroacetic acid or neutralized trichloroacetic acid at doses as low as 350 mg/kg/day for 90 days have produced decreased body weight and liver and kidney effects in male rats.(11,12) Male rats given trichloroacetic acid in the drinking water for 90 days, at a concentration providing daily doses of about 4, 35 or 350 mg/kg, had decreased body weights. At the high dose, increased liver and kidney weights and increased liver enzyme activity was also observed.(11) In another study, male rats given approximately 780 mg/kg/day of neutralized trichloroacetic acid in their drinking water had decreased body weight (approximately 17%) and liver weight (approximately 14%) after 90 days. Minimal to mild changes were seen in the liver and the lungs.(12) Administration of neutralized trichloroacetic acid at levels of 2000 mg/kg and greater in the diet produced body weight loss, lesions to mouth and gums, change in white blood cell count, lesions to liver and heart, skeletal muscle atrophy and impaired sperm formation. The nontoxic effect level was 500 mg/kg.(13) Study details are not available.

Carcinogenicity:

The International Agency for Research on Cancer (IARC) has determined that there is limited evidence in experimental animals for the carcinogenicity of trichloroacetic acid.(4,31)

Neutralized trichloroacetic acid was tested for carcinogenicity by oral administration in two studies using male mice. In both studies, the incidence of liver tumours (hepatocellular adenomas and carcinomas) was increased.(4,14)

Teratogenicity, Embryotoxicity and/or Fetotoxicity:

There is no specific information available for trichloroacetic acid. In one study, oral administration of neutralized trichloroacetic acid cause developmental effects, but only at maternally toxic doses (low dose 330 mg/kg/day).(15)

Reproductive Toxicity:

Injection of 500 mg/kg trichloroacetic acid into the body cavity of mice produced a slight increase in abnormal sperm head shape.(16) This route of exposure is not considered relevant to an occupational setting.

Mutagenicity:

Positive results (chromosomal aberrations and micronucleus tests in bone marrow cells) have been obtained in mice following the injection of trichloroacetic acid.(16) This positive effect was probably due to the pH of the injected solution, rather than a genotoxic effect. In a follow-up injection study with mice, a ten-fold higher dose of neutralized trichloroacetic acid did not cause similar mutagenic effects.(17) Reversible positive effects (DNA strand breaks) were observed in the liver cells of rats and mice treated orally with neutralized trichloroacetic acid.(18,19) In another study, negative results (DNA strand breaks) were observed in the liver, spleen and epithelial cells from the stomach and duodenum of mice or rats following the oral administration of neutralized trichloroacetic acid.(20)

DNA strand breaks were also not induced in human or rodent cells in vitro.(20) Trichloroacetic acid was not mutagenic to Salmonella typhimurium strains, in the presence or absence of metabolic activation (Ames test). However, trichloroacetic acid was mutagenic in a bacterial test when combined with the solvent DMSO.(4,16)

SECTION 16. OTHER INFORMATION

Selected Bibliography:

(1) Trichloroacetic acid. In: Documentation of the threshold limit values and biological exposure indices. 6th ed. American Conference of Governmental Industrial Hygienists, 1991. p. 1602-1604

(2) Grant, W.M., et al. Toxicology of the eye. 4th ed. Charles C. Thomas, 1993. p. 1446-1447

(3) Hayes, W.J. Pesticides studied in man. Williams and Wilkins, 1982. p. 537

(4) Trichloroacetic acid. In: IARC Monographs on the evaluation of the carcinogenic risk of chemicals to humans. Vol. 63. Dry cleaning, some chlorinated solvents and other industrial chemicals. International Agency for Research on Cancer, 1995. p. 291-314

(5) Davis, M.E. Effect of chloroacetic acids on the kidneys. Environmental Health Perspectives. Vol. 69 (1986). p. 209-214

(6) Muller, G., et al. Metabolism of trichloroethylene in man II: pharmacokinetics of metabolites. Archives of Toxicology. Vol. 32 (1974). p. 283-295

(7) The pesticide manual: a world compendium. 7th ed. The British Crop Protection Council, 1983. p. 11170

(8) Woodard, G., et al. The acute oral toxicity of acetic, chloracetic, dichloracetic, and trichloracetic acids. Journal of Industrial Hygiene and Toxicology. Vol. 23 (1941). p. 78-82

(9) RTECS record for acetic acid, trichloro-. Last updated: 9603

(10) Davis, M.E. Effect of chloroacetic acids on the kidneys. Environmental Health Perspectives. Vol. 69 (1986). p. 209-214

(11) Mather, G.G., et al. Subchronic 90 day toxicity of dichloroacetic and trichloroacetic acid in rats. Toxicology. Vol. 64, no. 1 (Oct. 1990). p. 71-80

(12) Bhat, H.K., et al. Ninety day toxicity study of chloroacetic acid in rats. Fundamental and Applied Toxicology. Vol. 17, no. 2 (Aug. 1991). p. 240-253

(13) Koenig, G., et al. Chloroacetic acids. In: Ullmann’s encyclopedia of industrial chemistry. 5th completely revised ed. Vol. A 6. VCH Verlagsgesellschaft, 1986. p. 537-552

(14) Herren-Freund, S.L., et al. The carcinogenicity of trichloroethylene and its metabolites, trichloroacetic acid and dichloroacetic acid, in mouse liver. Toxicology and Applied Pharmacology. Vol. 90 (1987) p. 183-189

(15) Smith, M.K., et al. Teratogenic activity of trichloroacetic acid in the rat. Teratology. Vol. 40 (1989). p. 445-451

(16) Bhunya, S.P., et al. Relative genotoxicity of trichloroacetic acid (TCA) as revealed by different cytogenetic assays: bone marrow chromosome aberration, micronucleus and sperm-head abnormality in the mouse. Mutation Research. Vol. 188 (1987). p. 215-221

(17) Mackay, J.M., et al. Trichloroacetic acid: investigation into the mechanism of chromosomal damage in the in vitro human lymphocyte cytogenetic assay and the mouse bone marrow micronucleus test. Carcinogenesis. Vol. 16, no. 5 (May 1995). p. 1127-1133

(18) Nelson, M.A., et al. Induction of strand breaks in DNA by trichloroethylene and metabolites in rat and mouse liver in vivo. Toxicology and Applied Pharmacology. Vol. 94, no. 1 (June 1988). p. 45-54

(19) Nelson, M.A., et al. Dichloroacetic acid and trichloroacetic acid- induced DNA strand breaks are independent of peroxisome proliferation. Toxicology. Vol. 58, no. 3 (Oct. 1989). p. 239-248

(20) Chang, L.W., et al. Analysis of DNA strand breaks induced in rodent liver in vivo, hepatocytes in primary culture, and a human cell line by chlorinated acetic acids and chlorinated acetaldehydes. Environmental and Molecular Mutagenesis. Vol. 20, no. 4 (1992). p. 277-288

(21) Chemical safety sheets: working safely with hazardous chemicals. Kluwer Academic Publishers, 1991. p. 873

(22) The Sigma-Aldrich library of chemical safety data. Ed. II. Vol. 2. Sigma-Aldrich, 1988. p. 3402C

(23) Verschueren, K. Handbook of environmental data on organic chemicals. 3rd ed. Van Nostrand Reinhold, 1996. p. 1758-1759

(24) Weast, R.C., ed. Handbook of chemistry and physics. 66th ed. CRC Press, 1985-1986. p. C-530, D-162, D-197, F-35

(25) Morris, E.D., et al. Acetic acid and derivatives: halogenated derivatives. In: Kirk-Othmer encyclopedia of chemical technology. 4th ed. Vol. 1. John Wiley and Sons, 1991. p. 169-170, 173-175

(26) Leo, A., et al. Partition coefficients and their uses. Chemical Reviews. Vol. 71, no. 6 (Dec. 1971). p. 556

(27) Urben, P.G., ed. Bretherick’s handbook of reactive chemical hazards. 5th ed. Vol. 1. Butterworth-Heinemann Ltd., 1995. p. 254

(28) Corrosion data survey: metals section. 6th ed. National Association of Corrosion Engineers, 1985. p. 128-9 to 129-9

(29) European Communities (EC). Commission Directive 2004/73/EC. Apr. 29, 2004

(30) Forsberg, K., et al. Quick selection guide to chemical protective clothing. 4th ed. Van Nostrand Reinhold, 2002

(31) International Agency for Research on Cancer (IARC). IARC monographs on the evaluation of carcinogenic risks to humans. Vol. 84. Some Drinking-water Disinfectants and Contaminants, including Arsenic. {Summary}. World Health Organization, Dec. 2002. Available on the World Wide Web: <193.51.164.11/htdocs/announcements/vol84.htm>

(32) Occupational Safety and Health Administration (OSHA). 2,2-Dichloropropionic Acid and Trichloroacetic Acid. In: OSHA Analytical Methods Manual. Revision Date: Oct. 31, 2001. Available at: <www.osha-slc.gov/dts/sltc/methods/toc.html>

Information on chemicals reviewed in the CHEMINFO database is drawn from a number of publicly available sources. A list of general references used to compile CHEMINFO records is available in the database Help.

Review/Preparation Date: 1996-12-23

Revision Indicators:

US transport       1998-03-01

Toxicological info 1998-06-01

TLV Comments    1998-06-01

Storage  1998-06-01

Engineering controls         1998-06-01

Emergency overview        1999-03-01

Handling 1999-03-01

WHMIS (proposed class)   1999-03-01

WHMIS (effects) 1999-03-01

WHMIS (disclosure list)     1999-03-01

WHMIS (detailed class)     1999-03-01

TLV-TWA            1998-06-01

EU risks 2002-02-12

EU safety           2002-02-12

PEL-TWA final     2003-12-04

Resistance of materials for PPE       2004-04-05

Carcinogenicity    2004-08-25

Bibliography        2005-01-05

EU classification   2005-01-05

EU comments      2005-01-05

Bibliography        2005-03-13

Passive Sampling Devices  2005-03-13

Sampling/analysis            2005-03-13

TRICHLOROACETIC ACID

(Group 3)

For definition of Groups, see Preamble Evaluation.

VOL.: 63 (1995) (p. 291)

CAS No.: 76-03-9

Chem. Abstr. Name: Trichloroacetic acid

  1. Summary and Evaluation

5.1 Exposure data

Trichloroacetic acid is produced commercially in small amounts by chlorination of acetic or chloroacetic acid. It is used principally in the form of the sodium salt, as a herbicide. Most human exposure to trichloroacetic acid occurs because of its metabolic formation from tetrachloroethylene, trichloroethylene, 1,1,1-trichloroethane, 1,1,2,2-tetrachloroethane and chloral hydrate. Trichloroacetic acid can also be formed during the chlorination of drinking-water.

5.2 Human carcinogenicity data

The available data were too limited to form the basis for an evaluation of the carcinogenicity of trichloroacetic acid to humans.

5.3 Animal carcinogenicity data

Trichloroacetic acid was tested by oral administration in the drinking-water in two studies in males of one strain of mice. In both studies, the incidence of hepatocellular adenomas and carcinomas was increased.

5.4 Other relevant data

Trichloroacetic acid has a longer plasma half-life in humans than in rodents, presumably because there is more binding to plasma proteins in humans. Much of an administered dose of trichloroacetic acid is excreted unchanged in the urine of rats and mice. Reductive dechlorination and glutathione conjugation are involved in the formation of the urinary metabolites, oxalate and thiodiacetic acid.

Little is known about the toxicity of this compound to humans. Single doses of high concentrations of trichloroacetic acid induce lipid peroxidation in the livers of rats and mice. Trichloroacetic acid causes hepatic peroxisome proliferation in both rats and mice in vivo and in cultured hepatocytes from mice and rats, but not from humans. Short-term, repeated administrations of trichloroacetic acid induced cell proliferation in the livers of mice but reduced cell proliferation in the livers of rats.

No data were available on the effects of trichloroacetic acid on human reproduction. In rats, fetotoxicity was observed at doses that are maternally toxic.

Trichloroacetic acid induced chromosomal aberrations and abnormal sperm in mice in one study. The results of studies on the induction of DNA strand breaks and micronuclei were inconclusive.

Trichloroacetic acid did not induce chromosomal aberrations in a single study or DNA strand breaks in cultured mammalian cells. Inhibition of intercellular communication has been reported. It was not mutagenic to bacteria.

5.5 Evaluation

There is inadequate evidence in humans for the carcinogenicity of trichloroacetic acid.

There is limited evidence in experimental animals for the carcinogenicity of trichloroacetic acid.

Overall evaluation

Trichloroacetic acid is not classifiable as to its carcinogenicity to humans (Group 3).

For definition of the italicized terms, see Preamble Evaluation.

Synonyms

Aceto-Caustin

Amchem Grass Killer

TCA

TCAA

TCA (acid)

Trichloracetic acid

Trichloroethanoic acid

Trichloromethanecarboxylic acid

Last updated 05/27/1997

See Also:

Trichloroacetic acid (IARC Summary & Evaluation, Volume 84, 2004)

Trichloroacetic acid solid (CHEMINFO)

Trichloroacetic acid solutions (CHEMINFO)

TRICHLOROACETIC ACID

(Group 3)

For definition of Groups, see Preamble Evaluation.

VOL.: 84 (2004) (p. 403)

CAS No.: 76-03-9

  1. Summary of Data Reported and Evaluation

5.1        Exposure data

Trichloroacetic acid is mainly used as a selective herbicide. It also finds use in the metal, plastics and textile industries and as an analytical reagent. It is used in the topical treatment of warts, cervical lesions and other dermatological conditions. Trichloroacetic acid is a major end metabolite of trichloroethylene and tetrachloroethylene. Wider exposure to trichloroacetic acid occurs at microgram-per-litre levels in drinking-water and swimming pools as a result of chlorination or chloramination.

5.2        Human carcinogenicity data

Several studies analysed risk with respect to one or more measures of exposure to complex mixtures of disinfection by-products that are found in most chlorinated and chloraminated drinking-water. No data specifically on trichloroacetic acid were available to the Working Group.

5.3        Animal carcinogenicity data

In four studies, neutralized trichloroacetic acid, when administered in the drinking-water to female and/or male mice, increased the incidences of hepatocellular adenomas and carcinomas. In a study in male rats, trichloroacetic acid did not increase the incidence of liver tumours or tumours at any other site. When administered in the drinking-water, trichloroacetic acid promoted the induction of hepatocellular adenomas and/or carcinomas in carcinogen-initiated male and female mice and of kidney tumours in male mice.

5.4        Other relevant data

The half-life of trichloroacetic acid, given orally or formed as a metabolite of trichloroethylene or trichloroethanol, is longer in humans than in rodents. Trichloroacetic acid may be reduced in vivo to dichloroacetic acid, but the artefactual conversion of trichloroacetic acid to dichloroacetic acid hinders any clear conclusions. A fraction of trichloroacetic acid is metabolized to carbon dioxide.

Trichloroacetic acid induces peroxisome proliferation in the livers of mice at doses within the same range as those that induce hepatic tumours. A brief stimulation of cell division is observed in the liver during the first days of treatment, but depressed cell replication results from chronic treatment. The initial increase in cell proliferation was correlated with decreased methylation of the promoter regions of the c-jun and c-myc proto-oncogenes and increased expression of these genes.

Effects of trichloroacetic acid on reproduction and development in rats have been reported, but were not confirmed in a subsequent study. In-vitro results suggest that trichloroacetic acid can produce teratogenic effects at high doses.

In male mice, trichloroacetic acid modified neither the incidence of mutations in exon 2 of H-ras in carcinomas, nor the mutational spectrum observed in tumours that bore a mutation in exon 2. In female mice, 27% of tumours promoted by trichloroacetic acid exhibited loss of heterozygosity at a minimum of two loci on chromosome 6.

In mouse liver in vivo, measurements of trichloroacetic acid-induced 8-hydroxydeoxyguanosine DNA adducts gave different results depending on the route of administration. Trichloroacetic acid induced abnormal sperm in mice in vivo in one study and chromosomal aberrations in mouse and chicken bone marrow in vivo. The results of in-vivo studies in rodents on the induction of DNA strand breaks and micronuclei were inconsistent. It induced the formation of micronuclei in newt larvae in vivo.

In human cells in vitro, trichloroacetic acid did not induce chromosomal aberrations or DNA strand breaks in single studies. In single studies on cultured rodent cells, trichloroacetic acid was weakly mutagenic; no effect was observed in a DNA strand-break assay or a single-cell gel assay. It also inhibited intercellular communication in cultured rodent cells. Trichloroacetic acid caused neither mutation in bacteria nor SOS repair.

5.5        Evaluation

There is inadequate evidence in humans for the carcinogenicity of trichloroacetic acid.

There is limited evidence in experimental animals for the carcinogenicity of trichloroacetic acid.

Overall evaluation

Trichloroacetic acid is not classifiable as to its carcinogenicity to humans (Group 3).

For definition of the italicized terms, see Preamble Evaluation.

Previous evaluation: Vol. 63 (1995)

Synonyms

  •       TCA
  •       TCA (acid)
  •       Trichloracetic acid
  •       Trichloroethanoic acid
  •       Trichloromethane carboxylic acid

Last updated: 29 September 2004

SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number:           63

CCOHS Chemical Name:   Nitrogen, liquid

Synonyms:

Molecular nitrogen

Nitrogen

Liquid nitrogen

Azote, liquide

Nitrogen (non-specific name)

Chemical Name French:    Azote (liquide)

Chemical Name Spanish:   Nitrógeno

CAS Registry Number:      7727-37-9

UN/NA Number(s):          1977

RTECS Number(s):           QW9700000

Chemical Family: Inorganic nitrogen compound / elemental nitrogen / molecular nitrogen

Molecular Formula:          N2

Structural Formula:          N#N (# denotes a triple bond)

SECTION 2. DESCRIPTION

Appearance and Odour:

Colourless, odourless, extremely cold liquid.

Odour Threshold:

Odourless liquid.

Warning Properties:

POOR – The bubbling of liquid nitrogen in containers and a fog in the vicinity, due to condensation of moisture in the air, are not reliable warning properties, since they are not always present.

Composition/Purity:

Liquid nitrogen is shipped as a cryogenic liquid at pressures below 1379 kPa gage in specially authorized, thermally insulated cylinders, in heavily insulated portable containers, and in bulk in thermally insulated tank trucks and tank cars.(1,6) Liquid nitrogen may contain small amounts of liquefied oxygen, argon and other inert gases, carbon monoxide, hydrocarbons such as methane and water. See CHEMINFO record 56E for information on nitrogen gas.

Uses and Occurrences:

Nitrogen is the main component of air, comprising 78 to 79% by volume. Liquid nitrogen is used primarily as an expendable refrigerant. It is also used in the food packaging industry for refrigeration, freeze-drying and quick-freezing of foods; for bright-annealing of steel and for chilling in aluminum foundries; cryopulverizing of plastics, rubber and spices; cryoforming of metals; shrink fitting of metal parts; in medicine for quick freezing of tissues and microorganisms, as a cryotherapeutic agent; and for preservation of biological samples; as a coolant in laboratories; and in low-temperature research.(1,2,3,4)

 

SECTION 3. HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW:

Colourless, odourless, extremely cold liquid. Will not burn. COMPRESSED GAS. Confined space hazard. Simple asphyxiant. Can displace oxygen in air. May cause frostbite.

POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:

Nitrogen gas is non-toxic at normal temperature and pressure. However, nitrogen is a simple asphyxiant. Simple asphyxiants displace oxygen in air and can cause symptoms of oxygen deprivation (asphyxiation) when present in high enough concentrations to significantly lower the oxygen concentration. Air normally contains approximately 78% nitrogen and 21% oxygen. The oxygen content must not fall below 18% or harmful effects will result.

Effects of oxygen deficiency are: 12-16%: breathing and pulse rate increase, muscular coordination is slightly disturbed; 10-14%: emotional upset, abnormal fatigue, disturbed respiration; 6-10%: nausea and vomiting, collapse or loss of consciousness; below 6%: convulsive movements, possible respiratory collapse and death. Since exercise increases the body’s need for oxygen, symptoms will occur more quickly during exertion in an oxygen-deficient environment.(11)

Should the victim survive the effects of breathing an oxygen- deficient atmosphere, some or all organs including the central nervous system and brain, may show damage due to oxygen deprivation. These effects may or may not be reversible with time, depending on the degree and duration of the oxygen deprivation and the extent of the tissue injury.(11,12)

Small amounts of liquid can evaporate into very large volumes of gas. For example, one litre of liquid nitrogen vaporizes to 695 litres of nitrogen gas when warmed to room temperature (21 deg C at 1 atmosphere).(1,7) In large amounts it may displace oxygen in the air and give rise to a hazardous situation. This is a particularly serious hazard in enclosed or confined spaces.

Prolonged breathing of extremely cold air may damage the lungs.(7) Super-cooled vapours, such as liquid nitrogen vapour, can cause thermal injury to the upper airways. Edema (accumulation of fluids), inflammation, charring and blisters can result with eventual dead mucosal tissue and ulceration in the areas of greatest exposure.(4)

Skin Contact:

Liquid nitrogen and the associated cold vapours and gases can produce effects on the skin similar to a thermal burn. Prolonged exposure of the skin or contact with cold surfaces can cause frostbite. There is no initial pain, but there is intense pain when the frozen tissue thaws.(7,13) Symptoms of mild frostbite include numbness, prickling and itching of the affected area. Symptoms of more severe frostbite include a burning sensation and stiffness of the affected area. The skin may become waxy white or yellow. Blistering, necrosis (dead skin) and gangrene have developed in several cases.

Unprotected skin can stick to metal that is cooled by cryogenic liquids. The skin can then tear when pulled away.(7)

Eye Contact:

Liquid nitrogen and the associated cold vapours and gases can cause frostbite of the eyes, even when the contact is very brief. Permanent eye damage or blindness can result. There are no reports of accidental injury from splash contact of liquid nitrogen with the eyes.(10)

Ingestion:

Ingestion is not an applicable route of exposure for liquid nitrogen.

Effects of Long-Term (Chronic) Exposure

 

No effects of long-term exposure have been reported.

Carcinogenicity:

No human or animal information is available.

The International Agency for Research on Cancer (IARC) has not evaluated the carcinogenicity of this chemical.

The American Conference of Governmental Industrial Hygienists (ACGIH) has not assigned a carcinogenicity designation to this chemical.

The US National Toxicology Program (NTP) has not listed this chemical in its report on carcinogens.

Teratogenicity and Embryotoxicity:

No human or animal information is available.

Reproductive Toxicity:

No human or animal information is available.

Mutagenicity:

No information is available.

Toxicologically Synergistic Materials:

No information is available.

Potential for Accumulation:

Nitrogen does not accumulate in the body.

Health Comments:

People working at low temperatures, such as workplaces where liquid nitrogen is used as a refrigerant, may be at risk of developing reduced body temperature. Symptoms may include slowing down of physical and mental responses; irritability; difficulty in speech or vision; cramps and shivers.(5,13) Susceptibility depends on the length of exposure, temperature and the individual.

 

SECTION 4. FIRST AID MEASURES

Inhalation:

Take proper precautions to ensure your own safety before attempting rescue (e.g. wear appropriate protective equipment, use the “buddy” system). Remove source of contamination or move victim to fresh air. If breathing is difficult, oxygen may be beneficial if administered by trained personnel, preferably on a doctor’s advice. If breathing has stopped, trained personnel should begin artificial respiration (AR) or, if the heart has stopped, cardiopulmonary resuscitation (CPR) immediately. Immediately transport victim to an emergency care facility.

Skin Contact:

Avoid direct contact. Wear chemical protective clothing if necessary. Quickly remove victim from source of contamination and briefly flush with lukewarm, gently flowing water until the chemical is removed. DO NOT attempt to rewarm the affected area on site. DO NOT rub area or apply dry heat. Gently remove clothing or jewellery that may restrict circulation. Carefully cut around any clothing that sticks to the skin, and remove the rest of the garment. Loosely cover the affected area with a sterile dressing. DO NOT allow victim to drink alcohol or smoke. Quickly transport victim to emergency care facility.

Eye Contact:

Avoid direct contact. Wear chemical protective gloves if necessary. Quickly remove victim from source of contamination. Immediately and briefly, flush with lukewarm, gently flowing water until chemical is removed. DO NOT attempt to rewarm. Cover both eyes with a sterile dressing. DO NOT allow victim to drink alcohol or smoke. Quickly transport victim to an emergency care facility.

Ingestion:

Ingestion is not an applicable route of exposure for liquid nitrogen in occupational situations.

First Aid Comments:

Provide general supportive measures (comfort, warmth, rest). Consult a doctor and/or the nearest Poison Control Centre for all exposures except minor instances of inhalation or skin contact. Some recommendations in the above sections, such as administration of oxygen, may be considered medical acts in some jurisdictions. These recommendations should be reviewed with a doctor and appropriate delegation of authority obtained, as required. All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.

SECTION 5. FIRE FIGHTING MEASURES

Flash Point:

Non-flammable liquid or gas

Lower Flammable (Explosive) Limit (LFL/LEL):

Not applicable

Upper Flammable (Explosive) Limit (UFL/UEL):

Not applicable

Autoignition (Ignition) Temperature:

Not applicable

Sensitivity to Mechanical Impact:

Stable liquid or gas. Not sensitive.

Sensitivity to Static Charge:

Non-flammable liquid or gas. Not sensitive.

Combustion and Thermal Decomposition Products:

None known

Fire Hazard Summary:

Nitrogen does not burn. However, containers may rupture or explode in the heat of a fire. Nitrogen can displace air to the point where there is not enough oxygen to breathe.(1) Cryogenic liquids can be particularly dangerous during fires because of their potential to rapidly freeze water. Careless use of water can lead to heavy icing, possibly blocking pressure relief valves.(7) Furthermore, the relatively warm water greatly increases the evaporation rate of the nitrogen. If large concentrations of nitrogen gas are present, the water vapour in the surrounding air will condense, creating a dense fog that may make it difficult to find fire exits or equipment.(15)

Extinguishing Media:

Use extinguishing media appropriate for surrounding fire.

Fire Fighting Instructions:

Move cylinder or container from fire area if it can be done without risk. Carefully use water in large quantities, preferably in spray form, to cool fire-exposed containers and equipment. Take care not to block pressure relief valves. Stay away from ends of tanks. If possible, avoid spraying cold areas of equipment. If it is desirable to evaporate a liquefied nitrogen spill quickly, water spray may be used to increase the rate of evaporation if the increased vapour evolution can be controlled. DO NOT discharge a solid stream of water into liquid nitrogen.

If liquid nitrogen is discharging into the air, judgment should be used in deciding whether to allow the gas to escape, or to cut off the gas flow, depending on which is safer.(1) Where asphyxiation is not a factor, it is preferable to let the gas escape.

NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION

NFPA – Health:     3 – Short exposure could cause serious temporary or residual injury.

NFPA – Flammability:        0 – Will not burn under typical fire conditions.

NFPA – Instability:            0 – Normally stable, even under fire conditions, and not reactive with water.

SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight:            28.013

Conversion Factor:

1 ppm = 1.14 mg/m3; 1 mg/m3 = 0.875 ppm at 25 deg C (calc.)

Physical State:    Gas

Melting Point:      -210 deg C (-346 deg F) at 1 atmosphere.(1,2,3,5)

Boiling Point:      -195.8 deg C (-320.5 deg F) at 1 atmosphere.(1,3,5,6)

Relative Density (Specific Gravity): Not applicable (gas)

Solubility in Water:          Poorly soluble (1.49% v/v at 25 deg C and 1 atmosphere).(6)

Solubility in Other Liquids: Soluble in liquid ammonia

Coefficient of Oil/Water Distribution (Partition Coefficient):     Not applicable

pH Value:           Not applicable

Vapour Density:   0.967 at 21.1 deg C and 1 atmosphere (air = 1) (1,3)

Vapour Pressure: Not applicable. Gas at room temperature.

Vapour Pressure at 50 deg C:        Greater than 7000 kPa (69 atm) (estimated from graph) (6b)

Saturation Vapour Concentration:   Not applicable. Gas at room temperature.

Evaporation Rate:            Rapid, unless the liquid nitrogen is contained in a well-insulated vessel.

Critical Temperature:       -147 deg C (-232.6 deg F) (1,3,5)

Critical Pressure: 3400 kPa (33.54 atmospheres) (1,6)

SECTION 10. STABILITY AND REACTIVITY

Stability:

Normally stable.

Hazardous Polymerization:

Does not occur

Incompatibility – Materials to Avoid:

NOTE: Chemical reactions that could result in a hazardous situation (e.g. generation of flammable or toxic chemicals, fire or detonation) are listed here. Many of these reactions can be done safely if specific control measures (e.g. cooling of the reaction) are in place. Although not intended to be complete, an overview of important reactions involving common chemicals is provided to assist in the development of safe work practices.

FATTY MATERIALS – Use of liquid nitrogen in cryogenic grinding of fatty materials can lead to an explosion.(8,9)

MAGNESIUM – A mixture of magnesium powder and liquid nitrogen reacts very violently when lit with a fuse, forming magnesium nitride.(8)

Hazardous Decomposition Products:

None

Corrosivity to Metals:

Not corrosive

Stability and Reactivity Comments:

For information on materials incompatible with nitrogen gas, see CHEMINFO record 56E for details.

If liquid nitrogen is exposed to air, oxygen from the air may condense into the liquid nitrogen. Liquid nitrogen contaminated with oxygen may present the same hazards as liquid oxygen and could react violently with organic materials, such as oil and grease.(8,9)

SECTION 11. TOXICOLOGICAL INFORMATION

Standard animal toxicity values are not available.

Eye Irritation:

Liquid nitrogen poured onto the eyes of rabbits for one or two seconds with the lids held apart, produced no discernable injury. When the exposure was extended to five seconds, slight lesions of the corneal were observed. By the next day, all eyes were entirely normal.(10)

SECTION 16. OTHER INFORMATION

Selected Bibliography:

(1) Compressed Gas Association. Handbook of compressed gases. 2nd ed. Van Nostrand Reinhold, 1981. p. 205-227, 412-417

(2) Kirk-Othmer encyclopedia of chemical technology. 3rd ed. Vol. 15. John Wiley & Sons, 1981. p. 932-941

(3) Nitrogen. (Data sheet I-742-89). National Safety Council, 1989. 4p.

(4) Rockswold, G., et al. Inhalation of liquid nitrogen vapour. Annals of Emergency Medicine. Vol. 11, no. 10 (Oct. 1982). p. 553-555

(5) British Cryogenics Council. Cryogenics safety manual: a guide to good practice. 3rd ed. Butterworth Heinemann, 1991. p. 1-51

(6a) Braker, W., et al. Matheson gas data book. Matheson Gas Products, Inc., 1980. p. 522-530

(6b) Yaws, C.L. Matheson gas data book. 7th ed. McGraw-Hill, 2001. p. 563

(7) Riklik, L. How to work safely with cryogenic liquids (P90-24E). CCOHS, 1990

(8) Bretherick, L. Bretherick’s handbook of reactive chemical hazards. 4th ed. Butterworths, 1990. p. 49-50, 1189, 1346-1347

(9) Hempseed, J.W. Safety considerations in using liquid nitrogen. Loss Prevention Bulletin. No. 097 (Feb. 1991). p. 1-3

(10) Grant, W.M. Toxicology of the eye. 3rd ed. Charles C.Thomas, 1986. p. 664-665

(11) Wilkenfeld, M. Simple asphyxiants. Environmental and Occupational Medicine. 2nd edition. Edited by Brown and Company, 1992. p. 535-538

(12) Casarett and Doull’s toxicology : the basic science of poisons. 3rd ed. Macmillan Publishing Company, 1986. p. 359-362

(13) Code of practice for safe operation of small-scale storage facilities for cryogenic liquids. (BS 5429 : 1976). British Standards Institution, 1976

(14) Position paper on the safe handling of cryogenic liquids. Canadian Standards Association, 1988

(15) Matheson guide to safe handling of compressed gases. 2nd printing. Matheson Gas Products, Inc., 1983. p. 216-225

(16) Fire protection guide to hazardous materials. 13th ed. Edited by A.B. Spencer, et al. National Fire Protection Association, 2002. NFPA 49

Information on chemicals reviewed in the CHEMINFO database is drawn from a number of publicly available sources. A list of general references used to compile CHEMINFO records is available in the database Help.

Review/Preparation Date: 1994-08-22

Revision Indicators:

Respiratory guidelines       1995-09-01

Resistance of materials     1995-09-01

EU number         1995-09-01

EU class 1995-09-01

TLV-TWA            1995-10-01

TLV comments    1995-10-01

US Transport      1998-03-01

TDG      2002-05-27

US transport       2002-12-06

Bibliography        2006-01-18

Vapour pressure at 50 deg C         2006-01-18

Relative density   2006-09-28

 

1-CHLORO-2,4-DINITROBENZENEICSC: 0416
Date of Peer Review: October 1999

1,3-Dinitro-4-chlorobenzene

2,4-Dinitrophenyl chloride

DNCB

 

CAS #97-00-7C6H3ClN2O4 / C6H3Cl(NO2)2
RTECS #CZ0525000Molecular mass: 202.6
UN #1577 

EC Index #610-003-00-4

 

TYPES OF HAZARD / EXPOSUREACUTE HAZARDS / SYMPTOMSPREVENTIONFIRST AID / FIRE FIGHTING
FIRECombustible. Gives off irritating or toxic fumes (or gases) in a fire.NO open flames.Water spray, foam, powder, carbon dioxide.
EXPLOSIONFinely dispersed particles form explosive mixtures in air.Do NOT expose to friction or shock.In case of fire: keep drums, etc., cool by spraying with water. Combat fire from a sheltered position.

 

EXPOSUREPREVENT DISPERSION OF DUST! STRICT HYGIENE!
InhalationBlue lips or finger nails. Blue skin. Dizziness. Headache. Laboured breathing. Nausea. Vomiting. Disturbed vision.Local exhaust or breathing protection.Fresh air, rest. Artificial respiration may be needed. Refer for medical attention.
SkinMAY BE ABSORBED! Redness. Pain. (Further see Inhalation).Protective gloves. Protective clothing.Remove contaminated clothes. Rinse and then wash skin with water and soap. Refer for medical attention.
EyesRedness. Pain.Face shield or eye protection in combination with breathing protection.First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then take to a doctor.
IngestionAbdominal pain. Blue skin. Dizziness. Headache. Laboured breathing. Nausea. Vomiting.Do not eat, drink, or smoke during work.Rinse mouth. Induce vomiting (ONLY IN CONSCIOUS PERSONS!). Wear protective gloves when inducing vomiting. Refer for medical attention.

 

SPILLAGE DISPOSALPACKAGING & LABELLING
Vacuum spilled material then remove to safe place. Do NOT let this chemical enter the environment. Chemical protection suit including self-contained breathing apparatus.Do not transport with food and feedstuffs. Marine pollutant.

EU Classification

Symbol: T, N

R: 23/24/25-33-50/53

S: (1/2-)-28-36/37-45-60-61

Note: [C]

UN Classification

UN Hazard Class: 6.1

UN Pack Group: II

EMERGENCY RESPONSESTORAGE
Transport Emergency Card: TEC (R)-61S1577-S or 61GT2-II

NFPA Code: H 3; F 1; R 4

Fireproof. Separated from strong oxidants, strong bases, food and feedstuffs. Cool.
 

IPCS

International

Programme on

Chemical Safety

Prepared in the context of cooperation between the International Programme on Chemical Safety and the Commission of the European Communities © IPCS, CEC 2005

 

SEE IMPORTANT INFORMATION ON BACK

 

 

1-CHLORO-2,4-DINITROBENZENEICSC: 0416

 

IMPORTANT DATA
PHYSICAL STATE; APPEARANCE:

PALE YELLOW CRYSTALS, WITH CHARACTERISTIC ODOUR.

 

CHEMICAL DANGERS:

May explosively decompose on shock, friction, or concussion. May explode on heating even in the absence of air. Reacts with strong oxidants and strong bases. On combustion, forms toxic and corrosive gases and fumes including hydrogen chloride and nitrogen oxides.

 

OCCUPATIONAL EXPOSURE LIMITS:

TLV not established.

MAK: sensitization of skin (Sh); (DFG 2004).

ROUTES OF EXPOSURE:

The substance can be absorbed into the body by inhalation and through the skin and by ingestion.

 

INHALATION RISK:

No indication can be given about the rate in which a harmful concentration in the air is reached on evaporation of this substance at 20°C.

 

EFFECTS OF SHORT-TERM EXPOSURE:

The substance irritates the eyes, the respiratory tract and is severely irritating to the skin. The substance may cause effects on the blood, resulting in formation of methaemoglobin. Exposure to high concentrations may result in death.

 

EFFECTS OF LONG-TERM OR REPEATED EXPOSURE:

Repeated or prolonged contact with skin may cause dermatitis. Repeated or prolonged contact may cause skin sensitization. The substance may have effects on the nervous system, resulting in impaired vision.

PHYSICAL PROPERTIES
Boiling point: 315°C

Melting point: 54°C

Density: 1.7 g/cm³

Solubility in water: none

Vapour pressure, Pa at 20°C: negligible

Flash point: 179°C

Auto-ignition temperature: 432°C

Explosive limits, vol% in air: 2.0-22

ENVIRONMENTAL DATA
The substance is very toxic to aquatic organisms.
NOTES
Card has been partly updated in October 2005. See sections Occupational Exposure Limits, Emergency Response.
ADDITIONAL INFORMATION
 

LEGAL NOTICENeither the CEC nor the IPCS nor any person acting on behalf of the CEC or the IPCS is responsible for the use which might be made of this information
© IPCS, CEC 2005

 

 

TRICHLOROACETIC ACIDICSC: 0586
Date of Peer Review: November 1998

Trichloroethanoic acid

Aceto-caustin

TCA

 

CAS #76-03-9C2HCl3O2 / CCl3COOH
RTECS #AJ7875000Molecular mass: 163.4
UN #1839 

EC Index #607-004-00-7

 

TYPES OF HAZARD / EXPOSUREACUTE HAZARDS / SYMPTOMSPREVENTIONFIRST AID / FIRE FIGHTING
FIRENot combustible. Gives off irritating or toxic fumes (or gases) in a fire.In case of fire in the surroundings: use appropriate extinguishing media.
EXPLOSION

 

EXPOSUREAVOID ALL CONTACT!IN ALL CASES CONSULT A DOCTOR!
InhalationSore throat. Cough. Burning sensation. Headache. Nausea. Vomiting. Shortness of breath. Laboured breathing. Symptoms may be delayed (see Notes).Ventilation (not if powder), local exhaust, or breathing protection.Fresh air, rest. Half-upright position. Artificial respiration may be needed. Refer for medical attention.
SkinPain. Redness. Blisters. Skin burns.Protective gloves. Protective clothing.Remove contaminated clothes. Rinse skin with plenty of water or shower. Refer for medical attention.
EyesPain. Redness. Severe deep burns.Face shield or eye protection in combination with breathing protection.First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then take to a doctor.
IngestionBurning sensation. Abdominal pain. Shock or collapse.Do not eat, drink, or smoke during work.Rinse mouth. Do NOT induce vomiting. Give plenty of water to drink. Rest. Refer for medical attention. See Notes.

 

SPILLAGE DISPOSALPACKAGING & LABELLING
Sweep spilled substance into water filled containers; if appropriate, moisten first to prevent dusting. Cautiously neutralize remainder with alkali such as sodium bicarbonate, sodium hydroxide. Then wash away with plenty of water. Personal protection: complete protective clothing including self-contained breathing apparatus.Unbreakable packaging; put breakable packaging into closed unbreakable container.

EU Classification

Symbol: C, N

R: 35-50/53

S: (1/2-)-26-36/37/39-45-60-61

UN Classification

UN Hazard Class: 8

UN Pack Group: II

EMERGENCY RESPONSESTORAGE
Transport Emergency Card: TEC (R)-80GC4-II+IIISeparated from food and feedstuffs. See Chemical Dangers. Cool. Dry. Well closed. Keep in a well-ventilated room.
 

IPCS

International

Programme on

Chemical Safety

Prepared in the context of cooperation between the International Programme on Chemical Safety and the Commission of the European Communities © IPCS, CEC 2005

 

SEE IMPORTANT INFORMATION ON BACK

 

 

TRICHLOROACETIC ACIDICSC: 0586

 

IMPORTANT DATA
PHYSICAL STATE; APPEARANCE:

COLOURLESS HYGROSCOPIC CRYSTALS, WITH PUNGENT ODOUR.

 

CHEMICAL DANGERS:

The substance decomposes on heating producing toxic and corrosive fumes including hydrogen chloride and chloroform. The solution in water is a strong acid, it reacts violently with bases and is corrosive to many metals.

 

OCCUPATIONAL EXPOSURE LIMITS:

TLV: 1 ppm as TWA; A3 (confirmed animal carcinogen with unknown relevance to humans); (ACGIH 2005).

MAK: IIb (not established but data is available); (DFG 2005).

ROUTES OF EXPOSURE:

The substance can be absorbed into the body by inhalation of its vapour and by ingestion.

 

INHALATION RISK:

A harmful contamination of the air will be reached rather slowly on evaporation of this substance at 20°C.

 

EFFECTS OF SHORT-TERM EXPOSURE:

The substance is corrosive to the eyes, the skin and the respiratory tract. Corrosive on ingestion. Inhalation of vapour may cause lung oedema (see Notes). The effects may be delayed. Medical observation is indicated.

PHYSICAL PROPERTIES
Boiling point: 198°C

Melting point: 58°C

Density: 1.6 g/cm³

Solubility in water: very good

Vapour pressure, Pa at 51°C: 133

Relative vapour density (air = 1): 5.6

Octanol/water partition coefficient as log Pow: 1.7
ENVIRONMENTAL DATA
NOTES
The symptoms of lung oedema often do not become manifest until a few hours have passed and they are aggravated by physical effort. Rest and medical observation is therefore essential. Immediate administration of an appropriate inhalation therapy by a doctor or a person authorized by him/her, should be considered. Card has been partly updated in October 2005. See sections Occupational Exposure Limits, EU classification, Emergency Response.
ADDITIONAL INFORMATION
 

LEGAL NOTICENeither the CEC nor the IPCS nor any person acting on behalf of the CEC or the IPCS is responsible for the use which might be made of this information
© IPCS, CEC 2005

 

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