HN1 (nitrogen mustard)

Last updated
HN1 (nitrogen mustard)
Nitrogen-mustard-HN1.png
HN1-3D-vdW.png
Names
IUPAC name
2-Chloro-N-(2-chloroethyl)-N-ethylethanamine
Other names
Bis(2-chloroethyl)(ethyl)amine
Identifiers
3D model (JSmol)
ChemSpider
MeSH bis(2-chloroethyl)ethylamine
PubChem CID
RTECS number
  • YE1225000
UNII
UN number 2810
  • InChI=1S/C6H13Cl2N/c1-2-9(5-3-7)6-4-8/h2-6H2,1H3 Yes check.svgY
    Key: UQZPGHOJMQTOHB-UHFFFAOYSA-N Yes check.svgY
  • CCN(CCCl)CCCl
Properties
C6H13Cl2N
Molar mass 170.08 g·mol−1
AppearanceColourless to pale yellow oily liquid
Odor Fishy, musty
Density 1.0861 g mL−1 (at 20 °C)
Melting point −34 °C (−29 °F; 239 K)
Boiling point 85.5 °C (185.9 °F; 358.6 K)
Related compounds
Related compounds
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).

Bis(2-chloroethyl)ethylamine is the organic compound with the formula C2H5N(CH2CH2Cl)2. Often abbreviated HN1, it is a powerful vesicant and a nitrogen mustard gas used for chemical warfare. HN1 was developed in the 1920s and 1930s to remove warts and later as a military agent. Because of the latter use, it is a Schedule 1 chemical within the Chemical Weapons Convention and therefore use and production is strongly restricted. It has never been used in warfare. [1]

Contents

It is an oily liquid with a colorless to pale yellow appearance and a faint fishy or musty odor. HN1 is also an alkylating agent. [1]

Reactions

Nitrogen mustards react via an initial cyclization to the corresponding aziridinium salt. The rate of this reaction is pH dependent because the protonated amine cannot cyclize. The aziridinium ion reacts with water in a slower reaction. At pH 8, the nitrogen mustards are essentially quantitatively converted to the aziridinium ion for subsequent slow reaction with water. In contrast, at pH 4 cyclization and hydrolysis show the classic form of reactions in series.[ citation needed ] Hydrolysis of HN1 produces toxic intermediates. [1]

HN1 reacts with iron alloys, corroding them at and above 65 °C (149 °F), and reacts with metals in general, producing hydrogen gas. This can potentially cause explosions. [1]

Toxicity

Because HN1 is an alkylating agent, it damages DNA, causes immunosuppression, and causes injury to areas that come into contact with it. Exposure to HN1 can be fatal, and its effects on skin and mucous membranes are worsened when they are moist. The alkylation effects cause damage to the spleen, bone marrow, and lymph nodes, which causes anemia, low white cell counts, and internal bleeding. The vesicant effects cause blistering and damage to the skin. [1]

The symptoms of exposure depend on the route of exposure. Eye exposure to vapor can cause lacrimation (tears), blepharospasm (eyelid twitching), irritation, itching, burning pain, dry feeling, and sometimes miosis (pinpoint pupils). More severe vapor exposure can also cause swelling and fluid buildup (edema) in the eyelids, increased pain, and redness. Very severe exposure to vapor or exposure to liquid can cause photophobia (aversion to light), corneal ulceration, and blindness. [1]

Inhaling the vapor causes symptoms that begin in the upper airway and expand to the lower airway. Increased concentrations cause worse symptoms. Mild inhalation exposure causes rhinorrhea (runny nose), sneezing, barking cough (a harsh cough that sounds somewhat like a dog barking), epistaxis (nosebleed), dyspnea (shortness of breath) that affects smokers and asthmatics, hoarseness that turns into toneless voice, ageusia (loss of taste), and anosmia (loss of smell); later on, sinus and nose pain develops. With more severe inhalation exposure, the airway becomes inflamed, pneumonia develops, and the respiratory epithelium can begin to have necrosis and slough off, forming a pseudomembrane that can occlude the airway. This occlusion can be fatal, as can the pneumonia. [1]

Skin contact with nitrogen mustard in low concentrations causes symptoms beginning with redness, then moving to blistering, itching, and burning pain. More severe exposure can cause necrosis (cell death) in the blisters, and systemic toxicity, which causes malaise, vomiting, exhaustion, and fever. Skin exposure that causes symptoms over more than 25% of the body area is often fatal. Though ingestion is uncommon, nitrogen mustard can burn the GI tract and cause nausea, vomiting, hemorrhagic diarrhea, and abdominal pain. [1]

Nitrogen mustard exposure does not cause symptoms until several hours to several days afterwards, but more severe exposure causes symptoms sooner. With severe exposure, eye injury can manifest within 1-2 hours, airway damage within 2-6 hours, and skin damage within 6-12 hours (sooner in hot or humid weather). Mild exposure takes longer to manifest symptoms: eye injury within 3-12 hours, airway damage within 12-24 hours, and skin damage up to 48 hours post-exposure. [1]

Long-term sequelae

Effects of nitrogen mustard exposure can be long-term or permanent; it is also a known carcinogen, reprotoxin, and developmental toxin after chronic and acute exposure, causing skin cancer and airway cancers in particular. Blindness from an acute exposure is usually temporary, resolving in days to months depending on severity. Chronic respiratory and eye infections are also common after acute nitrogen mustard exposure. Other consequences of acute exposure include ageusia, anosmia, pulmonary fibrosis, scarring, bronchitis, chronic respiratory disease, mental illness, and central nervous system damage. Consequences of chronic exposure beyond cancer include permanent kidney damage and immunosuppression. [1]

Treatment

Treatment for HN1 exposure is primarily supportive, since there is no antidote. First aid involves decontamination, irrigation, removing the affected person from the source of exposure, immediate medical attention, airway management (in cases of inhalation exposure), and medical monitoring of respiratory and cardiac function. If the affected person has trouble breathing (dyspnea) or stops breathing (apnea), ventilatory support and oxygen therapy can be helpful. If HN1 has been ingested, emetics (agents that induce vomiting) and gastric lavage are contraindicated, and nothing should be consumed by mouth because they could damage the gastrointestinal system. [1]

See also

Related Research Articles

<span class="mw-page-title-main">Lewisite</span> Arsenic compound and chemical weapon

Lewisite (L) (A-243) is an organoarsenic compound. It was once manufactured in the U.S., Japan, Germany and the Soviet Union for use as a chemical weapon, acting as a vesicant and lung irritant. Although the substance is colorless and odorless in its pure form, impure samples of lewisite are a yellow, brown, violet-black, green, or amber oily liquid with a distinctive odor that has been described as similar to geraniums.

Salt water aspiration syndrome is a rare diving disorder suffered by scuba divers who inhale a mist of seawater, usually from a faulty demand valve, causing irritation of the lungs. It is not the same thing as aspiration of salt water as a bulk liquid, i.e. drowning. It can usually be treated by rest for several hours. If severe, medical assessment is required. First described by Carl Edmonds.

<span class="mw-page-title-main">Blister agent</span> Chemicals that result in blistering and skin irritation and damaging

A blister agent, is a chemical compound that causes severe skin, eye and mucosal pain and irritation. They are named for their ability to cause severe chemical burns, resulting in painful water blisters on the bodies of those affected. Although the term is often used in connection with large-scale burns caused by chemical spills or chemical warfare agents, some naturally occurring substances such as cantharidin are also blister-producing agents (vesicants). Furanocoumarin, another naturally occurring substance, causes vesicant-like effects indirectly, for example, by increasing skin photosensitivity greatly. Vesicants have medical uses including wart removal but can be dangerous if even small amounts are ingested.

<span class="mw-page-title-main">Chemical burn</span> Medical condition

A chemical burn occurs when living tissue is exposed to a corrosive substance or a cytotoxic agent. Chemical burns follow standard burn classification and may cause extensive tissue damage. The main types of irritant and/or corrosive products are: acids, bases, oxidizers / reducing agents, solvents, and alkylants. Additionally, chemical burns can be caused by biological toxins and by some types of cytotoxic chemical weapons, e.g., vesicants such as mustard gas and Lewisite, or urticants such as phosgene oxime.

<span class="mw-page-title-main">Chlormethine</span> Chemical compound

Chlormethine, also known as mechlorethamine, mustine, HN2, and embikhin (эмбихин), is a nitrogen mustard sold under the brand name Mustargen among others. It is the prototype of alkylating agents, a group of anticancer chemotherapeutic drugs. It works by binding to DNA, crosslinking two strands and preventing cell duplication. It binds to the N7 nitrogen on the DNA base guanine. As the chemical is a blister agent, its use is strongly restricted within the Chemical Weapons Convention where it is classified as a Schedule 1 substance.

Phosgene oxime, or CX, is an organic compound with the formula Cl2CNOH. It is a potent chemical weapon, specifically a nettle agent, which is a type of blister agent. The compound itself is a colorless solid, but impure samples are often yellowish liquids. It has a strong, disagreeable and irritating odor. It is used as a reagent in organic chemistry.

<span class="mw-page-title-main">Abrin</span> Chemical compound

Abrin is an extremely toxic toxalbumin found in the seeds of the rosary pea, Abrus precatorius. It has a median lethal dose of 0.7 micrograms per kilogram of body mass when given to mice intravenously. The median toxic dose for humans ranges from 10 to 1000 micrograms per kilogram when ingested and is 3.3 micrograms per kilogram when inhaled.

<span class="mw-page-title-main">Pneumonitis</span> General inflammation of lung tissue

Pneumonitis describes general inflammation of lung tissue. Possible causative agents include radiation therapy of the chest, exposure to medications used during chemo-therapy, the inhalation of debris, aspiration, herbicides or fluorocarbons and some systemic diseases. If unresolved, continued inflammation can result in irreparable damage such as pulmonary fibrosis.

Acute severe asthma, also known as status asthmaticus, is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators (inhalers) and corticosteroids. Asthma is caused by multiple genes, some having protective effect, with each gene having its own tendency to be influenced by the environment although a genetic link leading to acute severe asthma is still unknown. Symptoms include chest tightness, rapidly progressive dyspnea, dry cough, use of accessory respiratory muscles, fast and/or labored breathing, and extreme wheezing. It is a life-threatening episode of airway obstruction and is considered a medical emergency. Complications include cardiac and/or respiratory arrest. The increasing prevalence of atopy and asthma remains unexplained but may be due to infection with respiratory viruses.

<span class="mw-page-title-main">Farmer's lung</span> Hypersensitivity pneumonitis

Farmer's lung is a hypersensitivity pneumonitis induced by the inhalation of biologic dusts coming from hay dust or mold spores or any other agricultural products. It results in a type III hypersensitivity inflammatory response and can progress to become a chronic condition which is considered potentially dangerous.

Occupational lung diseases comprise a broad group of diseases, including occupational asthma, industrial bronchitis, chronic obstructive pulmonary disease (COPD), bronchiolitis obliterans, inhalation injury, interstitial lung diseases, infections, lung cancer and mesothelioma. These can be caused directly or due to immunological response to an exposure to a variety of dusts, chemicals, proteins or organisms. Occupational cases of interstitial lung disease may be misdiagnosed as COPD, idiopathic pulmonary fibrosis, or a myriad of other diseases; leading to a delay in identification of the causative agent.

<span class="mw-page-title-main">HN3 (nitrogen mustard)</span> Chemical compound

2-Chloro-N,N-bis(2-chloroethyl)ethanamine, also known as trichlormethine, tris(2-chloroethyl)amine is the organic compound with the formula N(CH2CH2Cl)3. Often abbreviated HN3 or HN-3, it is a powerful blister agent and a nitrogen mustard used for chemical warfare. HN3 was the last of the nitrogen mustard agents developed. It was designed as a military agent and is the only one of the nitrogen mustards that is still used for military purposes. It is the principal representative of the nitrogen mustards because its vesicant properties are almost equal to those of HD and thus the analogy between the two types of mustard is the strongest. As a vesicant the use and production is strongly restricted within the Chemical Weapons Convention where it is classified as a Schedule 1 substance.

Potassium nitrate is an oxidizer so storing it near fire hazards or reducing agents should be avoided to minimise risk in case of a fire.

<span class="mw-page-title-main">Bird fancier's lung</span> Type of hypersensitivity pneumonitis

Bird fancier's lung (BFL), also known as bird breeder's lung, is a type of hypersensitivity pneumonitis. It can cause shortness of breath, fever, dry cough, chest pain, anorexia and weight loss, fatigue, and progressive pulmonary fibrosis. It is triggered by exposure to avian proteins present in the dry dust of droppings or feathers of a variety of birds. The lungs become inflamed, with granuloma formation. It mostly affects people who work with birds or own many birds.

<span class="mw-page-title-main">Phenyldichloroarsine</span> Chemical compound

Phenyldichloroarsine, also known by its wartime name phenyl Dick and its NATO abbreviation PD, is an organic arsenical vesicant and vomiting agent developed by Germany and France for use as a chemical warfare agent during World War I. The agent is known by multiple synonyms and is technically classified as a vesicant, or blister agent.

Acute inhalation injury may result from frequent and widespread use of household cleaning agents and industrial gases. The airways and lungs receive continuous first-pass exposure to non-toxic and irritant or toxic gases via inhalation. Irritant gases are those that, on inhalation, dissolve in the water of the respiratory tract mucosa and provoke an inflammatory response, usually from the release of acidic or alkaline radicals. Smoke, chlorine, phosgene, sulfur dioxide, hydrogen chloride, hydrogen sulfide, nitrogen dioxide, ozone, and ammonia are common irritants.

Chlorine gas poisoning is an illness resulting from the effects of exposure to chlorine beyond the threshold limit value.

<span class="mw-page-title-main">Nitrogen dioxide poisoning</span> Medical condition

Nitrogen dioxide poisoning is the illness resulting from the toxic effect of nitrogen dioxide. It usually occurs after the inhalation of the gas beyond the threshold limit value. Nitrogen dioxide is reddish-brown with a very harsh smell at high concentrations, at lower concentrations it is colorless but may still have a harsh odour. Nitrogen dioxide poisoning depends on the duration, frequency, and intensity of exposure.

<span class="mw-page-title-main">Lewisite 2</span> Chemical compound

Lewisite 2(L-2) is an organoarsenic chemical weapon with the formula AsCl(CH=CHCl)2. It is similar to lewisite 1 and lewisite 3 and was first synthesized in 1904 by Julius Arthur Nieuwland. It is usually found as a mixture of 2-chlorovinylarsonous dichloride (lewisite 1) as well as bis(2-chloroethenyl) arsinous chloride (lewisite 2) and tris(2-chlorovinyl)arsine (lewisite 3). Pure lewisite 1 is an oily, colorless liquid, however, the impure mixture can appear amber to black with an odor distinct to geraniums.

<span class="mw-page-title-main">Lewisite 3</span> Chemical compound

Lewisite 3(L-3) is an organoarsenic chemical weapon like lewisite 1 and lewisite 2 first synthesized in 1904 by Julius Arthur Nieuwland. It is usually found as a mixture of 2-chlorovinylarsonous dichloride as well as bis(2-chloroethenyl) arsinous chloride and tris(2-chlorovinyl)arsine. Pure lewisite 1 is an oily, colorless liquid, however, the impure mixture can appear amber to black with an odor distinct to geraniums.

References

  1. 1 2 3 4 5 6 7 8 9 10 11 The Emergency Response Safety and Health Database: NITROGEN MUSTARD HN-1. National Institute for Occupational Safety and Health. Accessed March 19, 2009.