Irritants - Riot Control Agents

The sole purpose of irritants (also known as tear gas, riot control agents, and lachrymators) is to produce immediate dermatological, respiratory, and ocular discomfort in order to render the victim incapable of fighting or resisting. Police forces use them for crowd control, and military forces currently use them mainly for training. These agents were used before World War I, and in that war, they were the first chemical agents used—well before the better-known chlorine, phosgene, and mustard gas. The United States used them during the Vietnam War to deny tunnel access to its enemies.[2]

The United States excludes these agents from the 1925 Geneva Convention banning other chemical and biological weapons. Dispersal is allowed in specific US military operations but only by presidential order.

Tear gas (CS) and chloroacetophenone (CN) are by far the most important pulmonary irritants. CN was the primary pulmonary irritant after World War I until the development of CS in 1928. CS was found to be more potent (10 times more potent as a lachrymator than CN) but less toxic. In approximately 1959, CS replaced CN as the principal military and law enforcement riot control agent.

CS is the familiar tear gas most often used by police for crowd control (eg, the police in the United Kingdom have used CS as an incapacitant for the past decade). CN has been available as Mace, a product that had been used for personal protection. Capsaicin, or pepper spray, has to some extent replaced CN as a personal protective agent, with less dangerous effects.[8]  

Although CS and CN are the most important agents in this class, several others require mention. Chloropicrin (PS) and bromobenzenecyanide (CA) were developed before World War I. Both largely have been replaced, as they were too lethal for their intended effects but not lethal enough to compete with the more effective blistering and nerve agents. PS is still seen occasionally as a soil sterilant, fumigant or grain disinfectant.[4, 7]

Attempts to make CN more effective resulted in the creation of CNB (CN, carbon tetrachloride, and benzene), chloroacetophenone in chloroform (CNC), and CNS (CN, chloroform, and PS). However, CS proved more effective and less toxic than any of the CN series and largely has replaced them. While the clinical effects of a CS spray may last for days, subjects sprayed with CS have shown no convincing physical evidence of pathology for up to 10 months afterward.[9]

Dibenz-(b,f)-1,4-oxazepine (CR) is a more recent tear gas, first synthesized in 1962. It reportedly is more potent and less toxic than CS. Part of its high safety profile is due to its low volatility, which minimizes its effects deep in the pulmonary system. However, it is still is not used widely. Pepper spray, or oleoresin capsicum (OC), is also considered a riot control agent. A 1% solution is sold commercially to the public, but 10% solutions exist. OC causes the release of a neuropeptide (substance P) that causes pain and inflammation. A recent review states that the neurogenic inflammation caused by capsaicinoid in the pepper spray is the cause of the compound's irritative effects.[10] However, at high concentrations and with prolonged exposure, fatalities with capsaicinoids have been reported.[11]  

The possibility of secondary contamination is very real. In one incident, CS was used to flush out possible stowaways on a cargo vehicle. When the cargo was finally delivered to 16 stores within Scotland, 21 workers experienced itching and running eyes, rhinorrhea, a burning sensation on the face and hands, and a burning throat.[12] In case studies, secondary exposures have also affected emergency department personnel and anesthetists.[3]

Onset of symptoms occurs in seconds to several minutes after exposure to pulmonary irritants. Most cases are brief and self-limited, and most persons do not seek medical care. Without continuing exposure, symptoms typically resolve spontaneously in 15-30 minutes, and most persons do not seek medical care. However, serious effects, including death, have been reported.[4, 5, 6, 7] See Presentation.

Riot control agents are solids with low vapor pressures that are dispersed as fine particles or in solution. CS and CN are SN2 alkylating agents and react at nucleophilic sites. Although the mechanism is presently unclear, injuries caused by this class of agents may be caused by inactivation of sulfhydryl-containing enzymes such as lactic dehydrogenase and a specific coenzyme in the pyruvate decarboxylase system (disulfhydryl form of lipoic acid).[3]

Research has indicated that these agents are extremely potent activators of the body's TRPA1 (a family of transient receptor potential ion channel) receptors (ie, mechanical stress sensors).[2, 13] Since anti‐inflammatory and analgesic effects have been observed for TRPA1 inhibitors in multiple models of chemical injury and inflammation, it is possible that TRPA1 inhibitors could alleviate at least some of the tear gas–induced effects. The conclusion of clinical trials using TRPA1 inhibitors in diabetic neuropathic patients is eagerly awaited with the hope that more advanced inhibitors will be made available for testing in other conditions, including irritant and tear gas agent exposures.[14]

No race- or sex-related susceptibility to pulmonary irritants exists. Chemical irritants, especially those deployed in aerosolized forms, are inherently indiscriminate and can affect not only the intended targets but also peaceful demonstrators, bystanders, nearby communities and residences,[15] emergency health care workers,[16] and law enforcement officers themselves. The majority of people injured are young adults, consistent with typical protest demographics.

Children are more vulnerable to severe injuries from chemical toxicity. The elderly and those with chronic diseases are also prone to worse outcomes.[17]

The prognosis for patients with irritant exposure is excellent. The few reported dangerous effects occur rapidly.

Short-term effects of pulmonary irritants predominate. Fatalities, albeit few, have occurred at high concentrations and with prolonged exposure.[17]   In fact, the risk of death is directly related to the agent, the concentration of the agent, the duration of exposure, the proximity to the source, and location (ie, indoors vs. outdoors).[2]

A systematic review of CS that included 90 cases of CS exposure reported the following distribution of effects[3] :

• Dermal - 61% of cases
• Ocular - 57%
• Respiratory - 40%
• Gastrointestinal - 13%
• Neurological -  7% 
• Other clinical effects - 17%

Complications include the following[4, 7] :

• Pulmonary edema
• Glaucoma
• Cataracts
• Blindness
• Death

A 2015 review of 10 riot control agent (RCA)–related deaths found that RCAs were the sole cause of death in three cases, a secondary cause in three (asthma, asphyxia), and contributory in four. Pepper spray (oleoresin capsicum; OC) was the RCA involved in eight of the cases, while chloroacetophenone (CN) and tear gas (CS) caused one apiece.[18]

Different types of symptoms tend to vary in their duration. A systematic review of CS exposure found the following typical durations[3] :

• Ocular symptoms and respiratory irritation - Minutes or a few hours
• Chest tightness - Up to 1 day
• Reactive airways dysfunction syndrome - Months and up to several years
• Erythema - A few days to 1 week
• Vesicular eruptions, blistering rash, or diffuse swelling - Usually days, but up to 4 weeks in some cases

In one study, a high rate (72.4%) of adult protesters with repeated or prolonged exposed to RCAs reported increased anxiety, startle response, fear, fatigue, or sadness/depressive feelings. Long-term persistent reactions in a minority of respondents were insomnia, nightmares, nausea, diarrhea with blood, and severe headaches.[15]

Exposure to tear gas has been associated with triggering or worsening existing health conditions including allergies, asthma, eczema, fibromyalgia, Hahimoto thyroiditis, rheumatoid arthritis, and herpes simplex virus.[15]

In rare cases, particular reactions may persist for much longer than usual (eg, dermatitis lasting for several months, headaches lasting several weeks).[19, 15]

Upon exposure to a riot control agent, the key steps are to remove oneself from the site of dissemination as quickly as possible—the mantra is to go "uphill, upwind, upstream"—and then begin the process of decontamination, should sufficent material remain in contact with eyes, skin, and clothes.

Symptoms caused by a riot control agent should subside within half an hour. Persistence of effects beyond that time suggests that the agent may, in fact, not be a relatively harmless riot control agent, but a more toxic substance such as lewisite or phosgene, in which case thorough decontamination is necessary.

For patient education information, see Chemical Warfare and Personal Protective Equipment.

The timing of symptom onset after exposure to tear gas (CS) varies, depending on the duration of exposure and the organ system involved. With dermal effects, for example, erythema may develop within a few minutes, whereas acute generalized exanthematous pustulosis may have a latency period of 1-2 weeks. Similarly, respiratory effects can occur immediately (eg, cough) or develop after about 3 weeks (eg, laryngeal obstruction).[3]  

Most cases are self-limited, lasting 15-30 minutes after clothing is removed and the person is in an open space.[2] Reconsider the diagnosis of riot control agent exposure if symptoms persist longer than 30 minutes. However, in one study, the majority of subjects who were directly sprayed with CS in the face still had respiratory and oral symptoms after 1 hour.[9]   

Typically, exposed persons feel a burning sensation in the eyes, nose, mouth, and even airway. The eye is the most sensitive organ involved and is the most immediately and severely affected of all the target organs. Eye involvement may include the following:

• Ocular pain, tearing, and severe blepharospasm are common; at high concentrations, 2-chloroacetophenone (CN) is known to cause corneal epithelial damage and chemosis.

• Conjunctival injection and periorbital edema may be noted

• More serious and even permanent eye injuries (eg, corneal abrasions, foreign bodies) can be caused by tear gas particles, other foreign particles, or the blast injury itself.

• Patients may complain of blindness because of the intense tearing and blepharospasm, but patients who can physically open their eyes have no significant change in visual acuity

Other manifestations are as follows:

• Nausea, vomiting, and diarrhea may occur
• Rhinorrhea, sneezing, and hypersalivation often occur as agents come in contact with sensitive mucous membranes.
• Patients also may report cough, chest tightness, dyspnea, and wheezing, but pulmonary function test results typically are not changed
• Exacerbation of a chronic pulmonary condition, such as asthma or chronic obstructive pulmonary disease, may occur
• Exercise exacerbates symptoms
• Psychological effects (eg, anxiety) also provoke increased response
• Tolerance to CS symptoms can develop with chronic low-grade exposures

Skin contact with a riot control agent results in erythema, tingling, and burning. Blistering may also occur after exposure to higher concentrations. Skin involvement tends to be more severe with CN, and may include irritation, bulla formation, and subcutaneous edema.[20] Dermal manifestations develop within minutes of exposure and last up to 1 hour after termination of exposure.

More severe skin injuries can occur in hot, humid environments with heavily sweating or wet patients or with prolonged or close-range exposures. First- or second-degree burns and delayed allergic contact dermatitis may be seen, especially with exposure to CN and CS.

Police and bystanders may be unintended victims of riot control agents. In a study by Watson and Rycroft, six police officers and one bystander developed contact dermatitis, leukoderma, exacerbation of seborrheic dermatitis, and aggravation of rosacea following exposure to CS.[21]

Serious effects, including death, have been reported. CN has accounted for five deaths due to pulmonary injury and/or asphyxia. A case report involved a 4-week-old infant who accidentally received a discharge of pepper spray (OC), which immediately led to respiratory distress, followed by apnea. The infant was resuscitated and ultimately recovered after much intensive care, including extracorporeal membrane oxygenation (ECMO).[22]

Severe effects (eg, pulmonary edema, chemical pneumonitis) usually occur only with prolonged exposure in an enclosed space. Such exposures can damage the respiratory tree. Upper airway mucosal necrosis and pulmonary edema have been reported.

Some studies have suggested that CS may be converted into cyanide in the peripheral tissues. However, the risk of cyanide toxicity seems to be minimal.[23]

There are limited data on the effects of tear gas during pregnancy, but the risk of fetal toxicity is thought to be minimal. There are no reports of tear gas in breast milk following exposure.[24]

Unintentional oral ingestions can occur, specifically in children. Abdominal cramps and diarrhea are common, but the ultimate course usually is uneventful. The lethal dose in one half of the exposed population (LD50) in animals is 200 mg/kg, which is an amount unlikely to be ingested.

Other gases irritating to the mucous membranes and respiratory system (eg, lewisite, phosgene oxime) may be confused with pulmonary irritants. Features that help with distinguishing these include the following:

• A history of gas exposure in use by law enforcement or military training suggests tear gas use.
• Eye symptoms are especially prominent in pulmonary irritant use.
• Significant respiratory findings are rare but may occur in high concentrations in an enclosed space, especially in pediatric and geriatric victims with preexisting comorbidities.

In a study of 2257 adults reporting exposure to tear gas during protests in Portland, Oregon in 2020, almost all respondents reported immediate health effects. In addition, 80.8% of participants reported delayed physical health issues 1 to 2 days after exposure. The most commonly reported delayed issues were related to lungs and/or chest and menstrual changes (eg, increased menstrual cramping, unusual spotting, increased bleeding), followed by gastrointestinal (eg, diarrhea, cramping), head, and eye issues.[15]  

Long-term effects, usually as a result of prolonged exposure, can include ophthalmological complications such as cataracts, glaucoma, and blindness, as well as pulmonary deterioration leading to respiratory failure.[7]

Physical findings in patients exposed to riot control irritants are as follows[2, 4, 5, 6, 7, 10] :

• Respiratory: Cough, chest tightness, sensation of suffocation, shortness of breath, increased respiratory rate, wheezing, rales, decrease in oxygen saturation, cyanosis, pulmonary edema, and respiratory arrest in young infants

• Cardiovascular: Tachycardia, hypertension (these are believed to be most likely a psychological response to the situations in which tear gases typically are used)

• Skin and mucous membranes: Erythema, pain, blistering of the skin, first- (possibly second-) degree burns of the skin

• Eyes: Conjunctival injection, redness, and irritation; corneal burns; pain; tearing; blurry vision; periorbital edema; lacrimation

• Oropharynx: Oral burns and irritation, sore throat, hoarseness, dysphagia, and hypersalivation

• Nasal: Rhinorrhea, burning, irritation, sneezing

Severity of manifestations varies with the age of the victim, comorbid factors, and duration of exposure.

 Short-term complications include the following[2, 4, 7] : 

• Pulmonary edema, bronchospasm, hemoptysis, chemical pneumonitis
• Hepatocellular damage
• Heart failure
• Second-degree burns
• Death

Long-term include the following[2, 4, 7] :

• Cataracts
• Glaucoma
• Blindness (note: hyphema, uveitis, necrotizing keratitis, secondary glaucoma, and cataracts have been reported, but since the exposure to the riot control agent was related to an explosive device, it is unclear whether these more serious complications were due to the agent or the delivery system. ^[2]
• Respiratory failure

Clinicians should don appropriate personal protective equipment (PPE) before triaging and assessing patients assumed to be contaminated with a riot control agent (RCA). Victims who have RCAs on clothes and exposed body parts require decontamination as a first step. 

Diagnosis of pulmonary irritant exposure is based on clinical findings. However, the following may provide useful information in some cases:

• Arterial blood gas and capnography measurements allow for confirmation of adequate ventilation
• A chest radiograph may be indicated in patients with significant respiratory complaints, especially if the offending agent is not known
• Perform a slit lamp examination with fluorescein on patients with significant eye complaints, especially if the patient experienced a close-range exposure
• An electrocardiogram (ECG) is indicated for patients with persistent respiratory complaints and/or chest discomfort, in the appropriate clinical setting

Laboratory studies are not indicated unless an exposure to a RCA was prolonged or the RCA-exposure diagnosis is in doubt.

Consider the following:

• Complete blood cell (CBC) count
• Serum chemistry profile
• Liver function studies
• Lactate level
• Toxicology screen

Consider the following:

• ABG/capnography: Baseline for those with prolonged and severe respiratory symptoms
• ECG: Particularly for the elderly patients or those with significant comorbidities

Consider the following:

• Decontamination of skin and eyes
• Basic and advanced airway techiques for evere respiratory compromise
• Slit-lamp examination

No antidote to riot control agents (RCAs) exists, so treatment is symptomatic and supportive. Treatment measures for RCA exposure include the following:

• Remove the patient from the source. Since aerosolized tear gas is heavier than air, HAZMAT rescuers should get the incapacitated victim off the ground as expeditiously as possible. ^[2]
• Remove clothes if clothing has been contaminated by RCAs.
• Ocular exposures initially require thorough eye decontamination. Flushing the eyes with water or saline for 10–20 min is the most often recommended for initial decontamination.
• Dermal exposures require simple soap and water decontamination for the most part. ^[2]  Potential decontamination agents have been studied, including aluminium hydroxide/magnesium hydroxide antacid, 2% lidocaine gel, milk, and baby shampoo, but none showed better efficacy than water. ^{[2, 25]}

Most people exposed to irritants do not seek medical care, and effects are self-limited. When persons seek care, first withdraw them from exposure. Responders should wear appropriate personal protective equipment (PPE). Decontamination should then proceed as follows:

• Remove contaminated external clothing.
• Acceptable decontaminating solutions are water or soap and water.
• Do not use hypochlorite; this relatively caustic solution may worsen the condition of skin injuries already suffered from exposure to irritants.
• Thoroughly flush eyes with water or saline; Patents may require a topical anesthetic to enable them to open their eyelids sufficiently for effective irrigation. Contact lenses should be removed before flushing.
• Devote specific attention to very young, infirm, and elderly patients, since their responses to these agents may be significant.
• Bronchodilator therapy may be used for those with postexposure bronchospasm.
• Warn patients that the pain worsens during decontamination.
• In patients with severe respiratory compromise, aggressive airway control, including invasive measures, may be required.

ED personnel should don proper personal protection equipment (PPE) to minimize accidental exposure. Secondary exposure during endotracheal intubation, extubation, and nasogastric tube insertion has been reported.[16]  A site should be established for the disrobing and general decontamination (see Prehospital Care) of the patients.

Initiate or continue care in the emergency department (ED) as follows:

• Flush the eyes of patients with eye complaints with normal saline or water to remove any particulate matter before fluorescein slit lamp examination for corneal abrasion.
• Treat more severe injuries, which occur in fewer than 1% of patients, in the usual fashion.
• Corneal abrasions can be treated with local antibiotics, oral analgesics, and close follow-up care.
• The rare eye foreign body may merit ophthalmologic consultation.
• Treat burns based on the severity and location of injury.
• Treat bronchospasm with bronchodilators.
• Topical/parenteral analgesia as needed.

Most patients with irritant exposure can safely be discharged from the ED, as the few reported dangerous effects occur rapidly.The rare patient with significant respiratory damage may require oxygen supplementation, aggressive bronchodilator therapy (if bronchospasm is present), and admission to the hospital, possibly a critical care unit.

Characteristically, hospital admission for extended medical care is not indicated.  Should hospitalization be required, consider alternative diagnoses.

Victims should be made aware that initial symptoms may be minimal or that there may even be a latent period.  Should any clinical deterioration occur the patient should be re-evaluated.

Medical follow-up is indicated for a minority of patients, including those with any of the following:

• Very young age
• Advanced age
• Comorbidities
• Significant dermal injuries
• Prolonged respiratory difficulties

Consultations with one or more of the following may be indicated:

• Ophthalmologist
• Burn specialist
• Mental health specialist
• Pulmonologist

Consider the following in long-term monitoring:

• Opthalmologist consultation with possible significant damage to the eyes
• Pulmonologist consultation should there be any long-term respiratory complications
• Mental health
• Burn care

In general, only decontamination with water is necessary when a patient's skin has been grossly exposed to riot control agents. Bronchodilators, analgesics, and pulmonary support may be needed, depending upon the severity of injury.

Diphoterine and vegetable oil  have chelating and amphoteric properties that show some promise in managing dermal exposures, but more studies are required to prove efficacy.[26]

Antibiotics may be reserved for dermal and pulmonary complications.  An antiobitic ointment may be helpful with ocular involvment.

Analgesics for pain, preferably non-steroidal agents;

Class Summary

Use only for patients with evidence of significant bronchospasm after exposure.

Albuterol 0.5% (Proventil, Ventolin)

Beta-agonist for bronchospasm refractory to epinephrine. Relaxes bronchial smooth muscle by action on beta 2-receptors with little effect on cardiac muscle contractility.

Class Summary

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions, may exist as well.

Ibuprofen (Motrin, Ibuprin)

Acts as an analgesic, antipyretic, and anti-inflammatory agent.

Class Summary

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained trauma or injuries.

Oxycodone/acetaminophen (Percocet, Roxicet, Roxilox)

Drug combination indicated for relief of moderate to severe pain.

Class Summary

Therapy must cover all likely pathogens in the context of the clinical setting.

Gentamicin 0.3 % solution (Genoptic, Ocu-Mycin)

Indicated for corneal abrasions. Aminoglycoside antibiotic used for gram-negative bacterial coverage.

Erythromycin ophthalmic (E-Mycin)

Indicated for corneal abrasions and infections caused by susceptible strains of microorganisms and for prevention of corneal and conjunctival infections.