Ophthalmology, Toxicology

Managing the Effects of Riot Control Agents

As protests have turned violent in response to the death of George Floyd, riot control agents have gained national attention. Exposures are now commonplace, and it's important for emergency physicians to understand the toxicity, clinical manifestations, and treatment of these chemicals. 

Riot control agents – also known as lacrimators, irritants, tear gas, and human repellents – are substances intended to irritate the mouth, eyes, skin, and respiratory tract. With a rapid onset, brief duration of irritation, and a wide therapeutic index, these chemicals are designed to render an individual or group of people temporarily disabled. 

The most common chemical incapacitants, 2-chloroacetophenone (CN; mace), o-chlorobenzylidene malonitrile (CS), and oleoresin capsicum (OC; pepper spray), have widely been used for personal self-defense as well as by law enforcement agencies for crowd control. These chemicals are solid at room temperature and may be dispersed as aerosols, foams, liquid sprays, or powder. Recently, in response to the death of George Floyd, these agents have gained national attention as exposures are now commonplace and the use of social media has spread true and false information about these substances. In this review, we outline the toxicity, clinical manifestations, and treatment of these commonly encountered agents. 

Mechanism of Injury
Mechanistically, both CN and CS are SN2-type alkylating agents which react with thiol and sulfhydryl-containing compounds, likely producing their toxicity by inhibition of crucial metabolic enzymes.1,2 Capsaicin, a naturally occurring lacrimator found in the oil of pepper plants (Capsicum anuum), is the active ingredient in OC. Capsaicin binds to an important target involved in the pathogenesis of OC known as transient receptor potential vanilloid channels (TRPV1) found within respiratory sensory fibers.3 OC exposure causes massive release of substance P, a pain neuropeptide, resulting in neurogenic inflammation and painful sensation following exposure.4 Interestingly, CS causes bradykinin release, which may be particularly relevant in the COVID-19 era and also in patients who are on ACE-inhibitors. The mechanism of injury of other riot control agents are not well elucidated.

Riot control agents are designed to immediately cause symptoms in multiple organ systems, most significantly involving the eyes and respiratory tract. All riot control agents produce a burning sensation and blepharospasm of the eyes, which renders a person functionally "blind" despite normal visual acuity. Further ocular exposure is typified by conjunctival injection, lacrimation, and photophobia.5-9 Firing of an agent at close range has caused permanent eye damage and blindness, either by blast force or possibly solid particles causing tissue damage in the cornea or conjunctiva.10,11 Inhalation of these chemicals causes increased secretions, dyspnea, cough, sneezing, and chest tightness. Subsequent nausea, vomiting, and diarrhea can result from swallowing of contaminated secretions. Outside of the ocular and respiratory systems, dermal manifestations follow a dose-dependent response and include tingling, burning, redness, and pruritus; skin symptoms are more common in CS exposures, while more threatening presentations including vesicle formation and second-degree burns are more representative of the more toxic CN.5-9 Transient tachycardia and hypertension are likely a symptom of pain and anxiety rather than a pharmacological mechanism.1

Less commonly, riot control agents including dibenzoxazepine (CR), chloropicrin (PS), and 10-chloro-5,10-dihydrodiphenarsazine (DM) are used. CR is similar to CS and CN but causes greater skin irritation. Skin exposed individuals can experience burning, redness, and vesicle formation dependent on dosage of toxic exposure. Exposed individuals typically disperse quickly, however deaths have been reported following exposure in closed spaces where egress is not possible.1,9,12 PS is another lacrimator that has caused human toxicity.13 DM causes lacrimation and vomiting. Symptoms are delayed, so dispersal of crowds takes longer. This leads to increased exposure and absorption. Observed symptoms are similar to other lacrimators however headache, malaise, nausea and vomiting may occur for an extended time.9,12

Symptom resolution typically occurs in less than 30 minutes; however, respiratory impairment, secretions, and cough may dissipate more slowly.4 Removal from the exposure and decontamination are the basis of treatment for riot control agents. Because tear gas particles are heavier than air, it is important to extract persons who may be found lying on the ground and allow the person to stand in a well ventilated or open area. 

There are no antidotes for any of these agents; thus, all treatment is aimed at symptomatic management. Clothing and other layers should be removed and sealed in airtight bags; care must be taken to avoid secondary exposure to police officers, nearby persons, and healthcare workers as particles may dry on skin and clothing.8 Mild soap and water can be used to wash any of these control agents off the skin. Transport of persons exposed to CS necessitates the police vehicle or ambulance to drive with the windows down to disperse remaining particles on skin. Ophthalmic treatment is based on copious irrigation with saline or normal water for 10-20 minutes, using topical anesthetics when needed. Consider an ophthalmology consult for fluorescein staining and a slit-lamp exam if symptoms persist post-irrigation or if a patient states they were exposed to an agent from a close range, as solid particles may mechanically disrupt ocular tissues. 

While skin exposures have been treated with alkaline solutions, baby shampoo, oil, milk, and lidocaine gel, the relative ubiquity of water combined with its similar efficacy make it the preferred treatment modality.16-18 Topical ophthalmic anesthetics, bronchodilators, and corticosteroids may be used in the severely affected.1 Although there are case reports of blindness, pulmonary disease, and death, the majority of persons exposed to riot control agents will experience minor symptoms that will resolve within 30-60 minutes of decontamination.19


  • CN was originally developed for use in WWI but has fallen out of favor due to toxicity. It is now sold commercially under the brand name Mace.
  • CS and OC are the most common riot control agents used in the United States.
  • U.S. military studies report laboratory evidence that CS can be metabolized to cyanide, suggesting that a patient exposed to high amounts of CS may also need to be treated for cyanide poisoning.9 
  • Studies have shown that CS exposure has a positive association with acute respiratory illnesses within a week of exposure.20
  • People who regularly eat hot peppers have less painful symptoms when exposed to OC.9 


  1. Medical Management of Chemical Casualties Handbook. 4th ed. Proving Ground, MD: US Army Medical Research Institute of Chemical Defense, Chemical Casualty Care Division; 2007. http://www.globalsecurity.org/wmd/library/policy/army/other/mmcc-hbk_4th-ed.pdf.
  2. Cucinell SA, Swentzel KC, Biskup R, et al. Biochemical interactions and metabolic fate of riot control agents. Fed Proc. 1971;30(1):8691.
  3. Caterina MJ, et al. The capsaicin receptor: a heat-activated ion channel in the pain pathway. Nature. 1997;389:816–824. [PubMed: 9349813]
  4. Schep LJ, Slaughter RJ, McBride DI. Riot control agents: the tear gases CN, CS and OC-a medical review. J R Army Med Corps. 2015;161(2):9499.
  5. Blain PG. Tear gases and irritant incapacitants. 1-chloroacetophenone, 2-chlorobenzylidene malononitrile and dibenz[b,f]-1,4-oxazepine. Toxicol Rev. 2003;22(2):103110.
  6. Olajos EJ, Salem H. Riot control agents: pharmacology, toxicology, biochemistry and chemistry. J Appl Toxicol. 2001;21(5):355391.
  7. Ballantyne B. Medical management of the traumatic consequences of civil unrest incidents: causation, clinical approaches, needs and advanced planning criteria. Toxicol Rev. 2006;25(3):155197.
  8. Blaho K, Winbery S. "Safety" of chemical batons. Lancet. 1998;352(9140):1633.
  9. Sidell FR. Riot control agents. In: Sidell FR, et al, eds. Medical Aspects of Chemical and Biological Warfare. Washington, DC: Office of the Surgeon General; 1997:307–324.
  10. Holopainen JM, Moilanen JA, Hack T, Tervo TM. Toxic carriers in pepper sprays may cause corneal erosion. Toxicol Appl Pharmacol. 2003;186(3):155162.
  11. Brown L, Takeuchi D, Challoner K. Corneal abrasions associated with pepper spray exposure. Am J Emerg Med. 2000;18(3):271272.
  12. Marrs TC, et al. Chemical warfare agents. Toxicology and Treatment. Chichester, UK: John Wiley & Sons, 1996.
  13. TeSlaa G, et al. Chloropicrin toxicity involving animal and human exposure. Vet Hum Toxicol. 1986;28:323–324. [PubMed: 3750814]
  14. Hay A, et al. Skin injuries caused by new riot control agent used against civilians on the West Bank. Med Confl Surviv. 2006;22:283–291. [PubMed: 17191624]
  15. Brewer NT, et al. Why people believe they were exposed to biological or chemical warfare: a survey of Gulf War veterans. Risk Analysis. 2006;2:337–345.
  16. Herman LM, et al. Treatment of mace dermatitis with topical antacid suspension. Am J Emerg Med. 1998;16:613–614. [PubMed: 9786549]
  17. Jones LA, et al. Household treatment for “chile burns” of the hands. J Toxicol Clin Toxicol. 1987;25:483–491.
  18. Suchard JR. Treatment of capsaicin (Mace?) dermatitis. Am J Emerg Med. 1999;17:210–211. 
  19. Haar RJ, Iacopino V, Ranadive N, Weiser SD, Dandu M. Health impacts of chemical irritants used for crowd control: a systematic review of the injuries and deaths caused by tear gas and pepper spray. BMC Public Health. 2017;17(1):831. Published 2017 Oct 19. doi:10.1186/s12889-017-4814-6
  20. Hout JJ, White DW, Artino AR, Knapik JJ. O-chlorobenzylidene malononitrile (CS riot control agent) associated acute respiratory illnesses in a U.S. Army Basic Combat Training cohort. Mil Med. 2014;179(7):793798.

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