The Biological Mechanisms of Tear Gas on the Human Body - New Jersey Anesthesia Professionals
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The Biological Mechanisms of Tear Gas on the Human Body

Tear gas, formally referred to as a lachrymator agent, produces a wide spectrum of acute and chronic health effects. The immediate effects of tear gas exposure at concentrations typically used by law enforcement include irritation to the eyes, nose, mouth, skin, and respiratory tract.1 Effects on the skin include itching, stinging, redness, and potential blistering and allergic responses.2 Direct exposure to the eye results in lacrimation, blepharospasm, itching, and burning.3 If inhaled, tear gas leads to immediate coughing, choking, salivation, and tightness in the chest.

Tear gas agents bind to a single target, TRPA1, an ion channel located on the plasma membrane of many cells. TRPA1 plays a role in the sensation of environmental irritants which give rise to modalities such as pain, cold, and itch, as well as protective processes such as airway resistance, coughing, and tearing. Initial neurobiological studies revealed TRPA1 as the target of mustard oil, the electrophilic, pain-inducing substance in mustard, wasabi, and horseradish.4 In additional experiments, TRPA1 was shown to respond to other electrophiles, such as the naturally occurring isothiocyanates and similar compounds in onions and garlic.4

The discovery of TRPA1 as the receptor for electrophilic irritants inspired another study – published in 2008 – that identified TRPA1 as the principal target of tear gas. In this study, Bessac et al used calcium imaging (a technique capable of monitoring the electrical activity of neurons in cell culture or in living tissue) to show that tear gas agents lead to the activation of membrane currents in neurons that display sensitivity to mustard oil.5 Furthermore, genetic ablation or pharmacological inhibition of TRPA1 in mice dramatically reduced tear-gas induced behaviors after exposure to the eyes and skin.5 Therefore, it is presumed that the TRPA1 receptor mediates the biological mechanisms of tear gas on the human body.

While there is extensive research on the acute effects of tear gas, there is a paucity of epidemiological studies on tear gas-exposed civilian populations and high risk groups. This is primarily due to the real-world conditions in which tear gas is used, which obscure critical factors such as concentration and duration of exposure and make it difficult to conduct effective and replicable studies. Many studies indicate that the effects of tear gas resolve within minutes after exposure. However, evidence for this conclusion comes from limited studies which only include healthy, male volunteers – without consideration of effects on other populations.3 Individuals with asthma or reactive respiratory disease, for example, could be at risk for more serious effects. One report on exposure at a nightclub suggests that patients with asthma displayed no greater sensitivity to tear gas than healthy individuals.6 In another study on exposure in South Korea, physicians indicated that patients with asthma and chronic obstructive pulmonary disease experienced deterioration of lung function.7 Furthermore, a case study reported that a 40-year-old man experienced acute myocardial infarction after exposure to pepper spray, which suggests that such agents could act as a triggering factor.8 

In summary, tear gas exposure results in a variety of health effects, such as irritation to the eyes, nose, mouth, and respiratory tract, which are mediated by TRPA1. Yet, the effects of tear gas agents on civilian and high risk populations remain unclear on the basis of available data and additional research may be necessary.


  1. Blain, P.G. 2003. Tear gases and irritant incapacitants. 1‐Chloroacetophenone, 2‐chlorobenzylidene malononitrile and dibenz[b,f]‐1,4‐oxazepine. Toxicol. Rev. 22: 103–110.
  2. Holland, P. & White R.G.. 1972. The cutaneous reactions produced by o‐chlorobenzylidenemalononitrile and ω‐chloroacetopheneone when applied directly to the skin of human subjects. Br. J. Dermatol. 86: 150–154.
  3. Beswick, F.W. , Holland P. & Kemp K.H.. 1972. Acute effects of exposure to orthochlorobenzylidene malononitrile (CS) and the development of tolerance. Br. J. Ind. Med. 29: 298–306.
  4. Jordt, S.E. , Bautista D.M., Chuang H.H., et al 2004. Mustard oils and cannabinoids excite sensory nerve fibres through the TRP channel ANKTM1. Nature 427: 260–265.
  5. Bessac, B.F. , Sivula M., von Hehn C.A., et al 2008. Transient receptor potential ankyrin 1 antagonists block the noxious effects of toxic industrial isocyanates and tear gases. FASEB J. 23: 1102–1114.
  6. Breakell, A. & Bodiwala G.G.. 1998. CS gas exposure in a crowded night club: the consequences for an accident and emergency department. J. Accid. Emerg. Med. 15: 56–57.
  7. Hu, H. , Fine J., Epstein P., et al 1989. Tear gas—harassing agent or toxic chemical weapon? JAMA 262: 660–663.
  8. Cil, H. , Atilgan Z.A., Islamoglu Y., et al 2012. Is the pepper spray a triggering factor in myocardial infarction? A case report. Eur. Rev. Med. Pharmacol. Sci. 16(Suppl. 1): 73–74.