Tear gas
Tear gas, formally known as riot control agents, encompasses chemical compounds such as 2-chlorobenzylidenemalononitrile (CS gas) and chloroacetophenone (CN), dispersed as aerosols or particulates to irritate the eyes, skin, and respiratory tract, inducing acute symptoms including excessive tearing, eyelid closure, coughing, throat burning, and disorientation that temporarily incapacitate targets without causing permanent structural damage in most exposures.[1][2][3][4] These agents function primarily through sensory irritation via mechanisms like alkylation of thiol groups in proteins, triggering inflammatory responses in mucous membranes.[5][3] Developed amid World War I chemical warfare research, tear gas prototypes were first deployed by French forces in 1914 to flush combatants from trenches, evolving from earlier irritant experiments into standardized munitions by the 1920s for police use in suppressing civil unrest, such as labor strikes and protests.[6][7] Post-war adoption by law enforcement agencies marked a shift from military to domestic applications, with CS gas supplanting CN due to its lower toxicity profile in open-air dispersal.[6][3] Primarily employed by security forces for non-lethal crowd control, tear gas munitions—ranging from grenades to sprays—aim to disperse gatherings by overwhelming sensory systems, though efficacy varies with environmental factors like wind and confinement, often failing to predictably de-escalate volatile situations.[8][3] Despite classification as humane alternatives to lethal force, controversies persist over health risks, with empirical data revealing potential for severe acute effects like pulmonary edema, corneal abrasions, and dermal necrosis in high-dose or prolonged exposures, alongside understudied long-term sequelae such as chronic respiratory impairment, particularly among asthmatics or in vulnerable populations; peer-reviewed analyses underscore that while fatalities are rare, the agents' safety margins erode in real-world, uncontrolled deployments.[3][9][10]Chemical Composition and Delivery
Primary Agents and Formulations
The primary chemical agents employed in tear gas, classified as riot control agents, include chloroacetophenone (CN), 2-chlorobenzalmalononitrile (CS), and dibenzoxazepine (CR), with CN and CS being the most widely used historically and currently.[1][3] These lacrimatory irritants target sensory nerves to induce temporary incapacitation through eye, skin, and respiratory irritation, rather than causing permanent tissue destruction.[11] Chloroacetophenone (CN), a ketone with the formula C₈H₇ClO, was first synthesized in 1871 and served as the standard tear gas agent during World War I, deployed by French and German forces starting in 1914.[8][6] CN formulations typically involve dissolution in solvents such as ethanol, ether, or propylene glycol at concentrations of 0.5% to 5%, often combined with dispersing agents like chloroacetone for aerosolization in sprays or grenades.[12][13] This agent produces a pungent odor and oily residue, with formulations designed for pyrotechnic dispersal via heat from exploding canisters to generate irritant particles of 5-10 micrometers in size.[14] 2-Chlorobenzalmalononitrile (CS), a nitrile compound with the formula C₁₀H₅ClN₂, was developed in 1928 by British chemists and introduced for riot control in the 1950s, supplanting CN due to lower toxicity and faster dissipation.[3][14] CS is a white crystalline solid at room temperature, formulated as micronized powders (particle size 5-16 micrometers) for thermal dispersion in grenades or as 1% solutions in volatile solvents like methyl isobutyl ketone or dichloromethane for personal sprays, with higher 5% concentrations used in some non-U.S. applications.[14][12] These formulations rely on propellants such as nitrogen or pyrotechnic mixtures to aerosolize the agent, ensuring rapid evaporation and reduced residue compared to CN.[14] Dibenzoxazepine (CR), synthesized in the 1960s, is a more potent sensory irritant with the formula C₁₃H₉NO, used in specialized formulations for its prolonged effects and lower effective dose, often dispersed as aerosols in solvents like propylene glycol.[11][3] Less common than CS or CN due to higher production costs and potential for greater skin penetration, CR formulations emphasize fine particle generation for inhalation exposure.[11] Other agents, such as chloropicrin (PS), have been used historically as fumigants with lacrimatory properties but are rarely primary in modern tear gas due to toxicity concerns.[1] Formulations across these agents prioritize stability, dispersibility, and minimization of environmental persistence, with empirical testing confirming efficacy at concentrations below lethal thresholds.[14][3]Deployment Methods and Technologies
Tear gas agents, such as CS, are disseminated primarily as aerosols via pyrotechnic, expulsion, liquid stream, or fog methods to achieve rapid incapacitation in crowd control scenarios.[15] Pyrotechnic delivery involves igniting a mixture that burns for 15 seconds to 2.5 minutes, using intense heat to vaporize the solid agent into a persistent submicron cloud, allowing for launchable grenades or projectiles that provide accurate placement and psychological deterrence through visible smoke.[15] This method is favored for outdoor use due to its range and duration but carries risks of fire ignition and uncontrollability once deployed.[15] [16] Expulsion-based systems employ a small explosive charge or mechanical force to burst the canister and eject micropulverized agent, enabling immediate area saturation without fire hazards, suitable for indoor or close-quarters applications.[15] These non-pyrotechnic munitions, such as flameless expulsion canisters or multi-chamber separating types like the Triple-Chaser, disperse agent over 10-20 meters and reduce throwable risks by design.[15] [17] Barrier-penetrating variants, classified by penetration capability (e.g., Type III for dual-layer plasterboard), use kinetic, pyrotechnic, or explosive dissemination when fired from 37-mm riot guns or 12-gauge shotguns, with tested ranges up to 50 meters.[16] Liquid dissemination propels a solvent-dissolved agent as a targeted stream or fog using compressed gas, offering portability for individual or small-group engagement but limited by wind drift and shorter effective range.[15] Fog dissemination, conversely, generates clouds via hot exhaust vaporizing liquid agent in portable devices, providing economical coverage at lower cost per gram compared to pyrotechnics, though susceptible to mechanical failure and operator exposure.[15] Projectile technologies dominate large-scale deployment, with 37-mm, 38-mm, or 40-mm munitions launched from single-shot or multi-barrel riot guns, achieving velocities around 61 m/s and ranges permitting high-angle fire for overhead dispersal.[16] [18] Examples include 40-mm cartridges weighing approximately 230 grams, designed for anti-riot guns to project burning or bursting payloads.[19] Hand-thrown grenades complement these for immediate, low-tech use, while emerging systems explore vehicle-mounted or aerial delivery, though traditional ground-based launchers remain standard for precision and safety protocols prohibiting direct individual targeting.[20][16]Historical Development
Early Invention and Military Origins
The employment of lacrimatory agents, precursors to modern tear gas, emerged as a tactical innovation during World War I, initially aimed at incapacitating enemy forces through eye and respiratory irritation rather than lethality. French forces pioneered their use on August 22, 1914, firing grenade projectiles containing ethyl iodoacetate into German positions near the border, marking the first documented deployment of such irritants in modern warfare.[21] This approach sought to flush troops from cover without the ethical or logistical burdens of more lethal munitions, though the agents' volatility and limited dispersal range constrained their immediate impact.[22] German military chemists, responding to French initiatives, developed and deployed xylyl bromide—a halogenated alkylbenzene compound known for inducing severe lacrimation and mucosal inflammation—as an artillery-delivered agent. The first large-scale attempt occurred on January 31, 1915, during the Battle of Bolimów against Russian lines, where approximately 18,000 shells filled with liquid xylyl bromide were fired; however, subzero temperatures caused the chemical to freeze inside the shells, rendering the attack largely ineffective and resulting in few casualties.[23][24] Subsequent refinements by both sides escalated production, with xylyl bromide and similar bromoacetone derivatives integrated into gas cloud and projectile systems to exploit trench warfare stalemates.[25] These agents, synthesized from industrial chemicals available pre-war, represented an early fusion of organic chemistry and battlefield application, driven by imperatives for non-persistent incapacitants amid the era's gas mask countermeasures.[26] The invention of these early lacrimators stemmed from 19th-century chemical research into alkyl halides and their irritant properties, but their weaponization was a direct product of World War I's arms race, with German firms like those affiliated with Fritz Haber accelerating development under military contracts. By 1915, the term "lachrymatory gas" entered tactical lexicon, distinguishing these from asphyxiants like chlorine, though boundary blurring occurred as formulations grew more toxic. Allied and Central Powers alike scaled production, with millions of rounds deployed by war's end, laying foundational precedents for irritant-based crowd and combat control despite the 1925 Geneva Protocol's later prohibitions on chemical warfare.[27]Transition to Civil Applications
Following World War I, tear gas agents, initially developed for military harassment, were repurposed for civilian crowd control due to their capacity to incapacitate without widespread lethality, appealing to law enforcement seeking alternatives to firearms amid labor unrest and urban riots. In the United States, the U.S. Army's deployment of chloroacetophenone (CN) gas during the 1921 Battle of Blair Mountain—where approximately 10,000 striking coal miners clashed with authorities in West Virginia—demonstrated its effectiveness in dispersing large groups, marking one of the earliest large-scale applications against civilians and influencing subsequent police adoption.[28][29] Private chemical firms, leveraging surplus wartime production, marketed CN-based munitions to police departments as a "humane" tool for turning orderly crowds into disorganized mobs, with demonstrations such as a 1921 Philadelphia police trial exposing officers to the agent to prove its controllability.[6][30] By the mid-1920s, U.S. law enforcement agencies began equipping with grenade and projector delivery systems, transitioning from ad hoc military loans to standardized civil inventories, as evidenced by sales records from manufacturers like the Lake Erie Chemical Company.[29] This shift was driven by post-war economic pressures and rising domestic protests, with CN supplanting earlier ethyl iodoacetate formulations for its stability and lower toxicity profile in open-air dispersal.[8] In Europe, the transition paralleled U.S. developments; French police had experimented with rudimentary chemical hand bombs as early as 1912 against organized crime, but systematic adoption accelerated post-1918 with interwar riot control needs, including xylyl bromide variants tested in colonial policing.[28] By the 1930s, tear gas had become a fixture in Western police arsenals, though its use against the 1932 U.S. Bonus Army veterans—dispersed by Army troops under presidential order—highlighted lingering military-civil overlaps and debates over proportionality.[31] Adoption was not uniform; some jurisdictions resisted due to concerns over unintended indoor exposures, but empirical success in quelling strikes without mass casualties solidified its role, paving the way for later agents like CS in the 1950s.[32][33]Major International Restrictions and Events
The Geneva Protocol, formally the Protocol for the Prohibition of the Use in War of Asphyxiating, Poisonous or Other Gases, and of Bacteriological Methods of Warfare, adopted on June 17, 1925, and entering into force on February 8, 1928, marked the first major international restriction on tear gas by prohibiting its use as a method of warfare following widespread deployment of irritant gases during World War I, where German forces fired approximately 18,000 xylyl bromide shells at Bolimów on January 31, 1915, and French troops used ethyl iodoacetate grenades against trenches.[34][23] By 2023, 146 states were parties to the protocol, though some reservations allowed retaliatory use. The Chemical Weapons Convention (CWC), opened for signature on January 13, 1993, and entering into force on April 29, 1997, further codified restrictions by banning the development, production, stockpiling, and use of chemical weapons, while classifying tear gas and other riot control agents (RCAs) as non-prohibited for law enforcement purposes but explicitly forbidding their use as a method of warfare under Article II(7), which defines RCAs as "any chemical which can produce rapidly in humans sensory irritation or disabling physical effects which disappear within a short time following termination of exposure."[35][36] Administered by the Organisation for the Prohibition of Chemical Weapons (OPCW), the treaty has 193 states parties as of 2023, with non-signatories including Egypt, North Korea, and South Sudan facing no such constraints on RCA use in conflict. Customary international humanitarian law reinforces this via Rule 75, prohibiting RCAs in both international and non-international armed conflicts as a warfare method, applicable even to non-CWC states.[37] Significant events underscoring these restrictions include U.S. deployment of tear gas in Vietnam War operations from 1962 onward, such as during the siege of Khe Sanh in 1968, which blurred lines between riot control and warfare, prompting President Nixon's November 25, 1969, renunciation of first-use for RCAs and herbicides in war, influencing CWC negotiations amid debates over their toxicity.[38] More recently, direct-fire misuse during civilian protests has sparked international scrutiny without yielding binding prohibitions on domestic applications; for instance, on November 26, 2019, Chilean police fired a tear gas canister at close range, blinding Fabiola Campillai and injuring over 400 others with eye trauma during Santiago protests, leading to a 2022 conviction for unlawful coercion but only domestic protocol reviews rather than global bans.[39] Similarly, 2022 crackdowns in Iran (over 500 deaths linked to chemical irritants per Amnesty documentation), Peru, and Sri Lanka highlighted lethal risks from indoor or excessive deployment, prompting non-binding calls from human rights groups for trade regulations, though no UN or treaty-level restrictions on police use emerged.[40] These incidents illustrate persistent tensions between permitted riot control and warfare prohibitions, with empirical data showing RCAs cause fatalities in confined spaces via asphyxiation or secondary fires, yet lacking enforcement mechanisms for domestic overreach.[41]Mechanisms of Action
Physiological Pathways
Tear gas agents such as o-chlorobenzylidene malononitrile (CS) and chloroacetophenone (CN) primarily induce sensory irritation through activation of the transient receptor potential ankyrin 1 (TRPA1) cation channel expressed on peripheral nociceptive neurons. These electrophilic compounds covalently modify cysteine residues within TRPA1's N-terminal domain, promoting channel opening, influx of calcium and sodium ions, and subsequent neuronal depolarization. This triggers action potentials along sensory afferents, particularly via the trigeminal nerve for facial and ocular effects, and vagal nerves for respiratory responses, resulting in rapid perception of burning pain and reflexive autonomic reactions.[42][43][44] In the ocular pathway, CS and CN penetrate the corneal epithelium and directly stimulate TRPA1-expressing trigeminal nerve endings in the cornea and conjunctiva, eliciting immediate blepharospasm, lacrimation, and conjunctival hyperemia within seconds of exposure. The irritation signals propagate centrally to induce photophobia and involuntary eye closure, impairing vision; this reflex serves to protect the eyes but incapacitates the individual. Unlike earlier misconceptions of acid hydrolysis (e.g., CN forming hydrochloric acid with moisture), the dominant mechanism is TRPA1-mediated neurogenic inflammation, with release of neuropeptides like substance P amplifying local edema and chemosis.[3][42][44] Respiratory effects follow inhalation of aerosolized particles, where agents deposit on mucosal surfaces of the upper and lower airways, activating TRPA1 on vagal C-fiber afferents and bronchial nociceptors. This leads to initial apnea or hyperpnea due to trigeminal-vagal reflexes, followed by cough, bronchoconstriction, and mucus hypersecretion as sensory nerves release calcitonin gene-related peptide (CGRP) and other proinflammatory mediators. High concentrations can overwhelm these pathways, causing laryngeal spasm or pulmonary edema via sustained inflammation, though effects typically resolve with agent clearance and ventilation.[3][43][42] Dermal exposure involves transcutaneous absorption and TRPA1 activation in cutaneous sensory endings, producing erythema, pruritus, and a burning sensation that peaks within minutes and persists for 15-30 minutes in ventilated conditions. CN tends to cause more pronounced vesication due to its higher reactivity, potentially leading to chemical burns via secondary protein alkylation, whereas CS effects are largely reversible sensory without epidermal necrosis at standard doses. Systemic absorption is minimal due to rapid metabolism, but confined spaces exacerbate pathway overload.[3][42][44]Sensory and Behavioral Impacts
Tear gas agents, primarily CS, induce sensory irritation by activating nociceptors in mucous membranes and skin, leading to intense burning sensations in the eyes, nose, mouth, and respiratory tract within seconds of exposure.[42] This irritation triggers reflexive responses such as profuse lacrimation, blepharospasm, and conjunctival inflammation in the eyes, often resulting in temporary functional blindness despite intact vision.[45] Nasal exposure causes rhinorrhea and a burning sensation, while inhalation provokes coughing, throat constriction, and bronchoconstriction, impairing airflow and exacerbating discomfort.[3] Skin contact elicits erythema and stinging, particularly in moist areas, though effects are generally milder and transient compared to mucosal sites.[46] These sensory disruptions culminate in behavioral incapacitation, as the overwhelming pain and reflexive actions—such as involuntary eye closure and gasping—hinder coordinated movement and sustained activity.[47] Exposed individuals typically exhibit a flight response, dispersing from the affected area to seek fresh air, which aligns with the agents' design to enforce temporary deterrence without permanent harm.[1] In crowd settings, this manifests as disorientation and reduced aggression, with studies noting that even low concentrations (e.g., 0.04% CS in air) suffice to compel evasion behaviors within 20-60 seconds.[48] Empirical observations from controlled exposures confirm that while voluntary tolerance is possible briefly, involuntary reflexes dominate, rendering purposeful resistance impractical.[49]Health Effects
Immediate and Short-Term Reactions
Exposure to tear gas agents, primarily CS (o-chlorobenzylidene malononitrile) and CN (chloroacetophenone), triggers rapid onset of sensory irritation targeting mucous membranes and skin. Immediate ocular effects include intense burning pain, profuse lacrimation, blepharospasm, conjunctival injection, and temporary blurred or impaired vision, often rendering affected individuals incapacitated for combat or flight within seconds of inhalation or contact.[45][50] Respiratory reactions manifest as immediate coughing, throat and nasal burning, increased secretions, bronchoconstriction, and dyspnea, with irregular breathing patterns reported in up to 70% of exposed subjects in controlled studies.[49][45] Skin exposure produces prompt erythema, stinging or burning sensations, and potential vesication, especially with CN, where liquid droplets can cause first- or second-degree chemical burns upon direct impact.[51][50] Systemic short-term responses may include nausea, vomiting, headache, and disorientation, persisting beyond initial dispersal due to residual agent on clothing or in enclosed environments.[49] Gastrointestinal irritation from inadvertent ingestion of contaminated hands leads to salivation and retching in approximately 20-30% of cases during acute exposure.[45] In empirical field data from civil unrest events, such as the 2019-2020 Santiago riots involving CS and oleoresin capsicum, over 80% of surveyed victims reported acute pain, vision impairment, and respiratory distress resolving within 20-60 minutes post-exposure, though higher concentrations extended symptoms to 1-2 hours.[49] Decontamination via flushing with water or saline typically accelerates recovery, but incomplete removal prolongs dermal erythema and pruritus for 1-7 days in sensitive individuals.[51][47] These reactions stem from the agents' irritant properties rather than toxicity at standard dispersal levels, with no peer-reviewed evidence of immediate lethality in healthy adults under open-air conditions.[42]Long-Term and Vulnerable Population Risks
Repeated or prolonged exposure to tear gas agents, such as CS gas, has been associated with chronic respiratory conditions including bronchitis, persistent coughing, wheezing, and dyspnea in some individuals. A study of Turkish military personnel exposed to CS gas during training found that exposed subjects exhibited a higher risk for chronic bronchitis compared to unexposed controls, with symptoms persisting beyond acute phases. Similarly, case reports have documented respiratory symptoms lasting up to two years following short-term exposure. However, comprehensive long-term epidemiological data remains limited, with many conclusions on safety derived from animal studies or acute human exposures rather than longitudinal human cohorts.[52][53][54] Vulnerable populations, including children, pregnant individuals, the elderly, and those with pre-existing respiratory conditions like asthma, face heightened risks from tear gas exposure due to physiological differences and reduced physiological reserves. In children and infants, exposure can lead to severe respiratory distress, exacerbated by smaller airways and immature detoxification mechanisms; a 1972 case report described a 4-month-old infant developing chemical pneumonitis after indirect exposure. Epidemiological data from Chile's 2019 social unrest indicated increased respiratory emergencies, particularly bronchial diseases, among infants and older adults following massive tear gas deployment.[55][56] For pregnant women, limited evidence suggests potential adverse reproductive outcomes, including associations with miscarriage in exposed populations in Bahrain, Palestine, and Chile, though causality remains unestablished due to confounding factors like concurrent violence. Individuals with asthma or hypertension may experience disproportionate effects, challenging earlier assertions of minimal impact; studies supporting safety claims often rely on low-dose or non-representative exposures. Elderly populations show elevated rates of bronchial exacerbations post-exposure, linked to age-related declines in lung function. Overall, while acute effects predominate in most cases, the scarcity of rigorous, population-specific long-term studies underscores uncertainties in risk assessment for these groups.[57][54][56]Empirical Evidence from Studies
A systematic review of injuries from tear gas and other chemical irritants in crowd control analyzed 31 studies involving 5131 exposed individuals, documenting 9261 total injuries, of which 8.7% were severe (requiring professional medical management, often ocular or respiratory), 17% moderate, and 74.3% minor.[9] Severe injuries were disproportionately ocular (153 cases of corneal abrasion or laceration) and respiratory (e.g., chemical pneumonitis), with tear gas implicated in 58% of severe cases across the dataset.[9] The review noted two fatalities directly attributed to tear gas: one from asphyxiation in a confined space and another from respiratory arrest in an asthmatic individual.[9] Controlled exposure studies on CS gas, the most common tear gas agent, demonstrate acute physiological effects via sensory nerve stimulation, primarily through TRPA1 receptor activation, leading to lacrimation, blepharospasm, throat burning, and transient respiratory distress resolving within 30-60 minutes in open air.[3][58] In a study of 38 volunteers exposed to CS spray, all experienced eye pain, nasal discharge, and skin irritation, but pulmonary function tests showed no significant changes post-exposure, with symptoms fully abating without medical intervention.[45] High-concentration or prolonged exposures in enclosed spaces, however, correlated with rare severe outcomes like reactive airways dysfunction syndrome or hemoptysis in case reports.[59] Epidemiological data from protest exposures indicate elevated respiratory emergencies post-tear gas deployment; a time-series analysis in an urban setting found a 20-30% increase in bronchial disease visits among vulnerable populations (e.g., elderly, asthmatics) on deployment days, with odds ratios peaking at 1.45 for emergency admissions.[60] Repeated occupational exposures in law enforcement personnel showed mildly diminished lung function via spirometry in some cohorts, though causality remains debated due to confounding factors like smoking.[3] A review of long-term effects highlighted insufficient prospective studies, with animal models (e.g., mice exposed to 30 mg/m³ CS for a year) revealing chronic laryngitis and tracheitis but no carcinogenesis.[54][33] Self-reported surveys from protest participants link tear gas exposure to reproductive health issues, with 83% of 199 exposed individuals (primarily women) reporting outcomes like menstrual irregularities or infertility attempts, adjusted odds ratio 3.0 for disruptions.[61][62] These associations, derived from retrospective data, warrant caution due to recall bias and lack of unexposed controls, though mechanistic plausibility exists via endocrine disruption hypotheses.[63] Ocular studies report persistent effects like symblepharon or corneal scarring in 1-2% of severe exposures, based on case series from mass events.[64] Overall, empirical evidence underscores dose-dependent irritancy with low lethality (fatality rate <0.1% in reviewed incidents) but gaps in long-term cohort data, particularly for vulnerable groups.[65][66]Practical Applications
Law Enforcement and Riot Control
Tear gas, encompassing riot control agents such as 2-chlorobenzalmalononitrile (CS) and chloroacetophenone (CN), is utilized by law enforcement agencies globally to incapacitate and disperse crowds during riots, protests, and civil disturbances. These agents induce acute irritation to the eyes, skin, and respiratory tract, resulting in temporary sensory overload that compels individuals to evacuate affected areas, thereby enabling officers to restore public order without immediate resort to deadly force.[3][1] Deployment occurs via pyrotechnic grenades, pressurized canisters, or munitions launched from 37mm or 40mm riot guns and mortars, allowing controlled dissemination from distances up to 100 meters to minimize direct exposure risks to personnel.[67][3] The inaugural application in policing traces to 1912 in Paris, France, where authorities employed hand-thrown chemical irritant bombs against organized criminal groups. Post-World War I, tear gas transitioned from military origins to civil use, with U.S. police demonstrations in 1921 marking its integration into standard riot control arsenals by the 1920s.[7][6] In the United States, notable deployments include the 1969 Stonewall riots in New York City, where police used tear gas to quell crowds outside the Stonewall Inn on June 28, and the May 4, 1970, events at Kent State University, Ohio, where it facilitated initial crowd movement prior to escalation.[68][69] Contemporary examples encompass widespread use during the 2020 protests following George Floyd's death, with agencies in over 50 U.S. cities deploying CS gas to manage assemblies exceeding 10,000 participants in some instances.[70] Empirical assessments affirm that exposure to CS at concentrations of 0.08–0.47 mg/m³—typical in riot scenarios—triggers incapacitation within 5–20 seconds via reflexive closure of eyes and involuntary coughing, achieving dispersal rates of 70–90% in open-air settings under favorable wind conditions.[42][20] Law enforcement protocols mandate training in agent characteristics, protective equipment like gas masks, tactical positioning to avoid blowback, and post-deployment decontamination with water or saline to mitigate secondary exposures.[71] In the U.S., federal oversight is absent, with usage dictated by local policies requiring proportionality; domestically, the 1993 Chemical Weapons Convention exempts law enforcement applications while prohibiting wartime use.[72][73] European frameworks similarly permit it under human rights-compliant guidelines, emphasizing necessity in proportionate responses to threats.[74]