Poisons Causing Temporary Blindness

Gassed. John Singer Sargent. 1919.

Poisonous powders and smokes that blind the enemy were well known and used by ancient commanders for millennia. The ancient Indian treatise Arthashastra (6th–3rd century BC) contains recipes for poisonous smokes causing blindness. Besides magical components such as a snake's head, peacock tail, or brown cow's bile, they included poisonous plants from the spurge family (Euphorbiaceae), whose vapors indeed cause chemical burns to human eyes followed by blindness[15].

The use of mustard gas in World War I showed that to force the enemy to lay down arms, it was completely unnecessary to drop tons of explosives or liquid chlorine on them. To make the opponent completely helpless, it was enough to simply deprive them of the ability to see. Having lost their sight, such soldiers were unable even to care for themselves, requiring constant care from civilians. Mortality from mustard gas did not exceed 2% and was mainly associated with secondary infections.

Severe eye injuries accompanied by necrosis, ulceration, and corneal clouding requiring prolonged treatment accounted for only 0.1% of cases. The remaining 99.9% of affected individuals had mild (75%) and moderate (25%) degrees of severity[16].

After the end of World War I, interest in blinding chemical agents did not wane. Military chemists from different countries tried to find a more "humane" alternative to vesicant substances. In 1926, V. Vogak in his book "Death... Death... Death... An Essay on the Development of Weapons Technology" describes a case of using an unknown blinding chemical agent:

Several classes of chemical agents causing reversible vision impairment are described:

• Vesicant and urticant chemical agents;
• Miotics — causing pupil constriction (miosis)
• Mydriatics — causing pupil dilation (mydriasis);
• Chemical agents causing reversible corneal clouding;
• Chemical and biological agents causing conjunctivitis and blepharitis.

Vesicant and Urticant Chemical Agents

In 1919, C.I. Reed from the Medical Division of the U.S. Chemical Warfare Service decided to test on himself what concentration of sulfur mustard would cause eye damage severe enough to render a person combat-ineffective.

Mild mustard gas eye injury. On the 7th day, conjunctivitis and eyelid swelling still persist.

To start, he evaporated just 12 mg of mustard gas in a 10 m³ chamber, and being fully confident that such a microscopic amount of mustard gas would definitely not harm him, he spent 45 minutes in the chamber. His confidence was based on numerous animal experiments that tolerated such concentration completely painlessly. What was his surprise when after 12 hours he developed severe blepharospasm accompanied by profuse tearing and photophobia. Severe scleral redness lasted about a week, for another two weeks C. Reed suffered from intense pain in the eye, mouth, and nose areas, and complete recovery took about 3 months. Besides the eyes, the respiratory tract mucous membranes were also severely affected, and the skin of the face and torso itched and peeled for almost a year after exposure.

Later, C. Reed established that staying 10–25 minutes in an atmosphere with a mustard gas concentration of just 0.5 mg/m ³ is sufficient for conjunctivitis development[9].

Mustard gas performed its task well but acted too slowly, plus it gave itself away with a specific sharp odor. Lewisite had the same disadvantages. Chemical agent KB-18 had a barely perceptible odor, but blindness after its exposure developed even later than after mustard gas. Phosgene oxime acted quickly but was unstable and for this reason was never adopted for service. Nitrogen mustards are best suited for temporary and reversible damage to vision organs, but their effect occurred after several hours.

Agents Causing Pupil Constriction (Miosis)

Alkyl fluorophosphates. Experiments on the effects of alkyl fluorophosphates on human vision were conducted in 1942 at the Chemical Defence Experimental Station (CDES) at Porton Down (United Kingdom). It was known that preparations of this group cause severe pupil constriction and accommodation disorders, and it was assumed they could be used to blind enemy personnel, especially at night.

Miosis

Diisopropyl fluorophosphate (DIF) and Diethyl fluorophosphate (DEF) were chosen for testing, which belong to the same class of nerve agents as sarin, soman, and VX, however, in subtoxic concentrations could be used as incapacitants.

Exposure to diisopropyl fluorophosphate (DIF) at a concentration of 41 mg·min/m³ caused throat irritation and chest tightness. Pupil diameter decreased insignificantly. Visual acuity did not worsen. When DIF concentration was increased to 99 mg·min/m³, for 3 hours after exposure the pupils were the size of a "needle's eye," light reflexes and accommodation were absent. Volunteers complained of vision deterioration, pain behind the eyeballs, and insomnia. The next day, the ability to see distant objects was restored, but "nearsightedness" even intensified. Pupil size completely returned to normal only after 5–6 days. The subjects' condition improved after instillation of 1% atropine solution. The calculated median lethal concentration LC₅₀ of DIF — 3000 mg·min/m³ is 30 times higher than the incapacitating concentration. Similar poisoning symptoms occurred after inhalation of diethyl fluorophosphate (DEF), but its effect was much weaker[1].

The report states that using DIF at night causes loss of combat effectiveness due to vision deterioration, however, the need to use high concentrations raises doubts about the possibility of using alkyl fluorophosphates as chemical agents[1].

Other organophosphorus chemical agents (sarin, soman, VX), in concentrations much lower than lethal, can cause temporary loss of combat effectiveness due to sharp vision deterioration, salivation, frequent urination and defecation. For example, sarin causes pupil constriction (miosis) and nasal mucous discharge at a concentration of just 0.4 mg·min/m³. Lethal injury requires doses 250 times greater.

Echothiophate
 

Bis-(triethyllead)
-fluorophosphate

Diisopropyl fluorophosphate
(DIF)

Diethyl fluorophosphate
(DEF)

Bis-(triethyllead)-fluorophosphate. During World War II, English chemists in Cambridge synthesized a "hybrid" whose molecule consisted of two halves — an organophosphorus chemical agent and an irritant from the trialkyllead group. The resulting bis-(triethyllead)-fluorophosphonate proved to be a powerful irritant, with a concentration of 1.7 mg/m³ for one minute causing severe irritation of nasal and throat mucous membranes, while higher concentrations caused miosis[2].

In 2012–2013, during the Syrian civil war, at least 14 cases of chemical weapon use were documented. It can be considered proven that in most cases, the cause of human poisoning was the nerve agent sarin. However, some media named other probable chemical agents, from ordinary chlorine to exotic "super-powerful tear gas" and psychochemical agents like BZ or Agent 15[11]. For example, the Syria Support Group (SSG) reported the use of a chemical agent called Echothiophate in the vicinity of Damascus and Aleppo[12]. By its chemical structure, echothiophate is a quaternary derivative of the insecticide and chemical agent amiton. This fairly common medication for glaucoma treatment acts like a nerve poison in large doses but is 25 times less toxic than sarin. A logical question arises: why use eye drops instead of standard sarin available in sufficient quantities in the Syrian army's arsenal? However, SSG sources invented an explanation for this too: Syrian President Bashar Assad, a former ophthalmologist, knew that echothiophate is one of the most powerful miotics, causing prolonged vision deterioration lasting about two weeks, rendering a person completely combat-ineffective.

Substances Causing Pupil Dilation (Mydriasis)

Mydriatics are a group of pharmacological preparations causing pupil dilation (mydriasis) and paralysis of the ciliary muscle located inside the eye that controls focusing (cycloplegia). Under the influence of mydriatics, temporary vision deterioration occurs, where a person sees surrounding objects as blurred and cannot focus their gaze. These preparations do not cause complete blindness.

Mydriasis

By mechanism of action, mydriatics belong to adrenomimetics and muscarinic antagonists. Depending on how long vision disorder persists, mydriatics are divided into three groups: short-acting (1–2 hours) — Tropicamide, medium duration (3–4 hours) — Cyclopentolate, and long-acting (5–6 hours) — Atropine.

The first known blinding substances of this type were alkaloids from plants of the nightshade family, such as henbane (Hyoscyamus niger), belladonna (Atropa belladonna), and jimsonweed (Datura stramonium). At the beginning of the last century, finely ground seeds of these plants were mixed with gunpowder and used to fill homemade bombs or blank cartridges. When firing such a cartridge, the finest plant dust containing alkaloids atropine or scopolamine got into the eyes and led to temporary vision deterioration.

Substance 301051

In 1947, the famous British military chemist A.H. Ford-Moore synthesized and studied the action of 40 mydriatics from the benzilate group. This work probably had military-practical significance, as its publication required permission from the UK Ministry of Defence[17].

In 2001, an article was published in a journal dedicated to aviation security discussing the theoretical possibility of using this group of substances in case of aircraft hijacking by terrorists[3].

In specialized literature devoted to temporary incapacitation agents, only one experimental substance from this group is mentioned under the code CAR 301,051[4].

Chemical Agent EA 1972

When affected by "urticant" chemical agents, temporary blindness develops due to the direct damaging effect of these substances on the eye's cornea with subsequent development of keratitis and corneal clouding. As a rule, such injuries are reversible, although they require prolonged treatment (see Phosgene oxime.)

Corneal clouding (Leukoma)

Agent EA 1972 (DG, TL 150). Dimethyl ester of diglycolic acid acts similarly, which even in small concentrations causes temporary blindness 20 minutes after exposure. The substance has no odor and does not cause eye irritation. As a rule, after 2–3 days the corneal clouding passes and vision is completely restored. Unlike vesicant and urticant chemical agents, DG exposure is completely painless.

Chemical agent EA 1972

This unusual effect was discovered by employees of the American company DuPont in the 1940s. The military immediately became interested in the new substance, assigning it the code DG and later — EA 1972. However, they considered the 20-minute period from the start of exposure to the onset of blindness too long[7]. Chemists working at this company, Loder and Woodhouse, attempted to synthesize a faster-acting chemical agent based on dimethyl diglycolate, but their attempts were unsuccessful[14].

The lethal dose EA 1972 for animals (mice) is 500 mg/kg with intraperitoneal injection and 1820 mg/m³ with 10-minute inhalation[5,6]. Diethyl and di(2-methoxyethyl) esters of diglycolic acid have similar effects[8].

Biological Agents

In 1990, Iraq began studying the acute hemorrhagic conjunctivitis (AHC) virus in a laboratory in Daura. However, according to the testimony of the chief virologist who headed the Iraqi biological program, attempts to cultivate the virus for further mass production were unsuccessful[13].

Enteroviral hemorrhagic conjunctivitis

Enterovirus-70 (EV-70) is the causative agent of epidemic hemorrhagic conjunctivitis. After an incubation period of 1 to 3 days, a person suddenly develops eye pain, photophobia, tearing, swelling and redness of the conjunctiva first in one eye, and after several days in the other eye. Conjunctivitis is accompanied by hemorrhages, more often under the mucous membrane of the upper eyelid, serous or sero-purulent discharge. General well-being usually does not suffer, recovery occurs in 1–2 weeks.

EV-70 belongs to highly contagious infections; in 1980–1982, major outbreaks of epidemic hemorrhagic conjunctivitis were recorded in tropical areas of Africa, Asia, North and South America, and Pacific islands.