Mass poisoning events with neurotoxic agents …

Douglas J Lanska MD MS MSPH

Neurotoxicology

Updated 06.24.2024
Expires For CME 06.24.2027

Mass poisoning events with neurotoxic agents

Author: Douglas J Lanska MD MS MSPH

See Contributor Disclosures

Mass poisoning events with neurotoxic agents

In This Article

Quick Link

Introduction

Overview

This article examines mass poisoning events from the 19th to 21st centuries. For the purposes of this article, mass poisoning will consider events of chemical poisoning involving at least 50 victims that result from the same source or circumstances, whether restricted to a single locale or more spatially dispersed, and whether restricted to a single point in time or serialized over a longer period (but usually within a few weeks or months). The poisons used in mass poisonings can be categorized by the circumstances of poisoning into (1) adulteration, (2) contamination, (3) recreational (usually with intended intoxicants), (4) occupational exposure (ie, poisoning of workers), (5) iatrogenic (ie, toxic substances are intentionally administered because the therapeutic benefit is believed to outweigh the risks from adverse effects of the substances), (6) environmental exposure (ie, with poisons released intentionally or otherwise into a shared environment), (7) mass suicide, (8) mass murder (with multiple subcategories: non-terrorism mass murder, terrorism mass murder, war crimes, genocide), and (9) unknown or unclear.

Key points

	• Mass poisoning is characterized by the occurrence of similar symptoms in a group of previously healthy people in a narrow time frame.
	• The poisons used in mass poisonings can be categorized by the circumstances of poisoning into (1) adulteration, (2) contamination, (3) recreational (usually with intended intoxicants), (4) occupational exposure (ie, poisoning of workers), (5) iatrogenic (ie, toxic substances are intentionally administered because the therapeutic benefit is believed to outweigh the risks from adverse effects of the substances), (6) environmental exposure (ie, with poisons released intentionally or otherwise into a shared environment), (7) mass suicide, (8) mass murder (with multiple subcategories: non-terrorism mass murder, terrorism mass murder, war crimes, genocide), (9) psychogenic, and (10) unknown or unclear.
	• Adulteration means to corrupt foods, drugs, or dietary supplements by adding a foreign or inferior substance, typically to prepare foods or drugs for sale by replacing more valuable ingredients with less valuable ones.
	• Neurotoxic adulterants repeatedly implicated in mass poisoning include arsenic (heavy metal) and triorthocresyl phosphate (organophosphate).
	• Neurotoxic contaminants implicated in mass poisoning include arsenic (heavy metal), organomercury compounds, pesticides, hexachlorobenzene, hexachlorophene, domoic acid, and bongkrekic acid.
	• Recreational exposures associated with mass poisoning predominantly involve methanol.
	• Non-terrorism mass murder by poisoning has employed arsenic, morphine, atropine, strychnine, diacetylmorphine (also called diamorphine; pharmaceutical heroin), cyanide, and tetramethylene disulfotetramine (tetramine).
	• Terrorism-related mass poisoning with neurotoxic poisons has involved the sarin nerve agent in two separate incidents in Japan in the mid-1990s.
	• War crimes associated with mass poisoning have involved the nerve agents sarin and tabun, as employed by Iraq in 1985 as it faced attacks from Iranian troops and poorly trained but loyal volunteers and again by Iraq in the Halabja massacre of Kurdish people in northern Iraq on March 16, 1988, during the closing days of the Iran-Iraq War.

Description

	• Mass poisoning is characterized by the occurrence of similar symptoms in a group of previously healthy people in a narrow time frame.
	• The poisons used in mass poisonings can be categorized by the circumstances of poisoning into (1) adulteration, (2) contamination, (3) recreational (usually with intended intoxicants), (4) occupational exposure (ie, poisoning of workers), (5) iatrogenic (ie, toxic substances are intentionally administered because the therapeutic benefit is believed to outweigh the risks from adverse effects of the substances), (6) environmental exposure (ie, with poisons released intentionally or otherwise into a shared environment), (7) mass suicide, (8) mass murder (with multiple subcategories: non-terrorism mass murder, terrorism mass murder, war crimes, genocide), (9) psychogenic, and (10) unknown or unclear.
	• Heavy metals have been implicated in mass poisonings in occupational poisoning (arsenic, lead, manganese, mercury), environmental poisoning (eg, arsenic, lead, mercury), mass murder (arsenic), and historically in iatrogenic poisoning (eg, mercury and arsenicals for syphilis).
	• Adulteration means to corrupt foods, drugs, or dietary supplements by adding a foreign or inferior substance, typically to prepare foods or drugs for sale by replacing more valuable with less valuable ingredients.

Poisoning is injury or death due to swallowing, inhaling, touching, or injecting various drugs, chemicals, venoms, or gases. Mass poisoning is characterized by the occurrence of similar symptoms in a group of previously healthy people in a narrow time frame. Similar to the definition of “mass” in mass murder or mass grave, mass poisoning refers to the poisoning of three or more victims in a single incident at a single location. However, this definition is problematic for multiple reasons: (1) the implication of “mass” is usually of a multitude of victims, many more than three; (2) requiring so few victims to meet the definition does not adequately distinguish mass poisoning from poisoning in general; and (3) a “single location” is too vague with an implication that is too restricted spatially. For the purposes of this chapter, mass poisoning will consider events of chemical poisoning involving at least 50 victims that result from the same source or circumstances, whether restricted to a single locale or more spatially dispersed, and whether restricted to a single point in time or serialized over a longer period (but usually within a few weeks or months).

This article will not comprehensively address iatrogenic poisoning (ie, toxicity from drugs that have not been adulterated when used appropriately from a medical perspective), which involves issues of drug evaluation, drug regulation, trade-offs between benefit and risk, and issues of manufacturing quality control. This article will also not cover radiation poisoning. Occupational, environmental, and psychogenic mass poisoning are addressed in separate Medlink Neurology articles.

The responsible toxic agent of a mass poisoning event may not be identified during the early stage of the event, especially if mass poisoning results from oral exposure. The toxicity of sources can be inherent to the agent itself or result from contamination.

Although most mass poisonings are unintended, many have resulted from intentional action (eg, adulteration of alcoholic beverages with methanol, adulteration of medical drugs with agents showing higher toxicity than the drug itself, mass murder, genocide).

Heavy metals have been implicated in mass poisonings in occupational poisoning (arsenic, lead, manganese, mercury), environmental poisoning (eg, arsenic, lead, mercury), mass murder (arsenic), and historically in iatrogenic poisoning (eg, mercury and arsenicals for syphilis). Other implicated substances in occupational mass poisoning events (eg, n-hexane) have affected much smaller numbers of people.

The poisons used in mass poisonings can be categorized by the circumstances of poisoning into (1) adulteration, (2) contamination, (3) recreational (usually with intended intoxicants), (4) occupational exposure (ie, poisoning of workers), (5) iatrogenic (ie, toxic substances are intentionally administered because the therapeutic benefit is believed to outweigh the risks from adverse effects of the substances), (6) environmental exposure (ie, with poisons released intentionally or otherwise into a shared environment), (7) mass suicide, (8) mass murder (with multiple subcategories: non-terrorism mass murder, terrorism mass murder, war crimes, genocide), (9) psychogenic, and (10) unknown or unclear (Table 1). Some substances can cause several different kinds of mass poisonings. For example, arsenic has caused mass poisonings by contamination, adulteration, occupational exposure, environmental exposure, and mass murder. Some events are not classifiable because the responsibility and intent are unclear.

Table 1. Categorization of Mass Poisoning Events*

Category of Poisoning	Subcategory	Intentional		Maximum scale (persons affected)
Category of Poisoning	Subcategory	Yes	No	Maximum scale (persons affected)
Adulteration		•		1,000
Contamination			•	1,000
Recreational		•		100
Occupational			•	1,000
Iatrogenic		•		10,000
Environmental		•	•	10,000,000
Mass suicide		•		1,000
Mass murder	Crime	•		1,000
	Terrorism	•		10,000
	War crime	•		10,000
	Genocide	•		10,000,000
Psychogenic				1,000
Unknown or unclear		?	?	100,000
* Notes: • Rare exceptions may differ in intention and maximum scale from that given in the table. • The information in the table primarily reflects historical information on poisonings that occurred in the 19th, 20th, and 21st centuries and does not reflect what malicious individuals or states may do in the future. • Some categories listed as not intentional may sometimes be intentional. For example, a company that fails to correct known problems that expose its workers to harmful substances does this with intent, driven by profit motives. Similarly, a company that knowingly releases toxic substances into the environment does this intentionally. • Also, the information reflects clinical poisoning rather than exposure, as, for example, virtually all people have been exposed to toxins such as lead and mercury. • Occupational, iatrogenic, and environmental mass poisoning are not considered in detail in this article. The occupational and environmental categories are considered in separate Medlink Neurology articles.

Adulteration

Adulteration means to corrupt foods, drugs, or dietary supplements by adding a foreign or inferior substance, typically to prepare foods or drugs for sale by replacing more valuable ingredients with less valuable ones. Adulterants are substances added to foods, drugs, and dietary supplements (either intentionally or by accident) but not listed as an ingredient. An adulterant may cause a product to be harmful or not work as it should.

In some cases, the adulterating substances can be toxic (eg, adding cheaper methanol to ethanol as was done during Prohibition in the United States and continues to be done in various countries, especially by poor individuals). The intent of adulteration is usually financial without an attempt to harm, but it may be financial with the recognition that the added substance is harmful (eg, the sale of ethanol adulterated with methanol to American Indians by unscrupulous white profiteers in the early 20th century), or it may be malicious (eg, acts of murder or terrorism).

The Plague of Adulteration: A Popular Complaint to a Popular Air

	Oh, have you heard the tales of late, How tradesmen all adulterate, There's scarce a thing now, sad to state, That's free of Adulteration. Your tea is mere chopped hay and sticks, Your Wallsend's safe to burn like bricks, With sand your sugar so they mix, That daily in your throat it sticks; Your coffee is chicory, beans, and bones, Your jeweller sells you paste for stones, In short whate'er you purchase owns Some taint of Adulteration
	Chorus: Hocus, pocus! fee, fo, fum! No wonder we all look so glum For nothing but ill-health can come From the Plague of Adulteration
	Your best kid-gloves are really rat, Your butter is pig's lard mixed with fat, Your mutton-pies are made of cat, By this plaguy Adulteration! Your beer is strychnine, salt and slops, And everything save malt and hops; And if you rashly call for wine, I would not that your fate were mine! Of lees and logwood port is made, And even worse things, I'm afraidm And sherry is now so tricked in trade, 'Tis nought but Adulteration.
	Chorus.— Hocus, pocus! &c.
	Where'er you go, whate'er you buy, Whatever “noted shop” you try, For genuine goods in vain you cry, Nought's sold but Adulteration. You ask for a loaf of wheaten bread, And they serve you with alum and “daff” instead, Which on your stomach lie like lead, And make a torment of your bed; If then in drugs you seek relief, You find they but increase your grief, Near every chemist's now a thief, And deals in Adulteration!
	Chorus.— Hocus, pocus! &c.
—Punch November 27, 1888, p. 214

Under the 1938 Federal Food, Drug, And Cosmetic Act (21 U.S. Code § 342) as amended, food, drugs, or dietary substances are considered adulterated if any of the following apply (summarized from the original lengthy legal verbiage):

	• Poisonous or unsanitary ingredients. If it bears or contains any poisonous or deleterious substance that may render it unsafe or injurious to health (including pesticide residue or food additives, any filthy, putrid, or decomposed substances) or if it was prepared, packed, or held under unsanitary conditions. • Absence, substitution, or addition of constituents.

		- If any valuable constituent has been omitted or substituted, wholly or in part. - If damage or inferiority has been concealed. - If any substance has been added, mixed, or packed with the product to increase its bulk or weight, to reduce its quality or strength, or to make it appear better or of greater value than it is.


	• Confectionery containing alcohol or a nonnutritive substance.
	• Dietary supplement containing a dietary ingredient that presents a significant or unreasonable risk of illness or injury.

Clinical applications

	• Neurotoxic adulterants repeatedly implicated in mass poisoning include arsenic (heavy metal) and triorthocresyl phosphate (organophosphate).
	• Neurotoxic contaminants implicated in mass poisoning include arsenic (heavy metal), organomercury compounds, pesticides, hexachlorobenzene, hexachlorophene, domoic acid, and bongkrekic acid.
	• Recreational exposures associated with mass poisoning predominantly involve methanol.
	• Non-terrorism mass murder by poisoning has employed arsenic, morphine, atropine, strychnine, diacetylmorphine (also called diamorphine; pharmaceutical heroin), cyanide, and tetramethylene disulfotetramine (tetramine).
	• Health professionals, including one British physician, have been implicated in serial mass murder using neurotoxic poisons.
	• Terrorism-related mass poisoning with neurotoxic poisons has involved the sarin nerve agent in two separate incidents in Japan in the mid-1990s.
	• War crimes associated with mass poisoning have involved the nerve agents sarin and tabun, as employed by Iraq in 1985 as it faced attacks from Iranian troops and poorly trained but loyal volunteers, and again by Iraq in the Halabja massacre of Kurdish people in northern Iraq on March 16, 1988, during the closing days of the Iran-Iraq War.
	• From 1939 to 1945, the Nazis developed increasingly efficient means of extermination with engine exhaust gas, carbon monoxide, and cyanide, as employed in genocidal intent during the Holocaust.
	• Unclassifiable poisoning with neurotoxic agents has often involved arsenic in the past, particularly in the 19th century, but in the United Kingdom as late as 1943.

Adulteration

Arsenic.

Table 2. Mass Poisoning Due to Adulteration with Arsenicals

Substance	Year	Place	Neurotoxic event
Arsenic	1858	Bradford, England	More than 200 people poisoned, with 21 deaths
Arsenic	1867	Wurzberg, Germany	373 to 400 people poisoned
Arsenic	1888	Hyères, France	500 people poisoned, with 15 fatalities, when wine was adulterated with white arsenic instead of gypsum.
Arsenic	1955	Japan	Morinaga milk poisoning: more than 700 infants poisoned, with more than 100 deaths.

Bradford sweets poisoning (1858). In the 1858 Bradford sweets poisoning, more than 200 people in Bradford, England, were poisoned with arsenic that had been accidentally incorporated into candies during preparation. The event contributed to the passage of the Pharmacy Act 1868 in the United Kingdom and legislation regulating the adulteration of foodstuffs.

William Hardaker, known as “Humbug Billy,” sold sweets from a stall in the Greenmarket in central Bradford. Hardaker purchased his supplies from Joseph Neal, who made the sweets (or “lozenges”). The lozenges were peppermint “humbugs” (ie, hard candies, especially ones flavored with peppermint), made from a base of sugar and gum with peppermint oil added for flavor. However, because sugar was expensive, Neal routinely substituted inexpensive powdered gypsum for some of the sugar (the gypsum was known as “daff” and, by weight, cost less than 8% of the cost of sugar). On October 30, 1858, Neal sent James Archer, a lodger at his house, to collect daff from druggist Charles Hodgson. Hodgson was at the pharmacy but was ill, so his young assistant, William Goddard, attended to Archer. Goddard asked Hodgson where the daff was and was told that it was in a cask in a corner of the attic. However, rather than daff, Goddard accidentally sold Archer 12 pounds (5.4 kg) of arsenic trioxide. The mistake remained undetected during the preparation of the sweets by James Appleton, an “experienced sweetmaker” employed by Neal. Appleton became ill during the process and remained ill for several days afterward, suffering with vomiting and pain in his hands and arms, but did not realize a poison caused it. Neal sold 40 pounds (18 kg) of lozenges to Hardaker. Although Hardaker tasted the sweets and promptly became ill, he nevertheless sold 5 pounds (2.3 kg) to patrons that night. Of those who purchased and ate the sweets, 21 people died, and 200 or so more became severely ill within a day.

"The Great Lozenge-Maker: A Hint to Paterfamilias" (1858)

Death, the poisonous candy maker, is shown mixing arsenic with a mortar and pestle. A barrel full of arsenic and a wooden box full of plaster of Paris are to either side, and a countertop with candies laid out is behind. Paterf...

The first deaths of two children were initially attributed to cholera, but the rapid increase in casualties soon showed that the lozenges from Hardaker's stall were responsible. Goddard was arrested and was questioned by magistrates in the Bradford courthouse on November 1. Goddard, Hodgson, and Neal were all subsequently committed for trial on a charge of manslaughter. Dr. John Henry Bell (1832-1906) identified arsenic as the cause of the mass poisoning, which was confirmed by forensic analytical chemist Felix Rimmington (1818-1897) (18; 55). Rimmington estimated that each humbug contained between 14 and 15 grains (910-970 mg) of arsenic, several times the lethal dose of 4.5 grains (290 mg). The prosecution against Goddard and Neal was later withdrawn, and Hodgson was acquitted at the York Assize on December 21, 1858 (An assize was a periodical court that sat at intervals in each county of England and Wales to administer civil and criminal law).

John Henry Bell MD (1832-1906)

Dr. John Henry Bell first identified arsenic as the cause of the Bradford sweets mass poisoning (1858). This photograph was included in his newspaper obituary and his obituary in the British Medical Journal in 1906. (Source: An...

The tragedy and public reaction served as a major stimulus to the passage of (1) the Pharmacy Act of 1868, which recognized the chemist and druggist as the custodian and seller of named poisons, and (2) the Sale of Food and Drugs Act of 1875, which regulated the adulteration of foods and drugs.

Triorthocresyl phosphate (TOCP). Numerous mass poisoning events have been attributed to triorthocresyl phosphate (TOCP; tri-O-cresyl phosphate) and organophosphate compound (Table 3) (172; 168; 73; 196; 114). Cresol (C7H8O) refers to any of the three methylphenols: ortho- (o-) cresol, meta- (m-) cresol, and para- (p-) cresol. Cresols are obtained from coal tar or petroleum, usually as a mixture (tricresol or cresylic acid) of the three stereoisomers. All three isomers are highly toxic. Triorthocresyl phosphate is an organophosphate with three orthocresol moieties bound to a phosphate. Like organophosphate nerve agents, triorthocresyl phosphate causes organophosphate-induced delayed neurotoxicity (OPIDN) that often manifests as spastic paraparesis.

2D skeletal model of ortho-cresol

(Source: Wikimedia Commons. Public domain.)
Nomenclature for benzene derivatives by position of substitution on the benzene ring

(Source: Wikimedia Commons. Public domain.)
Forms of cresol (methylphenol)

The three forms of cresol (methylphenol) with a methyl group on the 2, 3, and 4 positions on the benzene ring for ortho-, meta-, and para-cresol. (Source: Wikimedia Commons. User: Dr. T., 2009. Creative Commons Attribution 3.0 ...
2D skeletal model of triorthocresol phosphate

(Source: Wikimedia Commons. Public domain.)
Ball-and-stick model of triorthocresol phosphate

Key: Carbon (grey), hydrogen (white), oxygen (red), and phosphorus (orange). (Source: PubChem, National Institutes of Health, Bethesda, Maryland. Public domain.)

Jamaica ginger extract (Jake). Jamaica ginger extract, known in the United States by the slang name “Jake,” was a late-19th-century patent medicine, sold in drug stores and at roadside stands since the 1860s, that provided a source of ethanol during the Prohibition era because it contained approximately 70% to 80% ethanol by weight. During the early 1930s, at the end of the Prohibition Era (1920-1933), an estimated 30,000 men in the American South and Midwest developed arm and leg weakness and pain after drinking “Ginger Jake,” which contained a Jamaican ginger extract adulterated with TOCP (20; 21; 22; 33; 37; 53; 98; 47; 57; 65; 59; 39; 87; 86; 180; 186; 207; 28). The damage resulted in the limping “Jake Leg,” “Jake Leg Wobble,” “Jake Limber Leg,” or “Jake Walk,” which were terms frequently used in the blues music of the period (106; 195; 108): “Jake leg blues” (1928, 1930, 1934), “ Alcohol and Jake Blues” (1930), “Jake Leg Rag” (1930), “Jake Leg Wobble” (1930), “ Jake Liquor Blues” (1930), “Got the Jake leg too” (1930), and “Jake Walk Papa” (1933).

“He could be named Charley, and he could be named Ned, But if he drank this jake, it will give him the limber leg.”
	“Jake Leg Blues” Mississippi Sheiks Recorded June 11, 1930
“I can't eat, I can't talk Been drinkin' mean jake, Lord, now can't walk Ain't got nothin' now to lose Cause I'm a jake walkin' papa with the jake walk blues.”
	“The Jake Walk Blues” The Allen Brothers Recorded May 5, 1930

Trademark registration by Frederick Brown for Essence of Jamaica Ginger brand

(Courtesy of the Prints and Photographs Division, U.S. Library of Congress, Washington, D.C. Public domain.)
Sanford's Extract Jamaica Ginger

(Courtesy of the Prints and Photographs Division, U.S. Library of Congress, Washington, D.C. Public domain. Edited by Dr. Douglas J Lanska.)
Jamaica Ginger bottle

HW Wilson Ltd, St. John, New Brunswick, Canada. (Source: Photograph by Terry Lavigne. Public domain.)
Bottles of "Jamaica ginger," also called "Jake"

(Source: Wikimedia Commons. Photograph by User: Deltabeignet. Public domain. Edited by Dr. Douglas J Lanska.)
Investigator sampling Jamaica Ginger tainted with triorthocresol phosphate from a wholesale barrel

(Source: U.S. Food and Drug Administration. Public domain.)

In 1930, Jamaican ginger paralysis was linked to adulteration with TOCP by Maurice Isadore Smith MD (1887-1951), Principal Pharmacologist and Chief of the Section on Pharmacology in the Laboratory of Pathology and Pharmacology, Experimental Biology, and Medicine Institute, and Elias Elvove PhD (1883-1962), Senior Chemist, Laboratory of Chemistry, National Institutes of Health, United States Public Health Service (160; 159; 161; 155; 158; 162; 154; 155; 156; 157; 155; 157; 23; 24; 129). Smith and Elvove were both Russian emigres who were educated in the United States and later became influential scientists at the National Institutes of Health.

Maurice Isadore Smith MD (1887-1951)

Dr. Maurice Isadore Smith, Principal Pharmacologist and Chief of the Section on Pharmacology in the Laboratory of Pathology and Pharmacology, Experimental Biology and Medicine Institute (EBMI), National Institute of Health, Uni...
Elias Elvove PhD (1883-1962) (1)

Dr. Elias Elvove, Senior Chemist, Laboratory of Chemistry, National Institute of Health, United States Public Health Service. (Courtesy of the U.S. National Library of Medicine, Bethesda, Maryland. Public domain.)
Elias Elvove PhD (1883-1962) (2)

Dr. Elias Elvove, Senior Chemist, Laboratory of Chemistry, National Institute of Health, United States Public Health Service. (Source: Courtesy of the U.S. National Library of Medicine, Bethesda, Maryland. Public domain.)
Hygienic Laboratory Division of Chemistry with Dr. Elias Elvove, 1939

Dr. Elias Elvove is front row, third from left. The photograph was taken on the front steps of the National Institute of Health’s administration building in Washington, DC. In the front row are Dr. W Dayton Maclay, Dr. Ernest L...

Europe experienced outbreaks of TOCP poisoning with resultant neuropathy and some deaths from intentionally contaminated abortifacients in the 1930s, and South Africa experienced a similar outbreak in the 1950s (176; 140; 172).

Over a period of 3 weeks, in the fall of 1959, Morocco experienced an epidemic of paralysis from TOCP poisoning. Victims were poor Arab families poisoned by using olive oil adulterated with TOCP “by unscrupulous profiteers to increase its bulk” (151; 58; 134; 131; 178). TOCP was an ingredient of a detergent cleansing fluid used to flush jet engines and was acquired at a cheaper price than olive oil. The cheaper price of adulterated olive oil led to the selective poisoning of people with meager financial resources.

The Moroccan police seized all the olive oil available at that time in Morocco, which terminated the epidemic. Nevertheless, by the end of September 1959, 10,466 individuals had been afflicted.

Table 3. Mass Poisoning Events with Triorthocresyl Phosphate (TOCP) *

Year(s)	Place	Cases	Vehicle of TOCP	References
1899-1928	Europe	59	Phospho-creosote (used as a pharmaceutical for pulmonary disorders)	(140)
1930-1931	USA (Southeast)	30,000-50,000 (range of estimates: 20,000-100,000)	Jamaica ginger (ginger extract)	(47; 105; 104; 128; 129)
1930-1935	Europe	Approximately 300	Apiol with TOCP used as abortifacient	(176; 140)
1938	South Africa	68	Cooking oil	(144)
1940	Switzerland	80	Cooking oil	(188; 189)
1940-1946	Germany	More than 200	Cooking oil (“using the heavy oil from the German naval torpedo experimental station for cooking purposes”) and some occupational exposures	(48; 185; 63; 99)
1942-1943	Italy (Verona)	41	Cooking oil (suspected contamination with residual military engine oil)	(177)
1945	Great Britain (Liverpool and surrounding Merseyside)	17	Cooking oil	(71)
1955	South Africa	11	Apiol with TOCP as abortifacient	(172)
1959	Morocco	10,466	Olive oil (adulterated with jet engine lubricant from an American airbase)	(151; 58; 134; 131; 178; 184)
1960	India (Bombay)	58	Food	(187)
1962	India (West Bengal, Malda district)	More than 400	Flour	(40)
1966	Romania	12	Liquor	(181; 182; 183)
1967	Fiji	56	Flour	(167)
1971-1972	Vietnam	15-20	Cooking oil	(52)
1977-1978	Sri Lanka	More than 20	Gingili oil (consumed in a ritual at menarche and after childbirth)	(147; 147)
1988	India (Calcutta)	Approximately 600	Adulterated rapeseed (canola) oil	(169)
1995	China	74	Flour	(190)
*Notes: • Most of these events were due to adulteration of cooking oils, flour, or liquor. But the initial entry concerns iatrogenic poisoning, and two later episodes involved intentional, though misguided, addition of TOCP to apiol (green oil of parsley, the extracted oleoresin of parsley) to augment abortifacient effects (176; 140; 172). Apiol alone has been associated with deaths when used as an abortifacient (67; 135). • A few of these events might have been categorized as “contamination” rather than adulteration (eg, events during and after WWII when cooking oil may have been stored in drums with residual military engine oil).

Contamination

Arsenic.

English beer poisoning (1900). In 1900, a mass poisoning epidemic affected more than 6,000 people in England, who were poisoned by arsenic-tainted beer (51; 83; 138; 139; 84; 137; 81; 82; 132; 44; 54). Of those afflicted, 70 died. The food safety crisis was caused by arsenic entering the supply chain through impure sugar made with contaminated sulfuric acid. The illness was prevalent across the Midlands and North West England, with Manchester being the most heavily affected. Originally misdiagnosed as alcoholic neuropathy, the main epidemic was only recognized after 4 months.

In November 1900, Ernest Septimus Reynolds (1861-1926), Assistant Physician to the Manchester Royal Infirmary and Visiting Physician to the Manchester Workhouse Infirmary, announced “An epidemic of peripheral neuritis amongst beer drinkers in Manchester and district” and attributed this to arsenic poisoning (138; 139):

There is present in Manchester and district a wide-spread epidemic of peripheral neuritis, either sensory, vasomotor, or motor, or all three combined, associated with running of the eyes and nose (in many cases) and marked lesions of the skin. ... The disease is only met with in beer or porter drinkers. ... It is somewhat like the ordinary “alcoholic” paralysis at first sight, but differs from it in the greater amount of sensory and vasomotor disturbance, and especially in the presence of the peculiar skin lesions which are not present in alcoholic paralysis. ... We are thus reduced to arsenic as a cause of the symptoms, at any rate of the skin lesions, which in their multiform character can be explained by no known drug except arsenic. ... (Corroborating this clinical diagnosis) I found a considerable amount of arsenic in certain beer used in this district, and confirmed the observation next day. I have Professor Dixon Mann's authority for stating that ... he has also found arsenic in a different sample of beer. I have reason to believe that the source of the arsenic will be found to be the sulphur used in the hop industry (138; p 1493).

Reports confirming and expanding Reynold's observations appeared within weeks (51; 83; 84; 137). A Royal Commission chaired by Lord Kelvin (Sir William Thomson; 1824-1907) published its final report in 1903 (81; 82).

Foot of person with arsenic poisoning

Foot of person poisoned with arsenic contamination of beer, showing keratosis and erythema, with pigmentation. (Source: Kelynack TN, Kirkby W. Arsenical poisoning in beer drinkers. London: Baillière, Tindall and Cox, 1901. Publ...
Pigmentation of skin over breast in arsenic poisoning

Pigmentation of skin over breast and slight desquamation about nipple and areola in a woman poisoned with arsenic-contaminated beer. (Source: Kelynack TN, Kirkby W. Arsenical poisoning in beer drinkers. London: Baillière, Tinda...
Pigmentation over abdomen in arsenic poisoning

Pigmentation over abdomen, especially marked along lineae albicantes (whitish marks in the skin, especially of the abdomen and breasts, that often follow pregnancy), in a woman with arsenic-contaminated beer. (Source: Kelynack ...
Foot drop, muscle atrophy, cuticle thickening, and pigmentation in arsenic poisoning

"Dropping" of feet, slight atrophy of muscles, thickened and separating cuticle, and pigmentation in a person poisoned with arsenic-contaminated beer. (Source: Kelynack TN, Kirkby W. Arsenical poisoning in beer drinkers. London...
Fingernail ridging in arsenic poisoning

Transverse ridging of fingernails in a woman poisoned with arsenic-contaminated beer. (Source: Kelynack TN, Kirkby W. Arsenical poisoning in beer drinkers. London: Baillière, Tindall and Cox, 1901. Public domain.)
Paralysis and muscle wasting in arsenic poisoning

Paralysis of lower extremities with wasting of muscles and bilateral foot drop in a person poisoned with arsenic-contaminated beer. (Source: Kelynack TN, Kirkby W. Arsenical poisoning in beer drinkers. London: Baillière, Tindal...
Hand drop and muscle atrophy in arsenic poisoning (1)

"Dropped" hands from paralysis of extensors, with marked muscle atrophy in a woman poisoned with arsenic-contaminated beer. (Source: Kelynack TN, Kirkby W. Arsenical poisoning in beer drinkers. London: Baillière, Tindall and Co...
Hand drop and muscle atrophy in arsenic poisoning (2)

"Dropped" hands from paralysis of extensors, with marked muscle atrophy in a person poisoned with arsenic-contaminated beer. (Source: Kelynack TN, Kirkby W. Arsenical poisoning in beer drinkers. London: Baillière, Tindall and C...
Paralysis, muscle wasting, and pigmentation in arsenic poisoning

Paralyzed lower extremities, with marked muscle wasting and some pigmentation in a person poisoned with arsenic-contaminated beer. (Source: Kelynack TN, Kirkby W. Arsenical poisoning in beer drinkers. London: Baillière, Tindall...
Hand and foot drop in arsenic poisoning

"Dropped" hands and feet in a woman poisoned with arsenic-contaminated beer. (Source: Kelynack TN, Kirkby W. Arsenical poisoning in beer drinkers. London: Baillière, Tindall and Cox, 1901. Public domain.)
Pigmentation in arsenic poisoning

Pigmentation about the arm, axilla, and side of chest and over abdomen in a woman poisoned with arsenic-contaminated beer. (Source: Kelynack TN, Kirkby W. Arsenical poisoning in beer drinkers. London: Baillière, Tindall and Cox...
Extensive pigmentation in arsenic poisoning

Extensive pigmentation of the body in a woman poisoned with arsenic-contaminated beer. (Source: Kelynack TN, Kirkby W. Arsenical poisoning in beer drinkers. London: Baillière, Tindall and Cox, 1901. Public domain.)
Atrophic paralysis, wasting, and foot drop in arsenic poisoning

Atrophic paralysis, with marked wasting, and "dropped" feet in a person poisoned with arsenic-contaminated beer. (Source: Kelynack TN, Kirkby W. Arsenical poisoning in beer drinkers. London: Baillière, Tindall and Cox, 1901. Pu...
Paralysis, atrophy, thickened nails, and pigmentation in arsenic poisoning

Complete paralysis of the lower extremities with marked atrophy, thickened nails, and mild pigmentation of skin in a woman poisoned with arsenic-contaminated beer. (Source: Kelynack TN, Kirkby W. Arsenical poisoning in beer dri...
Muscle atrophy in arsenic poisoning

General muscular atrophy in a woman poisoned with arsenic-contaminated beer. (Source: Kelynack TN, Kirkby W. Arsenical poisoning in beer drinkers. London: Baillière, Tindall and Cox, 1901. Public domain.)
Wasting, atrophy, and hand and foot drop in arsenic poisoning

General wasting, extensive atrophy of the extremities, and "dropped" hands and feet in a woman poisoned with arsenic-contaminated beer. (Source: Kelynack TN, Kirkby W. Arsenical poisoning in beer drinkers. London: Baillière, Ti...
Ernest Septimus Reynolds (1861-1926)

Dr. Ernest Septimus Reynolds, Assistant Physician to the Manchester Royal Infirmary and Visiting Physician to the Manchester Workhouse Infirmary, announced "an epidemic of peripheral neuritis amongst beer drinkers in Manchester...
Sir William Thomson, Baron Kelvin (1824-1907)

Sir William Thomson, Baron Kelvin "resting on a binnacle and holding a marine azimuth mirror." (Source: Photograph by T. & R. Annan & Sons; restored by Adam Cuerden. National Galleries of Scotland Accession number: PGP ...

“L'affaire de la poudre Baumol” (“the Baumol powder affair,” 1952). This health scandal took place in France, mainly in the South West and Brittany, in 1952 (56; 89; 90). Because of a manufacturing error, a talc preparation for babies was contaminated with an arsenical compound, causing about 500 casualties, including 82 deaths. Baumol powder, as originally developed by the Francam laboratories in 1914, consisted of a combination of talc powder (talcum, a clay mineral composed of hydrated magnesium silicate) and zinc oxide with a lavender perfume. The Daney laboratories purchased the business in 1951. When they manufactured the baby powder, they accidentally replaced zinc oxide with arsenious anhydride (ie, the anhydride form of arsenous acid, or arsenic trioxide), which is used as a herbicide, pesticide, and rodenticide. The laboratory was found to be negligent with quality control, both of ingredients and finished products. The first health alerts were raised in the spring of 1952, and the product sale was banned in late October of the same year.

2D structural model of arsenous acid (arsenic trioxide)

The anhydride form of arsenous acid, arsenic trioxide, is used as a herbicide, pesticide, and rodenticide. (Public domain.)
3D ball-and-stick model of arsenous acid (arsenic trioxide)

Key: arsenic (purple), oxygen (red), hydrogen (white). The anhydride form of arsenous acid, arsenic trioxide, is used as a herbicide, pesticide, and rodenticide. (Public domain.)
Arsenic (III) trioxide

Arsenic (III) trioxide is a white powder that has been mistaken for edible substances with fatal consequences. (Public domain.)

Morinaga milk poisoning (1955). In the early summer of 1955, more than 2,113 bottle-fed Japanese infants were poisoned by arsenic, with more than 100 deaths, due to arsenic-contaminated milk powder produced by the Morinaga Company (50). The source of arsenic contamination was an industrial-grade disodium phosphate product added to cow's milk as a stabilizer to preserve constant acidity, but this was of low purity and contained significant amounts of sodium arsenate (Na₃AsO₄) (50).

Distribution of 2,113 cases of arsenic poisoning from contaminated dried milk in Okayama Prefecture, Japan, in 1955, by month and age

(Source: Dakeishi M, Murata K, Grandjean P. Long-term consequences of arsenic poisoning during infancy due to contaminated milk powder. Environ Health 2006;5:31. Creative Commons Attribution 2.0 Generic [CC BY 2.0] license, cre...
Sodium arsenate (Na3AsO4)

(Public domain.)

Table 4. Mass Poisoning by Contamination with Arsenicals

Substance	Year	Place	Neurotoxic event
Arsenic	1900	England (Midlands and North West)	English beer poisoning. Beer was contaminated with arsenic. Traced to sugar manufactured with sulfuric acid that was naturally contaminated with arsenic from Spanish pyrites. An epidemic of more than 6000 cases in London, including 70 deaths.
Arsenious anhydride (arsenic trioxide)	1952	France	“L'affaire de la poudre Baumol.” About 500 casualties, including 82 deaths.
Arsenic	1955	Japan	Morinaga milk poisoning. More than 2,100 infants were poisoned, with more than 100 deaths, due to arsenic-contaminated milk powder produced by the Morinaga Company.

Organomercury.

Table 5. Mass Poisoning by Contamination with Organomercury Compounds

Substance	Year(s)	Place	Neurotoxic event
Organic mercury	1955-1959	Iraq	Mercurial fungicide (ethyl mercury p-toluene sulphonanilide) caused 200 poisoning cases and 70 deaths (75; 06).
	1960	Iraq	Mercurial fungicide (ethyl mercury), used to treat seed grain, was used in bread. More than 1,000 people were affected (75; 06).
	1971	Iraq	Methylmercury, used as a fungicide to treat seed grain, was used in bread. Caused more than 5,000 severe poisonings and 450 hospital deaths (30; 29; 31; 13; 14; 12; 15; 16; 17; 93; 05; 07; 08; 10; 11; 41; 42; 80; 153; 61; 191; 46; 110).

Pesticides.

Table 6. Pesticide Mass Poisoning Events

Substance	Year	Place	Neurotoxic event
Aldicarb (pesticide)	1985	United States (California, other western states) and Canada (British Columbia)	More than 1,000 people experienced neuromuscular and cardiac problems after ingestion of melons contaminated with pesticide (74).

Hexachorobenzene. Hexachlorobenzene or perchlorobenzene, an aryl chloride compound, was used as a fungicide and pesticide until 1965 and was also used in the production of rubber, aluminum, and dyes and in wood preservation. As a fungicide, it was formerly used as a seed treatment, especially on wheat to control the fungal disease bunt.

Structural formula of the aryl chloride compound hexachlorobenzene (or perchlorobenzene)

(Public domain.)

Table 7. Mass Poisoning Due to Contamination with Hexachorobenzene

Substance	Year	Place	Neurotoxic event
Hexachorobenzene	1956	Turkey	Hexachlorobenzene, a seed-grain fungicide, led to the poisoning of 3,000 to 4,000 with a 10% case-fatality rate (191).

Hexachlorophene (disinfectant). In the “Affaire du talc Morhange” (Morhange talc affair) in 1972, 204 children in the northeastern French community of Morhange became ill, and 39 died in an epidemic of percutaneous poisoning. Affected children developed ulcerative skin lesions, diarrhea, encephalopathy with convulsions, and coma. The toxic agent was a contaminant of talc “baby powder”; because of a manufacturing error, the baby powder contained 6.3% hexachlorophene, an organochlorine compound. The cause of the epidemic was established by chemical analysis of the talc, high hexachlorophene levels and characteristic histological findings in affected children, and toxicity tests in animals (95; 96). In 1972, the U.S. Food and Drug Administration halted the production and distribution of products containing more than 1% hexachlorophene.

Structural formula of the organochlorine compound hexachlorophene

(Public domain.)
3D ball-and-stick model of the organochlorine compound hexachlorophene

(Public domain.)

Table 8. Mass Poisoning Due to Contamination with Hexachlorophene

Substance	Year	Place	Neurotoxic event
Hexachlorophene (disinfectant)	1972	France	In the “Affaire du talc Morhange,” 204 children became ill, and 39 died in an epidemic of percutaneous poisoning due to 6.3% hexachlorophene in talc baby powder (95; 96; 45).

Domoic acid.

Table 9. Mass Poisoning Due to Contamination of Mussels with Domoic Acid

Substance	Year	Place	Neurotoxic event
Domoic acid	1987	Canada (Prince Edward Island)	Ingestion of mussels contaminated with domoic acid caused 107 cases of amnestic syndrome and three deaths (130).

Bongkrekic acid.

Mozambique funeral beer poisoning (bongkrekic acid). Bongkrekic acid (also known as bongkrek acid) is a respiratory toxin produced in fermented coconut or corn mash that is contaminated by the bacterium Burkholderia gladioli pathovar cocovenenans. Bongkrekic acid is a highly toxic, heat-stable, colorless, odorless, unsaturated tricarboxylic acid that inhibits ADP/ATP translocase (the mitochondrial ADP/ATP carrier), preventing ATP from leaving the mitochondria to provide metabolic energy to the rest of the cell. Bongkrek acid, when consumed through contaminated foods, mainly targets the liver, brain, and kidneys. Most outbreaks are found in Indonesia and China, but the largest outbreak occurred in 2016 in Mozambique among attendees at a funeral who drank traditionally brewed pombe beer (a traditional fermented beverage made of sorghum, bran, corn, and sugar that is fermented with Schizosaccharomyces pombe yeast). A total of 230 were poisoned, and 75 people died.

Table 10. Mass Poisoning Due to Contamination with Bongkrekic Acid

Substance	Year	Place	Neurotoxic event
Bongkrekic (or bongkrek) acid	2015	Villages of Chitima and Songo, Mozambique	Mozambique funeral beer poisoning. On January 9, 2015, 230 were poisoned, and 75 people died after drinking contaminated beer at a funeral. All the people affected had consumed the local beer, pombe, which had been inadvertently contaminated by the bacterium Burkholderia gladioli, which produced the toxic compound bongkrekic acid (27; 62; 64).

Recreational exposures associated with mass poisoning

Methanol. Methanol poisoning can be unintentional to the person ingesting it (eg, with adulteration), or it can be intentional (eg, as a misguided attempt to ingest an intoxicating substance, or less commonly as an agent of suicide or murder). In some cases, categorizing the nature of the ingestion is problematic. In this section, we consider all cases of methanol poisoning resulting from drinking surrogate alcohol with a recreational intent.

Surrogate alcohol is a term for a product containing ethanol that is not meant for human consumption but is nevertheless intentionally consumed by humans. Consumption of surrogate alcohol may carry extreme health risks from toxic substances that may be present (eg, methanol or lead). Often those who seek out surrogate alcohol are either underaged, unable to afford consumable alcoholic beverages (eg, homeless alcoholics), or have no immediate access to drinking ethanol (eg, prison inmates and individuals in psychiatric wards).

Table 11. Recreational Mass Poisoning with Neurotoxic Poisons (Methanol)

Substance	Year(s)	Place	Neurotoxic event
Methanol	1904	Canada and United States	275 cases of methanol poisoning, including 153 cases of blindness and 122 deaths (38; 38)
	1911	Berlin, Germany	235 cases of methanol poisoning (cheap schnapps adulterated with methanol) among tramps or hoboes, with at least 72 deaths (133; 170). Traced to a distillery in Charlottenburg near Berlin. Five individuals were later arrested for manufacturing and distributing the adulterated liquor.
	1913	United States	720 cases of methanol poisoning due to ingestion, 390 (54%) died, 90 became totally blind, 85 were left with visual impairment, 6 to 10 had temporary blindness, 31 recovered, and about 114 did not have associated outcome data (32).
	1914	Bristol, England	An estimated 40 to 80 were poisoned, and 13 died.
	1951	Atlanta, Georgia, United States	433 cases of methanol poisoning with 38 deaths (34)
	1967	Madras, India	More than 500 cases (88)
	1978	Gujarat, India	100 deaths
	1981	Karnataka, India	308 poisoned
	1986	Gujarat, India	108 deaths
	1986	Italy	Hundreds of people poisoned, with 90 hospitalized and 23 deaths
	1987	Gujarat, India	200 deaths
	1988	Bombay (now Mumbai), India	97 poisoned and 28 deaths (101)
	1992	Odisha, India	More than 200 people poisoned
	1998	Phnom Penh, Cambodia	400 hospitalized and 70 deaths
	1998	Madagascar	200 deaths
	1999	Bahia state, Brazil	Estimates of 450 people hospitalized with 35 deaths
	2000	El Salvador	122 deaths
	2000	Nairobi, Kenya	More than 400 cases, with “around 140” deaths, and “at least 20 others became irreversibly blind” (26)
	2001	Pärnu, Estonia	The “Pärnu methanol poisoning incident.” 154 cases with 68 deaths and 43 left disabled after contents of stolen methanol canisters were used in the production of bootleg liquor (127; 126; 125).
	2002-2004	Oslo, Norway	51 hospitalized cases with nine deaths, plus nine who died outside of the hospital (72).
	2004	Mumbai neighborhood of Vikhroli, India	104 deaths from methanol poisoning
	2004	Shiraz, Iran	62 cases hospitalized, five suffered visual impairment (103).
	2006	León and of Chinandega, Nicaragua	801 cases treated with 48 deaths and 15 people blinded (197)
	2008	Karnataka and Tamil Nadu, India	148 people poisoned
	2009	Ahmedabad, Gujarat, India	“Hooch tragedy.” More than 241 poisoned. At one hospital, 63 men poisoned with 20 deaths (149). At another hospital, 178 hospitalized (175 men), but deaths not reported (76). Eight people, including three women, who were responsible for supplying the tainted liquor were subsequently arrested.
	2010	Southwestern Kabale District, Uganda	80 deaths from methanol-tainted waragi (“banana gin”)
	2011	Mat Prey Village, Cambodia	70 poisoned by drinking “a bad batch of “rice wine,” which actually turned out to be water mixed with pure methanol.”
	2011	Ecuador	124 poisoned of whom 21 died
	2011	Sangrampur, India	179 poisoned
	2011	Khartoum State, Sudan	71 deaths were reported among 13- to 25-year-old homeless youth (04)
	2012	Czech Republic	121 cases with 41 deaths and 20 survivors with visual or CNS sequelae (203; 205; 201; 200; 204; 206; 202; 142)
	2013	Rafsanjan, Iran	694 cases of methanol poisoning with eight deaths (66; 100)
	2013	Tripoli, Libya	1066 cases of methanol poisoning with 101 deaths (10%) (175; 141)
	2014	Havana, Cuba	100 poisoned with 11 deaths. Nearly a dozen arrested for distributing black-market liquor and “negligent homicide.”
	2014	Kenya (central)	341 cases of methanol poisoning with 100 deaths (29%) (141)
	2014	Kapsabet and Eldoret, Kenya (western)	64 cases of methanol poisoning with 13 deaths (20%) (141)
	2015	Laxmi Nagar slum in Malad, Mumbai, India	102 deaths and another 45 hospitalized with methanol poisoning
	2015	South Nigeria	84 poisoned with 70 deaths (124)
	2016	Irkutsk, in Siberia, Russia	In December, 123 people were hospitalized, and at least 78 died.
	2018	West Java, Jakarta, and Papua, Indonesia	100 deaths and 160 hospitalized
	2018	Bojnourd, Iran	73 patients (69 males) with methanol poisoning with eight deaths (10.8%) (02; 143; 97)
	2018	Iran	768 cases of methanol poisoning with 76 deaths (10.1%) (145) with later reports of nearly 1000 poisoned and 84 deaths.
	2019	China	52 poisoned, two died, and one had decreased visual acuity (136)
	2019	Northern states of Uttar Pradesh and Uttarakhand, followed by a second outbreak in Assam state, India	256 deaths with more than 200 additional people hospitalized in two separate outbreaks over 2 weeks.
	2020	Iran	Through March 18, 1463 cases of methanol poisoning (150). Through April 8, more than 3000 cases with 728 deaths (03). On April 27, the Iranian Health Ministry reported a total of 5,011 cases of methanol poisoning with 728 deaths through April 7, and 90 cases of blindness (Associated Press, April 27).
		Tehran, Iran	Approximately 2,200 cases with 296 deaths (13.5%) (166)
		Fars Province, Iran	797 cases of methanol poisoning with 97 deaths (145)
		Shiraz, Iran	Approximately 300 patients with methanol poisoning with 108 cases of methanol-induced optic neuropathy (85)
		Rafsanjan, Iran	694 cases of methanol poisoning with eight deaths
	2020	Mexico	More than 100 deaths from adulterated alcohol during ban on official sales of beer during COVID-19.

Although Iranian outbreaks of methanol poisoning were not new in 2020, their magnitude was nevertheless unprecedented and stemmed in part from internet claims that alcohol or methanol specifically could cure COVID-19. The Iranian government mandates that manufacturers of methanol add an artificial color to their products so the public can distinguish it from ethanol. Ethanol production is illegal in Iran. Some Iranian bootleggers add bleach to methanol to remove the added color before selling it as drinkable. Methanol is also used to adulterate traditionally fermented alcohol. All the methanol outbreaks for which data were available are listed above, rather than separating them and considering some as instances of adulteration. There have been numerous reports from Iran concerning the epidemic in 2020, but the documentation is poor, many reports consider “alcohol poisoning” without identifying how many actually had methanol toxicity, and many reports present overlapping or partially overlapping data, either spatially or temporally or both.

Non-terrorism mass murder by poisoning

Many examples of non-terrorism mass murder by mass poisoning were serial poisonings over a period of years by individuals who were medical professionals (ie, a nurse, midwife, or physician) (Bodó 2002a, 2002b; 152; 01; 192). An exception was the mass murders and mass “suicides” ordered of cult members at Jonestown, Guyana, in 1978 (see below). Another exception was a fast-food proprietor, who poisoned his competitor's breakfast snacks with the rodenticide tetramine, causing more than 340 poisonings and 42 deaths, all around September 14, 2002.

Dutch nurse and serial poisoner Maria Catherina van der Linden-Swanenburg (1839-1915)

(Source: Wikipedia. Public domain.)
American nurse and serial poisoner Jane Toppan (1854-1938)

(Source: Wikipedia. Public domain.)
Defendants in the arsenic poisoning cases of the Nagyrév area

Women walking in the Szolnok prison yard between 1929 and 1933. (Source: Bodó B. Tiszazug: A Social History of a Murder Epidemic. Boulder: East European Monographs, 2002b:185-6. Public domain.)
Structural formula of the rodenticide tetramethylene disulfotetramine (tetramine)

(Source: Wikipedia user: Shaddack, 2006. Public domain.)

Table 12. Non-Terrorism Mass Murder by Poisoning with Neurotoxic Substances

Substance	Year(s)	Place	Neurotoxic event
Arsenic	1880	St. Denis (near Paris), France	A baker's boy “wishing to avenge himself on his employer mixed arsenic with the bread and poisoned 270 people.”
?Arsenic	1880-1883	Leiden, Holland	Maria Catherina van der Linden-Swanenburg (1839-1915) was a Dutch nurse who murdered at least 27 people and was suspected of killing more than 90 people. Her motive was apparently financial. (Died in prison.) (192)
Morphine, atropine, and strychnine	1902	Massachusetts, United States	Jane Toppan (1854-1938) was an American nurse, nicknamed Jolly Jane, who confessed to poisoning 31 people (but may have killed as many as 100). Her motive was unclear, possibly sexual fetishism or sadism. (Committed to an asylum for life.) (01)
Arsenic	1914-1929	Nagyrév, Hungary	Zsuzsanna Fazekas (?-1929) was a Hungarian midwife, serial poisoner, and facilitator or promoter of homicidal poisoning by other women in the village of Nagyrév, Hungary. Fazekas began secretly persuading women to poison their husbands, using arsenic collected from the residue after boiling flypaper. The group of women was dubbed the “Angel Makers of Nagyrév.” Some of the women went on to poison their parents (and sometimes their children), either to eliminate a perceived burden or to receive an inheritance. There were somewhere between 40 to 300 murders from 1914 to 1929. Twenty-six of the Angel Makers were tried, among them Fazekas. Eight were sentenced to death, but only two were executed; another 12 received prison sentences. Fazekas reportedly committed suicide by hanging herself in November 1929. (35; 36)
Diacetylmorphine (also called diamorphine; pharmaceutical heroin)	1971-1998	Hyde, Greater Manchester, UK	Dr. Harold Frederick Shipman (1946-2004) was a British family practitioner who was nicknamed “Dr. Death” and the “Angel of Death.” He killed at least 218 people by poisoning and was estimated to have killed 250 but was tried for and convicted of killing 15. Most were elderly women, and his motive was at least partly financial--stealing jewelry and creating fraudulent wills, etc. (Committed suicide in prison.) (152)
Cyanide	1978	Jonestown, Guyana	“Jim” Jones (James Warren Jones; 1931-1978) ordered the poisoning of cult members in Jonestown, Guyana. A total of 907 died of cyanide poisoning; at least 70 had cyanide injected, apparently involuntarily, and one third of the victims were children.
Arsenic	1998	Wakayama, Japan	“Wakayama curry-poisoning incident.” Masumi Hayashi was arrested, convicted, and executed (in 2009) for poisoning 67 people, of whom four died. The motive was apparently insurance fraud.
Tetramethylene disulfotetramine (tetramine) sold as rat poison in China	2002	Nanjing, China	Snack shop proprietor Chen Zhengping (?-2002) became jealous of a competitor's snack bar and adulterated his competitor's foodstuffs, poisoning as many as 100 people, of whom 42 died. (Executed in October 2002.) (49; 01)

Cyanide use in the Jonestown massacre (1978). In 1978, the Peoples Temple Agricultural Project, better known by its informal name “Jonestown,” was a remote settlement in Guyana (the small remote country east of Venezuela), established by the Peoples Temple, a San Francisco-based cult under the leadership of “Jim” Jones (James Warren Jones; 1931-1978), who had been a political activist, preacher, and faith healer. On November 18, 1978, Jones orchestrated the deaths of more than 900 people at Jonestown, the nearby airstrip in Port Kaituma, and a Temple-run building in Georgetown, Guyana's capital city. The mass tragedy relied heavily on poisoning with cyanide-laced Flavor Aid, with many followers lining up to drink the lethal poison after being instructed to by cult leader Jones (an event that continues to be reflected in the popular expression of “drinking the Kool-Aid” to refer to a person who believes in a possibly doomed or dangerous idea, although most who employ the phrase seem unaware of its historical origin).

Guyana

(Source: "Addicted04" using Natural Earth, a public domain map dataset. Creative Commons Attribution 3.0 Unported [CC BY 3.0] license, creativecommons.org/licenses/by/3.0.)
The Peoples Temple Agricultural Project's places of interest in Guyana

(Source: Wikipedia. Edited by Dr. Douglas J Lanska.)
Cult leader Jim Jones at an anti-eviction rally Sunday, January 16, 1977

Photo taken in front of the International Hotel in San Francisco. Jones was a white minister who preached socialist and progressive ideas to a predominantly African-American congregation, called the Peoples Temple. (Source: Pho...

In total, 909 individuals died in Jonestown itself, all but two from apparent cyanide poisoning. Although Jones and some Peoples Temple members referred to “revolutionary suicide” on an audio tape of the event and in prior recorded discussions, at least 70 individuals at Jonestown were injected with poison, apparently against their will, and a third of the victims were minors. Moreover, the poisonings in Jonestown followed the murder of five others ordered by Jones at Port Kaituma, including the assassination of U.S. Congressman Leo Ryan (1925-1978) and murder-suicide ordered by Jones in Georgetown. Furthermore, Jones ordered guards armed with firearms and crossbows to shoot anyone who attempted to flee the settlement. Although some initial press descriptions of the event called it a “mass suicide,” this does not accurately reflect the manner of death for many of the victims; consequently, later sources refer to the deaths as mass murder-suicide, a massacre, or simply mass murder. Mass murder-suicide seems best to describe this atrocity.

Terrorism-related mass poisoning with neurotoxic poisons

Sarin. The nerve agent sarin (isopropyl methylphosphonofluoridate; also known as GB) was originally developed in 1938 in Germany as a pesticide. In its pure form, sarin is a clear, colorless, odorless, and tasteless liquid. Exposure to large doses of sarin may result in loss of consciousness, convulsions, paralysis, and respiratory failure, possibly leading to death. Low or moderate doses of sarin may produce some or all of the following symptoms within seconds to hours of exposure: rhinorrhea, ocular symptoms (eg, lacrimation, miosis, ocular pain, blurred vision), drooling, excessive sweating, respiratory symptoms (eg, cough, chest tightness, tachypnea), abdominal symptoms (eg, diarrhea, nausea, vomiting, abdominal pain), cardiovascular symptoms or signs (eg, bradycardia, tachycardia, hypotension, or hypertension), increased urination, confusion, drowsiness, weakness, and headache.

Sarin was used in two terrorist attacks in Japan in 1994 and 1995 by the cult Aum Shinrikyo, collectively poisoning more than 6000 people and killing 19 (199). After earlier failed attempts at developing and dispersing biological weapons (botulinum toxin and anthrax), the cult tested the development of sarin in a small laboratory beginning in November 1992 and then built a large chemical weapon production facility in the Fujigamine district of Kamikuishiki, labeled Satyan-7 (“Truth”).

The first attack occurred in a residential area of the city of Matsumoto, Japan, on June 27, 1994, when terrorists released about 12 liters of the nerve agent. Approximately 600 residents, rescue staff, and hospital personnel were poisoned; 58 were hospitalized, and seven who lived near the release died before reaching the hospital (inhalation caused instantaneous death by respiratory arrest in four of the victims) (107; 113; 112; 121; 146; 120; 179; 199). The geographical distribution of sarin victims was closely related to the direction of the wind (112). Muscarinic signs were common to all victims, whereas nicotinic signs were only seen in severely affected victims (112). Miosis was the most common sign (120). Laboratory findings for severely poisoned people included decreases in serum cholinesterase and acetylcholinesterase in erythrocytes (107; 173). Mild fever and epileptiform abnormalities on electroencephalogram were present for up to 30 days (107). Examination several weeks after the attack generally revealed no persisting abnormal physical findings in mildly exposed individuals (107), but surviving severely exposed individuals had worse outcomes, including one individual with persistent akinetic mutism 2 years after the attack (173). Acetylcholinesterase returned to normal within 3 months (107). Although subclinical miosis and neuropathy were present 30 days after exposure, almost all symptoms of sarin exposure disappeared rapidly and left no evident sequelae in most mildly exposed people (107).

Three weeks after the intoxication, 129 victims still had some symptoms, such as dysesthesia of the extremities (112). At that time, many victims had begun to experience asthenopia (ocular strain), which was even more frequent at 4 months. Although victims who reported sarin-related symptoms decreased by a year after the attack, some had persistent symptoms (112).

The cult employed a different nerve agent, VX, in late 1994 to assassinate up to 20 dissident members.

The second terrorist attack occurred on March 20, 1995, when cult members released sarin gas on the Tokyo subway, killing 12 and injuring more than 5,500 people, including subway users, subway workers, rescue personnel, and emergency room medical staff (25; 116; 117; 174; 123; 194; 179; 69; 199). Of those who died, two died in station yards, and another 10 died in hospitals within a few hours to 3 months after poisoning (199). Severely poisoned victims who did not immediately die arrived at the emergency department with cardiopulmonary or respiratory arrest with marked miosis and extremely low serum cholinesterase value (118). Common signs and symptoms in less severely poisoned victims included miosis, headache, dyspnea, nausea, ocular pain, blurred vision, vomiting, coughing, muscle weakness, muscle twitching, and agitation (118). Almost all patients showed miosis and related symptoms such as headache, blurred vision, and visual darkness (118).

In general, miosis and copious secretions from the respiratory and gastrointestinal tracts (muscarinic effects) were common in severely to slightly affected victims, whereas weakness and muscle twitches (nicotinic effects) appeared in severely affected victims (199). Leukocytosis and high serum CK levels were common clinical laboratory abnormalities in victims (199).

Ocular signs and symptoms resolved between 3 and 21 days after exposure; treatment with 0.5% tropicamide ophthalmic solution effectively decreased ocular pain (77).

Chronic complications included post-traumatic stress disorder (118; 79; 119; 171), insomnia (78), and neurocognitive impairment (psychomotor function and memory) (70; 115; 102), as well as a variety of nonspecific psychiatric and somatic symptoms (eg, fear or anxiety, headache, fatigue or fatigability, asthenia, shoulder stiffness, asthenopia, and blurred vision) (111; 122; 171). The prevalence of post-traumatic stress disorder was less than 8% after 5 years (199). Neuropathy and ataxia were observed in fewer than 10% of victims, but associated findings generally disappeared between 3 days and 3 months. EEG abnormalities persisted for up to 5 years (199). Other subclinical effects were evident in the central and autonomic nervous systems of survivors for months after the attack (109).

Oximes, atropine sulphate, diazepam, and ample intravenous infusion were effective treatments (199). Intravenous pralidoxime iodide reversed cholinesterase and symptoms quickly, even if administered 6 hours after exposure (199).

Table 13. Use of Neurotoxic Poisons in Terrorism

Substance	Year	Place	Neurotoxic event
Sarin nerve agent	1994	Matsumoto, Japan	The cult Aum Shinrikyo used the sarin nerve agent to poison approximately 600 residents, rescue staff, and hospital personnel; 58 were hospitalized, and seven who lived near the release died before reaching the hospital.
Sarin nerve agent	1995	Tokyo, Japan	The cult Aum Shinrikyo used the sarin nerve agent on the Tokyo subway to poison more than 5,500 people, killing 12 (199).

War crimes using neurotoxic agents for mass poisoning

The largest use of chemical weapon nerve agents in war was by Iraq in the Iran-Iraq War (1980-1988). Iraq used two nerve agents in the G series: GA or tabun (EA1205) and GB or sarin (EA1208). G-series nerve agents are a class of chemical warfare agents developed by German scientists before and during World War II. They are organophosphate compounds. The “EA” numbers stand for Edgewood Arsenal number designations for chemical warfare agents. From 1948 to 1975, the U.S. Army Chemical Corps conducted classified human subject research at the Edgewood Arsenal facility in Maryland to evaluate the impact of low-dose chemical warfare agents on military personnel and to test protective clothing, pharmaceuticals, and vaccines.

Structural formula for the organophosphate nerve agent tabun (GA, EA1205)

(Public domain.)
Ball-and-stick model of the organophosphate nerve agent tabun (GA, EA1205)

Key: carbon (black), hydrogen (white), nitrogen (blue), oxygen (red), phosphorus (orange). (Public domain.)
Structural formula for the organophosphate nerve agent sarin (GB, EA1208)

(Public domain.)
Ball-and-stick model of the organophosphate nerve agent sarin (GB, EA1208)

Key: carbon (black), fluorine (green), hydrogen (white), oxygen (red), phosphorus (orange). (Public domain.)

Iraq's use of nerve agents against Iran in the Iran-Iraq War (1980-1988). Iraq used the nerve gas tabun from 1985 as it faced attacks from Iranian troops and poorly trained but loyal volunteers.

Iraq's use of nerve agents in the Halabja massacre (1988). The Halabja massacre was a massacre of Kurdish people in Halabja in northern Iraq on March 16, 1988, during the closing days of the Iran-Iraq War. Iraqi warplanes and artillery pounded Halabja with mustard gas and the nerve agents sarin and tabun, apparently as punishment because some Kurdish guerrilla forces had joined the Iranian offensive (68). The incident was the largest chemical weapons attack directed against a civilian-populated area in history, killing between 3200 and 5000 people and injuring 7000 to 10,000 more, most of them civilians.

Table 14. Use of Neurotoxic Poisons in War Crimes

Substance	Year(s)	Place	Neurotoxic event
Nerve agents sarin and tabun	1980-1988	Iran-Iraq war

Genocide using neurotoxic agents for mass poisoning

Across the various genocides of history, genocide was not commonly implemented by poisoning but rather by forced starvation or execution with bullets, burning, or hanging. However, from 1939 to 1945, the Nazis developed increasingly efficient means of extermination with engine exhaust gas, carbon monoxide, and cyanide. Cyanide and carbon monoxide both bind to cytochrome c oxidase, inhibiting the protein from functioning and leading to the chemical asphyxiation of cells.

The cyanide anion is an inhibitor of the enzyme cytochrome c oxidase (or complex IV, EC 1.9.3.1), a large transmembrane protein complex of the electron transport chain located in the inner membrane of the mitochondria of eukaryotic cells. The cyanide anion attaches to the iron within this protein and prevents the transport of electrons from cytochrome c to oxygen. As a result, the electron transport chain is disrupted, meaning that the cell can no longer aerobically produce ATP for energy. Tissues that depend highly on aerobic respiration, such as the central nervous system and the heart, are particularly affected by this histotoxic hypoxia.

Cyanide use in the Holocaust. Zyklon B (German for Cyclone B) was the trade name of a cyanide-based pesticide invented in Germany in the early 1920s. It consisted of hydrogen cyanide (prussic acid), an eye irritant, and one of several adsorbents (eg, diatomaceous earth).

Structural formula of hydrogen cyanide

(Public domain.)
Ampoule of hydrogen cyanide

(Source: Wikimedia Commons User: Pok, 2024. Creative Commons Attribution 4.0 International [CC BY 4.0] license, creativecommons.org/licenses/by/4.0.)

The product was used by Nazi Germany during the Holocaust to murder approximately 1.1 million people in gas chambers installed at Auschwitz-Birkenau, Majdanek, and other extermination camps. Most of the victims were Jews (although the original tests were done on Russian prisoners of war); by far the majority killed using this method died at Auschwitz. Auschwitz received 23.8 tonnes (23,800 kg), of which 6 tonnes (6000 kg) were used for fumigation (delousing); the remainder of approximately 18 tonnes (18,000 kg) was used in the gas chambers or lost to spoilage (the shelf life was only 3 months).

Labels taken from canisters of Zyklon B from the Dachau gas installation

Photograph taken April 7, 1946, by Alfred H Booth. The first and third panels contain the German Pest Control Company emblem and the brand name Zyklon. The center panel reads "Poison Gas!" "Cyanide Preparation! [skull and cross...
Empty Zyklon B canisters

Empty Zyklon B canisters found by the Allies at Auschwitz-Birkenau Nazi extermination camp in 1945 at the end of World War II. (Source: Wikimedia Commons. Public domain. Cropped and edited by Dr. Douglas J Lanska.)

The gas chambers consisted of a sealed chamber into which a poisonous gas was introduced, usually carbon monoxide or hydrogen cyanide (Zyklon B), both of which specifically inhibit cytochrome c oxidase of the human mitochondrial respiratory chain (09; 43). Despite some pseudo-scientific claims by Holocaust deniers that cyanide was not used to exterminate prisoners, cyanide residuals have been demonstrated on the walls of the gas chambers in the former Auschwitz and Birkenau concentration camps using appropriate forensic methods (94; 60). Residuals of cyanide are also present on the walls of a concrete-walled gas chamber at the former Majdanek concentration camp in the form of the pigment Prussian blue (ferricyanide).

Reinforced concrete gas chamber (1)

Reinforced concrete gas chamber in the Nazi-operated Majdanek concentration camp, designed for killing prisoners by carbon monoxide, which was introduced through a tube, or Zyklon B (hydrogen cyanide), as evidenced by the resid...
Reinforced concrete gas chamber (2)

Reinforced concrete gas chamber in the Nazi-operated Majdanek concentration camp, designed for killing prisoners by carbon monoxide, which was introduced through a tube, or Zyklon B (hydrogen cyanide), as evidenced by the resid...
Structural formula of ferricyanide

2D structural formula of ferricyanide (hexacyanoferrate[III]), the anion (Fe[CN]₆₎³⁻. (Public domain.)
Ball-and-stick and space-filling models of ferricyanide

3D ball-and-stick (left) and space-filling (right) models of ferricyanide (hexacyanoferrate[III]), the anion (Fe[CN]₆)³⁻. Key: Carbon (black), iron (light purple), nitrogen (dark blue). (Public domain.)
Prussian blue (ferricyanide) sample

The pigment Prussian Blue, ferricyanide, was invented in 1706 and named after the country in which the invention took place (Prussia). (Public domain.)

The Nazis started using Zyklon B in extermination camps in early 1942 to murder prisoners during the Holocaust. German SS officer and commandant of the Auschwitz concentration camp Rudolf Hoess (also Höss, Höß, Hoeß; 1901-1947) had been testing and implementing methods to accelerate Hitler's order to systematically exterminate the Jewish population of Nazi-occupied Europe, known as the Final Solution. On the initial suggestion of one of his subordinates, Karl Fritzsch (1903-c1945), deputy and acting commandant at the Auschwitz concentration camp, Hoess introduced the pesticide Zyklon B to be used as the killing agent in the gas chambers. On April 15, 1946, Hoess testified at the International Military Tribunal at Nuremberg, where he gave a detailed accounting of his crimes. On May 25, 1946, Hoess was handed over to Polish authorities, and the Supreme National Tribunal in Poland tried him for murder. Hoess was convicted at his trial in March 1947, and he was sentenced to death by hanging, which was carried out on April 16 next to the crematorium of the former Auschwitz I concentration camp.

Three SS officers and war criminals socialize on the grounds of the SS retreat outside of Auschwitz, at “Solahütte,” 1944

From left to right they are: Richard Baer (Commandant of Auschwitz, 1911-1963), Dr. Josef Mengele (1911-1979), and Rudolf Hoess (the former Auschwitz Commandant, 1901-1947). Hoess was the Commandant when Zyklon B (hydrogen cyan...
Nazi SS Haupsturmfuehrer Karl Fritzsch (1903-c1945) at Auschwitz Concentration Camp

Fritzsch was deputy and acting commandant at the Auschwitz concentration camp. According to Rudolf Höss, Fritzsch first suggested using poisonous gas Zyklon B for the purpose of mass murder. Hauptsturmfuehrer was a Nazi Party p...
Rudolf Franz Ferdinand Höss (1901-1947)

Former German SS officer and commandant of the Auschwitz concentration camp Rudolf Franz Ferdinand Höss (also Höß, Hoeß, or Hoess; 1901-1947), during his trial in Warsaw, Poland, in 1947, after which he was declared guilty then...
War criminal Rudolf Hoess before execution (1)

War criminal Rudolf Hoess with his executioners walking to his gallows next to a crematorium in the Nazi Auschwitz death camp in Poland (1947). (Source: Photograph by press photographer Stanisław Dąbrowiecki, 1947. Public doma...
War criminal Rudolf Hoess before execution (2)

Moments before Rudolf Hoess was put to death for his war crimes at Auschwitz, 1947. (Source: Photograph by press photographer Stanisław Dąbrowiecki, 1947. Public domain.)

Table 15. Genocidal Poisoning with Neurotoxic Agents

Substance	Years	Place	Neurotoxic event
Carbon monoxide and later cyanide gas	1942-1945	Death camps in Germany, Austria, Poland	During the Holocaust, Nazi Germany used poison gases to murder approximately 1.1 million people, predominantly Jews, in gas chambers installed at Auschwitz-Birkenau, Majdanek, and other extermination camps, beginning in 1942. (The Nazis also used other means of extermination, so the total deaths included approximately 6 million Jews from 1941-1945. Separate Nazi persecutions killed a similar number of non-Jewish civilians and prisoners of war.)

Unclassifiable or unclear

Table 16. Unclassifiable Poisoning with Neurotoxic Agents

Substance	Year(s)	Place	Neurotoxic event
?Arsenic	1828-1830	Paris	The so-called “epidemie de Paris” of peripheral neuritis and acrodynia reportedly produced 40,000 deaths. Some have attributed this to arsenic poisoning, but the source has not been established, nor has the magnitude been validated (139).
Arsenic trioxide	1857	British Hong Kong	In the Esing Bakery incident (also called the “Ah Lum affair”), between 300 and 500 predominantly European residents of the colony were poisoned by bread produced by the Chinese-owned Esing Bakery. Although this was not likely accidental, the motive and the perpetrator are unclear.
Arsenic	1867	Wurzburg, Germany	373 people poisoned
Arsenic	1880	St. Denis (near Paris), France	More than 80 people ate bread contaminated with or adulterated with arsenic. The source of the arsenic and the motive, if intentional, were never clarified.
Arsenic trioxide	1943	St. Andrews University, Scotland	About half a pound of white arsenic (arsenic trioxide) was added to a batch of sausages. About 90 students were poisoned, some severely, although there were no deaths. “Further investigations by the public health authorities and the police failed to show how the arsenic had been put into the sausage mix, or even where the arsenic could have come from” (198).
?	1981	Madrid	*More than 25,000 were seriously poisoned, and more than 1,000 died. Attributed at the time to adulterated rapeseed or canola oil, hence the commonly used name “toxic oil syndrome” for this epidemic; however, a plausible toxin was never identified, and there is evidence of governmental interference (to protect Spain's native olive oil industry). Variously attributed to aniline derivatives in cooking oil (unlikely as this doesn't correspond with clinical features) and to organophosphate contamination (possibly on tomatoes).
*Because the Spanish epidemic in 1981 never had a plausible toxin identified, and because of evidence of governmental interference in the initial studies, the lack of similar epidemics elsewhere, etc., it seems that a final “answer” for this epidemic is unlikely. Because this was a “one-off” event, a detailed review is not given here.

Esing Bakery Incident or “Ah Lum affair” (1857). The Esing Bakery incident (92; 91) was a food contamination scandal in the early history of British Hong Kong. On January 15, 1857, during the Second Opium War (1856-1860), between 300 and 500 predominantly European residents of the colony were poisoned from bread produced by the Chinese-owned Esing Bakery. Victims fell ill with nausea, vomiting, stomach pain, and dizziness. Later testing concluded that the bread had been adulterated with large amounts of arsenic trioxide. There were no deaths immediately attributable to the poisoning, although three deaths that occurred the following year were ascribed to the long-term effects of arsenic poisoning. The quantity of arsenic involved was thought to be so high that the poison was vomited out before it could be fatally absorbed. A total of 52 Chinese men were detained and examined at the Central Police Station on January 21. The proprietor, Cheong Ah-lum (alternate transliterations of his name include Cheung instead of Cheong and A[-]lum, Allum, Ahlum, or Ah Lum instead of Ah-lum), was accused of plotting the poisoning but was acquitted in a jury trial. Despite this, Cheong was successfully sued for damages and was banished from the colony.

Esing Bakery, Hong Kong, 1857

The Chinese-owned Esing Bakery, Hong Kong, 1857, at the time of mass poisoning of between 300 and 500 predominantly European residents of the colony. (Source: Illustrated London News, March 28, 1857:286. Public domain.)
Questioning of the proprietor of the Esing Bakery regarding mass poisoning

Examination of Al-Lum Cheong, proprietor of the Esing Bakery, at the Police Office, Victoria, Hong Kong on the charge of poisoning. (Source: Illustrated London News, March 28, 1857:286. Public domain.)

Responsibility for the incident and its intention remain matters of debate; proposed explanations include accidental contamination or intended murder for either commercial sabotage, terrorism, or a war crime orchestrated by the Qing government. Chemical analyses at the time do not support an accidental cause because arsenic was found only in the bread itself, and in massive quantities, but not in the flour, yeast, pastry, or scrapings collected from the table. The poison must have been introduced shortly before baking. Moreover, the decision to poison European-style bread, which was generally not eaten then by the Chinese, served to target European victims with a readily available and fast-acting poison.

Qing governor Ye Mingchen (1807-1859)

London newspapers accused the Qing governor Ye Mingchen of masterminding the Esing Bakery poisoning incident in 1857. Ye was known for his resistance to British influence in Canton (Guangzhou) in the aftermath of the First Opiu...

Media

References

01: Aggrawal A. Mass poisonings. In: Payne-James JJ, Byard RW, editors. Encyclopedia of Forensic and Legal Medicine. 2nd ed. London: Elsevier Academic Press, 2016;3:300-6.
02: Aghababaeian H, Araghi Ahvazi L, Ostadtaghizadeh A. The methanol poisoning outbreaks in Iran 2018. Alcohol Alcohol 2019;54(2):128-30. PMID 30715164
03: Aghababaeian H, Hamdanieh L, Ostadtaghizadeh A. Alcohol intake in an attempt to fight COVID-19: a medical myth in Iran. Alcohol 2020;88:29-32. PMID 32693023
04: Al Alim AbdulRahim F, Al Shiekh A. Substance abuse and homelessness: mass methanol poisoning in Khartoum. Sudan Med J 2012;48(1):1-6.
05: Al-Damluji SF. Intoxication due to alkylmercury-treated seed--1971-72 outbreak in Iraq: clinical aspects. Bull World Health Organ 1976b;53 Suppl(Suppl):65-81. PMID 1086168
06: Al-Damluji SF. Organomercury poisoning in Iraq: history prior to the 1971-72 outbreak. Bull World Health Organ 1976a;53 Suppl(Suppl):11-3. PMID 788949
07: Al-Falluji N, Makkawi TA, Abou-el-azm IM, Sokkar IM, Darraji M. Experimental studies on organomercury poisoning in chickens in Iraq. Bull World Health Organ 1976;53 Suppl(Suppl):119-27. PMID 1086160
08: Al-Mufti AW, Copplestone JF, Kazantzis G, Mahmoud RM, Majid MA. Epidemiology of organomercury poisoning in Iraq. I. Incidence in a defined area and relationship to the eating of contaminated bread. Bull World Health Organ 1976;53 Suppl(Suppl):23-36. PMID 1086164
09: Alonso JR, Cardellach F, López S, Casademont J, Miró O. Carbon monoxide specifically inhibits cytochrome c oxidase of human mitochondrial respiratory chain. Pharmacol Toxicol 2003;93(3):142-6. PMID 12969439
10: Al-Saleem T. Levels of mercury and pathological changes in patients with organomercury poisoning. Bull World Health Organ 1976;53 Suppl(Suppl):99-104. PMID 1086172
11: Al-Tikriti K, Al-Mufti AW. An outbreak of organomercury poisoning among Iraqi farmers. Bull World Health Organ 1976;53 Suppl(Suppl):15-21. PMID 1086163
12: Amin-Zaki L, Elhassani S, Majeed MA, et al. Perinatal methylmercury poisoning in Iraq. Am J Dis Child 1976;130(10):1070-6. PMID 973609
13: Amin-Zaki L, Elhassani S, Majeed MA, Clarkson TW, Doherty RA, Greenwood M. Intra-uterine methylmercury poisoning in Iraq. Pediatrics 1974a;54(5):587-95. PMID 4480317
14: Amin-Zaki L, Elhassani S, Majeed MA, Clarkson TW, Doherty RA, Greenwood MR. Studies of infants postnatally exposed to methylmercury. J Pediatr 1974b;85(1):81-4. PMID 4854450
15: Amin-Zaki L, Majeed MA, Clarkson TW, Greenwood MR. Methylmercury poisoning in Iraqi children: clinical observations over two years. Br Med J 1978;1(6113):613-6. PMID 630256
16: Amin-Zaki L, Majeed MA, Elhassani SB, Clarkson TW, Greenwood MR, Doherty RA. Prenatal methylmercury poisoning. Clinical observations over five years. Am J Dis Child 1979;133(2):172-7. PMID 84530
17: Amin-Zaki L, Majeed MA, Greenwood MR, Elhassani SB, Clarkson TW, Doherty RA. Methylmercury poisoning in the Iraqi suckling infant: a longitudinal study over five years. J Appl Toxicol 1981;1(4):210-4. PMID 6892222
18: Anonymous. John Henry Bell MD MRCS. BMJ 1906;2(2386):735-6.
19: Anonymous. Ernest Septimus Reynolds MD FRCP. BMJ 1926;1:969.
20: Anonymous. “Jake” paralysis. N Engl J Med 1930;202(11):541.
21: Anonymous. Additional cases of Jamaica Ginger paralysis recently reported. N Engl J Med 1931;204(8):399.
22: Anonymous. “Ginger poison.” JAMA 1933;100(12):974.
23: Anonymous. Dr. Maurice I Smith retires after 30 years. NIH Record 1950;2(4):3.
24: Anonymous. Dr. Elvove, famed scientist, retires. NIH Record 1953:5(6):1.
25: Anonymous. Murder on the metro. Nature 1995;374(6521):392. PMID 7700333
26: Anonymous. Methanol-laced moonshine kills 140 in Kenya. Lancet 2000;2:1911.
27: Anwar M, Kasper A, Steck AR, Schier JG. Bongkrekic acid-a review of a lesser-known mitochondrial toxin. J Med Toxicol 2017;13(2):173-9. PMID 28105575
28: Aring CD. The systemic nervous affinity of triorthocresyl phosphate (jamaica ginger palsy). Brain 1942;65(1):34-47.
29: Bakir F, Al-Shahristani H, Al-Rawi NY, Khadouri A, Al-Mufti AW. Indirect sources of mercury poisoning in the Iraqi epidemic. Bull World Health Organ 1976;53 Suppl(Suppl):129-32. PMID 1086161
30: Bakir F, Damluji SF, Amin-Zaki L, et al. Methylmercury poisoning in Iraq. Science 1973;181(4096):230-41. PMID 4719063
31: Bakir F, Rustam H, Tikriti S, Al-Damluji SF, Shihristani H. Clinical and epidemiological aspects of methylmercury poisoning. Postgrad Med J 1980;56(651):1-10. PMID 7383945
32: Baskerville C. Wood alcohol: a report on the chemistry, technology and pharmacology of and the legislation pertaining to methyl alcohol. Reprint of appendix VI to second report of the New York State Factory Investigating Commission, submitted to the legislature January 15, 1913. Albany, New York: J B Lyons Company, 1913.
33: Bennett C. A group of patients suffering from paralysis due to drinking Jamaica ginger. South Med J 1930;23(5):371-4.
34: Bennett IL, Cary FH, Mitchell GL, Cooper MN. Acute methyl alcohol poisoning: a review based on experiences in an outbreak of 323 cases. Medicine (Baltimore) 1953;32(4):431-63. PMID 13110604
35: Bodo B. The poisoning women of Tiszazug. J Fam Hist 2002a;27(1):40-59. PMID 11789522
36: Bodo B. Tiszazug: a social history of a murder epidemic. Boulder: East European Monographs, 2002b:185-6.
37: Bowden DT. The incidence of “Jake” paralysis in Oklahoma. Am J Public Health 1930;20(11):1179-86.
38: Buller F, Wood CA. Poisoning by wood alcohol: cases of death and blindness from Columbian Spirits and other methylated preparations. J Am Med Assoc 1904;43:1058-296.
39: Burley BT. Polyneuritis from tricresyl phosphate. JAMA 1932;98(4):298-304.
40: Chaudhuri RN. Paralytic disease caused by consumption of flour contaminated with tricresyl phosphate. Trans R Soc Trop Med Hyg 1965;59:98-102. PMID 14287628
41: Clarkson TW, Amin-Zaki L, Al-Tikriti SK. An outbreak of methylmercury poisoning due to consumption of contaminated grain. Fed Proc 1976;35(12):2395-9. PMID 964390
42: Clarkson TW, Magos L, Cox C, et al. Tests of efficacy of antidotes for removal of methylmercury in human poisoning during the Iraq outbreak. J Pharmacol Exp Ther 1981;218(1):74-83. PMID 7241391
43: Cooper CE, Brown GC. The inhibition of mitochondrial cytochrome oxidase by the gases carbon monoxide, nitric oxide, hydrogen cyanide and hydrogen sulfide: chemical mechanism and physiological significance. J Bioenerg Biomembr 2008;40(5):533-9. PMID 18839291
44: Copping M. Death in the beer-glass: the Manchester arsenic-in-beer epidemic of 1900-1 and the long-term poisoning of beer. Brewing History 2009;132:31-57.
45: Coulomb B. The Morhange talc affair (1972-1981). VIEW Journal of European Television History and Culture 2020;9(18):1-13.
46: Cox C, Clarkson TW, Marsh DO, Amin-Zaki L, Tikriti S, Myers GG. Dose-response analysis of infants prenatally exposed to methyl mercury: an application of a single compartment model to single-strand hair analysis. Environ Res 1989;49(2):318-32. PMID 2473897
47: Crandall FG. Paralysis-from spurious Jamaica ginger extract: report on Los Angeles County outbreak. Cal West Med 1931;35(3):180-2. PMID 18741869
48: Critchley M. Orthocresyl phosphate poisoning. Lancet 1946;1:253.
49: Croddy E. Rat poison and food security in the People’s Republic of China: Focus on tetramethylene disulfotetramine (tetramine). Arch Toxicol 2004;78(1):1-6. PMID 14551672
50: Dakeishi M, Murata K, Grandjean P. Long-term consequences of arsenic poisoning during infancy due to contaminated milk powder. Environ Health 2006;5:31. PMID 17076881
51: Delepine S, Tattersall CH, Crawshaw JW, et al. The epidemic of peripheral neuritis traced to arsenical contamination of beer-making materials. BMJ 1900;2(2083):1587-94.
52: Denis DR. Jakewalk in Vietnam. Ann Intern Med 1977;86:665-6.
53: Dudley BT. The 1930 type of polyneuritis. N Engl J Med 1930;202(24):1139-42.
54: Dyer P. The 1900 arsenic poisoning epidemic. Brewery History 2009;130:65-85.
55: Fee E, Brown TM. John Henry Bell: Occupational Anthrax Pioneer. Am J Public Health 2002;92(5):756-7.
56: Galmiche B. L'affaire de la poudre Baumol: le souvenir de 82 bébés. Accessed June 21, 2024. https://france3-regions.francetvinfo.fr/bretagne/l-affaire-de-la-poudre-baumol-le-souvenir-de-82-bebes-941502.html. Franceinfo, 2016.
57: Gardner W. Jamaica ginger paralysis. South Med J 1931;24(2):97-101.
58: Geoffroy H, Pascal P, Slomic A. [On the “poisoning epidemic” of 1959 in Meknes, Morocco. (Mass poisoning caused by cresyl phosphate)]. Munch Med Wochenschr 1960;102:1494-504. PMID 13827342
59: Goodale RH, Humphreys MB. Jamaica ginger paralysis: autopsy observations. JAMA 1931;96(1):14-16.
60: Green RJ. A Foreword to the IFFR Report. Accessed August 22, 2021. https://phdn.org/archives/holocaust-history.org/auschwitz/chemistry/iffr/index.shtml. January 19, 2000.
61: Greenwood MR. Methylmercury poisoning in Iraq. An epidemiological study of the 1971-1972 outbreak. J Appl Toxicol 1985;5(3):148-59. PMID 4008862
62: Gudo ES, Cook K, Kasper AM, et al. Description of a mass poisoning in a rural district in Mozambique: The first documented bongkrekic acid poisoning in Africa. Clin Infect Dis 2018;66(9):1400-6. PMID 29155976
63: Habermann H. Das spastische Syndrom bei der o-Trikresylphosphatvergiftung [Spastic syndrome in o-tricresyl phosphate poisoning]. Dtsch Med Wochenschr 1948;73(9-12):122-4. PMID 18914565
64: Han D, Chen J, Chen W, Wang Y. Bongkrekic acid and Burkholderia gladioli pathovar cocovenenans: formidable foe and ascending threat to food safety. Foods 2023;12(21):3926. PMID 37959045
65: Harris S. Jamaica ginger paralysis (a peripheral polyneuritis). South Med J 1930;23(5):375-80.
66: Hassanian-Moghaddam H, Nikfarjam A, Mirafzal A, et al. Methanol mass poisoning in Iran: role of case finding in outbreak management. J Public Health (Oxf) 2015;37(2):354-9. PMID 24944254
67: Hermann K, Le Roux A, Fiddes FS. Death from apiol used as abortifacient. Lancet 1956;270(6929):937-9. PMID 13320936
68: Hiltermann JR. A Poisonous Affair: America, Iraq, and the Gassing of Halabja. Cambridge University Press, 2007.
69: Hoffman A, Eisenkraft A, Finkelstein A, Schein O, Rotman E, Dushnitsky T. A decade after the Tokyo sarin attack: a review of neurological follow-up of the victims. Mil Med 2007;172(6):607-10. PMID 17615841
70: Hood E. The Tokyo attacks in retrospect: sarin leads to memory loss. Environ Health Perspect 2001;109(11):A542. PMID 11762311
71: Hotson RD. Outbreak of polyneuritis due to orthotricresyl phosphate poisoning. Lancet 1946;1:207.
72: Hovda KE, Hunderi OH, Tafjord AB, Dunlop O, Rudberg N, Jacobsen D. Methanol outbreak in Norway 2002-2004: epidemiology, clinical features and prognostic signs. J Intern Med 2005;258(2):181-90. PMID 16018795
73: Inoue N, Fujishiro K, Mori K, Matsuoka M. Triorthocresyl phosphate poisoning--a review of human cases. J UOEH 1988;10(4):433-42. PMID 3062730
74: Jackson J, Stratton JW, Goldman LR, et al. Aldicarb food poisoning from contaminated melons--California. MMWR Morbidity and Mortality Weekly Report 1986;35(16):254-8. PMID 3083232
75: Jalili MA, Abbasi AH. Poisoning by ethyl mercury toluene sulphonanilide. Br J Ind Med 1961;18(4):303-8. PMID 14450973
76: Jarwani BS, Motiani PD, Sachdev S. Study of various clinical and laboratory parameters among 178 patients affected by hooch tragedy in Ahmedabad, Gujarat (India): a single-center experience. J Emerg Trauma Shock 2013;6(2):73-7. PMID 23723613
77: Kato T, Hamanaka T. Ocular signs and symptoms caused by exposure to sarin gas. Am J Ophthalmol 1996;121(2):209-10. PMID 8623892
78: Kawada T, Katsumata M, Suzuki H, et al. Insomnia as a sequela of sarin toxicity several years after exposure in Tokyo subway trains. Percept Mot Skills 2005;100(3 Pt 2):1121-6. PMID 16158698
79: Kawana N, Ishimatsu S, Kanda K. Psycho-physiological effects of the terrorist sarin attack on the Tokyo subway system. Mil Med 2001;166(12 Suppl):23-6. PMID 11778423
80: Kazantzis G, Al-Mufti AW, Al-Jawad A, et al. Epidemiology of organomercury poisoning in Iraq. II. Relationship of mercury levels in blood and hair to exposure and to clinical findings. Bull World Health Organ 1976;53 Suppl(Suppl):37-48. PMID 1086165
81: Kelvin WT, Hart Dyke W, Church WS, Thorpe TE, Cosmo Bonsor H, Whitelegge BA. Final report of the Royal Commission appointed to inquire into arsenical poisoning from the consumption of beer and other articles of food or drink. London: His Majesty's Stationary Office, 1903a.
82: Kelvin WT, Hart Dyke W, Church WS, Thorpe TE, Cosmo Bonsor H, Whitelegge BA. The final report of the Royal Commission on arsenical poisoning. Lancet 1903b;2:1674-8.
83: Kelynack TN, Kirkby W, Delépine S, Tattersall CH. Arsenical poisoning from beer drinking. Lancet 1900;2:1600-3.
84: Kelynack TN, Kirkby W. Arsenical poisoning in beer drinkers. London: Baillière, Tindall and Cox, 1901.
85: Khalili MR, Sadati MS, Jahanbani-Ardakani H. Outbreak of methanol-induced optic neuropathy amid COVID-19 pandemic. Graefes Arch Clin Exp Ophthalmol 2021;259(5):1375-6. PMID 32910310
86: Kidd JG, Langworthy OR. Jake paralysis: paralysis following the ingestion of Jamaica ginger extract adulterated with tri-ortho-cresyl phosphate. Bull Johns Hopkins Hosp 1933;52:39-65.
87: Kiely CE, Rich ML, Vonderahe AR. An epidemic of motor neuritis in Cincinnati, Ohio, due to drinking adulterated Jamaica ginger. Public Health Reports 1932;47(42):2039-63.
88: Krishnamurthy MV, Natarajan AR, Shanmugasundaram K, Padmanabhan K, Nityanandan K. Acute methyl alcohol poisoning: A review of an outbreak of 89 cases. J Assoc Phys India 1968;16(10):801-5. PMID 5715506
89: Le Douget A. Enquête sur le scandale de la poudre Baumol (1951-1959), la première catastrophe sanitaire française [An investigation into the Baumol powder scandal (1951-1959), the first French health catastrophe]. Fouesnant: Le Douget, 2016.
90: Le Joliff JC. The talc saga. Accessed June 21, 2024. https://cosmetotheque.com/en/2019/11/07/the-talc-saga. La Cosmétothèque, 2019.
91: Lee J. Poisoned Bread: The Esing Bakery incident of 1857 and racism in colonial Hong Kong. Armstrong Undergrad J History 2021;11(2):1-39.
92: Lowe K, McLaughlin E. “Caution! The bread is poisoned”: The Hong Kong mass poisoning of January 1857. Journal Imperial Commonwealth History 2015;43(2):189-209.
93: Maghazaji HI. Psychiatric aspects of methylmercury poisoning. J Neurol Neurosurg Psychiatry. 1974;37(8):954-8. PMID 4420813
94: Markiewicz L, Gubala W, Labedz J. A study of the cyanide compounds content in the walls of the gas chambers in the former Auschwitz and Birkenau concentration camps. Available at: https://phdn.org/archives/holocaust-history.org/auschwitz/chemistry/iffr/report.shtml. Accessed August 22, 2021. Z Zagadnien Nauk Sadowych [Problems of Forensic Sciences] 1994;30:17-27.
95: Martin-Bouyer G, Lebreton R, Toga M, Stolley PD, Lockhart J. Outbreak of accidental hexachlorophene poisoning in France. Lancet 1982;1(8263):91-5. PMID 6119504
96: Martin-Bouyer G, Stolley PD. Hexachlorophene poisoning. Lancet 1982;1(8281):1121. PMID 6122909
97: Mashallahi A, Mohamadkhani M, Ostadtaghizadeh A. Methanol poisoning outbreaks in Southern Iran in 2018: a lesson learned. Iran J Public Health 2021;50(7):1502-3. PMID 34568196
98: Merritt HH, Moore M. Peripheral neuritis associated with ginger extract ingestion. N Engl J Med 1930;203(1):4-12.
99: Mertens HG. Zur Klinik der Triorthokresylphosphatvergiftungen. (Zugleich Bericht über mehrere Fülle von Vergiftungen in einem Igelitherstellungsbetrieb.) [Clinical aspects of tri-orthocrésyl phosphate poisoning (including a report on several cases of poisoning in an Igelit factory). Note: Igelit was a type of soft polyvinyl chloride manufactured in the late 1930s by IG Farben, Germany.] Arch Psychiatr Nervenkr 1948;179:458-82.
100: Mirzaee V, Riahi Z, Sharifzahed Z, Parizi MK, Pour AA. Survey on methanol poisoning epidemic in Rafsanjan City in Year 2013. IMMINV 2017;2(3):84-9.
101: Mittal BV, Desai AP, Khade KR. Methyl alcohol poisoning: an autopsy study of 28 cases. J Postgrad Med 1991;37(1):9-13. PMID 1941700
102: Miyaki K, Nishiwaki Y, Maekawa K, et al. Effects of sarin on the nervous system of subway workers seven years after the Tokyo subway sarin attack. J Occup Health 2005;47(4):299-304. PMID 16096354
103: Moghadami M, Masoumpoor M, Tabei SM, et al. Therapeutic response to folinic acid in methanol poisoning epidemic in Shiraz. IJMS 2008;33(1):22-6.
104: Morgan JP. The Jamaica ginger paralysis. JAMA 1982;248(15):1864-7. PMID 6750161
105: Morgan JP, Penovich P. Jamaica ginger paralysis; forty-seven-year follow-up. Arch Neurol 1978;35(8):530-2. PMID 666613
106: Morgan JP, Tulloss TC. The Jake Walk Blues: a toxicologic tragedy mirrored in American popular music. Ann Intern Med 1976;85(6):804-8. PMID 793467
107: Morita H, Yanagisawa N, Nakajima T, et al. Sarin poisoning in Matsumoto, Japan. Lancet 1995;346(8970):290-3. PMID 7630252
108: Munsey C. Paralysis in a bottle (The “Jake Walk” story). Bottles and Extras 2006;Winter:7-12.
109: Murata K, Araki S, Yokoyama K, et al. Asymptomatic sequelae to acute sarin poisoning in the central and autonomic nervous system 6 months after the Tokyo subway attack. J Neurol 1997;244(10):601-6. PMID 9402534
110: Myers GJ, Davidson PW, Cox C, Shamlaye C, Cernichiari E, Clarkson TW. Twenty-seven years studying the human neurotoxicity of methylmercury exposure. Environ Res 2000;83(3):275-85. PMID 10944071
111: Nakajima T, Ohta S, Fukushima Y, Yanagisawa N. Sequelae of sarin toxicity at one and three years after exposure in Matsumoto, Japan. J Epidemiol 1999;9(5):337-43. PMID 10616267
112: Nakajima T, Ohta S, Morita H, Midorikawa Y, Mimura S, Yanagisawa N. Epidemiological study of sarin poisoning in Matsumoto City, Japan. J Epidemiol 1998;8(1):33-41. PMID 957569
113: Nakajima T, Sato S, Morita H, Yanagisawa N. Sarin poisoning of a rescue team in the Matsumoto sarin incident in Japan. Occup Environ Med 1997;54(10):697-701. PMID 9404315
114: National Research Council Committee on Neurotoxicology and Models for Assessing Risk. Environmental Neurotoxicology. Washington (DC): National Academies Press (US), 1992. PMID 25121283
115: Nishiwaki Y, Maekawa K, Ogawa Y, et al. Effects of sarin on the nervous system in rescue team staff members and police officers 3 years after the Tokyo subway sarin attack. Environ Health Perspect 2001;109(11):1169-73. PMID 11713003
116: Nozaki H, Aikawa N, Shinozawa Y, et al. Sarin poisoning in Tokyo subway. Lancet 1995a;345(8955):980-1. PMID 7715305
117: Nozaki H, Hori S, Shinozawa Y, et al. Secondary exposure of medical staff to sarin vapor in the emergency room. Intensive Care Med 1995b;21(12):1032-5. PMID 8750130
118: Ohbu S, Yamashina A, Takasu N, et al. Sarin poisoning on Tokyo subway. South Med J 1997;90(6):587-93. PMID 9191733
119: Ohtani T, Iwanami A, Kasai K, et al. Post-traumatic stress disorder symptoms in victims of Tokyo subway attack: a 5-year follow-up study. Psychiatry Clin Neurosci 2004;58(6):624-9. PMID 15601387
120: Okudera H. Clinical features on nerve gas terrorism in Matsumoto. J Clin Neurosci 2002;9(1):17-21. PMID 11749011
121: Okudera H, Morita H, Iwashita T, et al. Unexpected nerve gas exposure in the city of Matsumoto: report of rescue activity in the first sarin gas terrorism. Am J Emerg Med 1997;15(5):527-8. PMID 9270397
122: Okumura T, Hisaoka T, Naito T, et al. Acute and chronic effects of sarin exposure from the Tokyo subway incident. Environ Toxicol Pharmacol 2005;19(3):447-50. PMID 21783510
123: Okumura T, Takasu N, Ishimatsu S, et al. Report on 640 victims of the Tokyo subway sarin attack. Ann Emerg Med 1996;28(2):129-35. PMID 8759575
124: Onyekwere N, Nwadiuto I, Maleghemi S, et al. Methanol poisoning in South-South Nigeria: reflections on the outbreak response. J Public Health Afr 2018;9(1):748. PMID 30079165
125: Paasma R. Clinical study of methanol poisoning: handling large outbreaks, treatment with antidotes, and long-term outcomes. Tartu, Estonia: University of Tartu Press, 2013.
126: Paasma R, Hovda KE, Jacobsen D. Methanol poisoning and long term sequelae--a six years follow-up after a large methanol outbreak. BMC Clin Pharmacol 2009;9:5. PMID 19327138
127: Paasma R, Hovda KE, Tikkerberi A, Jacobsen D. Methanol mass poisoning in Estonia: outbreak in 154 patients. Clin Toxicol (Phila) 2007;45(2):152-7. PMID 17364632
128: Parascandola J. Pharmacology and public health: the Jamaica ginger paralysis episode of the 1930s. Pharm Hist 1994;36(3):123-31. PMID 11613494
129: Parascandola J. The Public Health Service and Jamaica ginger paralysis in the 1930s. Public Health Rep 1995;110(3):361-3. PMID 7610232
130: Perl TM, Bédard L, Kosatsky T, Hockin JC, Todd EC, Remis RS. An outbreak of toxic encephalopathy caused by eating mussels contaminated with domoic acid. N Engl J Med 1990;322(25):1775-80. PMID 1971709
131: Pfenninger A. [Poisoning in Morocco by tricresylphosphate: a myo-myelo-polyneuritis]. Rev Med Suisse Romande 1962;82:355-72. PMID 14486137
132: Phillips J, French M. The Pure Beer Campaign and arsenic poisoning, 1896-1903. Brewery History 1998;9(2):195-209.
133: Pinkus F. Die Massenerkranungen im Städtischen Asyl für Obdachlose in Berlin, 24. bis 31, 1911. Medizinische Klinik Wochenschrift für Praktische Ärzte 1912;8(1):41-6.
134: Primeau B. The rehabilitation of 10,000 victims of paralysis in Morocco by the League of Red Cross societies. Can Med Assoc J 1961;85(23):1249-52. PMID 14488784
135: Quinn LJ, Harris C, Joron GE. Apiol Poisoning. Can Med Assoc J 1958;78(8):635-6. PMID 20325694
136: Ran M, Li Y, Zhang L, et al. Clinical features, treatment, and prognosis of acute methanol poisoning: experiences in an outbreak. Int J Clin Exp Med 2019;12(5):5938-50.
137: Raw N, Barendt FH, Warrington WB. Epidemic arsenical poisoning amongst beer drinkers. Lancet 1901;1:10-12.
138: Reynolds ES. An epidemic of peripheral neuritis amongst beer drinkers in Manchester and district. Lancet 1900;2:1492-3.
139: Reynolds ES. An account of the epidemic outbreak of arsenical poisoning occurring in beer drinkers in the North of England and the Midland Counties in 1900. Med Chir Trans 1901;84:409-52. PMID 20896969
140: Roger H, Recordier M. Les polynévrites phosphocréosotiques (phosphate de créosote, ginger paralysis, apiol). Ann. Med 1934;35:44-63.
141: Rostrup M, Edwards JK, Abukalish M, et al. The methanol poisoning outbreaks in Libya 2013 and Kenya 2014. PLoS One 2016;11(3):e0152676. PMID 27030969
142: Rulisek J, Balik M, Polak F, et al. Cost-effectiveness of hospital treatment and outcomes of acute methanol poisoning during the Czech Republic mass poisoning outbreak. J Crit Care 2017;39:190-8. PMID 28291652
143: Salahshour B, Sadeghi S, Soltaninejad K. Analysis of methanol content in fake alcoholic beverages during a methanol mass poisoning outbreak (Bojnourd- Northeast of Iran, 2018). Asia Pac J Med Toxicol 2020;9(4):142-9.
144: Sampson BF. The strange Durban epidemic of 1937. S Afr Med J 1942;16:1-9.
145: Sefidbakht S, Lotfi M, Jalli R, Moghadami M, Sabetian G, Iranpour P. Methanol toxicity outbreak: when fear of COVID-19 goes viral. Emerg Med J 2020;37(7):416. PMID 32414710
146: Sekijima Y, Morita H, Yanagisawa N. Follow-up of sarin poisoning in Matsumoto. Ann Intern Med 1997;127(11):1042. PMID 9412293
147: Senanayake N. Tri-cresyl phosphate neuropathy in Sri Lanka: a clinical and neurophysiological study with a three year follow up. J Neurol Neurosurg Psychiatry 1981;44(9):775-80. PMID 7310416
148: Senanayake N, Jeyaratnam J. Toxic polyneuropathy due to gingili oil contaminated with tri-cresyl phosphate affecting adolescent girls in Sri Lanka. Lancet 1981;1(8211):88-9. PMID 6109132
149: Shah S, Pandey V, Thakore N, Mehta I. Study of 63 cases of methyl alcohol poisoning (hooch tragedy in Ahmedabad). J Assoc Physicians India 2012;60:34-6. PMID 23029719
150: Shokoohi M, Nasiri N, Sharifi H, Baral S, Stranges S. A syndemic of COVID-19 and methanol poisoning in Iran: time for Iran to consider alcohol use as a public health challenge? Alcohol 2020;87:25-7. PMID 32505493
151: Smith HV, Spalding JM. Outbreak of paralysis in Morocco due to ortho-cresyl phosphate poisoning. Lancet 1959;2:1019-21.
152: Smith J. The Shipman Inquiry. Accessed June 21, 2024. https://webarchive.nationalarchives.gov.uk/ukgwa/20090808163914mp_/http://www.the-shipman-inquiry.org.uk/images/sixthreport/SHIP06_COMPLETE_NO_APPS.pdf Sixth Report - Shipman: The Final Report, 2005.
153: Smith JC, Farris FF, Burg R. Chemical type of mercury in patients in the outbreak of organomercury poisoning in Iraq. Bull World Health Organ 1976;53 Suppl(Suppl):61-3. PMID 1086167
154: Smith MI. The pharmacological action of certain phenol esters, with special reference to the etiology of so-called ginger paralysis. Public Health Reports 1930;45(42):2509-24.
155: Smith MI. The estimation of tissue phenols: the distribution of phenol in the tissues of the normal and of the poisoned rabbit. Public Health Reports 1933a;48(5):1487-96.
156: Smith MI. Further studies on the pharmacology and neuropathology of certain phenol esters. Public Health Reports 1933b;48(6):137-8.
157: Smith MI. Triorthocresyl phosphate and polyneuritis. JAMA 1934;102(26):2045-6.
158: Smith MI, Elvove E. The epidemic of so-called ginger paralysis in Southern California in 1930-31. Public Health Reports 1931;46:1227-35.
159: Smith MI, Elvove E, Frazier WH. The pharmacological action of certain phenol esters, with special reference to the etiology of so-called ginger paralysis (Second Report). Public Health Reports 1930b;45:2509-24.
160: Smith MI, Elvove E, Valaer PJ, Frazier WH, Mallory GE. Pharmacological and chemical studies of the cause of so-called ginger paralysis: a preliminary report. Public Health Reports 1930a;45:1703-16.
161: Smith MI, Engel EW, Stohlman EF. Further studies on the pharmacology of certain phenol esters with special reference to the relation of chemical constitution and physiologic action. Washington DC: National Institute of Health Bulletin 1932;160:1-53.
162: Smith MI, Lillie RD. The histopathology of triorthocresyl phosphate poisoning: the etiology of so-called ginger paralysis (Third Report). Arch Neurol Psychiatr 1931;26:976-92.
163: Smith MI, Lillie RD, Elvove E, Stohlman EG. The pharmacologic action of the phosphorous acid esters of the phenols. J Pharmacol Exper Ther 1933;49(1):78-99.
164: Smith MI, Stohlman EF. The hydrolysis of the phenyl and cresyl phosphoric and phosphorous acid esters in alcoholic and aqueous systems. Public Health Reports 1933;48:734-9.
165: Smith MI, Stohlman EG. A comparative pharmacologic study of the three phosphoric esters of orthocresol. J Pharmacol Exper Ther 1934;51(2):217-36.
166: Soltaninejad K. Methanol mass poisoning outbreak: a consequence of COVID-19 pandemic and misleading messages on social media. Int J Occup Environ Med 2020;11(3):148-50. PMID 32225177
167: Sorokin M. Orthocresyl phosphate neuropathy: report of an outbreak in Fiji. Med. J Aust 1969;1:506-8.
168: Spencer PS, Schaumburg HH. Experimental and Clinical Neurotoxicology. Baltimore: Williams & Wilkins, 1980.
169: Srivastava AK, Das M, Khanna SK. An outbreak of tricresyl phosphate poisoning in Calcutta, India. Food Chem Toxicol 1990;28(4):303-4. PMID 2358255
170: Stadelman, Magnus-Levy A. Ueber die in der Weihnachtszeit 1911 in Berlin vorgekommenen Massenvergiftungen, Berliner Klinische Wochemschrift 1912;49(5):193-8.
171: Sugiyama A, Matsuoka T, Sakamune K, et al The Tokyo subway sarin attack has long-term effects on survivors: a 10-year study started 5 years after the terrorist incident. PLoS One 2020;15(6):e0234967. PMID 32574198
172: Susser M, Stein Z. An outbreak of tri-ortho-cresyl phosphate (T.O.C.P.) poisoning in Durban. Br J Ind Med 1957;14(2):111-20. PMID 13426434
173: Suzuki J, Kohno T, Tsukagosi M, Furuhata T, Yamazaki K. Eighteen cases exposed to sarin in Matsumoto, Japan. Intern Med 1997;36(7):466-70. PMID 9240494
174: Suzuki T, Morita H, Ono K, Maekawa K, Nagai R, Yazaki Y. Sarin poisoning in Tokyo subway. Lancet 1995;345(8955):980. PMID 7715304
175: Taleb ZB, Bahelah R. Viewpoint: methanol poisoning outbreak in Libya: a need for policy reforms. J Public Health Policy 2014;35(4):489-98. PMID 24831674
176: Ter Braak JW. Een 'epidemie' van polyneuritis van bijzonderen oorsprong. Nederlands Tijdschrift voor Geneeskunde 1931;75:2329-39.
177: Tosi L, Righetti C, Adami L, Zanette G. October 1942: a strange epidemic paralysis in Saval, Verona, Italy. Revision and diagnosis 50 years later of tri-ortho-cresyl phosphate poisoning. J Neurol Neurosurg Psychiatry 1994;57(7):810-3. PMID 8021666
178: Travers PR. The results of intoxication with orthocresyl phosphate absorbed from contaminated cooking oil, as seen in 4,029 patients in Morocco. Proc R Soc Med 1962;55(1):57-60. PMID 13922340
179: Vale A. What lessons can we learn from the Japanese sarin attacks? Przegl Lek 2005;62(6):528-32. PMID 16225116
180: Valear P. Discovery of toxic ingredient in Jamaica ginger. JAMA 1933;100(18):1450.
181: Vasilescu C. Motor nerve conduction velocity and electromyogram in triorthocresyl-phosphate poisoning. Rev Roum Neurol 1972;9(5):345-50. PMID 4664802
182: Vasilescu C. Triorthocresyl phosphate neuropathy. Arch Neurol 1979;36(7):455. PMID: 454258
183: Vasilescu C. Neuropathy after organophosphorus compounds poisoning. J Neurol Neurosurg Psychiatry 1982;45(10):942. PMID 7143020
184: von Albertini A, Gross D, Zinn WM, Ragaz B. Triaryl-Phosphate Poisoning in Morocco 1959. Experiences and Findings. Stuttgart: Georg Thieme. New York: Intercontinental Medical Book Corporation, 1968.
185: von Keyserlingk H. Nervenerkrankungen nach Oelvergiftungen (Triorthokresylphosphat) [Nerve diseases after oil poisoning (triorthocresyl phosphate)]. Med Klin 1947;42(1):27-9. PMID 20241217
186: Vonderahe AR. Pathologic changes in paralysis caused by drinking Jamaica ginger. Arch Neur Psych 1931;25(1):29-43.
187: Vora DD, Dastur DK, Braganca BM, et al. Toxic polyneuritis in Bombay due to ortho-cresyl-phosphate poisoning. J Neurol Neurosurg Psychiatry 1962;25:234-42. PMID 13926733
188: Walthard B. Zur Histologie der Triorthokresylphosphatvergiftung [On the histology of triorthocresyl phosphate poisoning]. Schweiz Arch Neurol Psychiatr 1946a;58(1):188. PMID 20297212
189: Walthard KM. Aperçu des résultats obtenus lors des derniers examens des malades intoxiqués en 1940 par le phosphate tri-orthocrésilique [An overview of the results obtained during the last examinations of patients intoxicated in 1940 by tri-orthocresilic phosphate]. [French]. Schweiz Arch Neurol Psychiatr 1946b;58(1):189-94. PMID 20297213
190: Wang L, Liu YH, Xu Y, Yin W, Huang YG. Thirteen-year follow-up of patients with tri-ortho-cresyl phosphate poisoning in northern suburbs of Xi'an in China. Neurotoxicology 2009;30(6):1084-7. PMID 19576241
191: Weiss B, Clarkson TW. Toxic chemical disasters and the implications of Bhopal for technology transfer. Milbank Q 1986;64(2):216-40. PMID 3520276
192: Weterings V. Swanenburg, Maria Catharina (1839-1915). Digitaal Vrouwenlexicon van Nederland. Amsterdam: Huygens ING, 2019.
193: Wood CA, Buller F. Poisoning by wood alcohol: cases of death and blindness from Columbian spirits and other methylated preparations. JAMA 1904:43: 972-7.
194: Woodall J. Tokyo subway gas attack. Lancet 1997;350(9073):296. PMID 9242833
195: Woolf AD. Ginger Jake and the blues: a tragic song of poisoning. Vet Human Toxicol 1995;37(3):252-4.
196: World Health Organization. Environmental health criteria for tricresyl phosphate. Geneva: World Health Organization 1990.
197: World Health Organization. Methanol poisoning emergency in Nicaragua. PAHO/WHO Emergencies News 2006:105:1.
198: Wright D. Arsenic at St. Andrews, 1943. Med Hist 1983;27(2):184-5. PMID 6345965
199: Yanagisawa N, Morita H, Nakajima T. Sarin experiences in Japan: acute toxicity and long-term effects. J Neurol Sci 2006;249(1):76-85. PMID 16962140
200: Zakharov S, Kurcova I, Navratil T, Salek T, Komarc M, Pelclova D. Is the measurement of serum formate concentration useful in the diagnostics of acute methanol poisoning? A prospective study of 38 patients. Basic Clin Pharmacol Toxicol 2015a;116(5):445-51. PMID 25308806
201: Zakharov S, Navratil T, Pelclova D. Fomepizole in the treatment of acute methanol poisonings: experience from the Czech mass methanol outbreak 2012-2013. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2014c;158(4):641-9. PMID 25482738
202: Zakharov S, Nurieva O, Kotikova K, Belacek J, Navratil T, Pelclova D. Positive serum ethanol concentration on admission to hospital as the factor predictive of treatment outcome in acute methanol poisoning. Monatsh Chem 2017;148(3):409-9. PMID 28344362
203: Zakharov S, Pelclova D, Navratil T, et al. Intermittent hemodialysis is superior to continuous veno-venous hemodialysis/hemodiafiltration to eliminate methanol and formate during treatment for methanol poisoning. Kidney Int 2014a;86(1):199-207. PMID 24621917
204: Zakharov S, Pelclova D, Navratil T, et al. Fomepizole versus ethanol in the treatment of acute methanol poisoning: Comparison of clinical effectiveness in a mass poisoning outbreak. Clin Toxicol (Phila) 2015b;53(8):797-806. PMID 26109326
205: Zakharov S, Pelclova D, Urban P, et al. Czech mass methanol outbreak 2012: epidemiology, challenges and clinical features. Clin Toxicol (Phila) 2014b;52(10):1013-24. PMID 25345388
206: Zakharov S, Pelclova D, Urban P, et al. Use of out-of-hospital ethanol administration to improve outcome in mass methanol outbreaks. Ann Emerg Med 2016;68(1):52-61. PMID 26875060
207: Zeligs MA. Upper motor neuron sequelae in “Jake” paralysis: a clinical follow up study. J Nerv Ment Dis 1938;87(4):464-70.
208: References especially recommended by the author or editor for general reading.

This is an article preview.
Start a Free Account
to access the full version.

Nearly 3,000 illustrations, including video clips of neurologic disorders.
Every article is reviewed by our esteemed Editorial Board for accuracy and currency.
Full spectrum of neurology in 1,200 comprehensive articles.
Listen to MedLink on the go with Audio versions of each article.

Questions or Comment?

MedLink®, LLC

3525 Del Mar Heights Rd, Ste 304
San Diego, CA 92130-2122

Toll Free (U.S. + Canada): 800-452-2400

US Number: +1-619-640-4660

Support: service@medlink.com

Editor: editor@medlink.com

ISSN: 2831-9125

Mass poisoning events with neurotoxic agents

Also Relevant

Arsenic neuropathy
Carbon monoxide poisoning
Hexacarbon neuropathy
Lathyrism, konzo, and tropical ataxic neuropathy
Lead neuropathy
- Lead poisoning in childhood
- Mercury neuropathy
- Metal neurotoxicity
- Methanol poisoning
- Neurologic disorders related to chemical warfare nerve agents
- Organophosphate neuropathy
- Shellfish poisoning
- Toxic peripheral neuropathies

Clinical Categories

Neurotoxicology

Mass poisoning events with neurotoxic agents

Introduction

Overview

Key points

Description

Table 1. Categorization of Mass Poisoning Events*

Adulteration

The Plague of Adulteration: A Popular Complaint to a Popular Air

Clinical applications

Adulteration

Table 2. Mass Poisoning Due to Adulteration with Arsenicals

Table 3. Mass Poisoning Events with Triorthocresyl Phosphate (TOCP) *

Contamination

Table 4. Mass Poisoning by Contamination with Arsenicals

Table 5. Mass Poisoning by Contamination with Organomercury Compounds

Table 6. Pesticide Mass Poisoning Events

Table 7. Mass Poisoning Due to Contamination with Hexachorobenzene

Table 8. Mass Poisoning Due to Contamination with Hexachlorophene

Table 9. Mass Poisoning Due to Contamination of Mussels with Domoic Acid

Table 10. Mass Poisoning Due to Contamination with Bongkrekic Acid

Recreational exposures associated with mass poisoning

Table 11. Recreational Mass Poisoning with Neurotoxic Poisons (Methanol)

Non-terrorism mass murder by poisoning

Table 12. Non-Terrorism Mass Murder by Poisoning with Neurotoxic Substances

Terrorism-related mass poisoning with neurotoxic poisons

Table 13. Use of Neurotoxic Poisons in Terrorism

War crimes using neurotoxic agents for mass poisoning

Table 14. Use of Neurotoxic Poisons in War Crimes

Genocide using neurotoxic agents for mass poisoning

Table 15. Genocidal Poisoning with Neurotoxic Agents

Unclassifiable or unclear

Table 16. Unclassifiable Poisoning with Neurotoxic Agents

Media

References

Contributors

Author

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Metal neurotoxicity

Medications and substances causing headache

Mercury neuropathy

Thallium neuropathy

Occupational neurotoxicology: metals

Occupational neurotoxicology: overview

Para-occupational poisoning

Alcohol abuse and its neurologic complications

This is an article preview.
Start a Free Account
to access the full version.