The Poisoner's Handbook

by Deborah Blum

Arguably the three most important atoms on Earth are carbon, oxygen, and hydrogen. Carbon provides the fundamental chemical base of every life-form on the planet, past and present. When fuels derived from the decomposed and fossilized life of the past—such as coal or gasoline—burn, they release carbon into the air. Oxygen is vital to keeping carbon-based life forms alive, barring a few odd creatures like anaerobic bacteria. And if two hydrogen atoms attach to a single oxygen atom, the result—H2O—is that gloriously necessary liquid called water.

  Mixed together, rearranged, and stretched out into long chains, elaborate arrangements, and simple atomic blocks, these three chemicals write the story of life on Earth. They form sugars, proteins, acids, hormones, enzymes—the list is nearly endless. That complex list also includes the familiar and risky family of alcohols.

  The primary alcohols, including methyl and ethyl, are straightforward arrangements of carbon, hydrogen, and oxygen. In the curious way of chemistry, the deadlier of the two compounds is more simply constructed. Methyl alcohol is CH3OH. It begins with a cluster of three hydrogen atoms encircling one of carbon. That cluster is firmly linked to an oxygen-hydrogen pair called a hydroxyl radical. Ethyl is a slightly bulkier compound: C2H5OH. Two carbons and five hydrogens form a chunky arrangement, once again attached to that highly reactive hydroxyl radical.

  Some fancier alcohols have more complicated structures, containing, for instance, more carbon atoms. But such elaborate alcohols were never destined to become the stuff of drinking legends, the magic ingredient in a golden brandy and soda, a copper-hued scotch and water, because they aren’t water soluble. It turns out that the extra carbon interferes with the molecular mixing process.

  The wonderfully soluble, amazingly intoxicating ethyl alcohol, derived from the fermentation of fruits, grains, and even vegetables, is by far the most popular member of the alcohol family. And the most thoroughly studied. Research interest in ethyl alcohol dates back to the eighth century, when alchemists working for the caliph of Baghdad started experimenting with distillation methods, leaving behind detailed observations on the flammable vapors of boiled wine.

  A good thousand years later scientists in nineteenth-century England identified ethyl alcohol’s chemical formula, learned to synthesize it and make it on an industrial scale. Mass-produced ethyl alcohol (also called ethanol) has uses far beyond potable spirits. Denatured, it can be used for everything from solvents to fuel. Even automobiles can run on alcohol; in fact, until Prohibition, the Model T Ford could be, and often was, adapted to run on ethanol. The practice fell out of favor once bootleggers started siphoning off the fuel from cars and repackaging it and the government enforcement division charged ethanol manufacturers with enabling criminal activities.

  Before Prohibition most people wouldn’t have considered drinking fuel alcohol. They had a choice of good corn whiskies like bourbon, grain alcohols from beer to scotch, hard apple cider, and fermented grape products from wine to brandy. When those drinks were legal, the government regulated the amount of alcohol they could contain. Beer, for instance, usually contained 2 to 6 percent alcohol, wine from 7 to 20 percent, and whiskey 40 percent. Bootlegged whiskey was a different matter. Some of the bottles confiscated by the police and analyzed at the Bellevue laboratories were 60 percent alcohol (a staggering 120 proof). And some were nothing but alcohol.

  Depending on one’s perspective, it was one of the benefits, or curses, of ten years of Prohibition: every drink was a stiff one.

  THAT DESCRIPTION took on an ironic meaning when considering corpses of those killed by ethyl alcohol. The cadavers tended, for reasons not quite clear to the pathologists, to stiffen in death, sometimes remaining rigid for days, while the other bodies in the morgue softened like wax on a summer day.

  Perhaps, the medical examiners speculated, that was because the high alcohol content suffusing the bodies preserved them, even pickled them. As Gettler once noted, it takes a determined drinker to imbibe a lethal amount of ethyl alcohol. The liquid lacks the viciously subversive makeup of its chemical cousin, methyl alcohol. If the two were a little more alike, frankly, alcohol consumption would never have caught on.

  When the enzymes in the liver break apart methyl alcohol, the result is the two poisons formic acid and formaldehyde. Ethyl alcohol, by contrast, dissolves rather easily into acetic acid, the bitter but basically harmless compound that is the primary constituent in vinegar, and the acid breaks down further into carbon dioxide and water.

  The graceful disintegration of ethyl alcohol means that, in moderate amounts, it usually metabolizes out of the body without causing any immediate harm or even calling much attention to itself. The risk increases, of course, with continual exposure. Like most alcohols, ethyl is an irritant—too much will inflame the stomach enough to induce nausea and vomiting. It also causes dehydration: “alcohol abstracts water from the tissues and precipitates proteins,” in Gettler’s careful phraseology. Chronic drinking, chronic irritation and dehydration can eventually lead to long-term damage, especially to the liver, which does most of the work in breaking down the alcohol so that it can be moved out of the body.

  As the pathologists in Charles Norris’s department discovered, people who chugged ethyl alcohol often didn’t live long enough to develop the signs of chronic liver destruction. Their autopsies revealed different damage: the stomach and esophagus were a deep, irritated red; tiny blooms of blood patterned the mucous lining of the stomach; the brain was bruised-looking and flushed with excess blood.

  The last fact caught Gettler’s attention, reminding him that alcohol crosses the blood-brain barrier. But what does it actually do once it permeates the brain? For all the bodies gathered up over the years, for all the drinkers scraped off city sidewalks, no one really knew the answer to that question.

  FOR GETTLER and the young chemists studying with him—a next generation of toxicologists who would become known in the profession as the Gettler Boys—the alcohol-poisoned cadavers, those literal stiffs, raised question after intriguing question.

  Pathologists routinely found the bloody evidence of ethyl alcohol damage in bodies collapsed on sidewalks or in stairwells. The city toxicologists routinely extracted alcohol from blood and brain. But they had no way to attach meaning to it. No one had figured out how much alcohol in the blood meant intoxication, much less how to calculate what various alcohol levels in the brain meant. The basic assumption was that of common sense: the higher the alcohol level in the blood, the greater the probable state of drunkenness.

  On the other hand, sometimes one person would appear to be intoxicated by a small amount of alcohol while another would seem remarkably steady even after enjoying a bounty of whiskey or a buffet of cocktails. People might talk of hard heads and experienced drinkers, but such variances made it very difficult for pathologists to figure out whether a man or woman was genuinely impaired by alcohol at the time of death.

  Gettler reasoned that the presence of alcohol in the blood wasn’t true evidence of drunkenness: the bloodstream didn’t affect behavior. It delivered materials to organs, like the brain, that did so. Equally logically, liquor found still sloshing in the stomach could have no impact at all. “It indicates merely that alcohol has been partaken of, but can in no way be taken as an index of intoxication,” Gettler wrote.

  The answer had to lie in the correlation between alcohol levels in the blood and in the brain: how much meant cheerful intoxication, and how much meant falling-down drunk? Along with his Gettler Boys, he decided that now was the right moment to solve the problem, and the fact that they were studying an illegal substance, in the midst of Prohibition, didn’t bother them at all.

  THE BLUES SONGS telling of poison started in 1930. From Tennessee came a mournful plaint of paralysis, a man who couldn’t walk or talk after drinking with friends. From Wisconsin sounded a bitter ode to the drink Ginger Jake. The writer worried that everyone he knew was now messed up by the cocktail.

  The same year, from Mississippi, singer Willie
“Poor Man” Loftus wailed, “Mama cried out and said, Oh Lord, there’s nothin’ in the world poor daddy can do, ’cause he done drank so much jake, he done got the limber leg, too. ”

  From Brooklyn arose another kind of sound—the angry crash of a raid, that May of 1930, when enraged Prohibition agents arrested a local operator who’d concocted a uniquely poisonous alcoholic drink in his small factory—barrels and barrels of Ginger Jake, shipped to southern states, the very drink that had inspired all those mournful songs.

  Mr. Walter Anderson, of Brooklyn’s Decker, Ingraham & Smith Pharmaceuticals, wasn’t the only operator making Ginger Jake or even the biggest swindler. Some of the larger Jake rings, investigators would discover, operated out of St. Louis and Cincinnati. But Anderson, by selling his mixture wholesale at $225 a barrel, putting it into two-ounce bottles that sold for thirty-five cents in drugstores, candy stores, and roadside stands, purveyed along with the ice cream and the pre-cut sandwiches, was getting rich enough.

  Jake was based on an old patent medicine, Jamaican Ginger, which was really ginger-flavored ethyl alcohol, between 70 and 80 percent by weight. Following the passage of the Eighteenth Amendment, the government had ordered Jamaican Ginger makers, like Anderson’s Brooklyn company, to reduce the alcohol and double the ginger. This Prohibition-approved recipe turned out to be a money-losing proposition, turning the concoction from a popular tonic (especially among those looking for a cheap drink) to a horribly bitter black syrup.

  Anderson’s license to make Jamaican Ginger had been revoked a year earlier, when Treasury tests showed he was spiking his product with extra alcohol. It became obvious that he hadn’t shut down, merely started another operation in secret, pretending to be making aftershave lotions while cooking up his lucrative supplies of Ginger Jake.

  Bootleggers had fiddled with Jamaican Ginger substitutes over the years, trying to keep them as cheap as possible. The new Jakes usually contained bottom-of-the-barrel ingredients—one short-lived formula included creosote and carbolic acid. But in early 1930, a pair of syndicate chemists from Boston found a better recipe, one based on an industrial compound known as a plasticizer, which was easy enough to steal from George Eastman’s Kodak Company in Rochester, New York, or from the Celluloid Company of Newark, New Jersey. It was this improved version that Anderson, among others, had adopted.

  The new additive was a compound used to keep plastics, such as those in photographic film, from becoming brittle. It combined those standard atoms—carbon, hydrogen, and oxygen—with phosphorus; its technical name was tri-o-cresyl phosphate. The name explains the structure: carbon, hydrogen, and oxygen bond into a ring-shaped structure called a cresol (also found in creosote), and phosphorus hangs on to the ring like an exhausted swimmer gripping a life preserver.

  In the new Jamaican Gingers the plasticizer combined with denatured alcohol to form a compound called an organophosphate. That potent combination was responsible for Jake’s newly powerful buzz. The dizzying sensation derived from the fact that the compound was also an efficient neurotoxin—as became almost immediately and horrifyingly evident.

  The Jake Leg epidemic, as people would call it, began in February 1930 with a sudden, inexplicable spate of paralysis cases in Oklahoma City. Doctors there first feared they were witnessing an outbreak of polio. But the men suddenly crowding into city hospitals, sixty-five in a single week, showed none of the predictable symptoms of that dread infection—the fever and stiffness, the muscle spasms and difficulty swallowing and breathing. They simply and in the strangest way began to lose control of their hands and feet.

  Some victims of this peculiar new outbreak could walk all right, but they had no control over the muscles that normally positioned the feet. They developed what came to be called the “jake walk”: raising their feet high, the toes flopping downward. Point toes, step, heel down, point toes—the men made a distinctive tap-click, tap-click sound as they walked. Other muscles flopped as well—the muscles below the knee, the ones that connected fingers and thumbs. But it was the tapping walk that gave the syndrome its best-known and most bitter nicknames: jake leg, jake foot, jakeitis, jakeralysis, and gingerfoot.

  By summer, physicians across the country were reporting the results of the handiwork of Jake dealers like the Brooklyn company: thousands of paralysis cases fanned across the South and Southwest, where Jamaican Ginger had made up a cheap cocktail, mixed with ginger ale, for many years. The Public Health Service counted more than two thousand Jake cases in Mississippi alone, nearly as many in Kansas, hundreds more in Kentucky, Oklahoma, Tennessee, Georgia, and Texas, and even an odd few in Rhode Island and Massachusetts.

  It took months for scientists to identify the plasticizer; they first suspected creosote, then carbolic acid, before they untangled the Ginger Jake chemistry. And when they realized that the crippling agent was the plasticizer, they were genuinely surprised. Organophosphates weren’t considered all that dangerous. Now Ginger Jake forced public health chemists to somewhat reluctantly reassess that idea. The studies that followed the epidemic, both through autopsies and through animal studies (in Oklahoma, the scientists did the work in chickens), showed that the compound was horrifyingly precise in its action. It chewed through a specific series of nerve cells in the spinal cord, the anterior horn cells. These were motor neurons; researchers would later find that people suffering from ALS suffered damage in these same cells.

  But Ginger Jake hardly dampened enthusiasm for a very promising new group of industrial chemical compounds that people usually didn’t drink. It didn’t take long for military scientists, in particular, to see the weaponlike potential in organophosphate compounds. By the end of the 1930s, Nazi researchers in Germany had developed four nerve gases—the most famous of which is sarin—all of which build on the kind of damage seen in the Ginger Jake tragedy, and which are so ugly in effect that most have never been used in warfare at all.

  IN NEW YORK CITY, where the preferred drink of 1930 was bootleg gin, the Jake epidemic proved mostly a curiosity, barring some unwanted attention paid to Brooklyn’s innovative chemical manufacturers.

  After busting Anderson and his Ginger Jake factory, dry agents discovered a liquor distribution ring that was cleverly using the cosmetics industry as a cover. For this project the chemist had purchased perfumes from around the country, stripped them down to the raw alcohol, boosted their intoxication factor with the same plasticizer used in Ginger Jake, repackaged the alcohol as perfume, and sent the packages to druggists, who sold them from under the counter to customers in the know, who unfortunately also developed a sinking paralysis.

  The head of the syndicate—identified by the government as Harry Mandell, alias Charles Harris, alias Ralph Lewis of Brooklyn—had put together an enviable national network. By the time the government finished hunting down his co-conspirators, more than one hundred druggists had been indicated in Kansas alone, along with Harris-Lewis-Mandell and seventeen other Brooklyn residents.

  James Doran, director of the Treasury Department’s Bureau of Industrial Alcohol, used the moment to remind the American drinking public that bootleggers were not their friends. Members of the alcohol syndicates, he suggested, would poison their mothers to make money. They were criminals, liars, and businessmen “evidently operating on a get-rich-quick basis.”

  That “get rich” part was all bootleggers cared about and all they ever would. And on that point, even Charles Norris and Alexander Gettler agreed with him—a rare moment of consensus between the medical examiner’s office and the Prohibitionist Doran.

  BY 1930, Gettler had assembled an encyclopedic list of cases for his research into the chemistry of drunkenness. Back in the 1920s he and one of his trainees, a promising chemist named Arthur Tiber, had begun that project on an optimistic note—they had an unlimited supply of test subjects since “intoxicated people were encountered every day” on the streets and alcoholic deaths were logged into the morgue every night.

  Once again Gettler was in the ri
ght department, the right building, and just the right job for this kind of research. The morgue was a repository of alcohol victims, accident victims, people shot to death, people drowned, and those claimed by illness and age. He had bodies to test for alcohol levels, and he had bodies to use for comparison purposes. When he tallied up his project, he found it had consumed more than five years of research and some six thousand brains.

  The work could best be described as gruesomely tedious.

  To establish baseline numbers, Gettler and Tiber would mince chunks of brain from people who had died of natural causes, sometimes using as much as half a pound of gray matter per test. They’d distill the gory sludge of tissue with steam, eventually collecting a clearish pink fluid. That fluid would be divided in half; they’d set one sample aside and test the other. Then they’d divide the remaining half into halves and test one portion of that. Again and again they would test and then retest these divisions, which chemists liked to call aliquot portions, dividing and redividing, trying to figure out how small a sample would still tell them what they wanted to know.

  Gettler’s steam distillation apparatus used a two-liter flask, where steam was generated, connected by glass tubes to a second vessel that contained the brain tissue. From there more glass tubes led to a condensing unit and then to a glass container that collected the dripping fluid of the final product. The whole assemblage was almost eight feet long and was housed under a hood. Eventually, as need for the tests grew, Gettler would fill an entire room of his laboratory quarters with the oversize alcohol-analysis devices.

  Each apparatus worked by mimicking the way the human body metabolizes ethyl alcohol into acetic acid. If a tissue sample contained alcohol, the acid would form in that spiderweb of glass tubes and drip into the last collection flask. If Gettler was working with a large quantity of alcohol, he didn’t need such elaborate measures; he could find ethyl alcohol more directly. But he was hunting for a way to find traces of the compound at a level long thought undetectable. Analyzing bare smears of brain tissue, he’d learned that the acetic acid test offered the most sensitive measurement available.