ALEXANDER GETTLER had another reason, though, for exploring the chemistry of ethyl alcohol. It was an important poison, absolutely, but it was also a fascinating one. It offered an illuminating case study in the peculiar, paradoxical nature of the planet’s chemistry: what sustained life could also kill it.
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—H
2
O—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 CH
3
OH. 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: C
2
H
5
OH. 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.