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 right 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.
In the third-floor laboratory Gettler and his assistants duplicated the tests until they were sure of one fact: the tissue of a normal brain always contains a trace of ethyl alcohol as a result of normal metabolic processes. And
trace
was the right word: at most, natural alcohol content in the brain is 2/1,000th of a percent.
But that number, that barest gleam of alcohol, gave them a baseline reading to compare to the brains of people who had consumed alcohol. That was the real question anyway—how much alcohol was added when people drank, when they drank a little, and when they drank way too much? How much did it take before the brain was, one might fairly say, soaking in the stuff?
“WELL, Doctor, isn’t it a fact that I can give the same amount of alcohol to two people, and one may become intoxicated and the other not?” Gettler was forever being asked that question by attorneys representing clients charged with public intoxication or drunk driving or any of the alcohol offenses that had continued, without fail, to plague the criminal justice system during Prohibition.
“My answer to that is, we are not analyzing what the man gets to drink.” As he’d said for years, he didn’t care about that, didn’t care what was in the bottle, the stomach, or the intestines, didn’t even fully count the blood-alcohol level. “We are analyzing for the alcoholic content of the brain. Once it gets to the brain, it has an effect, and that effect is proportionate to the amount present” in those tissues.
To correlate the amount of alcohol in the brain with drunken behavior, Gettler had pored over the remains of people identified as drunk at time of death, people who’d fractured their skulls falling down stairs, meandered in front of a hurrying automobile or tumbled onto train tracks and been collected in pieces. He’d matched them to witness statements gathered by the police, descriptions of those weaving, stumbling, and joking their way toward their final conclusion. For comparison, he’d also looked at the brains of people who’d consumed no alcohol, patients who’d died at Bellevue after lengthy hospitalizations, people whose tissues were guaranteed to contain no more than the normal baseline of ethyl alcohol.
All of that—the measurements of alcohol in the brain, the injuries, the behavior, the full context of those deaths—would go into the paper that he and Tiber published, which would be widely acclaimed as creating the first scientific scale of intoxication.
Gettler’s scale used the numerical plus sign + to indicate each level of drunkenness. Each plus stood for a level above normal: baseline brain alcohol plus one, plus two, plus three, or plus four. Spelled out, the scale read like this:
+ “In all cases in which there was an alcoholic content of the brain below 0.1 percent, the patients showed no obvious alcohol impairment.”
++ From 0.1 to 0.25 percent alcoholic content. Subjects showed slight inebriation: they were a little more aggressive than normal, a little less cautious in their behaviors. One man who had knocked back a couple of drinks, pitched into a bar fight, and was stabbed to death had a ++ rating.
+++ From 0.25 to 0.4 percent alcoholic content. In the hours before death, subjects were unsteady on their feet, loud, and judged drunk by everyone who saw them. A typical +++ was autopsied after he’d fallen down the stairs while drunk and broken his neck.
++++ From 0.4 to 0.6 percent alcoholic content. These subjects had died after becoming falling-down drunk. They had consumed so much liquor that they succumbed to ethyl alcohol poisoning, usually within several hours after reaching a hospital.
Gettler’s one-to-four scale of drunkenness was ideal for establishing intoxication at time of death, working as it did with brain tissue.
A companion rating scale—for the drunk drivers who survived a crash—would follow shortly. In 1931, an Indiana University toxicologist named Rolla Harger invented the “Drunk-o-Meter,” a device in which drinkers blew into a balloon, allowing chemists to analyze the vapors in their breath. Harger’s system, like Gettler’s, assigned intoxication values linked to behaviors measured at each level of chemical results.
The Prohibition era had been a great source of material for building an excellent science of alcohol intoxication.
IN NEW York City, according to press reports, two men in a First Avenue speakeasy died from alcohol poisoning in August. Six died and twenty-one were hospitalized in September, all sickened by wood alcohol served in a Brooklyn bar. In October another twenty were dead in Newark. They’d apparently skipped the redistilling process entirely and guzzled straight industrial alcohol.
In December 1930 James Doran acknowledged that the death rate was worsening, at least for “a certain type of person with uncontrollable appetite.” The latest holiday drink was a mixture that included the alcohol used in antifreeze formulas. The antifreeze cocktail was a favorite of rail riders, traveling laborers who liked to sneak their rides on cargo trains. They called the drink “derail” for its near-instant brand of intoxication. It killed a few of them, sure, but they were used to the effects of borderline alcohol. The rail riders admitted—or sometimes boasted—that they’d drunk Sterno on occasion, or bay rum aftershave if there was nothing else to be found.
“These deaths have been attributed to so-called poison liquor,” Doran acknowledged, “namely denatured alcohol, manufactured under government supervision.” In response to continued criticism—Charles Norris had taken to describing the United States as the land of hypocrisy—Prohibition chemists had invented a new formula, to be introduced in 1931, which they thought would be repulsive without actually killing people.
The new formula mixed petroleum products into the alcohol, pretty much the sludge left behind during gasoline processing. Noxious with the rotten-egg reek of hydrogen sulfide, they figured it would be unpleasant enough to discourage anyone conscious enough to get a whiff. To publicize the new approach, the Treasury Department invited journalists to come taste it. One experienced newshound immediately identified it as containing either benzene or ether. “It’s not as bad as some of the stuff you’ve been drinking,” Doran replied ironically, as the writer, clearly accustomed to the more usual versions of poisoned alcohol, chugged down another sample.
WHY WERE some people, journalists notoriously among them, seemingly able to guzzle alcohol without obvious effect? Why didn’t everyone fall flat after a marathon of martinis? These questions were asked enviously by hungover friends, resentfully by dry advocates. And they had perplexed scientists for decades.
Gettler could—and did—cite puzzled research papers dating back to the turn of the century. One of the most provocative, published in 1908, was a study of rats and rabbits that were provided a regular supply of ethyl alcohol. After the scientists had created a colony of alcoholic animals, they offered the same laboratory cocktails to animals with no previous exposure. The novice drinkers became stumbling drunk on the same amount of alcohol that no longer had any effect on the habituated rats and rabbits.
By doing a series of blood draws, the scientists found that their habitués had somehow learned to better process their drinking binges. The unaccustomed animals absorbed 20 percent more alcohol into their bloodstream in the first two hours than did the practiced ones. By the end of a day, first-time drinkers had blood-alcohol levels 66 percent higher than the experienced imbibers.
Working with his talented toxicology students, Abe Freireich (who would later become chief medical examiner for New York’s Nassau County), Gettler decided to see if he could provide a better understanding of how alcohol is metabolized by different kinds of drinkers. He chose dogs for their experiments.