by Deborah Blum
THE HOTEL MARGARET glittered like an enormous holiday ornament on the northeastern corner of Orange Street, in Brooklyn’s upscale Columbia Heights neighborhood. Built in 1889, according to the colorful plans of local architect Frank Freeman, the hotel was a twelve-story fantasy of limestone, brick, and terra-cotta, with copper balconies and arched rectangular windows that rose to an ornate peaked roof.
In the 1920S, the hotel offered both overnight accommodations—at a pricey twenty dollars a night—and residential apartments. The latter were so popular that the owners had built an annex to house the long-term residents, crafted in the same tones of copper, red, and gold, offering the same delivery of meals by white-coated waiters, the same copper-grilled elevators manned by uniformed porters, and the same nearly invisible maid service. The elegant Hotel Margaret blended seamlessly into the elegant mansions of the Heights.
At least until the day a retired carpet dealer and his wife were found dead on the bathroom floor of their annex apartment.
“AGED COUPLE Slain Strangely” read the New York Times headline on April 27, 1922, reflecting the bafflement of the police investigators. They’d found seventy-five-year-old Fremont M. Jackson and his sixty-year-old wife, Annie, crumpled on the black and white tile of their bathroom. Both were dressed in street clothes. She lay close to the sink, and he just inside the door.
The Jacksons had died badly. Their teeth were clenched, and their lips were stained with a dried bloody froth. Their faces were oddly bluish, and their skin was patterned over with livid red spots. The physician assigned to the case suspected a double suicide, perhaps by swallowing a quick-acting poison.
But investigators found not a trace of poison in the Jacksons’ rooms—no container, vial, or bottle—and no mysterious remnants in the bottom of a drinking glass. And the family members described the couple as happy and healthy, insisting that suicide was out of the question. The Jacksons had barely been married a year. After spending years alone, they had both been enjoying the companionship of a second marriage. Annie Jackson’s son sent a telegram from his Massachusetts home, proposing that his mother had died of food poisoning and that the shock of finding her body must have killed her husband.
On Norris’s order, one of the assistant medical examiners in the Brooklyn office did an autopsy. It hinted at cyanide, which was known to cause a kind of chemical suffocation and would explain the blue look of oxygen deprivation. But cyanide from where? It killed quickly, too quickly for them to have imbibed it elsewhere and then strolled back home. Police searched the apartment again, once more failing to find a trace of the poison.
“Mr. and Mrs. Jackson met their deaths by poisoning, but whether the drug was self-administered or sent to them is impossible just now to determine,” the medical examiner’s office announced. “The poison might have been administered in food or drink.” The doctor conducting the autopsy had removed both stomachs, placed them in specimen jars, and sent them from Brooklyn to Manhattan for analysis in Gettler’s laboratory. Until those results came in, investigators could “not determine what caused the death of the couple.”
But, truth to tell, they rather hoped it was something else, something less ugly than cyanide.
CYANIDES POSSESS a uniquely long, dark history, probably because they grow so bountifully around us.
They flavor the leaves of the yew tree, the flowers of the cherry laurel, the kernels of peach and apricot pits, and the fat pale crunch of bitter almonds. They ooze in secretions of arthropods like millipedes, weave a toxic thread through cyanobacteria, massed in the floating blue-green algae along the edges of the murkier ponds and lakes, and live in plants threaded through forests and fields.
Humans recognized early the murderous potential of cyanide-rich plants. Scholars have found references to “death by peach” in Egyptian hieroglyphics, leading them to believe that those long-ago dynasties carried out cyanide executions, perhaps by making a potion from poisonous fruit pits. Centuries later cyanide became more readily available in large and lethal quantities. That happened, in part, due to some experiments by a German painter who in 1704 was only trying to improve the colors on his palette.
The artist, one Heinrich Diesbach, was a born experimenter. He spent hours in the laboratory of a Berlin chemist, trying to create a new shade of red paint. He swirled together wilder and wilder mixtures, eventually mixing dried blood, potash (potassium carbonate), and green vitriol (iron sulfate), then stewing them over an open flame. He expected the flask to yield a bloody crimson, but instead a different brilliance appeared—the deep violet-blue glow of a fading twilight. Diesbach called the vivid pigment Berlin blue; English chemists would later rename it Prussian blue.
Almost eighty years later a Swedish chemist mixed Prussian blue with an acid solution, heated the witchy, foaming result, and produced a colorless gas, undetectable but for a faint smell of bitter almonds. The gas easily condensed into a clear liquid that, even diluted with water, was an exceptionally potent acid. That corrosive liquid became popularly known as Prussic acid, although scientists preferred to call it hydrocyanic acid (from the Greek words hydro for water and kyanos for blue).
The gas was hydrogen cyanide (HCN), a deceptively simple, spectacularly lethal bundle of hydrogen, carbon, and nitrogen atoms. It could be chemically treated to produce powdery white poisonous salts, usually potassium cyanide (KCN) or sodium cyanide (NaCN). As a group, the three cyanides quickly showed themselves valuable in industrial products. Hydrogen cyanide was used in pesticides, explosives, engraving, and tempering steel, as a disinfecting agent, in creating colorful dyes, and even in making nylon. Sodium cyanide became a favored tool of the mining industry, used to etch away useless rock and extract the gold contained inside. Potassium cyanide was also used in mining, as well as in photography, electroplating, and metal polishing.
Alexander Gettler, tracking cyanide problems in New York, kept a list of accidental poisonings, such as those caused when someone with an open cut on a hand polished the family silver. The exposure was low enough that most people, after becoming miserably sick, survived. But Gettler had logged one fatality, following a meal served by a cook who failed to thoroughly wash out a pot after polishing it to a gleam inside and out. Gettler worried—no, he knew—that people using cyanides didn’t appreciate how dangerous they were: “It is of considerable practical significance that hydrocyanic acid is a poison for all members of the animal kingdom.”
In other words, cyanides were useful, plentiful, easy to acquire—and astonishingly lethal.
STILL, most murderers tended to avoid cyanide—the poison left a too-obvious trail of evidence. The resulting corpse would be a textbook study in violent death, marked by bruising discoloration, twisted by the last convulsions, often eerily scented with cyanide’s characteristic warning perfume, a faint, fruity scent of almonds. (Researchers would later find that a fair number of people carry a genetic mutation that keeps them from smelling cyanide.)
It was more popular as a suicide choice due to its reputation for acting quickly. As Gettler wrote, “The symptoms of acute poisoning proceed with almost lightning-like rapidity. Within two to five minutes after ingestion of the poison, the individual collapses, frequently with a loud scream (death scream).” In lesser amounts the poison kills more slowly, if faster than most other toxic substances. The average survival after swallowing cyanide is between fifteen and forty-five minutes. Fast or slow, it is never a kind ending. The last minutes of a cyanide death are brutal, marked by convulsions, a desperate gasping for air, a rising bloody froth of vomit and saliva, and finally a blessed release into unconsciousness.
WHETHER SWALLOWED or inhaled, all members of the cyanide family kill in the same way—they shut down the body’s ability to carry or absorb oxygen. In the late 1890s one daring physician swallowed a light dose of potassium cyanide to test its effects. In Gettler’s day medical papers still cited his gasping cries that he was suffocating. Although the doctor survived, no one had repeated that exper
iment.
Cyanide’s action is murderously precise. It attaches with stunning speed to protein molecules in the blood—called hemoglobins—that carry oxygen throughout the body. Thus the poison is rapidly circulated by the bloodstream and delivered to cells through the body. There it shreds cellular energy mechanisms, breaks down cellular respiration, and causes rapid cell death due to oxygen starvation. Cellular respiration suffers an instant “paralysis,” as Gettler once put it, and the body begins to die. Enzyme production is stymied, electrical signals falter, and as muscle cells and nerve cells explosively fail, body-rattling convulsions frequently result.
After death, the bluish tones of oxygen deprivation mottle the skin. On autopsy, the blood shows such a dark red that it sometimes appears purple. The veins leading from lung to heart are engorged with blood—evidence of the heart’s desperate efforts to circulate more and more blood as the body seeks desperately for any stray trace of oxygen. In Gettler’s time, the easily available cyanide salts provided further specific evidence of the poison because they were so corrosive. If swallowed, they burned their way down. An autopsy of a cyanide victim found the mucous membranes of the lips, mouth, and esophagus darkened to a bloody, ragged red—especially if the poison had been taken without food to buffer the impact. The stomach became swollen, discolored, clotted with swampy, streaky mucus produced as the cyanide salts broke down.
In the four years since Gettler had become city toxicologist, he’d investigated seventy-nine cyanide deaths, scattered across the boroughs. Forty-nine had been suicides, usually by sodium cyanide. Sodium cyanide was the cheapest form of the poison and, as research would show, was more efficient than potassium cyanide. (Sodium atoms are much smaller than potassium atoms, making room for a larger proportion of cyanide in the compound.) Most of the other deaths Gettler reviewed were accidental. Hydrogen cyanide gas was routinely used to fumigate buildings or disinfect ships. Occasionally workers were killed by the gas, especially if they returned before it had cleared.
Investigators wondered about fumigation as they looked into the deaths of Fremont and Annie Jackson at the Hotel Margaret. But the manager assured them that no fume-producing activities had occurred in the critical time period. So if indeed cyanide had killed the Jacksons, they had to have swallowed it, which was why the stomachs had been so carefully removed for chemical testing.
GETTLER EXPECTED to find the usual wreckage left by the poison: the bloody, corrosive trail of cyanide through the digestive system. But it wasn’t there. The tissues from the dead couple were slightly decayed but basically healthy. Still, every toxicologist knew that people reacted differently to poisons, that any known rule of evidence had the occasional exception.
So he set about doing the finer chemical tests for the poison. His plan was to check the contents of the stomachs and the tissues of the stomach muscle separately. Cyanide in the stomach would indicate only that a person had swallowed the poison. Cyanide in the stomach walls would be evidence that it had been absorbed and might even reveal how much had entered the body.
Gettler’s detailed notes explained the procedure step by step. He stored the still-full stomachs in an icebox until he was ready to run his tests. He then removed the contents and separated them from the muscle tissue. From each stomach he took a healthy chunk of about 200 grams (some seven ounces) of muscle and minced it into a pinkish-gray paste. He then drained off the stomach contents into two liter-size flasks; he placed the tissue slush in two other flasks. He then dripped acid into the flasks, just a little, but enough to further break down the contents. He distilled the liquid in a steam bath and condensed it into another flask packed around with ice.
Any cyanide would be concentrated in the clear fluid contained by that last well-chilled flask.
One reliable way to then check for cyanide was called the Prussian blue test. To begin it, Gettler took a little of the distilled liquid, added some iron-rich salts, and heated the mixture. As it cooled, a muddy brown layer settled at the bottom of the flask. He then added hydrochloric acid, drop by drop, until the dirty sludge started to dissolve. If the sludge contained a high level of cyanide, a brilliant blue layer would almost immediately form in the flask. If there was only a trace of poison, there would be no blue flash. Instead the sediment would glint green before slowly turning blue.
Gettler ran the Prussian blue test on both the stomach tissue and the contents. He ran six other tests. No blue; no anything. They were all negative for cyanide. That meant the investigation was back where it had started, with two dead bodies and no good answers.
THE JACKSON CASE had all the appearance of one of those locked-room mysteries that writers of crime fiction like so much and that working detectives despise. In fact, the door to the Jacksons’ apartment had been locked; a maid had found the bodies when she opened it with a hotel key in order to clean the room.
But perhaps they’d missed some clue to a clever murder. The New York State court system alone offered plenty of examples, from other cases, of the creative ways killers tried to sneak poison into their victims’ food and drink.
In the previous few years alone, a Westchester man, irritated one evening because his wife wouldn’t fetch his cigarettes, had placed a box of poisoned candy on the sitting room table and waited for her to sample it. A fired Mayville county clerk had sent a box of homemade candy laced with cyanide to the woman who had replaced her. A White Plains woman, irritated by the neighbor’s barking dog, had substituted a bottle of milk containing cyanide for one that the milkman had delivered. A newly married woman in Olean hadn’t wanted a stepson so she’d sent the six-year-old boy a box of poisoned chocolates while he was vacationing in Missouri, nearly killing the child’s aunt, who ate a piece when her nephew shared his candy.
One of the most famous cyanide-by-mail murder cases in the United States had occurred in New York City at the turn of the twentieth century. It involved cyanide, had the son of a Civil War hero as the suspected murderer, and featured the city’s exclusive Knickerbocker Athletic Club as the backdrop to the crime.
Shortly before Christmas 1898, the club’s athletic director, Harry Cornish, received an unexpected package at home. It contained a nice little gift: a blue Tiffany box containing a bottle of Bromo-Seltzer inside a chased silver bottle holder. Cornish shared a house, owned by his aunt, with several other family members. A couple days after the holiday, his aunt developed a severe headache. Remembering the medicine he’d received in the mail, he mixed up a glass to relieve her pain. His aunt swallowed the tonic and then, to his horrified shock, collapsed to the floor, gasping for air, her face darkening to blue as she died.
Panicked family members called the doctor, who immediately detected the characteristic bitter almond smell in the medicine bottle. The resulting autopsy showed classic signs of cyanide poisoning. Anonymous poisonings by mail were usually hard to solve, but the investigators caught a break: Cornish had saved the wrapping that contained the package. A secretary at the Knickerbocker Club recognized the handwriting on the label. That led police directly to a disgruntled former club member named Roland Molineux, who had quit the club after quarreling with Cornish.
The thirty-one-year-old Molineux seemed an unlikely suspect. He was the elegant and well-educated son of a famous Civil War hero. Former Union Major General Leslie Molineux had fought in some of the war’s most critical missions, supporting Grant at Richmond and Sherman during his march through Georgia. The general was so well respected and so well liked that his reputation cast a warm and protective aura around his son. At first the police found the very notion that Roland Molineux was a killer ridiculous. But mounting circumstantial evidence changed their minds.
Molineux had an account at Tiffany & Co. and had made a purchase at the Fifth Avenue store in December, which would have provided him with the familiar blue box. He worked for a family dye company, had studied chemistry, and had a personal laboratory equipped with an array of poisons used in dyes—mercury, arsenic, and cyanide-rich
Prussian blue. His office was located within blocks of the post office from which the package had been mailed. And the son was nothing like his father: he was instead a man with an outsize sense of superiority. His quarrels with Cornish had involved the other’s refusal to expel “lesser” families from events. He’d written to the club asking for Cornish’s removal, describing him as a “vile, bad man.”
The police investigation turned up something even more disturbing. A month earlier, in November 1898, another member of the Knickerbocker Club had died unexpectedly. The dead man, Henry Barnet, had been pursuing a rather beautiful young woman whom Molineux wanted to marry. Barnet’s death had been considered a natural one; the death certificate blamed a sudden weakness of the heart. But now detectives discovered that Barnet had also received an anonymous package of medicine in the mail and died shortly after taking it. They exhumed Barnet’s body and discovered that the stomach and other organs contained a high concentration of cyanide.
Less than three weeks after Barnet’s death, Molineux had married the woman in question. The police were sure that Molineux had killed both people, but prosecutors decided to try him only for the death of Cornish’s aunt, where the evidence—including the handwriting sample—was stronger. The case went to trial in late 1899, and at its conclusion Roland Molineux was sent to Sing Sing to await execution.
But the prosecutor had made an unfortunate decision in his closing argument: he’d repeatedly talked to the jury of Barnet’s death, even though Molineux had not been charged in that case. He dramatically told the jurors that he could hear not one but two voices in the night calling to him for justice: Cornish’s tragically dead aunt, and Henry Barnet, “in the vigor of his youth and manhood, stricken down in that same manner . . . And will a jury of my countrymen quail before the honest and just verdict? I think not.”