Angel Killer: Deborah Blum Discusses Serial Stalker Albert Fish and eBook Publishing

by Deborah Blum

When first thinking that I might tell the story of Albert Fish – the cannibal killer who stalked New York City in the 1920s and '30s – all my friends advised against it. Did I really want to spend hours of my life with a subject this warped? “Call me if you if you really decide to write that book,” a long-time friend at NPR said. “So that I can talk you out of it.”

And yet the story haunted me. It tapped me on the shoulder when I was working on other projects. If you write for a living, you know what that means. I decided finally that I would write it but not as a full-length book.  So I pitched the shadowy, murderous path of Albert Fish as a long narrative story – an e-single – to the rising star digital publisher, The Atavist.

Last week, that story – titled Angel Killer – was the number-one selling non-fiction single on Amazon (number eight out of all Kindle singles). Partly, I think, because it’s just an incredible story of murder and detection and of scientists wrestling with their own definitions of justice regarding a madman. Partly, I hope, because I told it with style.

But also because this turned out to be just the right format for my story set in shadows.  I just participated in a panel on e-books at the National Association of ScienceWriters meeting in Raleigh, N.C.  I’m including a link to that session here because you can download a pdf there with all kinds of great information about e-publishing, from commissioned pieces like my own to self-publishing.

We talked about this newly wonderful opportunity to write a long-form story, a place where you could publish in the 10,000 to 20,000 word length (mine’s about 11,000) as opposed to a full-length book of 100,000 or more words. We talked about all the digital possibilities not available in print.  In the enhanced editions, for instance, Angel Killer contains video, audio (by me), music, interactive murder maps. We talked about what the future looks like for writers and publishers.

But here’s the thing. Every person on my panel agreed that in the end, it wasn’t the bells and whistles that made this most exciting. It was the story itself. And the opportunity to tell it a really good length, long enough to do it justice, but short enough to make it a fast read.  Which brings me back, of course, to the dark journey of Albert Fish and why I couldn’t quite let it go.

I’m not a writer who specializes in serial killers. I am a science writer who specializes in poisons and toxicology, so I do often tell stories that you might consider true crime. My book, The Poisoner’s Handbook, for instance, is subtitled “Murder and the Birth of Forensic Medicine in Jazz-Age New York.” And it was because I spent so much time researching criminal justice in that time period, that I encountered the crimes of Albert Fish.

At first his story looks like that of many serial killers. White, male, poor and poorly educated, abused as a child, angry. He was born in 1870 in Washington, D.C. scraped out a living as a painter and handyman for most of this life in New York City. He was thin, gray, a shadow man drifting through the city streets. He stalked, he killed, and for well over a decade, he got away with it. One of the nicknames for him, after he became infamous, was the Gray Man.

But he was crazier than most. And, yes, it’s hard to argue with that description of a cannibalistic serial killer who sends recipe-infused letters to the families of his victims. I say that because he was delusional. He suffered from hallucinations, heard voices, believed that he followed the instructions of vengeful angels (hence the title of my story.)

And the question of his sanity was why I became so interested. During his 1935 trial, that was the most important, really the only question about his future. Was he crazy enough to escape the electric chair at Sing Sing Prison? The psychiatrists for the defense didn’t see it as escape. They saw a desperately mentally ill man who had become a successful killer. They wanted him locked away, studied, used to gain new understanding of multiple murders. The state of New York, though, just wanted him dead.

As a result, the trial provided one astonishing scene after another of psychiatrists facing off over a killer’s sanity. Even today, the testimony of some of the state experts – one scientist described Fish’s habits as “just a matter of taste” – is some of the most egregious on record. It was that extreme scientific testimony, the question of how we define sanity that first caught my attention.

But it was the ethical, moral dilemma that kept me interested. How should we deal with the dangerously crazy in the criminal justice system? Is there a best answer for what to do with a killer like Albert Fish once we’ve managed to catch him? One person wrote me to say engraving his name on a tombstone was a good enough result. But of the defense psychiatrists at the time likened executing an insane old man to witch burning in the Salem trials of long ago.

So, that’s why I wanted to tell the story of Albert Fish. I wanted to put myself – in the way writers do – on that wooden bench with the jurors and see if I could answer that question.  And did I find it? Some days I know exactly what I’d do. And on others the story still taps on my shoulder, letting me know that I’m still wrestling with the question. But that’s okay.  A good story should haunt you for a while anyway.

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Eerie Deaths in Thailand of 2 Sisters

Wikipedia Commons

by Deborah Blum

The Phi Phi Islands sit off the western coast of Thailand, floating like jewels in a turquoise sea, a picture-perfect image of a tropical getaway. Director Danny Boyle filmed his 2000 psychothriller, The Beach, on the largest of those islands and if you know the movie, you know, despite the gem-like setting the story ends badly.

They say, though, that the movie put the largest of the islands, Ko Phi Phi Don, on the map as a tourist getaway, a reasonably priced home to glittering beaches and unlimited partying. And that’s undoubtedly what drew two young sisters from a small Canadian village, just north of the Maine border, to travel there for a summer break from their university studies.

Noemi Belanger was 26 and her sister, Audrey, 20, when they planned the June vacation. Both sisters lived in their hometown of Pohenegamook, Quebec. Did I mention that it was small, the kind of place where people know each other, stay close? The population is about 3,000 and both girls worked for their father, Carl, in his grocery store before starting university classes. They were happy girls, friendly, residents say, involved in their community, helping out at the local library, at public beaches.

This summer, they were ready to fly a little, indulge in a splashy vacation. So they saved their money and flew to Thailand in June, went to visit the Phi Phi Islands. And there, as a flood of mid-June news stories made obvious, things went very wrong. Very, very wrong.

The stories were puzzled, horrified. A story in Canada’s National Post described a hotel maid finding the sisters dead in their room, with lesions tracked across their bodies, their fingernails and toenails turned an odd grayish blue. They were huddled in their beds, relayed the Global Post, smeared with vomit and blood.

Rumors flew of an exotic poison, of a lurking killer. Dismissive statements from the police added to the sense of mystery. “We found many kinds of over-the-counter-drugs, including ibuprofen, which can cause serious effects on the stomach,” one investigator said, sounding as if packing painkillers was the real problem. Mysterious poison deaths of tourists visiting the Phi Phi Islands were recalled: the 2009 death of a Seattle woman, still unsolved today. The similar and also unexplained death of a 22-year-old woman from Norway the same year. An odd cluster of deaths in another Thai city during winter of last year, including a 23-year-old woman from New Zealand. The conspiracy theories expanded to include the unexplained deaths of two young women in Vietnam this summer. “Is this a cover-up?” asked a letter writer in the Bangkok Post after the police went on from the ibuprofen theory to one that involved food poisoning.

And not just any food poisoning. A leak from the investigation suggested that detectives were considering the possibility that the sisters had dined – somewhere – on either poisonous mushrooms or blowfish, sometimes called pufferfish or fugu. The fishes are considered a delicacy but they must be carefully prepared to exclude any contact with the liver or other internal organs, which contain an exceptionally potent neurotoxin called tetrodotoxin.

Neither of these suggestions, though, were an ideal match for the described symptoms. Tetrodotoxin is most famous for its ability to induce a corpse-like paralysis in victims; they may remain alert but unable to move or communicate, gradually suffocating as the lungs fail. Poisonous mushrooms tend to kill by gradually destroying the liver. As quickly as the suggestion was floated it seemed to disappear, leaving the questions to further simmer over the summer.

Until last week, when a preliminary autopsy report was announced, which apparently indicated a toxic level of exposure. According to news reports, toxicologists in Thailand now believed that the two sisters had been drinking a popular local cocktail that contains Coca-Cola, cough syrup, ground up leaves from the kratom tree, and the well-known mosquito repellent DEET and is admired for its hallucinogenic qualities. In their case, apparently, too much DEET had ended up in the drink.

Or as the tourism-focused island paper, Phuket Wan, wrote following the announcement:

Phi Phi is renowed as a rites-of-passage destination for 20-somethings and it transforms from a haven for day-trippers in the sunshine to a less beguiling island party after dark. Alcohol is just one of the many ingredients that Phi Phi’s party people mix in their buckets. Each bucket is a concoction of all kinds of juices and substances that are mixed into containers of various sizes and usually sucked through straws all night long.

It’s a nicely sinister portrait of cocktails in the Phi Phi islands. Still my first reaction was a kind of “DEET, really?” skepticism. We’re not talking about anything like tetrodotoxin here; this is a compound we routinely spray all over ourselves on camping trips and summer hikes. Our Environmental Protection Agency estimates that about 30 percent of the U.S. population uses a DEET-infused product every year. Plenty of us have accidentally swallowed a little during an over-enthusiastic assault on mosquitoes without getting sick (including myself). Not that you’d want to take it by the tumbler, of course. But it’s reasonable to ask whether it would take a tumbler to kill you

The short answer, yes, pretty close to that. DEET, by the way, stands for N.N-Diethyl-meta-toluamide, which is basically chemist-code for a formula that includes the familiar elements carbon, hydrogen, nitrogen and oxygen. It apparently works as a repellent by disrupting insect olfaction-detection systems. And an EPA analysis found that it is slightly toxic to birds, fish, and aquatic invertebrates and has”very low toxicity potential” in mammals, such as ourselves.

So, it’s not surprising that the Agency for Toxic Substances and Disease Registry reports that people have committed suicide with the repellent but only by drinking full “bottles of DEET” along with quantities of alcohol. In other words, The stories were puzzled, horrified. A story in Canada’s National Post described a hotel maid finding the sisters dead in their room, with lesions tracked across their bodies, their fingernails and toenails turned an odd grayish blue. They were huddled in their beds, relayed the Global Post, smeared with vomit and blood.

Rumors flew of an exotic poison, of a lurking killer. Dismissive statements from the police added to the sense of mystery. “We found many kinds of over-the-counter-drugs, including ibuprofen, which can cause serious effects on the stomach,” one investigator said, sounding as if packing painkillers was the real problem. Mysterious poison deaths of tourists visiting the Phi Phi Islands were recalled the 2009 death of a Seattle woman still unsolved today, and the similar and also unexplained death of a 22-year-old woman from Norway the same year. An odd cluster of deaths in another Thai city during winter of last year, including a 23-year-old woman from New Zealand. The conspiracy theories expanded to include the unexplained deaths of two young women in Vietnam this summer. “Is this a cover-up?” asked a letter writer in the Bangkok Post after the police went on from the ibuprofen theory to one that involved food poisoning.

And not just any food poisoning. A leak from the investigation suggested that detectives were considering the possibility that the sisters had dined – somewhere – on either poisonous mushrooms or blowfish, sometimes called pufferfish or fugu. The fishes are considered a delicacy but they must be carefully prepared to exclude any contact with the liver or other internal organs, which contain an exceptionally potent neurotoxin called tetrodotoxin.

Neither of these suggestions, though, were an ideal match for the described symptoms. Tetrodotoxin is most famous for its ability to induce a corpse-like paralysis in victims; they may remain alert but unable to move or communicate, gradually suffocating as the lungs fail. Poisonous mushrooms tend to kill by gradually destroying the liver. As quickly as the suggestion was floated it seemed to disappear, leaving the questions to further simmer over the summer.

Until last week, when a preliminary autopsy report was announced, which apparently indicated a toxic level of exposure. According to news reports, toxicologists in Thailand now believed that the two sisters had been drinking a popular local cocktail that contains Coca-Cola, cough syrup, ground up leaves from the kratom tree, and the well-known mosquito repellent DEET and is admired for its hallucinogenic qualities. In their case, apparently, too much DEET had ended up in the drink.

Or as the tourism-focused island paper, Phuket Wan, wrote following the announcement:

Phi Phi is renowed as a rites-of-passage destination for 20-somethings and it transforms from a haven for day-trippers in the sunshine to a less beguiling island party after dark.

Alcohol is just one of the many ingredients that Phi Phi’s party people mix in their buckets.

Each bucket is a concoction of all kinds of juices and substances that are mixed into containers of various sizes and usually sucked through straws all night long.

It’s a nicely sinister portrait of cocktails in the Phi Phi islands. Still my first reaction was a kind of “DEET, really?” skepticism. We’re not talking about anything like tetrodotoxin here; this is a compound we routinely spray all over ourselves on camping trips and summer hikes. Our Environmental Protection Agency estimates that about 30 percent of the U.S. population uses a DEET-infused product every year. Plenty of us have accidentally swallowed a little during an over-enthusiastic assault on mosquitoes without getting sick (including myself). Not that you’d want to take it by the tumbler, of course. But it’s reasonable to ask whether it would take a tumbler to kill you

The short answer, yes, pretty close to that. DEET, by the way, stands for N.N-Diethyl-meta-toluamide, which is basically chemist-code for a formula that includes the familiar elements carbon, hydrogen, nitrogen and oxygen. It apparently works as a repellent by disrupting insect olfaction-detection systems. And an EPA analysis found that it is slightly toxic to birds, fish, and aquatic invertebrates and has”very low toxicity potential” in mammals, such as ourselves.

So, it’s not surprising that the Agency for Toxic Substances and Disease Registry reports that people have committed suicide with the repellent but only by drinking full “bottles of DEET” along with quantities of alcohol. In other words, evidence is that it would take that tumbler full to kill you. I also looked at the other ingredients in the suspect cocktail, except for the Coca-Cola (which hasn’t contained cocaine for more than a century). The codeine in cough syrup could, in a high enough amount, add to a sleepy buzz. And kratom – while known to be hallucinogenic – can also bring on a numbing lethargy in too high a dose. It is generally, though, considered to be most risky for its addictive qualities than for its acute toxicity issues.

Which brings us back to the DEET theory of death. And that requires someone to pour a ridiculously large quantity of this pale yellowish liquid into a drink served to two sisters from Canada. Could someone be that careless? Sure, especially if they were enjoying the island brew themselves. Still, only the Belanger sisters died after that night on the beach; under this theory only one over-toxic cocktail was served. And that does raise a few other questions. For instance, why – as you may have noticed from my fatality list – is it mostly young women who are dying of mysterious chemical poisonings in a tropical paradise?

Even Phuket Wan (which seems remarkably tough-minded for a publication focused on tourism) seems unconvinced by the mosquito repellent hypothesis, noting that it would be unusual for only two people to be poisoned by a shared bucket drink.

Could it be a cover up, the paper asked, for a heavy-handed use of insecticide in the sisters’ room? Insecticides have been suspected in some of the other deaths. Could it be that island authorities were trying to hide the existence of a killer who was deliberately spiking drinks? Or, slightly less creepily, that the women had been killed by excessive use of insecticides by hotel management and that authorities were moving to protect reputations? “All options remain open,” the paper warned, until the authorities produce evidence of a much more meticulous investigation.

And, yes, you’ll find me in the “options remain open” camp as well. It may well be that this is as simple as it sounds, two trusting travelers from rural Canada drinking an untrustworthy bar drink.

Still, at the moment, if I felt a sudden urge to go party in the Phi Phi islands, you would find me insisting on a nicely capped container – and, I think, opening that bottle myself. Which, frankly, makes good sense -- most of the time anyway.

evidence is that it would take that tumbler full to kill you. I also looked at the other ingredients in the suspect cocktail, except for the Coca-Cola (which hasn’t contained cocaine for more than a century). The codeine in cough syrup could, in a high enough amount, add to a sleepy buzz. And kratom – while known to be hallucinogenic – can also bring on a numbing lethargy in too high a dose. It is generally, though, considered to be most risky for its addictive qualities than for its acute toxicity issues.

Which brings us back to the DEET theory of death. And that requires someone to pour a ridiculously large quantity of this pale yellowish liquid into a drink served to two sisters from Canada. Could someone be that careless? Sure, especially if they were enjoying the island brew themselves. Still, only the Belanger sisters died after that night on the beach; under this theory only one over-toxic cocktail was served. And that does raise a few other questions. For instance, why – as you may have noticed from my fatality list – is it mostly young women who are dying of mysterious chemical poisonings in a tropical paradise?

Even Phuket Wan (which seems remarkably tough-minded for a publication focused on tourism) seems unconvinced by the mosquito repellent hypothesis, noting that it would be unusual for only two people to be poisoned by a shared bucket drink.

Could it be a cover up, the paper asked, for a heavy-handed use of insecticide in the sisters’ room? Insecticides have been suspected in some of the other deaths. Could it be that island authorities were trying to hide the existence of a killer who was deliberately spiking drinks? Or, slightly less creepily, that the women had been killed by excessive use of insecticides by hotel management and that authorities were moving to protect reputations? “All options remain open,” the paper warned, until the authorities produce evidence of a much more meticulous investigation.

And, yes, you’ll find me in the “options remain open” camp as well. It may well be that this is as simple as it sounds, two trusting travelers from rural Canada drinking an untrustworthy bar drink.

Still, at the moment, if I felt a sudden urge to party in the Phi Phi islands, you would find me insisting on a nicely capped container – and, I think, opening that bottle myself. Which, frankly, makes good sense -- most of the time anyway.

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Cough Syrup, Dead Children, and the Case for Regulation

By Deborah Blum

Kathleen Hobson was eight years old when her mother unknowingly dosed her with poisonous cough syrup. She’d only taken a couple spoonfuls but when investigators came round, they still found nothing left to test. After the little girl died, her mother had set the bottle on fire and then thrown it into the trash.

Charlene Canady was just four when she died from the same medication. Her father had carefully packed the cough syrup bottle, waiting for justice to come calling. I always imagine him silent when he handed the bottle over, grief and his daughter’s name caught like a kind of suffocation in his throat.

Both little girls lived in Tulsa, Oklahoma, both came down with nasty little colds in the fall of 1937, and both died because they were dosed with a brand new medication, a popular, raspberry-flavored cough syrup. In all, the syrup would kill 11 people in Oklahoma, within a few weeks. Ten in Alabama. Ten in Georgia. Twenty-three in Mississippi. Nine in South Carolina. Seven in Texas. More in California, Ohio, Illinois, Missouri, Virginia, Louisiana, and more.

More than one hundred dead nationwide, in fact, and most of them children, Charlenes and Kathleens scattered across the United States like so much storm wreckage. “Nobody but Almighty God and I can know what I have been through these past few days,” a Louisiana doctor later wrote to the U.S. Food and Drug Administration, after six of his patients died in one week.

As FDA scientists would quickly realize, the syrup was lethal because it was sweetened by a compound known as diethylene glycol which kills by causing acute kidney damage. Both diethylene glycol and the obviously closely related compound, ethylene glycol (even more toxic) are best known today for their use as antifreeze agents and homicidal weapons on more than one occasion.

But at the time that Elixir Sulfanilamide came to be, produced by the S.E. Massengill Company of Bristol, Tennessee, that wasn’t well understood. There was actually no legal requirement that companies understand their products, much less safety test them.

The company chemist who designed the cough syrup by mixing a sulfa drug into the poisonous sweetener claimed to have no such knowledge. And as the company president, Samuel Massengill responded: “We have been supplying a legitimate professional demand and not once could have foreseen the unlooked-for results. I do not feel that there was any responsibility on our part.”

The resulting Elixir Sulfanilamide scandal – and it was, indeed, an incendiary, nation-rocking scandal at the time - is mostly forgotten today. But it shouldn’t be. Those rippling deaths, the feeble government response, the indifference of the manufacturer and its big business allies - provoked such a passionate outcry that a year later, the long-delayed U.S. Food, Drug and Cosmetics Act was signed by President Franklin Roosevelt.

The 1938 law was first major upgrade of 1906 legislation. The earlier law established the U.S. government as a guardian of the American people’s safety, set precedents in regulating toxic chemicals in food and drugs. But that turn-of-the century law was in many ways a piece of regulatory lace, full of exceptions and exemptions. The new law filled many of those holes, gave power to protective rules.

Now, for the first time, manufacturers were required to safety test their wares and could be held responsible for consumer death and injury. In the case of Elixir Sulfanilamide, the company could not be held liable for a single death. It could only be charged with mislabeling – elixirs were supposed to contain alcohol and the cough syrup contained none.

The 1938 law also required manufacturers to list ingredients on their labels in some detail – another first. One of my favorite books of the 1930s, 100,000,000 Guinea Pigs, by Arthur Kallet and F.J. Schlink, is basically a litany of the hidden dangers that preceded that rule: the toothpaste that contained so much potassium chlorate that it was possible to commit suicide by eating a single tube; the high levels of lead in hair dye,;and the use of the toxic element thallium in depilatory creams. One of the side effects of thallium poisoning is that hair falls out. Cosmetic manufacturers of the 1930s thus found it handy in hair-removal products. They expressed surprise at the small epidemic of baldness, paralysis and occasional death that resulted. But, as they reminded irate physicians, they could not be held responsible for that.

But although advocates like Kallet and Schlink spent years marshaling such evidence in an effort to persuade the government to give the FDA actual enforcement powers, they were stymied by business opposition until the Elixir Sulfanilamide scandal galvanized the country. In an essay for the Annals of Internal Medicine, toxicologist Paul M. Wax called it “one of the most consequential mass-poisonings of the twentieth century.”

And it’s that case that always comes to mind when I hear politicians trumpeting the wonders of an unregulated marketplace, as with the current Republican party mantra that we don’t need strong environmental protections or – at the most extreme vantage point – even a U.S. Environmental Protection Agency at all. Last year, along the same lines, conservative legislators were busily trying to defund the FDA as well.

The Washington Post’s Ezra Klein points out that Americans tend to sound anti-regulation when queried. But, he adds, if you press them on which oversight they’d like to give up, the picture becomes more complicated. Klein cites a Pew Research survey done in February which found that 53 percent of respondents wanted food and food product regulation increased – only seven percent thought it should be reduced. For environmental regulation, slightly more – a full 17 percent – argued for relaxing the rules. The survey was, actually, unable to locate a majority of American citizens seeking to be less well protected.

We hear legislators suggest that hard economic times demand the loosening of regulations. But don’t forget that our country was still mired in the long-reach of the Great Depression when that 1938 law was passed. The government recognized, even then, that protection of American citizens meant more than policing our cities and defending our borders. It meant dedicated protection of public health.

Do we sometimes wish that such protection was smarter, moved faster, was more richly knowledge-based? Less influenced by politics, on occasion, by corporate lobbyists? Of course, we do. But I see that as a call to keep the process as politics free as possible (dreaming, I know), to invest more in good risk research and to use that knowledge to improve protection against everything from food poisoning to chemical contamination.

We may not remember by name the Kathleen Hobsons and Charlene Canadays of our past. And as I said, the Elixir Sulfanilamide story, is mostly forgotten as well. But we should be grateful for the way it changed our lives. And we should occasionally acknowledge those lost children; whether we recognize it or not, their ghosts still walk among us today, reminding us of what is right.

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About Pepper Spray

By Deborah Blum

One hundred years ago, an American pharmacist named Wilbur Scoville developed a scale to measure the intensity of a pepper’s burn. The scale – as you can see on the widely used chart to the left – puts sweet bell peppers at the zero mark and the blistering habenero at up to 350,000 Scoville Units.

I checked the Scoville Scale for something else yesterday. I was looking for a way to measure the intensity of pepper spray, the kind that police have been using on Occupy protestors including this week’s shocking incident involving peacefully protesting students at the University of California-Davis.

As the chart makes clear, commercial grade pepper spray leaves even the most painful of natural peppers (the Himalayan ghost pepper) far behind. It’s listed at between 2 million and 5.3 million Scoville units. The lower number refers to the kind of pepper spray that you and I might be able to purchase for self-protective uses. And the higher number? It’s the kind of spray that police use, the super-high dose given in the orange-colored spray used at UC-Davis.

The reason pepper-spray ends up on the Scoville chart is that – you probably guessed this - it’s literally derived from pepper chemistry, the compounds that make habaneros so much more formidable than the comparatively wimpy bells. Those compounds are called capsaicins and – in fact – pepper spray is more formally called Oleoresin Capsicum or OC Spray.

But we’ve taken to calling it pepper spray, I think, because that makes it sound so much more benign than it really is, like something just a grade or so above what we might mix up in a home kitchen. The description hints maybe at that eye-stinging effect that the cook occasionally experiences when making something like a jalapeno-based salsa, a little burn, nothing too serious.

Until you look it up on the Scoville scale and remember, as toxicologists love to point out, that the dose makes the poison. That we’re not talking about cookery but a potent blast of chemistry. So that if OC spray is the U.S. police response of choice – and certainly, it’s been used with dismaying enthusiasm during the Occupy protests nationwide, as documented in this excellent Atlantic roundup - it may be time to demand a more serious look at the risks involved.

My own purpose here is to focus on the dangers of a high level of capsaicin exposure. But as pointed out in the 2004 paper, Health Hazards of Pepper Spray, written by health researchers at the University of North Carolina and Duke University, the sprays contain other risky materials:

Depending on brand, an OC spray may contain water, alcohols, or organic solvents as liquid carriers; and nitrogen, carbon dioxide, or halogenated hydrocarbons (such as Freon, tetrachloroethylene, and methylene chloride) as propellants to discharge the canister contents.(3) Inhalation of high doses of some of these chemicals can produce adverse cardiac, respiratory, and neurologic effects, including arrhythmias and sudden death.

Their paper focuses mostly, though, on the dangerous associated with pepper-based compounds. In 1997, for instance, researchers at the University of California-San Francisco discovered that the “hot” sensation of habeneros and their ilk was caused by capsaicin binding directly to proteins in the membranes of pain and heat sensing neurons. Capsaicins can activate these neurons at below body temperature, leading to a startling sensation of heat. Repeated exposure can wear the system down, depleting neurotransmitters, reducing the sensation of the pain. This knowledge has led to a number of medical treatments using capsaicins to manage pain.

Its very mechanism, though, should remind us to be wary. As the North Carolina researchers point out, any compound that can influence nerve function is, by definition, risky. Research tells us that pepper spray acts as a potent inflammatory agent. It amplifies allergic sensitivities, it irritates and damages eyes, membranes, bronchial airways, the stomach lining – basically what it touches. It works by causing pain – and, as we know, pain is the body warning us of an injury.

In general, these are short term effects. Pepper spray, for instance, induces a burning sensation in the eyes in part by damaging cells in the outer layer of the cornea. Usually, the body repairs this kind of injury fairly neatly. But with repeated exposures, studies find, there can be permanent damage to the cornea.

The more worrisome effects have to do with inhalation – and by some reports, California university police officers deliberately put OC spray down protestors throats. Capsaicins inflame the airways, causing swelling and restriction. And this means that pepper sprays pose a genuine risk to people with asthma and other respiratory conditions.

And by genuine risk, I mean a known risk, a no-surprise any police department should know this risk, easy enough to find in the scientific literature. To cite just three examples here:

1) Pepper Spray Induced Respiratory Failure Treated with Extracorporeal Membrane Oxygenation

2) Assessing the incapacitative effects of pepper spray during resistive encounters with the police.

3) The Human Health Effects of Pepper Spray.

That second paper is from a law enforcement journal. And the summary for that last paper notes: Studies of the effects of capsaicin on human physiology, anecdotal experience with field use of pepper spray, and controlled exposure of correctional officers in training have shown adverse effects on the lungs, larynx, middle airway, protective reflexes, and skin. Behavioral and mental health effects also may occur if pepper spray is used abusively.

Pepper spray use has been suspected of contributing to a number of deaths that occurred in police custody. In mid-1990s, the U.S. Department of Justice cited nearly 70 fatalities linked to pepper-spray use, following on a 1995 report compiled by the American Civil Liberties Union of California. The ACLU report cited 26 suspicious deaths; it’s important to note that most involved pre-existing conditions such as asthma. But it’s also important to note a troubling pattern.

In fact, in 1999, the ACLU asked the California appeals court to declare the use of pepper spray to be dangerous and cruel. That request followed an action by northern California police officers against environmental protestors – the police were accused of dipping Q-tips into OC spray and applying them directly to the eyes of men and women engaged in an anti-logging protest.

“The ACLU believes that the use of pepper spray as a kind of chemical cattle prod on nonviolent demonstrators resisting arrest constitutes excessive force and violates the Constitution,” wrote association attorneys some 13 years ago.

Today, the University of California-Davis announced that it was suspending two of the police officers who pepper-sprayed protesting students. Eleven of those students were treated by paramedics on scene and two were sent to a hospital in Sacramento for more intensive treatment.

Undoubtedly, these injuries will factor into another scientific study of pepper spray, another acknowledgement that top of the Scoville scale is dangerous territory. But my own preference is that we start learning from these mistakes without waiting another 13 years or more, without engaging in yet another cycle of abuse and injury.

Now would be good.

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A Colorful Little Tale of Halloween Poison

by Deborah Blum

I grew up on a dead-end street in Baton Rouge, Louisiana, where remnants of swampy forest surrounded the old wood-frame homes. Live oaks lined the streets. Spanish moss dripped from their branches. Snakes coiled under the ancient azaleas that edged the yards.

It was, in fact, the perfect setting for a haunted Halloween night. And there was this one house, you know, where the yard was so dense with bush and tree that it could barely be seen through its thicket of shadow. To trick-or-treat, you walked up the dark sidewalk toward a faint glow on the front porch, just the one lit window. The air hummed with passing insects and the porch creaked like Dracula’s coffin under your feet, the slow, dry eek of old wood.

Reader, you had to beware on Halloween night. Just a block over lived a maniacal dentist who liked to dress up like a werewolf on October 31 and fill his front hall with clouds of drifting fog created by dropping dry ice (super-chilled chunks of carbon dioxide) into water. Bwa-ha-ha, he would chortle as he opened the door, as the chilly wisps of fog drifted out around him.

But this silent house, dressed in darkness, was so much scarier. We children would gather in front of the gate, unable to walk alone through those prowling shadows. The crowd would form on the sidewalk: tiny pillowcase ghosts and jeweled princesses, small pirates and glittery fairies. When someone decided we’d achieved a safe number, we’d start edging toward the green door at the top of the porch steps. Whispering about what the old man who lived there would hand out – what dangerous treats might wait for us there.

This was the 1960s and even then, people told stories, warned their children, about the psychopaths out there who might drop poisoned candy into one’s hands. In the long history of the holiday, truthfully, this has almost never happened. But the very nature of Halloween – the witch at the door, the monster in the closet – lends itself to such ideas. Wasn’t there a crazy woman on Long Island in 1964, after all, who handed out arsenic to trick-or-treaters she thought too old for the candy hunt?

It hardly mattered that as Snopes points out, she didn’t kill anyone. And her deliberate poisoning attempt seems to be an odd exception to the general goodwill of the holiday. The psychopath at the door is an urban myth. Most of the poisonous Halloween stories turn out to be mistakes or far more personal tragedies. The worst is that of a Texas father who murdered his eight-year-old son in 1974 for insurance money.

He did so by putting cyanide into into the fruit-flavored sugar inside a Pixie Stick, one of the child’s favorites. In an attempt to make the death seem like a random poisoning, the father – Ronald Clark O’Bryan – also gave cyanide-laced candy to his daughter and three other children in his Deer Park neighborhood. These other lethal treats were collected by police as (fortunately) the children hadn’t touched them.

O’Bryan – nicknamed The Candyman by the Texas media – was executed by lethal injection ten years after his son’s death. But people remembered. And they forgot that the worst outbreak of Halloween candy poisoning had nothing to do suspected killers. The biggest poison outbreak – linked to Halloween of 1950 – was simply caused by orange food coloring used by candy manufacturers.

Scores of children across the country fell ill with severe diarrhea and welting rashes after eating candy and popcorn balls tinted by the FDA approved Orange Dye No. 1 ( also known as FD&C Orange No. 1, Acid Orange 20, and Orange 1). The “FD&C” indicates that the dye is used in food, drugs and cosmetics. Throughout the first half of the 20th century, Orange 1 was used primarily in candy, cookies, cakes, carbonated beverages, and meat-products such as hot dogs.

As federal investigators would discover upon investigation, the dye was also a rash-inducing occupational health hazard. Orange 1 belonged to a group of seven dyes first approved by the federal government in the year 1906, the first year that this country began regulating food safety. All seven of these dyes were coal-tar dyes, derived originally from the hydrocarbon byproducts of processed coal. Orange 1, for instance, contained benzene, today one of our better known toxic compounds.

But at that Halloween moment in 1950, no one had thought much about colored food. In fact, officials at the U.S. Food and Drug Administration suddenly realized that no one had really taken a good look at these turn-of-the-century food dyes for almost 50 years. The FDA promptly launched an investigation that found that, yes, Orange 1 was definitely poisonous: an oral dose of one gram of the dye per one kilogram of food killed two out of five mice in a day. A 20-week-experiment mixing the dye into rat food killed three of eight test rats.

The researchers also found that manufacturers were tossing the dye into candy corn and sugary little pumpkins with surprising enthusiasm. According to a 1954 article in The New York Times, one piece of candy was 1,500 parts per million pure Orange 1. Two years later, in 1956, the FDA delisted Orange 1 as well as Orange 2 (used to deepen the color of oranges) and Red Dye No. 32. Twelve other food colorings have been delisted since that time. This doesn’t reassure everyone; consumer advocates still worry over the health effects of food coloring.

But – take at least this reassurance: it’s been a long time since we saw children falling ill across the country because they indulged in an extra handful of candy corn, not realizing that its cheerful orange was a signal for trouble. We’re mostly smart enough to realize that regulating food safety offers more protection than worrying about the crazy man behind the door.

Which brings me back to my friends and I hesitating at that shadowy gate on a Halloween night in Louisiana. Let me tell you what happened, Halloween after Halloween. Slowly, we inched down the sidewalk, creaked up the steps, quavered at the door. Slowly, the door pulled open and the slightly tottering elderly man opened the screen to drop glossy red apples into our bags.

Every year it added an extra thrill to the night. But, reader, you had to beware on Halloween night. I’m almost positive they were just bright fall apples. But our parents wouldn’t let us eat them.

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