The Curious Case of the Poisoned Cows
Tuesday, 2012/07/03 | 09:59:40
June 29, 2012 |
On a bright morning in early June, a Texas rancher named Jerry Abel turned his small herd of cattle out to graze. The 18 cows moved hungrily into that field of fresh grass. Within a few hours, only three were still alive.
Abel’s 80 acre ranch sits just a little east of Austin and the story was strange enough that on Sunday a local CBS affiliate picked it up. “There was nothing you could do,” Abel told KEYE about his desperate efforts to save the animals. “Obviously, they were dying.”
The television reporter apparently saw the evil hand of science at work in the episode, at least that was definitely the message in the story: “Genetically modified grass linked to cattle deaths.“ Alternatively, she just didn’t do her homework because the grass in question – Tifton 85 - is not a GM product. It’s a decades old hybrid grass developed by Georgia agricultural scientists as a high-protein, easily digestible forage.
The CBS story was immediately circulated – and by circulated, I mean embraced – by anti-GM activists and bloggers. I wrote a summary of this for the Knight Science Journalism Tracker earlier this week which detailed both the activist enthusiasm for the story (one suggested that GM grass was practically producing chemical warfare agents) and the rapid corrective response from science writers who knew what “hybrid” actually meant. The you-got-this-wrong message was so strong that CBS News corrected the story within a day.
But my point here is not to review the media issue but to take a look at the Sherlockian mystery of how a pasture full of a well-known hybrid grass could suddenly turn so murderous. And I’ll give away part of the solution by reminding you of something we tend to forget in our obsession with the risks of synthetic chemistry and genetic engineering. What the Texas cow story reminds us – or should – is that naturally occurring chemistry can be just as wicked as anything we dream up in a laboratory.
There’s no debate over the poison that killed Mr. Abel’s cows. Hydrogen cyanide was found both in the cow’s bodies and in the grass itself. The veterinarian who autopsied the animals, called it prussic acid poisoning. Prussic acid is an old-time term for hydrogen cyanide (derived from hydrocyanic acid), dating back to some 18th century chemistry experiments in which a deep blue pigment used by artists, called Prussian Blue , was mixed with acid to generate the poison.
The foundation of any cyanide is a a cyano group – basically a carbon atom tripled bonded to a nitrogen atom (with the chemical symbol CN). Cyanides are natural joiners, attaching to other chemicals with enthusiasm. Thus we have the gases hydrogen cyanide (HCN) and cyanogen chloride (CNCl) and the salts – sodium cyanide (NaCN), potassium cyanide (KCN). All are acutely poisonous. And while I earlier mocked the anti-GM activist comparing Texas grass to chemical weaponry, both hydrogen cyanide and cyanogen chloride do have military designations. The military symbol for hydrogen cyanide is AK.
But don’t let that fool you into thinking that cyanides are a human invention. They aren’t. We just capitalized on an invention of nature itself, a chemistry shared by numerous plant species including some grasses. Why? Most scientists believe that plants developed this chemistry as a way of fending off predators, from insects to grazers. The plants store cyanides in an inactive form but they can release them under threat or stress.
The stored forms of cyanide in plants are called cyanogenic glycosides. Basically this tells us that the cyanide is bound to – neatly locked up by – sugars in the plant. Under stress, though, the cyanide-sugar bond can break and the poison can be released. How many plant species hold this potential? Thousands. After the Texas cattle story appeared, the scientist and blogger Mary Mangan sent me a link to a 1998 article in the journal Phytochemistry titled “Why Are So Many Food Plants Cyanogenic”?
The paper’s author, David A. Jones, points out that “There are now sufficient examples of plant defense by cyanogenesis for us to conclude that cyanogenesis is an important system of chemical defense in plants.” He then reviews an astonishing variety of food plants that contain these precursor poisons, including wheat, barley, oats, rye, French beans, kidney beans, lima beans, apples, peaches, plums, apricots, cherries, almonds, Macadamia nuts, quince, papaya, passion fruit, bamboo shoots, cassava root, taro root and more.
As Jones notes, in most cases we are eating plants in which the cyanides remain locked up by the surrounding sugars. Or they are found in parts of the fruit, say, that we normally don’t eat – the seeds of the apple, the pit of the peach. And we usually eat them in a small enough amount (dose) and at a gradual enough rate that our own metabolic enzymes can break them down into a relatively harmless state. I say relatively because there are some instances of harm from what Jones calls “chronic cyanide poisoning of humans”, but these tend to occur in high risk groups. People with sickle cell diseases, tobacco smokers, people with Leber’s disease (an inherited degeneration of the optic nerve) seems less able to detoxify cyanogenic compounds. As one example of this, Jones cites a number of Leber’s patients who went blind due to the cyanogens found in apple cider.
None of this, you’ve probably noted, involves people or animals suddenly dropping dead of cyanide poisoning. Most of that of course, is because we’re still talking about consumption of those sugar-bound poison molecules. But what if the plant is an unhappy plant? What if it’s suffering from sustained, damaging stress? And what if, under that stress, the glycosides unravel and release pure hydrogen cyanide?
As we all know, Texas is in the midst of a sustained and destructive drought. And as it turns out, there’s quite a bit of research showing that forage grasses can become surprisingly poisonous when they are stressed by heat and drought. To that end, I refer you to this article from the University of Wyoming titled, “Managing Forages to Minimize Prussic Acid Poisoning.” Or “Livestock and Prussic Acid Poisoning” from Ohio State University. Or “Preventing Prussic Acid Poisoning of Livestock” from Oregon State University. And as it also turns out, the Tifton 85 grass in Mr. Abel’s field is a hybrid of Bermuda grass and star grass. And star grass is one of those cyanogenic plant species we’ve just been discussing.
All of which suggests that Mr Abel’s cows were caught in a lethal interaction between some very old and very well known plant chemistry and an entrenched period of hot, dry weather. As you’ve noticed, this doesn’t solve for the entire mystery. Why this field and not other Texas fields planted with Tifton 85? One possibility is suggested by an investigation by Natural News, which points out that heavy use of nitrogen fertilizers can influence the cyanogenic process. Natural News, of course, is firmly in the anti-GM camp but even it concluded that “there appears to be no GMO, no secret experiments, no conspiracy.”
There’s a hint of disappointment in that line. But there shouldn’t be. Because this piece of scientific detective work leads us to a point that – as I said earlier – we too often forget: that we live in a chemical word, amazing, complicated, ingenious, and occasionally wonderfully, startlingly, and terrifyingly lethal.
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