The summer of 1972 was an unusually rainy season in the Corn Belt – the “I” states: Indiana, Iowa, Illinois – and many of the corn fields were infected by the fungus Fusarium graminearum, which in its anamorph lifecycle goes by the name Gibberella zeae (a much cooler name, if you ask me), and also infects wheat and barley (1). These things happen, and the corn was fed to the pigs anyways. But a funny thing happened on the way to the slaughterhouse, the pigs either vomited, or stopped eating, and lost weight. And no one likes an anorexic pig (2).

So in comes the U.S. Department of Agriculture to the rescue. From samples of infected corn they ground, extracted, separated and identified the culprit. They named it vomitoxin, because it caused pigs to, you know, vomit. Seriously. And if the pigs had diarrhea instead, they would have named it shitoxin. OK, I made that one up.

So just what is shitoxin…I mean vomitoxin? Vomitoxin, also known by the lame name deoxynivalenol, belongs to a family of mycotoxins (fungus derived toxins) called trichothecenes. The trichothecenes share the tricyclic backbone exemplified by vomitoxin on the left. Many of these mycotoxins are produced by the fungal genus Fusarium.

If you grow tomatoes, Fusarium may sound familiar, as Fusarium oxysporum is responsible for the fungal disease “fusarium wilt,” which is a vascular disease and causes leaves to yellow and die. Gardeners, like me, don’t like fusarium wilt.

Of the trichothecenes, and there’s nearly 200 of them, vomitoxin is relatively tame. It’s cousin though, T-2, is responsible for tens of thousands of deaths and has even been used as a biological weapon. So while you aren’t likely to die from vomitoxin exposure, it does constitute a serious economic and health liability.

Because of its hazards to livestock and humans, most countries have set thresholds for allowable vomitoxin concentrations in grain products. The U.S Food and Drug Administration has set a limit of 1 part per million (ppm, or 1000 ug vomitoxin/kg grain), while many other countries in Europe and Asia have set a limit of 0.5 ppm. In the U.S. economic losses due to vomitoxin exceed over 1 billion annually because of inferior quality of the grain and crop, feed, and livestock losses (3).

There’s really no getting around vomitoxin. Our grains and grain products, such as breads, crackers and cereals, have it. And unfortunately the trichothecene mycotoxins are stable to baking processes. In making bread, for example, vomitoxin concentration is only decreased 7% (4). The question to ask is how much are we exposed to and what is the impact to human health. Fortunately, this is a well-studied area, and has made what I thought was going to be a short, silly posting into something a bit more in depth than I wanted. Such is life.

A three-year study was conducted in the Jiangsu province of China to determine the vomitoxin prevalence and concentration in wheat crops (5). From 180 samples, 75% of them contained detectable levels of vomitoxin, ranging from 14 to 41,000 ug/kg, with an average of 488 ug/kg, or 0.488 ppm. These result are fairly typical, I just used a result from China because it seems that nearly everything in the U.S. is made in China.

So let’s travel from China to France, and explore how much vomitoxin is in the foods we eat. In a total diet study, 577 foods from mainland France, meant to be representative of the population’s diet, were analyzed for mycotoxins, including vomitoxin (6). Foods highest in vomitoxin were ones that you might expect, breads, pasta, and pastries, with concentrations of 132, 56, and 73 ug/kg, respectively. When applied to typical diets, the average French adult is exposed to 0.40 ug per kilogram of body weight per day (ug/kg bw/day), while a child is exposed to 0.55 ug/kg bw/day. The health-based guidance value for exposure is set at 1 ug/kg bw/day. These were just averages, and when looking at the 95th percentile of 0.75 and 1.0 ug/kg bw/day, for adults and children, there are many that meet or exceed the recommended exposure to vomitoxin.

You’re sick of the numbers, I get it. The take home message here is that we are all exposed to vomitoxin, every day, and there’s not much we can do about it, save for going Caveman. Never go full Caveman.

So what’s the harm in vomitoxin? We’ve already established that vomitoxin makes pigs throw up, and it has similar effects in cats and dogs, too. Humans are no exception either. In China between 1961 and 1981 there were 32 outbreaks of food poisoning associated with Fusarium infested wheat and corn (3). Of the 9300 people who consumed the infected grains, 6000 of them experienced symptoms of vomitoxin poisoning. The symptoms included nausea, vomiting, diarrhea, abdominal pain, and fever. All of these symptoms mimic those of “traditional” bacterial food-borne illness.

The mechanism behind vomitoxin toxicity, and associated GI disturbances, lies in its ability to destroy intestinal barrier functions (7). The intestinal barrier is the body’s largest and most important barrier, and facilitates the transport of nutrients into the body, while keeping toxins out. The selective barrier is made of protein-protein networks that link adjacent cells, and are known as tight junctions. The destruction of these tight junctions allows antigens and other toxins to enter the body and blood stream. The breakdown of tight junctions is associated with the onset and recurrence of chronic intestinal inflammation, which would be expected if antigens – anything that triggers an immune response – have free reign over the intestines. Diseases that follow this pattern are the well known inflammatory bowel disease (IBD) and celiac disease (8).

Think of your intestinal barrier as the Great Wall of China held together by tight junctions. Now imagine the tight junctions being destroyed and the Mongols invading. It’s just like that. The facilitator in breaking apart those tight junctions? That would be the Mongol’s secret weapon: vomitoxin. And it’s not just a high dose acute exposure that leads to the gastritis and intestinal distress symptoms, chronic low-level amounts of vomitoxin can disrupt the intestinal barrier and may be a factor in IBD, celiac disease, and food allergies (8).

So when someone suspects food poisoning, maybe they should consider vomitoxin toxicity, especially if they’ve had a grain heavy meal – like pasta made from flour milled by the farm down the road. And the current fad of “gluten-free” diets – perhaps people that have GI upsets after eating wheat products are just sensitive to vomitoxin, and it has nothing to do at all with gluten.

So there we go, an around-the-world voyage in explaining vomitoxin, something I stumbled upon that made me laugh because of its name. Who knew it was something so serious? And why can’t all toxin names be self-explanatory?

*** [Featured homepage image of Wheat Field by Jeff Golden (CC BY-SA 2.0)] ***

References:

1. Vesonder, R. F., A. Ciegler, and A. H. Jensen. “Isolation of the Emetic Principle from Fusarium-Infected Corn.” Applied Microbiology 26.6 (1973): 1008-1010

2. It’s true, I asked.

3. Pestka, James, and Alexa Smolinski. “Deoxynivalenol: Toxicology and Potential Effects on Humans.”Journal of Toxicology and Environmental Health, Part B 8.1 (2005): 39-69.

4. Giménez, Isabel, Jesús Blesa, Marta Herrera, and Agustín Ariño. “Effects of Bread Making and Wheat Germ Addition on the Natural Deoxynivalenol Content in Bread.” Toxins 6.1 (2014): 394-401.

5. Ji, Fang, Jianhong Xu, Xin Liu, Xianchao Yin, and Jianrong Shi. “Natural Occurrence of Deoxynivalenol and Zearalenone in Wheat from Jiangsu Province, China.” Food Chemistry 157 (2014): 393-97.

6. Sirot, Véronique, Jean-Marc Fremy, and Jean-Charles Leblanc. “Dietary Exposure to Mycotoxins and Health Risk Assessment in the Second French Total Diet Study.” Food and Chemical Toxicology52 (2013): 1-11.

7. Akbari, P., S. Braber, H. Gremmels, and P. Koelink. “Deoxynivalenol: A Trigger for Intestinal Integrity Breakdown.” The FASEB Journal 28.6 (2014): 2414-429.

8. Demeo, Mark T., Ece A. Mutlu, Ali Keshavarzian, and Mary C. Tobin. “Intestinal Permeation and Gastrointestinal Disease.” Journal of Clinical Gastroenterology 34.4 (2002): 385-96.