Sign Up for Our Newsletter


They’re Feeding WHAT to Cows?
'Poultry litter' is exactly what it sounds like: the filthy stuff scraped off the floor of a chicken coop. Feeding it to cattle (yes, that happens) risks the spread of mad cow disease—yet the FDA has done nothing to stop it.

This show on the Cartoon Network was funny. What cows are eating is not.

Anyone who pays even scant attention to where our food comes from is likely aware that some pretty unsavory things happen between the farm and your fork (see this month’s big story in Rolling Stone, for example). But some of these farming methods are more than just unappetizing: they could be deadly. One practice in particular could allow for the spread of bovine spongiform encephalopathy, or BSE, the gruesome and fatal neurodegenerative disorder more commonly known as mad cow disease.

The practice in question is feeding what’s known as “poultry litter” to farmed cattle. Poultry litter is the agriculture industry’s term for the detritus that gets scooped off the floors of chicken cages and broiler houses. It’s mainly a combination of feces, feathers, and uneaten chicken feed, but in addition, a typical sample of poultry litter might also contain antibiotics, heavy metals, disease-causing bacteria, and even bits of dead rodents, according to Consumers Union (the policy and action arm of the nonprofit that publishes Consumer Reports).

Aside from the fact that we’re feeding our cows chicken crap, this practice is worrisome because both the excrement and uneaten pellets of chicken chow found in poultry litter can contain beef protein, including ground-up meat and bone meal. Which means—if you can follow the gruesome flow chart here—that cows could be, indirectly, eating each other.

As the U.S. Department of Agriculture has made quite clear, cows really, really shouldn’t be doing that. Meat and bone meal containing infected bovine protein, the USDA says, is the chief culprit behind the spread of mad cow disease. (The closely related illness in humans is called variant Creutzfeldt-Jakob disease.)

The U.S. Food and Drug Administration wisely banned the practice of feeding the remains of dead cows to living ones back in 1997. But the agency has never prohibited feeding those same remains to chickens and other poultry, nor does it currently prohibit feeding poultry litter to cattle. And so, thanks to this ghoulish quirk of our Rube Goldberg-like regulatory mechanism—call it the Feedlot Feedback Loop, or maybe the Feedlot Feedback Loophole—cows are still at risk of consuming the suspect bovine proteins that inspired the 1997 ban in the first place.

“I’ve always been against the feeding of poultry litter back to ruminants [cows and their cud-chewing cousins],” says Linda Detwiler, who served as the USDA’s head of mad cow surveillance from 1996 to 2002 and who has more than 25 years of experience working with the disease. “If there was contamination with the BSE agent—through either spilled feed or feed that passed through undigested—there could be a potential of exposure to cattle.”

Just how much poultry litter actually gets collected, processed, and fed to cows isn’t precisely known. In 1967, the FDA declared that poultry litter could be classified as an “adulterated” form of livestock feed, a designation that effectively prohibited its interstate shipment and greatly curbed its use for such purposes. But in 1980, at the dawning of Reagan-era deregulation, the agency stopped policing its use and ceded the issue of how to handle poultry litter to state agricultural agencies.

Those agencies, alas, haven’t done a very good job of regulating it since then. According to a survey conducted by the Food Animal Concerns Trust, a Chicago-based organization that advocates for the welfare of farm animals, 21 of 32 responding state agencies reported that they neither monitored nor maintained any data on the amount of poultry litter being used as cattle feed in their jurisdictions. The FDA has estimated that between 1 million and 2 million tons of it are fed to U.S. cattle every year.

Aside from the fact that we’re feeding our cows chicken crap, this practice is worrisome because—if you can follow the gruesome flow chart here—it means that cows could be, indirectly, eating each other.

In early 2003, shortly after the first U.S. cow infected with bovine spongiform encephalopathy was discovered in Washington State, the FDA responded to mounting public anxiety by announcing that it would ban the use of poultry litter as cattle feed. But once Big Ag stepped in, the agency suggested a different course of action. There was no need for a permanent ban, the FDA concluded: just a promise by chicken-feed manufacturers that they would leave out the riskiest, most infectious bovine tissues, mainly from brains and spinal cords. (If this sounds familiar, it’s probably because the FDA said yesterday that it is taking a similar voluntary approach to the overuse of antibiotics in livestock, another potential human health risk.) Such promises on poultry litter notwithstanding, Detwiler says risky bovine tissue could still make its way into chicken feed. “The FDA is not requiring all the infectious parts to be [taken] out.”

The FDA did not respond to OnEarth’s requests for comment on this story.

Why does Big Ag want to keep feeding poultry waste to cows? That’s an easy one: It’s plentiful, expensive to dispose of by other means, and relatively rich in protein (however disgusting a form that protein may take). Feeding it to ruminant livestock represents a win-win for beef producers and poultry producers—just not for cows, or for anyone who happens to eat beef and care about its safety.

Which is why in August 2009, more than a dozen national consumer and animal welfare organizations formally petitioned the FDA to put an end to this practice once and for all. They cited recent studies by researchers at Harvard highlighting the risks. They cited bans already in place in a number of countries: Australia, New Zealand, Canada, and the European Union member states among them. They poked holes in the logic used by the FDA to demonstrate poultry litter’s safety and to justify its continued use. The agency’s self-imposed deadline for responding to the petitioners was February 2010. Those petitioners are still waiting for an answer.

Michael Hansen, a senior scientist at Consumers Union, was one of the petition’s signers. He describes the FDA’s lack of a formal response as “appalling.” In a closed-door meeting with agency officials that he attended last summer, he recalls, those officials blamed the delay on the massive backlog of other petitions currently demanding the agency’s attention. When they were reminded of exactly how long—nearly four years—Hansen and others had been waiting for a response, the officials seemed unfazed, Hansen says. Their blasé attitude “makes no sense,” in his words, given that the FDA had already acknowledged the potential hazards of feeding poultry litter to cows when it announced plans to ban the practice back in 2004. (Again, this might sound familiar: it has taken the FDA more than 30 years to act on the well-known risk of antibiotics use in livestock.)

Detwiler, who left the USDA in 2003 and now works as a global consultant on mad cow issues, believes that the FDA’s inactivity reflects a dangerous complacency surrounding the contemporary incidence of the disease. Safeguards put in place after Europe experienced a string of mad cow outbreaks in the 1980s and 1990s have mitigated many risk factors, she said, but that doesn’t mean protective agencies can let their guard down—especially now that new, atypical strains of BSE have entered the picture.

Wait—what’s that? Well, here in the United States, all three cows confirmed to have contracted BSE since 2003 have tested positive for an atypical strain of the disease, as opposed to the more widely studied (and better understood) “typical” strain. USDA officials maintain that atypical BSE findings in cows are actually cause for less concern, not more, because these officials, along with some in the scientific community, believe these atypical strains can only occur spontaneously and are rooted in genetic defects, rather than contaminated feed.

Detwiler, Hansen, and other scientists say there’s simply not enough evidence to support that belief. And it would seem that they’re not alone: the U.S. Centers for Disease Control and Prevention cautions that “transmission through feed or the environment cannot be ruled out.” What’s more, Detwiler and Hansen note, recent studies suggest that atypical BSE strains may be more virulent than the typical strain. “We have to be very careful,” Detwiler says. “I think scientists and public officials should point out that we still don’t know all there is to know.”

With only three U.S. cases of BSE-infected cattle detected in the last decade, the USDA claims that our current safeguards are sufficient. But as Hansen notes, the agency tests only one-tenth of one percent of the roughly 35 million U.S. cattle slaughtered annually. Given what we know about the presence of bovine tissue in poultry litter, and given what we don't know about how atypical BSE is contracted, we should at least let caution and prudence offset some of the information gap.

Other countries have banned feeding poultry litter to cows “for quite good reason,” Hansen says. “These diseases don’t go away until you take strong measures.”

Like this article? Donate to NRDC to support OnEarth's groundbreaking nonprofit journalism.

image of Brad Jacobson
Brad Jacobson is an OnEarth contributor, who covers energy, environment, and public health for the magazine. His reporting has appeared elsewhere in The Atlantic, In These Times, Salon, Columbia Journalism Review, Billboard, and other publications. He's also a regular contributor to the award-winning online news magazine AlterNet. Follow him on Twitter. MORE STORIES ➔
Comments (7)
Reader comments are moderated and may be edited or deleted if they violate our rules for civil discourse.
All comments offered in the spirit of civil discourse are welcome. Commercial spam, obscenity, and other rude behavior are not and will be removed. Due to our nonprofit status, we are also required to delete any express or implied statement endorsing or opposing any political party or candidate for political office. Valid email addresses are required. (OnEarth respects your privacy and will not use, lend, or sell your email address for any reason.)
I'm as put off as the next person at the idea of feeding poultry litter to cows just because it's poop, but I don't like hysteria just as much. Has anyone ever actually found one of those wacky Prions in poultry litter? I can't find any literature saying that they have. Ed
Do you think that might be because no one's bothering to look for them, as the story says?
I think the question should be, has anyone ever looked at feces, to see if the TSE prion is detectable ??? Detection of PrPCWD in Rocky Mountain Elk Feces Using Protein Misfolding Cyclic Amplification Bruce E Pulford,1 Terry Spraker,1 Jenny Powers,2 Margaret Wild2 and Mark D. Zabel1 1Department of Microbiology; Immunology and Pathology; College of Veterinary Medicine and Biomedical Sciences; Colorado State University; 2Biological Resource Management Division; United States National Park Service; CO, USA Key words: CWD, feces, PMCA, elk Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy affecting cervids, including mule and white-tailed deer (Odocoileus hemionus and virginianus), elk (Cervus elaphus nelsoni) and moose (Alces alces shirasi). The method of CWD transmission between hosts is unclear, though there is evidence that feces excreted by infected animals may play a role. Recently, CWD prions was detected in feces using bioassays in cervidized mice, which took many months to produce results. In this study, we use a more rapid procedure, protein misfolding cyclic amplification (PMCA), to test elk feces for the presence of PK-resistant cervid PrP (PrPCWD). Feces were collected from symptomatic and asymptomatic elk in several northern Colorado locations, homogenized, mixed with normal brain homogenate from Tg5037 mice (expressing cervid PrP) and subjected to up to 9 rounds of PMCA (1 round = 40 secs sonication/30 mins at 70% maximum power, 24 hours). Western blots were used to detect PrPCWD using BAR-224 anti-PrP antibody. Rectal and CNS tissue from the elk were IHC-labeled and examined for the presence of PrPCWD. Fecal samples from symptomatic and asymptomatic elk that tested positive by IHC showed characteristic PrPCWD bands on western blots following PMCA. In addition, PMCA detected PrPCWD in 25% of fecal samples from IHC-negative animals. These data suggest that PMCA may (1) prove useful as a non-invasive method to supplement or even replace IHC testing of cervids for CWD, and (2) identify additional asymptomatic carriers of CWD, the prevalence of which may be underestimated using IHC. Detection of subclinical infection in deer orally exposed to urine and feces (1) suggests that a prolonged subclinical state can exist, necessitating observation periods in excess of two years to detect CWD infection, and (2) illustrates the sensitive and specific application of sPMCA in the diagnosis of low-level prion infection. Based on these results, it is possible that low doses of prions, e.g. following oral exposure to urine and saliva of CWD-infected deer, bypass significant amplification in the LRS, perhaps utilizing a neural conduit between the alimentary tract and CNS, as has been demonstrated in some other prion diseases. In summary, we provide evidence for the presence of infectious prions in the brains of conventional prion-assay-negative deer orally exposed 19 months earlier to urine and feces from CWD-infected donor deer. This apparent low level of prion infection was amplified by sPMCA, confirmed by Tg[CerPrP] mouse bioassay, and detected only in the obex region of the brain. These results demonstrate the potential for CWD prion transmission via urine and/or feces, and highlight the application of more sensitive assays such as sPMCA in identification of CWD infection, pathogenesis, and prevalence. In contrast, CWD prions have been reported in saliva, urine and feces, which are thought to be responsible for horizontal transmission. While the titers of CWD prions have been measured in feces, levels in saliva or urine are unknown. Because sheep produce ~17 L/day of saliva and scrapie prions are present in tongue and salivary glands of infected sheep, we asked if scrapie prions are shed in saliva. We inoculated transgenic (Tg) mice expressing ovine prion protein, Tg(OvPrP) mice, with saliva from seven Cheviot sheep with scrapie. Six of seven samples transmitted prions to Tg(OvPrP) mice with titers of -0.5 to 1.7 log ID50 U/ml. Similarly, inoculation of saliva samples from two mule deer with CWD transmitted prions to Tg(ElkPrP) mice with titers of -1.1 to -0.4 log ID50 U/ml. Assuming similar shedding kinetics for salivary prions as those for fecal prions of deer, we estimated the secreted salivary prion dose over a 10-mo period to be as high as 8.4 log ID50 units for sheep and 7.0 log ID50 units for deer. These estimates are similar to 7.9 log ID50 units of fecal CWD prions for deer. Because saliva is mostly swallowed, salivary prions may reinfect tissues of the gastrointestinal tract and contribute to fecal prion shedding. Salivary prions shed into the environment provide an additional mechanism for horizontal prion transmission. Conclusions. This study documents the first aerosol transmission of CWD in deer. These results further infer that aerosolized prions facilitate CWD transmission with greater efficiency than does oral exposure to a larger prion dose. Thus exposure via the respiratory mucosa may be significant in the facile spread of CWD in deer and perhaps in prion transmission overall. Conclusion. Transepithelial transport of prions across nasal cavity mucosa begins within minutes of inhalation and can continue for up to 3 h. While M cells appear to transport prions across the follicular associated epithelium, larger amounts of prions are transported between the cells of the respiratory and olfactory epithelia, where they immediately enter the lymphatic vessels in the lamina propria. Thus, inhaled prions can be spread via lymph draining the nasal cavity and have access to somatic and autonomic nerves in the lamina propria of the nasal cavity. The increased efficiency of the nasal cavity route of infection compared with the oral route may be due to the rapid and prolonged transport of prions between cells of the respiratory and olfactory epithelia. Now that these experiments are completed we conclude that TSE infectivity is likely to survive burial for long periods of time with minimal loss of infectivity and restricted movement from the site of burial. These experiments emphasize that the environment is a viable reservoir for retaining large quantities of TSE infectivity, and reinforce the importance of risk assessment when disposing of this type of infectious material. Friday, December 06, 2013 2:39 PM Procedures for identifying infectious prions after passage through the digestive system of an avian species A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO CAMELUS) - SPONGIFORM ENCEPHALOPATHY 4.21 Three cases of SE’s with an unknown infectious agent have been reported in ostriches (Struthio Camellus) in two zoos in north west Germany (Schoon @ Brunckhorst, 1999, Verh ber Erkeg Zootiere 33:309-314). These birds showed protracted central nervous symptoms with ataxia, disturbances of balance and uncoordinated feeding behaviour. The diet of these birds had included poultry meat meal, some of which came from cattle emergency slaughter cases. SE1806 TRANSMISSION STUDIES OF BSE TO DOMESTIC FOWL BY ORAL EXPOSURE TO BRAIN HOMOGENATE 1 challenged cock bird was necropsied (41 months p.i.) following a period of ataxia, tremor, limb abduction and other neurological signs. Histopathological examination failed to reveal any significant lesions of the central or peripheral nervous systems... 1 other challenged cock bird is also showing ataxia (43 months p.i.). snip... 94/01.19/7.1 A notification of Spongiform Encephalopathy was introduced in October 1996 in respect of ungulates, poultry and any other animal. 4.23 MAFF have carried out their own transmission experiments with hens. In these experiments, some of the chickens exposed to the BSE agent showed neurological symptoms. However MAFF have not so far published details of the symptoms seen in chickens. Examination of brains from these chickens did not show the typical pathology seen in other SE’s. 4.24 A farmer in Kent in November 1996 noticed that one of his 20 free range hens, the oldest, aged about 30 months was having difficulty entering its den and appeared frightened and tended to lose its balance when excited. Having previously experienced BSE cattle on his farm, he took particular notice of the bird and continued to observe it over the following weeks. It lost weight, its balance deteriorated and characteristic tremors developed which were closely associated with the muscles required for standing. In its attempts to maintain its balance it would claw the ground more than usual and the ataxia progressively developed in the wings and legs, later taking a typical form of paralysis with a clumsy involuntary jerky motion. Violent tremors of the entire body, particularly the legs, became common, sparked off by the slightest provocation. This is similar to that seen in many BSE cases where any excitement may result in posterior ataxia, often with dropping of the pelvis, kicking and a general nervousness. Three other farmers and a bird breeder from the UK are known to have reported having hens with similar symptoms. The bird breeder who has been exhibiting his birds for show purposes for 20 years noticed birds having difficulty getting on to their perch and holding there for any length of time without falling. Even though the bird was eating normally, he noticed a weight loss of more than a pound in a bird the original weight of which was 5 pounds. 4.25 Histological examination of the brain revealed degenerative pathological changes in hens with a minimal vacuolation. The presence of PrP immunostaining of the brain sections revealed PrP-sc positive plaques and this must be regarded as very strong evidence to demonstrate that the hens had been incubating Spongiform Encephalopathy. OPINION on : NECROPHAGOUS BIRDS AS POSSIBLE TRANSMITTERS OF TSE/BSE ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 7-8 NOVEMBER 2002 OPINION 1. Necrophagous birds as possible transmitters of BSE. The SSC considers that the evaluation of necrophagous birds as possible transmitters of BSE, should theoretically be approached from a broader perspective of mammals and birds which prey on, or are carrion eaters (scavengers) of mammalian species. Thus, carnivorous and omnivorous mammals, birds of prey (vultures, falcons, eagles, hawks etc.), carrion eating birds (crows, magpies etc.) in general could be considered possible vectors of transmission and/or spread of TSE infectivity in the environment. In view also of the occurrence of Chronic Wasting Disease (CWD) in various deer species it should not be accepted that domestic cattle and sheep are necessarily the only source of TSE agent exposure for carnivorous species. While some information is available on the susceptibility of wild/exotic/zoo animals to natural or experimental infection with certain TSE agents, nothing is known of the possibility of occurrence of TSE in wild animal populations, other than among the species of deer affected by CWD in the USA. 1 The carrion birds are animals whose diet regularly or occasionally includes the consumption of carcasses, including possibly TSE infected ruminant carcasses. C:\WINNT\Profiles\bredagi.000\Desktop\Necrophagous_OPINION_0209_FINAL.doc snip... skroll down to the bottom ; Date: Mon, 11 Jun 2001 16:24:51 –0700 Reply-To: Bovine Spongiform Encephalopathy Sender: Bovine Spongiform Encephalopathy From: "Terry S. Singeltary Sr." Subject: The Red-Neck Ostrich & TSEs 'THE AUTOPSY' see full text and more ; Friday, February 25, 2011 Soil clay content underlies prion infection odds UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION CONGRESS SEPTEMBER 8-11 2010 just saying...kind regards, terry
As with everything else in the God forsaken country, it's all about the almighty dollar. No one gives a shit about the people until someone can say, "I told you so". Continuing this practice is sheer madness.
An excellent article. (Much better than Huffington's - if I may say!) The moment you stop being "indignant" about such outrageous events (as some commenters seem to be suggesting), the worse off we will all be. Keep up the pressure, OnEarth! Hope to see many more stories like this.
Hello Mr. Jacobson, My name is Ellie Kim, and I am a student intern for the Media Freedom Foundation, specifically under Mickey Huff, the director of Project Censored. I am compiling a list of contacts which includes authors featured in the Censored 2015 book. Your article, “They’re Feeding WHAT to Cows?” is a source for one of our top 25 censored stories of 2014. I was hoping to obtain an email address and/or phone number that we could reach you at for the book's purposes. Thank you for your help, Ellie Kim