Would you eat it? Chances are, you already have. Pink slime, or lean finely textured beef (LFTB) trimmings, is made from the leftover meat after all of the marketable cuts of beef have been harvested. These are undesirable because they are fattier, contain connective tissues, and are more highly susceptible to E. coli and salmonella contamination. This is where Beef Products Inc. (BPI) steps in and processes these trimmings by centrifuging at high speed to separate the meat from the fat and then sterilizes the separated product with gaseous ammonium hydroxide (ammonia plus water). This step increases the pH of the meat creating an intolerable environment for the bacteria. The USDA allows up to 15% of ground beef content to be LFTB and does not require any labeling to indicate that ammonium hydroxide-treated LFTB has been used as filler.
The recent uproar over LFTB was triggered last week when The Daily broke the news that the federal government was set to purchase ~7 million pounds of LFTB for the national school lunch program. This sparked concerned “mother of two Bettina Siegel to start an online petition on Change.org asking Secretary of Agriculure Tom Vilsack to please put an immediate end to the use of ‘pink slime’ in our children’s school food.” (1) Another petition is pushing for stricter labeling requirements for products that contain pink slime. This, however, is not the first time that LFTB has garnered negative attention. In December 2009, The New York Times examined how effective the ammonium hydroxide treatment eliminated E. coli and salmonella, while last season’s premiere of Jamie Oliver’s Food Revolution featured a segment in which he recreated how he imagined LFTB was made. While I stand with the public’s concern over the safety of LFTB as well as the demand for stricter labeling requirements so that consumers can make informed decisions, I do have a bone to pick with Jamie Oliver and food blogs covering this issue. If their agenda is to educate the public about LFTB then I think it is their duty to do it fairly and accurately.
Let’s start with Jamie Oliver
Here is the segment from last’s seasons premiere where he essentially admits he doesn’t know what he’s talking about (also, look for the woman in the shades who looks like she’s about to vomit and cry at the same time. I bet you she’d have that reaction if she saw how animals are butchered. period.):
So, let’s see at 2:12 he says, “This is how I imagine the process to be.” Imagine is not good enough. Then at 3:15, after dousing the meat with household cleaning ammonia (complete with skull and crossbones on the bottle) and some water, he admits, “I don’t know how much and the water. There’s a specific ratio but basically they wash this meat and that kills the E. coli and the salmonella and kind of pathogens.” Sure, dramatically bathing any food in ammonia that came from a bottle marked with a skull and crossbones is going to get your point across. Unfortunately for Jamie Oliver, ammonium hydroxide as a food additive is generally regarded as safe (GRAS) by the FDA and is found in a variety of food products. Furthermore, while his theatrical demonstration suggests that too much ammonia is used, the real issue, as the December 2009 New York Times articles reports, might be that not enough ammonia is used, since E. coli and salmonella was still found in some of BPI’s LFTB (2). According to BPI’s website, “By adding a tiny amount of ammonia (gas) to the beef, we raise the pH in the beef to help kill any harmful bacteria that could possibly be present.” He then later goes quasi-conspiracy theorist on us and criticizes the USDA. You can almost taste the contempt he has for his audience.
And now a word about food blogs…
I’ve seen a number of inaccuracies and misinformation being spread through blogs, in particular food blogs. The following excerpt from Eat Like No One Else struck me since it was biological in nature:
Let’s go back to why they use ammonia in the first place – to kill any E. coli bacteria. This is one of those fixing the problem we caused situations. E. coli is as natural as ammonia. We have it in our bodies right now. It became a problem when people started feeding corn to cows. This caused a mutation to occur with the E. coli bacteria in the cow, which lead to a strain that is harmful to us. Biologists from the USDA and Cornell University have known about this since 1998.
The harmful strain to which the blogger is referring is E. coli O157:H7. There is no evidence that the switch to feeding corn to cows caused a mutation that led to this harmful strain of E. coli. The O157:H7 strain is harmful because along its evolutionary path it picked up the ability to produce Shiga-like toxins, thus named because of its similarity to the Shiga toxin produced by another bacteria, Shigella dysenteriae. Shiga-like toxins bind to components on the outside of blood vessels, in particular those of the GI tract, kidneys, and lungs. The toxin is then pulled into the cells of the blood vessels where it shuts down the cellular factories (insert Bain Capital joke) that make proteins and results in cell death. Ultimately, this breaks down the lining and leads to bloody diarrhea typical of O157:H7 infection.
How did O157:H7 come to produce Shiga-like toxins? Through horizontal gene transfer. While we typically think of passing on genetic material as happening vertically from parent to child, or mother cell to daughter cell, there are exceptions. In bacteria, genetic material can be transferred “horizontally,” independent of reproduction. This can happen in several ways, a) transformation, where the bacteria takes up DNA from its environment, b) transduction, the integration of genetic material mediated by bacteriophages or phages (viruses that infect bacteria) or c) conjugation, direct transfer of genetic material from one bacteria to another through cellular contact. It’s through the second process that O157:H7 obtained the ability to produce Shiga-like toxins.
Some viruses, when they infect cells, can undergo either a lytic cycle or a a lysogenic cycle. Lytic cycles are characterized by the production of more viruses by hijacking the infected cell’s machinery. The infected cell will eventually burst and release more viruses into the environment. When viruses adopt a lysogenic program, they insert their genetic material into the genome of the infected cell thereby piggybacking on the cell’s DNA replication cycle in order to perpetuate. Under certain stressful conditions, these dormant viruses (prophages) can be coaxed into entering the lytic cycle to produce more viruses and abandon the infected cell that is under stress. With their penchant for popping in and out of genomes, you can think of viruses as nature’s recombinant DNA engineers.
Biologists have known that the E. coli O157:H7 E. strain became toxic through infection by Shiga-like toxin- converting phages for several reasons. First, the production of these viruses could be induced by subjecting the O157:H7 to irradiation (3). Furthermore, these viruses could in turn be harvested and infect a different E. coli strain and consequently confer the ability to produce Shiga-like toxins. Then in 2001, biologists sequenced the genome of O157:H7 and confirmed the presence of DNA sequences from Shiga-like toxin-converting phages (4).
Back to the biologists from Cornell. What they were studying was how cattle diet affected the acid resistance of E. coli. Normally, the acidity of our stomachs is inhospitable to many microorganisms. However, E. coli can survive extreme acidity if it is first habituated under mildy acidic conditions. When exposed to an acidic environment, E. coli responds by initiating an innate acid resistance program (5). This is no more a mutation than how our own body responds with a fever to infections. The researchers at Cornell observed that the pH in the colons of cattle fed corn was lower (more acidic) than that of cattle fed hay (6). This is because, in contrast to hay, the difficult-to-digest starch in corn passes through the cattle’s GI tract and ends up in the colon where it ferments and acidifies the environment. Therefore, the researchers hypothesized that any E. coli that ends up in the colon could become acid-resistant thereby increasing the likelihood of contaminating meat during slaughter as well as increasing the ability of the bacteria to survive the acid shock of our stomachs. What they found was that colonic E. coli from cattle fed corn were in fact acid-resistant. However, since the cattle they used in the study tested negative or the O157:H7 strain, they confirmed the ability of O157:H7 to become acid resistant in the lab. In contrast, E. coli from cattle fed grass or hay were less acid resistant and could not survive an “acid shock” comparable to the environment of the human stomach. This prompted the scientists to suggest that switching from corn to hay feed days before slaughter might reduce the load of acid- resistant E. coli. Unfortunately, many follow-up studies have yielded results that directly contrast the oft-cited study from Cornell and call into question the importance of acid-resistance in O157:H7 virulence (7,8).
Now, this is by no means a tacit defense of the meat industry, whose practices leave much to be desired. While much focus has been on the O157:H7 strain, there are other pathogenic strains of bacteria that are associated with the beef industry. To BPI’s credit, they have voluntarily started testing for 6 other strains of virulent E. coli following the 2011 outbreak in Germany. However, I do echo the demands made by the public (as well as Mr. Oliver and aforementioned food blogs) that the labeling requirements for products containing LFTB be of a higher standard so that consumers can make informed choices. That being said, how we inform the public must also be held to a high standard or we run the risk of undercutting and discrediting the importance of the message.
7. Hancock, D. & Besser, T. E. coli O157: H7 in hay-or grain-fed cattle. College of Veterinary Medicine (2006).
8. McWilliams, J. Beware the Myth of Grass-Fed Beef. Slate (2010).at <http://www.slate.com/articles/health_and_science/green_room/2010/01/beware_the_myth_of_grassfed_beef.2.html