Why Was Chicken the Primary Source of Arsenic Exposure in Children?

What was the National Chicken Council’s response to public health authorities calling for the industry to stop feeding arsenic-based drugs to poultry?

“Dietary practices influence our exposure to pesticides, toxic heavy metals, persistent organic pollutants, and industrial pollutants….A diet high in fish and other animal products, for example, results in greater exposure to persistent organic compounds and metals than does a plant-based diet because these compounds bioaccumulate up the food chain.” Researchers at UC Davis analyzed the diets of children and adults in California to see just how bad things have gotten.

Cancer benchmark levels were exceeded by all children—100 percent of children—for arsenic, the banned pesticides dieldrin and DDT, metabolite DDE, as well as dioxins, and not just by a little. As you can see at 0:51 in my video Where Does the Arsenic in Chicken Come From?, researchers found more than a hundred times the acceptable daily exposure for arsenic in preschoolers, school-aged children, parents, and older adults, about ten times the acceptable levels for various pesticides, and up to a thousand times the daily dose for dioxins. Where are all these toxins coming from?

The number-one source of dioxins in the diets of Californian preschoolers, kids, parents, and grandparents appears to be dairy for all age groups, followed by meat, and then white potatoes, refined grains, mushrooms, poultry, and fish.

These days, our DDT legacy is also mostly from dairy. Dieldrin was created as a safer alternative to DDT, but it was banned just two years later, in 1974, though it’s still found in our bodies, mostly thanks to dairy, meat, and, evidently, cucumbers.

Chlordane made it into the 1980s before being banned, though we’re still exposed through dairy (and cukes). Lead is — foodwise — also mostly from dairy, and mercury is not surprisingly mostly from tuna and other seafood. But the primary source of arsenic in children? Surprisingly, mostly from chicken. Why?

Let me tell you a tale of arsenic in chicken. Arsenic is “well known as a poison by anyone who reads mysteries or the history of the Borgias, and with its long and colourful history, arsenic is not something that people want in their food.” So, when a biostatistics student went to the USDA in 2000 in search of a project for his master’s degree, he decided to look into it. He found a startling difference: Arsenic levels in chicken were three times higher than in other meats. His veterinary colleagues weren’t at all surprised and explained that four different types of arsenic-containing antibiotic drugs are fed to poultry—and have been fed to them since 1944.

“While arsenic-based drugs had been fed to poultry since the 1940s, recognition of this source of exposure [for humans] only occurred after appropriate statistical analysis of the data”—that is, after this student churned through the data. It was published in 2004 and expanded upon in 2006. The National Chicken Council (NCC) was none too pleased, saying lots of foods are contaminated with arsenic. “By focusing specifically on chicken, IATP [the Institute for Agriculture and Trade Policy] makes it clear that it is producing a publicity-oriented document focused on the objective of forcing [chicken] producers to stop using these safe and effective products”—by which the NCC means these arsenic-containing drugs. In fact, the NCC admits to using them but says we don’t need to worry because chicken producers use organic arsenic, “not the inorganic form made infamous in ‘Arsenic and Old Lace.’” Okay, so we don’t need to worry—until, apparently, we cook it. When chicken is cooked, it appears that some of the arsenic drug in the meat turns into the ”Arsenic and Old Lace” variety. So, the Poison-Free Poultry Act of 2009 was introduced into Congress, flopped, and was followed by the subsequent introduction of the Poison-Free Poultry Act of 2011. Did the second attempt fare any better? No, legislators once again said pish posh to poison-poor poultry. So, in 2013, a coalition of nine organizations got together and sued the FDA, and by December 31, 2015, all arsenic-containing poultry drugs were withdrawn. As of 2016, arsenic is no longer to be fed to chickens. The bad news is that without giving birds the arsenic-containing drug roxarsone, chicken may lose some of its “appealing pink color.”

In the end, the poultry industry got away with exposing the American public to arsenic for 72 years. “It should be noted that the European Union has never approved drugs containing arsenic for animal consumption” in the first place, saying, Hmm, feed our animals arsenic? No thanks, nein danke, no grazie, non, merci.

Europe has also long since banned the “urgent threat to human health” posed by feeding farm animals millions of pounds of human antibiotics. As you can see at 5:30 in my video, feeding chickens en masse literally tons of drugs like tetracyclines and penicillins to fatten them faster is a problem that gets worse every year instead of better and dates back to 1951 when drug companies whipped out the ALL CAPS in advertisements,  promising “PROFITS…several times higher!”, a dangerous practice the poultry industry has gotten away with for 68 years…and counting.


If you don’t eat poultry and are feeling a little cocky, you may want to check out my 12-video series on arsenic in rice before you gloat too much:

Think feeding arsenic to chickens is weird? Check out Illegal Drugs in Chicken Feathers.

And for more on the critical public health threat posed by antibiotic overuse in animal agriculture, see:

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

What Explains the Egg-Cancer Connection

The reason egg consumption is associated with elevated cancer risk may be the TMAO, considered the “smoking gun” of microbiome-disease interactions.

“We are walking communities comprised not only of a Homo sapiens host, but also of trillions of symbiotic commensal microorganisms within the gut and on every other surface of our bodies.” There are more bacterial cells in our gut than there are human cells in our entire body. In fact, only about 10 percent of the DNA in our body is human. The rest is in our microbiome, the microbes with whom we share with the “walking community” we call our body. What do they do?

Our gut bacteria microbiota “serve as a filter for our largest environmental exposure—what we eat”—and, “technically speaking, food is a foreign object that we take into our bodies” by the pound every day. The “microbial community within each of us significantly influences how we experience a meal…Hence, our metabolism and absorption of food occurs through” this filter of bacteria.

However, as you can see at 1:22 in my video How Our Gut Bacteria Can Use Eggs to Accelerate Cancer, if we eat a lot of meat, including poultry and fish, milk, cheese, and eggs, we can foster the growth of bacteria that convert the choline and carnitine in those foods into trimethylamine (TMA), which can be oxidized into TMAO and wreak havoc on our arteries, increasing our risk of heart attack, stroke, and death.

We’ve known about this “troublesome” transformation from choline into trimethylamine for more than 40 years, but that was way before we learned about the heart disease connection. Why were researchers concerned back then? Because these methylamines might form nitrosamines, which have “marked carcinogenic activity”—cancer-causing activity. So where is choline found in our diet? Mostly from meat, eggs, dairy, and refined grains. The link between meat and cancer probably wouldn’t surprise anyone. In fact, just due to the industrial pollutants, like PCBs, children probably shouldn’t eat more than about five servings a month of meats like beef, pork, or chicken combined. But, what about cancer and eggs?

Studies going back to the 1970s hinted at a correlation between eggs and colon cancer, as you can see at 2:45 in my video. That was based just on so-called ecological data, though, showing that countries eating more eggs tended to have higher cancer rates, but that could be due to a million factors. It needed to be put to the test.

This testing started in the 80s, and, by the 1990s, 15 studies had been published, of which 10 suggested “a direct association” between egg consumption and colorectal cancer, “whereas five found no association.” By 2014, dozens more studies had been published, confirming that eggs may indeed be playing a role in the development of colon cancer, though no relationship was discovered between egg consumption and the development of precancerous polyps, which “suggested that egg consumption might be involved in the promotional” stage of cancer growth—accelerating cancer growth—rather than initiating the cancer in the first place.

This brings us to 2015. Perhaps it’s the TMAO made from the choline in meat and eggs that’s promoting cancer growth. Indeed, in the Women’s Health Initiative study, women with the highest TMAO levels in their blood had approximately three times greater risk of rectal cancer, suggesting that TMAO levels “may serve as a potential predictor of increased colorectal cancer risk.”

As you can see at 4:17 in my video, though there may be more evidence for elevated breast cancer risk with egg consumption than prostate cancer risk, the only other study to date on TMAO and cancer looked at prostate cancer and did indeed find a higher risk.

“Diet has long been considered a primary factor in health; however, with the microbiome revolution of the past decade, we have begun to understand how diet can” affect the back and forth between us and the rest of us inside, and the whole TMAO story is “a smoking gun” in gut bacteria-disease interactions.

Since choline and carnitine are the primary sources of TMAO production, the logical intervention strategy might be to reduce meat, dairy, and egg consumption. And, if we eat plant-based for long enough, we can actually change our gut microbial communities such that we may not be able to make TMAO even if we try.

“The theory of ‘you are what you eat’ finally is supported by scientific evidence.” We may not have to eat healthy for long, though. Soon, Big Pharma hopes, “we may yet ‘drug the microbiome’…as a way of promoting cardiovascular health.”

What did the egg industry do in response to this information? Distort the scientific record. See my video Egg Industry Response to Choline and TMAO.


This is not the first time the egg industry has been caught in the act. See, for example:

For background on TMAO see my original coverage in Carnitine, Choline, Cancer, and Cholesterol: The TMAO Connection and then find out How to Reduce Your TMAO Levels. Also, see: Flashback Friday: How to Reduce Your TMAO Levels.

This is all part of the microbiome revolution in medicine, the underappreciated role our gut flora play in our health. For more, see: 

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

How to Avoid BPA

The purported link between obesity and hormone-disrupting plastics chemicals like bisphenol A (BPA) was initially based in part on observations that the rise in chemical exposure seemed to coincide with the rise of the obesity epidemic, but that may only be a coincidence. Many other changes over the last half century, like an increase in fast-food consumption and watching TV, would seem to be simpler explanations. But why are our pets getting fatter, too? Fido isn’t drinking more fries or drinking more soda. Of course, the more we watch Seinfeld reruns, the less we may walk the dog, but what about our cats? They’re also getting fatter. Are we giving both them and our kids a few too many treats? That would seem to be an easier explanation than some pervasive obesity-causing chemical in the environment building up in the pet and person food chains.

How then do we explain the results of a study of more than 20,000 animals from 24 populations, showing they are all getting fatter? The odds that this could happen just by chance is about 1 in 10 million. The study’s “findings reveal that large and sustained population increases in body weight” are occurring across the board, even in those without access to vending machines or getting less physical education in schools. Perhaps some environmental pollutant is involved. I discuss this in my video How to Avoid the Obesity-Related Plastic Chemical BPA.

We’re exposed to a whole cocktail of new chemicals besides BPA, but the reason researchers have zeroed in on it is because of experiments showing that BPA can accelerate the production of new fat cells, at least in a petri dish. This was at more than a thousand times the concentration found in most people’s bloodstream, though. We didn’t know if the same thing happened at typical levels…until now. Most people have between 1 and 20 nanomoles of BPA in their blood, but even 1 nanomole may significantly boost human fat cell production. So, even low levels may be a problem, but that’s in a petri dish. What about in people?

Why not just measure the body weights of a population exposed to the chemical compared to a population not exposed to the chemical? There is virtually no unexposed population: BPA is everywhere. In that case, how about those with higher levels compared to those with lower levels? This is what researchers at New York University did, and the amount of BPA flowing through the bodies of children and adolescents “was significantly associated with obesity.” However, since it was a cross-sectional study, a snapshot in time, we don’t know which came first. Maybe instead of the high BPA levels leading to obesity, the obesity led to high BPA levels, since the chemical is stored in fat. Or, perhaps BPA is a marker for the same kinds of processed foods that can make you fat. What we need are prospective studies that measure exposure and then follow people over time. We never had anything like that…until now! And indeed, researchers found that higher levels of BPA and some other plastics chemicals were significantly associated with faster weight gain over the subsequent decade. So, how can we stay away from the stuff?

Though we inhale some from dust and get some through our skin touching BPA-laden receipts, 90 percent of exposure is from our diet. How can we tell? When we have people fast and drink water only out of glass bottles for a few days, their BPA levels drop as much as tenfold.

Fasting isn’t very sustainable, though.

What happens with a three-day fresh foods intervention, where families switch away from canned and packaged foods for a few days? A significant drop in BPA exposure. If we do the experiment the other way, adding a serving of canned soup to people’s daily diet, we see a thousand percent rise in BPA levels in their urine compared to a serving of soup prepared with fresh ingredients. That study used a ready-to-serve canned soup, which, in the largest survey of North American canned foods, was found to have about 85 percent less BPA than condensed soups, but the worst was canned tuna.


I previously touched upon bisphenol A in BPA Plastic and Male Sexual Dysfunction. Some companies make canned foods without BPA, for example, Eden Foods. (See Do Eden Beans Have Too Much Iodine? for more information.) You can also buy aseptic packaged beans or boil your own. Personally, I like pressure-cooking them.

For more on BPA, see:

Phthalates are another concerning class of plastics chemicals. I covered those in Avoiding Adult Exposure to Phthalates and What Diet Best Lowers Phthalate Exposure?.

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations: