A chemical is a chemical is a chemical

A chemical’s properties are not affected by whether it was made by God, Mother Nature, evolution, or a chemist in a lab coat.

There’s a certain irony to drinking a soy latte from a BPA-free mug, but that’s not something the chemophobic fear squad seems to understand. This fear-mongering crowd would have you believe that synthetic endocrine-disrupting chemicals (EDCs) are going to be the downfall of civilization as we know it (I admit, that’s hyperbolic, but so are many of their exaggerated claims). However, in a truly perfect example of inconsistent application of the precautionary principle and selective consideration of data and data gaps, they completely overlook the potential risks of phytoestrogens, naturally occurring endocrine-disrupting chemicals found in soy and other common foods.

Phytoestrogens are of particular concern because of the increased consumption of phytoestrogen-containing food. Sales of soy-based food products (tofu, tempeh, edamame, soy “milk”, soy “yogurt”, soy-based baby formula) have grown substantially since the late 1990s. Other sources of phytoestrogens include grapes and red wine, citrus fruits and juices, parsley, celery, pepper, kale, broccoli, onions, tomatoes, lettuce, apples, chocolate, green tea, beans, apricots, cherries, berries, spinach, and flax seed.

Data suggest that the exposure to EDCs from natural dietary sources may be higher than exposure to synthetic EDCs although this is a difficult comparison to make conclusively. Epidemiological studies of the health effects of both show mixed, complicated (i.e. confounded by associated factors), and mostly small results. Despite this nuance, we tend to view natural EDCs favorably, and synthetic EDCs unfavorably, despite having similar chemical properties. Source, not evidence, is the foundation for the difference in attitude toward natural and synthetic EDCs.

Now, this is not meant to make you afraid of eating soy, kale, berries and all these other foods, or of using your shampoo. I point this out to draw attention to the fact that that we tolerate a lot of risk in our lives and that exposure and risk are unavoidable parts of life. A simplistic dichotomy between the hazards of synthetic exposures and safety of natural exposures is often not based on evidence. There is truly no such thing as a risk-free, exposure-free life, even with so-called “all-natural” products. However, there are some simple and easy steps to reduce exposures if you are concerned, like avoiding soy-based products and use less plastic in food preparation and storage during sensitive developmental periods.

Reducing and mitigating risks where it is feasible to do so is reasonable, but it is often not a simple undertaking. For example, a recommendation to completely avoid phytoestrogen containing food would be misguided as evidence consistently shows that, despite concerns about exposure to phytoestrogens at certain times in life, a diet rich in a wide variety of fruits and vegetables produces a net benefit for health.

The similarities between natural and synthetic chemicals are often overlooked as we fall victim to our assumptions that natural is good and synthetic is bad. A chemical’s properties are not affected by how it was produced. Synthetic chemicals that have a biological effect are able to do so because they are able to mimic or interact with systems that exist in nature. Chemistry, not source, determines how a chemical acts in a biological system.

From a 2010 review, “The pros and cons of phytoestrogens”:

Phytoestrogens are intriguing because, although they behave similarly to numerous synthetic compounds in laboratory models of endocrine disruption, society embraces these compounds at the same time it rejects, often with vigor, use of synthetic endocrine disruptors in household products. Thus, phytoestrogens both expand our view of environmental endocrine disruptors and propound that the source of the compound in question can influence the direction and interpretation of research and available data. While the potentially beneficial effects of phytoestrogen consumption have been eagerly pursued, and frequently overstated, the potentially adverse effects of these compounds are likely underappreciated. The opposite situation exists for synthetic endocrine disruptors, most of which have lower binding affinities for classical ERs than any of the phytoestrogens but can sometimes produce similar biological effects. (emphasis mine)

In interpreting information about health effects of chemicals, wherever they come from, we must be aware of our biases in favor of the natural and against the synthetic to ensure that we analyze data objectively. Only when we consider evidence without bias can we arrive at sound recommendations and regulations.EDCs



Glyphosate toxicity: Looking past the hyperbole, and sorting through the facts. By Credible Hulk

You may at some point have heard people speak of glyphosate as being “less toxic than caffeine or table salt.” What they’re referring to when they say that is what we call its LD50, which a standard way of quantifying acute toxicity. A substance’s LD50 is the dose at which 50% of the subjects who ingest that amount will die of complications from an acute overdose, and it is measured in units of mass of the substance per unit mass of the subject (usually mg/kg). See, one of the most fundamental principles in all of toxicology is that “the dose makes the poison,” which was famously coined by Paracelsus, the father of toxicology.  Most substances have some amount beyond which they become toxic. Many substances that are benign, beneficial, or even essential to human health in one range of concentration will become harmful if taken in sufficiently large amounts. Even water can be toxic if you drink enough of it. So, you can’t just look at it as though there were some toxic things in the world and some non-toxic things, or that something that is toxic at one dose is bad in any dose, simply because that’s not how toxicology works.

Here you can find a very brief introduction to concepts in toxicology, but for now, suffice it to say that students are generally taught about three main types of toxicity: acute, chronic and subchronic.

By the acute standard of LD50, glyphosate (albeit not necessarily round up brand mind you, which also contains surfactants) is indeed less toxic than either caffeine or table salt.

It has an LD50 of 5600 mg/kg based on oral ingestions in rats, according to EPA assessments, placing it in Toxicity Category III. The EPA ranks chemicals in four categories, I being the most toxic and IV being the least.

To compare, caffeine has a much lower LD50 of 192 mg/kg based on oral ingestion in rats. Similarly, sodium chloride (table salt) has an LD50 of about 3000 mg/kg. Rotenone, which is used on some organic farms (though less so in the US in recent years), has an LD50 162-1500 mg/kg, and Copper sulfate, which also sometimes used on certain organic farms, has an LD50 of  30mg/kg. This is permissible by organic certification due in part to the fact that it is completely naturally occurring, which of course has little to do with its safety or environmental effects. The purpose of these comparison is not to make caffeine and table salt, which most people take for granted as being fairly safe, seem dangerous, nor is it to demonize these other pesticides to make them seem unacceptable; rather, the purpose is to show that idea that glyphosate is this abnormally dangerous toxic substance, a notion popular among many laypeople, simply isn’t accurate.

However, that was only a matter of acute toxicity. Many opponents are willing to concede that the acute risks are fairly minimal, but they worry about the risks of long term low-level exposure. The EPA took that into account as well.  The EPA dealt with this issue by setting maximum safe levels of residues called “tolerances.” The USDA tests crops each year to make sure that herbicide residues do not exceed the permitted tolerance levels. If any crops contain residue amounts higher than tolerance levels, the USDA reports the information to the FDA, who has the regulatory power to recall foods, levy fines and take other actions to prevent the foods from reaching consumers.

In case you’re wondering how these tolerances were arrived at, the EPA tested glyphosate on numerous animal species. They then used the result from the MOST sensitive species tested as the basis for setting the Reference Dose. The RfD represents the level at (or below) which daily aggregate dietary exposure over a lifetime will not pose appreciable risks to human health.

The RfD is determined by using what’s called the “toxicological end point” or the “NOEL” (No Observable Effect Limit) for the most sensitive mammalian toxicological study. The EPA uses an uncertainly factor of 100 in deriving it (which is pretty high in order to be conservative) so as to ensure the sufficiency of the RfD, and based on the assumption that certain segments of the human population could be as much as 100 times more sensitive than the species represented by the toxicology tests. In rat studies on glyphosate, doses of up to 31 mg/kg/day were administered with no observable adverse effects at all, and dog studies have gone as high as 500 mg/kg/day with no negative effects.

The EPA’s assumption about how much people would eat was very conservative. In order to insure you don’t get over 2 mg per kg per day they use a “worst case” dietary risk model of an individual eating a lifetime of food derived entirely from glyphosate-sprayed fields with residues at their maximum levels.

Here are examples of the residues of Glyphosate permitted on our food:

Vegetable, bulb, group 3-07 – 0.20 ppm

Vegetable, cucurbit, group 9 – 0.5 ppm

Vegetable, foliage of legume, subgroup 7A, except soybean 0.2ppm

Vegetable, fruiting, group 8-10 (except okra) 0.10ppm

Vegetable, leafy, brassica, group 5 – 0.2ppm

Vegetable, leafy, except brassica, group 4 – 0.2ppm

Vegetable, leaves of root and tuber, group 2, except sugar beet tops 0.2ppm

Vegetable, legume, group 6 except soybean and dry pea 5.0ppm

Vegetables, root and tuber, group 1, except carrot, sweet potato, and sugar beet 0.20ppm

Note that most are all less than one part per million.

Now to put that in perspective, let’s assume you are a vegetarian and eat a mix that is on the extreme high end and you consume food which is at an average of 5 ppm per day.

So 200 grams of food would yield 1 mg of glyphosate.

You weigh 70 kg or 154 lbs.

To get 2 mg per kg you would need to get 140 mg of glyphosate residue.

So you would need to eat 200 * 140, or 28,000 grams of this 5 ppm produce to get to the 2 mg per kg per day level.

There are 28 grams in an ounce, so that’s 1,000 ounces.

There are 16 oz in a pound, so you would need to eat 62 lbs of produce.

We’re talking about EACH DAY here, and even if you managed that, that would only get you to a level that is 100 times less then the NOEL level in the most sensitive species tested.

Supposing you wanted to do similar calculations on your own upon looking up the EPA tolerances for a particular food item. How would you do that? How about I just derive the formula for you, and you can plug and chug for any given food based on its tolerance (even though, in actuality the residues will seldom be right up at the cutoff level). That way, this formula will apply no matter what the specific tolerances are for the item in question.

Let the Tolerance level of a particular food = x ppm,

which conveniently also equals 1mg/kg,

(which btw is one of the reasons I love the SI system of units).

Let m1= your mass in kg.

We want to see how much of a given food we would have to consume such that our intake of glyphosate residues exceeds 2 mg/kg,

so let m2 = the mass (in kg) of that food you’d have to consume each day to reach 2mg/kg.

So, we have

m2*x = m1*2 mg/kg.

Solving for m2 yields

m2 = 2*m1/x

So, supposing for example that the tolerance of a given crop is 10 ppm, and say you are only 50 kg (about 110 lbs).

Then the mass of that food you’d have to eat every day to exceed 2 mg/kg would be 2*50/10 = 10 kg = 22 lbs per day. Easy, right?

For someone my size, it’d have to be over 52 lbs a day just of that one product, and for an extended period of several years, and even then, only if the farmers were really pushing the limits of what they could get away with, which obviously wouldn’t make much sense from a business standpoint, since that stuff costs them money, and the whole reason they use it is to be more efficient: that is, to get the greatest output for the least input.

Another issue worth addressing is the recent IARC and WHO reclassification of glyphosate as a Class 2A carcinogen. The IARC classification process isn’t designed to serve as a statement on risk analysis, and for that reason, it did not take into account actual common usage practices. They placed glyphosate in the 2A category, which includes “probable” (albeit unconfirmed) carcinogens such as emissions from frying food, hairdresser products and burning wood. It mainly pertains to application protocols rather than minuscule trace amounts in food.

Consequently, banning glyphosate as a knee jerk reaction to its recent classification would be similar to never going out of the house in the daytime because sunlight is carcinogenic. Actually, it would be even less sensible because sunlight is in an even higher class of carcinogen than glyphosate. Think about it. It’s in the same classification as manufacturing glass, burning wood, emissions from high temperature frying, and work exposure as a hairdresser. Alcohol and sunlight are both higher on their carcinogen scale than glyphosate, and neither of those cause cancer with conservative exposure either.

Should proper precautions be taken during application procedures? Of course. Are the trace amounts in food, which are usually on the order of parts per million (ppm) or less even prior to being washed, a threat to consumers? No. The bottom line is that hazard is not the same thing as risk, and the latter is dependent largely upon exposure levels as well as type of exposure.

Moreover, as Kate Guyton, one of the scienists behind IARC’s classification stated:

“I don’t think home use is the issue. It’s agricultural use that will have the biggest impact. For the moment, it’s just something for people to be conscious of.”

Basically, what that means is that it’s the people actually applying the herbicide who are thought to be at increased risk. But applicators have their own set of protocols and certification requirements, and they are generally pretty well-versed in how to properly apply glyphosate.

The Farmer’s daughter USA wrote an informative and easy to understand piece on this. It may also be worthy seeing what various other scientists had to say about the reclassification of glyphosate and what they think it means in this article here.

It’s also worth noting that the IARC also classifies some organic pesticides as carcinogenic, and so do studies at the UC Berkeley.

Does that mean that they cause cancer at in the amounts consistent with actual practical usage?

Not necessarily. But the extreme emphasis some people are putting on glyphosate’s reclassification to the exclusion of the other “natural” compounds is quite a double standard, and double standards are pretty good indication of a strong bias on the part of the people making the most noise about it.

There are legitimate concerns over the evolution of glyphosate-resistant weeds. In fact, it’s one of the few of the common criticisms of glyphosate and GR crops that has any legitimate merit to it, but that’s an issue that affects all methods of weed control (even hand tilling), and although weed resistance has slightly increased, the RATE at which herbicide resistant weeds have been developing since the rise in glyphosate resistant GMO crops has not increased. It has always been an issue, and there are ways of dealing with it, but that’s a discussion for another day.

In closing, the take home message is that glyphosate is not the monumentally dangerous herbicide that its opponents have hyped it up to be. When the proper application procedures are practiced by applicators and usage on food crops are kept within the regulatory parameters, it is fairly innocuous, particularly when compared to many of its more toxic alternatives, many of which were phased out in conjunction with the rise in glyphosate’s popularity. Opponents of glyphosate often seem to hold this unfounded notion that, if they can manage to get glyphosate banned or simply willingly abandoned, then it would mean an improvement in both food and environmental safety, but the truth is it would likely be the exact opposite of that. Weeds are a legitimate problem in farming that has to be dealt with one way or another. In its absence, it would have to be replaced with something else, and it would likely be something more caustic: not less.


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