Line 4Line 4 Copyic/close/grey600play_circle_outline - material

What can we say about exposure to glyphosate?

With regard to glyphosate, it seems the IARC did not consider the overwhelming scientific and medical evidence demonstrating that glyphosate is not a human carcinogen. This includes the largest epidemiological study of farmers ever undertaken, the U.S. National Cancer Institute’s Agricultural Health Study, which failed to find a relationship between glyphosate and cancer. Agencies around the world, including the US EPA and the highly respected German BfR (Agency for Risk Assessment, conducting the EU evaluation of glyphosate) have concluded that there is no risk of cancer with glyphosate use. BfR updated its comprehensive assessment as recently as January 29, 2015 and has criticized the IARC assessment.

In short, the weight of the evidence strongly indicates that glyphosate does not cause cancer— in humans or in animals.  The evidence comes from the Ag Health Study which uses a design that is considered the best epidemiology approach for examining the impact of a chemical on actual cancer rates (Blair et al., 2015), and did not find an association with cancer (De Roos  et al., 2005). 

It is also important to realize that the IARC assessment is what toxicologists call a “hazard assessment,” meaning that a particular chemical might cause a problem under some circumstances.  Paracelsus, the "father" of modern day toxicology, said, "The dose makes the poison."  In other words, to translate hazard into risk, you need to know something about dose — a dimension that is critical to understanding potential health impacts of glyphosate on cancer or other clinical conditions. The few animal studies cited by IARC were not repeatable, had tumors at the incidence historically observed for controls and are misquoted by the IARC.

In this case, we can’t compare the human dose of glyphosate to doses that cause cancer in animals because glyphosate does not cause cancer in animals – the evidence supports the opposite conclusion.  We can compare exposure to doses shown to be safe in animals based on a “no effect level.”  For glyphosate, the US EPA establishes a safe level of intake for humans, or Allowable Daily Intake (ADI), based on a no effect level, applying a 100-fold safety factor and conservatively assuming the highest possible residues in all the food you consume.

So, first, to state the obvious, the concept of dose doesn't even come into play if there is no exposure. In other words, if one is never in contact with (i.e. exposed) a chemical, then one cannot possibly receive a dose. If there is a container of glyphosate in your garage, sitting unopened on a shelf, no one is being exposed to it. Likewise, aspirin in the bottle won’t help your headache.

If contact with a chemical does occur (inhaled, ingested or on skin), it is possible that the chemical may enter the body and result in a "dose." But simply receiving a dose isn't enough – that dose needs to be high enough and prolonged enough for medical consequences to occur. Likewise, an aspirin tablet may help your headache, but 1/100 of an aspirin tablet won’t.

Further, once a chemical does get absorbed into the body, it can be broken down (metabolized) by or excreted from the body. Metabolism can produce problems if the breakdown products are more toxic or reactive, and some chemicals can persist in the body – but what about glyphosate? Absorbed glyphosate is not metabolized in humans, is not fat soluble, and does not accumulate in the body over time, but rather is excreted unchanged in the urine.

What can we say about exposure to glyphosate?  For the public with exposure via foods, we know that the “worst case” estimates, assuming that permitted crops are treated by all growers and have maximum allowable residues, put us at about 1/5 of the ADI.  Actual use is far less, and most crops have well below maximal levels, so true exposure is far less than this.  In fact, urinary monitoring data available for the US and Europe (which works very well for glyphosate) suggests typical exposures less than 1/100 of the ADI. We also have studies in farmers and farm families (Farm Family Exposure Study) that demonstrate that the majority of farmers had no detectable glyphosate in urine following application, and that wives (all the farmers in this study happened to be male) and children had very low levels and no detectable rise in levels (unless they assisted in application).  Farmers who did apply glyphosate had exposures well within the ADI. 

Finally, what about consumers using glyphosate products in the lawn and garden setting? Certainly, the farmer data should be very reassuring given the scope of agricultural use compared to typical home application. Even, Kate Guyton, the IARC officer responsible for the IARC session looking at glyphosate said: “"I don't think home use is the issue," pointing out the higher exposure potential for farmers and professional applicators.

Overall, it appears that IARC has overreached in its opinion by failing to consider the vast body of literature supporting the notion that glyphosate is not a carcinogen. Further, “the dose makes the poison,” and the IARC, even if they are correct, has failed to place potential hazard into a context of actual risk.  Real-life exposures to glyphosate via food and the environment are small – the ADI is 100 times less than a dose that causes no observable adverse effect in animals, and most people seem to have exposures more than 100-times less than the ADI. Even farmers applying glyphosate fall within the ADI and consumer use exposures, while not studied in the detail we have for farmers, can reasonably be expected to be similar or smaller.

The weight of evidence strongly suggests that glyphosate does not cause cancer – and if it does, a look at the dose demonstrates a lack of medically significant exposure.  Users and the public can be confident that labeled uses of glyphosate products pose no meaningful risk of cancer.