With respect to glyphosate herbicide, it is clear that IARC disregarded the large body of scientific and medical evidence demonstrating that glyphosate does not cause cancer in humans or animal. This evidence includes the largest epidemiological study of farmers ever done, the U.S. National Cancer Institute’s Agricultural Health Study. This study, following a large group of farmers forward in time, and using a design that is considered the best epidemiology approach for examining the impact of a chemical on actual cancer rates (Blair et al., 2015), has failed to find any relationship between glyphosate and cancer (De Roos et al., 2005). Agencies around the world, including the U.S. EPA and the highly respected German BfR (Agency for Risk Assessment, conducting the EU assessment 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 in March issued a strong criticism of the IARC assessment.
Importantly, 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 U.S. 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.
First, note that if one is never in contact with (i.e. exposed to) a chemical, 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. 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. An aspirin tablet may help your headache, but 1/100 of an aspirin tablet won’t. Further, once a chemical is absorbed into the body, it can be broken down (metabolized) or excreted. Metabolism of some chemicals can produce problems if the breakdown products are more toxic or reactive, and some chemicals can persist in the body – but what about glyphosate? Glyphosate is not metabolized in humans, is not fat soluble, and does not accumulate in the body over time, but is excreted unchanged in the urine.
What can we say about exposure to glyphosate? For food intake by the general public the “worst-case” estimates, assuming that all growers treat all permitted crops and all have maximum allowable residues, put us at about 1/5 of the ADI. Because actual use is far less and because most crops have well below the maximal allowable levels true exposure is far less than this. Urinary monitoring (which works very well for glyphosate) in the U.S. and Europe 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 farmers in this study happened to be male) and children had very low levels and no detectable rise in levels unless they actually helped to apply glyphosate. Even the farmers who applied glyphosate had exposures well within the ADI for the general population.
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. More reassuring, 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.
I believe IARC has overreached in its opinion by failing to consider the vast body of literature demonstrating glyphosate is not a carcinogen. Certainly, they are out of position on this issue relative to 40 years of authoritative regulatory safety assessments. Further, even if the IARC is correct, they have failed to put this 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. In my opinion, IARC needs to work with regulatory experts around the globe and revisit the safety of glyphosate.
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.