Glyphosate (GP) was introduced into the market in the early 1970s. It is a widely approved and widely used herbicide. If it caused injury during foreseeable use then liability insurance would be involved. Given both professional and amateur usage, the foreseeable uses would be many and non-compliant standards of use would be unsurprising. Generic and specific causation would be the key tests of liability.
Recent interest in causation includes requests to regulators to label foods as containing traces of glyphosate on the grounds that it may cause cancer. This would have a significant impact on sales of food and glyphosate.
This follows on from a 2015 decision made by the International Agency for Research on Cancer (IARC) to classify glyphosate as a probable human carcinogen. Californian law requires that it adopts IARC decisions.
The DeWayne Johnson (aged 46) claim for non-Hodgkin lymphoma (NHL) recently reached a key step in awarding damages. The claimant made use of suggestions of profiteering, conspiracy, secrecy and oppression to help influence a jury. There was written evidence that the manufacturer had been concerned about public opinion. Indeed it would be quite proper for a manufacturer to discuss potential adverse public opinion and the effect this has on regulators and failure to consider this could lead to action by shareholders. For those interested in rational arguments about causation there will be an appeal.
The Radar service has been following the Glyphosate (GP) causation science.
In 1993 the USEPA pronounced that glyphosate “does not pose unreasonable risks or adverse effects to humans or the environment”. Once adsorbed to soil it is broken down by soil microbes.
In 2009, GP was listed as a potential endocrine disruptor to be added to a long list of other widely used chemicals. Endocrine science is highly uncertain both in its conduct and in interpretation of evidence generated. This is ideal for those motivated to talk about what-ifs and could-be’s. The manufacturers involved were on increased notice that pressure would be brought to bear on regulators.
There is clear evidence that plants metabolise GP. Animals that eat GP in fodder excrete it. It does not accumulate in animals.
In the EU the permitted level in foods was around 20 mg/kg but varies with food type. 0.05 mg/kg is the detection limit. Food surveys show that exposure is usually around 17% of the ADI value. Such limits are set by noting the lowest level of exposure where some biological effect can be seen in rats or other test animals and then dividing by a safety factor of 100 or so. The biological effect e.g. an enlarged liver, is rarely significant enough to be described as a legal injury. The regulator is probably correct to observe that if there can be no biological effect then there can be no injury. A precautionary approach.
At the time of the IARC decision the Radar report noted that the evidence in support of the conclusion was not available for scrutiny and that other recent reviewers did not agree with IARC. Having reviewed their evidence, Radar agreed that a lack of mutagenicity, unclear results on possibly irrelevant DNA damage in humans, the very high levels of exposure needed to obtain an effect in rabbits, and lack of dose response evidence of cancer in mice except in mice that develop cancer in response to almost any chemical stressor would tend to suggest GP is an improbable carcinogen per se. That is, the probability of objective reviewers finding generic causation is less than 50%.
IARC is not bound by the doubled risk test. Any evidence at all of a statistical association can be sufficient for IARC to decide there is evidence of increased risk in humans. If at the same time massive unrepresentative doses cause cancer in especially genetically vulnerable mice then IARC is within its mandate to decide GP is a probable human carcinogen. A precautionary approach.
The common law does not adopt a precautionary test of causation.
Proof of exposure
Traces of glyphosate are ubiquitous. The recently introduced practice of drying crops with GP just before harvest could increase residual levels. Surveys of food stuffs find residues at around 20% of the permitted level.
Provable significant exposures are usually confined to application activities and self-harm.
In the financial year 2005-2006 there were 169 hospital episodes of accidental poisoning by an exposure to pesticides (http://www.hesonline.nhs.uk ); of these 93% were emergency admissions and 70% occurred to children under the age of 15 years. There were also 109 episodes of intentional self-poisoning by an exposure to pesticides; of these 88% were emergency admissions and 84% were aged between 15 and 59 years. Proof of exposure in these cases is objective.
Licensed applicators keep records.
Courts are persuaded by logically consistent witness evidence.
Non-Hodgkin lymphoma (NHL):
There are around 13,000 new diagnoses each year in the UK. A rate of 20 per 100,000. Around 3,400 cases are diagnosed each year in the under 65s. In men, 9% of cases manifest before the age of 46.
Trend analysis shows that the UK rate of NHL has nearly trebled since 1975. If this is a real effect and not just a change in diagnostic practices or an increasing lack of competing causes of disease, a cause should be sought. The slope of the year on year trend is the same for both male and female. After correcting for age, the trend is most pronounced in those aged over 80 and reduces gradually with age. There is no annual trend at all in those aged below 60. In epidemiology this is a classic sign of an environmental factor having caused some of the manifest cases.
Age corrected incidence rates have not doubled in any age group over the past 20 years.
Age corrected mortality rates have doubled since 1971 but plateaued in 1990. The same mortality trends have been seen in men and women alike. At the same time GP use has continued to grow.
If generic causation is accepted the case moves on to consider specific causation.
Given that people not exposed to GP also suffer from NHL, the correct statistical test of specific causation is the doubled risk test. That is, the claimant has to show that his exposure history would normally double the risk of NHL. In the absence of any dose response data in humans such statistical proof is impossible. Extrapolating from animal experiments is the next option, but is highly uncertain. Given the general lack of any cancer response to GP in exposed animals the only way to support the case is to ignore most of the evidence.
If the claimant can show that NHL is a non-stochastic disease then he may be able to argue material contribution. If so, almost any proven exposure two decades before cancer manifestation would pass the test. In this case damages would usually be awarded in proportion to exposure.
By selectively omitting most of the evidence a case can be made for GP being a possible human carcinogen. If all the evidence is considered with the appropriate degree of expertise the case is not strengthened. The generic causation test would not be passed by an objective assessor.
By selectively omitting most of the evidence a method can be proposed that could assist with specific causation. The claimant would have to show that evidence of a dose response effect for a different cancer seen in especially vulnerable mice at very high doses was pertinent to his NHL. This would be pure speculation.
A proposed breach of duty (if needed) would usually be credible given the lack of precision in exposure records and frequently non-compliant uses of a product which was regarded as safe.
The jury decision is not unexpected but is unlikely to be upheld by an experienced assessor of evidence.
 CAS number: 1071-83-6, official name: N-(phosphonomethyl) glycine.
 On the 10th of April 2018 the Californian authorities, working to proposition 65, recorded a view that there was no significant risk at 1,100 micrograms per day. That is, 1.1 milligrams per day. The rule comes into effect on the 1st of July 2018. From that date, business would need to label products with warnings if there was a foreseeable risk of excess exposure. No significant risk is defined as being below 1 excess cancer for every 100,000 people exposed for a lifetime. https://oehha.ca.gov/media/downloads/crnr/glyphosatensrlfsor041018.pdf
 0.5 mg/kg body weight per day. This level varies across different jurisdictions and varies upon evidence review. It was recently increased.
 https://www.bfr.bund.de/cm/349/does-glyphosate-cause-cancer-expert-group-to-address-diverging-assessments-within-the-who.pdf . See also EFSA Journal (2015) Vol.13(11) : 4302
 IARC performed a meta-analysis of case control studies of non-Hodgkin lymphoma and came to a risk ratio of 1.3 (1.03 to 1.65). A more directly interpretable cohort study found no significant association with NHL.
 http://www.cancerresearchuk.org/cancer-info/cancerstats/types/nhl/incidence/ . 36% of NHL cases will die of the disease. There are many forms of NHL.