Additional information about organophosphates (OPs) and what happened on our farm that led to Wrather v. Farnam Companies – please note that (a) this is our lay understanding of the science (in other words, consult a scientist if you want to be certain of the details), and (b) we leave it to the reader (as we left it to the jury) to draw conclusions about a relationship between the OP absorption and the horses’ problems.

OPs interfere with nerve impulse transmission (chemical warfare poisons such as Sarin are OPs).  They work primarily by depressing the body’s levels of cholinesterase, an enzyme that acts to “clean up” behind the vital neurotransmitter acetylcholine.  When there is not enough cholinesterase to do the job, the acetylcholine builds up and neurotransmission becomes hyperactive and erratic.  Many or most bodily systems depend on the proper functioning of neurotransmitters, including the immune system, growth regulation, and thyroid function. OPs cross the placental barrier and cross the blood-brain barrier. 

OP intoxification can be the result of an acute exposure or a long-term chronic exposure. Acute toxicity results from a large dose all at once. One measure of the acute toxicity of an OP is its “LD50”, which is defined as the amount of the OP required to kill 50% of the population exposed to it. It is usually measured in “mg of toxicant/kg of animal body weight”. Signs of acute OP toxicity in horses include “convulsions, profuse salivation, tremors, muscle weakness … exhaustion and death.”  Veterinary Treatments and Medications for Horsemen, Equine Research Inc. pub. 1977, p. 539.  Years ago horses were dewormed with OPs, and the dangers were clearly recognized (just ask any vet).  Such wormers were never considered safe for pregnant mares because they could cause abortion and/or other reproductive abnormalities. 

Feed-through fly control using OPs involves long-term, low-level chronic exposure rather than acute exposure, and the symptoms of intoxification may be different or more subtle.  Recent research in environmental toxicology has also revealed something called an “inverse dose response” – certain chemicals can induce a greater physiological effect at small doses than at large ones.  In addition, OPs are fat-soluble and may be accumulated in lipid-rich tissues (fat, brain, etc.).  It has been suggested that when this has occurred, the toxins may “flood” the system when fat is mobilized rapidly for caloric needs. 

We fed Equitrol (or occasionally a similar product from another manufacturer) from about 1996 through August 2000 during fly season which is here about March through October/November.  In the summer of 2000, we read an article in The Horse Journal questioning the safety of feed-through fly control and explaining that testing cholinesterase levels would reveal whether horses were absorbing the OP’s into their systems. We tested the cholinesterase of selected horses while on the Equitrol®, discontinued the Equitrol®, and tested again about 8 weeks later. The results of these tests can be found in Table 5 of the July 2, 2002 EPA memorandum (see link). It is evident from the table that Equitrol® significantly depressed cholinesterase levels in our horses. In our lawsuit, we presented to the jury evidence of the following categories of problems:

          1. “Hyperexcitability” and other neurological dysfunctions, in some horses rather like panic              attacks, in others rather like learning disabilities, sometimes ataxia

          2. Stunted and retarded growth

3. Reproductive problems (delivery abnormalities such as dystocia and uterine inertia; dysmature foals; foals with abnormal blood work; birth defects; angular deformities serious enough to require surgery; difficulty/inability in conceiving; abortion; resorption)

4. Immunosuppression and autoimmune problems (including canker in a yearling filly living in a clean grass pasture, leukemia, severe pneumonias in horses with no obvious pneumonia risk factors)

5. Laminitis (severe relapses in horses with formerly manageable chronic conditions)

6. Low thyroid

7. Exercise intolerance/labored breathing

8. Growth-related orthopedic abnormalities

9. High incidence of fractures, other injuries and illness

10. Severe persistent diarrhea

11. Colic

In a number of these categories we were able to provide "during OP use vs. after OP use" numbers as a percentage of total horses.  Here is that information – note that this is just the incidence of problems, without attributing cause:

1.     Reproductive abnormalities/problems (any listed in 3 above):  In pregnancies in which the mares were exposed during pregnancy, 16 problems from 31 live foals (52%).  In those not involving exposure during pregnancy, 5 problems in 25 live foals (20%).  The difference is statistically significant at the .05 level (fewer than 5 chances in 100 that the difference is due to random chance).

2.     Stunted or retarded growth:  Of youngsters exposed for 2 or more fly seasons prior to age four, 29 of 30 foals (97%) are stunted or had visibly retarded growth until taken off the product (the other foal died from a neck deformity).  Of the 2001 foal crop (in utero exposure only) and horses not exposed, 3 of 27 appear abnormal (1 of 27 just plain small).  Statistically significant at the .0001 level (fewer than 1 chance in 10000 that the difference is due to random chance).

3.     Orthopedic and musculoskeletal abnormalities prior to intense training:  Of exposed horses, 22 of 58 (38%) had problems.  Of horses not exposed, 2 of 24 (8%) had problems.  Statistically significant at the .012 level (fewer than 12 chances in 1000 that the difference is due to random chance).

4.     Infections/infectious disease (not counting foot abscesses or routine foal sniffles):  Of horses exposed, 30 of 58 (52%) had illnesses.  Of horses not exposed, the number was 4 of 24 (18%). Statistically significant at the .014 level (fewer than 14 chances in 1000 that the difference is due to random chance).

Some of these problems appear to be permanent or very long term, namely stunted growth of course, neurological deficits, altered immune system responses, low thyroid, and some cases of diarrhea (intestinal tract may be damaged by chronic diarrhea, leading to a permanent problem). The horse who had the very rare leukemia died last September, over three years after we stopped using the feed-through fly control, and on post-mortem there were depressed levels of cholinesterase in her brain (and no evidence of any recent exposure to any OP at all – she was tested for every known one).

 
Those who feed such a product might wish to test their horses' levels of cholinesterase, as  we did.  If feeding it now, do the tests, then take the horses off it for 8 weeks and test again (takes 6 to 8 weeks for the blood levels to normalize).  If not feeding it at present but intending to, do the tests and then test again a couple of weeks into feeding.  The tests cost about $70 each -- if you want to save some money and are willing to rely on others’ data, read the EPA memo (which doesn't even include Dr. Madigan's data because the memo predates that study). The EPA memo summarizes that every test to date of a horse on Equitrol has showed depressed cholinesterase.  Label changes have been pending since the date of that memo (2002), but so far we have not seen any notification to consumers that precautions might be in order.