Weighing Studies, Research and Findings
In my previous post, I showed how DuPont tried to discredit our expert witnesses, and to claim that Johnny Castillo’s blindness wasn’t a result of its toxic fungicide, but due to other causes. We were able to show that DuPont was wrong here, but it was a difficult process. Still, we soldiered on.
With all other potential environmental causes discounted by the opposition’s own denials during the discovery process, I next placed the focus on Benlate.
• I already had Donna’s testimony about her exposure to the spray.
• I had the DuPont rat studies, which proved it was a teratogen in rats.
• I had the outside studies that were conducted at the University of California and other places, which showed that benomyl and Benlate were both teratogens in rats.
• I had DuPont’s skin transmission studies.
• I had in-vitro tests that showed cell death—known as apoptosis—occurring at such small amounts as twenty-two parts per billion.
• I even had studies that showed neurite retraction (preventing cells from communicating) occurring at three parts per billion.
All of the in-vitro studies were admitted into evidence as both generally accepted and relevant. General acceptance and relevance were very easy to prove, since DuPont itself, along with literally every major drug manufacturer, uses the exact same type of tests.
What was really in question was the alleged need for epidemiology where none had previously existed. When drugs are being tested, epidemiological studies make sense, because you know who is taking the drug and who is not. You can give it to humans and study the impact by following the population.
In a case like the Castillos’, such a study was not possible. Pregnant women who were exposed to Benlate between seven and 10 weeks into their pregnancies were very rare and extremely hard to find, as were children born with Johnny’s condition. Statistics show only 1 in 10,000 have this condition. Therefore, testing this type of chemical exposure is not only difficult but also dangerous to pregnant women, and ethically impermissible.
There was a textbook that DuPont expert Dr. Holmes agreed was authoritative. It laid out the scheme and interplay between epidemiology and animal studies, taking those two things into account and dividing them into two categories: definitive evidence and adequate evidence.
Under the definitive evidence category, the textbook stated that if you were going to definitively prove developmental toxicity, you needed to have sufficient epidemiological studies from a scientific community that found a cause-and-effect relationship. To definitively prove there was no apparent effect, you needed epidemiological studies that had sufficient power. You also had to look at a variety of developmental end points.
The only study of any significance to this case that we were able to uncover was an Italian study that satisfied neither point: it did not have sufficient power, and did not look at multiple end points.
DuPont had claimed that Johnny Castillo should have had more than one malformation. However, in every microphthalmia rat study we had found, the majority of rats had only one malformation, not multiple malformations.
Dr. Brent’s position regarding adequate evidence for potential human developmental toxicity required at least one well-executed animal study showing developmental toxicity, or strong suggestive evidence from epidemiological studies.
Of course, in this case there were multiple well-executed animal studies, such as the University of California study. In fact, Dr. Staples himself, and other doctors in this case for the defense, had said the methodology of those studies was proper and that the tests were well conducted.
We were making our case, but we would have to deal with yet another roadblock from DuPont, which I will write about in my next blog.
You can find a lot more about the science of this case, and the complexities of representing clients in a chemical-company suit, in my book, Blindsided , from which this blog post is adapted.