BELLEVILLE – “Studies have shown,” say lawyers on television linking weed killer paraquat to Parkinson’s disease. But doctors have hunted for that link a long time without finding it.
Doctors who carried out an immense project to resolve the mystery once and for all concluded 10 years ago that it needed further research.
They found some evidence of a link between Parkinson’s and weed killer rotenone, diagnosing the disease 2.5 times as often among users.
Online advocates pull that statistic from the study and pin it on paraquat.
Two studies showed a possible link between Parkinson’s disease and combinations of herbicide exposures and other causes.
One stated that no single chemical could reproduce characteristics of the disease.
St. Clair County jurors will learn the science at a paraquat trial starting May 10. Associate Judge Kevin Hoerner will preside.
The big study came from eight doctors at Parkinson’s Institute in California, nine other American doctors, and three from other nations.
Lead author Caroline Tanner first laid out the background.
Tanner wrote that mitochondrial dysfunction and oxidative stress were implicated as mechanisms underlying Parkinson’s disease.
She wrote that rotenone inhibits a mitochondrial complex and paraquat causes oxidative stress.
Despite decades of laboratory study, neither rotenone nor paraquat had been definitively associated with the disease in humans.
“Previous studies have reported associations with paraquat, but results are inconsistent and in general, studies included few exposed cases,” Tanner wrote.
She listed studies from 1990 and 2005 that found an association and studies from 1987 and 1997 that didn’t.
Her team enjoyed access to about 80,000 farmers in Iowa and North Carolina through a group the government created for purposes of health research.
They identified 170 persons who might have the disease based on self reports and mortality files, and assessed them in their homes.
They diagnosed the disease in 115, and 110 provided complete information.
They picked a control group of 358 persons.
They found paraquat use before diagnosis for 23 in the study group and 49 in the control group, indicating a rate 53 percent higher for paraquat users.
Tanner wrote that the disease was diagnosed at a younger age among those who used oxidative stressors, 64 years for one group and 59 for the other.
That statistic mixed other oxidative stressors with paraquat.
A table showed the difference for paraquat without other stressors at 62 to 59.
“Our findings, considered together with earlier results, suggest that paraquat use plays a role in human Parkinson’s disease,” Tanner wrote.
She wrote that paraquat and rotenone were linked experimentally and the study connected the dots to human populations.
She wrote that the study had limitations, in that they couldn’t confidently exclude effects of agents other than those they studied.
She wrote that they couldn’t rule out a possibility that the results were attributable to combined exposures.
She wrote that they couldn’t use laboratory measures to estimate exposure because the measures are poor predictors of long term use.
“Thus, although we recognize that retrospective exposure assessment has limitations, it is often the best approach for studying lifelong exposure in an adult population in connection with a rare disease,” she wrote.
“Additionally, we were able to investigate only persons willing to participate.”
Last October, the U.S. Environmental Protection Agency extended paraquat’s registration for 15 years.
The agency allows only certified applicators to use it.