The government has been using a Parkinson’s-related poison in Montana’s waterways since 1948

Does FWP use a level of rotenone that would kill a human drinking treated water? Probably not, Duncan is right about that. But the risks are not black and white. A disease like Parkinson’s has chronic effects that sometimes don’t manifest themselves until many years later. When a chemical used by a government on public waterways has even a small potential to cause chronic disease or pose a health hazard, government agencies and the public should be well informed of the risks.

Regarding wildlife, FWP took no precautions to prevent eagles or other predators from eating the dead fish after poisoning them with rotenone. FWP told the Public Herald in October 2021 that rotenone-treated fish are left uncollected after treatments and are allowed to float to the surface to line river banks and lake edges until they eventually decompose – prime prey for the numerous fish-eating wildlife in the surrounding areas.

The FWP environmental report on the fate of dead fish states:

“Terrestrial scavengers contribute to the disappearance of carcasses, and fish killed by piscicides pose no health risk to organisms that consume them. Previous treatments have shown that fish killed by rotenone decay quickly and are difficult to locate even a few days after treatment.”

FWP’s conclusions on the effects of rotenone on wildlife aftertreatment are often based on test model studies conducted in the 1980s:

“Rotenone has a half-life of 14 hours at 24 °C and 84 hours at 0 °C (Gilderhus et al. 1986, 1988), which means that half of the rotenone is deactivated and no longer toxic in this time.”

However, according to Microbac Laboratories, the breakdown of rotenone is not as simple as FWP reports. Depending on a variety of conditions – i.e. sunlight, temperature and sediment – Rotenone can decompose quickly (within 24 hours) or months.

“Because of all these factors [bold added] Aquatic systems treated with Rotenone cannot be considered non-toxic until the systems have been analyzed for Rotenone and its breakdown products, as well as other chemicals found in various rotenone formulations. The analytical methods used to determine the levels of rotenone (and other chemicals) must be sensitive enough to detect these compounds at low ppb levels and specific enough to ensure the identification of each compound.”

A 2015 study from New Zealand using the “Gamma distribution to determine the half-life of rotenone when applied to freshwater” had similar concerns. This study examined whether a more sensitive test model would change the dissipation results of rotenone in a treated water body. It turned out that using this model, the half-life of rotenone was ten times longer (or approximately 50 days) compared to the usual method of determining half-life.

What if federal and state governments used more sensitive models to test rotenone post-treatment? What would the results be?

In the food chain, studies of rotenone by use are limited.

A report for Washington State notes that up to 0.696 parts per million (ppm) of rotenone has been detected in dead fish residue – citing Philip A. Gilderhus’ 1986 study, which Montana uses for its own assessments – and that these concentrations were low enough to be insignificant for wildlife feeding on the carcass.

For humans, the EPA in 2007 identified an acute nutritional risk of rotenone toxicity as 0.01117 mg/kg/day (milligrams per kilogram per day), but has yet to determine an acute nutritional risk for terrestrial wildlife. In an independent 2002 study in rats, an injection of low-dose rotenone at 1.5 mg/kg per day for two months was sufficient to induce Parkinson’s disease symptoms.

After studies linking rotenone to Parkinson’s disease in 2004, the EPA required a “subchronic (28-day) inhalation neurotoxicity study” for human health because it was registered as a product for personal and agricultural use. In response, the industry withdrew its registration of rotenone for all uses other than piscicide, negating the need for the EPA to conduct a human health study.

As of 2022, the EPA’s Health Effects Division (HED) sought to minimize the growing body of independent studies identifying Rotenone’s relationship to Parkinson’s disease, stating publicly, “There was insufficient epidemiological evidence to conclude that there is a clear associative or causal relationship between rotenone exposure and Parkinson’s disease.” The assessment of HED was based on eight selected studies – excluding most of the work.

Overall, the chronic effects of rotenone toxicity in the food supply are not well understood. EPA reports generally cite its ability to either be rapidly broken down or converted to non-toxic excretable substances.

The biology professor Dr. However, according to John Stolz, director of the Center for Environmental Research and Education at Duquesne University, who has studied the effects of chemicals in the food supply, federal and state declarations of rotenone’s toxicity are not enough.

“The bottom line is that they don’t want to pay people to catch the fish,” says Dr. Proud. “They just want to throw chemicals in there to kill everything. It’s the same as atrazine in the sense that they don’t want to hire workers to pick weeds – so spray atrazine instead. But then you find out that atrazine is a hormone that causes problems. Or in the case of glyphosate, that it’s now being detected in children’s Cheerios.”

dr Stolz believes that the indiscriminate use of a toxic chemical impacts the food web and that safer methods should be employed.