In two recent articles, Joel Hood from the Chicago Tribune and Adam Jensen of the Tahoe Daily Tribune report on rotenone, a fish poison used in lakes and rivers across the country to kill invasive fish species. Both articles ignore information on human health or ecosystem concerns associated with rotenone.
Rotenone is a powerful neurotoxin that kills fish and other aquatic organisms by shutting down energy production in cells. Lab studies show that at low doses over time, rotenone selectively kills dopamine-producing nerve cells grown in petri dishes. Loss of these cells leads to Parkinson’s disease, and researchers routinely use rotenone to induce Parkinson’s disease in research animals.
A few human studies have linked Parkinson's disease with exposure to rotenone and other neurotoxic pesticides. One study that looked at people living in Texas found significantly increased risk of Parkinson's disease with any occupational or environmental use of rotenone in the prior year as well as an increased risk from using pesticides, including rotenone, during the last year while gardening.
However, more studies in humans are needed to fully understand the health risks of rotenone exposure and to evaluate the sources of exposure after a waterway is doused. At risk for exposure are people applying rotenone, anyone who may use treated water recreationally, and the general public if drinking water is contaminated following rotenone applications.
When the U.S. Environmental Protection Agency reviewed rotenone in 2007, it noted that, "using the existing database, EPA cannot quantitatively assess a potentially critical effect (neurotoxicity) at doses to which rotenone users could be exposed." Essentially, neurological impacts of rotenone were not considered in EPA's assessment, despite the fact that neurological impacts are the main issue of concern with rotenone. To account for this lack of information, EPA added a 10 times uncertainty factor to set approved concentrations for rotenone.
Importantly, rotenone has not been evaluated for effects on fetal development, although studies with
other neurotoxins show that fetal exposure can increase a person’s risk for neurodegenerative disease, like Parkinson's, later in life.
In his article, Jensen noted that there are "concerns about rotenone's effect on invertebrates and whether the pesticide will persist in the creek beyond the few days a year projected by Fish and Game." Hood writes, "Biologists have used rotenone for decades to eradicate fish and control their movement, and they say it is not believed to be dangerous to humans or wildlife."
But when rotenone is applied to a river or lake with the intention of eradicating a target fish species, all fish, amphibians and invertebrates are vulnerable to extermination. Rotenone is not selective. Therefore, it is extremely dangerous to wildlife. Moreover, the loss of aquatic species eradicates the food supply for birds and other near-shore animals. This can
interrupt bird diversity, nesting and reproduction for several years.
In addition to leaving out the health and ecosystem impacts of rotenone, neither journalist reported on whether or not rotenone actually works to achieve the fish eradication objectives set forth by water managers. In 1997, the California Department of Fish and Game applied rotenone to Lake Davis to control northern pike. Initially, the treatment worked, but
two years later the pike returned.
After the 1997 poisoning, the town of Portola had to switch its water supply from Lake Davis to wells due to rotenone poisoning in the lake. The debacle led to a
$9.2 million settlement between California and Portola. Today, California continues to use rotenone against northern pike, despite the dramatic costs and ineffectiveness of this approach.
To mention these potential health and environmental effects would have strengthened the article and added an additional dimension to the still controversial use of rotenone.
