Last updated June 7, 2018 at 2:36 pm
Research reveals common pesticides affect mitochondrial function.
People genetically predisposed towards developing Parkinson’s disease are adversely affected by even very low levels of some common agricultural pesticides, Canadian research has shown.
The results – published in the journal Federation of American Societies for Experimental Biology – are the first to determine how the link between pesticides and Parkinson’s works in human cells, and prompts a call for tighter regulations concerning the use of the chemicals.
As early as 1998, epidemiological studies started uncovering a link between the prevalence of Parkinson’s and exposure to certain agrochemicals – particularly paraquat and maneb.
A separate line of investigation around the same time established that people carrying a mutation of a gene known as alpha-synuclein, located on chromosome four, had a higher-than-average risk of developing the disease.
Circumstances in which both factors are combined results in a massively increased chance of the condition manifesting.
Risks add up
“People exposed to these chemicals are at about a 250 per cent higher risk of developing Parkinson’s disease than the rest of the population,” says Scott Ryan from the University of Guelph in Ontario, lead author of the new study.
“We wanted to investigate what is happening in this susceptible population that results in some people developing the disease.”
To do so, Ryan and his colleagues resorted to stem cells. The researchers established two cohorts, the first using cells derived from Parkinson’s patients known to be carrying the alpha-synuclein mutation, and second from standard embryonic stem cells into which the mutation was introduced by means of gene-editing.
Both sets of cells were induced to create dopamine-producing neurons, which are primarily affected by Parkinson’s. The neurons were then exposed to varying levels of the target agrochemicals.
It was found that the chemicals prevent the cell mitochondria from functioning correctly, depriving the neurons of essential energy and leading them to fail.
“Until now, the link between pesticides and Parkinson’s disease was based primarily on animal studies as well as epidemiological research that demonstrated an increased risk among farmers and others exposed to agricultural chemicals,” explains Ryan.
“We are one of the first to investigate what is happening inside human cells.”
The researchers discovered that the alpha-synuclein mutation effectively turbo-charged the cells’ reaction to the chemicals, causing mitochondrial function to fail at exposure levels much lower than those contained in Canadian Environmental Protection Authority regulations.
Cells that did not carry the mutation needed higher doses before function was impaired.
Ryan adds that the results indicate that current one-level-fits-all advice for chemical exposure needs to be ditched.
“This study shows that everyone is not equal, and these safety standards need to be updated in order to protect those who are more susceptible and may not even know it,” he says.