Results of a new animal study suggest inhaling low levels of Paraquat may allow the chemical to enter the brain, causing changes to the sense of smell that are consistent with the trajectory of Parkinson’s disease.
What is Paraquat?
Paraquat, including brand-name products Gramoxone, Blanco, and Cyclone SL 2.0, is used by farmers and ranchers to control weeds and as a post-harvest drying agent. As a restricted-use herbicide, the weedkiller is not available for home use.
Paraquat is highly toxic if inhaled, ingested, or allowed to come in contact with the skin. But despite restrictions on its use, including a requirement that it only be mixed and applied by individuals who have undergone specialized training, about 100 Paraquat poisonings occur in the United States every year, resulting in at least one death annually since 2012.
Paraquat has also been linked to an increased risk of Parkinson’s disease through studies involving agricultural workers exposed to the weedkiller and research showing it can destroy dopamine-producing neurons in mice. Unfortunately, the U.S. Environmental Protection Agency does not take low-level exposure into account when setting herbicide regulations. Meanwhile, animal studies assessing exposure risk rarely examine the effect of inhaled pesticides.
Inhaled Paraquat Accumulated in Olfactory Bulb
For this latest study, researchers at the University of Rochester in New York sought to compare the amount of Paraquat accumulated in various organs of mice when inhaled at low levels.
“Inhalation can provide a direct route of entry to the brain,” said Timothy Anderson, a graduate student at the University of Rochester and first author of the study,
“If you inhale something and it goes into your nose,” he continued, “it can actually enter the neurons responsible for sense of smell, and travel into the brain.”
Over 28 days, Anderson and his team exposed male and female mice to aerosolized Paraquat for four hours a day, five days a week. At predefined time points, they measured levels of the herbicide in the animals’ lungs, kidneys, and four regions of the brain — the olfactory bulb, striatum, midbrain, and cerebellum.
While Paraquat accumulated in all of the tissue examined, the highest concentrations were detected in the olfactory bulb, indicating that the herbicide had been inhaled. Brain levels of the herbicide did not return to near pre-exposure amounts until 28 days after the final exposure. Paraquat was undetectable in the brain around nine months after the last exposure.
Early Parkinson’s Symptoms Include Changes to Sense of Smell
To determine whether this impacted the animals’ sense of smell, the study authors also trained the mice to drink from water containing one particular scent while avoiding water of another scent. Both scents were then mixed in various ratios to test how well exposed mice could discriminate between the two.
No significance was seen in the number of incorrect choices made by exposed female mice, indicating no major changes to their sense of smell. However, male mice that had inhaled Paraquat were more likely to make an incorrect choice than the male mice that had not been exposed, even at time points corresponding to undetectable levels. It also appeared that the olfactory impairment experienced by the exposed mice continued for months after their last exposure.
As an early sign of Parkinson’s, olfactory impairment may serve as a sensitive indicator of pesticide exposure in humans.
“These data,” the researchers concluded, “support the need for the establishing protective regulations for applying neurotoxic pesticides, such as [Paraquat], to protect public health.”
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