Neurotransmission targets of per-and polyfluoroalkyl substance neurotoxicity: Mechanisms and potential implications for adverse neurological outcomes
Open accessAbstract
Per- and polyfluoroalkyl substances (PFAS) are a group of persistent environmental pollutants that are ubiquitously found in the environment and virtually in all living organisms, including humans. PFAS cross the blood-brain barrier and accumulate in the brain. Thus, PFAS are a likely risk for neurotoxicity. Studies that measured PFAS levels in the brains of humans, polar bears, and rats have demonstrated that some areas of the brain accumulate greater amounts of PFAS. Moreover, in humans, there is evidence that PFAS exposure is associated with attention-deficit/hyperactivity disorder (ADHD) in children and an increased cause of death from Parkinson's disease and Alzheimer's disease in elderly populations. Given possible links to neurological disease, critical analyses of possible mechanisms of neurotoxic action are necessary to advance the field. This paper critically reviews studies that investigated potential mechanistic causes for neurotoxicity including (1) a change in neurotransmitter levels, (2) dysfunction of synaptic calcium homeostasis, and (3) alteration of synaptic and neuronal protein expression and function. We found growing evidence that PFAS exposure causes neurotoxicity through the disruption of neurotransmission, particularly the dopamine and glutamate systems, which are implicated in age-related psychiatric illnesses and neurodegenerative diseases. Evaluated research has shown there are highly reproduced increased glutamate levels in the hippocampus and catecholamine levels in the hypothalamus and decreased dopamine in the whole brain after PFAS exposure. There are significant gaps in the literature relative to the assessment of the nigrostriatal system (striatum and ventral midbrain) among other regions associated with PFAS-associated neurologic dysfunction observed in humans. In conclusion, evidence suggests that PFAS may be neurotoxic and associated with chronic and age-related psychiatric illnesses and neurodegenerative diseases. Thus, it is imperative that future mechanistic studies assess the impact of PFAS and PFAS mixtures on the mechanism of neurotransmission and the consequential functional effects.
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PFAS exposure is associated with neurological effects, including ADHD, cognitive decline, Parkinson's, and Alzheimer's, with high risk in children and the elderly.
“| Neurological | ADHD, cognitive decline, Parkinson's, Alzheimer's. | High | Children, elderly | Long-term cognitive impairment | [225] |”
From Industrial Applications, Environmental Fate, Human Exposure, and Health Effects of PFAS (2025) · cites this paper as [225]
The Abstract reports evidence associating PFAS exposure with ADHD in children and Parkinson’s- and Alzheimer’s-related mortality in elderly populations. “PFAS Alter Behavioral Function” reports learning and memory deficits, including in adult mice exposed during development. The paper does not establish a uniformly high risk for children and the elderly or demonstrate long-term cognitive impairment in those human populations; it also describes the ADHD association as controversial. (LLM, conf=0.86)
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Flagged first, then by citations
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Cited by
Sorted by citations
Li, S., Qin, S., Zeng, H., Chou, W., Oudin, A., Kanninen, K. M., Jalava, P., Dong, G., & Zeng, X. (2024) · Eco-Environment & Health · doi:10.1016/j.eehl.2024.08.002 · Cited by 54 · see citing works
Industrial Applications, Environmental Fate, Human Exposure, and Health Effects of PFAS
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- Authors
- Brown-Leung, J. M., & Cannon, J. R.
- Affiliations
- Purdue University West Lafayette (US)
- Corresponding author
- Cannon, Jason R.
- Venue
- Chemical Research in Toxicology
- Publisher
- American Chemical Society (ACS)
- Published
- 2022-08-03
- Volume
- 35
- Issue
- 8
- Pages
- 1312-1333
- ISSN
- 0893-228X (ISSN-L)
- 1520-5010
- PMC
- PMC10446502
- OpenAlex
- W4289654250
- Cited by
- 164
- References
- 109
- Citations by year
- 2026: 58 · 2025: 53 · 2024: 36 · 2023: 15 · 2022: 2
- FWCI
- 1.87
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Chemical Research in Toxicology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (AG068787)
- Topics
- Physical Sciences › Environmental Science › Environmental Chemistry › Per- and polyfluoroalkyl substances research
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmaceutical Science › Fluorine in Organic Chemistry
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
- Keywords
- per- and polyfluoroalkyl substances, neurotransmission, dopaminergic system, glutamatergic system, blood-brain barrier, neurodegenerative diseases, Parkinson's disease, Alzheimer's disease, attention deficit hyperactivity disorder, catecholamines, hippocampus, hypothalamus, nigrostriatal pathway, PFAS mixtures, brain accumulation
- MeSH terms
- Aged, Animals, Child, Dopamine, Environmental Pollutants, Fluorocarbons, Glutamates, Humans, Synaptic Transmission, Neurotoxicity Syndromes, Rats
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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