Evidence map›Paper›PMID 41382278›Full record

ArticleMolecular neurodegeneration2025

The pesticide chlorpyrifos increases the risk of Parkinson's disease.

Kazi Md Mahmudul Hasan, Lisa M Barnhill, Kimberly C Paul, Chao Peng, William Zeiger, Beate Ritz, Marisol Arellano, Michael Ajnassian, Shujing Zhang, Aye Theint Theint and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular neurodegeneration, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Kazi Md Mahmudul HasanDepartment of Neurology, David Geffen School of Medicine at UCLA, 710 Westwood Plaza, Los Angeles, CA, 90095, USA.
Lisa M BarnhillDepartment of Neurology, David Geffen School of Medicine at UCLA, 710 Westwood Plaza, Los Angeles, CA, 90095, USA.
Kimberly C PaulDepartment of Neurology, David Geffen School of Medicine at UCLA, 710 Westwood Plaza, Los Angeles, CA, 90095, USA.
Chao PengDepartment of Neurology, David Geffen School of Medicine at UCLA, 710 Westwood Plaza, Los Angeles, CA, 90095, USA.
William ZeigerDepartment of Neurology, David Geffen School of Medicine at UCLA, 710 Westwood Plaza, Los Angeles, CA, 90095, USA.
Beate RitzDepartment of Epidemiology, University of California-Los Angeles, Los Angeles, CA, 90095, USA.
Marisol ArellanoDepartment of Neurology, David Geffen School of Medicine at UCLA, 710 Westwood Plaza, Los Angeles, CA, 90095, USA.
Michael AjnassianDepartment of Neurology, David Geffen School of Medicine at UCLA, 710 Westwood Plaza, Los Angeles, CA, 90095, USA.
Shujing ZhangDepartment of Neurology, David Geffen School of Medicine at UCLA, 710 Westwood Plaza, Los Angeles, CA, 90095, USA.
Aye Theint TheintDepartment of Neurology, David Geffen School of Medicine at UCLA, 710 Westwood Plaza, Los Angeles, CA, 90095, USA.
Gazmend EleziPasarow Mass Spectrometry Laboratory, The Jane and Terry Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at UCLA, Los Angeles, CA, 90095, USA.
Hilli WeinbergerPasarow Mass Spectrometry Laboratory, The Jane and Terry Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at UCLA, Los Angeles, CA, 90095, USA.
Julian P WhiteleggePasarow Mass Spectrometry Laboratory, The Jane and Terry Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine at UCLA, Los Angeles, CA, 90095, USA.
Qing BaiDepartment of Neurology and Pittsburgh Institute for Neurodegenerative Disease, University of Pittsburgh School of Medicine, Pittsburgh, PA, 15213- 3301, USA.
Sharon LiDepartment of Neurology, David Geffen School of Medicine at UCLA, 710 Westwood Plaza, Los Angeles, CA, 90095, USA.
Edward A BurtonDepartment of Neurology and Pittsburgh Institute for Neurodegenerative Disease, University of Pittsburgh School of Medicine, Pittsburgh, PA, 15213- 3301, USA.
Jeff M BronsteinDepartment of Neurology, David Geffen School of Medicine at UCLA, 710 Westwood Plaza, Los Angeles, CA, 90095, USA. jbronste@mednet.ucla.edu.

Funding

PARKINSON'S DISEASES SUSCEPTIBILITY GENES AND PESTICIDESR01ES010544 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI RITZ, BEATE R. · 2000 to 2015
$5.7M
Microbiome, Pesticides and Parkinsons in LatinosR01ES031106 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI RITZ, BEATE R. · 2020 to 2025
$3.8M
NIEHS NIH HHS R01 ES010544NIEHS NIH HHS R01 ES031106
6 · The paper itself

Abstract

backgroundPesticides as a class have been associated with an increased risk of Parkinson’s disease (PD), but it is unclear which specific pesticides contribute to this association and whether it is causal. Since chlorpyrifos (CPF) exposure has been implicated as a risk factor for PD, we investigated its association to incident PD and if this association is biologically plausible using human, rodent, and zebrafish (ZF) studies.

methodsThe association of CPF with PD was performed using the UCLA PEG cohort (829 PD and 824 control subjects), the pesticide use report and geocoding the residence and work locations to estimate exposures. For the mammalian studies, 6 months old male mice were exposed to CPF by inhalation (consistent with human exposures) for 11 weeks and behavioral and stereological pathological analyses were performed. Transgenic ZF were utilized to determine the mechanism of CPF neurotoxicity.

resultsLong-term residential exposure to CPF was associated with more than a 2.5-fold increased risk of developing PD. Mice exposed to aerosolized CPF developed motor impairment, dopaminergic neuron loss, microglial activation, and an increase in pathological α-synuclein (α-syn). Using ZF, we found that CPF-induced dopaminergic neuron loss was at least partially due to autophagy dysfunction and synuclein accumulation, as knocking down LC3 recapitulated the dopaminergic neuron loss and restoring autophagic flux or eliminating synuclein reduced neuronal vulnerability.

conclusionsCPF exposure is associated with an increased risk of developing PD and relevant exposures in animal models establish biological plausibility. In addition to establishing a new risk factor for PD, we identified new therapeutic targets for disease modification.

Indexed as

ChlorpyrifosInsecticidesParkinson DiseasePesticidesalpha-SynucleinAnimalsDisease Models, AnimalDopaminergic NeuronsFemaleHumansMaleMiceMice, Inbred C57BLRisk FactorsZebrafishalpha-SynucleinChlorpyrifosInsecticidesPesticides

Identifiers

PMID41382278
PMCPMC12801438

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.