Pesticides and Parkinson Disease (Pest-PD) — NCT06420310

Pest-PD: Pesticides and Parkinson Disease (NCT06420310)

Overview

The Pest-PD study (NCT06420310) is a case-control cross-sectional prevalence study conducted by [Hospital Universitario de Burgos](https://clinicaltrials.gov/study/NCT06420310) in Spain. The study aims to determine whether individuals exposed to pesticides have a higher prevalence of preclinical and prodromal Parkinson's disease compared to unexposed controls. This is an epidemiological study investigating the environmental etiology of [Parkinson's disease](/diseases/parkinson-disease) through the lens of pesticide exposure as a major modifiable risk factor.

Pest-PD: Pesticides and Parkinson Disease (NCT06420310)

Overview

The Pest-PD study (NCT06420310) is a case-control cross-sectional prevalence study conducted by [Hospital Universitario de Burgos](https://clinicaltrials.gov/study/NCT06420310) in Spain. The study aims to determine whether individuals exposed to pesticides have a higher prevalence of preclinical and prodromal Parkinson's disease compared to unexposed controls. This is an epidemiological study investigating the environmental etiology of [Parkinson's disease](/diseases/parkinson-disease) through the lens of pesticide exposure as a major modifiable risk factor.

Unlike interventional clinical trials, Pest-PD is an observational study that will assess biomarker and clinical sign prevalence in pesticide-exposed vs. unexposed populations. The mechanistic focus aligns with the broader literature implicating pesticide exposure as a dominant environmental driver of [Parkinson's disease risk](/mechanisms/environmental-toxins-parkinson-risk)[@tang2024][@ball2019].

Trial Details

| Attribute | Value |
|-----------|-------|
| NCT Number | NCT06420310 |
| Acronym | Pest-PD |
| Official Title | Prevalence of Preclinical and Prodromal Parkinson Disease in Subjects Exposed to Pesticides |
| Study Type | Observational (Case-Control) |
| Overall Status | Recruiting |
| Study Start Date | April 2024 |
| Estimated Primary Completion | September 2028 |
| Estimated Study Completion | December 2028 |
| Target Duration | 3 Years |
| Enrollment | 260 (estimated) |
| Condition | Pesticide-Induced Parkinsonism |
| Biospecimens | Blood samples with DNA |
| Data Sharing | No IPD sharing |

Scientific Rationale

Pesticides and Neurodegeneration

Epidemiological evidence has consistently demonstrated that pesticide exposure significantly increases [Parkinson's disease](/diseases/parkinson-disease) risk. Key mechanistic pathways include:

Prodromal PD Assessment

The study focuses on detecting [prodromal Parkinson's disease](/diseases/parkinson-disease) — the pre-diagnostic phase characterized by non-motor symptoms that precede motor diagnosis by years to decades. Key prodromal markers include:

• Olfactory dysfunction: Hyposmia is one of the earliest and most prevalent prodromal signs
• REM sleep behavior disorder (RBD): Strongly predictive of synucleinopathies
• Constipation and GI dysfunction: Reflects early alpha-synuclein pathology in the enteric nervous system
• Depression and anxiety: May precede motor symptoms
• Subtle motor signs: Bradykinesia, gait changes, micrographia (pre-motor PD)

Study Design

Structure

Pest-PD Study Design
├── Cases: Farmers with occupational pesticide exposure
│ └── N ≈ 130 individuals
└── Controls: Un-exposed individuals
└── N ≈ 130 individuals

• Observational Model: Case-Control
• Time Perspective: Cross-sectional
• Sampling Method: Non-probability sample
• Target Population: Subjects not diagnosed with PD living in the Burgos region, Spain

Key Elements

Eligibility Criteria

Inclusion Criteria

• Cases: Farmers with occupational exposure to pesticides
• Controls: Individuals with no occupational pesticide exposure
• Age range: 45–55 years
• Healthy volunteers: Yes

Exclusion Criteria

• Subjects without signed informed consent form
• Subjects with significant neurological conditions (other than prodromal signs)
• Prior diagnosis of [Parkinson's disease](/diseases/parkinson-disease) or parkinsonism

Biological Sample Collection

The study collects blood samples from both cases and controls, including DNA for genomic analysis. This biospecimen collection enables:

• Genetic analysis: Examining gene-environment interactions, including [GBA](/diseases/gba-related-parkinsonism), [LRRK2](/genes/lrrk2), [SNCA](/genes/snca), and other [Parkinson's disease](/diseases/parkinson-disease) risk genes
• Biomarker studies: Neurofilament light chain (NfL), alpha-synuclein in blood/serum, and other neurodegenerative markers
• Epigenetic profiling: DNA methylation studies to assess pesticide-induced epigenetic modifications

Outcome Measures

Primary Outcome

| Measure | Description | Time Frame |
|---------|-------------|------------|
| Prodromal PD prevalence | Presence of early non-motor symptoms associated with preclinical/prodromal [Parkinson's disease](/diseases/parkinson-disease) | Over the last year |

Study Endpoints

The study will compare:

• Prevalence of prodromal PD signs in pesticide-exposed vs. unexposed groups, stratified by age and gender
• Biological biomarker profiles in exposed vs. unexposed cohorts
• Risk of presenting early [Parkinson's disease](/diseases/parkinson-disease) after adjustment for clinical covariates

Location

| Facility | City | Country | Status |
|----------|------|---------|--------|
| Hospital Universitario de Burgos | Burgos | Spain | Recruiting |

Principal Investigator

Esther Cubo, MD, PhD
Hospital Universitario de Burgos
Contact: +34 947 256 533 | mcubo@saludcastillayleon.es

Significance for NeuroWiki

Mechanistic Context

The Pest-PD study directly supports the environmental etiology section of [Environmental Toxins and Parkinson's Disease Risk](/mechanisms/environmental-toxins-parkinson-risk). Key mechanistic connections:

• Pesticide → mitochondrial dysfunction → alpha-synuclein aggregation → dopaminergic neuron loss: This pathway chain is well-established in the literature[@betarbet2000][@tang2024]
• Epigenetic modifications: Pesticide exposure changes gene expression related to [Parkinson's disease](/diseases/parkinson-disease) without changing DNA sequence
• Gene-environment interactions: Individual genetic susceptibility (e.g., [GBA](/diseases/gba-related-parkinsonism), [SNCA](/genes/snca) multiplications) modulates pesticide toxicity

Cross-Linking Opportunities

This trial page provides anchor points for:

• [Environmental risk factors mechanism page](/mechanisms/environmental-risk-factors)
• [Parkinson's disease etiology section](/diseases/parkinson-disease)
• [Occupational health and neurodegeneration](/mechanisms/environmental-toxins-parkinson-risk)
• [Prodromal Parkinson's disease biomarkers](/mechanisms/prodromal-parkinson-markers) (if such a page exists)

Broader Research Context

The Pest-PD study complements several other research streams in the NeuroWiki knowledge base:

Research Team

Hospital Universitario de Burgos serves as the lead sponsor and coordinating center. The study represents a collaborative effort between neurology, epidemiology, and occupational medicine specialists in Spain.