VOLUME 30, ISSUE 1 • March 2026. Full issue »

Tomatoes and Parkinson’s disease: An old hypothesis revisited
In 1989, Jacob Sage proposed that tomatoes might contribute to the etiology of Parkinson’s disease (PD) [1]. At the time, his hypothesis mainly served as a provocative, tongue-in-cheek illustration of the challenges in identifying the causes of PD. In our paper 2], we discuss why this hypothesis may have been less far-fetched than originally thought.
Specifically, evidence linking pesticide exposure to the etiology of PD is mounting fast [3, 4]. Various epidemiological studies have found associations between PD and certain pesticides, which is further supported by pre-clinical studies [5-7]. While most studies have focused on occupational exposure, emerging evidence indicates that people living near agricultural fields or consuming pesticide-treated products may also encounter risks [8, 9].
Interestingly, at least some of these very same pesticides are used in the cultivation of tomatoes. To gain insight into the pesticide profile used in tomato production, we analyzed pesticide use data from California — a major tomato-producing state [10]. We found that many of the most commonly used pesticides on tomatoes have been previously linked to PD (Table 1). Moreover, the increasing number of pesticides applied over the years raises concerns about cumulative or even synergistic neurotoxicity, where the combined effects of multiple pesticides could amplify neurotoxicity [11, 12]. In addition, countries with the highest growth in tomato cultivation, including China, India, and the United States, also have a rising prevalence of PD, which suggests that contaminated tomatoes could be contributing to the worldwide growth of PD.
We fully acknowledge that the evidence presented in our paper is circumstantial and that our hypothesis remains speculative. While we do not claim that tomatoes — or specifically the pesticides used on them — are an actual cause of PD, we believe that the growing use of pesticides in agriculture and their potential (cumulative) neurotoxic effects merit serious consideration. It is crucial to critically look at current pesticide regulations and risk assessments, which often do not consider the long-term neurotoxic effects of individual compounds, and especially the combined effects of multiple compounds [13]. Future research should focus on real-world exposures, including more adequate risk assessment, with a specific focus on interactions between environmental exposures, including the potential for cumulative and synergistic toxicity. Findings could help inform much-needed preventative measures to mitigate the growing burden of PD worldwide.
Table 1: Top pesticides applied on tomatoes across California by pounds applied (2010–2020).
| Pesticide | Linked to PD [14–20] | Chemical class | Mode of action |
|---|---|---|---|
| Trifluralin | Yes | Dinitroaniline | Non-systemic |
| Metam-sodium | Yes | Dithiocarbamate | Non-systemic |
| Chlorothalonil | Yes | Polychlorinated aromatic | Non-systemic |
| Sulfur | Yes | Chalcogen | Non-systemic |
| Glyphosate, isopropylamine salt | Yes | Phosphonoglycine | Systemic |
| Glyphosate, potassium salt | Phosphonoglycine | Systemic | |
| Kaolin | Aluminosilicate | Non-systemic | |
| Potassium N-methyldithiocarbamate | Dithiocarbamate | Non-systemic | |
| S-metolachlor | Chloroacetanilide | Systemic | |
| Chloropicrin | Yes | Halonitroalkane | Systemic |
| 1,3-Dichloropropene | Yes | Organochlorine | Non-systemic |
| Metolachlor | Chloroacetanilide | Systemic | |
| Imidacloprid | Neonicotinoid | Systemic | |
| Mancozeb | Yes | Dithiocarbamate | Non-systemic |
| Carbaryl | Yes | Carbamate | Non-systemic |
| Copper hydroxide | Yes | Inorganic compound | Non-systemic |
| Dimethoate | Yes | Organophosphate | Systemic |
| Pendimethalin | Yes | Dinitroaniline | Non-systemic |
| Methyl bromide | Yes | Organobromine | Systemic |
| Diazinon | Yes | Organophosphate | Systemic |
| Ethephon | Yes | Organophosphate | Systemic |
| Chlorine | Halogen | Non-systemic |
Top pesticides used on tomatoes by total pounds of active ingredient applied each year from 2010 to 2020. Source: California’s Pesticide Use Report (PUR) database [10]. For each pesticide, it is indicated whether it has been previously linked to Parkinson’s disease (PD), along with its chemical class and whether it is systemic or non-systemic.
References
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- Bogers JS, Paul KC, Dorsey ER, Bloem BR. Tomatoes and Parkinson’s disease – an old hypothesis revisited. Medical Hypotheses. 2026;206.
- Atterling Brolin K, Schaeffer E, Kuri A, Rumrich IK, Schumacher Schuh AF, Darweesh SKL, et al. Environmental Risk Factors for Parkinson's Disease: A Critical Review and Policy Implications. Mov Disord. 2025;40(2):204-21.
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- California Department of Pesticide regulation (CDPR). Pesticide Use Report (PUR) data Available from: https://www.cdpr.ca.gov/pesticide-use-in-california/.
- Paul KC, Krolewski RC, Lucumi Moreno E, Blank J, Holton KM, Ahfeldt T, et al. A pesticide and iPSC dopaminergic neuron screen identifies and classifies Parkinson-relevant pesticides. Nat Commun. 2023;14(1):2803.
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- Gatto NM, Cockburn M, Bronstein J, Manthripragada AD, Ritz B. Well-water consumption and Parkinson's disease in rural California. Environ Health Perspect. 2009;117(12):1912-8.
- Narayan S, Liew Z, Paul K, Lee PC, Sinsheimer JS, Bronstein JM, et al. Household organophosphorus pesticide use and Parkinson's disease. Int J Epidemiol. 2013;42(5):1476-85.
- Manthripragada AD, Costello S, Cockburn MG, Bronstein JM, Ritz B. Paraoxonase 1, agricultural organophosphate exposure, and Parkinson disease. Epidemiology. 2010;21(1):87-94.
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