We are interested in all the ways that it is possible to slow, stop, and reverse Parkinson’s.  Much of our focus is on treatments, but treatments are only part of the story. A vital step for Cure Parkinson’s is to stop people from getting Parkinson’s in the first place.

There is strong evidence indicating that exposure to pesticides, paraquat in particular, is associated with the risk of developing Parkinson’s.

Exposure to paraquat produces oxidative stress, causing mitochondrial dysfunction and inflammation, which contribute to dopamine cell degeneration. The loss of dopamine cells leads to Parkinson’s.  Although paraquat use is banned in the EU and UK, it is manufactured in the UK for export to the USA, South America and Asia.

Given that the number of people living with Parkinson’s globally is set to double by 2040 and with that the exponential increase in related healthcare costs, permanently banning paraquat’s use internationally would be one simple step that could help to cut the numbers of people getting Parkinson’s and reduce the cost of treating people.  

Based on the information that is available, we believe the UK Government has a duty of care to act now and stop the manufacture and distribution of toxic chemicals that have led to a neurological health crisis. Cure Parkinson’s has highlighted the urgent need for a thorough, public-health related consultation as part of a major public dialogue on the chemicals we’re exposed to, involving a broad audience including DEFRA, Department of Health, DTI, health charities and the general public.

Cure Parkinson’s took part in the public consultation document ‘Sustainable Use of Pesticides: Draft National Action Plan’ which closed on 26 February.

We are grateful to those who added their voice to this consultation.

Pesticide Action Network UK (PAN UK), who have a particular focus on urban pesticide use, have also lobbied the government.

Cure Parkinson’s is working with  Parkinson’s UK and both organisations have responded. We await further news on this important debate. 


For Further Reading:

 

Barlow, B. K., Richfield, E. K., Cory-Slechta, D. A., & Thiruchelvam, M. (2004). A fetal risk factor for Parkinson’s disease. Dev Neurosci, 26(1), 11-23. doi:10.1159/000080707

Bastias-Candia, S., Di Benedetto, M., D’Addario, C., Candeletti, S., & Romualdi, P. (2015). Combined exposure to agriculture pesticides, paraquat and maneb, induces alterations in the N/OFQ-NOPr and PDYN/KOPr systems in rats: Relevance to sporadic Parkinson’s disease. Environ Toxicol, 30(6), 656-663. doi:10.1002/tox.21943

Bastias-Candia, S., Zolezzi, J. M., & Inestrosa, N. C. (2019). Revisiting the Paraquat-Induced Sporadic Parkinson’s Disease-Like Model. Mol Neurobiol, 56(2), 1044-1055. doi:10.1007/s12035-018-1148-z

Cicchetti, F., Lapointe, N., Roberge-Tremblay, A., Saint-Pierre, M., Jimenez, L., Ficke, B. W., & Gross, R. E. (2005). Systemic exposure to paraquat and maneb models early Parkinson’s disease in young adult rats. Neurobiol Dis, 20(2), 360-371. doi:10.1016/j.nbd.2005.03.018

Cook, A. R., Botham, P. A., Breckenridge, C. B., Minnema, D. J., Sturgess, N. C., & Travis, K. Z. (2016). Neurotoxicity of paraquat and paraquat-induced mechanisms of developing Parkinson’s disease. Lab Invest, 96(9), 1028-1029. doi:10.1038/labinvest.2016.80

Cory-Slechta, D. A., Thiruchelvam, M., & Di Monte, D. A. (2008). Letter regarding: “Paraquat: the red herring of Parkinson’s disease research”. Toxicol Sci, 103(1), 215-216; author reply 217-218. doi:10.1093/toxsci/kfm309

Costello, S., Cockburn, M., Bronstein, J., Zhang, X., & Ritz, B. (2009). Parkinson’s disease and residential exposure to maneb and paraquat from agricultural applications in the central valley of California. Am J Epidemiol, 169(8), 919-926. doi:10.1093/aje/kwp006

Dinis-Oliveira, R. J., Remiao, F., Carmo, H., Duarte, J. A., Navarro, A. S., Bastos, M. L., & Carvalho, F. (2006). Paraquat exposure as an etiological factor of Parkinson’s disease. Neurotoxicology, 27(6), 1110-1122. doi:10.1016/j.neuro.2006.05.012

Goldman, S. M., Kamel, F., Ross, G. W., Bhudhikanok, G. S., Hoppin, J. A., Korell, M., . . . Tanner, C. M. (2012). Genetic modification of the association of paraquat and Parkinson’s disease. Mov Disord, 27(13), 1652-1658. doi:10.1002/mds.25216

Mandel, J. S., Adami, H. O., & Cole, P. (2012). Paraquat and Parkinson’s disease: an overview of the epidemiology and a review of two recent studies. Regul Toxicol Pharmacol, 62(2), 385-392. doi:10.1016/j.yrtph.2011.10.004

McCormack, A. L., Thiruchelvam, M., Manning-Bog, A. B., Thiffault, C., Langston, J. W., Cory-Slechta, D. A., & Di Monte, D. A. (2002). Environmental risk factors and Parkinson’s disease: selective degeneration of nigral dopaminergic neurons caused by the herbicide paraquat. Neurobiol Dis, 10(2), 119-127. doi:10.1006/nbdi.2002.0507

Miller, G. W. (2007). Paraquat: the red herring of Parkinson’s disease research. Toxicol Sci, 100(1), 1-2. doi:10.1093/toxsci/kfm223

Ossowska, K., Wardas, J., Smialowska, M., Kuter, K., Lenda, T., Wieronska, J. M., . . . Wolfarth, S. (2005). A slowly developing dysfunction of dopaminergic nigrostriatal neurons induced by long-term paraquat administration in rats: an animal model of preclinical stages of Parkinson’s disease? Eur J Neurosci, 22(6), 1294-1304. doi:10.1111/j.1460-9568.2005.04301.x

Pezzoli, G., & Cereda, E. (2013). Exposure to pesticides or solvents and risk of Parkinson disease. Neurology, 80(22), 2035-2041. doi:10.1212/WNL.0b013e318294b3c8

Ritz, B. R., Manthripragada, A. D., Costello, S., Lincoln, S. J., Farrer, M. J., Cockburn, M., & Bronstein, J. (2009). Dopamine transporter genetic variants and pesticides in Parkinson’s disease. Environ Health Perspect, 117(6), 964-969. doi:10.1289/ehp.0800277

Sanchez-Ramos, J. R., Hefti, F., & Weiner, W. J. (1987). Paraquat and Parkinson’s disease. Neurology, 37(4), 728. doi:10.1212/wnl.37.4.728

Spivey, A. (2011). Rotenone and paraquat linked to Parkinson’s disease: human exposure study supports years of animal studies. Environ Health Perspect, 119(6), A259. doi:10.1289/ehp.119-a259a

Tangamornsuksan, W., Lohitnavy, O., Sruamsiri, R., Chaiyakunapruk, N., Norman Scholfield, C., Reisfeld, B., & Lohitnavy, M. (2019). Paraquat exposure and Parkinson’s disease: A systematic review and meta-analysis. Arch Environ Occup Health, 74(5), 225-238. doi:10.1080/19338244.2018.1492894

Tanner, C. M., Kamel, F., Ross, G. W., Hoppin, J. A., Goldman, S. M., Korell, M., . . . Langston, J. W. (2011). Rotenone, paraquat, and Parkinson’s disease. Environ Health Perspect, 119(6), 866-872. doi:10.1289/ehp.1002839

Thompson, M. D., & Zhang, X. F. (2016). Response to: Neurotoxicity of paraquat and paraquat-induced Parkinson’s disease. Lab Invest, 96(9), 1030-1034. doi:10.1038/labinvest.2016.83

Uversky, V. N. (2004). Neurotoxicant-induced animal models of Parkinson’s disease: understanding the role of rotenone, maneb and paraquat in neurodegeneration. Cell Tissue Res, 318(1), 225-241. doi:10.1007/s00441-004-0937-z

Zhang, X. F., Thompson, M., & Xu, Y. H. (2016). Multifactorial theory applied to the neurotoxicity of paraquat and paraquat-induced mechanisms of developing Parkinson’s disease. Lab Invest, 96(5), 496-507. doi:10.1038/labinvest.2015.161

PLEASE NOTE:

Cook et al (2016) is SYNGENTA’s response, along with the excellent rebuttal by Thompson & Zhang (2016).

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