Herbicides and Pesticides Linked to Parkinson’s Disease

Research is now confirming that Parkinson’s disease is linked to pesticide and herbicide chemical exposures. Let’s take a look at the evidence.

Glyphosate boosts Parkinson’s risk

In a 2018 study, researchers from Brazil’s University of Campinas tested 10 commercial brands of infant formulas. They found glyphosate residues at levels ranging from .02 to .17 milligrams per kg. in the formulas. The researchers linked the glyphosate and its metabolite, aminomethylphosphonic acid to Parkinson’s:

“Recently, glyphosate and its metabolite aminomethylphosphonic acid (AMPA) have been identified as possible contributors to the emergence of various diseases such as autism, Parkinson’s and Alzheimer’s diseases, as well as cancer.”

Glyphosate (e.g., RoundUp) has been linked to Parkinson’s in other studies. A 2013 study found that because glyphosate inhibits the P450 enzymes, and it builds up in tissues, it damages cells and produces brain toxicity.

A 2006 study followed 55,931 people who worked in agriculture. They found those who handled pesticides and herbicides the most had about double the risk of Parkinson’s disease.

Paraquat linked to Parkinson’s

A 2013 study from UCLA confirmed that exposure to the herbicide Paraquat is linked with a heightened risk of Parkinson’s disease. This combines with other research finding that herbicides and pesticides increase the risk of Parkinson’s.

The researchers, from UCLA’s Fielding School of Public Health, studied 357 Parkinson’s disease cases along with 754 control subjects – adults from Central California. The researchers determined increased exposure to the herbicide Paraquat through geographic mapping of their home addresses, together with agricultural use of the chemical on nearby farms. The research found that those living closer to farms that sprayed the herbicide were found to have a 36% increased risk of Parkinson’s.

However, those who experienced a head injury combined with increased Paraquat exposure tripled their chances of having Parkinson’s disease.

Researchers from Mexico’s Unidad de Medicina Familiar also studied cases of Parkinson’s together with exposure to the herbicide Paraquat among Mexican workers. They also found a positive association between exposure to this chemical and Parkinson’s disease.

Paraquat is N,N′-dimethyl-4,4′-bipyridinium dichloride.

Rotenone linked to Parkinson’s

A study from Korea’s Yonsei University studied the broad spectrum pesticide Rotenone – and how it damages nerve cells and pathways.

The researchers found that Rotenone induces cell death in a process called with G2/M cell cycle arrest. G2/M cell cycle arrest blocks the process of mitosis that enables cells and their DNA to replicate – and more importantly among nerve cells – repair any DNA damage.

Thus the insecticide basically blocks the ability of the nerve cell to repair itself – lending to the cells eventually dying off or mutating.

Benomyl blocks brain cell processes

Meanwhile, researchers from UCLA’s David Geffen School of Medicine found that the fungicide Benomyl will block multiple cell processes. One of these blocks the production of aldehyde dehydrogenase (ALDH).

ALDH increases the dopamine metabolite 3,4-dihydroxyphenylacetaldehyde, which produces degeneration among neurons associated with the production of dopamine. One of the central dopamine-producing centers exists in the brain – the substantia nigra located within the midbrain.

When the nerve cells located in this region die off or become otherwise deranged, they stop producing dopamine and other neurotransmitters that help control coordination and movement throughout the body. A lack of these neurotransmitters will produce the shakiness and eventual loss of coordination characteristic amongst progressed Parkinson’s patients.

Parkinson’s and occupational pesticides

A 2012 review of research from Belgium’s Catholic University of Louvain confirmed that Parkinson’s disease is linked to occupational exposure to pesticides.

The researchers, working with the Louvain Center for Toxicology and Applied Pharmacology, analyzed studies between 1985 and 2011 that looked at pesticide exposure by workers who handled pesticides. These included farm workers who sprayed pesticides.

The research found that those who handled pesticides were significantly more likely to contract Parkinson’s disease. In four studies, where the Parkinson’s diagnoses were confirmed by neurologists, those handling pesticides had an average of over two-and-a-half times the risk of contracting Parkinson’s disease. The increased risk ranged from 46% higher to almost four-and-a-half times higher among the workers.

Three cohort studies, which followed larger populations and compared them to the general population, concluded that workers handling pesticides had close to twice the risk of contracting Parkinson’s disease than the rest of the population. (The general population typically also has constant contact with pesticide residue in the form of foods and household pesticides.)

One of these cohort studies showed workers handling pesticides had almost three times the rate of contracting Parkinson’s disease.

Their meta-analysis found that all twelve studies individually and combined, established a link between pesticide exposure and Parkinson’s disease.

After calculating meta-data ratios and relative risk, the researchers found that Parkinson’s disease incidence as diagnosed by a neurologist was more than two-and-a-half times for those exposed to more pesticides compared to those less exposed. Other risk calculations showed the increased incidence of Parkinson’s disease to range from nearly double to 28% – which was the average of all cases studied.

But when the research focused upon farm workers involved in the growing of bananas, pineapples or sugarcane, the incidence of Parkinson’s disease more than doubled that of lower-exposure individuals.

The researchers concluded:

“The present study provides some support for the hypothesis that occupational exposure to pesticides increases the risk of Parkinson’s disease.”

Neurotoxic pesticides

Today over five billion pounds of pesticides are applied to our crops, households and other areas we share with insects. As we’ve discussed, many of these pesticides have been shown to be neurotoxic – they damage nerves and nerve transmission.

Three-quarters of the twelve most dangerous chemicals (aka the “dirty dozen”) used by man are pesticides according to the Stockholm Convention on Persistent Organic Pollutants.

Many of these pesticides have been proven to be neurotoxins. Organochlorine hydrocarbons are one of the most widely used types of pesticides in commercial farming enterprises. These include DDT (dichlorodiphenyltrichloroethane), which is banned in the U.S. but not in many other countries where lots of our food is grown. DDT’s analogs such as dicofol and methoxychlor are also in use.

Other neurotoxic organochlorine hydrocarbons include hexachlorocyclohexane, lindane, gamma-hexachlorocyclohexane, endosulfan, chlordane, heptachlor, aldrin, dieldrin, endrin, kelevan, mirex, chlordecone, toxaphene and isobenzan. Most of these will cause changes to the central nervous system by altering potassium, sodium or calcium ion channels.

Today many of the organochlorines have been replaced by organophosphates, but these will alter neurons by blocking acetylcholinesterase enzymes. Cholinesterase enzymes are acetylcholine inhibitors. Increased acetylcholine availability leads to excessive to neuron firing, resulting in nerve excitability, long term nervousness, nerve weakness and even paralysis. And yes, neurotoxic conditions such as Parkinson’s disease.

This was confirmed in a study from the University of California, Berkeley that tested Mexican-American mothers and their children living in agricultural regions with higher pesticide exposure. The researchers monitored 202 mother-and-daughter pairs for relative levels of paraoxonase, acetylcholinesterase, and butyrylcholinesterase enzymes and their respective activity among neurons.

The researchers confirmed that pesticide exposures not only affect adult acetylcholinesterase levels, but also affect children under the age of nine years old more than adults. They also concluded that children born of pesticide-exposed parents have even lower levels of acetylcholinesterase – relating to the higher risks of nerve disorders.

Other pesticides, such as imidacloprid and related neonicotinoids are neurotoxins in turn bind to nicotinic acetylcholine receptors – important to healthy nerve firing. These pesticides are also suspected in bee colony collapse disorder.

Manufacturers of neonicotinoid pesticides have claimed that the chemicals will not affect human acetylcholine receptors. However, a study by researchers from the Tokyo Metropolitan Institute of Medical Science released this February found that the neonicotinoids imidacloprid and acetamiprid “had greater effects on mammalian neurons than those previously reported in binding assay studies.”

Pesticide residues for the rest of us

As for those of us not handling pesticides on the job or at home, pesticide residues are found on a majority of commercially grown foods. In a review of the research by Cornell University’s Dr. David Pimentel, 73% to 90% of conventional fruits and vegetables contain pesticide residues, with at least 5% of those pesticide levels above FDA tolerance amounts.

While the cost of organic foods might be a tad higher in the store, the price paid in the long run for pesticides in terms of liver disorders and nervous disorders such as Parkinson’s – as well as environmental damage to our bees, waterways and soils – makes the real price for organic foods much more competitive to conventional, pesticide- and herbicide-laden foods.

REFERENCES:

Rodrigues NR, de Souza APF. Occurrence of glyphosate and AMPA residues in soy-based infant formula sold in Brazil. Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2018 Feb 20:1-8. doi: 10.1080/19440049.2017.1419286.

Ryu HW, Oh WK, Jang IS, Park J. Amurensin G induces autophagy and attenuates cellular toxicities in a rotenone model of Parkinson’s disease. Biochem Biophys Res Commun. 2013 Mar 29;433(1):121-6.

Mostafalou S, Abdollahi M. Pesticides and human chronic diseases: evidences, mechanisms, and perspectives. Toxicol Appl Pharmacol. 2013 Apr 15;268(2):157-77.

León-Verastegui AG. Parkinson’s disease due to laboral exposition to paraquat. Rev Med Inst Mex Seguro Soc. 2012 Nov-Dec;50(6):665-72.

Fitzmaurice AG, Rhodes SL, Lulla A, Murphy NP, Lam HA, O’Donnell KC, Barnhill L, Casida JE, Cockburn M, Sagasti A, Stahl MC, Maidment NT, Ritz B, Bronstein JM. Aldehyde dehydrogenase inhibition as a pathogenic mechanism in Parkinson disease. Proc Natl Acad Sci U S A. 2013 Jan 8;110(2):636-41.

Anthony Samsel and Stephanie Seneff. Glyphosate’s Suppression of Cytochrome P450 Enzymes and Amino Acid Biosynthesis by the Gut Microbiome: Pathways to Modern Diseases. Entropy 2013, 15(4), 1416-1463; doi:10.3390/e15041416.

F Kamel, CM Tanner, DM Umbach, JA Hoppin, MCR Alavanja, A Blair, K Comyns, SM Goldman, M Korell, JW Langston, GW Ross, DP Sandler; Pesticide Exposure and Self-reported Parkinson’s Disease in the Agricultural Health Study, American Journal of Epidemiology, Volume 165, Issue 4, 15 February 2007, Pages 364–374, https://doi.org/10.1093/aje/kwk024

Pan-Montojo F, Schwarz M, Winkler C, Arnhold M, O’Sullivan GA, Pal A, Said J, Marsico G, Verbavatz JM, Rodrigo-Angulo M, Gille G, Funk RH, Reichmann H. Environmental toxins trigger PD-like progression via increased alpha-synuclein release from enteric neurons in mice. Sci Rep. 2012;2:898.

Lee PC, Bordelon Y, Bronstein J, Ritz B. Traumatic brain injury, paraquat exposure, and their relationship to Parkinson disease. Neurology. 2012 Nov 13;79(20):2061-6.

Van Maele-Fabry G, Hoet P, Vilain F, Lison D. Occupational exposure to pesticides and Parkinson’s disease: a systematic review and meta-analysis of cohort studies. Environ Int. 2012 Oct 1;46:30-43.

Lundius EG, Stroth N, Vukojević V, Terenius L, Svenningsson P. Functional GPR37 trafficking protects against toxicity induced by 6-OHDA, MPP+ or rotenone in a catecholaminergic cell line. J Neurochem. 2013 Feb;124(3):410-7.

Van Maele-Fabry G, Hoet P, Vilain F, Lison D. Occupational exposure to pesticides and Parkinson’s disease: a systematic review and meta-analysis of cohort studies. Environ Int. 2012 Oct 1;46:30-43.

Gonzalez V, Huen K, Venkat S, Pratt K, Xiang P, Harley KG, Kogut K, Trujillo CM, Bradman A, Eskenazi B, Holland NT. Cholinesterase and paraoxonase (PON1) enzyme activities in Mexican-American mothers and children from an agricultural community. J Expo Sci Environ Epidemiol. 2012 Jul 4.

Kimura-Kuroda J, Komuta Y, Kuroda Y, Hayashi M, Kawano H. Nicotine-like effects of the neonicotinoid insecticides acetamiprid and imidacloprid on cerebellar neurons from neonatal rats. PLoS One. 2012;7(2):e32432.

Pimentel D. Environmental and Economic Costs of the Application of Pesticides Primarily in the United States. Environment, Development and Sustainability. 2005. 7: 229-252.

Adams C. The Living Cleanse: Detoxification and Cleansing Using Living Foods and Safe Natural Strategies. Logical Books, 2011.