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Parkinson’s Disease And Chemical Exposure

Analyses By Publication Year Periods

Paraquat Herbicide Exposure and Parkinson’s Disease

Studies of NHL showed higher sRR estimates in later publication years. Additionally, slightly higher sRR for PC and NHL were found for self-reported exposures and expert-level assessments in later publication years. These changes are not explained by concurrent changes in type of study design casecontrol studies, which showed the highest sRR regardless health outcome, were less frequently applied in later NHL studies and equally applied in early and late PC publications . Publication year will partly correlate with years of pesticide exposure, and might thus reflect changes in used active ingredients and levels of exposure over time . Nevertheless, publication year correlates better with time of outcome assessment for chronic diseases . As the disease classification system for NHL changed in 2000 to cover subtypes of NHL, the inclusion of more specific health outcomes in recent studies might have enabled the detection of associations previously undiscovered. Moreover, in present analyses later NHL studies applied less frequently group-level assessments and/or self-reported exposures, and more frequently expert-level assessments. Thus, higher sRR estimates seen in later NHL publications might partly reflect an increased probability of less error-prone exposure assessment methods to yield less towards-the-null biased associations. However, the superiority of expert-level assignments is dependent on the exposure information available.

Parkinsons And Occupational Pesticides

A 2012 review of research from Belgiums Catholic University of Louvain confirmed that Parkinsons 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 Parkinsons disease. In four studies, where the Parkinsons diagnoses were confirmed by neurologists, those handling pesticides had an average of over two-and-a-half times the risk of contracting Parkinsons 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 Parkinsons disease than the rest of the population.

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

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

The researchers concluded:

Links Between Chemical Exposure And Parkinson’s

Within the last decade or so, there has been scientific evidence that directly or indirectly connects exposure to certain chemicals as a correlation to the onset of PD. Although there are ongoing studies into the conclusive cause and effect of the suspected toxins found in various chemicals in question, there have been few definitive answers.

Congress and the Department of Veterans Affairs have however extended the presumption of disability to military and civilians associated with the exposure. It goes without saying that some of our bravest men and women served our country faithfully and honorably.

As a grateful nation, we have an obligation to take care of those who served and who gave their lives in her defense. There are many exposure cases pending decisions and scientific evidence being compiled but I will defer my comments to two of the most common studies that have been decided.

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Metal Elements And Pesticides As Risk Factors For Parkinson’s Disease

Common miRNA association between Parkinson’s Disease and pesticides exist.

Pesticide-deregulated miRNAs affect PD-related molecules, e.g. -synuclein.

There exist an association between essential, non-essential metals and PD.

UPS and mitochondrial impairment, oxidative stress, gene mutation and -Syn aggregation are prime mechanisms involved in essential, non-essential metals neurotoxicity in PD.

Data Extraction From Articles


In addition to data from the systematic review, we extracted for the meta-analyses from each article the reported risk estimate, study population, sample size, number of cases and controls, type of pesticide and type of exposure variable . Included articles and extracted data are provided in . References to included articles and applied exposure assessment method are described in .

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Contact The Lyon Firm Today

Parkinsons disease is a brain disorder that causes shaking, stiffness, and difficulties with balance and coordination. Approximately one million people in the U.S. have Parkinsons disease , with 50-60,000 new annual diagnoses. Symptoms generally worsen over time, and as the disease progresses, people may have mental and behavioral changes, trouble sleeping, depression, memory difficulties, and chronic fatigue.

Parkinsons disease can be triggered when nerve cells in the area of the brain that controls movement are damaged or die. These nerve cells usually produce a brain chemical called dopamine. When the cells are damaged, they produce less dopamine and thus the movement of the person is affected. Scientists still theorize what causes these cells to die.

People with Parkinsons also lose important nerve endings that control many automatic functions of the body, like heart rate and blood pressure. The loss of these nerve endings may help explain some distinct features of Parkinsons, such as fatigue, irregular blood pressure, and the disruption of the digestive tract.

Other medicine used to treat Parkinsons symptoms include dopamine agonists that mimic the role of dopamine in the brain, MAO-B inhibitors that slow down an enzyme that breaks down dopamine in the brain and Anticholinergic drugs that help reduce tremors and muscle rigidity.

Paraquat Linked To Parkinsons

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

The researchers, from UCLAs Fielding School of Public Health, studied 357 Parkinsons 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 Parkinsons.

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

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

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

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Limitations Of The Study

There are a number of limitations to this study. First, some gut metabolites that were identified, but not validated, are not necessarily irrelevant to PD, but rather the hitherto studies regarding targeted metabolomics did not cover all metabolites in human feces. The more targeted metabolomics studies toward all the detected metabolites should be further conducted. Second, the analyses could not address doseresponse relationship of metabolites. Our discussions on the association between fecal metabolite levels and increasing PD risk were based on the results of the previous literature. Third, identification of metabolites via a number of curated gene interactions, but not all PD-associated genes in humans have been determined, and the metabolitegene interactions should be elucidated in further studies.

Tce Exposure And Parkinsons

Environmental Exposures in Veterans with Parkinson’s Disease

HiI am interested if anyone with PD has had any contact with the degreasing fluid Genklene or any TCE .I am in the process of litagation concerning working exposure.Could you possibly contact me as it could be very beneficial to you and you family.removed by admin to protect users identity.

Hello I had a Saturday job in dry cleaners for about a year in approx 1965 then went on to be a hairdresser for 4 years where we used carbon tetrachloride to clean all the wigs and hairpieces popular then.I have been diagnosed since 2013. Hope this is of interest.

Yes. I am sure I used it as degreaser during my time in RN we used to call it Trike!

Yep, you probably did. In RAF we also called it , we had large trike baths for decreasing. Trike or to give its proper name Trichloroethylene is a TCE. It also came I other names during my 24 years but basically all were derived from the same basic chemicals.I am going to call Veterans Welfare or Royal British Legion later today, in between work, they can give us free advice and also help us file a case under forces compensation scheme or depending on your dates of service it may be under the war pension scheme. I will let you know how I get on

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Application Of Protein Analysis Through Evolutionary Relationships

To gain insight into the specific function of PD that may be influenced by the validated metabolites, we identified disease-specific biological process gene ontology terms and pathways for the metabolites using PANTHER tools.

First, we used the PANTHER tool to identify enriched GO terms represented by the 106 genes contained in the CTD term Parkinsons Disease due to the stability and sorting hierarchical relations by the PANTHER system . The PD gene set was directly inputted for GO enrichment analyses in the gene ontology consortium website2 that is connected to the PANTHER analysis tool. The options of Homo sapiens and biological process were chosen. The GO terms of the FDR < 0.05 were displayed. Second, the main biological processes were selected to exclude redundancy according to the FDR values and hierarchical relations between enriched functional classes. The top five GO terms with the minimum FDR values were chosen as the main biological processes of PD according to the results of enrichment analyses, because the closer the FDR values to zero, the more significant the particular GO terms associated with the PD gene set. Notably, based on hierarchical relations, when the FDR values of two terms were quite close and one term was a child node of the other, we chose the parent term. Then, enriched GO terms represented by the 106 PD genes were identified.

The Organochlorine Pesticides: The Case Study Of Dieldrin

Brief History of Use

Mechanism of Action

One of the primary mechanisms of action of dieldrin is to bind to, and block the gamma-aminobutyric acid A receptor-chloride channel complex . GABA is an inhibitory neurotransmitter in the central nervous system and opens GABAA channels to chloride in order to hyperpolarize cells. Dysfunction in these receptors result in over-excitation, seizures, and death. Studies have shown some activity as a mitochondrial toxicant and endocrine disruptor, and dieldrin has been reported to disrupt the mitochondrial electron transport chain and to act as weak estrogen receptor agonists and antagonists in estrogen and androgen transactivation assays. Detailed structure-activity relationships have also been investigated for dieldrin in terms of cellular interactions and dieldrin was found to disrupt a wide number of cellular processes including the dopamine synthesis pathway that were dependent upon both its stereochemistry and structure . Thus, while dieldrin is a potent GABAA receptor antagonist, the modes of action for dieldrin are diverse in the CNS.

Epidemiological Evidence

Cellular and Molecular Responses

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Measures Of Pesticide Exposure

In order to move beyond a broad assessment of direct pesticide application, the recalled pesticide products were classified into specific functional types and chemical classes. The chemical or trade name of each pesticide product was input into the Pesticide Action Network pesticides database to obtain its primary function and the chemical class of the main active ingredient. This database has been used for classification in other pesticide studies . For each functional type and chemical class, individuals were classified as ever exposed to the relevant class or type, ever exposed to any other pesticide, and never exposed to any pesticide.

In the residential history section of the environmental risk factor questionnaire, individuals were asked to “list the cities, towns, or communities in which you have lived for the majority of each year from childhood to now.” For each location, individuals were then questioned on their years of residence, whether they lived on or next to a farm, whether they drank well-water, and if so, the years of drinking well-water. Individuals who reported drinking well-water at any residence prior to their reference age were classified as ever exposed to well-water consumption. Cumulative duration was then determined and categorized into tertiles of exposure and a referent level of never being exposed.

Other Chemicals That Can Cause Parkinsons Disease


Paraquat, an herbicide that has been used in everything from commercial agriculture to home groundskeeping, has also been linked to an increased risk for Parkinsons disease.

Paraquat became a popular alternative to Roundup weed killer after Roundup became associated with non-Hodgkins lymphoma and other cancers.

Unfortunately, Paraquat is not the safer alternative it was once thought to be, as studies have linked Paraquat to Parkinsons disease after direct or environmental exposure.

Those at increased risk of Parkinsons disease due to Paraquat exposure include:

  • Agricultural workers

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Have You Been Exposed To Paraquat

If you have developed Parkinsons disease, or symptoms, due to paraquat exposure, you likely have grounds to file suit against the paraquat manufacturers who harmed you including:

  • Syngenta Group
  • Chevron Phillips Chemical Company, LLC
  • Drexel Chemical Company
  • HELM Agro US, Inc.
  • And more.

According to the National Law Review, the first of these lawsuits was filed in October 2017 in Illinois. Our legal team at Wilson Law, P.A. is proud to announce that we are accepting cases in North Carolina and will file paraquat lawsuits for residents suffering catastrophic injury due to toxic exposure. There are several different herbicides throughout the nation that contain paraquat, the most common of which is Syngentas Gramoxone SL 2.0 Herbicide. Para-SHOT, Helmquat, and Devour are other common weed killers in which paraquat is an active ingredient.

To learn more, please visit our paraquat litigation page here.

Rotenone Linked To Parkinsons

A study from Koreas 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.

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Fox Foundation Offers Guide For Using Medical Marijuana

A number of environmental and lifestyle factors such as smoking or exposure to heavy metals have been implicated in the development of Parkinsons. Diet and exposure to agricultural chemicals also have been implicated as important factors affecting Parkinsons risk. However, to date, individual studies have considered diet or chemical exposure, rather than looking at both factors concurrently.

To address these research gaps, we conducted a hospital-based case-control study in the province of Brescia, Northern Italy. We aimed to assess the association of nutritional factors and agrochemical exposure with the risk of , the researchers wrote.

The teams analysis included data on 347 people with Parkinsons and 389 without the disease . The Parkinsons patients were slightly older on average , and were generally more likely to have a family history of Parkinsons or a history of exposure to agricultural chemicals or metals. Parkinsons patients also were generally more likely to have been born in the province of Brescia.

The researchers constructed statistical models to look for the associations between various factors and Parkinsons risk. In addition to data on diet and chemical exposures, this included data on sex, age, socio-economic status, head injury, family history, smoking, metals exposure, and SCNA gene variations.

The models also showed that people with a reported history of exposure to agricultural chemicals were nearly twice as likely to get Parkinsons.

Does Trichloroethylene Cause Cancer

Does Paraquat Exposure Cause Parkinson’s Disease?

Trichloroethylene is classified as a carcinogen and cancer of the cervix, non-Hodgkin lymphoma, autoimmune diseases, cholangiocarcinomas, renal cell carcinoma, lung cancer, and cancer lymphatic system, male breast tissue cancer, fetal cardiac defects, and lead to mitochondrial dysfunction. The direct relationship to developing Parkinsons has been overlooked because exposure to TCE can happen decades before it manifests itself and cancer. While some exposed patients can show symptoms immediately, most others may unknowingly live or work in contaminated areas for most of their adult lives before developing any symptoms related to Parkinsons disease.

Patients living in sites already known to be contaminated with hazardous materials such as TCE are especially at high risk of exposure. Some countries such as Canada already heavily regulate TCE, and the chemical is also banned in the EU without special permits. It is estimated that over 1 Billion pounds of toxic chemicals are still used annually around the world. In 2018, more than 120 Million pounds of TCE were released into the environment, mainly from industrial sites, which contaminate soil, water, and air. It is estimated that trichloroethylene products can be found in over 25% of groundwater in developed nations, with that number possibly doubling for developing nations.

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New Proof Of Environmental Link To Parkinson’s Disease

Researchers based their study on previous findings that show exposure to environmental toxins may raise the risk of developing the disease by increasing the rate of oxidative stress. Oxidative stress is related to the body’s ability to eliminate free radicals in the body and can result in cell damage within the body.

In the study, researchers showed that flies lacking forms of the DJ-1 gene were normal under standard conditions. But when they were exposed to high doses of the herbicide paraquat and insecticide rotenone, which have previously been linked to Parkinson’s disease, the flies suffered from extreme oxidative stress and died.

Researchers say these findings suggest that a loss of DJ-1 gene function increases sensitivity to chemicals that cause oxidative stress.

Together, researchers say the results shed new light on the biological connections between the inherited and sporadic forms of Parkinson’s disease and may lead to more effective treatments.

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