Environmental Toxins Linked To Parkinson’s
New Studies Support Link Between Chemicals and Parkinson’s Disease
Researchers say the findings support evidence of a possible link between environmental toxins and Parkinson’s disease and may help explain why some people with genetic risk factors for the disease get it while others do not.
Parkinson’s disease is a common neurological disorder that can occur randomly or as the result of inherited gene mutations.
In the study, which appears in Current Biology, researchers looked at fruit flies lacking both forms of a gene that is associated with the inherited form of Parkinson’s disease. These specially bred fruit flies became extremely sensitive to the herbicide paraquat and the insecticide rotenone and died after exposure.
How Parkinson’s Affects Daily Life And Overall Health
Dr. Karmon shares, “Parkinson’s disease affects patients’ lives in many ways. The most prominent effects are slowness, stiffness, vibration and disturbance in stability. These disorders can cause difficulty in daily functioning, difficulty in hand function, difficulty walking with the risk of falls, difficulty swallowing and difficulty speaking. In addition to these characteristics, there are also many non-motor characteristics pain, constipation, urinary incontinence, falls, sleep disorders, poor mood and even impaired thinking.”
Environmental Factors In Parkinsons Disease
Here are environmental factors that may play a role in the development of Parkinsons disease:
Although environmental exposure to these and other toxins is of continued research interest, its hard to determine if any one substance is a culprit. Most often, individual cases of Parkinsons disease result from a complex interplay between genetics and environmental and other factors.
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Pesticide And Herbicide Exposure
A strong link has been shown between PD and exposure to pesticides and herbicides. We need more Parkinsons-specific research to better understand what causes PD and to work to prevent it and help eliminate the risk of getting the disease, when it comes to all environmental risk factors and whether genetics can cause an increased risk in developing Parkinsons.
One herbicide that has been linked to Parkinsons is paraquat, a widely used commercial herbicide in the U.S. that is banned in 32 countries, including the European Union and China. The Parkinsons Foundation, along with the Unified Parkinsons Advocacy Council, signed two letters to the U.S. Environmental Protection Agency encouraging them to cancel the registration of paraquat based on strong scientific research linking the herbicide to Parkinsons disease. In October 2020, the EPA re-approved paraquat for use in the U.S. Without additional action, paraquat will remain legal for sale and use in the U.S. for the next 15 years.
What Are The Symptoms
The best-known symptoms of Parkinson’s disease involve loss of muscle control. However, experts now know that muscle control-related issues aren’t the only possible symptoms of Parkinson’s disease.
Motor symptoms which means movement-related symptoms of Parkinsons disease include the following:
Additional motor symptoms can include:
- Blinking less often than usual. This is also a symptom of reduced control of facial muscles.
- Cramped or small handwriting. Known as micrographia, this happens because of muscle control problems.
- Drooling. Another symptom that happens because of loss of facial muscle control.
- Mask-like facial expression. Known as hypomimia, this means facial expressions change very little or not at all.
- Trouble swallowing . This happens with reduced throat muscle control. It increases the risk of problems like pneumonia or choking.
- Unusually soft speaking voice . This happens because of reduced muscle control in the throat and chest.
Several symptoms are possible that aren’t connected to movement and muscle control. In years past, experts believed non-motor symptoms were risk factors for this disease when seen before motor symptoms. However, theres a growing amount of evidence that these symptoms can appear in the earliest stages of the disease. That means these symptoms might be warning signs that start years or even decades before motor symptoms.
Non-motor symptoms include:
Stages of Parkinsons disease
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Chemicals Used To Create Pd Model
To clarify the pathophysiological process of PD and to evaluate the efficiency of PD-targeted medicines, sophisticated models have been developed that use a panel of chemicals to reproduce and imitate the neurodegeneration process of PD. We introduce four chemicals that were applied to create the PD model for their capability to cause PD-like neuron impairments and symptoms . The ability of these chemicals to induce ferroptosis will also be discussed with special attention paid to their effects in SH-SY5Y human neuroblastoma cells since these cells possess properties of dopaminergic neurons, and, therefore, have a long history of use as an in vitro model in studies on PD . Early studies using SH-SY5Y cells as an in vitro model of chemically-induced PD showed that apoptosis is the main mode of cell death induced by PQ , rotenone , 6-OHDA , and MPP+ . This might be, at least in part, to the fact that apoptosis was the only mode of cell death that could be examined using marker proteins as well as electron and fluorescence microscopy when the studies were performed. However, recent research progress has shown that SH-SY5Y cell death due to PD-inducing chemicals involves forms of cell death other than apoptosis.
Chemically Induced Models Of Parkinsons Disease: History And Perspectives For The Involvement Of Ferroptosis
- Department of Forensic Medicine, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan
Ferroptosis is a newly discovered form of necrotic cell death characterized by its dependency on iron and lipid peroxidation. Ferroptosis has attracted much attention recently in the area of neurodegeneration since the involvement of ferroptosis in Parkinsons disease , a major neurodegenerative disease, has been indicated using animal models. Although PD is associated with both genetic and environmental factors, sporadic forms of PD account for more than 90% of total PD. Following the importance of environmental factors, various neurotoxins are used as chemical inducers of PD both in vivo and in vitro. In contrast to other neurodegenerative diseases such as Alzheimers and Huntingtons diseases , many of the characteristics of PD can be reproduced in vivo by the use of specific neurotoxins. Given the indication of ferroptosis in PD pathology, several studies have been conducted to examine whether ferroptosis plays role in the loss of dopaminergic neurons in PD. However, there are still few reports showing an authentic form of ferroptosis in neuronal cells during exposure to the neurotoxins used as PD inducers. In this review article, we summarize the history of the uses of chemicals to create PD models in vivo and in vitro. Besides, we also survey recent reports examining the possible involvement of ferroptosis in chemical models of PD.
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What Raises Someone’s Risk For Parkinson’s
It’s a complex picture, but you may be more likely to get Parkinson’s based on:
Age. Since it mostly affects people 60 and older, your risk goes up as the years go by.
Family history. If your parent, brother, or sister has it, you’re a little more likely to get it.
Job. Some types of work, like farming or factory jobs, can cause you to have contact with chemicals linked to Parkinson’s.
Race. It shows up more often in white people than other groups.
Serious head injury. If you hit your head hard enough to lose consciousness or forget things as a result of it, you may be more likely to get Parkinson’s later in life.
Gender. Men get it more than women. Doctors aren’t sure why.
Where you live. People in rural areas seem to get it more often, which may be tied to chemicals used in farming.
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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Importance Of Parkinsons Advocacy
Not to be all doom and gloom. This is a serious issue that affects a lot of people with PD and other diseases including myself. Personally, I feel that scientific research is closing in on certain causes for developing PD and the acknowledgment by our government agencies.
I encourage you to be your own advocate. Stand up for your rights to a healthy environment and ask questions of those that include positions of influence and demand answers. Although these are two examples of recognized links to PD, I realize there are other case studies of intentional or unintentional toxic contamination of our environment. If we take action today, we can make the future better for our children and grandchildren.
Other Causes Of Parkinsonism
“Parkinsonism” is the umbrella term used to describe the symptoms of tremors, muscle rigidity and slowness of movement.
Parkinson’s disease is the most common type of parkinsonism, but there are also some rarer types where a specific cause can be identified.
These include parkinsonism caused by:
- medication where symptoms develop after taking certain medications, such as some types of antipsychotic medication, and usually improve once the medication is stopped
- other progressive brain conditions such as progressive supranuclear palsy, multiple systems atrophy and corticobasal degeneration
- cerebrovascular disease where a series of small strokes cause several parts of the brain to die
You can read more about parkinsonism on the Parkinson’s UK website.
Page last reviewed: 30 April 2019 Next review due: 30 April 2022
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What Are The Early Warning Signs Of Parkinson’s Disease
Parkinsons warning signs can be motor symptoms like slow movements, tremors or stiffness. However, they can also be non-motor symptoms. Many of the possible non-motor symptoms can appear years or even decades ahead of motor symptoms. However, non-motor symptoms can also be vague, making it difficult to connect them to Parkinson’s disease.
Non-motor symptoms that might be early warning signs include:
- Sleep problems such as periodic limb movement disorder , rapid eye movement behavior disorder and restless legs syndrome.
What Medications And Treatments Are Used
Medication treatments for Parkinsons disease fall into two categories: Direct treatments and symptom treatments. Direct treatments target Parkinsons itself. Symptom treatments only treat certain effects of the disease.
Medications that treat Parkinsons disease do so in multiple ways. Because of that, drugs that do one or more of the following are most likely:
Several medications treat specific symptoms of Parkinson’s disease. Symptoms treated often include the following:
- Erectile and sexual dysfunction.
- Hallucinations and other psychosis symptoms.
Deep brain stimulation
In years past, surgery was an option to intentionally damage and scar a part of your brain that was malfunctioning because of Parkinsons disease. Today, that same effect is possible using deep-brain stimulation, which uses an implanted device to deliver a mild electrical current to those same areas.
The major advantage is that deep-brain stimulation is reversible, while intentional scarring damage is not. This treatment approach is almost always an option in later stages of Parkinson’s disease when levodopa therapy becomes less effective, and in people who have tremor that doesnt seem to respond to the usual medications.
Researchers are exploring other possible treatments that could help with Parkinsons disease. While these arent widely available, they do offer hope to people with this condition. Some of the experimental treatment approaches include:
One Of The First Studies To Look At Human Cells
At least 30 alterations in this gene have been associated with Parkinsons, and -synuclein protein clumps are a well-documented, albeit poorly understood, hallmark of the disease.
For the new research, the scientists also worked with normal embryonic cells that they modified using genetic editing to replicate the -synuclein genetic mutation.
Prof. Ryan explains why using human cells makes this study particularly valuable. Until now, he says, the link between pesticides and Parkinsons disease was based primarily on animal studies as well as epidemiological research that demonstrated an increased risk among farmers and others exposed to agricultural chemicals.
We are one of the first to investigate what is happening inside human cells, explains Prof. Ryan.
Stem cells are undifferentiated cells that go on to individualize into specific types of cells. Prof. Ryan and his colleagues used the two types of stem cells to derive dopamine-producing nerve cells from them.
Then, they exposed these dopaminergic neurons which are known to be affected the most by Parkinsons disease to the two pesticides.
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What Else Do We Know
As scientists try to learn whats at the root of Parkinsons, theyre looking far and wide to pick up clues where they can.
Theyve found that people with Parkinsons tend to have something called Lewy bodies in their brain. These are unusual clumps of a protein called alpha-synuclein. The protein itself is normal, but the clumps are not. And theyre found in parts of the brain that affect sleep and sense of smell, which could explain some symptoms of Parkinsons not related to movement.
Your gut may also have a part in it, as some of its cells make dopamine, too. Some doctors think that this might be where the earliest signs of Parkinsons show up, but that idea needs more research.
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Parkinsons Disease And Covid
Many people in the disease community have wondered: how will COVID-19 impact my treatment and condition? In this case, Bloem notes that patients with Parkinsons disease are not any more likely to contract COVID-19 than anyone else. However, he does believe that patients who get COVID-19 are more likely to experience severe symptoms. Parkinsons symptoms can become less severe with exercise and physical activity, or more severe due to stress. In a co-authored article, Bloem explains that:
Non-motor issues such as insomnia or constipation may also worsen due to a lack of physical activity. Promoting home-based and adequately dosed exercises, such as cycling on a stationary bicycle, is therefore more important than ever before.
However, he hopes that this pandemic shows people that more research needs to be done on Parkinsons disease, and that more data needs to be discovered on the impact of these situations on patients. Read the full article in Journal of Parkinsons Disease.
Other Causes Include A Combination Of Factors
According to Dr. Petrossian, “In most cases, PD is likely due to a combination of aging, genetic changes that confer susceptibility, and exposure to certain environmental triggers. Many triggers have been theorized to play a role such as repetitive head trauma, long-term exposure to chemicals such as pesticides or solvents, and other yet unknown atmospheric or dietary chemicals. What we know with certainty is that the brain and nervous system undergo changes such as the atrophy of specific brain cells, changes in brain chemicals, and an abnormal accumulation of misfolded proteins in the remainder of brain cells.”
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What Can I Expect If I Have This Condition
Parkinsons disease is a degenerative condition, meaning the effects on your brain get worse over time. However, this condition usually takes time to get worse. Most people have a normal life span with this condition.
You’ll need little to no help in the earlier stages and can keep living independently. As the effects worsen, youll need medication to limit how the symptoms affect you. Most medications, especially levodopa, are moderately or even very effective once your provider finds the minimum dose you need to treat your symptoms.
Most of the effects and symptoms are manageable with treatment, but the treatments become less effective and more complicated over time. Living independently will also become more and more difficult as the disease worsens.
How long does Parkinsons disease last?
Parkinsons disease isnt curable, which means its a permanent, life-long condition.
Whats the outlook for Parkinsons disease?
Parkinson’s disease isn’t fatal, but the symptoms and effects are often contributing factors to death. The average life expectancy for Parkinson’s disease in 1967 was a little under 10 years. Since then, the average life expectancy has increased by about 55%, rising to more than 14.5 years. That, combined with the fact that Parkinson’s diagnosis is much more likely after age 60, means this condition doesn’t often affect your life expectancy by more than a few years .
Cellular Pathophysiology Of Pd
Figure 1. Cellular iron metabolism. Ferric iron is transported into cells via binding to transferrin receptor and subsequent endocytosis, while ferrous iron enters cells through divalent metal transporter1 . Within the endosomes, Fe3+ is reduced to Fe2+ through the action of the six-transmembrane epithelial antigen of the prostate and released into the cytosol via DMT1. Ferritin is served as the intracellular reservoir of iron. In DA neurons, neuromelanin works as the iron storage protein instead of ferritin. Fe2+ stored in ferritin/NM is released into the cytosol as the cytosolic labile iron pool via ferritinophagy. Excess in the cytosolic labile iron pool leads to the export of excess iron via ferroportin. In Parkinsons disease patients as well as PD models, cellular iron uptake and release were increased and decreased, respectively, in DA neurons. Also, ferritinophagy is upregulated in the PD model. All of these contribute to the increase of cytoplasmic labile iron pool, which leads to an increase of ferroptosis susceptibility of DA neurons in PD.
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