The growing link between environmental toxins and Parkinson’s disease

A recent study revealed that Parkinson's disease is caused by environmental toxins, which trigger inflammation, mitochondrial damage and oxidative stress even decades after exposure.

Environmental toxins are increasingly acknowledged as a significant risk factor for the development of Parkinson’s disease. The rising incidence of the disease is thought to parallel the growth of industrialization and associated exposures to environmental toxins.

These toxins are shown to trigger inflammation, mitochondrial damage, and oxidative stress. Due to the specific vulnerability of dopaminergic cells to these factors, environmental toxins are implicated in the neuronal cell death associated with Parkinson’s disease development.

The role of pesticides

Long linked to Parkinson’s disease, pesticides are associated with neurotoxicity in various ways. Paraquat, rotenone, and glyphosate are just a few of the many culprits identified through epidemiological studies as toxins that increase Parkinson’s risk, especially among those with occupational exposures, such as agricultural workers.

Pesticides have been shown to compromise the integrity of the intestinal barrier, leading to intestinal and systemic inflammations. This results in an accumulation of misfolded alpha-synuclein and neurodegeneration.

A separate neurotoxicity mechanism from inflammation includes the production of free radicals, causing direct cellular damage and affecting the neuronal removal of damaged or degraded proteins, further increasing cellular damage.

A study found that 23% of Parkinson’s cases in both men and women were associated with exposure to pesticides, herbicides, or military-type chemical exposures.

Military chemicals and industrial solvents

Agent Orange and trichloroethylene (TCE) are known toxins targeting veterans. Agent Orange, a powerful herbicide used by US military forces during the Vietnam War to eliminate forest cover and crops, contains dioxin, which has been linked to Parkinson’s disease. The same type of dioxin was also released in the Seveso disaster and in Taranto.

TCE, an industrial solvent found in food, air, and water, is increasingly recognized as a potential cause of the exponential increase in Parkinson’s disease cases observed in recent decades. TCE presence in drinking water has been documented, and a study found that veterans exposed to unsafe levels of TCE had a 70% higher risk of developing Parkinson’s disease even decades after exposure.

Air pollution and fine particulate matter

Another significant environmental etiology for a multitude of health problems is fine particulate matter associated with air pollution. Fine particulate matter has been shown to cross the blood-brain barrier and can generate an immune response, observable by evaluating cytokine levels in the blood and cerebrospinal fluid.

These cytokines are mediators of inflammatory signaling, promoting tissue swelling, leading to cell death and vascular damage.

Researchers at the Barrow Neurological Institute (Phoenix – AZ) confirmed a strong national association between Parkinson’s disease and fine particulate matter using geospatial analytical techniques.

The study observed that regional differences in the incidence of Parkinson’s disease might reflect regional differences in particulate composition, with some areas containing more toxic components than others.

Environmental exposures are increasingly recognized as risk factors in the pathogenesis of Parkinson’s disease, and numerous studies have demonstrated how these exposures are contributing to the rising incidence of the disease.

Source: Journal of Parkinson’s Disease

The article draws upon studies published and recommendations from international institutions and/or experts. We do not make claims in the medical-scientific field and report the facts as they are. Sources are indicated at the end of each article.
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