• Dogyote@slrpnk.net
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    4 days ago

    I wish they collected water samples and tested them. Right now I’m not fully convinced it’s the water.

    • perestroika@slrpnk.netM
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      2 days ago

      I agree that they should have, but they were running a retrospective study without field research activity. :(

      As the article suggests, one way of validating would be comparing effects in different countries.

      in the US, pesticide application to golf courses can be up to 15 times higher compared with countries in Europe.

      In a global meta-analysis searching for correlation between any kind of well water consumption and PD, results were globally inconclusive, but locally (Asia) a positive correlation existed.

      https://pmc.ncbi.nlm.nih.gov/articles/PMC8687678/

      The strongest link I am aware of between chemical exposure and Parkinson’s disease is this one:

      https://journals.sagepub.com/doi/10.3233/JPD-225047

      Occupational or hobby exposure to significant quantities of trichloroethylene (used in dry cleaning clothes, degreasing metal and previously used in anesthesia) was linked to a 500% increase in risk of PD.

      In addition, a small epidemiological study found that occupational or hobby exposure to the solvent was associated with a 500% increased risk of developing PD. In multiple animal studies, the chemical reproduces the pathological features of PD.

      Exposure is not confined to those who work with the chemical. TCE pollutes outdoor air, taints groundwater, and contaminates indoor air. The molecule, like radon, evaporates from underlying soil and groundwater and enters homes, workplaces, or schools, often undetected. Despite widespread contamination and increasing industrial, commercial, and military use, clinical investigations of TCE and PD have been limited. Here, through a literature review and seven illustrative cases, we postulate that this ubiquitous chemical is contributing to the global rise of PD and that TCE is one of its invisible and highly preventable causes. Further research is now necessary to examine this hypothesis.

      I’m not aware if trichroloethylene (or a similar molecule) can result from breakdown of pesticides. What I know is that several pesticides and neurotoxins are organic chlorine compounds - a class of chemicals that shares a similarity with trichloroethylene.

      A study in Greece compared organochlorine exposure with PD occurrence:

      https://pmc.ncbi.nlm.nih.gov/articles/PMC7225589/

      Their results:

      Higher levels of DDE were detected among PD patients in comparison to controls by using logistic regression analysis to control for confounders [Odds Ratio, OR (95 % confidence interval, C.I.)]: 2.592,(1.29–5.21)], whilst lower levels of HCB were detect among PD patients [OR,95 %CI:0.176(0.09−0.35)].

      Our data suggest that exposure to specific OCs is related to the risk of PD. Further studies, using real exposure data, are needed in order to confirm and extend these findings.