Thursday, June 5, 2025

Acrid Burning Herbicide Smell of ALS and neurogenerative diseases! No thanks "True Green"

 I noticed Panera's weed free lawn with the little herbicide signs had a strong acrid burning smell - the same as the herbicide aisle at Lowes! Only I was in the car some 50 feet from the lawn at Paneras. So I wondered what causes this acrid burning smell? I tracked it down to this "broadleaf herbicide"
Broadleaf herbicides primarily target the enzyme acetolactate synthase (ALS). ...Yes, certain enzyme herbicides, particularly those that inhibit acetolactate synthase (ALS), are known to cause damage to the SOD1 enzyme in humans, increasing the risk of ALS. SOD1 is a crucial antioxidant enzyme that protects against oxidative stress, and its damage can contribute to the progression of ALS... ALS (acetolactate synthase) inhibitor herbicides are toxic to plants because they block the biosynthesis of branched-chain amino acids, essential for growth
Is this the same ALS disease that my friend and former boss's dad (who had a hobby farm) died from? tragically yes. 
citing
So what would appear to be a hysterical reaction to pesticides is now considered to be a significant correlation for 90% of ALS victims.
Only 10 % of the ALS cases can be attributed to a familial trait or gene (Mathis et al., 2019). Identifying etiologic factors could help to prevent ALS and focus studies of interventions to block progression.
  In Washington State, U.S., ALS diagnosis 1990–1994 was associated with job histories coded for exposure to agricultural chemicals among men (OR 2.8 95 %CI 1.3–6.1 for high vs. no exposure) (McGuire et al., 1997).

 https://biology.stackexchange.com/questions/20006/why-doesnt-the-herbicide-2-4-d-damage-lawn-grass

The herbicide is used to kill broadleaf weeds, which are dicots, while monocot grasses, such as sorghum and corn, are more resistant. That's because grasses inactivate 2,4-D inside the plant, while broadleaf dicots do not.

 However, the underlying molecular mechanism of how auxinic herbicides selectively kill dicots and spare monocots is not understood yet (Grossmann 2000; Kelley and Riechers 2007; McSteen 2010). The mechanisms of auxin biosynthesis, transport, and signal transduction are conserved in monocots and dicots make this question more complex (McSteen 2010). Early research has proposed that the selectivity of auxinic herbicide is because of either limited translocation or rapid degradation of exogenous auxin, altered vascular anatomy, or altered perception of auxin in monocots (Monaco et al. 2002; Kelley and Riechers 2007). Auxin transport is influenced by plant vascular systems (Mattsson et al. 1999; Scarpella et al. 2006). The difference in vascular tissue structure between dicots and monocots may contribute to the selectivity of auxinic herbicides. In monocot stems, the vascular tissues (the phloem and xylem) are scattered in bundles, and lack a vascular cambium; in dicot stems, the vascular tissues are form ed in rings and possess a cambium.

 https://ucanr.edu/site/herbicide-symptoms/acetolactate-synthase-als-or-acetohydroxy-acid-synthase-ahas-inhibitors

 the most common inherited form of ALS, one caused by mutations in a gene called SOD1. Indeed, RIPK1 levels were elevated in those cells too. ...The findings suggest that RIPK1 may be involved in a range of other neurodegenerative diseases marked by axonal damage, including multiple sclerosis, certain forms of spinal muscular atrophy, and even Alzheimer’s disease.

 https://news.harvard.edu/gazette/story/2016/08/harvard-researchers-pinpoint-enzyme-that-triggers-cell-demise-in-als/

  In this study, the researchers note, “[W]e identified pesticides applied to crops in the area of residences associated with risk of ALS in a large healthcare claims network. Our analysis identified several herbicides, insecticides, and fungicides that have been implicated in the literature as being neurotoxic as potential ALS risk factors. Other less-studied pesticides that we identified also may warrant further investigation in the laboratory to assess mechanisms, their potential as etiologic contributors to sporadic ALS risk, and as targets for exposure mitigation.”

  chronic exposure to sublethal (low) levels of pesticides adversely affects the central nervous system (CNS). Specifically, researchers identify agricultural chemical exposure as a cause of many adverse CNS impacts. In addition to CNS effects, pesticide exposure can impact a plethora of neurological diseases. These diseases include amyotrophic lateral sclerosis (ALS) and Parkinson’s diseasedementia-like diseases such as Alzheimer’s, and other effects on cognitive function.

Even with residential uses of glyphosate and uses of chlorpyrifos on food crops (already banned for residential use) ending in February 2022, these compounds will remain in the environment for years, further contaminating the ecosystem. Moreover, the pesticide marketplace still contains many chemicals that cause neurotoxic health effects. 

Although the study demonstrates ALS incidents are highest in the Midwest, where pesticide use is most chemically intensive, proximity to agricultural fields does not generally result in higher rates of ALS. In fact, geospatial analysis suggests certain chemical compounds used in agricultural areas, especially the Midwest, have neurotoxic effects that increase disease risk.

 

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