ThereseFlower, I'm not sure which blood test you were referring to; was that post meant for a different thread?
Not dead yet, I made a point of looking out my notes on trichloroethylene which I put together for my legal case against the company I worked for. It explains the mechanism by which the halocarbon solvent blocks normal cellular aerobic respiration, so inducing glycolytic energy production and chronic fatigue. It is able to prevent the formation of a specific enzyme, pyruvate dehydrogenase, required for the Krebs cycle to work. I only learned about the connection between trichloroethylene inhalation and Parkinson's disease after I wrote it.
I would leave work filled with energy but be completely exhausted by the time I reached home; I would remain in this state until I returned to work again. At the time I had no idea what the cause of this was and physicians, whom I repeatedly consulted about it, just told me not to worry about it. Towards the end of the year 2000 I stumbled across a book on chronic fatigue (Tired all the time, by Dr Ronald L Hoffman) which detailed how trichloroethylene (TCE), a solvent which we used in enormous quantity in our job, replaced a part of the Krebs cycle whenever someone is exposed to it. It inhibits pyruvate dehydrogenase via its metabolite, dichloroacetic acid, triggering the glycoxylate shunt; bypassing the carbon dioxide producing steps of the tricarboxylic cycle for energy production. Another trichloroethylene metabolite, S-(1,2-Dichlorovinyl)-L-cysteine (abbv; DCVC), stimulates compensatory utilization of glycerol, lipid, and amino acid metabolism which provides intermediate substrates which enter downstream in the glycolytic pathway or the tricarboxylic acid cycle. The consequence of this is that, during periods of direct exposure, the bodies energy levels are temporarily restored to normal before they collapse again after exposure ceases. The metabolite also has the effect of inducing kidney damage, including being linked to toxic nephropathy. This occurs by activating CD4+ T cells which promote immunoglobulin G (IgG; a lupus related antibody which induces lupus anticoagulant syndrome; a condition which I have tested positive for) production. The IgG has been found to bind to foreign molecules attached to podocytes in the kidneys, so inducing membranous nephropathy. Trichloroethylene, as a halocarbon possessing dioxin-like properties, is both genotoxic and mutagenic. Polymorphisms of the NAT2 (TCE is mutagenic of this gene) and GSTmu genes (TCE induced renal toxicity occurs primarily through GST conjugation and bioactivation by renal cysteine-lyase) have also been identified as risk factors in the development of membranous nephropathy as a consequence of hydrocarbon exposures. Trichloroethylene is the solvent, previously used in office correction fluid, which was found to be the cause of officeworkers becoming extremely fatigued and sick many years ago. Oxalic acid is another metabolite of trichloroethylene and is also implicated in the development of nephropathy. Trichloroethylene is also linked to the development of metabolic Parkinson’s disease.
During the 1940’s and 50’s a researcher named Eugene Kennedy formulated the Kennedy pathway for phospholipid synthesis. This found that solvent exposures resulted in aberrant phospholipid synthesis of types such as phosphorylcholine and phosphorylethanolamine which have both been linked to the development of both antiphospholipid and lupus antibodies such as I have tested positive for in regards to my blood clotting.