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Manganese Poisoning from Ephedrone (MCAT)

Hammilton

Bluelighter
Joined
Sep 2, 2008
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I wanted to post this here to warn people before they inject or smoke methcathinone / ephedrone made with KMnO4. It is an extremely bad idea. Manganese poisoning cannot be reversed once it happens, and symptoms will often continue to get worse slowly and may not stop progressing. I have probably poisoned myself with manganese but it's too soon to know how bad it'll be (I'm keeping my fingers crossed, while I was exposed to very high levels, it was over a *fairly* short period of time). I did not do so with ephedrone, however, but via another route.

If there is anyone here who has developed manganism from using ephedrone, please send me a PM, I have questions for someone who developed the condition by using this drug.

The last study looks interesting, if nothing else it's probably loaded with excellent ref's.

Ham

Acta Neurol Scand. 2007 Jun;115(6):385-9.
Irreversible motor impairment in young addicts--ephedrone, manganism or both?
Sikk K, Taba P, Haldre S, Bergquist J, Nyholm D, Zjablov G, Asser T, Aquilonius SM.
Source
Department of Neurology and Neurosurgery, University of Tartu, L. Puusepa 2, Tartu 51014, Estonia. [email protected]
Abstract
BACKGROUND:
Parkinsonian syndrome related to intravenous use of a "designer" psychostimulant, derived from pseudoephedrine using potassium permanganate as the oxidant, has been observed in drug addicts in Estonia.
OBJECTIVE:
To describe the symptomatology of four young patients, history of drug administration and chemical analysis of a drug batch.
METHODS:
Mental and motor function and quality of life were scored and ephedrone was analyzed using electrospray mass spectrometry. Manganese content of the final synthetic mixture was analyzed using Inductively Coupled Plasma-Atomic Emission Spectrometry.
RESULTS:
None of the four cases scored below the dementia threshold in MMSE, while other ratings (UPDRS, H&Y, PDQ-39) corresponded to disabilities seen in relatively advanced Parkinson's disease. The ephedrone yield of the reaction was approximately 44% and the mixture was found to contain 0.6 g/l of manganese.
CONCLUSIONS:
The cases were exposed to extreme manganese load. Their symptomatology is probably identical to manganism. The role of ephedrone is presently unknown. Physicians must be aware of early signs of manganism in patients within social risk groups.

Mov Disord. 2008 Nov 15;23(15):2224-31. doi: 10.1002/mds.22290.
Parkinsonism and dystonia caused by the illicit use of ephedrone--a longitudinal study.
Selikhova M, Fedoryshyn L, Matviyenko Y, Komnatska I, Kyrylchuk M, Krolicki L, Friedman A, Taylor A, Jäger HR, Lees A, Sanotsky Y.
Source
Institute of Neurology, Reta Lila Weston Institute of Neurological Studies, UCL, United Kingdom.
Abstract
A neurological syndrome characterized by levodopa unresponsive bradykinesia, retropulsion with falls backwards, dysarthria, gait disturbance, dystonia, and emotional lability was identified in 13 male opiate addicts following the prolonged intravenous use of ephedrone (methcathinone), a central nervous stimulant prepared from pseudoephedrine, potassium permanganate, and vinegar. The natural history, response to treatment, and clinical features has been studied, and MR and dopamine transporter SPECT brain imaging were carried out. Pubic hair was sampled for manganese. The clinical and radiological picture closely resembled previous reports of chronic manganese poisoning and increased mean manganese level in pubic hair observed for at least 1 year after cessation of ephedrone. Odor identification was intact. Cognitive assessment showed a mild executive dysfunction and a mild depression. DaTSCANs were all normal. The neurological syndrome bears some similarities to PSP but differs from Parkinson's disease. Delayed neurological progression despite discontinuation of ephedrone occurred in one-third of cases. Ephedrone poisoning should be considered as a possible cause of secondary Parkinsonism in young adults, particularly from Eastern Europe.
PMID: 18785245 [PubMed - indexed for MEDLINE]

Environ Health Perspect. 2010 Aug;118(8):1071-80. doi: 10.1289/ehp.0901748. Epub 2010 Apr 19.
Manganese and Parkinson's disease: a critical review and new findings.
Guilarte TR.
Source
Neurotoxicology and Molecular Imaging Laboratory, Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA. [email protected]
Abstract
BACKGROUND:
Excess accumulation of manganese (Mn) in the brain results in a neurological syndrome with cognitive, psychiatric, and movement abnormalities. The highest concentrations of Mn in the brain are achieved in the basal ganglia, which may precipitate a form of parkinsonism with some clinical features that are similar and some that are different to those in Parkinson's disease (PD). Recently, scientists have debated the possibility that Mn may have an etiological role in PD or that it may accelerate the expression of PD.
OBJECTIVE:
The goal of this review was to examine whether chronic Mn exposure produces dopamine neuron degeneration and PD or whether it has a distinct neuropathology and clinical presentation.
DATA SOURCE:
I reviewed available clinical, neuroimaging, and neuropathological studies in humans and nonhuman primates exposed to Mn or other human conditions that result in elevated brain Mn concentrations.
DATA EXTRACTION:
Human and nonhuman primate literature was examined to compare clinical, neuroimaging, and neuropathological changes associated with Mn-induced parkinsonism.
DATA SYNTHESIS:
Clinical, neuroimaging, and neuropathological evidence was used to examine whether Mn-induced parkinsonism involves degeneration of the nigrostriatal dopaminergic system as is the case in PD.
CONCLUSIONS:
The overwhelming evidence shows that Mn-induced parkinsonism does not involve degeneration of midbrain dopamine neurons and that l-dopa is not an effective therapy. New evidence is presented on a putative mechanism by which Mn may produce movement abnormalities. Confirmation of this hypothesis in humans is essential to make rational decisions about treatment, devise effective therapeutic strategies, and set regulatory guidelines.
 
So an actionable takeaway is that people who take methcathinone made by someone else should do an extra solvent wash just in case, as this stuff is pretty likely to be made by amateurs who are following a recipe rather than conducting a synthesis-proper.

ebola
 
Given that manganese isn't used in the manugfacture of 4-methylamphetamines, I don't think you need to worry.
 
Manganese, no. KMnO4, yes.
Pretty simple to get 4-MMC when you've got 4-Methylephedrine and KMnO4. What is the research chemical community's preferred method of making MMC?


This is of course primarily a problem for IV users, but could also be a problem for snorters and smokers. Mn is known to access the brain via nerves in the nose, but unlike snorting a drug that can't pass the BBB well, Mn is very bad in the brain. Smoking it may pose less of a problem than snorting for that reason, along with the fact that super high heat isn't being used. I'm uncertain how high the heat would need to be before much Mn would vaporize, but I don't think they're reached here.

However if you were to use KMnO4 as an oxidizer in a fuel... well, you're probably vaporizing quite a lot (mistake #1) so don't do it in an even semi-enclosed area (mistake #2).
 
What is the research chemical community's preferred method of making MMC?

I thought it was bromination of 4-methyl-propiophenone, and amination of the resulting bromoketone. No ephedrines needed.
 
Sure, but if what ktp says is accurate, and 4-methyl-ephedrines are being sold in bulk, you can bet the majority will become 4-MMC.
 
There exist plenty of other ways to oxidise secondary alcohols that don't involve Mn. Also, wouldn't an acid/base extraction significantly decrease Mn content, as it's present as a nonpolar salt?

On Sciencemadness there is even a way to oxidise 2ndaries with fucking household bleach and a nickel salt. The Ni precipitates out as a nanoparticle, so work up is pretty easy - filter it out... and extract the bleachy muck with a nonpolar solvent, and add HCl.

(Also also, I would not be surpised if the 4-methylephedrine is being made by reduction of the ketone anyway, to skirt existing laws banning beta-keto but not beta-hydroxy phenethylamines)
 
ktp's comment has really taken this thread off topic!

Anyway, this isn't a question of what's possible, but of what will actually happen. If 4-methyl-ephedrine is being sold in bulk, whether it's being bought for personal use or for "modified resale," the vast majority will be buying KMnO4 in the form of green sand iron filter cleaner. I'd be awfully surprised if even one person used the nickel peroxide method you refer to (http://pubs.acs.org/doi/abs/10.1021/jo01052a026), but I don't think it'd be as easy as making an aqueous solution of sodium hypochlorite and nickel sulfate then pouring in your 4-ME (actually, that's a great code name, but nothing anyone would want to consume!). I would think that the sodium hypochlorite would be bad for 4-ME, I think you'd need to first produce your nickel peroxide, clean it up, and then add it to an aqueous, alkaline solution of 4-ME.

I would be careful with drying nickel peroxide. It'd be a somewhat novel way to go out with a bang!


It should be very easy to clean out the residual Mn content of oxidized ephedrines. Whether people do so properly or not is another story. Additionally, the amounts of Mn needed to produce damage are very small. There is some evidence to indicate that in areas with high Mn content in water, the steam from a hot shower may contain enough Mn to cause damage. It's not so much the one or two exposures, it's the chronic administration of the compound that is really the problem, and with addicts, chronic admin is the norm!
 
I don't think it'd be as easy as making an aqueous solution of sodium hypochlorite and nickel sulfate then pouring in your 4-ME

Trust me on this one - it is. And the 'aqueous solution of hypochlorite' is household bleach direct from the bottle. The prepared nickel peroxide is actually a poor oxidant because it only gives you something like 0.5 moles oxidant per mole of prepared complex. Plus, trying to filter and recover it out of a messy aqueous solution is a fucking mess.

Thankfully as an 'inorganic' peroxide, it's suprisingly non-energetic. There are records of people preparing hundreds of grams of the stuff for the pruduction of retinal (vitamin A). That Nakagawa paper is actually the old one. This is the one i was referring to. (it also works really well if you just keep it wet)

There is some evidence to indicate that in areas with high Mn content in water, the steam from a hot shower may contain enough Mn to cause damage.

Citation on that? Why do people use KMnO4 to clean water filters, if it's so toxic? (By the by, it's purple, not green)
 
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Huh? The filters are green sand filters, the KMnO4 is purple. I have plenty, I'm well aware...

The KMnO4 is used to remove build up, it's not passed back into the water supply.

The green sand filters contain green sand coated with manganese oxide. This reacts with soluble iron (FeO2?) and manganese (not sure what state it's present in) to make them insoluble (FeO2 to FeO3, I think). I believe the KMnO4 is used to recoat the green sand with insoluble MnO2, but to be honest, i'm not 100% sure how it works. My water is so bad that it didn't work and had to go with H2O2 as an oxidizer.

Ha
 
Med Hypotheses. 2005;65(3):607-16.
Neurotoxicity of inhaled manganese: public health danger in the shower?
Elsner RJ, Spangler JG.
Source
Wake Forest University School of Medicine, Department of Family and Community Medicine, Medical Center Blvd., Winston-Salem, NC 27157-1084, USA.
Abstract
CONTEXT:
Manganese (Mn) is an essential trace element but is neurotoxic at high doses. Showering with Mn-laden water has never been evaluated as a central nervous system (CNS) delivery vector for Mn, even though intranasally administered Mn in laboratory animals circumvents the blood-brain barrier and passes directly into the brain via olfactory pathways.
OBJECTIVE:
To review the literature on Mn and attempt to quantify potential human CNS exposure to manganese from showering.
DATA SOURCES:
We systematically searched Medline 11/9/02 and again on 3/9/04. The following search terms were used: manganese, water, drinking water, shower, showering, bath, bathing and inhalation, then combined with "water or drinking water or showering or shower or bathing or inhalation."
STUDY SELECTION:
Animal experimental investigations, human epidemiological studies, and consensus and governmental reports were utilized.
DATA EXTRACTION:
Data were extracted by both authors and extrapolations to humans were calculated by one of us (JGS) controlling for age, length of exposure and known respiratory differences between rats and humans.
DATA SYNTHESIS:
During a decade of showering in Mn-contaminated water, models for children and adults show higher doses of aerosolized Mn (3-fold and 112-fold greater, respectively) than doses reported to cause Mn brain deposition in rats.
CONCLUSIONS:
Long-term shower exposure to Mn-laden water may pose a significant risk for CNS neurotoxicity via olfactory uptake in up to 8.7 million Americans. If our results are confirmed, regulatory agencies must rethink existing Mn drinking water standards.
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