Toxicology of Butane

[JimiHawK*]

Last night when i was quite stoned i had an urge to do more drugs. However, nothing was available to me at the time apart from a can of butane that i had for my lighter.

I hesitated at first remembering all the negative things i heard from media and drug users alike but decided to go through with it anyway. I covered the nozzle with my duvet to act like a filter (it was to prevent getting frostbitten) inhaled through my mouth until i felt the effects which were nearly identical to Nitrous Oxide but slightly "different" and weaker. (initial sinking feeling, followed by ringing in the ears, euphoria, visual distortions etc)

Of course, it felt fucking good so i did it twice more before going to bed.

The similarities to Nitrous Oxide were substantial, and butane costs less than one tenth the price it does for cream chargers. It is also more convenient as you don't need a cracker. The difference for me however was that i thought Nitrous Oxide was completely harmless apart from Vitamin B12 deficiency resulting from chronic use. From looking at the posts on BL it seems most of you guys have a similar view.

Before doing more, i needed to know more about Butane. I wanted to know if all those "your going to become stupid" "irreversible brain damage" etc claims had any basis of truth. So for the last few hours i trawled through various reports and medical literature. What i have gathered was that butane had all the risks/effects associated with Nitrous Oxide and other inhalants (anoxia/hypoxia,cardiac arrest,asphyxia etc) but didn't directly "make you stupid" as it's not metabolized by the body. The euphoria/other effects results from CNS depression as butane (along with Nitrous Oxide) is an asphyxiant.

Basically what i want to know is :

1. Any further empirical+anecdotal evidence about Butane
2. Can Butane be used safely as a recreational inhalant just like NOS?
3. Will occasional use of Butane greatly affect my intelligence/cognitive functions?



Cheers %)

 

[mad_scientist]

I haven't seen any research that looked at butane specifically. Most research on "inhalants" doesn't really distinguish between use of butane, spray paint, glue and petrol, even though these substances are often used by different people in different ways, and undoubtedly have varying toxicity.

Anecdotally and from my not insignificant experience with inhalant users, I would support the popular view that paint, glue and petrol undoubtedly cause neurotoxicity and do tend to result in severe chronic harm when used to excess. People with a long history of huffing glue or petrol do certainly seem to suffer symptoms that would be consistent with brain damage and do not fully recover even after prolonged abstinence.

Butane on the other hand I'm not so sure about the neurotoxicity, it is certainly a very dangerous drug and I had one friend die from it back in high school, and a few more that came close many times. High doses of butane cause respiratory depression just as bad or worse than an opiate overdose, and it also causes cardiac arrhythmia and can induce acute heart failure. So in this respect I would say butane is much, much more dangerous than nitrous oxide.

However judging from the heavy butane users I have known, it doesn't seem to cause brain damage even after heavy and prolonged use, or at least I would say the brain damage is less severe from butane than from frequent use of ecstasy or methamphetamine. I think it would obviously have potential to cause brain damage through hypoxia following respiratory arrest though.

 

[MattPsy]

Note Jimihawk - a substance need not be metabolized in order for it to be toxic, be that neurotoxic, or otherwise.
With these hydrocarbon inhalants I understand the main problem is potential cell damage caused by them dissolving in lipid cell membranes and then forcefully bubbling out, maybe breaking the cell. Also, acting as lipid solvents isn't cool in itself, when in the body...

I tried butane (from a balloon, much like one uses N2O) a couple of times to see what inhalants were like (other than that, i've only tried diethyl ether, in the class of inhalants...) - I quite liked it to be perfectly honest - but at the same time it felt good I could tell it was not benign. Felt quite fuzzy headed after it'd worn off, maybe even for the next few days.
When it comes on I got a big warm rush that started in my chest and spread across my body like a wave. When it reached my head (~T+3 seconds) I got significant euphoria and red+green+purple fractal CEVs. Waves of hot/cold across the limbs. Main effects over by T+2 minutes, lingering effects for 30 minutes. (for me)

 

[Adrenochrome]

Wow sounds more visually intense then Diethyl Ether,
However, I love status quo of my plasma membranes, so I'm hesitant to consider even thinking of trying this.

 

[Riemann Zeta]

Butane, hexane, heptane, etc...are all neurotoxic to a certain degree (as mentioned above, they are lipophilic organic solvents) and are all potent carcinogens. I believe they are slightly less neurotoxic--and less carcinogenic--than benzene, tolulene and xylene, but should not even be considered in the same class as nitrous oxide, as they are all far more dangerous. No aliphatic solvent should be considered a viable drug, period.

 

[Adrenochrome]

Butane, hexane, heptane, etc...are all neurotoxic to a certain degree (as mentioned above, they are lipophilic organic solvents) and are all potent carcinogens. I believe they are slightly less neurotoxic--and less carcinogenic--than benzene, tolulene and xylene, but should not even be considered in the same class as nitrous oxide, as they are all far more dangerous. No aliphatic solvent should be considered a viable drug, period.

I don't meen to be rude but, What about ethanol and diethyl ether? or GHB?

(does alphatic solvent EF= alphatic hydrocarbon solvent?)

 

[mad_scientist]

Well ethanol is neurotoxic and carcinogenic, and probably most other solvents are when used as drugs. But dose and frequency of use would be key factors in how much damage eventuates.

 

[MattPsy]

GHB is not a lipid solvent. It's pretty damn far in the other direction, actually.

Diethyl ether, well, it's certainly a lipid solvent, so I would expect it's about as toxic as butane is.

 

[Adrenochrome]

Well ethanol is neurotoxic and carcinogenic, and probably most other solvents are when used as drugs. But dose and frequency of use would be key factors in how much damage eventuates.

Anything to indicate that Diethyl Ether is a carcinogen?

 

[Pomzazed]

I was thinking butane will be metabolyzed by oxidation yielding a dione compound (although i have no reference) in the same manner as hexane poisoning by its metabolite, check "hexane" in wikipedia.

 

[vecktor]

I was thinking butane will be metabolyzed by oxidation yielding a dione compound (although i have no reference) in the same manner as hexane poisoning by its metabolite, check "hexane" in wikipedia.

n-butane is likely to be oxidised to butanol and then to various other further oxidised creatures I didn't find human data, but the enzymes are pretty ubiquitous. butanol is found in alcoholic spirits where it is refered to a fusel oil these are the higher alcohols responsable for a lot of alcoholic drinks' hangover effects.
bear in mind that commercial butane is not simply n-butane its a mixture of straight and branched chain hydrocarbons all with a similar boiling point.

It is not something to play with as it has been strongly linked to heart muscle sensitisation, it basically makes the heart super sensitive to adrenaline and can lead to sudden cardiac arrest and death, even if you have previously used it without adverse effects.
It is also very likely to lead to brain damage by hypoxia.
Butanes chief action is to act as a simple asphyxiant, so a lot of the effects are due to lack of oxygen as butane displaces oxygen. this is the same as nitrous oxide, nitrous oxide produces unconsciousness through oxygen deprivation rather than anything else.

My advice, use it to refill your lighter or extract stuff nothing more.

http://www.inchem.org/documents/pims/chemical/pim945.htm#SectionTitle:6.5 Elimination and excretion

 

[LuxEtVeritas]

so basically all these drugs work by inducing catecholamine release (or other psychoactive brain pathways?) in response to acute hypoxia?

and the safest hypoxia inducing substance that is common is inhaled NO?

C&P'd as they may be of interest to some:

J Neurochem. 2006 Jun;97(6):1676-89. Links
Nitric oxide, cell bioenergetics and neurodegeneration.Moncada S, Bolaños JP.
The Wolfson Institute for Biomedical Research, University College London, London, UK. [email protected]

Following stimulation of NMDA receptors, neurons transiently synthesize nitric oxide (NO) in a calcium/calmodulin-dependent manner through the activation of neuronal NO synthase. Nitric oxide acts as a messenger, activating soluble guanylyl cyclase and participating in the transduction signalling pathways involving cyclic GMP. Nitric oxide also binds to cytochrome c oxidase, and is able to inhibit cell respiration in a process that is reversible and in competition with oxygen. This action can also lead to the release of superoxide anion from the mitochondrial respiratory chain. Here, we discuss recent evidence that this mitochondrial interaction represents a molecular switch for cell signalling pathways involved in the control of physiological functions. These include superoxide- or oxygen-dependent modulation of gene transcription, calcium-dependent cell signalling responses, changes in the mitochondrial membrane potential or AMP-activated protein kinase-dependent control of glycolysis. In pathophysiological conditions, such as brain ischaemia or neurological disorders, NO is formed excessively by NMDA receptor over-activation in neurons, or by inducible NO synthase from neighbouring glia (microglial cells and astrocytes). Elevated NO concentrations can then interact with superoxide anion, generated by the mitochondria or by other mechanisms, leading to the formation of the powerful oxidant species peroxynitrite. During pathological conditions activation of the NAD(+)-consuming enzyme poly(APD-ribose) polymerase-1 (PARP-1) is also a likely mechanism for NO-mediated energy failure and neurotoxicity. Activation of PARP-1 is, however, a repair process, which in milder forms of oxidative stress protects neurons from death. Thus, whilst NO plays a physiological role in neuronal cell signalling, its over-production may cause neuronal energy compromise leading to neurodegeneration.

PMID: 16805776 [PubMed - indexed for MEDLINE]

Essays Biochem. 2007;43:29-42.Links
Nitric oxide and hypoxia.Galkin A, Higgs A, Moncada S.
The Wolfson Institute for Biomedical Research, The Cruciform Building, University College London, Gower Street, London WC1E 6BT, U.K.

NO (nitric oxide) can affect mitochondrial function by interacting with the cytochrome c oxidase (complex IV) of the electron transport chain in a manner that is reversible and in competition with oxygen. Concentrations of NO too low to inhibit respiration can trigger cell defence response mechanisms involving reactive oxygen species and various signalling molecules such as nuclear factor kappaB and AMP kinase. Inhibition of mitochondrial respiration by NO at low oxygen concentrations can cause so-called metabolic hypoxia and divert oxygen towards other oxygen-dependent systems. Such a diversion reactivates prolyl hydroxylases and thus accounts for the prevention by NO of the stabilization of hypoxia-inducible transcription factor. In certain circumstances NO interacts with superoxide radical to form peroxynitrite, which can affect the action of key enzymes, such as mitochondrial complex I, by S-nitrosation. This chapter discusses the physiological and pathophysiological implications of the interactions of NO with the cytochrome c oxidase.

PMID: 17705791 [PubMed - in process

 

[fastandbulbous]

Butane, hexane, heptane, etc...are all neurotoxic to a certain degree (as mentioned above, they are lipophilic organic solvents) and are all potent carcinogens. I believe they are slightly less neurotoxic--and less carcinogenic--than benzene, tolulene and xylene, but should not even be considered in the same class as nitrous oxide, as they are all far more dangerous. No aliphatic solvent should be considered a viable drug, period.

Yet they still occasionally use cyclopropane as an inhalation anaesthetic in people with dodgy livers due to sensitivity or bad reactions to fluorocholohydrocarbon (aka halothane hepatitis) inhalation anaesthetics like halothane & sevoflurane

 

[Riemann Zeta]

Indeed, cyclopropane is an inhalational anaesthetic, just like diethyl ether. Most aliphatic compounds (especially aromatic or highly lipophilic ones) act as NMDA receptor pore blockers. For example, benzene/tolulene, PCP, long-ish-chain alkanes, diethyl-ether, EtOH, MK-801) all have dissociative psychedelic and anaesthetic properties. Almost any small lipophillic compound seems to act as a weak NMDA receptor antagonist at a high enough concentration, even amphetamine. Paradoxically, certain ultra-small, highly polar molecules, like Mg++ and N2O are also NMDA pore blockers. I wonder what makes the NMDA receptor ion-shunting pore so promiscuous--a whore among classical neuronal receptor loci?

Edit: I certainly did mean N2O and not NO2. The former is nitrous oxide, the later is a caustic, poisonous gas. Sorry about the typo

 

[fastandbulbous]

Paradoxically, certain ultra-small, highly polar molecules, like Mg++ and NO2 are also NMDA pore blockers. I wonder what makes the NMDA receptor ion-shunting pore so promiscuous--a whore among classical neuronal receptor loci?

Do you mean N2O (nitrous oxide) as nitrogen dioxide is just plain nasty & poisonous and getting a lungful of that would destroy your lugs so badly that anything else doesn't even enter into the equation?

 

[mad_scientist]

Ooh yeah thats not a mistake you want to make. I remember reading one of those Darwin Awards about two guys that stole a cylinder of nitrogen dioxide thinking it was nitrous oxide and started huffing it...I believe one of them died and the other one is now hooked up to a machine to breathe for him for the rest of his life....

 

[JimiHawK*]

Interesting, so the inhalants which i previously thought were harmless (ether and N2O) actually do cause damage, and are some what similar to butane/etc?

but should not even be considered in the same class as nitrous oxide, as they are all far more dangerous. No aliphatic solvent should be considered a viable drug, period.

If you don't mind, could you explain this further?

I was thinking butane will be metabolyzed by oxidation yielding a dione compound (although i have no reference) in the same manner as hexane poisoning by its metabolite, check "hexane" in wikipedia.

According to this, butane is excreted unmetabolized

Although metabolism normally results in detoxification, enhanced toxicity may also result. This
is especially true of solvents and other volatile compounds; aspects of the toxicity of, for example,
acetonitrile, carbon tetrachloride, chloroform, dichloromethane, hexane, methanol, trichloroethylene and
possibly halothane can be attributed to the formation of toxic metabolites (see Table 4). Many other
compounds including butane, many fluorocarbons, tetrachloroethylene and 1,1,1-trichloroethane, are
largely excreted unchanged in expired air.

Compound , Principle Metabolites
Butane , 2-Butanol, butanone (both <1 percent)

Link to article : http://www.unodc.org/pdf/technical_series_1997-01-01_1.pdf

 

[wungchow]

After personally using in excess of 4L of diethyl ether during a short (1-2 month) period, I can safely say that it doesn't cause noticeable brain damage on that dosage scale... i'm still able to do differential equations and vector calculus like a champ..

the oxygen atom present in ether probably has something to do with it's relative lack of toxicity compared with pure hydrocarbons such as toluene, butane, hexane, etc.

 

[Riemann Zeta]

Interesting, so the inhalants which i previously thought were harmless (ether and N2O) actually do cause damage, and are some what similar to butane/etc?

Well, N2O is not at all similar--aside from B12 depletion and risk of ischemia if you don't use balloons, it is relatively safe. The jury is still out on diethyl-ether; there are not many modern articles on its pharmacodynamics. It is definitely safer than the pure naked hydrocarbon solvents, but that doesn't mean it is perfectly harmless. I assume that its toxicology is much like that of ethanol, but it is probably more carcinogenic than ethanol. In addition, it has a steeper dose-response curve, so watch out for respiratory depression.

 

[wungchow]

yeah i wish there were more articles on the pharmacology of ether. but from my own experimentation it seems to be relatively benign, if the dose is titrated correctly (each dose being a small pour of droplets onto a rag.) this enables one to experience the full spectrum of effects without being overwhelmed.

the worst part about ether is the horrid stench that remains in your breath, sweat, and flatulence for the next 6-12 hours.