• N&PD Moderators: Skorpio

Documented dangers of haloalkanes?

56-MDDMT

Greenlighter
Joined
Nov 17, 2009
Messages
8
Documented dangers of inhalents?

Don't get me wrong, I think duster is a fucking retarded Idea, but when i was looking at a lot of these inhalant anaesthetics, http://en.wikipedia.org/wiki/Inhalational_anaesthetic

they look a suspiciously similar to some of the compounds used in computer duster, one of them is just an ether of tetraflouro-ethane. many of them are the exact same compounds except there is a flourine replaced with chlorine etc. I was wondering the actual toxicity of them, rats had a slightly higher incidence of heart disease with a constant low level in the atmosphere over several months.

Does anyone know of any studies or reasons for the much higher perception of danger with these cleaning compounds vs their anaesthetic analogues? (chloroform will actually rape your kidneys on a similar note)

What about butane and things like that? they that dangerous, would they not be oxidised to their specific carbonyl compounds, propane-> acetone, methane-> formaldehyde and then formic acid, ethane--> ethylalehyde (produced when you drink alcohol) and finaly acetic acid
So the problem with this is that apparently cyclopropane is fine as an anestetic!

Before anybody claims I am a fucktard, I am not going to try this! In general inhalants are a very bad idea, with the exception of alkylnitrites and nitrous oxide, I do not intend to try this. I only want a reason as to why these closely related compounds are more toxic, chemical, or pharmacological.
 
Last edited:
Don't know much about chemistry but I'm all but certain there's damn good reason not to huff any kind of gas/solvent other than maybe nitrous (or poppers... somebody must like them :D). But even with that lack of knowledge I would think that - although yhey may well have some similarities with gases used for anaesthesia - "the exact same compounds except there is a flourine replaced with chlorine etc" bit means they are not the exact same compounds so have different properties.

Also, they are also used under very controlled settings by highly trained people. Not quite the same set-up as your average huffer even if they were somehow miraculously safe. Which they aren't for a myriad of reasons - Wiki tells me just the same as it tells you - just bad news all round. Maybe ADD would be more suited for a question like this?
 
This is something I've wondered myself.

I assume that, obviously, the safety protocol that exists during the administration of general anesthesia in a hospital setting is far greater than that which exists in some idiotic huffing teenager's garage. Of course, the general anesthetics that are given in hospitals are not without risks, but if there are complications, they have the resources to help the patients. Also, general anesthesia is usually a once-in-a-long-time sort of deal--it's not a kid huffing duster over and over until he passes out in a pool of his own vomit.

Aside from these obvious points, I wonder if these general anesthetic gases are truly loads safer than that found in computer duster. I assume, if anything, only marginally.
 
Duster, diflouroethane has killed on quite a few occasions. forensic toxicology papers suggest that like some of the early (now discontinued) anaesthetics it sensitizes the heart to catecholamines like adrenaline and can result in sudden death.

Am J Forensic Med Pathol. 2006 Mar;27(1):58-60.
Fatal cardiac arrhythmia after repeated exposure to 1,1-difluoroethane (DFE).

Avella J, Wilson JC, Lehrer M.

Department of Forensic Toxicology, Suffolk County Office of the Medical Examiner, Hauppauge, New York 11788, USA. [email protected]

A 42-year-old man was found dead after repeated exposure to 1,1-difluoroethane (DFE, Freon 152a), a propellant found in CRC Duster, a product intended for the removal of dust and lint. Toxicologic analysis detected DFE in femoral blood 136.3 mg/L, brain 117.5 mg/kg, liver 87.6 mg/kg, lung 60.3 mg/kg, adipose 235.7 mg/kg, and vitreous fluid 25.1 mg/L. The cause of death was determined to be a fatal cardiac arrhythmia due to intoxication with 1,1-difluoroethane. After comparison to previously published cases involving DFE, we suggest that analysis of adipose tissue for DFE and similar compounds, along with blood and other tissues, may be useful in distinguishing between acute versus chronic exposure. Adipose may also be a valuable alternate specimen for detection in cases where loss or elimination from blood is likely to have occurred.
http://www.ncbi.nlm.nih.gov/pubmed/16501351

J Forensic Sci. 2004 May;49(3):627-9.
Sudden death caused by 1,1-difluoroethane inhalation.

Xiong Z, Avella J, Wetli CV.

Department of Pathology, State University of New York at Stony Brook, Stony Brook, NY, USA. [email protected]

A 20-year-old man was found dead on the floor next to a computer, with a nearly full can of "CRC Duster" dust remover located next to the deceased on the floor, and an empty can of the same product on the computer desk. Toxicologic evaluation using either gas chromatography/mass spectrometry (GC/MS) or gas chromatography/flame ionization detector (GC/FID) method identified the active ingredient 1,1-difluoroethane (Freon 152a) in all tissues analyzed. Tissue distribution studies revealed highest concentration in central blood, lung, and liver. It is believed that the 1,1-difluoroethane inhalation was the cause of death.
http://www.ncbi.nlm.nih.gov/pubmed/15171188

one other very serous issue is oxygen deprivation , which is something that doesn't occur in anaesthesia because it is closely monitored.

also see http://www.springerlink.com/content/9m40n27334789h51/

Duster is clearly more dangerous than halothane and similar medicinal agents.
 
Oh yes, I am just wondering about the gram for gram difference in toxicity between these compounds. undoubtedly if someone was playing with medical anaesthetics in their garage like kids do with duster you would have shit happening too. Besides I bet there is a lot of other crap in those duster cans than just what is on the label, whereas medical stuff is almost pure. I know that a small change in a molecule can kill, however I just want to know why, a lot of this stuff doesn't quite follow if you know what I mean.

Cyclopropane, why? I dont understand that one, the ring structure is highly stressed and should be oxidised and broken by the body into into an oxygenated alkene, like 1, or 2-propanol or acetone. it should follow a similar route to the breakdown of propane, which is said to be bad to huff. But consider this now, the body always gets rid of hydrocarbons by oxidising them over and over again, ethanol(toxic) goes to acetaldehyde(toxic) and then to acetic acid(non-toxic), and finally to water and carbon dioxide. Benzene turns into an epoxide (always poisonous, this is why you don't huff gas), tolouene(toxic) into benzalehyde(kinda toxic) and then to benzoic acid (non-toxic). Wikipedia says that methane and ethane are non-toxic and says nothing about propane and butane being toxic, it lists risks of huffing on butanes page, but no toxicity and all of the risks are not related to the compound they are freezing liquids and asphyxiation related.

The metabolic processes seem that they would not generate toxic crap if there were any taking place, I just have seen no hard evidence of the dangers.

Oh btw I do know that halogenated stuff is typically bad, but what about hydrocarbons?
 
It seems like most volatile anesthetics have been replaced in human medicine. I'm guessing the toxicity has to do with their mechanism of action, which is still to be determined, IIRC.
 
Oh yes, I am just wondering about the gram for gram difference in toxicity between these compounds. undoubtedly if someone was playing with medical anaesthetics in their garage like kids do with duster you would have shit happening too. Besides I bet there is a lot of other crap in those duster cans than just what is on the label, whereas medical stuff is almost pure. I know that a small change in a molecule can kill, however I just want to know why, a lot of this stuff doesn't quite follow if you know what I mean.

Cyclopropane, why? I dont understand that one, the ring structure is highly stressed and should be oxidised and broken by the body into into an oxygenated alkene, like 1, or 2-propanol or acetone. it should follow a similar route to the breakdown of propane, which is said to be bad to huff. But consider this now, the body always gets rid of hydrocarbons by oxidising them over and over again, ethanol(toxic) goes to acetaldehyde(toxic) and then to acetic acid(non-toxic), and finally to water and carbon dioxide. Benzene turns into an epoxide (always poisonous, this is why you don't huff gas), tolouene(toxic) into benzalehyde(kinda toxic) and then to benzoic acid (non-toxic). Wikipedia says that methane and ethane are non-toxic and says nothing about propane and butane being toxic, it lists risks of huffing on butanes page, but no toxicity and all of the risks are not related to the compound they are freezing liquids and asphyxiation related.

The metabolic processes seem that they would not generate toxic crap if there were any taking place, I just have seen no hard evidence of the dangers.

Oh btw I do know that halogenated stuff is typically bad, but what about hydrocarbons?

perhaps you shouldn't rely on wikipedia for all your information, this information is really not difficult to find.

butane toxicology:

http://www.inchem.org/documents/pims/chemical/pim945.htm

the toxicity doesn't have a lot to do with metabolism

11.1 Case reports from literature

Ventricular fibrillation
A 15 year old boy habitually inhaled butane by spraying it on
to a towel and inhaling to gain a euphoric state. The
effects normally took 20 minutes to wear off. A few moments
after one such sniffing episode he suffered severe anterior
chest pain, screamed, ran downstairs and collapsed. When the
ambulance arrived he was pulseless and apnoeic. CPR was
started and on arrival to hospital he was in VF and had DC
cardioversion 3 times in 30 minutes. He was given
intravenous (IV) lignocaine, atropine and calcium. ECG
showed sinus tachycardia with left-bundle-branch block.
Within 2 hours the QRS complex reverted to normal and there
was widespread ST segment elevation. He was ventilated for
36 hours due to cerebral oedema and made a complete recovery
in 4 weeks (Gunn et al., 1989).

Myocardial infarction
A 15 year old boy was found unresponsive and cyanosed after
inhaling butane from a plastic bag. CPR was given, he was
intubated and ventilated. He was in VT and VF which was
treated with lignocaine, CPR and cardioversion. On arrival
at hospital he was in asystole; sodium bicarbonate,
adrenaline, atropine, naloxone and lignocaine were given, he
converted to sinus tachycardia. He had generalised tonic
clonic seizures, treated with diazepam, phenytoin and
phenobarbitone. It was determined by ECG that he had suffered
an anterolateral MI and was treated with dobutamine and
captopril. CT scan showed bilateral hemispheric infarcts.
He was ventilated for 13 days. During his hospital admission
his cardiac status improved but he suffered memory and
personality problems at the time of discharge (Bauman et al.,
1991)).


Hemiparesis
A 15 year old boy inhaled half a can of butane then fell to
the ground with his right leg 'dead'. On examination he was
alert and orientated with a marked right sided hemiparesis,
power was reduced to grade 1/5 in both arm and leg. Within
24 hours the power in the right hand and forearm was grade
3/5 and he was able to stand with assistance. On discharge 5
days later he had pronounced upper limb proximal muscle
weakness and hemiplegic gait. CT scan was normal

fun
 
Indeed.

However all of my searches (try "butane intoxication") yielded things such as the following http://www.wickedroots.com/Vaporizers/Neurotoxic-Effects-Butane-Gas.html

Because butane gas inhalants enter through the pulmonary system, they immediately enter into the blood supply and within seconds produce intoxication. The acute effects of inhalants include dizziness, hypertension (increased blood pressure), tachycardia (increased heart rate), impaired coordination, disorientation, temporal distortion, confusion, thick slurred speech, delirium, hallucinations, assaults and suicide attempts. Depending upon the inhalant, recovery may take minutes to hours or may not occur at all. Single episode use can be fatal because of oxygen displacement from red blood cells, hypoxia and asphyxiation. Victims of pulmonary effects are often found with a paper bag over the head.

Chronic inhalant abuse destroys motor neurons that send commands from the brain to the hands and feet. As these motor neurons fail, varying degrees of motor impairment result, including a decreased ability to perform manual and mental tasks. For example, toluene vapors produce high levels of this lipid soluble chemical, particularly in the brain. Toluene abusers present symptoms of motor uncoordination, fatigue, mental impairment, and increasingly greater degrees of permanent central nervous system damage. Most inhalants produce some degree of hepatotoxicity (liver damage). Halogenated hydrocarbons, such as freon, cause severe hepatotoxicity.

Nothing is said for the chronic toxicity of butane(only tolouene and halogenated hydrocarbons are mentioned), the only dangers stated are asphyxiation and perhaps increased sensitivity to adrenaline

Even your source says the following-

7. TOXICOLOGY

7.1 Mode of action

It is a simple asphyxiant and causes toxicity by
displacing oxygen (Ellenhorn and Barceloux, 1988). There are
no direct systemic effects.

It also says that many of the heart problems may have been attributed to cold fluid stimulating the vegus nerve in the throat, inducing heart problems. Also, I was not using Wikipedia as my only source, I had done several searches on toxicity before but came up with what your source seems to indicate, procedural dangers(falls, spraying cold butane in the throat, asphyxiation) and incidences of other deaths from some odd symptoms. However, since these inhalants are CNS depressants this could also be attributed to a synergistic affect with other depressants or medications, or perhaps individual sensitivity.

There has been so far no proof(studies) to say that if butane was administrated with 20 percent O2 in an environment where cold fluid would not spray in the throat will produce chronic or acute toxicity, there are some indications it increases adrenaline sensitivity(perhaps sensitivity to all phenethylamines, maybe meth or ritalin was involved in some of the other deaths?).

However, just because it is not proved to be toxic we should not assume it is safe. We should always assume a substance is toxic unless proven safe by scientific studies.

P.S. No need to be so trite and condescending.
 
Nothing is said for the chronic toxicity of butane(only tolouene and halogenated hydrocarbons are mentioned), the only dangers stated are asphyxiation and perhaps increased sensitivity to adrenaline

It also says that many of the heart problems may have been attributed to cold fluid stimulating the vegus nerve in the throat, inducing heart problems. Also, I was not using Wikipedia as my only source, I had done several searches on toxicity before but came up with what your source seems to indicate, procedural dangers(falls, spraying cold butane in the throat, asphyxiation) and incidences of other deaths from some odd symptoms. However, since these inhalants are CNS depressants this could also be attributed to a synergistic affect with other depressants or medications, or perhaps individual sensitivity.

There has been so far no proof(studies) to say that if butane was administrated with 20 percent O2 in an environment where cold fluid would not spray in the throat will produce chronic or acute toxicity, there are some indications it increases adrenaline sensitivity(perhaps sensitivity to all phenethylamines, maybe meth or ritalin was involved in some of the other deaths?).

However, just because it is not proved to be toxic we should not assume it is safe. We should always assume a substance is toxic unless proven safe by scientific studies.

P.S. No need to be so trite and condescending.

The cardiac sensitisation has clearly occurred in cases where butane isobutane was sprayed into a bag or onto a towel, therefore no direct contact with cold liquid, that much is obvious just by looking at the précis in the reference above.
I have no doubt that a proper search of the toxicology literature would turn up more examples of sudden death caused directly by abuse of butane and similar simple alkanes.

I suggest that in some individuals, even individuals who have previously abused butane without serious adverse effects, inhalation of butane can cause sudden cardiac problems and death.

there is no proof that inhalation of butane is in any way safe, in fact most of the evidence points towards the quite opposite conclusion.

Butane obviously produces acute intoxication. 8)

or perhaps that's being too trite and condescending. :|
 
I thought this was supposed to be about haloalkanes, why has all the focus revolved around butane?
 
I thought this was supposed to be about haloalkanes, why has all the focus revolved around butane?

no idea.

maybe because the most commonly abused haloalkane was bad?

perhaps the thread title should change to documented danges of inhalants
 
good idea. There seems to be the idea that alkylnitrites are safe. Are they?

edit: I guess they are, or almost always are. strange, because I've found little to be as horrible and disgusting as cyclohexyl nitrite.
 
good idea. There seems to be the idea that alkylnitrites are safe. Are they?

edit: I guess they are, or almost always are. strange, because I've found little to be as horrible and disgusting as cyclohexyl nitrite.

Isobutyl Nitrite while on LSD is fucking awesome. Almost as good as N2O. And SO much cheaper.
 
I have heard alkyl and amyl nitrites are safe, but I have not researched it.

Also, as I have said above. I have do not believe butane to be safe, and I have explicitly said i thought it was dangerous. There is some evidence that says that it is dangerous. However, this is all evidence based on a few reports. I don't think we should say the butane directly causes cardiac arrest, It seems to have a Correlation. Could it also be that those 4 or 5 reports of teenagers dyeing while huffing were also on an amphetamine stimulant based drug for ADHD, adderol for instance is similar a stereo-isomer of amphetamine and Ritalin is vaguely related. These could interact with further interact in a synergistic manner with the sensitising butane. Or, these kids could have been chronic users, N2O is known to deplete levels of vitamin B12 causing neurotoxicity. Is it not possible that butane could have a similar effect on other vitamins or enzymes? There may be a relation between the two factors but good statistical practices tell us that correlation does not imply direct causation.

for instance, If a government study found out that homes with lower usage rates of electricity yield children that do better in school. It would be skipping steps and research to say that "the more power your house uses the dumber your children will be" It could be due to the fact that televisions and computers take quite a bit of energy to run and the homes with high usage rates of electricity is because of high tv watching rates, which might indicate that the children are watching too much tv or learning the bad habit from their parents.
 
More than a slightly stupid analogy.

1. If a kid has amphetamine, it's unlikely that he'll be abusing butane. possible, but rather unlikely.

2. It's really unlikely that given all of the reports of issues with similar alkane inhalation that the drug doesn't directly cause it.
 
Top