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Available on Amazon
also on all local Amazon sites, just change .com for the local version (.co.uk, .jp, .nl, .de, .fr etc.)


Inhaling volatiles and gases

Category: Events


Involuntary and voluntary

Introduction and description

Volatile inhalants are all  liquid at room temperature, but evaporate easily and become gases, which means they are easily inhaled deliberately or by accident.

All of these substances share the property of being hydrophobic i.e., as liquids, they are not freely miscible with water, and as gases they dissolve in oils better than in water. It is this latter property that appears to give them their effects in our bodies, because they stimulate without actually chemically altering our cells. 

The cells are principally water, thus any substance which repels water is not going to be absorbed by the cell only ‘stimulates’ it.  Thus these chemicals act like tiny little mechanical stimulators of the cells in our brain.

In effect, they do not work via specific receptors, although they may trigger a whole host of reactions as a result of their initial action.  The main volatile inhalants are as follows

Acetylglycinamide chloral hydrate
Chloral hydrate
Diethyl ether
Ethanol (Alcohol)
Ethyl chloride

Nitric oxide
Nitrous oxide
Vinyl ether

Freon is also occasionally included in this list, the most common representative is dichlorodifluoromethane (R-12 or Freon-12).

Gasoline (Petrol) - Overall, a typical gasoline is predominantly a mixture of paraffins (alkanes), naphthenes (cycloalkanes), and olefins (alkenes).

Kerosene is Paraffin – an alkane

I have added a section of Solvents, fuels, aerosols and adhesives which provides a bit more detail on some of these categories of volatile inhalants

There is also a section on  Aerosols and ‘dusters’ as well as just  Solvents which covers things like acetone, butanol, dichloromethane, ethanol and methanol, Glue and other contact adhesives and Starter fluid

The mechanism by which anaesthetics in general work has long been a subject for debate.  Although all classified as anaesthetics, the means by which they work differs and this is probably why such confusion exists. 

Thus it is not helpful to talk about ‘anaesthetics’ as some sort of generic grouping – or for that matter as a means of  helping a person to obtain a loss of consciousness prior to surgery, the groups of chemicals have to be classified  according to their receptor or cell activity and the so called ‘volatile inhalants’ act in a way very different from those based on receptors for example such as ketamine

How it works

Most chemicals act by affecting a receptor.  None of the volatile inhalants act this way. 

Instead they directly affect the brain and once affected, a chain of subsequent chemical actions then result which do involve neurotransmitters and which thus affect receptors.  It can thus be extremely confusing when one reads the scientific literature on these substances as they appear to affect any number of receptors.  But they don’t, what is actually happening is that a chain reaction affecting the other receptors then results leading to a whole host of extra activities in the brain and in the body from muscle relaxation to atonia to nervous sensation suppression.

In order to understand how they work we need to follow the sequence of action.

Because the action is very complex I have placed the scientific papers that support this description in a separate section you can refer to at leisure – see Volatile inhalants background scientific papers


Inhalants are taken by ‘volatilization’, you do not have to heat or burn them, they will vapourise naturally.   

Dispersal to the brain

Once the substances have been inhaled they travel very quickly to the brain.  Due to their small molecular size and high lipid solubility, these substances readily transfer across the blood brain barrier.

The brain receives a large proportion of the total cardiac output, averaging something like 50.8 ml/100 gms/minute, but blood flows in different areas vary considerably.  In other words, although the blood flows throughout the brain, the actual distribution of any chemical in the brain will not be the same.

The brain itself has a relatively high lipid content, but the actual content varies a lot between the different anatomic structures or organs.  In the chart left we can see the different lipid contents of each brain structure.

If we look at this chart, the hypothalamus, the corpus callosum and the reticular formation should be the three organs most affected by the inhalants along with the internal capsule,  and papers on the subject confirm that this is exactly what happens………

When you look at the research papers, it is clear that all the various inhalants show many similarities in their distribution and action on the brain.  In effect, although there is some difference between each of the substances  in that their lipid/blood solubility can be different – the organs affected are the same, only the degree to which they are affected differs.

Initially the circulation sends the substances to ‘grey matter’, but then the high lipid content of organs with fibre bundles causes a shift to the organs shown at the top of the list above.

One research paper, however, found a curious fact.  The hypothalamus should in theory retain the substance, but it doesn’t.  Over time the substances seem to dissipate from this organ but are retained in the reticular formation.  Thus once the effects have become stable, it is the brain stem and thus the reticular formation that shows the greatest impact from these substances

We now need to turn to the section on the Brain and its functions

The effects

These chemicals are a threat and they are a threat of enormous proportions because they have been able to enter the brain relatively easily. 

I have placed this mechanism under the heading of overload because that is what the body is facing – an overdose of enormous proportions and an overloading of all the systems it needs for its defence.  But its effect overall is one of total suppression, this we will see in a moment.  In effect, the amount is such that it knocks out functions.

Let us now hypothesise that initially the inhalants stimulate the function of the Will so that it starts to prepare the body to counter-act this massive attack on the key centre of consciousness. 

Thus it will send out a whole load of neurotransmitters that tell the body to shut down all but essential services – so most of the nervous sensations will need to go and we should also lose muscle control as well as changing things like our breathing rhythm and body temperature. 

This is exactly what happens , the body goes into a sort of tickover mode so that all the Will’s resources can be concentrated on repelling this overwhelming threat

 And the overall result is that the following happens 

How much they are suppressed depends on the dose we are given.  If it is partial we go into a sort of half sleep cycle, if it is more we do the equivalent of sleep and become unconscious,  if it is too much we go into a coma and eventually we may die.  So tricky stuff.  For an anaesthetist the dose is key.  There may also be release of neurotransmitters to relieve pain – endorphins for example if we run the risk of dying.  This is why some people get relief and a feeling of almost pleasure from inhalation [accidental or not]  – not spiritual at all.

References and further reading

  • Meyler’s Side Effects of drugs
  • Autoradiographic distribution of volatile anesthetics within the brain – Drs N Cohen, Kao L Chow, and Lawrence Mathers
  • EROWID's inhalants section


All these observations relate substances other than  nitrous oxide  The observations for nitrous oxide are grouped within the separate section inhaling  nitrous oxide.  It has a completely different profile from all these former substances.

In this section we find the observations for chloroform, ether, freon, toluene, gasoline, butane, chloral hydrate and a number of other solvents and little used anaesthetics.  Most of these show that the consequences of use of these products rarely provides much more than synaesthesia.  When it does provide more the person is close to a near death experience – in some cases they have a near death  experience, which means these products really only provide an experience close to death.  There are numerous instances I have found where they have a real death experience.

The health consequences from any regular use of these products is also catastrophic, brain damage, liver damage, kidney damage,  and so on .  The corpus callosum is particularly attacked by these types of volatile inhalants.  It may be of interest to turn to the description for Manic depressives [bipolar disorder] and see the effect of attack on the corpus callosum.  If any permanent damage is done the person could become a manic depressive or schizophrenic.

VOLATILE SUBSTANCE ABUSE - Practical Guidelines for Analytical Investigation of Suspected Cases and Interpretation of Results
- R.J. Flanagan, P.J. Streete, J.D. Ramsey
In general, the acute central nervous system depressant and cardiotoxic effects of volatile
substances are similar, being related more to their physical properties than to their chemical structure. The occurrence of toxicity such as peripheral neuropathy and hepatorenal damage, however, often results from metabolism and can differ markedly between compounds with ostensibly similar structures. Volatile substance abuse is characterised by a rapid onset of intoxication and a relatively rapid recovery; a "high" can be maintained for several hours by repeated "sniffing". As with the ingestion of ethanol, euphoria, disinhibition and a feeling of invulnerability may occur. Higher doses often lead to less pleasant and more dangerous effects. Changes in perception may precede bizarre and frightening hallucinations while tinnitus, ataxia, agitation and confusion are often reported; dangerous delusions such as those of being able to fly or swim may also occur. Nausea and vomiting with the risk of aspiration can occur at any stage. Flushing, coughing, sneezing and increased salivation are further characteristic features. Coma, depressed respiration and even convulsions may ensue in severe cases (Meredith et al. 1989).

Related observations