Perfect Poisons

[MickeyFinn]

There has been a lot of talk about untraceable poisons and the like ont his forum. From ricin to saxitoxin and botulism to tetanus. Sure, an untraceable poison would be the trump card in all assassination games. But what about accidental poisonings written off by the ME as accident? After all, unless you have access to CIA arsenals, such things as saxitoxin can not be readily obtainable as it takes tons of ocean shellfish to make a single gram. Of course if you had a well developed lab and a lot of time on your hands you could always synthesize it. So here's a list I made of "accidental" poisonings. PLease feel free to add pros and cons to these methods:

1---Methyl Alcohol: A little methyl alcohol goes a long way in taking someone out.

Pros: Alcoholics won't notice it slipped in moonshine. Police and MEs will attribute it to a bad bootlegging operation.

Cons: More than one person usually gets poisoned from bad bootlegging ops, unless the person made it and tried ithimself. It's kinda hard to set up a still in someone's backyard without them knowing.

2--- Botulism: With over 300,000 hospitalized instances of food poisoning a year, it's an ideal accident.

Pros: Since such a little amount can kill, it's easy to slip into anyone's food. By the time they get sick enough to go to the hospital, it may be too late.

Cons: How can you make it? Several recipes including the "spoiled food" recipe in the terrorist manual exist on the web.

3---- Abrin: protein poison requiring less dosage than ricin to kill.

Pros: Easily found and harvested. So small to be virtually untraceable itself in autopsy. It is a protein poison, and not an alkaloid.

Cons: The symptoms left behind may point to the abrin even if the abrin can not e found (such is the case as ricin). Finding a way to introduce it as an "accidental" poison. Not everyone is going to be making prayer beads and accidentally stick themselves with a needle containing the abrin from stringing prayer beads together.

4--- Tetrodotoxin: Puffer fish delicacy.

Pros: It's natural, and with a little luck can be caught by average fishermen. Or it can be bought from chemical companies, or one can purchase the whole fish.

Cons: It can be traced in an autposy. However if the stomach contents show pufferfish, it will be attributed to an amateur trying to cook and eat the fish improperly.

5--- Poison dart frogs: The golden poison dart frog will actually kill, not make you sick.

Pros: They can be purchased online. They can be found in the jungles of south america.

Cons: It must be introduced into the bloodstream by someone either handling one and the poison being absorbed in the cut from the frogs skin. You most likely will have to take osmeone on aj ungle trip to make it look really natural and accidental.

6--- Jungle Ants: these things are almost an inch long each. 1 bite will make a man cry, 2 will send him to the hospital, 5 will kill him.

Pros: It's a natural critter. The toxin works fast, and they can be aggresive.

Cons: It lives in the jungle so you have to take someone on a jungle trip. Most likely the ants must be introduced to someone sleeping who isnt suspecting them. (Coating them in honey perhaps?)

7--- The Deathcap mushroom: a classic "accident"

Pros: Easily obtainable. Will be written off most likely as an accidental death. Very time delayed. Initial symptoms last for 36 hours or so then go away, but death occurs within 1-12 days from liver and kidney failure. Many deaths are attributed each year because of amateur mushroom hunters mistakingly pic and eat it. Drug users may eat it if chopped up or they have never had "shrooms" before.

Cons: Someone has to really like mushrooms, or trust you enough to eat them when served. Recovery is possible if medical treatment is given early.


That's the list I've come up with so far. I'd be interested in hearing from others who give more examples, or add to the pros and cons of this list, or simply wanting to add their own methods of delivery, etc.

Mickey Finn

[simply RED]

If GABA receptor blocker is used or ATP-ase inhibitor
it will be abosutely impossible to determine the cause of death...

The structure of the receptors is unknown and ATP ase inhibition is just fun. The enzyme is huge and has many active centers and..........

Very possibly adenosine phosphate - acetate will inhibit the ATP- ase when it forms amide bonds with active NH centers. CO-NH is strong bond , OP-N never forms.

adenosine-O-POOH-O-COOCH3 ? or adenosine-O-POOH-CH2-COOCH3 if the first is unstable. Never tried it anyway... too dangerous it seems to be...

[xyz]

Sure, poison dart frogs can be purchased online, but it won't do you any good (or anyone else any harm ;) )

Their toxicity comes from the diet of insects that they eat in the jungle, once they're removed from the jungle they slowly become harmless over a period of a few months.

I also can't help but have doubts about your "jungle ants", as we have ants that size here in Australia and their stings are less painful than bee stings. Giving a species name would help...

Back to the subject though, does anyone know if nitrous oxide exposure is detectable in a post mortem examination (in the amounts required to cause unconsciousness)? I would assume that it probably can be detected. If not however, it can't be too hard to gas someone to unconsciousness with N2O and then to death with CO2 (undetectable).

Or if they're a deep sleeper maybe you could connect a medical oxygen mask to a regulated CO2 tank and put in on them as they sleep.

[Silentnite]

Or if they are a party student you could mask it as an accidental overdose. I remember trying Ballooning a while ago. Dumb yes, but interesting. Only reason to try it is a decent Darth Vader impression. Anyways. A quick excerpt:



Risky Business
Contrary to common drug lore, nitrous oxide is highly addictive and at times lethal. Because of N20's oxygen depleting properties, death often occurs when abusers inhale pure N20 in tight spaces, such as cars, closets and other confined, poorly ventilated areas.
Users seeking a more potent high place a plastic bag over their heads, then burst a cracker inside.
"It's the kids who are uneducated about nitrous oxide who end up doing it alone and in small spaces," Karim says. "The problem for them is as much their delivery system as the drug itself. If they're lucky, hopefully someone will notice that they've passed out. If not, they may actually die from asphyxiation."

Such was the case with Richard Guy, a third-year Massachusetts Institute of Technology (MIT) student who died while inhaling nitrous oxide stolen from a campus lab. The physics major was found dead in his dorm room August 31, 1999, with a garbage bag over his head.

Short-Term Damage
Common short-term risks of nitrous oxide use include frostbite on the lips, nose and esophagus due to the rush of high-powered pressurized gas.

Additional short-term side effects are:
a migraine-like headache that lingers for several hours
drowsiness
nausea

Not to mention:
Hypothermia -- occurs due to the sudden decrease in temperature associated with the release of nitrous oxide. The body's oxygen content depletes, and hypothermia ensues.
Hypoxia -- in other words, starving the body's red blood cells of oxygen. Hypoxia causes the user to feel a sense of euphoria, become incoherent and eventually pass out. Ingesting N20 that hasn't been mixed with oxygen can lead to hypoxia. (You'll never ingest straight nitrous oxygen in the dentist's chair. Medical professionals are very careful to mix it with oxygen to avoid fainting.)

Long-Term Damage
Research on addicted dentists has shown that frequent, large doses of nitrous oxide can result in brain damage and paralysis.

Other types of permanent damage associated with long-term nitrous oxide use include:
loss of motor control
inability to walk
numbness in the limbs, particularly the legs and feet
vitamin B12 depletion
folic Acid interference, something very dangerous for pregnant women
possible immune and reproductive system disturbance
accidental asphyxiation (suffocation)
http://drdrew.com/Topics/article.asp?id=1214

[MickeyFinn]

Sure, poison dart frogs can be purchased online, but it won't do you any good (or anyone else any harm ;) )

Their toxicity comes from the diet of insects that they eat in the jungle, once they're removed from the jungle they slowly become harmless over a period of a few months.

I also can't help but have doubts about your "jungle ants", as we have ants that size here in Australia and their stings are less painful than bee stings. Giving a species name would help...



I did not know about the frogs losing toxicity. Interesting though. As for the ants true names Im not quite sure. They were pointed out to my by a jungle guide on a tour I took while in costa rica. I'm not sure of what sort of ants you have in australia, but these little buggers seemed to the guide afraid, and a few of the locals who spotted some back at the hotel, so I guess their claims were pretty much right. I'll try to find them online.

SO Carbon Dioxide is untraceable? I suppose if you get someone to pass out from drinking alcohol you could place a co2 mask on them and let them dream away to the next life.

[Myrol]

Well, a very hard detectable poison could be heavy water!

Its not well known why heavy water kills people but it works if you have around a Liter handy :D Take the victims water can whilst he makes sport and refill the can completely with heavy water. After beeing dehydrated he will die mostly within 2h due to an heart-attack.

The mainproblem for the ?pathologes? (vocabulary!) is the all-present but not detectable heavy water. Perhaps they will search for potassium chloride due to the heart-attack but theres no real chemical method to detect heavy water against ordinary water! Only if they do some physical tests with some body-liquids they could probably find a little diffierence in boiling point etc.

If someone is poisoned with white phosphorous they boil the victims stomach-content to look for luminescating particels. Quite disgusting job if you're asking me!

[SweNMFan]

About the heavy water

wikipedia it

Health threat

Heavy water is not considered toxic, but some metabolic reactions require light water, so consumption of exclusively heavy water can cause illness. This can be thought of as similar to inhalation of pure nitrogen, the primary component of air -- it is not the nitrogen that is dangerous, but rather the lack of oxygen. Poisoning is unlikely except in unusual industrial and scientific situations.

Experiments with mice have shown that the main effect of heavy water's slightly different reaction rate is to inhibit mitosis, causing progressive damage of tissues that need rapid regeneration. After several days of ingesting only heavy water, the body fluids contain about 50% heavy water. At this point symptoms begin to appear, owing to the decrease in cell division rates of rapidly dividing tissues, such as hair roots and stomach linings. Aggressive cancers might also go into remission, but the effect is not believed to be pronounced enough to make this a useful therapy.

[akinrog]

Well, a very hard detectable poison could be heavy water!


Obtaining it may be problematic. In addition, this substance (D2O) must be kept sealed since it absorbs normal H isotopes from air moisture and gets diluted over the time.

Chloroform comes to my mind. If administered to a sleeping victim by placing a towel saoked with chloroform on his/her mout/nose, s/he shall pass out. However it is detected by the forensic scientiests if suspected, I believe.

[Chris The Great]

Water containing tritium will be a lethal poison due to the extreme radioactivity, as well as that it won't be able to be distinguished from normal water in a normal investigation (although the body may glow slightly if enough is ingested).

You could also spray it as it will absorbed through the skin and lungs, like normal water.

The problem is that tritium is more expensive than plutonium IIRC, at least per gram.

[meselfs]

Nice discussion, but the perfect poison for me is still good old tetramethylene disulfotetramine.

It can be prepared from home with very inconpicious chemicals and simple equipment, and it's LD50 for rats is 0.2 mg/kg.

Only trouble is it acts in maybe 2 hours causing obvios convultions, and has an antidote.

[tom haggen]

Just out of curiosity what is the atomic number of tritium?

[akinrog]

Just out of curiosity what is the atomic number of tritium?
Tom, since it's an isotope. Do you expect atomic number be different from ordinary hydrogen? Atomic weight is, of course, different. But atomic number is all the same. HTH

[The_Duke]

This is a very interesting thread indeed with very smart people posting very smart posts but it would seem as if everyone is overlooking the fact that each poison is different and acts different making them (most of them) unique. Poisons can kill, scar, mutilate, deform, cause blistering burning, and they can also be delivered by different means in different forms, meaning that while one poison is perfect for one target and one set of circumstances, it may be the last choice for another assignment or purpose.

So we ask ourselves questions like what is the perfect poison for a delayed poisoning? or a fast acting poison? what is the perfect deadliest poison? and the most untraceable? What is the best way to deliver these perfect poisons and so on. So while it’s great that everyone can tell us there what there favorite poison is, it is better to elaborate and explain why and what it is that makes that poison perfect for that purpose.

I really like the jungle ants idea. :D

Here is my two pennies worth, does anyone have change for a dime?

[SweNMFan]

Nice discussion, but the perfect poison for me is still good old tetramethylene disulfotetramine.

It can be prepared from home with very inconpicious chemicals and simple equipment, and it's LD50 for rats is 0.2 mg/kg.

Only trouble is it acts in maybe 2 hours causing obvios convultions, and has an antidote.

The problem with TETS is that it isn't THAT easy to make. Unless you are in China nobody would suspect TETS in the first place .. and about the antidote

There is no specific antidote but the use of vitamin B6 together with dimercaptopropane sulfonate (DMPS) has been successful in treating rodents poisoned with tetramine (Guan et al 1993; Zhang et al 2001). However, the clinical efficacy in human patients is not conclusive.

[meselfs]

Ah ok. I remember reading about some sort of treatment, confusing it with a specific antidote.

The procedure for making it is kinda long, that's what makes it hard. Otherwise, we're talking chemicals and equipment that most people here have...

[simply RED]

Simplify it for me. How to make sulfamide at home, or some another chemical is used?

[SweNMFan]

Go and read the Tetramethylenedisulfotetramine http://www.roguesci.org/theforum/showthread.php?t=4054 thread

T-2 mycotoxin seems to be pretty "simple" to make but with a LD50 of 2-4mg/kg not as potent as TETS..

[meselfs]

Simplify it for me. How to make sulfamide at home, or some another chemical is used?

SO2 + Cl2 ---Activated carbon---> SO2Cl2

SO2Cl2 + 2NH3 ------> SO2(NH2)2 + 2HCl

SO2(NH2)2 + 4H2CO ---60% H2SO4---> TETS


I haven't really tried this. I'm doubtful about the second step: Won't HCl formed react with yet unreacted NH3? Also, note that the NH3 must be anhydrous, else you'll get sulfuric acid.

[SweNMFan]

The second step is

SO2Cl2 + 4 NH3 = 2NH4Cl + SO2(NH2)2
135.0 68.1 107.0 96.1

Ive cleaned up the synth from a messy PDF Handbook of Preparative Inorganic Chemistry vol 1 and it is in the TETS thread

[john_smith]

Well what about phosphine? Is it actually undetectable (at least that's what "Silent Death" says) ? As for delayed "poisonong", carcinogenics would probably work best.

[meselfs]

Well what about phosphine? Is it actually undetectable (at least that's what "Silent Death" says) ? As for delayed "poisonong", carcinogenics would probably work best.

Concerning gasses, my favorite is Flourine Monoxide (or was it another oxide? I remeber there was a stable oxide of flourine that was very toxic. See Merck).

[FUTI]

phosphine smells like garlic so I guess it does have odour...
as for F2O...you couldn't pick some more reactive oxidant couldn't you? Stable is relative term.

[bipolar]

I was just reading the news and found out about Acontine a toxic substance extracted from the roots of an asian plant called Aconite may have been used by the Israeli's to poison Arafat says british intelligence. It says it can not be detected in the body 12 hours after ingestion. I found a place where you can buy the root concentrate online from a chinese herb shop. I read it takes 2 to 4 grams of root for a lethal dose, so less of the concentrate. It is supposed to dissolve rapidly in liquids. Also you can google for aconite seeds and find some.

Here is where to buy 100 grams for $16.99 of the root concentrate.http://www.1stchineseherbs.com/search.pl?q=aconite

[nbk2000]

A sensible thing to do, IMHO, would be to mix a sedative in with any poison that'd cause symptoms that'd have the victim running to the hospital soon enough for any type of effective treatment to be applied.

For instance, with strychnine or TETS, tremors and other symptoms would have them going hours before death would ensue. So, by mixing in something like GHB to knock them out, they'd die without having the opportunity to get help (assuming they're alone) or being able to tell anyone just exactly what happened to them recently (such as seeing you. ;))

[MickeyFinn]

There are numerous ways to kill with posions, yes. But my original hopes were to discuss perfect poisons that can be applied either untraceably or with less than suspect means when they fulfill their purpose. I did some research on the actonine mentioned in a previous post, and it sounds decent as an untraceable poison I never heard of. Carcinogen causing poisons are nice too, but take a long time and are not guaranteed to kill as cancer is treated successfully everyday.

Anyone else have any delivery methods of poisons to share?

[McVeigh]

does someone know any good book about poisons - makinng and using them????

[nbk2000]

If you mean a book specifically on the subject of poisoning for the purpose of murder, then I'll tell you that I've never seen one worth the paper it was printed on, everything by Paladin (PUNK) Press specifically included in this designation.

Now, if you mean books on the synthesis of chemicals that happen to be extremely toxic to sentient mammals ;), then there are several books that are of great utility. Specifically those by B.C. Saunders and Mario Sartori (both on the FTP).

Also, search for a link here on RS.org to the 'Digital Library of India' and, from there, find a book on poisons from the 19th century that's VERY detailed on the subject. :)

As for perfect poisons, think like an immortal...time...and lots of it.

If you're after a specific target, poisons are still detectable even if they leave no metabolic traces, simply by motive.

Now, if you think like an immortal and use time to your advantage, then the target GROUP is easily eliminated, where your individual target motive signal gets lost in the group motive noise. ;)

If you're not being picky, say (for instance) you wanted to eliminate an entire generation of future untermensch's, then you can choose things that take years to take effect (carcinogenic, mutagenic, teratogenic, etc) and slllooooooowwwly expose the target to them. Never enough at one time to cause immediate effects that'd get noticed, but the effects would be noticed by the dramatically decreased live-birth rate and increased birt-defect rate of those that are born in that region.

Water is the stuff of life, correct? All water in the city goes through pipes and comes in contact with gasket seals, correct?

Well, as an immortal (and all immortals are rich :p), you would buy a pipe or gasket manufacturing concern, add the 11 secret herbs and carcinogens to the materials, and then underbid everyone else (since you're not concerned about a profit) for the contract to install these materials in ghetto housing projects.

Thousands of less roaches every year equals 10's of millions less every century. :D

[Silentnite]

Depending on which poison you use, if its a powder, could you sprinkle it on their car door? Or if you know where they live, sprinkle some on their garbage can. If it won't stick could you maybe use vasoline?

Another idea, mix some DMSO, Poison, and a sedative, and put it in a stamp inkpad that's been properly drained. Go to a club or something, and switch the one they use to show your age.

Either one probably wouldn't work, but I really like the idea of using DMSO, and a sedative(good one NBK!).

Any word on how to dissolve the Actonite?

So far, this is what I have on it, sorry if its too long:


---Synonyms---Monkshood. Blue Rocket. Friar's Cap. Auld Wife's Huid.
---Part Used---The whole plant.
---Habitat---Lower mountain slopes of North portion of Eastern Hemisphere. From Himalayas through Europe to Great Britain.

Aconite is now found wild in a few parts of England, mainly in the western counties and also in South Wales, but can hardly be considered truly indigenous. It was very early introduced into England, being mentioned in all the English vocabularies of plants from the tenth century downwards, and in Early English medical recipes.

---Description---The plant is a hardy perennial, with a fleshy, spindle-shaped root, palecoloured when young, but subsequently acquiring a dark brown skin. The stem is about 3 feet high, with dark green, glossy leaves, deeply divided in palmate manner and flowers in erect clusters of a dark blue colour. The shape of the flower is specially designed to attract and utilize bee visitors, especially the humble bee. The sepals are purple - purple being specially attractive to bees - and are fancifully shaped, one of them being in the form of a hood. The petals are only represented by the two very curious nectaries within the hood, somewhat in the form of a hammer; the stamens are numerous and lie depressed in a bunch at the mouth of the flower. They are pendulous at first, but rise in succession and place their anthers forward in such a way that a bee visiting the flower for nectar is dusted with the pollen, which he then carries to the next flower he visits and thereby fertilizes the undeveloped fruits, which are in a tuft in the centre of the stamens, each carpel containing a single seed.

In the Anglo-Saxon vocabularies it is called thung, which seems to have been a general name for any very poisonous plant. It was then called Aconite (the English form of its Greek and Latin name), later Wolf's Bane, the direct translation of the Greek Iycotonum, derived from the idea that arrows tipped with the juice, or baits anointed with it, would kill wolves - the species mentioned by Dioscorides seems to have been Aconitum lycotonum. In the Middle Ages it became Monkshood and Helmet-flower, from the curious shape of the upper sepal overtopping the rest of the flower. This was the ordinary name in Shakespeare's days.

The generic name is said to have been derived from , a dart, because it was used by barbarous races to poison their arrows, or from akone, cliffy or rocky, because the species grow in rocky glens. Theophrastus, like Pliny, derived the name from Aconae, the supposed place of its origin. The specific name, Napellus, signifies a little turnip, in allusion to the shape of the roots.

---Cultivation---The chief collecting centres for foreign Aconite root have been the Swiss Alps, Salzburg, North Tyrol and Vorarlberg. Much was also formerly collected in Germany. Supplies from Spain and Japan are imported, so that the demand for English Aconite is somewhat restricted. The official Aconite is directed by the British Pharmacopceia to be derived only from plants cultivated in England, and a certain amount of home-grown Aconite has been regularly produced by the principal drug-farms, though good crops are grown with some difficulty in England, and cultivation of Aconite has not paid very well in recent years.

Aconite prefers a soil slightly retentive of moisture, such as a moist loam, and flourishes best in shade. It would probably grow luxuriantly in a moist, open wood, and would yield returns with little further trouble than weeding, digging up and drying.

In preparing beds for growing Aconite, the soil should be well dug and pulverized by early winter frosts - the digging in of rotten leaves or stable manure is advantageous.

It can be raised from seed, sown 1/2 inch deep in a cold frame in March, or in a warm position outside in April, but great care must be exercised that the right kind is obtained, as there are many varieties of Aconite- about twenty-four have been distinguished - and they have not all the same active medicinal properties. It takes two or three years to flower from seed.

Propagation is usually by division of roots in the autumn. The underground portion of the plants are dug up after the stem has died down, and the smaller of the 'daughter' roots that have developed at the side of the old roots are selected for replanting in December or January to form new stock, the young roots being planted about a foot apart each way. The young shoots appear above ground in February. Although the plants are perennial, each distinct root lasts only one year, the plant being continued by 'daughter' roots.

This official Aconite is also the species generally cultivated in gardens, though nearly all the species are worth growing as ornamental garden flowers, the best perhaps being A. Napellus, both white and blue, A. paniculatum, A. Japonicum and A. autumnale. All grow well in shade and under trees. Gerard grew four species in his garden: A. lyocotonum, A. variegatum, A. Napellus and A. Pyrenaicum.

---Part Used---Collection and Drying. The leaves, stem, flowering tops and root: the leaves and tops fresh, the root dried. The leaves and flowering tops are of less importance, they are employed for preparing Extract of Aconitum, and for this purpose are cut when the flowers are just breaking into blossom and the leaves are in their best condition, which is in June.

The roots should be collected in the autumn, after the stem dies down, but before the bud that is to produce the next year's stem has begun to develop. As this bud grows and forms a flowering stem, in the spring, some of the lateral buds develop into short shoots, each of which produces a long, slender, descending root, crowned with a bud. These roots rapidly thicken, filled with reserve material produced by the parent plant, the root of which dies as the 'daughter' roots increase in size. Towards the autumn, the parent plant dies down and the daughter roots which have then reached their maximum development are now full of starch. If allowed to remain in the soil, the buds that crown the daughter roots begin to grow, in the late winter, and this growth exhausts the strength of the root, and the proportion of both starch and alkaloid it contains is lessened.

On account of the extremely poisonous properties of the root, it is considered desirable that the root should be grown and collected under the same conditions, so that uniformity in the drug is maintained. The British Pharmacopceia specifies, therefore, that the roots should be collected in the autumn from plants cultivated in Britain and should consist of the dried, full-grown 'daughter' roots: much of the Aconite root that used to come in large quantities from Germany was the exhausted parent root of the wild-flowering plants.

When the roots are dug up, they are sorted over, the smallest laid aside for replanting and the plumper ones reserved for drying. They are first well washed in cold water and trimmed of all rootlets, and then dried, either entire, or longitudinally sliced to hasten drying.

Drying may at first be done in the open air, spread thinly, the roots not touching. Or they may be spread on clean floors or on shelves in a warm place for about ten days, turning frequently. When somewhat shrunken, they must be finished more quickly by artificial heat in a drying room or shed near a stove or gas fire, care being taken that the heated air can escape at the top of the room. Drying in an even temperature will probably take about a fortnight or more. It is not complete till the roots are dry to the core and brittle, snapping when bent.

Dried Aconite root at its upper extremity, when crowned with an undeveloped bud, enclosed by scaly leaves, is about 3/4 inch in diameter, tapering quickly downwards. It is dark brown in colour and marked with the scars of rootlets. The surface is usually longitudinally wrinkled, especially if it has been dried entire. The root breaks with a short fracture and should be whitish and starchy within. A transverse section shows a thick bark, separated from the inner portion by a well-marked darker line, which often assumes a stellate appearance. Aconite root as found in commerce is, however, often yellowish or brownish internally with the stellate markings not clearly shown, probably from having been collected too early. It should be lifted in the autumn of the second year.

Aconite root is liable to attack by insects, and after being well dried should be kept in securely closed vessels.

---Chemical Constituents---Aconite root contains from 0.3 to 1 per cent alkaloidal matter, consisting of Aconitine - crystalline, acrid and highly toxic - with the alkaloids Benzaconine (Picraconitine) and Aconine.

Aconitine, the only crystallizable alkaloid, is present to the extent of not more than 0.2 per cent, but to it is due the characteristic activity of the root. Aconite acid, starch, etc., are also present. On incineration, the root yields about 3 per cent ash.

The Aconitines are a group of highly toxic alkaloids derived from various species of Aconite, and whilst possessing many properties in common are chemically distinguishable according to the source from which they are obtained. The Aconitines are divided into two groups: (1) the Aconitines proper, including Aconitine, Japaconitine and Indaconitine, and (2) the Pseudaconitines - Pseudaconitine and Bikhaconitine.

This disparity between Aconites is a very important matter for investigation, though perhaps not so serious from a pharmaceutical point of view as might at first appear, since in the roots of several different species the alkaloid is found to possess similar physiological action; but this action varies in degree and the amount of alkaloid may be found to vary considerably. It is considered that the only reliable method of standardizing the potency of any of the Aconite preparations is by a physiological method: the lethal dose for the guinea-pig being considered to be the most convenient and satisfactory standard. Tinctures vary enormously as to strength, some proving seven times as powerful as others.

The Aconite which contains the best alkaloid, A. Napellus, is the old-fashioned, familiar garden variety, which may be easily recognized by its very much cut-up leaves, which are wide in the shoulder of the leaf - that part nearest the stem - and also by the purplish-blue flowers, which have the 'helmet' closely fitting over the rest of the flower, not standing up as a tall hood. All varieties of Aconite are useful, but this kind with the close set in helmet to the flower is the most valuable.

The Aconite derived from German root of A. Napellus appears to possess somewhat different properties to that prepared from English roots. The German roots may be recognized by the remains of the stem which crown the root. They are also generally less starchy, darker externally and more shrivelled than the English root and considered to be less active, probably because they are generally the exhausted parent roots.

---Medicinal Action and Uses---Anodyne, diuretic and diaphoretic. The value of Aconite as a medicine has been more fully realized in modern times, and it now rank as one of our most useful drugs. It is much used in homoeopathy. On account of its very poisonous nature, all medicines obtained from it come, however, under Table 1 of the poison schedule: Aconite is a deadly poison.

Both tincture and liniment of Aconite are in general use, and Aconite is also used in ointment and sometimes given as hypodermic injection. Preparations of Aconitc are employed for outward application locally to the skin to diminish the pain of neuralgia, lumbago and rheumatism.

The official tincture taken internelly diminishes the rate and force of the pulse in the early stages of fevers and slight local inflammations, such as feverish cold, larnyngitis, first stages of pneumonia and erysipelas; it relieves the pain of neuralgia, pleurisy and aneurism. In cardiac failure or to prevent same it has been used with success, in acute tonsilitis children have been well treated by a dose of 1 to 2 minims for a child 5 to 10 years old; the dose for adults is 2 to 5 minims, three times a day.
---Note---The tincture of Aconite of the British Pharmacopoeia 1914 is nearly double the strength of that in the old Pharmacopoeia of 1898.

Externally the linament as such or mixed with chloroform or belladonna liniment is useful in neuralgia or rheumatism.

---Poisoning from, and Antidotes---The symptons of poisoning are tingling and numbness of tongue and mouth and a sensation of ants crawling over the body, nausea and vomiting with epigastric pain, laboured breathing, pulse irregular and weak, skin cold and clammy, features bloodless, giddiness, staggering, mind remains clear. A stomach tube or emetic should be used at once, 20 minims of Tincture of Digitalis given if available, stimulants should be given and if not retained diluted brandy injected per rectum, artificial respiration and friction, patient to be kept lying down.

All the species contain an active poison Aconitine, one of the most formidable poisons which have yet been discovered: it exists in all parts of the plant, but especially in the root. The smallest portion of either root or leaves, when first put into the mouth, occasions burning and tingling, and a sense of numbness immediately follows its continuance. One-fiftieth grain of Aconitine will kill a sparrow in a few seconds; one-tenth grain a rabbit in five minutes. It is more powerful than prussic acid and acts with tremendous rapidity. One hundredth grain will act locally, so as to produce a well-marked sensation in any part of the body for a whole day. So acrid is the poison, that the juice applied to a wounded finger affects the whole system, not only causing pains in the limbs, but a sense of suffocation and syncope.

Some species of Aconite were well known to the ancients as deadly poisons. It was said to be the invention of Hecate from the foam of Cerberus, and it was a species of Aconite that entered into the poison which the old men of the island of Ceos were condemned to drink when they became infirm and no longer of use to the State. Aconite is also supposed to have been the poison that formed the cup which Medea prepared for Theseus. (Note---Aconite and Belladonna were said to be the ingredients in the witches' 'Flying ointments.' Aconite causes irregular action of the heart, and Belladonna produces delirium. These combined symptoms might give a sensation of 'flying.'---EDITOR)

Various species of Aconite possess the same narcotic properties as A. Napellus, but none of them equal in energy the A. ferox of the East Indies, the root of which is used there as an energetic poison under the name of Bikh or Nabee. Aconite poisoning of wells by A. ferox has been carried out by native Indians to stop the progress of an army. They also use it for poisoning spears, darts and arrows, and for destroying tigers.

All children should be warned against Aconite in gardens. It is wiser not to grow Aconite among kitchen herbs of any sort. The root has occasionally been mistaken for horse-radish, with fatal results - it is, however, shorter, darker and more fibrous - and the leaves have produced similar fatal results. In Ireland a poor woman once sprinkled powdered Aconite root over a dish of greens, and one man was killed and another seriously affected by it.

In 1524 and 1526 it is recorded that two criminals, to whom the root was given as an experiment, quickly died.

The older herbalists described it as venomous and deadly. Gerard says: 'There hath beene little heretofore set down concerning the virtues of the Aconite, but much might be saide of the hurts that have come thereby.' It was supposed to be an antidote against other poisons. Gerard tells us that its power was 'So forcible that the herb only thrown before the scorpion or any other venomous beast, causeth them to be without force or strength to hurt, insomuch that they cannot moove or stirre untill the herbe be taken away.' Ben Jonson, in his tragedy Sejanus, says:
'I have heard that Aconite
Being timely taken hath a healing might
Against the scorpion's stroke.'

Linnaeus reports Aconite to be fatal to cattle and goats when they eat it fresh, but when dried it does no harm to horses, a peculiarity in common with the buttercups, to which the Aconites are related. Field-mice are well aware of its evil nature, and in hard times, when they will attack almost any plant that offers them food, they leave this severely alone.

---Other Varieties---Japanese Aconite - syn. Aconitum Chinense - is regularly imported in considerable quantities. It used formerly to be ascribed to A. Fischer (Reichb.), but is now considered to be derived from A. uncinatum, var. Faponicum (Regel.) and possibly also from A. volubile (Pallas). It has conical or top-shaped, gradually tapering tuberous roots, 1 to 2 inches long, 1/3 to 1 inch in thickness at the top, externally covered with a brown, closely adhering skin internally white. Dried roots do not contain much alkaloid, if steeped when fresh in a mixture of common salt, vinegar and water. The poisonous alkaloid present is called Japaconitine, to distinguish it from the official Aconitine and the Pseudaconitine of A. laciniatum. Japaconitine is similar in constituents and properties with the Aconitine of A. Napellus.

Indian Aconite root or Nepal Aconite consists of the root of A. laciniatum (Staph.). It is also called Bikh or Bish, and is collected in Nepal. It is much larger than the English variety, being a conical, not suddenly tapering root, 2 to 4 inches long and an inch or more at the top, of a lighter brown than the official variety, the rootlet scars much fewer than the official root. Internally it is hard and almost resinous, the taste intensely acrid and is much shriveiled longitudinally. This root yields a very active alkaloid, Pseudoaconitine, which is allied to Aconitine and resembles it in many of its properties; it is about twice as active as Aconitine. Indian Aconite root was formerly attributed to A. ferox (Wall). Their large size and less tapering character sufficiently distinguish these from the official drug.

Other varieties of Aconite are A. chasmanthum (Staph.), known in India as Mohri, which contains Indaconitine, and A. spicatum, another Indian species containing Bikhaconitine, resembling Pseudaconitine.

Russian Aconite, A. orientale, grows abundantly in the Crimea and Bessarabia. It has a small, compact, greyish-black root with a transverse section similar to that of A. Napellus. Its taste is hot and acrid. When treated by a process which gave 0.0526 per cent of crystalline Aconitine from a sample of powdered root of A. Napellus, the dried root of A. orientale yielded 2.207 per cent of total alkaloids, which were, however, amorphous. The total alkaloid has not yet been investigated further.

A. heterophyllum (Wall), Atis root, is a plant growing in the Western temperate Himalayas. This species does not contain Aconitine and is said to be non-poisonous. Its chief constituent is an intensely bitter alkaloid - Atisine - possessing tonic and antiperiodic principles. A. palmatum, of Indian origin, yields a similar alkaloid, Palmatisine.

The province of Szechwen in West China grows large quantities of medicinal plants, among them A. Wilsoni, which is worth about 4s. per cwt., of which 55,000 lb. a year can be produced in this province; A. Fischeri, about four times the price, of which rather less are yearly available, and A. Hemsleyan, about the same price as the latter, of which about 27,000 lb. are available in an average year.

---Other Species---The Anthora, or Wholesome Aconite described by Culpepper, is a small plant about a foot high, with pale, divided green leaves, and yellow flowers - a native of the Alps. Its stem is erect, firm, angular and hairy; the leaves alternate and much cut into. The flowers are large, hooded with fragrant scent, growing on top of the branches in spikes of a pale yellow colour, smaller than the ordinary Monkshood and succeeded by five horn-like, pointed pods, or achenes, containing five angular seeds. It flowers in July and the seeds ripen at the end of August. The root is tuberous.

Culpepper tells us that the herb was used in his time, but not often. It was reputed to be very serviceable against vegetable poisons and 'a decoction of the root is a good lotion to wash the parts bitten by venomous creatures.' . . . 'The leaves, if rubbed on the skin will irritate and cause soreness and the pollen is also dangerous if blown in the eyes .'

As a matter of fact, this species of Aconite by no means deserves its reputation of harmlessness, for it is only poisonous in a less degree than the rest of the same genus, and the theory that it is a remedy against poison, particularly that of the other Aconites, is now an exploded one.

Parkinson, speaking of the Yellow Monkshood, calls it:
'The "counter-poison monkeshood" - the roots of which are effectual, not only against the poison of the poisonful Helmet Flower and all others of that kind, but also against the poison of all venomous beasts, the plague or pestilence and other infectious diseases, which raise spots, pockes, or markes in the outward skin, by expelling the poison from within and defending the heart as a most sovereign cordial.'

The so-called Winter Aconite, Aeranthis hyemalis, is not a true Aconite, though closely allied, being also a member of the Buttercup family, whose blossoms it more nearly resembles.

Also see:
DELPHINIUM
FIELD LARKSPUR
STARVEACRE.

From http://www.botanical.com/botanical/mgmh/a/aconi007.html

EDIT: I didn't realize this has been posted already on. But from what I saw it didn't have this information. I'll leave it to the mods discretion as to whether or not it should stay...

[SweNMFan]

Just don't waste time and money on DMSO + Ricin as it will not work, the ricin molecules are to big to get past the skin effectively. The Minnesota Patriots Council tried that against US Marshals..
And a internet urban myth started

[nbk2000]

I belive the MW of skin-transferable poisons has to be under 700. There's other untis of measure used for such things but I don't remember what they are.

[Blackout]

1---Methyl Alcohol: A little methyl alcohol goes a long way in taking someone out.

Pros: Alcoholics won't notice it slipped in moonshine. Police and MEs will attribute it to a bad bootlegging operation.

Cons: More than one person usually gets poisoned from bad bootlegging ops, unless the person made it and tried ithimself. It's kinda hard to set up a still in someone's backyard without them knowing.

An alcoholic won't makes the difference between beer and 95-96% alcohol and he will die from an overdose after an ethyl coma.
Methyl alcohol is an uban legend, http://ruscuisine.com/cooking-forums/viewtopic.php?mode=viewtopic&topic=329&forum=1&start=0

[simply RED]

Methyl alcohol is very good poison and not an urban legend.
The statistics talk!

[MickeyFinn]

Methyl alchohol, aka methanol, is most certaintly not an urban legend. If you think so then a couple hundred russians who imbibed bad vodka containing methanol and over 2 dozen that died from its ingestion will most certaintly disagree with you there.
That is just one of the newest widespread cases I have heard of recently, sometime last year I believe.

On another topic I remember reading about people in SPain in the early 80s who ingested rapeseed oil and slowly deteriorated away. The doctors were baffled as all tests were negative. Have tests since been developed to find rapeseed oil or is it tstill pretty much untraceable in the body as it slowly kills somoene?

[arnold]

Just don't waste time and money on DMSO + Ricin as it will not work, the ricin molecules are to big to get past the skin effectively. The Minnesota Patriots Council tried that against US Marshals..
And a internet urban myth started

So, what about DMSO + aconitine or colchicine or nicotine?

Which of them would be the best one?

[Storm on the Horizon]

Just out of curiosity what is the atomic number of tritium?

Tritiums atomic number is 1.

(Same as the hydrogen that it's an isotope of. NBK)

[controlphreak]

I don't know about the DMSO + aconitine mix specifically, however, it was written here - http://www.henriettesherbal.com/eclectic/kings/aconitum_aconitine.html - that mixing it with lard and applied to the unbroken skin created heat and a numbing sensation. That would have to be applied for several minutes.

It also stated that the broken skin would feel a burning sensation, so the aconitine + DMSO would not work I think. Though their tests used lard, the principle is still the same if I am not mistaken.

[Jacks Complete]

Does anyone know what DMSO alone feels like? I know it is used for horses and also in some "heat rubs". I would assume that it would feel warm anyway, since the enhanced blood flow to the area would warm the skin, tipping off the target.

Methanol is toxic to the liver, and sends people blind. Small amounts are easily netralised by drinking ethanol, so giving some to a drunk isn't going to work, and giving a drunk neat ethanol is fairly daft too, since they are going to notice unless they are blind drunk/unconcious, and if they are in that state you can easily kill them without fear anyway, without doing something that an autopsy might pick up.

Tritium's atomic number is 1, like Hydrogen, but it has a mass number of 3, due the the extra neutrons. Hence it is an isotope of Hydrogen.

[nbk2000]

I've read that heavy water is an undetectable poison.

The deuterium, which substitutes for the hydrogen in normal water, interferes with cellular processes, causing slow death.

Given the cost and amount needed, plus the time to administer the needed doses, this is something only people with money and patience could use.

Something along the lines of 'the nephew who'll inherit after the rich uncle dies' scenario.

http://yarchive.net/med/heavy_water.html

[arnold]

Poisons are a very good and universal weapon for selective assassination. However, there is a serious problem with delivering them without notice. That point can ce achieved using poison mixed with DMSO. But what poison to use? I hard that nicotine and nicotine sulfate are good skin penetrators, so mixed with dmso would be absorbed quicker than alone.

A good idea to deliver such a poison mix is to splash it onto someone's doorknob. But, would the one touch enough for the victim to get killed? Personally, I doubt. A I right?

What about a poisoned letter idea (applying a mixed poison to a piece of paper and mailing it to somebody)?

[sdjsdj]

Perhaps an effective long-term poisoning strategy could involve tainting a battery-powered air freshener (Something like this (http://www.naturex.ca/index.php?act=viewDoc&docId=7)?) with a potent yet volatile toxin capable of passing through the skin, then planting it in the target's home. after a cursory glance around the possible candidates, I belive that Dimethylmercury (http://en.wikipedia.org/wiki/Dimethylmercury) is an ideal solution; VERY toxic, yet hard to detect if well concealed, and (probably) slow acting enough that by the time it takes effect, you can be a long, long way away.

[Jacks Complete]

That is rather a good idea, very close to NBK's non-lethal idea for detering hobo's and others from your "condemned" building hide-away.

In a house, you could easily use a mains powered unit, or just "top up" the existing one, if it exists.

Anyone want to comment on the choice of a mercury compound? After all, they are anything but subtle. Also, there is no point putting it in a dispenser, simply spraying some in a bedroom would be enough to be fatal, even without the heater. Perhaps sometihing more common and easily obtained, but with a lower vapour pressure, or that is solid at room temperatures, would be better.

[akinrog]

Anyone want to comment on the choice of a mercury compound? After all, they are anything but subtle. Also, there is no point putting it in a dispenser, simply spraying some in a bedroom would be enough to be fatal, even without the heater. Perhaps sometihing more common and easily obtained, but with a lower vapour pressure, or that is solid at room temperatures, would be better.

I would recommend dimethyl mercury: a very volatile and transdermal compound. But IMHO heavy metals are no-no in poisoning business, since they are easily detectable.

However in case of dimethyl mercury, it's better to expose the target to its fumes for a prolonged period of time at doses way smaller than lethal dose. Mercury compounds induce insanity since they destroy nerve cells. In this fashion it's possible to incapacitate a person without actually killing him/her.

Another thought is to expose target to Nickel carbonyl or nitrosamine fumes. These are really nasty compounds: former is a tumoregenic and later is carcinogenic substance. :eek: Regards.

[sdjsdj]

Perhaps a Barbital (http://en.wikipedia.org/wiki/Barbital) aerosol, sprayed into the air for a few hours every night by a more complex diffuser could provide the desired cumulative effect; the trouble would be judging the dose to eventually kill without alarming the target into attending a hospital, as any serious blood testing would show up the substance(s) administered.
EDIT;
Perhaps for a more subtle kill, compounds such as tetra-ethyl lead or vitamin A could be administered over a long period in this way. After all, their general environmental presence would make it virtually impossible to detect foul play after the eventual overdose.

[Chris The Great]

Dimethylmercury takes months to kill, so exposing the target once will only cause death months later. If done right, there will be no way to link back to the initial poisoning because it was so long ago.

They will know that the person has been poisoned but there will be no way to find out who did it.

[akinrog]

They will know that the person has been poisoned but there will be no way to find out who did it.

One important point is to think like pigs. Pigs have been trained to think like criminals. If a suspicious death takes place, they shall first investigate friends / enemies / rivals around the victim.

So if the poisoner has a relation with the victim and pigs determine the possible motive, they can cage him/her.

In addition, I remember an episode of forensic inspectors broadcast on discovery where a man used a nitrosamine to poison his ex-girl friend but accidentally poisoned his ex-girlfriend's entire family. As a result of poisoning one of her kids and her brother were dead.

Although nitrosamines quickly decompose into metabolismic products. Forensic scientists could determine what kind of poison was used in poisoning based on the destruction of the liver, since nitrosamines quickly destroy liver causing hepatic fibrosis. After screening all possibilities and determined that ex-boyfriend once assaulted the woman's house and after finding out that the culprit was working in a cancer research facility, therefore can get that nitrosamine, they busted him.

The guy even carried out tests on animals to determine lethal dose and owners of the animals filed a complaint about him.

In short, even if the poison is not detectable they can bust the poisoner, if there is a motive, if there is an evidence that a poison is used and if culprit has possibility to access the chemical. Regards.

[arnold]

So that you have you have to wait a long period of time before commiting the crime. Then pigs won't be able to make the connection and even they make it will seem a believeless evidence for the judge.

What about my idea with dmso/nicotine? All of your ideas are good , but require entering the home. With my idea one NEED NOt to enter the home and if the pigs can't make the connection to the victim it may give a perfect results.
Think out about it!

[ozboy]

A nice little book called Silent Death by Uncle fester is available at,

nw0.info / eBooks and Audio Books / Banned_Books .

Definately worth a look at.

[teshilo]

A nice little book called Silent Death by Uncle fester is available at,

nw0.info / eBooks and Audio Books / Banned_Books .

.
Firstly: these link dont work ...:rolleyes:
Secondly: Silent Death by Steve Preysler (Uncle Fester his pseudo)
more related to basement WMD principles.More best David Harber "Assorted Nasties"And good poisoning depend from many factors..Classics Grigoriy Rasputin case: He got more than one gramm KCN :rolleyes: :rolleyes: and dead ater few shots and few strikes.

[Defendu]

link dont work

http://nw0.info/?p=eBooks%20and%20Audio%20Books/Banned_Books/

by Steve Preysler

Actually his surname is spelled Priesler.

[ozboy]

Firstly, thanks for fixing the link!

Secondly, I put it down as Uncle Fester so that everyone could find it in the list. (There are quite a few books on it).

[Cobalt.45]

Does anyone know what DMSO alone feels like? I know it is used for horses and also in some "heat rubs". I would assume that it would feel warm anyway, since the enhanced blood flow to the area would warm the skin, tipping off the target.

DMSO alone does feel warm, and has a noticeable "garlic- like" taste that one will experience shortly after application.

[FullMetalJacket]

If GABA receptor blocker is used or ATP-ase inhibitor
it will be abosutely impossible to determine the cause of death...


ATPase inhibitors are the basis of nearly every animal neurotoxin, especially atraxotoxins in Australian Funnelweb spiders.

Believe me, they are very identifiable.

[meyer25]

If rapid action and complicated detection are desired, I'd rely on anatoxin A.
It could be made by cultivating Anabaena flos-aquae, an ubiquitous freshwater algae.

If slow action would be of importance, I'd use aflatoxins (which hardly would be linked to a suspect) or 2,3,7,8-TCDD (not too pure, in order to mimic some chemical waste exposure on long term).

A rapid-acting skin-penetrating poison would be 4-chlorophenylsilatrane, 4-CN-TBOB, TBPS or a similar lipophilic cage convulsant. No need for DMSO in my opinion.

Identification of these (without a direct hint) would be very complicated, given the number of possibilities.

[nbk2000]

It's always good to expand unfamiliar acronyms.

For instance, TBPS (T??? B??? P??? S???).

jpet.aspetjournals.org/cgi/reprint/244/3/802.pdf, BTW.

[meyer25]

I'm sorry.

4-CN-TBOB stands for t-butylbicycloortho-(4-cyanobenzoate), TBPS for t-butylbicyclophosphorothionate.

Similar agents (cage convulsants of 4-alkylbicyclophosphate type) have been discussed in thread "Bicyclic Phosphates - Poor Man's Nerve Agents".

[simply RED]

Do you have some more information for:
t-butylbicycloortho-(4-cyanobenzoate), t-butlbicyclophosphorothionate?

LD50 and synthesis will be highly appreciated.

Do you think that replacmant of "t-butyl" part with "(CH3)3N(+)" will enhance the toxicity?

FullMetalJacket, the ATP-ase is a very complex structure, there are thousand possible ways to disrupt its functions.
No one is going to investigate such a complex case of poisoning anyway, come to the reality!

The australian funnelweb spider's venom is a mixture of many chemicals. Which one is ATP-ase inhibitor?

[FullMetalJacket]

Well, the Australasian Funnelweb or Sydney Funnelweb's primary toxin is robustotoxin, which just jams open the sodium channels.

[kamaz]

I've got an interesting idea. Put the ricin powder to piece of paper, then to envelope and mail it to a target. When the target pulls the letter he disperse a deadly cloud of ricin around his face. He will be practically dead.

The problem is: how to safely, cheaply and accurately enough grind the ricin to such tiny powder?

[Syke]

I think that you guys are overcomplicating things by trying to get a way to deliver a rare and conspicuous superpoison. The best way to poison something/one is to us a common enviromental poison. Look around your targets living area and find or plant the toxin in question. Investigators are much more likely to explain away the death of joe shmoe away with accidental mercury poisoning or pesticides since they wont think of a nobody as being important enough to assassinate.

[nbk2000]

I believe the name of the topic is 'Perfect Poisons', not 'Good Enough Poisons'. ;)

[Syke]

True but most marks arent going to come into a poison such as ricin in their everyday life. A poison is going to be more helpful if it goes unnoticed otherwise things can get complicated for the poisoner.

[FullMetalJacket]

I've got an interesting idea. Put the ricin powder to piece of paper, then to envelope and mail it to a target. When the target pulls the letter he disperse a deadly cloud of ricin around his face. He will be practically dead.

The problem is: how to safely, cheaply and accurately enough grind the ricin to such tiny powder?

Atomizing a milk slurry into a blast of freeze-drying was how they used to powder anthrax at places like Porton Down. A bit of bentonite clay powder in the mixture dissipated the static charge of the particles to give you better dispersion, too.

[cyclosarin]

As mentioned in the dimethylmercury article, this poison has been known to kill many weeks after exposure.

If analysis of the victim revealed mercury poisoning would it be possible to make it look like an environmental cause; perhaps by lacing a water supply or local stream with methylmercury and make it look like an undetected chemical spill such as that in Minamata?

[Corona]

http://members.tripod.com/~Prof_Anil_Aggrawal/poiso008.html


What do you guys think? Will such a small dose of something this crudely made (abrin), do in someone?
----------
The powder is then made into a paste with spirit and water, and long needles are fashioned out of this paste. The needles are about 1.5 cm in length - about the length of your thumbnail- and weigh about 100 mg on an average. These needles are then dried in the sun. When dry, they are known as suis or sutaris and are ready for use.

The killer uses these needles for killing. He may hold one or two such suis in his palm between his closely held fingers (the way one holds a cigarette; only much more tightly). The victim is then slapped in such a way that the suis penetrate the flesh. The effect is similar to giving an injection of abrin to the victim, and is thus obviously quite effective. You might be surprised to know that even animals are killed by this method.
------------------------------------------

Please read all of the article....

Here is some more. Very interesting (at least, for me).

http://members.tripod.com/~Prof_Anil_Aggrawal/

And...

http://members.tripod.com/~Prof_Anil_Aggrawal/index1.html

[FUTI]

I would never put betwen my fingers something that can kill through skin penetration, but as far as I remember abrin is quite toxic. I didn't check MSDS data, but that is trivial and I guess you already done it yourself, so I just want to point to the obvious flaw in the method of aplication.

[Corona]

I fully agree with you. It seems like one hell of a stupid risk to hold it between your fingers like described.

I was wondering that if true, this seems to be something that unsophisticated village folk are capable of doing... extracting enough abrin to kill, without using chemicals to isolate, extract or purify.

The final product... though much cruder than what some people here might have come up with... is still enough to do away with someone. Meaning you can be as sloppy as Kurt Saxon with his ricin (or sloppier) and still get something usable (for abrin)?

I know how poisonous this thing is supposed to be (only from what I've read here)... it still takes a bit of effort for it to sink in, thats all.

[20920474]

You guys have named a lot of poisons, still, one of the most easy to get is nicotine poisoning. Any guy with half a brain can make this stuff, get your hands on some chewing tobacco and put in a little jar of water, obviously, the less water, the more concentrated= easier to get out the nicotine. Let it sit overnight. Next, pour your shit coloured water+nicotine into a coffee filter above a can, let it sit for maybe six hours, next, squeeze the coffee filter above the can so the rest of the water+nicotine comes out of the filter, get rid of the coffee filter. Now that all you have is the can with the browny water, let the water evaporate, you will be left with a thick, suropy like substance that is pure nicotine, should it be to thick add a bit of water. This poison can kill with only a few drops, its best to put it into the vicims coffee or something to disguise the taste.

[random136]

20920474, written like a true newbie, your description is a paraphrased version of the information found in The Anarchist Crapbook. Please try reading this thread from start to finish before sharing any more of your wisdom.

Also, use our wonderfull search function to find one (if not several) threads discussing the real process involved in extracting nicotine. Finally, note that, as an alkaloid, nicotine can easily be identified forensically, making less then desirable poison with no redeeming qualities.

[teshilo]

Yes. As discussed in thread related nicotine extraction ,water hydrolise it..

[nbk2000]

Mr copy/paste is no longer amoung us. All hail the Beast! :)

[beirut]

Chloroform comes to my mind. If administered to a sleeping victim by placing a towel saoked with chloroform on his/her mout/nose, s/he shall pass out. However it is detected by the forensic scientiests if suspected, I believe.

Chloroform would affectively kill someone if too much is administered, plenty of people learned this back when it was used as an an anaesthetic, but administering it with a soaked rag could give away it's presence. Chloroform has been known to cause sores when skin is immersed in it. I would think that a wetted rag would be enough exposure to cause this. You'd have to find another way to deliver it into the body.

[random136]

Good first post beirut. May I direct the attention of anyone interested in using chloroform as a weapon to the following thread:

http://www.roguesci.org/theforum/battlefield-chemistry/1540-chloroform-bomb.html?highlight=chloroform

Especially Post #10 made by nbk. He gives a plausible, simple method to use chloroform in a faster more efficient manner. Generally speaking, it is no good for work where you wish to leave no trace, since the medical community is quite familiar with the substance, what with the many decades worth of studies.

[rayman]

I have been giving this some thought ( my job gives me plenty of thinking time most days ), and since this is the " Battlefield Chemistry " area, most of these ideas are junk, you would I assume want to knock out/ kill your enemy in the least amount of time where as somthing that may kill in 3 months is all fine and dandy, that would not help you on a battle field or in a war setting ... UNlLESS you where attempting to assassinate one commander/general in particular and had time and means to do so

What I realy wanted to comment on thought is there is no " perfect poison " I think that many poisons are usable if thought is put into what you want to achieve, make them sick, kill now, kill next week giving you time to distance your self from the act, make ill for some length of time before death as you realy want them to suffer

[fafner]

Substance P.
End of the 60',discussions have started on the risk of bioregulators being used as CW agents. These types ofof substances do not belong to the group of toxins but are,nonetheless,grouped with them since their possible use is similar.
They are closely related to substances normally found in the body and may be undedectable.
A characteristic of them is that they are active in extremely low doses and freqently have rapid effect.

One sample of this agents is Substance P,a polypeptide(molecular weight=1,350 D)which is active in doses of less than one microgramme!

Substance P causes, for example, a rapid loss of blood pressure which may cause spontane unconsciousness

++++++++++

Congratulations!

You've just won the Copy/Paste award of the month for your post! :)

Your skillz in copying text from SIPRI's The Problem of Chemical and Biological Warfare is dazzling!

As your prize, you get a one-way, all-expenses paid trip to Monster Island, where you'll get to meet the NBK (Naturalius Born Killium), a voracious meat-eating predator that hunts there.

[Bilbe]

Simplify it for me. How to make sulfamide at home, or some another chemical is used?

This doesn't look simple to me, (2.1 Chem. Bsc)

SO2 + Cl2 ---Activated carbon---> SO2Cl2

Are both gasses so to make this work I would expect the need for pressure? This will be expensive and hard.

SO2Cl2 + 2NH3 ------> SO2(NH2)2 + 2HCl

Anhydrous NH3 is a pain to work with I am having this difficulty right now. Using it in 2* excess would make up for the loss through acid base reaction (which will be the dominant reaction)

[eelfland]

If a person is known to be a drinker of ethanol, it would be a fairly simple matter to load the person up on it to the point of unconsciousness and then pour enough more of it in to produce death, either through simple alcohol poisoning or by aspiration of vomitus. It can also be administered via enema after the victim is unconscious. If you're on hand for the vomiting, you could simply cover the victim's mouth with him/her facing upward, making sure the vomit got aspirated.

People frequently die by accidental self-administered alcohol poisoning, and if the victim's not around to tell anybody otherwise, there is no evidence to show that it wasn't accidental.

"Perfect."

[ciguy007]

If someone were to hang around forensic toxicology organizations, one would find that after a few drinks, the subject of the perfect poison always comes up. The most "perfect) poison would be said to leave no abnormal symptoms, act quickly, be undetectable.

One might consider carbon dioxide - used to knock out animals prior to slaughter, used to kill (euthanize) un-wanted laboratory animals. Theoretically, simply holding a bag of finely-ground dry ice over the face of a sleeping victim could cause hypercarbia and death. Certainly if someone happened to have been sedated by some chemical (ethanol for instance), carbon dioxide could theoretically be administered - hypercarbia stimulates respiratory rate thereby increasing exposure to an inhaled substance which can quickly cause loss of consciousness and death.

Of course, elevated carbon dioxide concentrations are typically found in post-mortem blood - when one quits breathing (from whatever reason) blood oxygen levels fall and blood carbon dioxide levels rise - an unremarkable finding at autopsy.

[Vitalis]

Carbon Dioxide is hardly a perfect poison. Sure if you can get a person drunk/ drug them into a stupor, it would be easy to OD them on CO2. Otherwise it's tricky to poison someone with it, as they tend to wake up when their heart starts pounding and they feel the other symptoms of CO2 poisoning.

[xex]

From what I've seen people that die in their cars from exhaust are very pink. I don't know if that's because of the CO2 or CO but it's pretty obviously different than natural causes.

The case would be closed quickly if there was a probably natural cause.

[Kaydon]

That would be carbon monoxide. It takes a long time (8 hours or so) to die from it, from say a automobile/diesel. The good thing about it, is it leaves no odor and has no color. If for example you had to take someone out, and wanted to use CO, get them while they're sleeping :)

Edit: I read a few weeks ago about some african drug called Jenkem or something similar. You put feces and urine in a bottle and put a balloon over the top and let it ferment in the sun. You would then take the balloon off, kept closed, and inhale the gasses. Supposebly it knocks you out and then afterwards you have hallucinogenic affects. I see potential to use this to drug someone/something in order to get past it. Unlikely to die from it, but definitely leave you in the clear for a while. I even read you can have the affects days after inhalation of the gas.

http://en.wikipedia.org/wiki/Jenkem

http://www.google.com/search?source=ig&hl=en&rlz=&q=jenkem&btnG=Google+Search

[Hirudinea]

From what I've seen people that die in their cars from exhaust are very pink. I don't know if that's because of the CO2 or CO but it's pretty obviously different than natural causes.

The case would be closed quickly if there was a probably natural cause.

From what I understand the body uses CO the same way it uses O2 in the body, it is more reactive with hemoglobin in the body so given an equal amount the blood will take up CO before O2, and since it leaves the body a pink colour the victim dosn't look hypoxic, white, when they're being poisoned. (By the way that's a plot point in the movie Coma.)

I read a few weeks ago about some african drug called Jenkem or something similar. You put feces and urine in a bottle and put a balloon over the top and let it ferment in the sun. You would then take the balloon off, kept closed, and inhale the gasses. Supposebly it knocks you out and then afterwards you have hallucinogenic affects.

Sounds like they're just getting buzzed from a lack of oxygen from inhaling methane.

[Alexires]

Only fucking niggers would come up with the idea of getting high on their own excrement. *shakes head*.

I quite like the alcohol enema, if nothing else, it would be amusing.

One could always put some kind of heavy metal (lead or something as common) in their water purifier (everyone seems to have one these days) or in their pipes. Heavy metal poisoning would of course be found in autopsy, but just blamed on bad plumbers if they did eventually find the lead in the pipes.

Just a question to people more knowledgeable than I, how deep does a local anaesthetic penetrate? It might be possible to get someone into an alcohol induced sleep, apply some local anaesthetic and then inject them with something and they might not be able to feel it.

Otherwise, use Nitrous as a general and do the same thing.

[Joxer]

Perhaps you mean a topical anaesthetic?
A local is an injection.

[Man Down Under]

Here's an interesting one, and quite cheap to boot!

Source: http://members.aol.com/organichem/my_pages/history.htm


On January 20, 1974, Sunday, we made two plant batches of methyl iodide at 72-l scale (19-gal), both going smoothly. I looked after these preparations , the subsequent distillations and the drying of the distilled methyl iodide. Helen, my wife and partner in this grand enterprise, worked in the same large room with me that day doing batches of the first-step reaction (A-1 reaction) in a large flask (JPG: 45K).

In the midst of the bustle, I cut my finger on a glass tube when it broke as I tried to insert it into a holed stopper. The finger bled profusely and required three tight adhesives bandages to stop the bleeding. What happened next, we surmised many weeks later, was that I spilled some methyl iodide on the bandaged finger. Since methyl iodide is a local anesthetic, one feels no pain as you would with alcohol on a cut. Furthermore, the methyl iodide which boils a few degrees above body temperature cannot evaporate quickly as it would if you merely spilled some on skin open to the air. This conjecture is supported by the fact that when the physicians removed the bandage after I was admitted to the hospital, they found a large vesicant blister on the finger. But I am getting ahead of my story.

Just as we were preparing to close up and go home for dinner, I began to lose my balance in a way that had never happened before. I, at first, thought that I was just very over-tired because I had been feeling tired much of the day.

The next morning as Helen prepared to go to her regular job (high-school-guidance counselor), I told her that I was feeling a little off that morning and that I would stay in bed. By the time she came back that evening, I was really tired but wasn't bad enough to cause her tremendous alarm. But that night I thrashed all over the bed with violent nausea. She made arrangements to take me to the Neurological Institute at Columbia Presbyterian Medical Center in New York City early the next morning.

By that time, I was pretty disoriented. My last rational thought as I sat in a wheel-chair was that I must be very sick, but, if I could just tie that shoelace which had just become untied, then perhaps things weren't so bad after all. I couldn't do it! The next four weeks were a blur of confusing fantasies with some hallucinations and misunderstandings of events transpiring around me. I "woke up" four weeks later.

This malady was the result of methyl-iodide poisoning. Helen was not affected at all; yet we spent that Sunday working together in our plant. At first the neurologist thought that I had some kind of malfunction (or tumor, perhaps) of the cerebellum. A young resident Jerry Apel (now a nephrologist at Columbia Presbyterian) took an interest in my predicament and, after asking Helen about all the chemicals we used, searched out the effects caused by poisoning by methyl iodide. Helen later told me that she told him that I had told her that methyl iodide was the only chemical about whose toxicity I wasn't sure. Or perhaps it was just a process of elimination. The remainder of the chemicals would not be expected to cause the same kinds of symptoms.

At any rate, he found reports of six prior cases of poisoning by methyl iodide resulting in three deaths and two long-term-disability cases. The sixth, a Spaniard, was reported to be asymptomatic within about four months. These reports did suggest that the best treatment was no treatment: just keep the patient alive and let nature take its course. One of the major symptoms which arises in cases like this is the onset of what psychology books refer to as toxic psychosis which in my case was an induced paranoia. The result of this was that I didn't believe anyone that I was suffering from something as mundane as methyl-iodide poisoning.

After six weeks in the hospital, I was released to go home. I had improved considerably. I could walk without falling, but all the muscles were weak as if my brain could not communicate effectively with them. Even the heart muscle was weakened, because every time I stood up for more than a minute or two, I would feel a kind of "rattling" in my brain and discovered that I couldn't think as clearly as when I was reclining or even sitting (result of oxygen-deprivation to the brain). I had entered weighing 180 LBS and left weighing 160. People around me making the normal amount of noise caused me pain from the level of noise - - - and I feared the whole world was out to get me but couldn't figure out why. I rationalized that the reason I wasn't murdered immediately was that they wanted to scare me to death. I tried to put up a brave front to show them it wouldn't work, but my fear surfaced occasionally. In addition to being weak, I was so uncoordinated that writing my own name resulted in an illegible scrawl. It remains pretty illegible even to me to this day. Trying to write several lines or to type several lines with a mechanical typewriter led to severe chest pains as if someone had been tightening steel bands around my chest.


Methyl Iodide! :)

[megalomania]

Hmm, I don't know if methyl iodide poisoning will actually do this except in a small number of rare cases. Perhaps there are not enough recorded cases either. I wonder if there have been any treatments developed in the last 30 years?

[akinrog]

Hmm, I don't know if methyl iodide poisoning will actually do this except in a small number of rare cases.

I believe the author or narrator of the story gave some misleading information.

According to SIRI toxicity index, methyl iodide is little toxic, but, alas, methyl diiodide is quite toxic in oral administration, which makes it easier to assume that muscular or venous administration shall be much more effective.

Check this out :
http://www2.siri.org/msds/tox/f/q76/q73.html

In the toxic effects part, it says behavioral, which I believe quite similar to above. So I speculate that the substance in the above story must be methylene diodide not methyl iodide. Regards.

[Man Down Under]

The story says that the MeI was pretty much injected by a serious cut with glass tubing, and then held in the wound by tight bandages.

By reading the rest of the site, you see that it IS MeI, not methylene or diiodide anything else.

[akinrog]

By reading the rest of the site, you see that it IS MeI, not methylene or diiodide anything else.

You might be right but experience shows that not everything you read or see on the net is accurate.

Of course it's possible that the story is accurate but in these days of war on terror, misguidance is also a probability.

[Man Down Under]

Considering how the site is an AOL homepage, hasn't been updated in years, and was written by a professional chemist, I don't think 9/11 has anything to do with it.

It'd be easy enough for someone with the chemicals and a stray animal to test out. :)

[megalomania]

Methyl iodide, iodomethane, methylene iodide, or whatever you want to call it, here are some safety snippets I have collected:

Ranked as one of the most hazardous compounds (worst 10%) to ecosystems and human health.

In humans, acute (short-term) exposure to methyl iodide by inhalation may depress the central nervous system (CNS), irritate the lungs and skin, and affect the kidneys. Massive acute inhalation exposure to methyl iodide has led to pulmonary edema. Acute inhalation exposure of humans to methyl iodide has resulted in nausea, vomiting, vertigo, ataxia, slurred speech, drowsiness, skin blistering, and eye irritation. Chronic (long-term) exposure of humans to methyl iodide by inhalation may affect the CNS and cause skin burns.

Acute Effects:
* Massive acute inhalation exposure to methyl iodide has led to pulmonary edema. Depression of the CNS, irritation of the lungs and skin, and effects on the kidneys may result in acutely exposed humans. (3-5)
* Acute inhalation exposure of humans to methyl iodide has resulted in nausea, vomiting, vertigo, ataxia, slurred speech, drowsiness, skin blistering, and eye irritation. (2,3,5,6)
* Tests involving acute exposure of rats and mice have shown methyl iodide to have moderate to high acute toxicity by inhalation, and high acute toxicity by ingestion. (6)

Chronic Effects (Noncancer):
* Chronic inhalation exposure to methyl iodide may affect the CNS in humans. (4)
* Prolonged dermal contact with methyl iodide may cause skin burns in humans and animals. (1,4)
* EPA has not established a Reference Concentration (RfC) or a Reference Dose (RfD) for methyl iodide.

ACUTE HAZARDS / SYMPTOMS: Inhalation
Cough. Sore throat. Headache. Dizziness. Drowsiness. Weakness. Confusion. Diarrhoea. Nausea. Vomiting. Symptoms may be delayed. The symptoms of central nervous system do not become manifest until days or weeks after exposure. Insufficient data are available on the effect of this substance on human health, therefore utmost care must be taken.

Toxicity
LD50 oral-rat: 200 mg/kg or 50 mg/kg
TLV: 10 ppm air
Toxic, and cutaneously absorbed. When fumes are inhaled, the lung liver, kidney, and central nervous system are damaged, resulting in dizziness, sleepiness, nausea, diarrhea, speech disorder, ataxia, muscle convulsion, etc.
Acute poisoning is caused at 100 ~ 500 ppm in air, and death at 6000 ~ 8600 ppm.

Iodomethane has LD50 for oral administration to rats 76 mg/kg and in the liver it undergoes rapid conversion to S-methylglutathione.[5]

Breathing iodomethane fumes can cause lung, liver, kidney and central nervous system damage. It causes nausea, dizziness, coughing and vomiting. Prolonged contact with skin causes burns. Massive inhalation causes pulmonary edema.

NIOSH REL: 2 ppm (10 mg/m3) TWA [skin]; NIOSH considers methyl iodide to be a potential occupational carcinogen as defined by the OSHA carcinogen policy [29 CFR 1990].
Current OSHA PEL: 5 ppm (28 mg/m3) TWA [skin]
1989 OSHA PEL: 2 ppm (10 mg/m3) TWA [skin]
1993*1994 ACGIH TLV: 2 ppm (12 mg/m3) TWA [skin], A2

Original (SCP) IDLH: 800 ppm

Basis for original (SCP) IDLH: The chosen IDLH is based on the mouse 57*minute LC50 of 860 ppm [Buckell 1950 cited by Patty 1963].

Existing short*term exposure guidelines: 1991 American Industrial Hygiene Association (AIHA) Emergency Response Planning Guidelines (ERPGs):

ERPG*1: 25 ppm (60*minute)

ERPG*2: 50 ppm (60*minute)

ERPG*3: 125 ppm (60*minute)

ACUTE TOXICITY DATA:

Lethal concentration data see: http://0-www.cdc.gov.pugwash.lib.warwick.ac.uk/niosh/idlh/74884.html

Other animal data: In a subchronic study, no rats died following exposures to 150 ppm for 6 hours/day for 3 days [Monsanto 1986].
Human data: None relevant for use in determining the revised IDLH.
Revised IDLH: 100 ppm

Basis for revised IDLH: The revised IDLH for methyl iodide is 100 ppm based on acute inhalation toxicity data in animals [Bakhishev 1975; Buckell 1950; Monsanto 1986]. [Note: The 30*minute and 57*minute LC50 data were used rather than the 4*hour LC50 data so as not to magnify the conservatism already present in the correction factors. NIOSH recommends as part of its carcinogen policy that the "most protective" respirators be worn for methyl iodide at concentrations above 2 ppm.]

REFERENCES:
1. Bakhishev GN [1975]. Relationship between chemical structure and toxicity for some halogenated aliphatic hydrocarbons. Fiz Akt Vesh 7:35*36 (in Russian).
2. Buckell M [1950]. The toxicity of methyl iodide: I. Preliminary survey. Br J Ind Med 7:122*124.
3. Deichmann WB, Gerarde HW [1969]. Table 67. Acute inhalation toxicity of alkyl iodides. In: Toxicology of drugs and chemicals. New York, NY: Academic Press, Inc., p. 756.
4. Monsanto [1986]. Methyl iodide: pilot, 4*week, and 13*week inhalation toxicity studies in rats (ML*81*015, ML*81*084, ML*81*274). 1982*1986. [Unpublished report]. St. Louis, MO: Monsanto Company, Department of Medicine and Environmental Health.
5. Patty FA, ed. [1963]. Industrial hygiene and toxicology. 2nd rev. ed. Vol. II. Toxicology. New York, NY: Interscience Publishers, Inc., p. 1256.
6. von Oettingen WF [1955]. The halogenated aliphatic, olefinic, cyclic, aromatic, and halogenated insecticides, their toxicity and potential dangers. Washington, DC: U.S. Government Printing Office, U.S. Public Health Service Publication No. 414, pp. 30*32.

Toxicology
May be fatal if inhaled, swallowed or absorbed through skin. Highly toxic. May cause cancer. Possible teratogen. Vesicant. May cause harm to the unborn child. Readily absorbed through the skin. May cause sensitization. Severe irritant. Narcotic. Typical PEL ca. 5 ppm.

Toxicity data
ORL-RAT LD50 76 mg kg-1
IHL-RAT LC50 1300 mg/m3/4h
IPR-RAT LD50 101 mg kg-1
SCU-MUS LD50 110 mg kg-1

This last part is very relevant since this data is only a few months old:
see http://www.panna.org/fumigants/mei for the original info
The U.S. Environmental Protection Agency (EPA) registered methyl iodide on October 5th, 2007. The State of California entered methyl iodide into its evaluation process on August 22nd, 2007. The registrations of methyl iodide (also known as iodomethane) are as a new chemical touted as a replacement for methyl bromide for soil fumigant applications. EPA registered methyl iodide despite a concerted effort resulting in a September 25 letter from dozens of distinguished chemists saying that it is “astonishing” that the EPA is considering “broadcast releases of one of the more toxic chemicals used in manufacturing into the environment.” Although EPA announced it would “address recent questions prompted by the pending registration of iodomethane,” it went ahead with the registration a few days later. However, it took the unusual step of registering methyl iodide for only one year. This provides some hope for a reversal of the decision.

Fumigant pesticides are volatile, drift-prone chemicals injected into the soil at application rates of 50-400 pounds per acre. The maximum application rate for methyl iodide is 175 pounds per acre. Chemically related to methyl bromide—a fumigant scheduled for phaseout under the Montreal Protocol because of its ozone-depleting potential—methyl iodide is much more reactive than methyl bromide, reacting with air and water before it can be transported to the stratospheric ozone layer. [1] For this reason, methyl iodide is not an ozone-depleting chemical; nevertheless, there are a number of reasons why EPA should have refused the registration of this chemical.
Help Reverse Methyl Iodide Registration

Arysta LifeSciences is the registrant for the chemical. A preliminary risk assessment was released in January 2006, with a public comment period that closed on February 21, 2006. PANNA submitted both general and technical comment letters to EPA on this pesticide. You can download these letters here:

* Download PANNA's Technical Comment letter on methyl iodide (pdf)
* Download PANNA's General Comment letter on fumigants (pdf)

In addition, over 12,500 individuals weighed in to tell EPA that they did not want this toxic chemical used in their communities and workplaces.

On April 19, 2006, the US EPA announced that it was denying registration for methyl iodide in 2006, and that the chemical might be reconsidered in 2007.

On September 28, 2007, US EPA announced that it had “conducted a thorough scientific evaluation of the soil fumigant iodomethane.” But—apparently in response to the aforementioned September 25 letter from dozens of distinguished scientists to EPA Administrator Stephen Johnson, asking that registration be delayed while an independent panel of scientists assessed the evidence—the Agency briefly delayed registration.

* Quick Background Information on Methyl Iodide
* EPA Health Risk Assesment Report

Recent News on Methyl Iodide Registration:

* Rita Beamish AP article picked up by Fox News, picked up by the Mercury News too, September 25, 2007, prior to registration
* Marla Cone article in LA Times following registration, October 6, 2007
* Stephanie Hoops article in Ventura County Star following registration, October 7, 2007
* Witty opinion piece in the Santa Barbara Independent, October 11, 2007 (note that chloropicrin, not methyl bromide, is a chemical warfare agent)
* New Pesticide, Old Problem, October 12, 2007 (mp3)
Farmers have wanted a replacement for a pesticide that's being phased out because it destroys the planet's ozone layer. Now, EPA has approved a substitute but some leading scientists say that pesticide is highly toxic and too dangerous to use in fields. Living on Earth's Jeff Young reports from Washington.

Public Health Will Be Endangered if Methyl Iodide Begins to be Used

Enough is known about this chemical to predict that its use for soil fumigation will result in unhealthful human exposures. A history of mass poisonings involving other fumigants is part of the basis for this prediction.

For a recent example, consider the 121 people who were poisoned in Nevada on September 26, 2007, even as EPA was days away from its decision on methyl iodide. EPA's proposed buffer zones for iodomethane are at most 500 feet. The farmworkers who were poisoned were in a field half a mile from the one being fumigated. One can readily see from this incident that EPA's maximum 500-foot buffer zones are a fraction of the size that would be required to prevent recurrences of poisonings. Unfortunately, "feasibility" dictates the buffer zone sizes as much as health protection.

Real-world incidents are corroborated by EPA's detailed models which show that the buffer zones they have settled on are inadequate a few percent of the time for those who are unfortunate enough to be in the downwind direction. The game of roulette depends principally on the weather on the day of the fumigation. Light winds and clear skies near sunset lead to "inversions" which keep fumigants escaping from the ground from dispersing. Under these conditions, the models show and real-world incidents confirm that unhealthy concentrations of fumigant gas build up over the field and then slowly drift into neighboring communities.

Unless EPA's decision to approve methyl iodide as a soil fumigant is reversed, farmworkers, rural communities, and new suburbanites whose properties face or abut fields will be at risk, particularly those in States with high fumigant use—California, Washington and Florida. Public health protection should be the primary consideration for pesticide registration, and EPA should use the 1-year registration as an opportunity to reverse its decision on methyl iodide.

Methyl Iodide is Chemically Reactive
Methyl iodide is widely used in chemical synthesis because of its extraordinary ability to react with electron-rich molecules. Specifically, it reacts readily with biomolecules like DNA, the genetic material in cells, in a process that alters the structure of DNA and

Chemists use special techniques to protect themselves while handling even small quantities of methyl iodide in the laboratory.
Source: PANNA Archives

leads to mutations. Synthetic chemists treat this chemical with great respect, handling it only in a hood under an inert atmosphere and using specially sealed bottles and syringes for transfer to ensure that none of this highly toxic chemical escapes. The proposed release of massive amounts of this chemical into the environment is contrary to safe chemical management practices.

Methyl Iodide Will Contaminate Air and Water

Because methyl iodide is highly volatile, it is as drift-prone as other fumigants.[2] As a result, bystander inhalation exposure will be high if this chemical is applied as a soil fumigant. Methyl iodide is also a volatile organic compound (VOC) that will contribute to ground-level ozone, which is known to exacerbate asthma and other respiratory diseases.

Soil fumigation with methyl iodide poses a risk of groundwater contamination as well. A study of methyl iodide-treated soils demonstrated that cumulative volatilization losses from sandy loam soils ranged from 94% of the amount applied in non-tarped soils to 75% in soils covered with high-barrier tarps. [3] Tarping increased downward movement of the pesticide into the soil, which increased leaching into groundwater. The half-life of methyl iodide in soil depends on soil type, from 42 to 63 days for sandy loam soils and 9 to 13 days in soils rich in organic matter. [4]

Methyl Iodide is Acutely Toxic

Methyl iodide affects the nervous system, the lungs, liver, and kidneys. Symptoms of acute poisoning from inhalation include dizziness, sleepiness, nausea, diarrhea, slurred speech, lack of coordination, and muscle convulsions. [5] Methyl iodide is six times more acutely toxic than methyl bromide, and about twice as toxic as 1,3-dichloropropene (Telone).[6] To date, neither U.S. EPA nor California’s Department of Pesticide Regulation have set an acceptable level of human exposure for this chemical, but the National Institute of Occupational Safety and Health has set an eight to ten-hour worker (adult male) exposure limit of 10 mg/m3 based on the chemical's acute toxicity. [6] "Acceptable" exposures for children developed through risk assessment are typically 10-1,000 times lower than those for healthy adult males. EPA has listed methyl iodide as a Hazardous Air Pollutant generally known or suspected to cause serious health problems.

Methyl Iodide is a Carcinogen

The chemical reactivity of methyl iodide mentioned above has biological consequences. Vapors of methyl iodide induce DNA damage and are “mutagenic to bacteria in the presence or absence of an exogenous metabolic system” (the Ames test). [7] Methyl iodide is also commonly used to create mutant mammalian cell lines in the laboratory. [8] Radioactive labeling studies in rats demonstrate DNA damage to the lungs and digestive tract specifically caused by methyl iodide. [9] Because of this chemical reactivity, the National Institute of Occupational Safety and Health (NIOSH) recommended that methyl iodide be considered as a potential occupational carcinogen, [10] and the state of California lists it as a chemical "known to the State of California to cause cancer." [11]

The International Agency for Research on Cancer (IARC) indicates that: "No epidemiological data relevant to the carcinogenicity of methyl iodide were available. There is limited evidence in experimental animals for the carcinogenicity of methyl iodide." Because of this lack of data, IARC lists this chemical as "unclassifiable" as to its carcinogenicity. [12] While there are no recent cancer studies in the primary literature, the older animal studies cited and described by IARC indicate that cancers resulted from exposure to this chemical in all experiments at most dose levels tested, and in some instances from only a single moderate exposure.[13]

"Groups of BD rats (substrain and sex unspecified), about 100 days old, received weekly subcutaneous injections of 10 (16 animals) or 20 mg/kg body weight (eight animals) methyl iodide (purity unspecified) in arachis oil for about one year (total dose, 500 or 900 mg/kg body weight), or a single subcutaneous injection of 50 mg/kg body weight (14 animals), and were observed for life. Four and two animals in the first two groups, respectively (25%), died of pneumonia. Subcutaneous sarcomas occurred in 9/12 rats injected with 10 mg/kg body weight, in 6/6 rats injected with 20 mg/kg body weight and in 4/14 rats given a single injection of 50 mg/kg body weight. No subcutaneous tumor was reported to have occurred in control rats ... injected with arachis oil alone. Local tumors occurred more than one year after the first injection; histologically, these were fibrosarcomas and spindle-cell and round-cell sarcomas. In most cases ... pulmonary and lymph-node metastases were observed."
[IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work).V41 218 (1986)]

Click here to download a summary of the animal studies that have been done to date.

In its recent risk assessment [14] EPA found that methyl iodide caused thyroid tumors, but invoked a previously unheard of cancer ranking -- "Not likely to be carcinogenic to humans at doses that do not alter rat thyroid hormone homeostasis." Download the EPA Cancer Assessment. It is worth noting that the Cancer Assessment Review Committee used only a single study to come to this conclusion -- a study in which 62-66% of the rats in both the control group and the high dose group died during the experiment and only 52-54% of the rats in the other dose groups survived (see p. 11 in the Cancer Assessment), bringing into question the scientific validity of the study. Of particular concern is that the registrant, Arysta LifeSciences, determined the number of tumors caused by methyl iodide only for animals that survived beyond the first year of the study. (See page 7 in the Cancer Assessment, footnote to table 1). In addition to the thyroid tumors observed in the survivors of the study, large and significant changes were observed in thyroid hormone levels, which are intimately tied to metabolic disorders and immune function. EPA did not evaluate the possible health outcomes of these changes. Other toxic effects noted by EPA include respiratory tract and salivary gland lesions, neurological toxicity, reduced body weight, and developmental toxicity (manifested as fetal losses and decreased live births). Download the EPA Health Effects Assessment.

Methyl Iodide Interferes with Metabolic Processes

Several studies indicate that at intermediate doses, methyl iodide interferes with both lipid and glucose metabolism. Injection of male rabbits with 57 mg/kg of MeI for 2 days resulted in a five-fold increase in plasma triglyceride levels, with a significant increase in the very low density lipoprotein (the "bad cholesterol") and accumulation of fatty deposits in the liver. [15]

Another study showed that when methyl iodide was injected into rabbits, basal levels of insulin and glucagons increased, and plasma glucose levels responded abnormally to insulin and glucose injections, indicating disturbances in the regulation of carbohydrate metabolism. [16]

Resources

1. S.R. Yates, Methyl Iodide as a Replacement for Methyl Bromide: Environmental Implications, Agricultural Research Service, U.S. Department of Agriculture, October 15, 1996.
2. The vapor pressure of methyl iodide is 400 mm Hg, compared to 1,800 mm Hg for methyl bromide, 18 mm Hg for MITC and 29 mm Hg for 1,3-dichloropropene (Telone).
3. J. Gan, et al., J. Env. Qual. 1997, 26: 1107–15, as cited in the Hazardous Substances Data Bank, National Library of Medicine.
4. J. Gan and S.R. Yates, J. Agr. Food Chem., 1996, 44: 4001–8, as cited in the Hazardous Substances Data Bank, National Library of Medicine.
5. Methyl Iodide Product Information, Iodine.com.
6. a) Documentation of the Threshold Limit Values and Biological Exposure Indices, American Conference of Governmental Industrial Hygienists, Inc., 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991, p. 1013.
b) Methyl Iodide, Chemical Health and Safety Data, U.S. National Toxicology Program.
7. Methyl Iodide (Iodomethane), Air Toxics Website, U.S. EPA.
8. M.M. Moore, D. Clive, Environ. Mutagen., 1982, 4: 499-519.
9. Carbon-14 labeling studies indicate that methyl iodide methylates DNA, with DNA adducts detected in the stomach, forestomach, liver and lung of male and female rats exposed to [14C]-methyl iodide orally or by inhalation. IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man, Geneva: World Health Organization, International Agency for Research on Cancer, 1999, 71: 506.
10. Monohalomethanes: Methyl Chloride, Methyl Bromide, Methyl Iodide, National Institute for Occupational Safety and Health, September 27, 1984, page 22.
11. California Proposition 65 list, California Office of Environmental Health Hazard Assessment.
12. IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man, Geneva: World Health Organization, International Agency for Research on Cancer, 1986, 41: 222.
13. IARC monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man, Volume 15 (1977), 41 (1986) and 71 (1999).
14. Iodomethane Preliminary Risk Assessment, US EPA, Docket ID #EPA-HQ-OPP-2005-0252, Go to Docket.
15. H. Matsui, et al., Sangyo Igaku, 1982, 24: 85-89.
16. H. Matsui, et al., Hormone Metab. Res. 1982, 14: 676-67.

See the complete list of resources about pesticide drift.

[ccw8076]

Along the poisons route, heavy metal toxicity is only found if tested for a specific metal. There are different tests for say, lead and mercury, and only the most commonly found compounds are tested for. If you really want to kill someone silently, than I would recommend this:

Gold Sodium Thiomalate is a medical compound used to treat arthritis, it isn't used in the states much, but in Mexico and Canada it is plentiful. If you say, sprinkle some of it on the victim's corn flakes a little at a time for a couple of weeks, the victim will succumb to heavy metal toxicity of GOLD. Gold is NEVER tested for during an autopsy, I should know. And unless the target is high priority, the doctors will pass the death off as anything but gold poisoning. The best part of this scenario is that once the heavy metals have been tested, they will be ruled out entirely and therefore any other symptoms relating to the toxicity will be ignored. You go scot free. And no complicated syntheses, and no schedule 1 substance violations.

[ciguy007]

It not only acts rapidly (see press coverage of Kevorkian's early experiments), it is (when pure) odorless, colorless and tasteless. In high concentrations it can cause rapid loss of consciousness. Furthermore about 15% of the people intoxicated to the point of loss of consciousness develop irreversible neurologic sequelae. It's not just a cause of hypoxia. If you experimentally collect dog blood, bubble CO through it until it's 100% carboxyhemoglobin, spurge the CO dissolved in the liquid with an inert gas (say, helium) you can exchange-transfuse a dog using the 100% carboxyhemoglobin up to a concentration of over 50% before you see any symptoms of hypoxia (35% is typically associated with death); and you will not see other neurologic signs.

CO is a brain white matter poison in addition to being a hemoglobin-inactivator. I think its actual and potential toxicity has been underestimated in this forum.

[Torvaun]

No doubt CO is deadly, but it's also fairly obvious. The point of this thread is to leave medical examiners scratching their heads. On that note, I used to work with an ex-pharmacist who had done a great deal of cancer work. He had worked with a chemotherapy drug (which I can't think of right now, to my dismay) which had a maximum safe dose of one molecule. Anyone else know what this one is?

[Charles Owlen Picket]

I think someone was pulling your leg. If you actually have an interest, you could do a hunt for: "DOSE-RESPONSE RELATIONSHIPS IN TOXICOLOGY" and find out the real levels involved and they actually couldn't be a molecule (well, "anti matter" if you like Star Trek) ....TTBoMK.

The most potent poison in the world...
Botulin toxin is possibly the most acutely toxic substance commonly known, with a lethal dose of about 200-300 pg/kg, meaning that somewhat over a hundred grams could kill every human on earth (for perspective, the rat poison Strychnine, often described as highly toxic, has an LD50 of 1 mg/kg, or 1 billion pg/kg).

[Bugger]

I have thought of what would be a completely undetectable poison, if one were to want to kill someone, but make it look like "natural causes" occurring during sleep. This would be plain old CO2, obtainable in large quantities as "dry ice" from firms that compress and solidify or liquefy CO2 emissions from industrial furnaces or thermal power stations. It is undistinguishable from the small amount of CO2 that occurs in the atmosphere, unlike CO (which does not occur naturally in appreciable amounts, and the presence of which may be suspected from a body's color, and thence from pathological examination of the blood for CO content).

To use it, one would have to get a large chunk of "dry ice" in the evening, and, shortly before the victim usually goes to bed, somehow get inside and hide the stuff in his bedroom. The "dry ice" would evaporate as gaseous CO2 during the night, driving away all the oxygen present along with that which would normally diffuse into the bedroom, suffocating the victim but leaving no visible trace of a cause. However, it would work only if all the doors and windows of the bedroom were closed and fairly airtight, so it would be most likely to work in winter in areas which have cold winters.

CO2 poisoning fairly frequently happens when people abseil or climb down into deep vertical shafts in which CO2, which is heavier than air, accumulates from such sources as vehicle exhausts, industrial fuel burning, volcanic emissions, and fires. Such places can be natural pothole-type caves with no outlet at the bottom, old mines with no ventilation system, large industrial tanks, and large sewers.

[Jetex Kid]

Sodium azide is an uncommon poison that may be commonly found among Rogue Scientists, and it works.

The neighbor's aging 80-pound hound bayed relentlessly, day and night. The American judicial establishment does not do barking dogs, except in a lengthy, expensive and uncertain way, which invites alternatives.

First time, one-half gram in a gelatin capsule in chicken. 24 hours later, after no apparent effect, the dose was doubled and wrapped in irresistable bacon. 24 hours after that the barking was very weak and finally ceased. He went out barking to the end.

Probably one gram would have sufficed, which would be a ratio of about 35000-to-1. I think an instant death arouses suspicion, and 24 hours deterioration appears more natural. Also, I doubt they'd look for azide.

A dual-threat chemical that really works.:D

[Charles Owlen Picket]

In bio- science labs azide is generally (commonly) used to clean out Petri dishes and slides; to keep cultures from coming back after autoclaving. At the one gram level to 100lbs body weight it is considered not to be a serious poison on the level of bio-grades; the LD50 if I remember is pretty high like LD50 37 mg kg-1. That's pretty much like any common toxin. The issue with azide is that it is a skin permeable solid but it's not a real heavy duty toxin.
I won't even touch the issue of poisoning a neighbor's dog.....

[Jetex Kid]

Charles, your suggested LD50 of 37mg/kg would seem to be about right. Rosco recounted a female student dying from just one whiff (of HN3?), but I think that's an urban legend. No, azide is not a super poison, but it is efficient in convenient-size doses.

And Charles, unless you are deaf, you too would touch the issue of poisoning the neighbor's dog if this dog lived next to you. I do this of necessity, not for fun.:(

[Jetex Kid]

In WWII, when submarines were forced by to stay underwater too long, 0.5% concentration of CO2 was regarded as potentially fatal, though slow. I assume the 0.5% is volumetric. One cup o’ dry ice would generate 0.5% in a room of 1,000 cubic feet, excluding air changes. I’d have guessed much more. This concentration would cause a very rapid heartbeat and the victim would probably leave the room to seek medical attention. When workers go into a hole and then fall down dead, the concentration is probably well over 0.5%.

Possibly a better way to produce CO2 would be by surreptitious burning to convert O2 to CO2. I also wonder if CO victims might not often be victims of CO2 poisoning as well. However, CO2 poisoning remits with fresh air, and CO poisoning does not.

[ciguy007]

White Phosphorous anyone?

There used to be a rodenticide called "Stearns Electric Paste." It was a preparation of white phosphorous in a greasy carrier - looked a lot like peanut butter. Instructions were to spread it on bread, cut bread into small cubes and place them where rats (oh yeah and small children - duh!) could find them.

We saw a couple of cases that presented first as upper respiratory infections or otitis media. See the kid, prescribe some antibiotics, send them home. A week later they're back and in worse shape. Blood work shows evidence of bone marrow damage. Multi-organ failure follows with death very likely (in my case series n=2 both died).

There was even a somewhat cheesy movie entitled "luminous poison" made about it. The movie exaggerated, but at the end of the day white phosphorous is a very potent protoplasmic poison with a significant latent period, and a prolonged often fatal course.

By the way - regarding methanol: ethanol will block metabolism of methanol to formaldehyde and formic acid. We used to deliberately keep methanol exposures clinically drunk with IV or oral ethanol until they could be dialyzed. There are only a few conditions and/or substances which cause the ion-gap acidosis you see with methanol - a fairly trivial diagnosis if there is a clinical toxicologist or even a competent ER doc around.

[mike-hunt]

Thought I would ad a few ideas of my own on poisoning. I like the idea of making the poisoning look accidental as opposed to undetectable as mentioned in the starting post by Mickey Finn . Few things are completely undetectable and even less will be in ten years time. One relatively easy way if the person is taking any medication that is fatal at a high dose is by replacing a single dose of medication with a concentrated dose. With most medications a high percentage of the medicine is filler where a normal dose may be 10 mg a normal size tablet or cap is around .5grm and a pure or concentrated dose possibly fatal. easy to do with cap's .

The idea of poisonous animals, insects ect is also interesting. In my aria I can think of at least 2 spiders and 2 snakes that would be put down to accidental death but was wondering what if the creature was not common to the area e.g. an Australian death adder bite in the US or American rattler in Australia ? Using venom not commonly found in the aria would make it extremely unlikely that the cause is found as well as the antidote transported to the patient in time .When the cause is found after death it is more likely to be put down to an escaped pet then suspicious death .People love weird pets and as most are illegally purchased investigating where the spider/snake came from would lead to dead ends for police.

[Telkor]

There are some poisons which may be nearly undetectable.

One example ist Nitrosamines. Very toxic, but they are totally decomposed in humann metabolism within a short time. (approximately some hours). Very nasty stuff.
Or KCl injection. As the KCl concentration in blood will rise anyway post mortem, it can't be detected directly. But as it's a really painful procedure, it'll certainly be noticed.

[Giroro]

Potassium is a good one too, my old biology teacher told me this one (wonder why she got the sack...), that if you dissolve Potassium into water, and inject it into someones blood, whilst they sleep, they'll die within 4 hours, and whilst the autopsy will show high levels of Potassium, this will be attributed to the fact that post-humously, the body naturally produces Potassium, so it'll be put down as an unknown death.

Cons: If the autopsy surgeons find no trace of poison, they may (being intelligent), attribute it to pre-humous Potassium injection.

[Hinckleyforpresident]

Potassium is a good one too......

Surely anybody doing an autopsy worth their stuff would check the blood pH and notice that the victim was very very basic.

The same effect could be obtained by simply dissolving KOH or NaOH in water.

[chembio]

What about potassium permanganate? I once read somewhere that 20 grams of KMnO4 could be fatal to most people.

So maybe an aqueous solution containing more than 20g of the stuff could be delivered into the target via injection/IV?

Also, I once cultivated a supposedly highly-toxic plant called 'Angel's Trumpets' Brugmansia sp.. The tropane alkaloids it contains are a form of hallucinogen, but I wonder what they could do if administered intravenously? I'm thinking along the lines of several syringes of sap extract here.

Plus, it's a common tropical shrub, so any possible victims might be written off as having accidentally poisoned themselves by handling it. Heck, give someone a pot of the flowers as a gift, then off them :p


Just my 2 cents :)

[joffe]

What about potassium permanganate? I once read somewhere that 20 grams of KMnO4 could be fatal to most people

That doesn't seem like a great idea to me. If you need 20 grams of it to administer a fatal dose, it can hardly be classified as a poison. And if you dissolve it in an aqueous solution, you'll have to increase the dosage accordingly.
So how are you planning to administer the poison to the victim? I can't see any other way than strapping him to a bed and administer it via IV and he might no lie down willingly. And it's hardly a subtle substance either - his veins will probably turn purple.

[Roy Paci]

if you dissolve Potassium into water, and inject it into someones blood, whilst they sleep, they'll die within 4 hours,


Mmmh.. I think that when talking of potassium we only need to consider the meq of K+ we are administering. And if I'm wrong I just threwn some years of my life away.
But we need to consider the duration of the administration. A pair of healthly kidneys can overcome variations of electrolytes concentration in the blood. So you have to inject K+ quicker than kidneys can piss it off your blood.

And pH varies a lot in a corpse!

[Bugger]

Also, I once cultivated a supposedly highly-toxic plant called 'Angel's Trumpets' Brugmansia sp.. The tropane alkaloids it contains are a form of hallucinogen, but I wonder what they could do if administered intravenously? I'm thinking along the lines of several syringes of sap extract here. Plus, it's a common tropical shrub, so any possible victims might be written off as having accidentally poisoned themselves by handling it. Heck, give someone a pot of the flowers as a gift, then off them.
I have that plant (white trumpet lily tree) growing wild on my property in New Zealand. It requires fertile soil, moderately high rainfall, and an absence of frost.

[n1000]

On the same vein as utilizing CO2 as a poisioning agent. If you've got access to the target's sleeping room or could slip a mask on, why not just use pure nitrogen gas? The unopposable urge to breathe when you hold your breath, for example, is triggered by a buildup of CO2 causing gasping, and epinephrine release...certain to wake you up. A remotely triggered valve on even a modestly sized N2 tank could purge a room of oxygen quite quickly, someone sleeping inside would inevitably suffocate to the point of brain damage or death without waking

On an unrelated note, I think that these long acting poisons offer much potential. Benzene smells nice, and chronic exposure could be achieved using a benzene-based perfume in one of those plug-in air-fresheners.

Lowered blood count, anemia, damage to bone marrow...ultimately leukemia. It's a nice flat molecule which can slip between nucleobases, breaking DNA strands.. I believe it has nasty effects on the liver, kidneys and brain too.

I don't need to mention how accessible the stuff is, I mean... C6H6 for crying out loud! It blows my mind that the biologically ubiquitous 6 membered aromatic ring is so damn bad for you!

[Roy Paci]

I can't understand your point on CO2.
If your point about N2 is: no CO2 breathen, no urge for breathing, you are wrong.

Low oxygen--->hypoxia(anaerobic methabolism-----> acidosis)--->feeling of distress, tachipnea, polypnea, tachicardia, raising pulmonary arterial vessels pressure to elevate lungs perfusion

If hypoxia is mantained, pulmonary oedema. Any of the reported consequences of hypoxia is reversible by having the subject going to an ambient with a normal concentration of O2.


IMO the feeling of discomfort is strong enough to wake someone up.
You can try placing a plastic bag on you head. The CO2 speeds up things but doesn't modify them substantially. At one point you'll be feeling like you've been holding your breathe for a long time and will find it's annoying. Before loosing consciousness remove the bag(operate in order to get the plastic bag opening spontaneously if you pass over and you are alone). In a couple of breathes your status is almost completely restored.


Like when climbing mountains over 3000.

[ccw8076]

I believe that the concept of a "perfect poison" only really applys when used in the context of a subsequent police investigation. If your poison is a N2 tank or some CO2 apparatus, then the police will hardly think that the person died naturally; and if your method of poisoning leads the police to your doorstep, then it cannot be truly considered a "perfect" method of assassination. That is why the original posts in this thread dealt with toxins with no traces.

Also, if you used straight nitrogen, the blood would eventually become saturated, and the police would be aware they were looking for someone who had ready access to nitrogen, and the time and inclination to rig a such a system in the victims home.

[ironhyde]

Palytoxin and Maitotoxin looks like good candidates for perfect toxins

[Telkor]

What about ergot toxins?

Horribly toxic, undetectable after a few hours, and a huge variety of symptoms.

[Hinckleyforpresident]

What about ergot toxins?

Horribly toxic, undetectable after a few hours, and a huge variety of symptoms.

Ergotism - or St. Anthony's Fire - doesn't always kill... It is far more likely to make you go nuts and give you nasty seizures and convulsions. However, ergotism can constrict blood vessels, and cause gangrene (potentially lethal) as a result.

Generally speaking, ergotism is a recognized ailment. It is sometimes confused with mercury poisoning though.

On a slightly different note; how about distilled water as a perfect poison? When injected into the bloodstream, dH2O will cause blood cells to rupture - sometimes leading to death.

[ccw8076]

On a slightly different note; how about distilled water as a perfect poison? When injected into the bloodstream, dH2O will cause blood cells to rupture - sometimes leading to death.

While this is true for red blood cells, cells which make up the lining of the vessels themselves will not succumb to hemolysis in pure water, and practically speaking, it would take an enormous amount of pure water simply injected into the blood stream to cause the kind of damage which would lead to a condition either of hypoxia or a massive blood clot. In either of those cases, the conditions can be treated relatively quickly and are fairly easily detectable.

Long-shot though, if you injected distilled water mixed with potassium ions, to greatly speed passage of water along the aquaporins, in the internal carotid artery, which is just slightly above the 4th cervical, then you could potentially cause a lethal clot in the blood brain barrier.

[Alexires]

Otherwise set up a drip to inject water on the way to the brain. Target the bit that is most vulnerable as opposed to flooding the whole body.

*chuckle* Person is brain dead, but everything else is untouched.

Edit: That's random. It appears we appreciate the same literature, ccw.

[Vitalis]

Perhaps I'm mistaken, but I thought the point of the "Perfect Poisons" thread was to determine a poison that would cause death and not be detectable after death or at least be easily explained as to why the substance was in the person's body.

20g of KMnO4 couldn't be easily explained, nobody would ingest that amount by accident.

Same goes for injecting several syringes of Tropane Alkaloid containing plant material. The injection wounds would be obvious, plus the amount of alkaloid in the body would be insanely high. Unless the person was known as an idiot who would do anything to get high, nobody will believe they got such a huge amount of Tropane Alkaloid in their body.

If your mark enjoys their fugu, I would like tetrodotoxin, a little extra in their fish goes a long way...


What about potassium permanganate? I once read somewhere that 20 grams of KMnO4 could be fatal to most people.

So maybe an aqueous solution containing more than 20g of the stuff could be delivered into the target via injection/IV?

Also, I once cultivated a supposedly highly-toxic plant called 'Angel's Trumpets' Brugmansia sp.. The tropane alkaloids it contains are a form of hallucinogen, but I wonder what they could do if administered intravenously? I'm thinking along the lines of several syringes of sap extract here.

Plus, it's a common tropical shrub, so any possible victims might be written off as having accidentally poisoned themselves by handling it. Heck, give someone a pot of the flowers as a gift, then off them :p


Just my 2 cents :)

[Telkor]

Ergotism - or St. Anthony's Fire - doesn't always kill... It is far more likely to make you go nuts and give you nasty seizures and convulsions. However, ergotism can constrict blood vessels, and cause gangrene (potentially lethal) as a result.



Ergotism is caused by a chronic low dose exposure, but most of the ergot toxines affect neurotransmitters and will be lethal at a high dose.

Ergine, for example, would cause a circulatory collapse.

[ironhyde]

hello people i was googling on palytoxin and found this on wiki

Palytoxin targets the sodium-potassium pump protein by binding to the molecule such that the molecule is locked in a position where it allows passive transport of both the sodium and potassium ions, thereby destroying the ion gradient that is essential for most cells.

Typical symptoms of palytoxin poisoning are angina-like chest pains, asthma-like breathing difficulties, tachycardia, unstable blood pressure, hemolysis (destruction of red blood cells), and an electrocardiogram showing an exaggerated T wave. The onset of symptoms is rapid, and death usually follows just minutes after.

more on it here
http://en.wikipedia.org/wiki/Palytoxin
so i was thinking if somebody was poisoned with this then pigs may not suspect anythiny.:D:confused:

[Hinckleyforpresident]

Ergotism is caused by a chronic low dose exposure, but most of the ergot toxines affect neurotransmitters and will be lethal at a high dose.

Ergine, for example, would cause a circulatory collapse.

Could you cite a reference for the toxicity of ergine and other lysergic acid amides? I have never heard of compounds in the same class as LSD being potentially lethal. To my knowledge, the LD50's for all of them are way to high to ever reasonably OD.

However, clavine compounds can kill. But even still, the alkaloid contents of most ergot-compound containing plants and fungi is very low. And the majority of the alkaloids extracted would be LSA's, not lysergic clavines. So either the victim would have to unknowingly ingest a large amount of the raw plant/fungus, or the criminal would have to extract from a large amount of biomass.

Here is a reference for the toxicity of clavines (link (http://www.curehunter.com/public/pubmed6442580.do)).


Pharmacological investigations of the ergot alkaloid of the group of clavines, elymoclavine, isolated from Claviceps sp. cp. II showed the following results: The LD50 for mice for 24 h was 350 (228-535) mg/kg and for rats 145 (81-258) mg/kg. Elymoclavine induced a dose-dependent stereotypy (doses of 2 to 10 mg/kg) in rats and mice which was antagonized by haloperidol and pimozide. It prevented the development of haloperidol catalepsy in rats and produced rotations contralateral to the striatal lesions with 6-OHDA which were antagonized by pimozide and partly by cyproheptadine. Elymoclavine, like bromocriptine, decreased the plasma level of prolactin. Furthermore, elymoclavine increased the exploratory activity of rats in open field; this effect was antagonized by haloperidol and was essentially influenced by many substances acting on different transmitter systems (NA, DA, GABA). Elymoclavine inhibited the picrotoxin and electroshock convulsive seizures but potentiated the pentylenetetrazol ones in mice as these effects were differently influenced by pimozide, haloperidol, 5-HTP, atropine and phentolamine. 100 and 250 micrograms/kg of elymoclavine produced a considerable and persisting decrease of the blood pressure in anaesthetized cats. At 1 X 10(-6) M, without producing any per se effect, elyoclavine decreased the contractile effects of acetylcholine, nicotine, BaCl2 and PGE1 as well as the field electrical stimulation-induced contractions in an isolated segment from guinea-pig ileum. The observed effects of elymoclavine are mainly due to its dopaminergic agonist action. It seems, however, that influences on other transmitter receptors also underlie the mechanism of action of this ergot alkaloid.

[Alexires]

hello people i was googling on palytoxin and found this on wiki
.... may not suspect anythiny.:D:confused:

While you are at it, how about you look up capitalisation, spelling, punctuation and I/i failure on your one week break from The Forum?

[Telkor]

Could you cite a reference for the toxicity of ergine and other lysergic acid amides? I have never heard of compounds in the same class as LSD being potentially lethal. To my knowledge, the LD50's for all of them are way to high to ever reasonably OD.



Well, LSD itself isn't very toxic for humans.
A dose about 0,3 gram would kill an elephant (most likely through respiratory arrest), while a human being would survive.

However, other ergolines are more toxic. An amount of 5-10 gram of Claviceps purpurea are lethal, that equates 10-100 mg of toxines, depending on concentration.

The less toxic amides and similar derivatives can also be decomposed with light to become more toxic.

Ergolines can be extracted from ergots or morning glory with a tincture of ethanol and white spirit.


References:

http://www.landwirtschaft-mlr.baden-wuerttemberg.de/servlet/PB/menu/1156947_l1/index.html

http://www.thunemann.de/martin/lsd/Kapitel2.htm

[fluoroantimonic]

Well if you're looking for an effective poison sodium monofluoroacetate (known as 1080) fits the bill nicely. Depending on how suspicious the death is, there is a good chance that it would never be detected.

"If the treatment is delayed until severe symptoms of poisoning appear, the patient is almost certain to die."

"Currently there are no very effective decontamination treatments or antidotes for
1080."

300mg will surely be deadly to a human in a couple hours. The symptoms are somewhat similar to a heart attack, but I don't know if an experiences professional would mistake it for heart attack. As far as I have found it has basically never been used as a murder weapon, so I seriously doubt anyone would think of it as a suspect until it was much too late, if at all. It is quite soluble in water and has no color or taste supposedly.

I don't know if there is a test that detects it in the body after death, it is mostly retained unchanged, a small fraction is metabolized to fluorocitrate which is what fucks up on of the enzyme that run the Krebs cycle. Even if there was a test for it I doubt it would be performed, its symptoms are not particularly distinct.

Getting ahold of some might not be easy though, it is not widely used anymore (unless you're in New Zealand). It can apperently be made by direct fluorination of malonic acid in water, but that would be a major headache. But then again you wouldn't need much...

[mike-hunt]

Hears an interesting site I found for a venom supplier.
Http://www.latoxan.com/
I couldn't add it to above post #101 as edit feature has expired.

I wonder how customs would respond if I attempted to import 10 grams of death adder or rattle snake venom into Australia? :D

[Vitalis]

Yea, ordering poisons from a poison selling website usually attracts unwanted attention... ;)


I wonder how customs would respond if I attempted to import 10 grams of death adder or rattle snake venom into Australia? :D

[Alexires]

Getting ahold of some might not be easy though, it is not widely used anymore (unless you're in New Zealand).

It is pretty common in Aus, practically lying around forests and parks.

Find a farmer with a rabbit problem, I'm sure he would be able to help you out.

[ccw8076]

Okay,

I just had a thought. Ethidium Bromide is a compound that is used in gel electrophoresis. It is so used because it directly adheres to a double stranded DNA molecule. It has the perfect capability of a great poison. If one could add a nitrile (c-N) molecule to it, then you could theoretically have cyanide inside of the nucleus of a cell, and mutating DNA. It would not be a "perfect" poison say, but it would be a very effective way to kill someone, as it is nigh impossible to un-mutate a DNA molecule

"Ethidium bromide is thought to act as a mutagen because it intercalates into double stranded DNA, thereby deforming the molecule. This is believed to block or trip biological processes occurring on DNA, like DNA replication and transcription." -wikipedia

http://en.wikipedia.org/wiki/Ethidium_bromide

[Bugger]

Well if you're looking for an effective poison sodium monofluoroacetate (known as 1080) fits the bill nicely. Depending on how suspicious the death is, there is a good chance that it would never be detected.(cut)
300mg will surely be deadly to a human in a couple hours. The symptoms are somewhat similar to a heart attack, but I don't know if an experiences professional would mistake it for heart attack.(cut)
Getting ahold of some might not be easy though, it is not widely used anymore (unless you're in New Zealand). It can apperently be made by direct fluorination of malonic acid in water, but that would be a major headache. But then again you wouldn't need much...
1080, or CH2FCOONa, is the poison of choice here in New Zealand for killing the introduced Australian brushtail opossum on a large scale, especially for aerial application from fixed-wing aircraft or helicopters. This species of opossum is New Zealand's number one introduced pest, because of the enormous damage they do to native tree species (which do not contain any eucalyptus oil to discourage browsing), because they eat ripe fruit in orchards, because they take the eggs of native birds, and because they spread bovine tuberculosis among cattle with which they can come into contact.

They were introduced into New Zealand's North and South Islands (but not the smaller islands) because some idiot about 100 years ago thought that their fiber and pelts would make a great fur industry, This, however, has proved to be only marginally economic because of the rugged terrain of the bush where they mostly live. Because 1080 does not kill immediately, harvesting them for fur is instead done by either trapping or instant-killing cyanide paste instead.

They are, surprisingly, a protected species in Australia, despite the enormous damage they must do there also; except for Tasmania where hunting and poisoning and trapping them is allowed. The Tasmanian sub-species, more prized due to its longer and darker fur, was the one introduced into New Zealand's South Island. They, and other marsupials, are not found on offshore Australian islands like Norfolk Island, Lord Howe Island, MacQuarie Island, and Christmas Island.

[fluoroantimonic]

especially for aerial application from fixed-wing aircraft or helicopters.

They used to use it here in Alaska in a similar application to kill off wolves when they got to thick. Pack a bunch of beaver carcasses with it and chuck them out of an airplane every so often. Come back and and there'd be a whole ring of dead animals around it, many of them not wolves. Back in the good old days...

Another poison I like the sounds of is nicotine. Being deadly in 50-100mg doses and being very easily absorbed through skin gives some interesting possibilities. Also its absorption is known to be greatly enhanced by thinks like DMSO. Interestingly skin that has been treated with "Nair" has much faster absorption and is more likely to cause an overdose.

[iHME]

Nicotine is pretty classic probably.
I have read from a 70 ties trash novel how someone poisoned some other with nicotine in coffee, so the idea is hardly new.

Nicotine does have it's benefits, the dry distillation from tobacco is easy, a 7th grader could do it. (our science teacher demo'ed it for us back then)

If the victim is a chain smoker or similar the unnaturally high nicotine levels MIGHT go unnoticed. But I would not count on it.

[hatal]

I have topic related question. Dichloromethane (used as paintstripper) supposed to have pain-relieving properties in moderated doses (if inhaled) and higher exposure can result in death. Thickie-pedia also states it is not flammable but it produces poisonous gasses if burned. I haven't been able to find more information except the CAS-sheet. Does anyone have a few sources on dichloromethane and its combustion?

[Telkor]

I have topic related question. Dichloromethane (used as paintstripper) supposed to have pain-relieving properties in moderated doses (if inhaled) and higher exposure can result in death. Thickie-pedia also states it is not flammable but it produces poisonous gasses if burned. I haven't been able to find more information except the CAS-sheet. Does anyone have a few sources on dichloromethane and its combustion?

DCM is quite similar to Chloroform.

It will decompose into Phosgen gas and cause severe (or lethal) damage to the lungs.

[fluoroantimonic]

Dichloromethane (used as paintstripper) supposed to have pain-relieving properties in moderated doses (if inhaled) and higher exposure can result in death.
So will most other chlorinated solvents...

Thickie-pedia also states it is not flammable but it produces poisonous gasses if burned.

Also, so will almost any chlorinated solvent, and IIRC the products consist of a complex mix of various nasty chlorocarbons, some oxides, and maybe some phosgene.

[Vitalis]

As mentioned, nicotine would do it, but if it's in DMSO you better be careful not to get any on yourself. Or you could inject it. It's an alkaloid so it will taste like shit and show up easy in any blood-work.

Nobody would buy that even a heavy smoker smoked so much that they poisoned themselves to death by nicotine poisoning.

[FUTI]

Getting high on DCM would be so fucking stupid taking into acount how quickly he would take your kidneys out of business.

Friend of mine was taking those nicotine patches in attempt to quit smoking. Let's say that according to witness report leaving patch on your skin when you go to sleep is certain to cause strange and wild dreams. So I guess person would notice something is deeply wrong there if someone apply DMSO solution of nicotine on them.

[-=HeX=-]

As for nicotine, being a smoker I can testify to its wierd effects. Once, after not smoking for a week, I had twenty in one 'session', chain smoking them sans filter. I ended up with a splitting headache, cramps, nausea and a really sore throat. The cigarettes were a strong brand, 'Banson and Hedges Gold' and normally I would only have one or two. After 5 or so I had the 'Nicotine Rush' (the term sed by my associates) from hell, and my perception was a bit messed up. Not my smartest thing to do... If thats only from inhaling the stuff, god only knows what ingestion is like. A member here tried the nicotine syrup to off himself and only ended up with a headache and a feeling of being 'Buzzed'.

NBK posted about DCM being part of a CW he came up with, search 'MCX, the triple threat agent' or something like that. I read a post saying how a spraygun loaded with DCM sould be used where you want to knock someone out, but where killing is acceptable too. I also read of how DCM was even considered as an anastethic for surgury.

I have seen in many places that DCM decomposes to phosgene, could refluxing DCM at slightly over its decomp. temp be a method of making crude phosgene? I envision a reflux condenser with the DCM and Anti-Bump granules (dont know why we use them, but my chemistry textbook always includes them in refluxing) in the round bottom flask and the reflux column attached to that with a condenser. The DCM would be refluxed for a while then the phosgene or impurities distilled off. Would that work?

Here is a qute from wiki on the toxicity of DCM:

Dichloromethane is the least toxic of the simple chlorohydrocarbons, but it is not without its health risks as its high volatility makes it an acute inhalation hazard. Dichloromethane is also metabolised by the body to carbon monoxide potentially leading to carbon monoxide poisoning. Prolonged skin contact can result in the dichloromethane dissolving some of the fatty tissues in skin, resulting in skin irritation or chemical burns.

Least harmful? I wonder if the more harmful ones are OTC? Here is a link to a toxicology report on it: http://www.atsdr.cdc.gov/toxprofiles/tp14.pdf its from the US department of Health and Human resources. It has a fair lot on its effects on children from a quick flick through. Here is its MSDS: http://www.temarry.com/MSDS/Dichloromethane_msds.htm

Here is its LD50: LD50 (ORAL, RAT) IS 1500-2500 MG/KG
and some other interesting data:
Signs/Symptoms Of Overexp: IRRITATION, NAUSEA, VOMITING, HEADACHE,
DIZZINESS, SKIN DEFATTING AND BURNS, ELEVATED CARBOXYHEMOGLOBIN LEVELS, WEAKNESS.

That was copied from its MSDS. Here is its Sigma page: http://www.sigmaaldrich.com/catalog/search/ProductDetail/ALDRICH/270997

More links with good data on DCM:
http://msds.chem.ox.ac.uk/DI/dichloromethane.html
http://www.jtbaker.com/msds/englishhtml/D2895.htm
http://www.sigmaaldrich.com/sigma/datasheet/proligo_msds2_dca-deblock.pdf
http://www.inchem.org/documents/jecfa/jecmono/v48aje17.htm
http://www.lomb.com.au/Dichloromethane.pdf

Its decomp is 120 degrees celcius so I would reflux at 130 degrees celcius.
Here is a link on its decomp:
http://pubs.acs.org/cgi-bin/abstract.cgi/esthag/2001/35/i06/abs/es0011414.html

COCl2 is phosgene BTW. I wonder where the NOx came from...

I personally think that Parathion and DMSO mixed makes a good toxin, an associate placed 1ml on a stray dogs spine, it died in 15 minutes or so. Sick bastard... At least it was not a dog! Here in ireland we have cases of clikdren drinking herbicide occasionally, most die painfully within a week, even with medical attention. I will research more when I have the time to do so.

I also like ingestion of PS (chloropicrin) as a 'pain' toxin. it causes extreme pain as it erodes the intestinal lining, causing them to 'shit blood' fot a long time. And PS is easily OTC, as Mr Samosa showed in his 'Jam Jar Chloropicrin synth'.

Thats all from me for now, I should have more later. Hope the typo's are few and far between.

[FUTI]

Hex nice thinking few good idea and couple misconceptions. DCM boils at 44 degrees Celsius AFAIR. You can't heat it to 130 degrees Celsius. You can distill it through a tube which is heated to that temperature though, but be cautious not to cause explosion or fire. Making COCl2 is partial combustion, don't make is complete disaster. Anti-bump granules are there to prevent splashing of liquid caused by overheating... generally you are placing a source or point where will the steam bubbles will form in your liquid. Trichlorethylene and Chloroform are more toxic and that is true, but DCM still have chronic exposure problems in major league. I apologize as I strayed outside of topic, but DCM as junkie juice was hilarious.

DMSO and Acetonitrile are solvent of choice when you want skin penetration... the second one was used in USSR for weaponization of some CW agents I think.

[javainmycoffee]

What about KCl.

It is undetectable because it disassociates into Potassium and Chloride ions in the body. Both of which are naturally in the body. They use it in lethal injection of prisoners (pray for NBK) in conjunction with a barbiturate and a muscle relaxant. The last two are simply for redundancy and to assure the mourning family that the is no pain.:rolleyes:

The mechanism of action is to depolarize muscles, specifically the heart, causing cardiac arrest. The lethal injection dosage is 100 mEq, but I don't know how that translates to molarity. All I know is that it is small.

Pros: Sold as a table salt substitute for sodium challenged people, occurs naturally in the body anyway, small dosage is needed

cons: Must be injected

[iHME]

Now, did you read the whole thread? Did you? Well KCl injection was mentioned and discussed a few pages back.

[javainmycoffee]

It was more mentioned than discussed. I wanted to add some more information on it because I don't think enough was given.

I read and searched the thread by the way.

[sandm4n]

I read that if you ingest a few seed of this plant causes instant death to humans....read it for yourselfs (pardon my bad english)
I also read and did some research on VX the nerve agent used by the military, to survive from a drop of this nerve agent you have to be given the antidote almost instantly after the drop has touched your skin otherwise you will die, the major problem is, it is very dangerous and hard to produce this nerve agent. Only scientist with the proper technology and modern laboratory advances produce it....

[totenkov]

Datura is very unlikely to kill you; let alone instantly. There have been a few report deaths, but those who did where administered astronomical doses. Datura is a strong dissociative and deliriant. I can testify to these effects because I have had a horrid experience with the plant.

I cannot say for certain the exact amount because I was already extremely impaired. It was made into a tea, extremely bitter and unpleasant. The effects came on slowly, in such a way that I did not realize I was hallucinating until my friend made me aware of it. For the next 4 hours I was extremely uncomfortable, twitching, itchy and very unaware of my surroundings. I began to fall into a "dream like" state, like I was falling in and out of consciousness and awareness as we know it. The effects were horrid. With auditory and visual hallucinations that kept on getting more intense. It was like I was stuck in a vacuum, unable to get out; trapped in these horrid effects for what seemed like centuries.

After a complete 6 hours I was coherent enough to converse with people around me. I was exhausted and still very uncomfortable. Apparently I would start talking, make absolutely no sense, rambling and babbling like a lunatic. Wanting to jump up and run, thankfully I was with people that are excellent sitters and were able to restrain me.

It was foolish, poorly thought out, and a stupid decision to try the substance, however it gave me new faith that there are things in this world that will still knock me on my ass. :p

That being said, if you attempt to poison someone with Datura, you will send them through a hellish experience, however chances are they will live to talk about it.

[sandm4n]

Datura is very unlikely to kill you; let alone instantly. There have been a few report deaths, but those who did where administered astronomical doses...


You are very correct; I have done a little more research on Datura, and found out that in order to consume a fatal dose and die instantly you have to ingest about 3 or 4 seeds of this plant. Yet I do not think a intelligent person would eat that many seeds and not realize it.

I don't know if it has been mentioned here, but a plant called Oleander is known to be the deadliest plant on the planet. It contains various toxins; including nerioside, oleandroside, saponins, and cardiac glycosides. Just one leaf can kill an adult.

Another deadly plant is Rosary Pea, its red seeds contain the very known lectin called Abrin, only one seed will cause death in a short period of time.

Daphne, also called Spurge Laurel is very toxic also, consumption of the leaves or fruits will cause nausea and violent vomiting, followed by internal bleeding, coma and death. It is very rich in the toxin Mezerein.

**************************

Poorly written posts lead to bans. I will not be making your posts more readable in the future.

-Hinckleyforpresident

[Intrinsic]

I don't know if it has been mentioned here, but a plant called Oleander is known to be the deadliest plant on the planet. ----- Just one leaf can kill an adult.


What is your source for this? I found a handful of references on the toxicity, and the couple of LD50s I found referenced were all greater than 150mg/kg. This hardly seems to qualify it as "the deadliest plant on the planet". (Although I did see that particular quote on wikipedia). :rolleyes:


It is well known that abrin (and along the same lines, ricin) is acutely toxic. Both are commonly stated to having LD50s of 1-3ug/kg. These are both from plants, although how much toxin each seed might hold I couldn't find. Do you have a reference to how much toxin is in each leaf of Oleander?

[hatal]

Tropane alkaloids extracted from nightshades are a much better choice than just using the juice of datura. There is a hugh variety of highly toxic tropane alkaloids. There is also an extraction a synth posted somewhere.

[Cobalt.45]

What is your source for this? I found a handful of references on the toxicity, and the couple of LD50s I found referenced were all greater than 150mg/kg. This hardly seems to qualify it as "the deadliest plant on the planet". (Although I did see that particular quote on wikipedia). :rolleyes:
This is off topic, but if the only source that can be sited is wiki, the subject in question should be still in doubt. Serious doubt.

Wiki alone is not a valid source, IMO. There should be a mandate that if wiki is the sole source, it has to be disclosed. Of course, sources should be sited in any event.

[hatal]

Personally I dont trust Thickie at all, not mention in the field of science. Its credibilty is far from acceptable. But its still a valuable tool to find the "obvious" quickly and related material.

[Telkor]

Nicotine is pretty classic probably.
I have read from a 70 ties trash novel how someone poisoned some other with nicotine in coffee, so the idea is hardly new.

Nicotine does have it's benefits, the dry distillation from tobacco is easy, a 7th grader could do it. (our science teacher demo'ed it for us back then)

If the victim is a chain smoker or similar the unnaturally high nicotine levels MIGHT go unnoticed. But I would not count on it.

I wonder if somebod tried to hide some pure nicotine or nicotine sulphate in a cigarette. It wouldn't be noticed that easily, and the victim would inhale pretty much of it.

[c.Tech]

the major problem is, it is very dangerous and hard to produce this nerve agent. Only scientist with the proper technology and modern laboratory advances produce it....

:rolleyes: I believe lots of the people on this forum are very skilled, some have even synthesizesd nerve agents before.

It can be done but isn't very practical.

I wouldn't like to handle nerve agents. But you will need atropine shots ready if you do chose to make it, that will put use to your datura. :)

[Vitalis]

IMO, synthesizing nerve agents is just attempted by most to try to be a hot-shot. A biological agent would be easier and if contagious it does the work for the attacker after released by some crazy nutjob.

[megalomania]

I have research experience with organophosphorus chemistry under the tutiledge of a highly skilled expert PhD chemist, and we have discussed chemical weapon synthesis at length. Even he balks at the thought of making a nerve agent. These compounds are just too dangerous to even experiment with. I highly doubt anyone outside of our fedgov visitors have synthesized a nerve agent.

Blood, vomit, or blister agents perhaps, but not nerve gasses. I am not saying it can't be done, it certainly can, but the risk of accident is not worth it. If you are suicidal, as in suicide bomber suicidal, this would be one hell of a way to go out. International media coverage would be outstanding.

I wonder if they screen for chemical weapons on airlines? A small vial of nerve gas would be very easy to smuggle on board. When released into the small enclosed space of an airplane everyone on board would be dead in a matter of minutes, maybe less. A few hijackers with atropine might live long enough to crash the plane into something, but that plane will crash one way or another.

[slarter]

The military used to conduct CW training at Huntsville, AL where they would dress you out in the M3 TAP Suit (Toxicological Agent Protective) walk you into a small room on the range with a rabbit in a cage, where they would crack a small ampule of Nerve agent (GB IIRC). Within seconds the rabbit would start twitching and would be dead in about a minute. :eek: One of the scariest things imaginable. The only thing I fear more than chemical weapons are biological ones.

[joffe]

Talking about CW onboard airlines. The late Pakistani Brigadier Mohammad Yousaf claimed that Pakistan's former dictator Zia-ul Haq was assassinated when a military transport plane carrying him and several aides crashed. The assassination was carried out as follows; one of the pilots' coffee thermos was replaced with one filled with sarin. An obvious inside job, but it shows that nerve gas and airplanes are a bad combination.

[Telkor]

Crocin and Safranal might be suitable.

Though Saffron itself isn't very toxic (20 grams are lethal), the pure Terpenes will work well, and cause the symptoms of a Hepatic encephalopathy:

Confusion, euphoria, followed by apathy, damage to the CNS, organ failure, finally coma and death. Necrosis and haemorrhage may occur.

Safranal can be synthesized using citral, but extracting will be easier.

[TheSavageHyena]

Originally Posted by sandm4n
I have done a little more research on Datura, and found out that in order to consume a fatal dose and die instantly you have to ingest about 3 or 4 seeds of this plant. Yet I do not think a intelligent person would eat that many seeds and not realize it.

I somehow doubt you did any research on Datura or any of the other tropane alkaloids. Although the required doses vary highly from plant to plant, 3 or 4 seeds will hardly even produce any notable effects.

I suspect that perhaps 3 seed pods would cause ill effects (bearing in mind each pod may contain 50-100 seeds). The seeds resemble that of a bell peppers'.

http://www.erowid.org/experiences/exp.php?ID=850
(2 tbsp. vs. 135lbs)
http://www.erowid.org/experiences/exp.php?ID=17700
(150 seeds)
http://www.erowid.org/experiences/exp.php?ID=61125
(4 tsp. vs. 140lbs)

These people lived to tell about it, not to mention the countless references and a very helpful FAQ section.

Originally Posted by totenkov
After a complete 6 hours I was coherent enough to converse with people around me. I was exhausted and still very uncomfortable.

Compared to the many reports I've read, you got off very easy. 6 hours is a long time to trip out but very short lived by Nightshade standards. The first report I cited shows the subject tripping out for 2 1/2 days IIRC.

As was noted here before. This plants' use as a weapon would be best utilized if the tropane alkaloids were extracted and concentrated requiring a very small (physical) dose. It is a very versatile plant that grows in almost every back yard, so availability is never a question.

[pacer]

Obtaining it may be problematic. In addition, this substance (D2O) must be kept sealed since it absorbs normal H isotopes from air moisture and gets diluted over the time.

Chloroform comes to my mind. If administered to a sleeping victim by placing a towel saoked with chloroform on his/her mout/nose, s/he shall pass out. However it is detected by the forensic scientiests if suspected, I believe.

Ok, I know I am new here, but I have been surfing for awhile...and I have yet to find the answer to this question I have...

How long is Chloroform detectable in the body?

[Alexires]

pacer - UTSFE. I don't blame you for not finding it though, it was difficult to track down. Here is your answer.

"Chloroform is well absorbed, metabolized, and eliminated rapidly by mammals after oral, inhalation, or dermal exposure (IPCS, 2000b). In humans given a single oral dose of 0.5 g chloroform, about 50-52% of the dose was absorbed, and virtually all of the absorbed dose was metabolized to carbon dioxide. Blood levels peaked after 1.5 h and declined in line with a two-compartment model with half-lives of 13 and 90 min, respectively (Fry et al., 1972).

Following a single inhalation exposure to approximately 5 mg [38Cl]chloroform, volunteers absorbed about 80% (Morgan et al., 1970). The relative contributions of dermal and pulmonary uptake have been studied in individuals taking showers, using post-exposure exhaled air concentrations to estimate uptake. These were 6-21 µg/m3 for normal showering and 2.4-10 µg/m3 if exposure during showering was restricted to the inhalation route ("inhalation-only" showers). This difference was statistically significant and indicated that the contributions of dermal and inhalation exposures were approximately equivalent (Jo et al., 1990)."

From http://www.inchem.org/documents/cicads/cicads/cicad58.htm#7.0