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According to the United Nations, Syria imported 1,916,504 kilograms of "Propyl alcohol and isopropyl alcohol" in 2010, 1,705,420 kilograms in 2009, 926,139 kilo

According to the United Nations, Syria imported 1,916,504 kilograms of "Propyl alcohol and isopropyl alcohol" in 2010, 1,705,420 kilograms in 2009, 926,139 kilograms in 2008, and so on... ...To quote another here. Isopropyl alcohol is not an organophosphate precursor. https://cyber.sci-hub.hk/MTAuMTAwMi9zbGN0LjIwMTcwMjc2Mw==/quagliano2018.pdf https://cyber.sci-hub.hk/MTAuMTAwMi9zbGN0LjIwMTcwMjc2Mw==/qu... Precursors of CW agents are chemicals which have relatively small molecules, that may be used for the synthesis of other toxic products such as organophosphorous pesticides.[1,2] Direct precursors of nerve agents are those chemicals that can be converted to nerve agents in one or two synthetic steps, and are those under strict surveillance by OPCW. Industrial com- pounds such as organophosphates (pesticides mainly), phos- gene, chlorine, and cyanide are precursors that are not difficult to obtain.[3] On the other side, synthesis of methylphosphono- fluoridates (G-agents) and V-agents is not direct because of the absence of a large-scale commercial source of the key organo- phosphorous precursors: methylphosphonyl dichloride (Me- POCl2) and methylphosphonyl difluoride (MePOF2). However, impure nerve agent could be easily synthesized, as it was in the case of terrorist attacks in Tokyo subway in Japan in 1995. Precursors for sarin, tabun, and G-series agents are sources of fluorine, usually bifluorides. Ammonium or Sodium bifluoride for example, is absolutely a precursor (although it has some non-essential, legitimate industrial uses) For sarin, you must have a source of fluorine atoms, so it can be sensible to control export of bifluoride compounds. While alcohol is used, it’s like trying to control the production of beer by interdicting water instead of malted barley. While malted barley has many uses, it’s not essential and its major use is fermentation. Water meanwhile, is essential and ubiquitous. The key precursors for organophosphates involve the donated fluorine; no fluorination, no organophosphate weapons. As a bonus the fluorine compounds used are dangerous, and imported/exported in much smaller quantities than alcohol. Without bifluorides, you can still have industry, medicine, etc. Without isopropyl you can’t even have hand sanitizer. Blackbagboys: Oh for sure, it’s hard to imagine why there would be high demand for the most common disinfectant in a war zone. That’s incredibly suspicious, and clearly points to the production of sarin. (/s) Come on, this blog isn’t talking about anything reasonable, it’s calling rubbing alcohol a CW precursor.

jmblpati 8y ago
Your claim about fluorine being essential for organophosphate nerve agents is incorrect. The original nerve agent, tabun, contains no fluorine at all for example. Neither do VX, parathion, or paraoxon. The mechanism behind organophosphate poisoning lies entirely in the phosphate part of the molecule. Among the enzymes present in the human body are a large class known as serine hydrolases. These enzymes hydrolyze chemical bonds in a wide variety of compounds (such as sugars, proteins, and lipids), and their function critically depends on a nucleophillic serine amino acid in the enzyme's structure. This serine attacks the bond to be hydrolyzed, freeing one half of the victim molecule and leaving the other half attached to the enzyme. Then water comes in and breaks the bond between the serine and the second half to restore the enzyme and in sum hydrolyze the original bond. Organophosphate nerve agents act by entering the active site of a serine hydrolase. They are attacked by the active site serine to release a counterion (which depends on the specific nerve agent) and a phosphate ester of the enzyme. However, this enzyme ester can only be hydrolyzed extremely slowly-- the enzyme cannot be restored to its original form, and the entire enzyme is nonfunctional. Now, the released counterion could be many things (it just needs to be something that will leave if pushed out by the hydrolase serine). On the other hand, it should not be too eager to leave like something like chlorine would be: if it was the potential nerve agent would be attacked by things like water before getting to the hydrolase, wasting the agent. Thus, a balance needs to be struck between something easy to displace but not too easy to displace. This gives the classic functional groups present in most nerve agents and organophosphate pesticides: fluoride, cyanide, thiols, and phenolates. By the way, fluorides and fluoride minerals are virtually impossible to regulate trade in: they have a large variety of legitimate uses from toothpaste to aluminum production, and fluorspar is a fairly common mineral in the world. What is usually regulated instead are the phosphorus precursors such as phosphorus trichloride and red phosphorus as well as some chlorinating agents like thionyl chloride.
- pcrh 8y ago
  Just for your information, the mechanism of organophosphate nerve agent toxicity does not involve serine hydrolyases. It involves acetylcholinesterase. https://chemm.nlm.nih.gov/nerveagents.htm https://chemm.nlm.nih.gov/nerveagents.htm

jmblpati 8y ago

Your claim about fluorine being essential for organophosphate nerve agents is incorrect. The original nerve agent, tabun, contains no fluorine at all for example. Neither do VX, parathion, or paraoxon. The mechanism behind organophosphate poisoning lies entirely in the phosphate part of the molecule. Among the enzymes present in the human body are a large class known as serine hydrolases. These enzymes hydrolyze chemical bonds in a wide variety of compounds (such as sugars, proteins, and lipids), and their function critically depends on a nucleophillic serine amino acid in the enzyme's structure. This serine attacks the bond to be hydrolyzed, freeing one half of the victim molecule and leaving the other half attached to the enzyme. Then water comes in and breaks the bond between the serine and the second half to restore the enzyme and in sum hydrolyze the original bond. Organophosphate nerve agents act by entering the active site of a serine hydrolase. They are attacked by the active site serine to release a counterion (which depends on the specific nerve agent) and a phosphate ester of the enzyme. However, this enzyme ester can only be hydrolyzed extremely slowly-- the enzyme cannot be restored to its original form, and the entire enzyme is nonfunctional. Now, the released counterion could be many things (it just needs to be something that will leave if pushed out by the hydrolase serine). On the other hand, it should not be too eager to leave like something like chlorine would be: if it was the potential nerve agent would be attacked by things like water before getting to the hydrolase, wasting the agent. Thus, a balance needs to be struck between something easy to displace but not too easy to displace. This gives the classic functional groups present in most nerve agents and organophosphate pesticides: fluoride, cyanide, thiols, and phenolates. By the way, fluorides and fluoride minerals are virtually impossible to regulate trade in: they have a large variety of legitimate uses from toothpaste to aluminum production, and fluorspar is a fairly common mineral in the world. What is usually regulated instead are the phosphorus precursors such as phosphorus trichloride and red phosphorus as well as some chlorinating agents like thionyl chloride.

pcrh 8y ago
Just for your information, the mechanism of organophosphate nerve agent toxicity does not involve serine hydrolyases. It involves acetylcholinesterase. https://chemm.nlm.nih.gov/nerveagents.htm https://chemm.nlm.nih.gov/nerveagents.htm