专家:所谓“神经性毒气”属“重大误判”(图)

津爆核心区可以产生神经性毒气

先说什么是神经性毒气。

神经毒气_百度百科：神经性毒剂属有机磷或有机磷酸酯类化合物（organophosphorus compounds，organoposphates）。神经性毒剂属有机磷或有机磷酸酯类化合物（organophosphorus compounds，organoposphates）。这类毒剂特别对脑、膈肌和血液中乙酰胆碱酯酶（acetylcholine，Ach）在体内过量蓄积，从而引起中枢和外周胆碱能神经系统功能严重紊乱。因其毒性强、作用快，能通过皮肤、粘膜、胃肠道及肺等途径吸收引起全身中毒，加之性质稳定、生产容易、使用性能良好，因此成为外军装备的主要化学战剂。最具代表性的四个神经性毒剂是塔崩（tabun）、沙林（sarin）、梭曼（soman）和维埃克斯（VX）。美军将含有P-CN健和P-F健的前三者称为G类毒剂。代号分别为GA、GB和GD，将含有P-SCH2CH2N(R)2键的化合物称为V类毒剂，如VX、VE、VG、VS及VR等。

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  Nerve Gas

█ JUDYTH SASSOON

Nerve gases, or nerve agents, are mostly odorless compounds belonging to the organophosphate family of chemicals. Nerve gasses are either colorless or yellow-brown liquids under standard conditions. Two examples of nerve gases that have gained some notoriety through their powerful physiological effects are Sarin and VX. Even in small quantities, nerve gases inhibit the enzyme acetylcholinesterase and disrupt the transmission of nerve impulses in the body. Acetylcholinesterase is a serine hydrolase belonging to the esterase enzyme family, which acts on different types of carboxylic esters in higher eukaryotes. Its role in biology is to terminate nerve impulse transmissions at cholinergic synapses. It does this by rapidly hydrolysing the neurotransmitter, acetylcholine, which is released at the nerve synapses. Inhibition of the acetylcholinesterase results in the excessive buildup of acetylcholine in, for example, the parasympathetic nerves leading to a number of important locations in the body: the smooth muscle of the iris, ciliary body, the bronchial tree, gastrointestinal tract, bladder and blood vessels; also the salivary glands and secretory glands of the gastrointestinal tract and respiratory tract; and the cardiac muscle and endings of sympathetic nerves to the sweat glands. An accumulation of acetylcholine at parasympathetic sites gives rise to characteristic muscarinic signs, such as emptying of bowels and bladder, blurring of vision, excessive sweating, profuse salivation and stimulation of smooth muscles. The accumulation of acetylcholine at the endings of motor nerves leading to voluntary muscles ultimately results in paralysis.

Nerve gases are highly toxic, stable, and easily dispersed. They produce rapid physiological effects both when absorbed through the skin or through the respiratory tract. They are also fairly easy to synthesize and the raw materials required for their manufacture are inexpensive and readily available. This means that anyone with a basic laboratory can produce them. Nerve gases are, therefore, a significant concern for authorities as they are an easily available weapon for terrorist groups.

In 1936, the German chemist Gerhard Schrader of the I. G. Farbenindustrie laboratory in Leverkusen first prepared the agent Tabun (ethyl-dimethylphosphoramidocyanidate). At the time, Schrader was leading a program to develop new types of insecticides, working first with fluorine-containing compounds such as acyl fluorides, sulfonyl fluorides, fluoroethanol derivatives and fluoroacetic acid derivatives. Schrader's research eventually led to the synthesis of Tabun as an extremely powerful

agent against insects. Schrader found that as little as 5 parts per million (ppm) of Tabun killed all the leaf lice used in his experiments. Soon after Schrader's experiments, the potential use of this substance as an agent of war was realized.

In 1939, a pilot plant for Tabun production was set up at Munster-Lager, near the German Army training grounds at Raubkammer. In January 1940, Germany began the construction of a full-scale plant, code named Hochwerk, at Dyernfurth-am-Oder (now Brzeg Dolny in Poland). A total of 12,000 tons of Tabun was produced during the ensuing three years (1942–1945) and at the end of WWII, large quantities were seized by the Allied Forces. In addition to Tabun, Schrader and his colleagues produced some 2000 new organophosphates, including Sarin in 1938 and the third of the "classic" nerve agents, Soman, in 1944. These three nerve agents, Tabun, Sarin and Soban, are known as G-agents. The manufacture of Sarin was never fully developed in Germany and only about 0.5 tons were produced in a pilot plant before the end of WWII in 1945.

After 1945, a great deal of research began to focus on understanding the physiological mechanisms of nerve gas action, so that more effective means of protection could be devised against them. However, these efforts also allowed for the development of new and more powerful agents, closely related to the earlier ones. The first official publications on these compounds appeared in 1955. The authors, British chemists Ranajit Ghosh and J. F. Newman, described Amiton, one of the newly developed nerve agents, as being particularly effective against mites. At this time, researchers were devoting a great deal of energy to studying organophosphate insecticides both in Europe and in the United States. At least three chemical firms independently studied and quantified the intense toxic properties of these compounds during the years 1952–53 and some of them became available on the market as pesticides. By the mid-1950s, following in the wake of the intensive research activity, a new group of highly stable nerve agents had been developed. These were known as the V-agents and were approximately ten-fold more poisonous than Sarin. The V-agents can be numbered among the most toxic substances ever synthesized. VX, a persistent nerve gas, was discovered by Ghosh and was touted as being more toxic than any previously synthesized compound. Since the discovery of VX, there have been only minor advancements in the development of new nerve agents.

A contemporary use of nerve gas occurred during the Iran-Iraq war of 1984–1988. In this conflict, the United Nations confirmed that Iraq used Tabun and other nerve gases against Iran. This incident is a prime example of how the technology of chemical weapons was shared during the Cold War. The Soviets would arm their allies while the U.S. did the same for its allies. Iraq was a benefactor and implemented its chemical stockpiles during this period. Another contemporary incident of nerve gas use occurred in Japan in 1995. Members of the Aum Shinrikyo cult introduced Sarin gas into Tokyo's subway system. This incident gives an example of the possible new roles that nerve gases may play in the future, as tools of terrorism rather than the weapons of powerful nations.

  气态氰化氢是毒气，但可能不算神经性毒气。毒气列表见：

List of highly toxic gases - Wikipedia, the free...

氰化氢会引起神经性效应。但引起神经性效应的毒气一定是神经性毒气吗？

Chronic Toxicity Summary for Hydrogen Cyanide -...

Occupational epidemiological studies of hydrogen cyanide exposure are complicated by the mixed
chemical environments, which are created by synthetic and metallurgic processes. However, several
reports indicate that chronic low exposure to hydrogen cyanide can cause neurological, respiratory,
cardiovascular, and thyroid effects (Blanc et al., 1985; Chandra et al., 1980; El Ghawabi et al., 1975).
Although these studies have limitations, especially with incomplete exposure data, they also indicate that
long-term exposure to inhaled cyanide produces CNS and thyroid effects.

El Ghawabi et al. (1975) studied 36 male electroplating workers in three Egyptian factories exposed to
plating bath containing 3% copper cyanide, 3% sodium cyanide, and 1% sodium carbonate. Breathing
zone cyanide concentrations ranged from 4.2 to 12.4 ppm (4.6 to 13.7 mg/m3
), with means from 6.4 to 10.4
ppm (7.1 to 11.5 mg/m3
), in the three factories at the time of this cross-sectional study. The men were
exposed for a duration of 5 to 10 years, except for one man with 15 years exposure. Twenty non-exposed
male volunteers were used as controls. None of the subjects, controls or workers, currently smoked
cigarettes. Complete medical histories were taken, and medical exams were performed. Urinary levels of
thiocyanate (a metabolite of cyanide) were utilized as a biological index of exposure. Thyroid function was
measured as the uptake of radiolabeled iodine, since thiocyanate may block the uptake of iodine by the
thyroid leading to iodine-deficiency goiters. Frequently reported symptoms in the exposed workers
included headache, weakness, and altered sense of taste or smell. Lacrimation, abdominal colic, and lower
stomach pain, salivation, and nervous instability occurred less frequently. Increased blood hemoglobin and
lymphocyte counts were present in the exposed workers. Additionally, punctate basophilia were found in
78% (28/36) of the exposed subjects. Twenty of the thirty six exposed workers had thyroid enlargements,
although there was no correlation between the duration of exposure with either the incidence or the degree
of enlargement. Thyroid function test indicated significant differences in uptake between controls and
exposed individuals after 4 and 24 hours. Urinary excretion of thiocyanates correlated with the breathing
zone concentrations of cyanides. Symptoms persisted in 50% of the dyspneic workers in a 10-month
nonexposure follow up period. This study reported a LOAEL of 6.4 ppm (7.1 mg/m3
) for the CNS
symptoms and thyroid effects.
Another retrospective study (Blanc et al., 1985) examined 36 former silver-reclaiming workers with long­
term exposure to hydrogen cyanide fumes. The authors found significant trends between the incidence of
self-reported CNS symptoms during active employment (headache, dizziness, nausea, and bitter almond
taste), the symptoms reported post-exposure, and a qualitative index of exposure retroactively defined by
the investigators as low-, moderate-, or high-exposure through work histories. Some symptoms persisted
for 7 months or more after exposure. None of the workers had palpable thyroid gland abnormalities, but
clinical tests revealed decreases in vitamin B12 absorption and folate levels and statistically significant
increases in thyroid-stimulating hormone levels, which in combination with the CNS effects, suggest long­
term adverse effects associated with cyanide exposure.