Matsumoto attack

St Luke s Hospital showed an elevated creatine phospho-kinase (CPK) and leukocytosis in 11% and 60% of patients, respectively. In severe cases in the Matsumoto attack, hyperglycemia, ketonuria, and low serum triglycerides due to toxicity of sarin on the adrenal medulla were observed (Yanagisawa et al, 2006). 

The Matsumoto sarin attack occurred on June 27, 1994, one year before the Tokyo subway sarin attack, and although the group responsible for the Matsumoto attack was not known at the time of the Tokyo subway attack, emergency doctors in Japan knew that the diagnosis and treatment of sarin poisoning should follow that of accidental organophosphorus poisoning. 

In the Tokyo subway sarin attack, the amount of atropine sulfate administered was markedly smaller than what has been proposed in the past. The reason for this may be that the concentration of sarin used in the attack was low, at 35%. Large quantities of sarin of a higher concentration were thought to have been used in the Matsumoto attack, and intubation was difficult due to airway spasm and excessive airway secretion. Therefore, if the use of a nerve agent is suspected clinically, at a minimum, atropine sulfate should be administered as quickly as possible. It is therefore important to establish a system whereby antidotes can be administered early during pre-hospital care. 

According to inpatient records from St. Luke s Hospital, the most common laboratory finding related to sarin toxicity was a decrease in plasma cholinesterase (ChE) levels in 74% of patients. In patients with more severe toxicity, plasma ChE levels tended to be lower, but a more accurate indication of ChE inhibition is the measurement of erythrocyte ChE, as erythrocyte acetylcholinesterase (AChE) is considered "true ChE" and plasma ChE is "pseudo-ChE." However, erythrocyte ChE is not routinely measured, whereas plasma ChE is included in many clinical chemistry panels thus, it can be used as a simple index for ChE activity. In both the Matsumoto and Tokyo subway sarin attacks, plasma ChE served as a useful index of sarin exposure. In 92% of hospitalized patients, plasma ChE levels returned to normal on the following day. In addition, inpatient records from St. Luke s Hospital showed an elevated creatine phosphokinase and leukocytosis in 11% and 60% of patients, respectively. In severe cases such as the Matsumoto attack, hyperglycemia, ketonuria, and low serum triglycerides due to tire toxic effects of sarin on the adrenal medulla were observed (Yanagisawa et al, 2006). 

The agent used in the attack was not recognised until about 2.5 h after the attack when the classic nerve agent toxidrome was recognised by physicians who had attended the patients in the Matsumoto attack. 

Until now examples for catalytic reactions involving ferrates with iron in the oxidation state of -l-3 are very rare. One example is the hexacyanoferrate 8-catalyzed oxidation of trimethoxybenzenes 7 to dimethoxy-p-benzoquinones 9/10 by means of hydrogen peroxide which was published by Matsumoto and Kobayashi in 1985 [2]. Using hexacyanoferrate 8 product 9 was favored while other catalysts like Fe(acac)3 or Fe2(S04)3 favored product 10 (Scheme 2). The oxidation is supposed to proceed via the corresponding phenols which are formed by the attack of OH radicals generated in the Fe/H202 system. 

Multichemical resistanse of the conifer Podocarpus gracilior (Podocarpaceae) to insect attack. Kubo, 1. Matsumoto, T. Klocke, J.A. J. Chem. Ecol, 1984, 10, 547-559. 

The only reported incidents of nerve agent poisoning, where biomedical samples have been obtained, are those resulting from terrorist dissemination of sarin in Matsumoto (1994) and the Tokyo subway (1995), plus an assassination using VX, also in Japan (60). In contrast to the CW incidents involving sulfur mustard, many of the biomedical samples associated with these terrorist attacks were collected within hours of the event. 

TMS derivative by GC/FPD in urine collected over 7 days from casualties of the Tokyo attack (43). Concentrations were not reported but the estimated exposures were 0.13-0.25 mg of sarin in a comatose patient and 0.016-0.032 mg in less severely intoxicated patients. Using LC/MS/MS and a more rigorous method of quantitation, /-PrMPA was detected underivatized in serum at concentrations of 3-136ng/ml in four casualties of the Matsumoto incident and 2-100ng/ml in 13 casualties of the Tokyo attack (59). All samples were taken within 2.5 hours of hospitalization. High levels of /-PrMPA correlated with low levels of butyryl-cholinesterase activity. Other positive analyses associated with these incidents were obtained by identification of inhibited cholinesterase, and are reported in Part B. 

Application of the fluoride-reactivation method to serum samples of victims from the Tokyo subway attack, and of the Matsumoto incident, yielded, sarin concentrations in the range of 0.2-4.1ng/ml serum (44). Evidently, these casualties had been exposed to an organophosphate with the formula i-PrO(CH3)P(0)X, presumably with X = F (sarin). 

In June 1994 and again in May 1995 the Japanese cult group Aum Shinrikyo created much havoc when they released the deadly nerve agent sarin in two Japanese cities. In the first attack in Matsumoto, Japan, sarin vapor was released in a residential area where judges unfriendly to the cult resided. Seven people died as a consequence of this nerve agent exposure, and 500 people were injured. The 1995 attack occurred in the Tokyo subway system. Several coordinated releases of this potentially deadly vapor resulted in more than 5,000 visits to local emergency departments. Fortunately, the vast majority of exposed victims had few if any symptoms and there were only a handful of fatalities (Tucker, 2006 for further discussion, see chapter 19—Biological and Chemical Terrorism A Unique Threat). 

Terrorists have expressed an interest in nerve agents and have deployed them in attacks on unprotected civilians (Rotenberg and Newmark, 2003). A Japanese religious cult, Aum Shinrikyo, independently manufactured numerous chemical and biological agents. The first such attack with sarin occurred in Matsumoto in 1994 and the Tokyo subway in 1995. Thousands of people were affected and dozens of people died (Nagao et al, 1997 Ohtomi et al, 1996 Okumura et al, 1998 Yokoyama et al, 1998). In... 

Matsumoto (1994), 600 people were poisoned and hospitalized, and seven died (Morita et al, 1995 Nakajima et al, 1997 Yoshida, 1994). The attack in the Tokyo subway (1995) resulted in 5,500 people seeking hospital evaluation and 12 deaths (Bajgar, 2006). An interesting terroristic act was described by Tsuchihashi et al (2005) - a fatal intoxication with VX administered percutaneously. 

The Tokyo subway sarin attack occurred in 1995, following the Matsumoto sarin attack, and served as a wake-up call for anti-NBC (nuclear, biological, and chemical) terrorism policy throughout the world. In the 10 years since the attack, efforts to combat NBC terrorism have focused on rapid and effective measures to respond to attacks employing nerve agents such as sarin. 

This chapter has discussed sarin toxicity based on experiences of the attacks in Matsumoto and the Tokyo subway, and also the Iran-Iraq war. This section provides some conclusions drawn from the toxicological issues related to sarin. 

Given the low concentration and means of dispersal, the Tokyo subway sarin attack can be referred to as a passive attack. The implication of such an assumption is therefore that mankind has not yet witnessed a full-scale sarin attack in any major city. While valuable information can certainly be gained from the Tokyo subway sarin attack, the experience obtained from the more aggressive Matsumoto sarin attack and the Iran-Iraq war should also be considered when developing initiatives directed at dealing with a potential full-scale attack in the future where the effects will be more serious. 

Miyaki, K., Nishiwaki, Y., Maekawa, K., Ogawa, Y., Asukai, N., Yoshimura, K., Etoh, N., Matsumoto, Y., Kikuchi, Y., Kumagai N., Omae, K. (2005). Effects of sarin on the nervous system of subway workers seven years after the Tokyo subway sarin attack. J. Occup. Health 47(4) 299-304. 

Distribution, metabolism, and elimination of sarin in humans appear to resemble findings in animals. Minami and colleagues (1997, 1998) detected the sarin metabolite IMPA in urine of humans after the terrorist attack in Tokyo in 1995. They found peak levels of IMPA or methylphosphonic acid in urine 10-18 h after exposure. The levels of IMPA in urine correlated with the clinical symptoms. They also found evidence of distribution of sarin to the human brain in four of the 12 people who died after exposure. IMPA and MPA were detected in patients from the Matsumoto sarin exposure (Nakajima et al, 1998). 

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