Destruction of OPA from munitions demilitarization in supercritical water oxidation: kinetics of total organic carbon disappearance.

The destruction of OPA from munitions demilitarization has been accomplished in supercritical water oxidation (SCWO) with oxygen as oxidant in an isothermal continuous-flow reactor. The experiments were conducted at a temperature of 689-887 K and a fixed pressure of 25 MPa, with a residence time that ranged from 7 s to 14 s. The destruction efficiency was measured by total organic carbon (TOC) conversion. At the reaction condition, the initial TOC concentrations of OPA were varied from 1.41 mmol/L to 19.57 mmol/L and the oxygen concentrations were varied from 15.03 mmol/L to 81.85 mmol/L. Experimental data showed that all the TOC conversions were >80% under the above experimental conditions. The kinetics of TOC disappearance, which is essential for the design, optimization, and control of reliable commercial SCWO reactor was developed by taking into account the dependence of the oxidant and TOC concentration on the reaction rate. A global TOC disappearance rates expression was regressed from the data of 38 experiments, to a 95% confidence level. The resulting activation energy was determined to be 44.01 +/- 1.52 kJ/mol, and the pre-exponential factor was (1.67 +/- 0.45) x 10(2) L(1.14) mmol(-0.14) s(-1). The reaction orders for the TOC and the oxidant were 0.98 +/- 0.01 and 0.16 +/- 0.02, respectively.

Effects of combinational prophylactics composed of physostigmine and procyclidine on soman-induced lethality, seizures and brain injuries.

The antidotal, anticonvulsant and neuroprotective effects of physostigmine (PhS) and procyclidine (PC), the combinational prophylactics for organophosphate poisoning, were evaluated. For the investigation of dose-response relationship in rats and guinea pigs, various doses (0-6 mg/kg) of PC in combination with a fixed dose (0.1 mg/kg) of PhS were pretreated subcutaneously 30 min prior to subcutaneous poisoning with soman. Procyclidine in combination with PhS exhibited remarkable synergistic effects in a dose-dependent manner, leading to 1.92-5.07 folds of protection ratio in rats and 3.00-4.70 folds in guinea pigs. On the other hand, a low effect (1.65 fold) was achieved with the traditional antidotes atropine (17.4 mg/kg) plus 2-pralidoxime (30 mg/kg) treated immediately after soman poisoning, compared with a marked protection (5.50 fold) with atropine (17.4 mg/kg) plus HI-6 (125 mg/kg) in unpretreated rats. Noteworthy, the combinational prophylactics greatly potentiated the effect of atropine plus 2-pralidoxime to 6.13 or 12.27 folds and that of atropine plus HI-6 to 12.00 or 21.50 folds with 1.0 or 3.0 mg/kg of PC, respectively. A high dose (100 µg/kg, 1.3×LD(50)) of soman induced severe epileptiform seizures in rats pretreated with HI-6 (125 mg/kg), resulting in brain injuries in discrete brain regions under histopathological examination in 24 h. Interestingly, such seizures and excitotoxic brain injuries were fully prevented by pretreatment with PhS (0.1 mg/kg) and PC (1 mg/kg). Taken together, it is proposed that the prophylactics composed of PhS and PC could be a promising regimen for the prevention of lethality, seizures and brain injuries induced by soman poisoning.