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The objective of the present study was the development of the morphological criteria for the diagnostics of fatal intoxication with the herbal smoking blends (spices) using the samples of the biological materials obtained from the victims of pyrrolidinovalerophenone poisoning. The samples were taken from 13 autopsied cadavers of 11 men and 2 women at the age from 26 to 39 years based at the Astrakhan Regional Bureau of Forensic Medical Expertise during the period from 21011 to 2015. The diagnosis of pyrrolidinvalerpphenon poisoning was verified to the letter. The materials obtained during the standard autopsy procedure were used for the forensic genetic studies in the combination with the mandatory routine forensic chemical investigations with the application of the gas chromatographic techniques. Polymorphism of the morphological picture was attributable to the differences in the chemical composition of the poisons and the combination of narcotic and alcoholic intoxication. The signs of chronic intoxication manifested themselves in the form of mixed gliosis and various lesions of brain neurons. The variety of clinical symptoms and the morphological picture of pyrrolidinovalerophenone poisoning are responsible for different forms of tanatogenesis which suggests the necessity of further research on the mechanisms underlying the toxic effects of herbal smoking blends.

Mustard gas (sulfur mustard [SM], bis-[2-chloroethyl] sulfide) is a vesicating chemical warfare agent and a potential chemical terrorism agent. Exposure of SM causes debilitating skin blisters (vesication) and injury to the eyes and the respiratory tract; of these, the respiratory injury, if severe, may even be fatal. Therefore, developing an effective therapeutic strategy to protect against SM-induced respiratory injury is an urgent priority of not only the US military but also the civilian antiterrorism agencies, for example, the Homeland Security. Toward developing a respiratory medical countermeasure for SM, four different classes of therapeutic compounds have been evaluated in the past: anti-inflammatory compounds, antioxidants, protease inhibitors and antiapoptotic compounds. This review examines all of these different options; however, it suggests that preventing cell death by inhibiting apoptosis seems to be a compelling strategy but possibly dependent on adjunct therapies using the other drugs, that is, anti-inflammatory, antioxidant, and protease inhibitor compounds., (© The Author(s) 2014.)

Context: Sulfur mustard is a blister agent that can cause death by pulmonary damage. There is currently no effective treatment. N-acetyl-L-cysteine (NAC) has mucolytic and antioxidant actions and is an important pre-cursor of cellular glutathione synthesis. These actions may have potential to reduce mustard-induced lung injury., Objective: Evaluate the effect of nebulised NAC as a post-exposure treatment for inhaled sulfur mustard in a large animal model., Materials and Methods: Fourteen anesthetized, surgically prepared pigs were exposed to sulfur mustard vapor (100 μg.kg⁻¹), 10 min) and monitored, spontaneously breathing, to 12 h. Control animals had no further intervention (n = 6). Animals in the treatment group were administered multiple inhaled doses of NAC (1 ml of 200 mg.ml⁻¹ Mucomyst™ at + 30 min, 2, 4, 6, 8, and 10 h post-exposure, n = 8). Cardiovascular and respiratory parameters were recorded. Arterial blood was collected for blood gas analysis while blood and bronchoalveolar lavage fluid were collected for hematology and inflammatory cell analysis. Urine was collected to detect a sulfur mustard breakdown product. Lung tissue samples were taken for histopathological and post-experimental analyses., Results: Five of six sulfur mustard-exposed animals survived to 12 h. Arterial blood oxygenation (PaO₂) and saturation levels were significantly decreased at 12 h. Arterial blood carbon dioxide (PaCO₂) significantly increased, and arterial blood pH and bicarbonate (HCO₃⁻) significantly decreased at 12 h. Shunt fraction was significantly increased at 12 h. In the NAC-treated group all animals survived to 12 h (n = 8). There was significantly improved arterial blood oxygen saturation, HCO₃⁻ levels, and shunt fraction compared to those of the sulfur mustard controls. There were significantly fewer neutrophils and lower concentrations of protein in lavage compared to sulfur mustard controls., Discussion: NAC's mucolytic and antioxidant properties may be responsible for the beneficial effects seen, improving clinically relevant physiological indices affected by sulfur mustard exposure., Conclusion: Beneficial effects of nebulized NAC were apparent following inhaled sulfur mustard exposure. Further therapeutic benefit may result from a combination therapy approach.

Cases of deaths in manure or septic tanks are rare in legal-medical practice, more frequently as unfortunate occupational accidents. Poisoning with toxic gases, especially with hydrogen sulfide, is reported as the cause of death, while the exhaustion of oxygen in the air is omitted with the simultaneous excess of carbon dioxide. In such cases, determination of the direct cause of death constitutes a big problem because post-mortem examination does not reveal the specific changes. A case of acute collective poisoning by gases in a manure storage tank is presented of 5 agricultural workers, 2 of whom died. While explaining the cause of poisoning and deaths, toxicological blood tests were performed in the victims of the accident, as well as gases inside the manure storage tank. The post-mortem examinations and toxicological blood tests performed did not allow determination of the direct cause of death. Toxicological tests of gases from inside the manure tank showed a very low concentration of oxygen, with a simultaneous very high concentration of carbon dioxide, and a considerable level of hydrogen sulfide. The cause of fainting of three and deaths of two workers was not the poisoning with hydrogen sulfide, but oxygen deficiency in the air of the tank.

Exposure to sulphur mustard (SM) gas may have extensive immediate effects on the respiratory system. However, long-term effects are far less known. This case report describes a Kurdish male child who was exposed to SM gas during a chemical attack in Iraq at 5 yrs of age. In the acute phase, the child developed severe respiratory symptoms with a chemical pneumonia. Extensive burning of the skin occurred. In the course of 10 yrs, lung function deteriorated progressively to a forced expiratory volume in one second of 30% of predicted value. Severe air-trapping occurred. The lung function abnormalities were not reversed by treatment with corticosteroids or bronchodilators. Infectious exacerbations of the child's lung disease occurred. High resolution computed tomography scan showed multiple bronchiectasis. The histological picture of an open lung biopsy was best described as a "chronic bronchiolitis".

Changes in the rat brain macroglia produced by a natural gas from Astrakhan source containing hydrogen sulphide were studied immunocytochemically (glial fibrillar acid protein). Primary response was from oligodendroglia, dose increase followed by reaction from the astroglia.

Fatal intoxications with butane and/or propane are rare although the inhalation of such liquid gases in order to induce hallucinations is not uncommon amongst youngsters, the number of which is difficult to evaluate. Thus the possibility of gas intoxication should be taken into consideration in all cases of unclear death of youngsters, in which case the macroscopic and histological findings will be unspecific whereas the chemical-toxicological analyses, especially of the native brain, lung and liver tissue, lead to definite conclusions.

A poultry research facility that housed 2400 Peterson x Hubbard cross broilers (48 pens of 50 chicks each) experienced 4% mortality within 24 hr of chick placement. Mortality started within 4 hr of placement, and within 72 hr, cumulative mortality had reached 52%. Mild dyspnea was the only clinical sign noted in some chicks prior to death. The primary gross lesion noted in the chicks submitted was moderate to severe pulmonary congestion. The lungs of four of these chicks sank in formalin, and blood-tinged fluid was noted in the mouth and nares of two chicks. The microscopic lesions noted in the affected chicks were moderate to severe pulmonary edema and congestion. The diagnosis indicated to the submitter was that pulmonary edema caused by exposure to an unidentified noxious gas caused the death of the chicks. The poultry house environment was tested for sulfur dioxide, oxides of nitrogen, carbon monoxide, carbon dioxide, and volatile organic compounds (as produced by combustion engines); all tests were negative for significant levels of these compounds. A second broiler flock was placed in the same facility and the mortality at 6 wk was 11%, which was greater than the 2.5%-4.7% mortality seen in the previous four flocks on the farm. Further investigation revealed that the only change in management practice in this facility prior to the onset of the severe mortality problem was the replacement of 48 heat lamp bulbs (one for each pen). The new heat lamp bulbs were polytetrafluoroethylene (PTFE) coated. PTFE gas intoxication has been reported in several exotic avian species, but this intoxication has not been previously reported in a poultry flock.

A man had a quarrel with his wife. Suddenly he collapsed and became cyanotic. The woman supposed him to be dead. Because she was afraid of familiar requital, she opened the gas-cock of the cooking-range to pretend a suicide; methane emitted. The autopsy revealed a fresh cardiac infarction. Postmortem chemical analysis established methane in the blood. The question was, whether the methane had any importance for the death. By experimental inhalation of a methane-air-mixture (3%) we could expose, that the methane concentration in postmortem blood didn't have any relevance for the death.

The gross postmortem features of two victims (a 17-year-old and a 33-year-old male, both of Chinese descent) who died shortly after an ammonia-gassing exposure, are presented. The findings of extensive thermal burns on the body surfaces and on the lips, conjunctivitis and opaque cornea on both eyes, oedematous and congested lungs with large areas of haemorrhages, etc, were consistent with injuries inflicted by a corrosive gas such as ammonia. The postmortem toxicological findings of elevated blood ammonia levels supported the postmortem findings. The pulmonary and femoral blood ammonia levels (0.26 mg/mL and 0.65 mg/mL) of decedent one were at least 371 times and 928 times respectively higher than normal. Similarly, the pulmonary and femoral blood ammonia levels (0.51 mg/mL and 0.43 mg/mL) of decedent two were at least 728 times and 614 times respectively higher than normal.

Methylene chloride is a major component of paint and varnish strippers. Due to its high volatility, its use in unventilated or poorly ventilated confined spaces poses a serious health hazard as a result of accumulation of the solvent vapour. At high levels, methylene chloride can cause severe central nervous system depression and ultimately death, as illustrated in this case report. The importance of adequate forced ventilation, utilisation of proper personal protective equipment and enforcement of a permit-to-work system during work with solvents in confined spaces is emphasised.

In 1984 and 1985, a total of eleven Iranian patients were transferred to hospitals in Munich, Germany, after a reported gas attack in the Iran-Iraq war. The initial symptoms and pretreatment in Teheran, Iran, as well as the admittance examination data, the clinical courses of the patients, and the clinical laboratory data in Germany, are reported. The main injuries were to the skin, the eyes, and the respiratory tract. One patient stopped breathing suddenly on the third day of treatment (eight days after the exposure). A large piece of mucous membrane blocking a bronchus was removed during an immediate bronchoscopy, but attempts at resuscitation failed. The most important autopsy findings in this case were severe pseudomembranous inflammation of the trachea and the bronchial tubes. The histological findings are reported. Chemical proof of the poison (mustard gas) was established. A review of the history of chemical warfare, the physical and chemical properties of mustard gas, and a literature survey of clinical findings (including, especially, experiences from World Wars I and II) contribute to the understanding of the actual cases.

Ricardo T., aged 20 years, was a passenger in a Varig air-craft which suffered an accident on July 11th 1973. A fire developed on board whilst the plane was in the air, at about 3 p.m. After emergency landing, rescue workers (firemen and emergency ambulance teams) discovered only two survivors amongst the 122 passengers. One was in his forties and died a few moments later. The other (Ricardo) was rapidly transported to the surgical and traumatological intensive care unit of the Henri Mondor Hospital. At the time of arrival, he was in stage 1 coma with skin burns (3rd degree), burns of the airway and a high carbon monoxide blood level. Treatment consisted of assisted ventilation for 24 hours, with intermittent bronchial lavage used to eliminate ashes and calcinated debris, then for 10 days, spontaneous ventilation without intubation, with a tele-expiratory counter-pressure of 4 milibar in a mini-chamber (globe) enriched in oxygen. Intravenous hyperalimentation was started during the first few hours, continued on the 24th day by enteral alimentation. Initial chest XRays showed heavy flaky appearances, predominantly in the hilar region, and more marked on the right. At about the 15th day, XRay showed fibrous with predominance of signs of the apex. These sequellae were confirmed by respiratory function tests which gave objective evidence of a diffusion disturbance with decrease in membrane permeability coefficient. Repetition of RFT indicated a decrease in mechanical problems. On August 31st (on the 51st day) Ricardo was able to return to Rio in a good general condition, dorso-lumbar burns having healed. There was a dysphonia of mixed origin: scarred infiltrate of the vocal cords, but with normal mobility, and a decrease in vital capacity of --30%. Seen again in September 1978, Ricardo was found to be well with normal activity and slight effort dyspnea. Chest XRays showed signs of residual fibrosis.

Mustard gas or Yperite, an old and formerly well known chemical warfare agent was recently used against human beings in the Middle east. Some of the victims were transferred to European University Hospitals for intensive treatment. They all showed vesication of the skin and also the typical symptoms of severe damage of the respiratory mucosa. The macroscopical and microscopical observations after war gas exposure and the detection of mustard gas in biological material are reported.

The skin lesions seen in patients exposed to toxic war gases (dichlorethyl sulfide) are described. Histologic and electron microscopic findings are presented. The clinical course of the lesions is discussed.

A case of Diazomethane intoxication has been reported. Diazomethane is gaz commonly used by pharmacological and industrial chemist. This case of intoxication is rare, since only 15 other cases have been published up to now. A review of the literature leads leads describe the clinical feature of such an intoxication by gaz inhalation. When Diazomethane is inhaled it induces respiratory and general disorders. In some cases, it be fatal, and, in some other cases, when a second exposure happens, bronchial asthma may appear. Post mortem studies show pulmonary oedema lesions with important inflammatory reaction localized in the peribronchia. It must be emphasized that direct aggression is probably responsive of toxical discorders, but increase of the symptoms consecutive to a second exposure are related to allergical mechanisms.

Three cases of xylene poisoning occurred after prolonged inhalation of paint fumes. Analysis showed that xylene comprised more than 90% of the solvent in the paint, the total solvent comprising 34% of the paint by weight. One patient was dead on admission, while the other two recovered after at least 15 hours' loss of consciousness. Both patients had transient liver cell damage, and one temporary impairment of renal function.