Search

A Hypo helmet is a fabric hood soaked with an aqueous solution of two sodium salts for the detoxication of chlorine that was developed during the First World War. Herein, we report on a lecture, developed for non-chemistry majors that used the Hypo helmet to highlight the physical and chemical properties of chlorine. The lecture consisted of the following three components: (1) a brief introduction to the First World War (the Chemists' War), (2) video demonstrations of the generation of chlorine by mixing bleaching powder and hydrochloric acid and the detoxication of chlorine using a dummy Hypo helmet, and (3) students' written impressions of the lecture. The students' written impressions revealed two things: the lecture on chlorine and the Hypo helmet was well received, and most of the students (71 %, N = 82) did not know that chlorine was used as a poisonous gas during the First World War. [ABSTRACT FROM AUTHOR]

At present, the death cases of simple asphyxiant gas acute poisoning are increasing sharply. Common asphyxiant gases in death cases include nitrogen, helium, carbon dioxide, methane, propane, laughing gas, etc. Simple asphyxiant gas has no affinity for biological matrices and escapes quickly, which puts forward new requirements for autopsy procedures, selection and collection of samples, laboratory analysis and identification. This paper reviews the research and development process of death cases caused by simple asphyxiant gas acute poisoning and put forwards the collection and analysis strategy of the samples in such cases. The most valuable biological samples in such cases should be lung tissues associated with the airways, followed by brain tissue and cardiac blood. Gaseous samples from the esophageal cavity, tracheal cavity, pulmonary bronchi, gastric and cardiac areas are also recommended as valuable samples. In the case of postmortem examination, the gas should be injected into gas sample bag directly. Biological materials such as tissue and blood should be directly sealed in head-space vials and analyzed by using the headspace gas chromatography-mass spectrometry. [ABSTRACT FROM AUTHOR]

Objective. To study the first aid and nursing methods of patients with coal gas poisoning and explore the nursing effect. Method. The clinical data of 50 patients with carbon monoxide poisoning admitted to the emergency department of our hospital from February 2011 to August 2016 were retrospectively analyzed. The patients with severe toxic pulmonary edema were selected as the sample population, and all patients were equally divided by drawing lots. The two groups were divided into the study group and control group. The patients in the control group were given routine nursing intervention, while the patients in the study group were given routine nursing intervention. After the timely treatment of doctors in our hospital and the careful nursing of nursing staff, 45 patients in 50 patients were cured and discharged; 3 patients died of asphyxia due to long poisoning time. Two patients died of severe complications. Result. The total effective rate and oxygenation index of the study group were significantly different from those of the control group (P < 0.05). Conclusion. In the clinical nursing work of patients with severe carbon monoxide toxic pulmonary edema, the nursing effect of emergency cluster therapy is ideal. Patients with carbon monoxide poisoning have obvious age, gender, poisoning causes, and seasonal characteristics. It is an important means to carry out targeted publicity and education in daily life and take effective preventive measures to prevent carbon monoxide poisoning. Once poisoning occurs, timely treatment should be carried out, and careful nursing should be provided to help patients get rid of the danger. [ABSTRACT FROM AUTHOR]

We investigated the effects of poisoning and restoration of PdCuSi-metallic glass (MG), which is a sensing material that offers low power consumption and fast response times when used in capacitive MEMS hydrogen sensors. Four poisoning gases were used: hexamethyldisilazane (HMDS), H 2 S, SO 2 , and NO 2. Exposure to H 2 S resulted in metal sulfide forming at the surface of the PdCuSi-MG, although the sulfur did not diffuse into the PdCuSi-MG. Exposure to NO 2 only resulted in the nitrogen being adsorbed without bonding to metals. The poisoning elements were desorbed by heating. Exposure to H 2 S and SO 2 degraded the hydrogen sensitivity in terms of resistance of the PdCuSi-MG, although exposure to HMDS and NO 2 only slowed down the response time. These degradations were recovered by heating. We next examined forming a refresher layer under PdCuSi-MG in a hydrogen sensor. The hydrogen sensitivity of the H 2 S-exposed hydrogen sensor was restored by performing a refresh operation for a few minutes. • Poisoning by HMDS, H 2 S, SO 2 and NO 2 of PdCuSi-metallic glass (MG) was investigated. • Exposure to H 2 S led to formation of metal sulfide at only the surface of PdCuSi-MG. • At 200 °C, metal sulfide changed to SO X , which desorbed from PdCuSi-MG surface. • Degraded hydrogen properties of PdCuSi-MG restored by heating. • MEMS hydrogen sensor's reduced sensitivity was restored by using a refresher layer. [ABSTRACT FROM AUTHOR]

Introduction: While a number of developed countries have witnessed a decline in carbon monoxide (CO) deaths and increasing numbers of opioid-related fatalities, it is not known whether these or other trends have occurred in New Zealand. The aim of this study was, therefore, to review deaths due to poisoning in New Zealand, describe the causative substances, and identify any trends. Methods: Retrospective study reviewing New Zealand's poison-related death findings recorded in the National Coronial Information System (NCIS) database over the 6-year period 2008–2013. Results: We identified 1402 poisoning-related deaths recorded in the NCIS database representing a mortality rate of 5.4 deaths/100,000 population per year. The mortality rate due to poisoning was higher in males (6.96/100,000) than females (3.83/100,000). Fatalities peaked in the 40–50-year age group with the highest proportion of intentional deaths occurring in people aged 80–90 years. Pharmaceuticals accounted for 731 fatalities (52%) and chemicals 431 (31%), with multiple exposures occurring in 399 cases (28.5%). While CO was the leading cause of death throughout the period (n = 303, 21.6%), there was a significant reduction in the rate of CO fatalities from 1.69/100,000 population in 2008 to 0.94/100,000 in 2013 (IRR (95% CI) 2013/2008 0.56 (0.37–0.83)). There was, however, no statistically significant change in either the opioid-related death rate or the total number of deaths. Methadone was the leading pharmaceutical cause of fatality and the third most common cause overall, followed by morphine and codeine, with zopiclone and clozapine equally ranked as the sixth most common cause. Conclusion: While New Zealand has not suffered an "opioid epidemic" and has experienced a significant decline in CO deaths, the overall death rate due to poisoning has remained high. The development of accessible, timely, and relevant toxicovigilance systems would support the early implementation of interventions to reduce the leading causes of fatal poisoning. [ABSTRACT FROM AUTHOR]

[Display omitted] • Zn exerts an unusual promotion effect on SCR performance over Mn-HPW at > 180 °C. • Introducing HPW protects effectively acid sites on Mn from Zn poisoning. • Moderate decrease in redox performance of Zn/Mn-HPW alleviates NH 3 over-oxidation. • Both E-R and L-H mechanisms are applicative to Zn/Mn and Zn/Mn-HPW at 120 °C. • Only E-R route is involved in the reaction for Zn/Mn and Zn/Mn-HPW at 210 °C. MnO x -based catalysts are highly efficient for selective catalytic reduction (SCR) of NO x with NH 3 at low temperatures, but Zn contained in industrial flue gas may poison conventional SCR catalysts, and MnO x -based catalysts usually have low Zn tolerance. Herein, phosphotungstic acid-modified MnO x (denoted as Mn-HPW) was prepared to study the Zn tolerance. It was found that the deposition of Zn on Mn-HPW decreases the SCR activity at < 180 °C, but both NO x conversion and N 2 selectivity are enhanced at 180–300 °C, and > 95% NO x conversion can be achieved on Zn/Mn-HPW. Relevant catalysts were characterized and the results reveal that the decline in the activity at < 180 °C is related to the decrease in the quantities of Mn4+, Mn3+, and chemisorbed oxygen as well as the decreased capacities for adsorbing and activating NH 3 and NO x. The unusual improvement of SCR performance on Zn/Mn-HPW at 180–300 °C is mainly attributed to two aspects: (i) HPW can protect effectively the surface acid sites from Zn poisoning; (ii) The decrease in oxidation properties alleviates the over-oxidation of NH 3 , promoting the participation of more NH 3 in SCR. [ABSTRACT FROM AUTHOR]

Context:This study assessed the results of diffusion-weighted imaging (DWI) at presentation for acute charcoal-burning carbon monoxide (CO) poisoning and investigated whether the initial DWI results can predict long-term neurologic outcomes. Methods:The study included 128 patients who suffered from CO poisoning after burning charcoal and underwent DWI. These patients were divided into two groups based on imaging results: a normal DWI group and an abnormal DWI group. Data regarding clinical courses and long-term neurologic outcomes (persistent severe neurologic sequelae) were collected and compared. Results:The rate of abnormal DWI findings at presentation was 23.4%, and the most common site of abnormalities was the globus pallidus. All lesions in abnormal DWI had decreased apparent diffusion coefficient (ADC) values. The long-term neurologic state was assessed at a median follow-up of 19.5 months, and the frequency of poor long-term neurologic outcome was significantly higher in the abnormal DWI group (40.0% in the abnormal DWI group vs. 1.0% in the normal DWI group;p < .001). Abnormal DWI (odds ratio [OR]): 31.3, 95% confidence interval [CI]: 2.5–397) and old age (OR 1.1, 95% CI: 1.001–1.13) were independent factors for poor long-term neurologic outcomes, whereas the Glasgow Coma Scale score at presentation (OR: 0.7, 95% CI: 0.6–0.9) was negatively associated with the risk of poor long-term neurologic outcome. Conclusions:In cases involving CO poisoning due to charcoal burning, DWI at presentation may help predict the long-term neurological outcome after discharge. [ABSTRACT FROM PUBLISHER]

Objectives: The aim of this study has been to assess the characteristics of acute poisoning deaths in Poland over a period of time 2009-2013.Material and Methods: The analysis was based on the data obtained from the patient records stored in toxicology departments in 6 cities - Łódź, Kraków, Sosnowiec, Gdańsk, Wrocław and Poznań. Toxicological analyses were routinely performed in blood and/or urine. Major toxic substances were classified to one of the following categories: pharmaceuticals, alcohol group poisonings (ethanol and other alcohols), gases, solvents, drugs of abuse, pesticides, metals, mushrooms, others. Cases were analyzed according to the following criteria: year, age and gender of analyzed patients, toxic substance category and type of poisoning. The recorded fatal poisonings were classified according to the International Classification of Diseases.Results: The record of 261 deaths were retrospectively reviewed. There were 187 males (71.64%) and 74 females (28.36%) and the male to female ratio was 2.52. Alcohol group poisonings were more frequently responsible for deaths in men compared to all poisonings, 91.1% vs. 71.6%, respectively (p < 0.05), and pharmaceutical agents were more frequently responsible for deaths in women, 47.4% vs. 28.4%, (p < 0.05). Methanol was the most common agent in the alcohol group poisonings, accounting for 43.75% (N = 49), followed by ethylene glycol, 39.29% (N = 44), and ethanol, 16.96% (N = 19).Conclusions: Epidemiological profile data from investigation of poisoning deaths in Poland may be very useful for the development of preventive programs. Int J Occup Med Environ Health 2017;30(6):897-908. [ABSTRACT FROM AUTHOR]

Objective: The aim of this paper is to provide an overview of the delayed neurologic syndrome of carbon monoxide poisoning and its clinical importance in psychiatric settings.Method: A brief review of carbon monoxide poisoning is presented with a focus on the delayed neurologic syndrome and a case of deliberate self- poisoning is described.Results: As in the case described, the delayed manifestations of carbon monoxide poisoning can resemble a relapse of psychiatric illness.Conclusions: In cases of carbon monoxide poisoning it is important to consider the delayed neurologic syndrome as misdiagnosis could lead to inappropriate treatment and worsened outcome. [ABSTRACT FROM AUTHOR]

[Display omitted] • Poisoning effects of lead on NO and dioxins removal over VWTi catalyst were investigated. • Pb2+destroyed the V = O and V-OH bonds through the formation of -V-O-Pb bonds. • The formation of V-O-Pb bonds reduced the number of acidic sites on catalyst surface. • The formation of PbSO 4 led to a poor regeneration performance of the poisoned catalyst. V 2 O 5 -WO 3 /TiO 2 (VWTi) catalyst is widely used for simultaneously eliminating the NO and dioxins from the iron ore sintering flue gas. However, the catalyst is confronted with deactivation by heavy metals during operation. Here, we studied the effects of PbCl 2 and PbO on catalytic elimination NO and dioxins over VWTi catalyst based on the presence of lead species in sintering flue gas. Variations of catalytic activity, surface acidity, and regeneration performance were evaluated. The results confirmed that the deactivation degree was in correlation with the lead content, the influence of the existing forms of lead on the catalyst surface on denitrification, and dioxin removal activities were following the sequence: PbO > PbCl 2. The introduction of lead species could occupy acidic sites on the catalyst surface, resulting in a decrease in the V5+/V4+ molar ratio, the surface chemisorbed oxygen, and the amount of acid on the catalyst surface. XRD investigations show that the formation of PbSO 4 precipitates by the reaction of lead ions with sulfate groups on the catalyst's surface reduced the number of acidic sites provided by sulfate groups. Besides, the formation of PbSO 4 on the catalyst's surface also led to the failure of lead ion removal by regeneration treatment, consequently resulting in the catalytic activity can handly be effectively repaired. [ABSTRACT FROM AUTHOR]

Carbon monoxide (CO) poisoning is still a health problem all over the world. Informing users about symptoms and suggesting annual inspection of CO producing devices will result in CO poisoning reduction. The goal of this study was to evaluate awareness about CO poisoning symptoms and its prevention ways in Iranian population. In this study, a total of 700 patients' family members attended Imam Khomeni hospital were asked to enroll in the study. A structured questionnaire was used including demographic characteristics, devices which were used at home, awareness of CO poisoning symptoms, awareness of CO detectors, the last time that tubal patency of devices are checked, if it is helpful to open the window to fix gas leak and if surveying devices by an expert at the beginning of the cold season is recommended. A total of 635 participants completed questionnaires. The most used device was gas water heater followed by gas heater. Five hundred and nine reported that they are aware of CO poisoning symptoms (80.1%), 398 (62.6%) stated that it is possible to detect CO leak and 566 (89.1%) told CO detectors would be helpful for reduction of mortality from CO poisoning. Fifty percent of participants had not checked their devices since they have bought their devices. Five hundred and thirty-six (84.4%) reported that opening window could help CO leak, and 596 (93.8%) agreed that an expert checked their fuel-burning devices at the beginning of the winter. Iranian people are not aware of all CO poisoning symptoms. Developing a national strategy for CO surveillance and people education will be helpful. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide is a colorless gas and has a strong odor of rotten eggs. It is absorbed by the upper respiratory tract mucosa, and it causes histotoxic hypoxemia and respiratory depression by exerting an inhibitory effect on cytochrome oxidase. To evaluate the role of toxicological data in distinguishing between the H2S blood concentration secondary to lethal poisoning and the endogenous H2S produced during putrefaction, we compared the postmortem H2S concentrations of six fatal H2S poisoning cases (8.7-28.6 mg/L) with the postmortem concentrations of endogenous H2S of 12 subjects who died from other causes (traffic-related deaths) (2.2-32.7 mg/L). These results will be of interest to the forensic community as it underlines the importance of considering circumstantial evidence along with the toxicological and pathological findings in the identification of H2S lethal poisoning. [ABSTRACT FROM AUTHOR]

The article presents a study that examines the carbon monoxide (CO) poisoning in the United Arab Emirates. The study investigates 46 cases of CO poisoning presenting at emergency departments from 2007 to 2009 of the two main hospitals in Al Ain city through interviews, hospital records and surveys. It reveals that 52 percent of the cases are were males and 80 percent were foreign nationals.

Cyanide causes intracellular hypoxia by reversibly binding to mitochondrial cytochrome oxidase a3. Signs and symptoms of cyanide poisoning usually occur less than 1 minute after inhalation and within a few minutes after ingestion. Early manifestations include anxiety, headache, giddiness, inability to focus the eyes, andmydriasis. As hypoxia progresses, progressively lower levels of consciousness, seizures, and coma can occur. Skin may look normal or slightly ashen, and arterial oxygen saturation may be normal. Early respiratory signs include transient rapid and deep respirations. As poisoning progresses, hemodynamic status may become unstable. The key treatment is early administration of 1 of the 2 antidotes currently available in the United States: the well-known cyanide antidote kit and hydroxocobalamin. Hydroxocobalamin detoxifies cyanide by binding with it to form the renally excreted, nontoxic cyanocobalamin. Because it binds with cyanide without forming methemoglobin, hydroxocobalamin can be used to treat patients without compromising the oxygen carrying capacity of hemoglobin. INSET: CCN Fast Facts. [ABSTRACT FROM AUTHOR]

Introduction. Ingestion of concentrated hydrogen peroxide (H2O2) has been associated with venous and arterial gas embolic events, hemorrhagic gastritis, gastrointestinal bleeding, shock, and death. Although H2O2 is generally considered a benign ingestion in low concentrations, case reports have described serious toxicity following high concentration exposures. Hyperbaric oxygen (HBO) has been used with success in managing patients suffering from gas embolism with and without manifestations of ischemia. Methods. Poison center records were searched from July 1999 to January 2010 for patients with H2O2 exposure and HBO treatment. Cases were reviewed for the concentration of H2O2, symptoms, CT scan findings of portal gas embolism, HBO treatment, and outcome. Results. Eleven cases of portal gas embolism were found. Ages ranged from 4 to 89 years. All but one ingestion was accidental in nature. In 10 cases 35% H2O2 was ingested and in 1 case 12% H2O2 was ingested. All abdominal CT scans demonstrated portal venous gas embolism in all cases. Hyperbaric treatment was successful in completely resolving all portal venous gas bubbles in nine patients (80%) and nearly resolving them in two others. Ten patients were able to be discharged home within 1 day, and one patient had a 3.5-day length of stay. Conclusions. HBO was successful in resolving portal venous gas embolism from accidental concentrated H2O2 ingestions. [ABSTRACT FROM AUTHOR]

BACKGROUND: We aimed to evaluate 39 patients with CO poisoning followed-up in terms of clinical and laboratory findings. The study focused on examining the relationship between clinical status, carboxyhemoglobin and lactate level as well as determining the existence of myocardial ischemia. METHODS: Thirty nine cases between 1.5 months- 17 years old were enrolled prospectively. Demographics, source of carbon monoxide, time of admission, complaints, history of syncope, previous oxygen treatments, clinical findings and blood gas analysis were recorded. To evaluate myocardial ischemia electrocardiogram, creatine kinase myocardial band and troponin-I levels were measured. Echocardiogram was applied to cases with elevated myocardial enzymes. The relationship between neurological symptoms and cardiac damage with carboxyhemoglobin and lactate levels were evaluated. RESULTS: There was a positive correlation between carboxyhemoglobin and lactate levels of cases who had not taken oxygen before admission (r=0.621, p) CONCLUSION: Elevated lactate level is correlated with neurological symptoms and should be consider in carbon monoxide poisoning. While carboxyhemoglobin level is an important factor to diagnose and follow-up the measurement of carboxyhemoglobin levels alone may be insufficient to rule out the diagnosis. There should be studies with larger group of patients regarding the need of routine myocardial enzymes evaluation in cases that do not have clinical and electrocardiographic findings. [ABSTRACT FROM AUTHOR]

After rescue and transport a patient with severe carbon monoxide poisoning (CO-Hb concentration 82%) was treated by hyperbaric oxygen (HBO) therapy in a pressure chamber. During decompression the patient suffered cardiac arrest due to massive acidosis, hyperpotassaemia, haemoconcentration and elevated CO-Hb level. After successful resuscitation and cardiopulmonary diagnostics, HBO therapy was continued for prophylactic treatment of delayed neurological sequelae. Three months after completing treatment and discharge from hospital there were no neurological sequelae. [ABSTRACT FROM AUTHOR]

Despite advances in carbon monoxide detection in the residential setting, this product of incomplete combustion continues to present a significant hazard to children. The clinician must have a high index of suspicion if a patient presents even with vague symptoms and signs that are consistent with carbon monoxide poisoning, which may produce both immediate and delayed effects. Treatment should focus on immediate administration of 100% oxygen, with consideration for hyperbaric oxygen. [Copyright &y& Elsevier]

The article presents information on the study of acute welding exposure and its causes. The purpose of the study is to analyze and examine the correlation of fine particulate matter exposure along with Deoxyribonucleic acid (DNA) alteration and oxidative strain among boilermakers who are exposed to welding emissions. These welding fumes are the major contributors of occupational disorders to the employees, especially to the staff who are working in the field of welding and these welding fumes can cause metal fume fever, pneumonia, and occupational asthma.

The potency of newly developed oximes (K074, K075) and commonly used oximes (obidoxime, trimedoxime, and HI-6) to counteract tabun or cyclosarin-induced acute toxic effects was studied in mice. The therapeutic efficacy of trimedoxime and both newly developed oximes (K074, K075) was significantly higher than the potency of obidoxime and the oxime HI-6 in the case of acute tabun poisonings. On the other hand, the oxime HI-6 was significantly more efficacious than other studied oximes when mice were intoxicated with cyclosarin. The findings support the hypothesis that the therapeutic efficacy of oximes depends on the type of nerve agent. Due to their therapeutic efficacy, both newly developed K oximes can be considered to be promising oximes for the antidotal treatment of acute tabun poisonings, while the oxime HI-6 is still the most promising oxime for the treatment of acute cyclosarin poisonings due to its high potency to counteract cyclosarin-induced acute toxic effects. [ABSTRACT FROM AUTHOR]

Objectives: Carbon monoxide (CO) toxicity causes significant central nervous system and cardiac injury. Although the neurological damage caused by CO toxicity is extensively described, the mechanisms underlying myocardial insult are unclear. The authors used an externally perfused isolated rat heart model to examine the effects of a physiological saline solution (Krebs Henseleit HEPES, KHH) aerated with CO on cardiac function. Methods: Fifteen rats were equally divided into three groups: the control group (KHH + 100% O2), the nitrogen control group (KHH + 70% O2, 30% N2), and the CO group (KHH + 70% oxygen, 30% CO). Left ventricular peak systolic pressure (LVPsP), end diastolic pressure (LVEdP), and coronary perfusion pressure were measured while the isolated heart was paced and perfused on a modified Langendorf apparatus. Results: Left ventricular generated pressure (LVGP = LVPsP − LVEdP) decreased in the nitrogen control and CO groups compared to the control group. There was higher LVGP in the recovery phase between the nitrogen control group compared to the CO group. Both groups had increased lactic acid levels in the experimental phase. Conclusions: Carbon monoxide with hypoxia and hypoxemic hypoxia both result in similar depression of cardiac function. Hearts poisoned with CO with hypoxia do not recover function to the extent that hearts rendered hypoxic with nitrogen do when perfused with 100% oxygen after the insult. This suggests that CO causes direct myocardial toxicity distinct from the effects of hypoxia. [ABSTRACT FROM AUTHOR]

Methanol poisoning in Australia is now very rare as methanol has been removed from methylated spirits. In acute intoxication methanol may result in a wide range of damage to the central nervous system. Few cases have been imaged with MRI. We present two cases and their striking neuroimaging findings with a discussion of the published work on methanol poisoning. [ABSTRACT FROM AUTHOR]

A case study about carbon monoxide poisoning was used help students gain a greater understanding of the physiology of oxygen transport by the blood. A review of student answers to the case questions showed that students can use the oxygen-hemoglobin dissociation curve to make meaningful determinations of oxygen uptake and delivery. However, the fact that many students had difficulty locating the effect of carbon monoxide poisoning in the process of external respiration suggests that these students have not built a robust model of how oxygen distributes itself between the plasma and hemoglobin. This suggests that more determined emphasis on how oxygen enters the blood and how it is partitioned between hemoglobin and the plasma would help students develop more accurate mental models of how oxygen moves from the lungs to the tissues. [ABSTRACT FROM AUTHOR]

Sulphur mustard (SM) is an alkylating chemical warfare agent that was widely used during the World War I and in the Iran–Iraq conflict. Delayed complications of SM in different organs and their severity correlations have not previously been reported. Dermatological, ophthalmological, neurological and respiratory examinations, as well as spirometry, gasometry, high resolution computed tomography scanning of the chest, electromyography, nerve conduction velocity, cell blood counts, flow-cytometric analyses, and measurement of serum immunoglobulins and complement factors were performed on all severely SM poisoned veterans in the province of Khorasan, Iran. Haematological and immunological studies were also performed on a control group consisting of 35 healthy male subjects. The severity of dermal, ocular and respiratory complications were classified into four grades and their correlations with each other as well as with the haematological and immunological parameters were determined, using Spearman's rank correlation test. Forty male patients (aged 43.8 ± 9.8 years) with confirmed SM poisoning 16–20 years after the exposure were studied. The most common complications were found in the lungs (95%), peripheral nerves (77.5%), skin (75%), and eyes (65%). WBC, RBC, haematocrit (HCT), IgM, C3, and the percentages of monocytes and CD3+ lymphocytes were significantly ( P < 0.042) higher and the percentage of CD16 + 56 positive cells was significantly ( P = 0.006) lower in the patients than in the control group. The severity of respiratory complications revealed a significant correlation with the severity of ocular complications ( r = 0.322, P = 0.043), as well as with the haemoglobin ( r = 0.369, P = 0.024) and HCT ( r = 0.470, P =0.003). Although late complications of SM poisoning in the skin, eyes, and respiratory system are mainly due to its direct toxic effects, the neuromuscular, haematological and immunological complications are probably the result of systemic toxicity. [ABSTRACT FROM AUTHOR]

Mustard gas or sulfur mustard (SM) is an alkylating chemical warfare agent that was widely used during the World War I and in the Iran-Iraq conflict. We aimed to study late toxic effects of SM on the respiratory system of severely intoxicated Iranian veterans. Respiratory examination, spirometry, arterial blood gas (ABG) analysis, and high resolution computed tomograpghy (HRCT) of the chest were performed on all severely SM-poisoned veterans in the province of Khorasan, Iran. HRCT abnormalities were classified into four grades based on the number of lung lobes involved. ABG and spirometric results were compared with each other, as well as, with the severity grades of HRCT abnormalities, using Spearman's rank correlation test. Forty male subjects with confirmed SM poisoning 16 to 20 years ago, were studied. Main respiratory complications were diagnosed as chronic obstructive pulmonary disease (COPD) (35%), bronchiectasis (32.5%), asthma (25%), large airway narrowing (15%), pulmonary fibrosis (7.5%), and simple chronic bronchitis (5%) patients. While there was a significant correlation (p 2 . We concluded that SM-induced respiratory complications tend to progress over the years. While spirometry is a valuable diagnostic tool for evaluation of pulmonary impairment during regular follow-ups, ABG and HRCT are more objective and should be more considered for evaluation of the severity and for diagnosis of the respiratory complications. [ABSTRACT FROM AUTHOR]

To describe diagnostics, therapy, and sequelae of acute carbon monoxide (CO) toxicity because of a motor vehicle generator in 4 dogs and 2 cats. Four dogs and 2 cats presented for recumbency, disorientation, dyspnea, and stiffness after an estimated 6–8 hour exposure to exhaust from a generator. Diagnostics included a serum carboxyhemoglobin levels evaluation, arterial blood gas analysis, pulse oximetry readings, and blood pressure measurements. Initial therapy included oxygen (O2) administration, intravenous bronchodilators, fluids, and a hemoglobin-based O2 carrying (HBOC) molecule. Following administration of the HBOC, 4 of the 6 animals showed dramatic clinical improvement. Two weeks after hospital discharge, the owner reported potential hearing deficits in all animals. Brain auditory evoked response (BAER) tests were conducted in all surviving animals and some degree of hearing impairment was documented in all cases, with complete clinical resolution noted 6 weeks later. This report describes the therapeutic use of an HBOC in acute isolated CO toxicity (i.e. without the complications of smoke inhalation). In addition, delayed nervous system dysfunction was documented in all surviving animals. [ABSTRACT FROM AUTHOR]

Abstract: We report on a patient with delayed carbon monoxide encephalopathy who presented with severe cognitive impairment associated with MRI findings of extensive demyelination of the cerebral white matter after a silent period of three weeks from acute intoxication. Despite the severe signs of structural and functional cerebral impairment in the sub-acute stage, the clinical course was favorable but for residual mild dysfunction of the frontal lobes. [Copyright &y& Elsevier]

Estimates of unintentional deaths from carbon monoxide (CO) poisoning can be obtained from national mortality data. We explored ways of accurately estimating CO-related deaths from International Classification of Diseases, 9th Revision (ICD-9) coded U.S. mortality data. We evaluated and identified CO-related ICD-9 codes and created five classes of codes for case ascertainment that represented a continuum of the degree of certainty that the ICD-coded death was truly CO-related. We conducted single (underlying) cause-of-death and multiple-cause-of-death analysis using 20 years of data (1979-1998), and calculated sensitivity and positive predictive value using different criteria for case ascertainment. Single-cause analysis provided accurate estimates only when we used CO-exclusive E-codes, however this method failed to identify approximately one third of the CO-related deaths over the study period. Single-cause analysis overestimated the number of CO-related deaths when we used E-codes that were not exclusive to CO exposure. Identification of true CO-related deaths required multiple cause-of-death analysis and use of the CO nature-of-injury code, N986, to confirm suspected cases. Sensitivity of N986 was 99.5%, and positive predictive value of the individual E-codes in single cause-of-death analysis ranged from 1.5% to 92%. Estimating CO-related deaths from ICD-coded data requires a thorough understanding of the ICD codes, coding rules, and of the limitations imposed by case selection criteria and single cause-of-death analysis. [ABSTRACT FROM AUTHOR]

Presents a study to examine fatal and nonfatal unintentional, non-fire-related carbon monoxide exposures by analyzing data on emergency department visits from the National Electronic Injury Surveillance System All Injury Program and 2001-2002 death certificate data from the National Vital Statistics System. Description of the study; How males were more likely to die from carbon monoxide poisoning; Need for efforts to educate the public about preventing carbon monoxide exposure.

The manufacture and application of aluminium phosphide fumigants pose risks of inhalation exposure to phosphine gas. This article presents a case report of suspected inhalation exposure to phosphine gas in a manufacturing facility for aluminium phosphide fumigants, which was associated with acute dyspnoea, hypotension, bradycardia and other signs of intoxication. These symptoms resolved within several hours after removal from exposure. A review of the data on human exposures to phosphide fumigants identifies both pesticide applicators and individuals in the vicinity of application to be at risk of accidental exposure and injury from phosphine inhalation. More recent reports have identified risks of phosphine gas inhalation in association with the clandestine production of methamphetamine. Toxicodynamic effects of phosphine result from the inhibition of cytochrome c oxidase and subsequent generation of reactive oxygen species. There remain unanswered questions relating to the toxicokinetics of phosphine, as well as the assessment of human exposure utilizing biomarkers. As initial signs and symptoms of intoxication from phosphine gas may be nonspecific and transient, there is a need for improved recognition of the potential hazards associated with phosphide fumigants and phosphine gas. [ABSTRACT FROM AUTHOR]

Nerve agents are organophosphate compounds similar to those used as pesticides but with much higher toxicity. They all block the activity of the enzyme acetylcholine esterase. Victims are intoxicated by absorption of the toxin via exposed skin or, more commonly, via inhalation of the poisonous gas. The resultant clinical picture is of hyperstimulation of both the nicotinic and muscarinic cholinergic system, which, if not promptly treated, leads to severe muscle paralysis, cardiac brady-asystole, hypersecretion from secretory glands, respiratory failure, seizures, coma and death. If antidotal drugs are promptly administered, the clinical severity of the poisoning is attenuated or complete abortion of symptoms is obtained. The main therapeutic strategies include atropine and oximes that counteract the nerve-agent-induced muscarinic and nicotinic cholinergic symptoms, respectively. Anticonvulsants and sedatives are used to treat central nervous system acetylcholine esterase disarray. This review summarizes the biochemistry and pathophysiology of anticholinesterase poisoning, the relevant clinical manifestations and the currently available therapeutic strategies. [ABSTRACT FROM AUTHOR]

This comprehensive response was invited by the Editor ofEmergency Medicine Australasiato allow our Group from Salt Lake City, Utah to review the two articles‘Where to now with carbon monoxide poisoning?’ by Scheinkestelet al. and the accompanying Commentary:‘The dilemma of managing carbon monoxide poisoning’ by Emerson published in the April issue ofEmergency Medicine Australasia. [ABSTRACT FROM AUTHOR]

The neuropathological sequelae of carbon monoxide (CO) poisoning cannot be explained by hypoxic stress alone. CO poisoning also causes adduct formation between myelin basic protein (MBP) and malonylaldehyde, a reactive product of lipid peroxidation, resulting in an immunological cascade. MBP loses its normal cationic characteristics, and antibody recognition of MBP is altered. Immunohistochemical evidence of degraded MBP occurs in brain over days, along with influx of macrophages and CD-4 lymphocytes. Lymphocytes from CO-poisoned rats subsequently exhibit an auto-reactive proliferative response to MBP, and there is a significant increase in the number of activated microglia in brain. Rats rendered immunologically tolerant to MBP before CO poisoning exhibit acute biochemical changes in MBP but no lymphocyte proliferative response or brain microglial activation. CO poisoning causes a decrement in learning that is not observed in immunologically tolerant rats. These results demonstrate that delayed CO-mediated neuropathology is linked to an adaptive immunological response to chemically modified MBP. [ABSTRACT FROM AUTHOR]

Copyright of Canadian Geotechnical Journal is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Canadian Geotechnical Journal is the property of Canadian Science Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Presents a study which examined the epidemiology of acute carbon monoxide poisoning in a Spanish region. Methods; Results; Discussion.

Describes the epidemiology of unintentional carbon monoxide poisoning deaths in the U.S. Factors that can be attributed to the decrease in the rate of unintentional death from carbon monoxide poisoning; Effects of carbon monoxide on people; Trends in unintentional deaths caused by carbon monoxide poisoning; Demographic characteristics of the victims.

Evaluates male and female patients exposed to sarin poisoning during the Tokyo subway incident in Japan, focusing on the chronic neurobehavioral effects of this sarin poisoning. Number of tests conducted; What results revealed in relation to analysis covariance; Perception that a chronic effect on psychomotor performance was caused by acute sarin poisoning.

Reports on the features of severe sarin poisoning in Matsumoto, Japan. Presence of miosis and neuropathy; Use of epileptiform electroencephalography to record damages.