Chronic Carbon Monoxide Poisoning Research Articles

NANOCOMPOSITE-BASED THIN FILM CARBON MONOXIDE SENSORS

Over the past decade, organic semiconductors have been of great interest in basic research and practical applications. Composites based on organic materials have become widespread due to their unique properties and partial biodegradability: they are also suitable as sensitive materials — sensors for detecting various gases. One such gas is carbon monoxide or a different carbon monoxide. Carbon monoxide occurs wherever conditions exist for incomplete combustion of carbon-containing substances. One of the industrial industries where carbon monoxide is emitted in large volumes is the oil and gas industry. The main source in this industry are flares for combustion of associated gases, during the operation of gas turbine plants, as well as exhaust gases from internal combustion engines of construction, drilling equipment, vehicles, etc. Due to the high toxicity of carbon monoxide, it is necessary to create highly sensitive materials for CO sensors. So, when inhaling small concentrations of carbon monoxide (up to 1000 mg/m3), a person feels heaviness in the head, dizziness, nausea, a feeling of pleasant exhaustion, due to which a person cannot soon leave the affected area, and with prolonged (2–3 months) contact with CO, chronic carbon monoxide poisoning is possible at a concentration of 10-50 mg/m3. Therefore, the search for a new material having high sensitivity and selectivity to carbon monoxide is relevant. The purpose of this study is to develop a highly sensitive electronic gas sensor for detecting carbon monoxide at room temperature. The films were made by irrigation from a polymer solution containing graphene oxide and carbon nanotubes. The morphology of the surface of thin polymer films was investigated, spectral chemical analysis was carried out, voltampere characteristics of sensors were measureed0 and an IoT (Internet of Things) solution for remote monitoring was developed. The results show a good response and repeatability of the results at room temperature, allowing the thin films of the graphene polymer-CNT oxide composite to be considered a promising electronic sensor material for CO detection.

Three-step analysis of symptoms of carbon monoxide poisoning in pre-hospital medical response teams

Diagnosing chronic carbon monoxide poisoning can be a challenge for medical response teams. It is charaterised by unclear symptoms, which develop in a manner similar to many chronic cardiological or neurological diseases, and has consequences that can occur up to several months later. As a result, the character of such poisoning is often under¬estimated in daily practice. Multiple interventions and working under pressure does not always allow for a detailed analysis of many factors. It is therefore vital to develop solutions that allow for quick assessment of whether a patient has been exposed to carbon monoxide poisoning. Three-step analysis of the symptoms of poisoning is an ideal exam¬ple. This consists of a consultation on exposure to carbon monoxide poisoning, the presence of symptoms suggesting hypoxia due to poisoning, and determining the carboxyhaemoglobin index using equipment carried by the medical response team. Emergency procedures based on these three elements result in rapid identification of people suffering from carbon monoxide poisoning who require oxygen therapy, and the transportation of such people to specialised units for hyperbaric oxygen therapy. This system of analysis can also be used as part of a standard examination for assessing the exposure of a patient to carbon monoxide, both in hospital emergency departments and in medical response teams.

Chronic carbon monoxide poisoning. A report of two cases

If acute carbon monoxide poisoning is a well-known emergency situation, this is not the case for chronic poisoning. The missed diagnosis of acute CO poisoning is a well-known problem but the identification of a chronic poisoning is very challenging. Knowledge and awareness of chronic poisoning is less defined and probably there is a great number of patients with undiagnosed chronic CO poisoning. It is possible that in case of missed diagnosis because of non-specific symptoms, chronic CO poisoning could be responsible for significant morbidity. We describe the case of a married couple who were rescued almost simultaneously, to show this clinical condition.

Repeated unconsciousness due to chronic carbon monoxide poisoning in an older patient: a case report.

Objective: Although much is known about acute carbon monoxide (CO) poisoning, little is known about chronic CO poisoning. Chronic CO poisoning is often diagnosed based on the patient’s living environment and medical history. Herein, we report the case of an older patient who presented with repeated unconsciousness due to chronic CO poisoning.Case presentation: A 90-year-old man was brought to the emergency department after being found at home with a disturbance of consciousness. Arterial blood gas measurements in room air revealed a carboxyhemoglobin level of 18.0%. Impaired consciousness was caused by chronic CO poisoning. The patient received high-flow oxygen therapy, which promptly improved his condition. According to his family, briquette kotatsu was the cause of chronic CO poisoning.Conclusion: Although high-flow oxygen therapy has been said to be less effective than hyperbaric oxygen therapy in CO poisoning treatment, recent studies have demonstrated that high-flow oxygen has similar effects and benefits. Thus, in institutions that do not have hyperbaric oxygen, high-flow oxygen may be sufficient to treat patients with CO poisoning, as seen in the present case. It should be noted that briquette kotatsu can lead to CO poisoning. This case highlights the need for clinicians to consider patients’ living conditions.

Serum Netrin-1 and Asymmetric Dimethylarginine as Biomarkers of Acute and Chronic Carbon Monoxide Poisoning

Diagnosis of carbon monoxide (CO) poisoning is done traditionally by detecting carboxyhemoglobin (COHb) level. However, the severity of clinical manifestations is unrelated to the absolute levels of COHb. Netrin-1 (Net-1) is a protein with anti-inflammatory and anti-apoptotic properties while asymmetric dimethylarginine (ADMA) is an oxidative stress indicator. This study aimed at assessing and comparing between Net-1, ADMA and COHb as biomarkers in CO poisoning. This cross-sectional clinical study was carried out on 30 acutely CO poisoned adults admitted to Benha Poisoning Control Unit, Benha University Hospitals; 30 chronic CO exposed workers at four different car service centres, plus 30 healthy controls. Results showed a positive correlation between serum levels of Net-1 and ADMA and the severity of acute CO poisoning both on admission, and after oxygen therapy. There was a positive correlation between COHb level and both serum levels of Net-1 and ADMA in chronic cases. In conclusion: COHb level can only support the initial diagnosis of acute CO poisoning. Both ADMA and Net-1 are better biomarkers in assessing the severity of acute CO poisoning, where ADMA is better than Net-1. In diagnosis of chronic CO poisoning, both ADMA and Net-1 are as dependable as COHb.

DTI-Correlated Parkinsonism after Chronic Carbon Monoxide Poisoning (P4.006)

DTI-Correlated Parkinsonism after Chronic Carbon Monoxide Poisoning (P4.006)

Chronic exposure to carbon monoxide in two elderly patients using a kotatsu, a traditional Japanese charcoal‐based heater

We report on two elderly patients with cognitive impairments, for whom chronic carbon monoxide (CO) exposure was suspected based on elevated carboxyhaemoglobin levels in their serum. On their initial visits, cognitive impairment and brain magnetic resonance imaging findings in both patients were compatible with the diagnosis of Alzheimer's-type dementia. However, after discontinuation of the use of a kotatsu, a charcoal-based heater, their serum carboxyhaemoglobin levels normalized and their physical symptoms resolved. Their cognitive function also slightly improved. The causal relationship between physical symptoms and cognitive impairment after chronic CO poisoning is uncertain; however, it is possible that chronic exposure to low CO levels exacerbated the clinical manifestation in our patients.

Carbon Monoxide Exposure During Pregnancy.

Carbon monoxide (CO) is the leading cause of poisoning in the United States and is associated with high maternal and fetal mortality rates. Given the nonspecific signs and symptoms of toxicity, cases may go unsuspected or attributed to other etiologies. As CO adversely affects both mother and fetus, it is important for practitioners to recognize and treat poisoning in a timely manner. We seek to assist practitioners with understanding the physiology and recognizing the presentations of both acute and chronic CO poisoning, as well as provide information on diagnosis and treatment options. We also conducted a review of cases described in the literature during the past half century to show varying presentations and treatment methodologies. A qualitative literature search was conducted using PubMed and Google Scholar for articles published between 1970 and 2014 that assessed cases of CO poisoning during pregnancy. Excluded studies were not in English or contained nonhuman subjects. Nineteen published reports of CO poisoning during pregnancy described in varying levels of detail were found in the literature from 1971 to 2010. Carbon monoxide poisoning requires a high degree of suspicion. Diagnosis is made based on initial history and physical evaluation and assessment of environmental CO levels; presenting carboxyhemoglobin levels may be poor indicators of severity of disease. Oxygen therapy should be initiated promptly in all possible cases with consideration of hyperbaric oxygen therapy in cases of significant maternal exposure. Treatment requires a longer duration for fetal CO elimination than in the nonpregnant patients. Importantly, practitioners should educate pregnant patients on prevention.

An epidemiological study of acute carbon monoxide poisoning in the West Midlands.

OBJECTIVES: To describe the epidemiology of carbon monoxide (CO) poisoning in a defined population, identifying those at greatest risk from acute poisoning resulting in admission to hospital or death. METHODS:...

MRI of the brain in chronic carbon monoxide poisoning.

We examined 13 patients with chronic carbon monoxide (CO) poisoning by magnetic resonance imaging (MRI); all of them had been in an explosion in a coal mine 25 years previously. Symmetrical globus pallidus lesions were observed in 12, as was degeneration of the white matter, with focal cortical atrophy. The temporal parietal and occipital lobes were usually affected, the parietooccipital region being the most frequently and extensively damaged. Of the 12 patients with white matter degeneration 7 had definitely asymmetrical cortical and subcortical lesions. There were 6 patients with dilated temporal horns, probably due to atrophy of the hippocampal gyri. A history of CO inhalation and an awareness of the typical distributions of lesions are important for recognition of the effects of CO poisoning, especially when patients are in the chronic stage.

Chronic occult carbon monoxide poisoning.

Chronic occult carbon monoxide poisoning can be a lethal complication of being in a confined environment. The subtlety of the symptoms and the need for immediate care make the role of the emergency department triage nurse essential in helping to facilitate the diagnosis. Posttreatment nursing care also involves instructing the victim and cohabitants on prevention, recognition of signs and symptoms, and the need to monitor for aftereffects.

Cerebral Damage due to Endogenous Chronic Carbon Monoxide Poisoning caused by Exposure to Methylene Chloride

Cerebral Damage due to Endogenous Chronic Carbon Monoxide Poisoning caused by Exposure to Methylene Chloride

Ceruloplasmin activity in rat serum after carbon monoxide poisoning, methemoglobinemia and repeated bleeding

Ceruloplasmin activity in rat serum was markedly inhibited by acute (58 ± 5% COHb) or chronic (36 ± 10 and 50 ± 6% COHb) carbon monoxide (CO) poisoning. Sodium nitrite- (50 ± 5% Met-Hb) or m-dinitrobenzene ( m-DNB)-induced methemoglobinemia (51 ± 6% Met-Hb) did not change the N-dimethyl- p-phenylenediammonium-dichloride oxidizing activity significantly, while decrease of total hemoglobin concentration by 31% from repeated withdrawal of blood produced a distinct increase. The CO effect did not appear to be due to decrease of the oxygen transport capacity of hemoglobin.

Chronic carbon monoxide poisoning: effects on performance of the isolated right ventricle

Rats were exposed continuously for 21-35 days to 500 ppm carbon monoxide (37.4-39.2% HbCO). Aerobic resting force (RF)-active isometric twitch force (AF) curves of isolated right ventricle preparations were constructed at 27 degrees C. CO and control groups are nearly identical when expressed as percent of maximal AF over the range of RF used. There are no significant differences in AF either at the peak of the curve or at RF = 1 g. During 15 min of anoxia AF declines at both RF's used. Increased anoxic tolerance is apparent in all CO preparations when anoxic AF is plotted as percent of preanoxic AF. The effect is most marked at RF = 1 g, where time to one-half preanoxic AF is 12.6 +/- 0.9 vs.9.3 +/- 0.8 min for CO-exposed and controls, respectively. However, no significant differences in "absolute" AF are seen between the groups at either level of RF at any minute during anoxia. Aerobic recovery of CO preparations is markedly enhanced at 1 g RF. Anoxic tolerance and aerobic recovery differences, however, are smaller at the peak of the RF-AF curve. Effects on time to peak AF and maximal rate of rise of AF are not marked at either level of RF in CO preparations.

Hypoxia and bedcovers.

To the Editor.— The letter of Major Allen B. King appearing inTheJournalJune 26, 1972, on the subject of hypoxia and hypercapnia 1 from bedcovers was of particular interest to me because it suggests the probable pathophysiology underlying a type of headache that I have studied in a number of patients. This headache may awaken the patient from sleep during the night, or is present upon first awakening in the morning. It is generalized with bifrontal preponderance, and is similar to the headache of chronic carbon monoxide poisoning. 2 Because of the timing of its occurrence almost every morning upon awakening or during the night, it frequently raises suspicion of a brain tumor. However, on questioning these patients, it is found that they have the habit, as described by Dr. King, of pulling bedcoverings over the head upon retiring. I have thus referred to the resulting headaches as, turtle

Electron microscopic studies on the rebral lesions of rats in experimental carbon monoxide poisoning.

In experimental carbon monoxide poisoning, more marked and widespread pathological changes in the brain were seen in the white matter as compared with the gray matter. No essential difference, in the appearance of cerebral alterations, was detected between acute and chronic carbon monoxide poisoning. It was confirmed that the changes resulting from chronic poisoning showed a higher degree of severity as compared with those resulting from acute poisoning.

The solubilization of deoxyhemoglobin S.

The fundamental defect responsible for sickle-cell disease was recognized by Pauling and his co-workers' as a mutated hemoglobin. A single genetic change2 leads to the synthesis of hemoglobin S which contains a valine residue (instead of glutamic acid') at position 6 of the 13-chain.4-8 Hemoglobin S (Hb S) is thus composed of two normal a-chains and two modified 1-chains and may be written a! A 6v&l 8 In contrast to a normal red blood cell, a sickle cell loses the characteristic biconcave disk shape upon deoxygenation. The distortion in cell shape is caused by gel formation of the deoxyHb S in the cell. The phenomenon may also be observed in stroma-free deoxyHb S solutions.9 Certain hydrocarbons (methane, ethane, and propane) reverse gel formation from deoxyHb S solutions and unsickle sickled cells. On this basis, Murayama'0 proposes hydrophobic bonding as the driving force for the association process. Sickle-cell anemia is a serious disease, its sequellae arising from the abnormal behavior of the sickled cells in the circulation. Individuals afflicted with the disease (perhaps 40,000 in the United States alone) are subject to anemia, recurrent crises, and early death.I Occasional transfusions are the only generally useful supportive measure.12 Drastic techniques like chronic carbon monoxide poisoning,'3 raising the blood pH,'4-'6 oxidation of part of the Hb S to methemoglobin S,17 or supposed inhibition of glucose-6-phosphate dehydrogenase with phenothiazines'8' 19 have little or no clinical value. We have suggested that the introduction of glutamic acid residues into Hb S (a transformation) might diminish the ease of gel formation.a We now report that the solubility of Hb S (Itano2l) can be augmented in the predicted way. Glutamic acid residues can be introduced by reaction of the protein with the Ncarboxyanhydride of glutamic acid.22-24 With a sufficient number of added glutamic acid moieties, the solubility of the modified deoxyHb S exceeds that of deoxyHb A (normal hemoglobin). Methods and Results. -Bloods were drawn from outpatients at Bronx Municipal Hospital Center and Lincoln Hospital, Bronx, New York. All patients were SS and had not been transfused for at least five months. Hb S solutions were prepared from bloods by removal of plasma, washing cells with isotonic buffer, lysis with an equal volume of water, shaking after addition of half a volume of toluene, and separation of the Hb S solutions by centrifugation at 17,000 g. Concentrations were determined spectroscopically with a Cary model 14 spectrophotometer (em8 14,200). All Hb S solutions were maintained at 40 until use. The N-carboxyanhydride of glutamic acid, 1 (NCA 1), was generously supplied by Drs. Ralph Hirschmann and Robert Denkewalter of the Research Laboratories, Merck, Sharp and Dohme, Inc., Rahway, New Jersey. The NCA 1 was transported and stored at -80°. For utilization in the experiments, the stored material

Neurologic manifestations of chronic carbon monoxide poisoning.

ALTHOUGH acute carbon monoxide intoxication is a florid, well known and easily recognized entity, chronic poisoning with carbon monoxide is an insidious disease, more difficult to recognize, but no less dramatic. The preponderance of work on this subject in recent years has come from France and Scandinavia, where it is considered to be a serious problem.1 2 3 Public-health officials in the United States are becoming increasingly aware that chronic carbon monoxide poisoning is frequently encountered,4 particularly in view of the steadily increasing use of gasoline engines. The following case is reported to illustrate presenting symptomatology and diagnostic difficulties that may be . . .

Coronary artery disease.

In this article I will use the terms artery disease, pectoris, insufficiency, and interchangeably and synonymously. Angina pectoris can be manifested by almost any kind of pain and results from a disproportion between the oxygen demand and the oxygen supply of the myocardium. On this basis, many factors may operate in angina pectoris. It may be the result of: 1. Coronary sclerosis, coronary ostial closure, or inflammatory changes in the coronary arteries. 2. Chronic severe anemia or acute anemia, when the blood is unable to carry oxygen to the myocardium, or when the patient is suffering from chronic carbon monoxide poisoning. 3. A severe disease of the mitral or aortic valves, when the minute volume output of the heart cannot be maintained under exertion. Here the stroke volume is so decreased that, no matter how rapidly the rate may increase, the total output of blood

Some observations on serum-copper in chronic carbon monoxide poisoning.

Some observations on serum-copper in chronic carbon monoxide poisoning.