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Clinical manifestation, effects, diagnosis, monitoring of carbon monoxide poisoning and toxicity

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Kingston Rajiah at University of Ulster
Kingston Rajiah
Elizabeth M Mathew
Elizabeth M Mathew
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Abstract

Carbon monoxide is a product of incomplete combustion of organic matter with insufficient oxygen supply to enable complete oxidation to carbon dioxide (CO 2) and is often produced in domestic or industrial settings. In this study the clinical manifestation, effects, diagnosis and toxicity of carbon monoxide poisoning were reviewed. Research suggests that the intracellular uptake of carbon monoxide is an important mechanism for neurologic damage. As a result upon the review of many articles and research journals, it is identified that carbon monoxide may be quantitated in blood using spectrophotometric methods or chromatographic techniques in order to confirm the diagnosis of poisoning in hospitalized victims or to assist in the forensic investigation of a case of fatal exposure. A brain computed tomography (CT) scan may be normal in early stages or show signs of cerebral edema. Public education on the safe operation of appliances, heaters, fireplaces and internal combustion engines is required for prevention of CO poisoning. Carbon monoxide detectors with alarms can improve home safety and their use is recommended by various safety organizations.
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African Journal of Pharmacy and Pharmacology Vol. 5(2), pp. 259-264, February 2011
Available online http://www.academicjournals.org/ajpp
DOI: 10.5897/AJMR11.006
ISSN 1996-0816 ©2011 Academic Journals
Full Length Research Paper
Clinical manifestation, effects, diagnosis, monitoring of
carbon monoxide poisoning and toxicity
Kingston Rajiah1* and Elizabeth Mampally Mathew2
1International Medical University, No. 126, Jalan Jalil Perkasa 19, Bukit Jalil, 57000 Kuala Lumpur, Malaysia.
2Mallige College of Pharmacy, No 71, Silvepura, Bangalore, 560090 Karnataka, India.
Accepted 7 January, 2011
Carbon monoxide is a product of incomplete combustion of organic matter with insufficient oxygen
supply to enable complete oxidation to carbon dioxide (CO2) and is often produced in domestic or
industrial settings. In this study the clinical manifestation, effects, diagnosis and toxicity of carbon
monoxide poisoning were reviewed. Research suggests that the intracellular uptake of carbon
monoxide is an important mechanism for neurologic damage. As a result upon the review of many
articles and research journals, it is identified that carbon monoxide may be quantitated in blood using
spectrophotometric methods or chromatographic techniques in order to confirm the diagnosis of
poisoning in hospitalized victims or to assist in the forensic investigation of a case of fatal exposure. A
brain computed tomography (CT) scan may be normal in early stages or show signs of cerebral edema.
Public education on the safe operation of appliances, heaters, fireplaces and internal combustion
engines is required for prevention of CO poisoning. Carbon monoxide detectors with alarms can
improve home safety and their use is recommended by various safety organizations.
Key words: Carbon monoxide, toxicity, hemoglobin.
INTRODUCTION
Carbon monoxide has been unknowingly used by
humans since prehistoric times, for the smelting of iron
and other metallic ores. The gas was used for executions
by the Greek and Romans in “classical antiquity”, and
was first described by the Spanish doctor Arnaldus de
Villa Nova in the 11th century. In 1776, the French
chemist de Lassone produced CO by heating zinc oxide
with coke (fuel), but mistakenly concluded that the
gaseous product was hydrogen as it burned with a blue
flame. The gas was identified as a compound containing
carbon and oxygen by the Scottish chemist William
Cumberland Cruikshank in the year 1800. Its toxic
properties on dogs were thoroughly investigated by
Claude Bernard around 1846 (Cobb and Etzl, 1991).
SOURCES OF CARBON MONOXIDE
The human body produces carbon monoxide as a
*Corresponding author. E-mail: kingrajiah@gmail.com.
by product of hemoglobin degradation, resulting in
baseline carboxyhemoglobin (COHb) saturation of 1 to
3% in non-smokers and 10 to 15% amongst heavy
smokers. A smoker is exposed to 400 to 500 ppm of CO
while actively smoking (Cobb and Etzl, 1991). According
to ten years review of carbon monoxide related deaths,
more than half of unintentional deaths were caused by
motor vehicle exhaust (Cobb and Etzl, 1991). Burning of
charcoal, wood, kerosene, or natural gas for heating and
cooking also produces carbon monoxide (Raub et al.,
2000). In army setting, poisoning is usually seen in high-
altitude areas where unwary soldiers often sleep in
closed tents with burning bhukharis (charcoal/kerosene)
kept inside (Grace and Platt, 1981). Carbon monoxide
can occur in the presence of other factors, complicating
its management. It is a major contributor in thousands of
smoke inhalation deaths that occur each year.
People, who work with methylene chloride as paint
stripper, can be poisoned because the fumes are readily
absorbed and converted to CO in the liver (Meredith and
Vale, 1988). In such cases, peak COHb levels may be
delayed and prolonged because of on going production of
CO from liver.
260 Afr. J. Pharm. Pharmacol.
TOXICITY OF CO
The amount of CO absorbed by the body depends on
minute ventilation, duration of exposure and concen-
tration of CO in the environment. Carbon monoxide
quickly binds with hemoglobin with an affinity greater than
that of oxygen to form COHb. The resulting decrease in
arterial oxygen content and shift of the oxyhemoglobin
dissociation curve to the left explains the acute hypoxic
symptoms (primarily neurologic and cardiac) seen in
patients with acute poisoning (Mehta et al., 2001). But the
toxic effects of CO cannot be explained by these
processes alone, as COHb levels do not correlate well
with symptoms, outcomes or the phenomenon of delayed
neurologic sequelae (Ely et al., 1995). Research
suggests that the intracellular uptake of carbon monoxide
is an important mechanism for neurologic damage. When
carbon monoxide binds to cytochrome oxidase, it causes
mitochondrial dysfunction resulting into oxidative stress
related damage (Prockop and Chichkova, 2007). The
release of nitric oxide from platelets and endothelial cells,
which forms the free radical peroxynitrite, can further
inactivate mitochondrial enzymes and damage the
vascular endothelium of the brain (Myers and Synder,
1985). The end result is lipid peroxidation of the brain,
which starts during recovery from carbon monoxide
poisoning. With reperfusion of the brain, leukocyte
adhesion and the subsequent release of destructive
enzymes and excitatory amino acids all amplify the initial
oxidative injury (Burney, 1982). The net result is cognitive
defects, particularly in memory and learning with
movement disorders that may not appear for days
following the initial poisoning.
Carbon monoxide exposure has an especially dele-
terious effect on pregnant women, because of the greater
sensitivity of the foetus to the harmful effects of the gas.
The final COHb levels in the foetus significantly exceed
the level of the mother (Remick and Miles, 1997). The
excessive left shift of foetal COHb curve makes tissue
hypoxia more severe by releasing less oxygen to the
foetal tissues (Sato et al., 1990). Although the terato-
genicity of CO is controversial, the risk of foetal injury is
increased (Remick and Miles, 1997; Sato et al., 1990).
Once CO exposure is discontinued, dissociation of COHb
occurs and CO is excreted through the lungs. At
atmospheric pressure, the COHb half-life is 4 to 6 h
which decreases to 40 to 80 min on breathing 100%
oxygen.
Effects of CO
Patients can successfully recover from acute CO poison-
ing only to return, days later with serious neurological
problems, ranging from subtle cognitive deficits (apparent
on neuropsychological testing) to gross incapacitating
movement disorders, resulting from carbon monoxide’s
predilection for basal ganglia (Tibbles, 1996). Within
a day of high CO exposure, neuroimaging can show
decreased density in the central white matter and globus
pallidus. Autopsies have shown involvement of cerebral
cortex, hippocampus, cerebellum, and substantia nigra.
Neurologic sequelae may be evident immediately or may
occur after a lucid interval of up to three weeks. The
incidence of such sequelae can be as high as 40% (for
memory impairment), and they may persist for more than
a year. Children may present with behavioral or learning
problems, while the elderly appear to be more
susceptible to devastating consequences (Burney, 1982;
Sato et al., 1990).
The development of neurologic sequelae cannot be
reliably predicted. However, most cases are associated
with loss of consciousness in the acute phase of
intoxication (Hark and Kennedy, 1998). The standard CO
neuropsychological screen battery helps in objective
evaluation of such patients.
Severe CO poisoning
The symptoms of low level chronic CO intoxication are
non-specific, and unlikely to arouse suspicion of CO as
the cause. It can also exacerbate the preexisting
diseases like ischaemic heart disease or dementia (Sato
et al., 1990). Patients present with bizarre behavioural
abnormalities declining intellect, memory disturbances,
chronic cough or diarrhoea. The condition is often
misdiagnosed as chronic fatigue syndrome, a viral,
bacterial, pulmonary, gastrointestinal infection or immune
deficiency. Patients may occasionally present with
polycythemia or increased hematocrit. COHb is usually
not excessively elevated.
Clinical manifestations
Clinical manifestations of acute CO poisoning can be
vague and may closely mimic various nonspecific viral
illnesses. CO poisoning usually affects many people at
the same time. The acute symptoms of CO poisoning are
reflected in the susceptibility of the brain and heart.
Initially, patients may complain of headache, dizziness,
nausea, emotional liability, confusion, impaired judgment,
clumsiness and syncope (Ely et al., 1995; Myers and
Synder, 1985; Burney, 1982). Vomiting may be the only
presenting symptom in infants and may be misdiagnosed
as gastroenteritis. Coma or seizures can occur in patients
with prolonged CO exposure (Hark and Kennedy, 1998).
Elderly patients, especially those with coronary artery
disease, may have accompanying myocardial ischaemia,
which may result in frank myocardial infarction (Sato et
al., 1990). Prolonged exposures resulting in coma or
altered mental status may be accompanied by retinal
hemorrhages and lactic acidosis (Ely et al., 1995).
Myonecrosis can occur but it rarely leads to
compartment syndrome or renal failure. Cherry-red skin
color associated with severe carbon monoxide
Raijiah and Mathew 261
Table 1. Comparison of clinical features between Mehta et al and Pooled data Ely et al.
Clinical features Mehta et al. (n = 25)%
of patient
Pooled data (Ely et al., Myers et al.,
and Burney) (n = 196)% of patient
Drowsiness and/ or confusion 48 43
Coma 24 6
Hemiparesis 24 6
Seizures 12 -
Angina pectoris 8 9
Dyspnoea/ tachypnoea 80 40
Tachycardia 64 -
Cherry red skin 24 -
Table 2. Levels of COHb and clinical manifestations
Concentration (%) Symptoms
35 ppm (0.0035) Headache and dizziness within six to eight hours of constant exposure.
100 ppm (0.01) Slight headache in two to 3 h.
200 ppm (0.02) Slight headache within two to three hours; loss of judgment.
400 ppm (0.04) Frontal headache within one to 2 h.
800 ppm (0.08) Dizziness, nausea, and convulsions within 45 min; insensible within 2 h.
1,600 ppm (0.16) Headache, tachycardia, dizziness, and nausea within 20 min; death in less than 2 h.
3,200 ppm (0.32) Headache, dizziness and nausea in five to ten minutes. Death within 30 min.
6,400 ppm (0.64) Headache and dizziness in one to two minutes. Convulsions, respiratory arrest,
and death in less than 20 min.
12,800 ppm (1.28) Unconsciousness after 2 to 3 breaths. Death in less than 3 min.
poisoning is seen in only 2 to 3% of symptomatic cases
(Burney, 1982). Various clinical features for evaluation of
such cases are shown in Table 1.
Skin may develop erythematous lesions and bullae
especially over bony prominences. Severe poisoning
often leads to hypotension and pulmonary edema with
the former is the most reliable marker of overall prognosis.
The acute effects produced by carbon monoxide in
relation to ambient concentration in parts per million are
listed in Table 2.
Diagnosis
Physicians should be alert for the symptoms of carbon
monoxide poisoning, especially during the winter, when
risk of continued prolonged exposures may be greater.
Patients who present with flu-like symptoms (that is
headache, nausea, and dizziness) should be questioned
about the use of gas or oil based heating appliances at
home or work. The same symptoms occurring in
housemates are also a warning sign of environmental
exposure. Criteria for admission and prolonged
observation of such cases are shown in Table 3. A hand
held breath analyzer can be used to quickly rule out
carbon monoxide poisoning. However, the incidental
presence of ethanol can result in a false-positive reading.
Comatose patients can be monitored for rhabdomyolysis
by measuring creatine kinase (CK) levels. A brain
computed tomography (CT) scan may be normal in early
stages or show signs of cerebral oedema. Subsequently
CT may show symmetrical bilateral hypodensities of the
basal ganglia, particularly of the globus pallidus and
substantia nigra. The other abnormalities may be
subcortical white matter hypodensities, cerebral cortical
lesions, hippocampal lesions, and loss of gray-white
differentiation.
The electro encephalogram usually demonstrates
diffuse slowing which is of little prognostic value. Single
photon emission computed tomography (SPECT) has
also been used in CO poisoning cases.
Detection in biological specimens
Carbon monoxide may be quantitated in blood using
spectrophotometric methods or chromatographic techni-ques. This
is done in order to confirm a diagnosis of poisoning in hospitalized
victims or to assist in the forensic investigation of a case of fatal
exposure.
Carboxyhemoglobin blood saturations may range up to 8 to 10%
in heavy smokers or persons extensively exposed to automotive
exhaust gases. In symptomatic poisoned patients they are often in
the 10 to 30% range, while persons who succumb may have
postmortem blood levels of 30 to 90% (Sato et al., 1990).
262 Afr. J. Pharm. Pharmacol.
Table 3. Criteria for admission and prolonged observation.
1. Loss of consciousness.
2. Neurological deficit at any time.
3. Clinical or electrocardiographic signs of cardiac compromise.
4. Metabolic acidosis.
5. Abnormal chest radiograph.
6. COHb level >25%,COHb level >15% with a history of cardiac disease
or > 10% in a pregnant patient.
7. PO<60 mm Hg.
Table 4. Indications for HBO therapy in CO poisoning.
1. Comatose patients.
2. Any period of unconsciousness.
3. Any abnormal score on the Carbon monoxide neuropsychological screening battery.
4. Patients with COHb levels >40%.
5. Cardiovascular involvement (chest pain, ECG changes arrhythmias).
6. History of ischaemic heart disease and COHb levels >15%.
7. Pregnant patients with COHb levels >15%.
8. Patients who do not respond to 100% oxygen after 4 to 6 h.
9. Patients with recurrent symptoms up to three weeks after exposure.
TREATMENT
The initial treatment of patients with symptomatic carbon
monoxide poisoning is relatively straightforward. Non-re-
breather mask supplies 100% oxygen to quickly clear
COHb from the blood and this therapy reduces the half-
life of COHb from about 4 to 5 h to 1 h (Grace and Platt,
1981). Oxygenation at a peripheral setup can be given
with a simple oro-nasal plastic mask at a flow rate of 6 to
10 litres/minute which gives oxygen concentration of
about 35 to 50%. Oxygen delivery with face mask with
reservoir corticosteroids, mannitol, hypothermia and
hyperventilation has been recommended in serious cases
of CO poisoning but their benefit has not been proved.
HBO therapy
Hyperbaric oxygen therapy (HBO) for the treatment of
carbon monoxide (CO) poisoning was first discussed by
Haldane in the 1890s and was first used in the 1960s
(Smith, 1962). At the time, CO toxicity was thought to
result entirely from the relative anemia and hypoxia
imposed by the formation of carboxyhemoglobin (CO-
Hgb) (Haldane, 1972). We now know that the
pathophysiology of CO poisoning is much more complex
and involves direct toxicity at the cellular level (Kao and
Nanagas, 2005). Mechanisms and potential treatments
for CO poisoning are an area of active basic science and
animal research. Clinically intriguing is a syndrome of
apparent recovery followed approximately 2 weeks later
by behavioral and/or neurologic deterioration. This is
known as delayed neurologic sequelae (DNS) and it may
be debilitating and permanent (Thom and Keim, 1989;
Min, 1983; Myers et al., 1985; Prockop; 2005). The exact
cause and incidence of DNS remains elusive as does of
a precise definition. Indications for HBO therapy in CO
poisoning is given in Table 4.
Chem-optical (gel cell) technology
Chem-optical technology (or gel cell or biomimetic
technology) alarms use a type of sensor that simulates
haemoglobin in the blood.
Electrochemical alarm
Electrochemical alarms work by converting the carbon
monoxide electrochemically to carbon dioxide, which
generates an electrical current that is taken as a measure
of the gas concentration. Electrochemical alarms are
usually powered by a battery lasting about five years.
Semiconductor technology
These alarms use semiconductors or tin dioxide
technology to detect carbon monoxide levels. Unlike the
alarms above, semiconductor detector alarms do not
require any replacement sensors. The British Standards
Institute (BSI) is a national standards body, responsible
for ensuring products meet certain agreed standards of
safety. BSI standard BS7860 is the one for monitors that
detect carbon monoxide at levels well before they
become dangerous for humans (Tibbles, 1996). Preven-
tion requires public education on the safe operation of
appliances, heaters, fireplaces and internal combustion
engines. Increased awareness amongst soldiers posted
to cold/high altitude areas about the dangers of using
sigris and bhukharis in enclosed places like
tents/bashas/barracks/rooms will go a long way in
preventing CO poisoning and deaths.
Burned victims, with evidence of smoke inhalation from
an enclosed fire, should undergo testing for COHb levels.
During winters, CO poisoning should be suspected in
patients presenting with flu-like symptoms (for example
headache, dizziness and nausea), which they may not
attribute to a faulty furnace or other heating sources.
Carbon monoxide detectors with alarms can improve
home safety and their use is recommended by various
safety organizations.
PREVENTION
Carbon monoxide detectors are available from most local
hardware. They can provide an audible high-pitched
alarm when high levels of carbon monoxide are detected
or provide an alarm plus a digital display of the
concentration of carbon monoxide detected in units of
'parts per million' (ppm). Three types of carbon monoxide
detectors are available.
CONCLUSIONS
Carbon monoxide poisoning is a multi-system condition
and can cause a confusing constellation of clinical
features, precipitating presentation to general practi-
tioners, accident and emergency departments, acute care
physicians, general surgeons, neurologists and even
psychiatrists. With increasing specialization within the
medical profession the diagnosis may be missed by the
specialist who fails to recognize the significance of
pathology outside his or her own area of interest. The
benefits of prompt diagnosis are threefold. Firstly,
recommended therapy, in the form of 100% normobaric
oxygen in all cases and hyperbaric oxygen in cases of life
threatening poisoning can be instigated.
Secondly, as illustrated by this case, unnecessary
expensive and painful investigations can be avoided.
Thirdly, and perhaps most importantly, the dire cones-
quences of discharging a patient home to, or allowing
others access to a potentially fatal environment can be
avoided.
Raijiah and Mathew 263
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... When CO gas enters into the body through the process of respiration, it combines with hemoglobin present in blood cells and is converted into carboxyhemoglobin (CoHb), therefore the oxygen carrying ability in the nerves of the body decreased. Other effects of exposure to CO in the environment on the human body are cardiological problems, neurological damage, coughing, souring, headache, dizziness and nausea etc [3] . ...
... In the MnOx catalyst at the transmittance conditions, eight peaks were obtained. The IR band (3590 cm −1 ) shows the presence of -OH group, (3040 cm −1 and 2350 cm −1 ) shows the presence of COO group, (1640 cm −1 and 1530 cm −1 ) shows the presence of MnO 2 group and (1250 cm −1 and 525 cm −1 ) shows the presence of CO 3 2 − group respectively. ...
... In the CuOx catalyst at the transmittance conditions, six peaks were obtained. The IR band (3529 cm −1 ) shows the presence of -OH group, (2994 cm −1 ) shows the presence of -NH group, (1699 cm −1 ) shows the presence of C = O group, (1388 cm −1 ) shows CO 3 2 − group and (615 cm −1 and 577 cm −1 ) shows the presence of CuO 2 group respectively. ...
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... After absorption, 90% of CO is taken up by hemoglobin, 10% binds to myoglobin and cytochrome oxidase, and less than 1% is dissolved in plasma (Henz and Maeder, 2005). Carbon monoxide binds to hemoglobin, forming carboxyhemoglobin (COHb), as it has 200-300 times more affinity to hemoglobin than oxygen (Rajiah and Mathew, 2011). Its deleterious effects are observed mostly in organs with high oxygen demands, such as brain and heart (Wolf et al., 2017). ...
... Hypoxic and oxidative stresses predispose to cerebrovascular, cardiovascular, and neurological insult . Also, carboxyhemoglobin increases the sticking of white blood cells to endothelial surfaces, especially in the brain tissue, leading to leukocyte-dependent inflammatory reactions with white matter demyelination and focal necrosis (Rajiah and Mathew, 2011). ...
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Background: Carbon monoxide (CO) is an odorless, tasteless and colorless gas that causes a potentially fatal illness with a tremendous burden due to significant mortality and morbidity. Carbon monoxide poisoning leads to the development of delayed neurological sequelae (DNS). Aim: To assess the possible risk factors that can predict the development of DNS after acute CO poisoning. Subjects and methods: The patients were recruited between January 2018 and December 2018. The study included 37 cases with acute CO poisoning. The medical history was taken thoroughly. Patients underwent general and neurological clinical assessments with laboratory investigations, including arterial blood gases (ABG), carboxyhemoglobin (COHb), cardiac enzymes, and serum lactate. At the time of admission, all patients were subjected to an electrocardiogram (ECG) and brain imaging (CT or MRI) of the brain. They were followed up three and six months after discharge for complete neurological examination and cognitive functions assessment using the Mini-Mental State Examination (MMSE). Results: Two patients died, both presenting with coma and hemodynamic instability. Five cases were excluded due to a lack of comprehension and refusal to follow-up. Out of the 30 patients who completed the follow-up, 67% survived with no complication, while DNS developed in 33% of the patients. Several predictors for development of DNS were identified. They included lower Glasgow coma score, duration of CO exposure, high COHb level, decrease in blood pH, elevated serum levels of creatine kinase and lactate, and abnormalities in brain structure. The time of DNS development extended to six months post-exposure. Conclusion: We conclude that several clinical and laboratory parameters can predict DNS. Recommendations: proper and accurate clinical and laboratory evaluation of any suspected case of acute CO poisoning should be performed especially those parameters proved to be predictors for DNS. The follow-up of cases should continue at least for six months post-exposure.
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... After absorption, 90% of CO is taken up by hemoglobin, 10% binds to myoglobin and cytochrome oxidase, and less than 1% is dissolved in plasma (Henz and Maeder, 2005). Carbon monoxide binds to hemoglobin, forming carboxyhemoglobin (COHb), as it has 200-300 times more affinity to hemoglobin than oxygen (Rajiah and Mathew, 2011). Its deleterious effects are observed mostly in organs with high oxygen demands, such as brain and heart (Wolf et al., 2017). ...
... Hypoxic and oxidative stresses predispose to cerebrovascular, cardiovascular, and neurological insult . Also, carboxyhemoglobin increases the sticking of white blood cells to endothelial surfaces, especially in the brain tissue, leading to leukocyte-dependent inflammatory reactions with white matter demyelination and focal necrosis (Rajiah and Mathew, 2011). ...
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Full-text available
  • Aug 2021
Background: There is a surge increase in grills-fast food outlet in the urban areas that plays an essential role in producing air pollution. Chronic accumulation of carbon monoxide might affect the airway and destroy alveolus as well as correlated with the disturbance of lung function. Objective: The purpose of this study is to compare the occupational CO levels, HbCO, and lung functions between grill and non-grill street vendors. Methods: This was an observational analytic study with a case-control design. The subjects were grill street vendors and non-grill street vendors in Medan city who fulfilled several inclusion criteria. The questionnaire was used to determine some characteristics, while smokerlyzer, and ELISA for expiration CO level and blood CO level, spirometer was used to determining lung function. Logistic regression was performed with p-value < 0.05 considered to be significant using SPSS ver 24.0. Results: A total of 50 subjects enrolled into this study with the majority of subjects in the case group were in red (40%) zone in CO exhaled test with the results in pulmonary function test, predominantly restrictive (56%) and mixed-type (40%) with the mean value of HbCO was 486.16 (ng/mL). Meanwhile, the majority of subjects were green zone with mixed type of lung function disturbance in the control group with 540.15 (ng/mL) as HBCO mean value. Grilled street vendors have a higher level of exhaled CO level (p- value: 0.03) without significant difference in HbCO and lung functions (p-value > 0.05). Age, smoking status, HbCO, and lung function did not significantly affect the CO level (p-value: 0.05). Conclusion: There was a significant difference in exhaled CO level between grill-and non-grill street vendors without significant difference in HbCO and lung functions.
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... On day 5, the "direct" strategy should be more preferred/ favored than any other strategy if at all the animals have learned and been able to recall the actual location of the target hole. It appears that neurobehavioral tests can be relied upon in the assessments of subtle neurologic dysfunctions resulting from CO poisoning (Rajiah & Mathew, 2011). ...
Effects of Mosquito coil Smoke Inhalation on Spatial Memory in Mice
Article
Full-text available
  • Jun 2020
  • Niger J Physiol Sci
Background: Mosquito coil (MC) is widely used to repel mosquitoes in order to prevent malaria in many malaria-endemic countries. Although we are fully aware and concerned about carbon monoxide (CO) and its toxicity, exposure to CO from common, though occult sources like MC smoke is often overlooked. Equally, the adverse health effects, especially to the brain, are usually underestimated. Objective: To assess the effects of exposure to CO from MC smoke inhalation on spatial memory in mice. Methods: Sixteen, adult, male, mice, were randomly assigned to either the experimental or the control group; each having 8 mice. The experimental group was exposed to the MC smoke (Wavetide, China) that was allowed to burn inside the gas chamber (75 cm x 50 cm x 50 cm) for 15 minutes, daily, for 14 days. Digital CO meter (PCMM05 Pyle) was used to measure the amount of CO and Barnes maze protocol to assess the spatial memory. Results: Our results indicate that burning MC for 15 minutes produced up to 312 parts per million (ppm) of CO and raised the blood carboxy-hemoglobin (COHb) level by 15.8%. This is higher than the WHO recommended limit (<100 mg/m3 or 87 ppm for 15 min.) of CO exposure and the %COHb level of <2%. Mosquito coil smoke was also associated with impaired spatial memory. However, the dose and duration of exposure did not significantly affect weight gain in the mice. Conclusion: Although widely used to prevent malaria, MC could serve as a potential source of CO and other neurotoxins that could be harmful to the brain; the use and toxicity of which is mostly overlooked even by the public health professionals.
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... Hence, CO poisoning affects our whole body. 3 The pathophysiology of CO poisoning is as follows: first, due to the difference in oxygen affinity, CO leads to relative anemia, tissue asphyxia, and hypoxia; second, CO disrupts oxidative phosphorylation by binding to cytochrome c oxidase in mitochondria, which reduces cellular respiration and causes cellular hypoxia; third, CO increases the adhesion of white blood cells to endothelial surfaces and leads to leukocyte-dependent inflammatory changes and lipid peroxidation. This results in cellular edema, focal necrosis, and reperfusion injury. ...
Evaluation of hepatic injury in acute carbon monoxide-poisoned patients in emergency department
Article
Full-text available
Introduction The affinity of hemoglobin for carbon monoxide (CO) is 250 times higher than that for oxygen. Therefore, exposure to CO leads to a reduction in oxygen delivery to tissues, resulting in cellular hypoxia and affects whole body. Hepatic dysfunction in critically ill patients is related to poor outcome, but few studies have been conducted on this subject that occurs after CO poisoning. This study aims to conduct a study of hepatic injury in CO-poisoned patients in emergency department (ED). Methods This retrospective observational study collected data from patients who were diagnosed with acute CO poisoning at the ED between June 2011 and May 2018 in local tertiary-care hospital (Wonju, Republic of Korea). The primary end point of this study was to describe the prevalence of hepatic injury in acute CO-poisoned patients. The secondary goals were to investigate the recovery trends of hepatic injury caused by acute CO poisoning and the relation to neurologic outcome and mortality. Results Eight hundred ninety-four patients were enrolled in the final analysis, 128 cases (14.3%) had subclinical hepatic injury and 15 (1.6%) cases had hepatic injury. The relationship with mortality was not statistically significant. However, the hepatic injury group was higher incidence of intensive care unit admission and other complications. Patients in the hepatic injury group recovered through conservative management within 1 week of being admitted to the ED. Conclusions While CO-induced hepatic injury is relatively uncommon, it can be associated with complications and poor neurologic outcome. However, CO-induced hepatic injury was not found to have a statistically significant effect on mortality rate.
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Metaverse ve Sağlık Hizmetleri
Chapter
  • Mar 2023
Önümüzdeki birkaç on yılda hayatımızın birçok alanına girmesi öngörülen yeni sanal dünya Metaverse’e karşı araştırmacıların ilgisi gün geçtikçe artmaktadır. Birçok alan ile Metaverse ilişkisinin anlatıldığı yayınlarda yer alan konulardan birinin de sağlık hizmetleri olduğu görülmektedir. Metaverse yapılanması henüz erken aşamada olmakla birlikte sağlık hizmetlerinin dönüşümü ve iyileştirilmesi bakımından sunduğu fırsatlar alana duyulan ilgiyi artırmaktadır. Dünya Ekonomik Forumu (WEF) yayınladığı raporda mevcut sağlık hizmeti sunum modelinin giderek sürdürülemez hale geldiğini ve dijital hizmetlerin tanıtılmasının, önümüzdeki on yılda sağlık hizmetlerinin dönüşümünde en önemli belirleyicilerden biri olduğunu belirtmektedir (World Economic Forum, 2016). Sağlık İçin İnsan Kaynakları Dublin Deklerasyonu raporunda ise 2030 yılı projeksiyonunda yaklaşık 18 milyon hekim, hemşire ve diğer sağlık çalışanlarına gereksinim duyulacağına vurgu yapılmıştır (Heaney, 2017). Büyük ölçekli teknoloji şirketlerinin dijital sağlığa yaptıkları yatırımlar, VR ve AR kullanımıyla gelişen artan sayıda girişim ve cerrahi, ortamın nasıl değişebileceğine ışık tutmakta yanı sıra beceri ve yetkinlikleri geliştirmede yararlanılabilmektedir. Bu bağlamda Metaverse’ün sağlık eğitimi, sağlık bakımı, sağlık çalışanları arasında iş birliği ve katılımcıların sağlığı bakımından etkileri yanı sıra sunduğu fırsatlar ve zorluklar bildirilmektedir. Tüm bu nedenlerle Metaverse’ün sağlık hizmetlerinde kullanımı ve bu yöndeki araştırmaların sayısı her geçen gün artmaktadır. Bu bölüm, Metaverse kavramına, bu kavramın sağlık hizmetleri ile olan ilişkisine dair projeksiyon sunmayı amaçlamaktadır.
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Waste to Energy: An experimental comparison of burning the waste-derived bio-oils produced by transesterification and pyrolysis methods
Article
  • Dec 2021
  • ENERGY
In the present research, waste cooking oil biodiesel (WB) and waste pyrolysis oil (WPO) are produced via transesterification and pyrolysis methods. Then the produced WB and WPO are blended at the volumetric percentages of 25, 50, 75, and 100% into the conventional diesel fuel. These fuel blends are tested on a single-cylinder diesel engine under the varying engine loads (1, 2, 3, and 4 kW) at a constant crankshaft speed of 1500 rpm. The results show that both WB and WPO blended fuels decrease the brake thermal efficiency and higher exhaust gas temperature than diesel fuel. As the WB content in the test fuel increases, CO, HC, and smoke emissions gradually decrease due to the high oxygen content of WCO, but NOx emission increases. In terms of exhaust emissions, the reverse trend is noticed for WB blended test fuels (high CO, HC, and smoke, but low NOx) with the lack of oxygen atoms for WPO substitutes. As the percentage of WPO in the test fuel is increased, CO, HC, and smoke emissions gradually increase in comparison to those of diesel fuel, while NOx emissions exhibited a reverse trend. In comparison to that of reference diesel fuel, the highest thermal efficiency declines are found to be 22% for WB100 and 19% for WPO100. WPO100 leads to the significant increment in the HC, CO, and smoke emissions by 59, 36, and 31%, respectively. Compared to diesel fuel, WB100 ensures the highest CO, HC, and smoke emission reduction by 45, 62, and 47%, respectively. On the other hand, the maximum increase in NOx emission is found to be 46% for WB100 test fuel, while the maximum decrease is found to be 25% for WPO100 test fuel as compared to that of diesel fuel. In terms of engine performance and exhaust pollutants excluding NOx emission, it is well-noticed that the WB substitutes present more promising results than those of WPO substitutes. Accordingly, the present research proves that the transesterification method is more suitable for biofuel production than the pyrolysis method.
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Could Gnomoniopsis castaneae Be Used as a Biological Control Agent against Insect Pests?
Article
Full-text available
  • Apr 2021
Gnomoniopsis castaneae is the cause of the chestnut brown rot but has been also regarded as an important mortality factor for the chestnut gall wasp Dryocosmus kuriphilus. The question to whether G. castaneae could serve as a natural biocontrol agent against insect pests is investigated in the present study. We used three serious insect pests as experimental model insects: Plodia interpuctella and Trogoderma granarium, which are important pests of stored products, and Myzus persicae, a cosmopolitan, serious pest of annual and perennial crop plants. Although chemical pesticides represent effective control means, they are also related to several environmental and health risks. In search for alternative pest management methods, scientific interest has been focused, inter alia, on the use of entomopathogenic fungi. While Isaria fumosorosea has long been recognized as an effective control agent against several pests, G. castaneae has been very little studied. The present study examined whether and to what extent G. castaneae and I. fumosorosea exhibit insecticidal activity against fourth-instar larvae of P. interpunctella and T. granarium and adults of M. persicae. Mortality was examined in interrelation with dosage and time exposure intervals. Both fungi exhibited pesticidal action. However, G. castaneae induced noteworthy mortality only at very high doses. In general, we concluded that G. castaneae failed to cause high insect pathogenicity at normal doses and may not be an efficient biocontrol agent compared with other entomopathogens. On the other hand, our study reiterates the pathogenic potential of I. fumosorosea. More studies are needed to further our insight into the potential of EF species as a component of IPM.
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A new naphthalimide-Pd(II) complex as a light-up fluorescent chemosensor for selective detection of carbon monoxide in aqueous medium
Article
  • Mar 2020
  • INORG CHIM ACTA
A fluorescent light-up probe, MENap-Pd, was designed and synthesized to detect CO in aqueous buffer medium (pH 7.2, 37 °C). This detection was highly selective and sensitive towards CO. The probe prompted a more than 9-fold ‘turn-on’ fluorescence response to CO through the demetallation of the nonfluorescent Pd(II) complex, MENap-Pd to generate free fluorescent ligand, MENap in the reaction medium. The fluorescence response is highly selective towards relevant reactive oxygen, nitrogen, and sulfur species and also various cationic, anionic, and neutral species present in biological system. The limit of detection (LOD) of this probe for CO sensing (CORM-2) is calculated as 1.4 μM with a linear range of 0–60 μM concentration of CORM-2.
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Carbon monoxide poisoning
Article
Full-text available
  • Nov 2004
  • EMERG MED CLIN N AM
CO is an insidious poison with many sources of exposure. CO poisoning produces diverse signs and symptoms, which often are subtle and can be misdiagnosed easily. Failure to diagnose CO poisoning may result in significant morbidity and mortality and allow continued exposure to a dangerous environment. In the ED, a high index of suspicion must be maintained for occult CO exposure. Headache, particularly when associated with certain environments, and flulike illness in the wintertime with symptomatic cohabitants should raise the index of suspicion in the ED significantly for occult CO poisoning. Emergency treatment of CO poisoning begins with inhalation of supplemental oxygen and aggressive supportive care. HBOT accelerates dissociation of CO from hemoglobin and may prevent DNS. Absolute indications for HBOT for CO poisoning remain controversial, although most would agree that HBOT is indicated in patients who are comatose, are neurologically abnormal, have a history of loss of consciousness with their exposure, or have cardiac dysfunction. Pregnancy with an elevated CO-Hgb level (>15-20%) also is widely considered an indication for treatment. HBOT may be considered in patients who have persistent symptoms despite NBO, metabolic acidosis, abnormalities on neuropsychometric testing, or significantly elevated levels. The ideal regimen of oxygen therapy has yet to be determined, and significant controversy exists regarding HBOT protocols. The emergency physician may be confronted with the diffcult decision regarding disposition and even transfer to a hyperbaric facility. Often the local medical toxicologist, poison control center, or hyperbaric unit can assist the emergency physician with the decision-making process.
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The evolutionary rate variation among genes of HOG-signaling pathway in yeast genomes
Article
Full-text available
  • Jul 2010
  • BIOL DIRECT
Responses to extracellular stress are required for microbes to survive in changing environments. Although the stress response mechanisms have been characterized extensively, the evolution of stress response pathway remains poorly understood. Here, we studied the evolution of High Osmolarity Glycerol (HOG) pathway, one of the important osmotic stress response pathways, across 10 yeast species and underpinned the evolutionary forces acting on the pathway evolution. Although the HOG pathway is well conserved across the surveyed yeast species, the evolutionary rate of the genes in this pathway varied substantially among or within different lineages. The fast divergence of MSB2 gene indicates that this gene is subjected to positive selection. Moreover, transcription factors in HOG pathway tend to evolve more rapidly, but the genes in conserved MAPK cascade underwent stronger functional selection. Remarkably, the dN/dS values are negatively correlated with pathway position along HOG pathway from Sln1 (Sho1) to Hog1 for transmitting external signal into nuclear. The increased gradient of selective constraints from upstream to downstream genes suggested that the downstream genes are more pleiotropic, being required for a wider range of pathways. In addition, protein length, codon usage, gene expression, and protein interaction appear to be important factors to determine the evolution of genes in HOG pathway. Taken together, our results suggest that functional constraints play a large role in the evolutionary rate variation in HOG pathway, but the genetic variation was influenced by quite complicated factors, such as pathway position, protein length and so on. These findings provide some insights into how HOG pathway genes evolved rapidly for responding to environmental osmotic stress changes. This article was reviewed by Han Liang (nominated by Laura Landweber), Georgy Bazykin (nominated by Mikhail Gelfand) and Zhenguo Lin (nominated by John Logsdon).
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Carbon monoxide poisoning: Neurologic and psychiatric sequelae
Article
Full-text available
  • Oct 1977
  • Can Med Assoc J
Poisoning with carbon monoxide is a frequent means of suicide and has an estimated mortality of 30%. However, there have been few case reports of neuropsychiatric sequelae in survivors. The authors report the case of a young woman with parietal lobe signs 6 months after she had attempted suicide with a combination of barbiturate overdose and carbon monoxide poisoning. The purpose of this report is to call attention to these signs, which may the mistaken for signs of a psychiatric disorder, and to discuss the importance of the barbiturate overdose in this case.
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Unintentional carbon monoxide - Related deaths in the United States, 1979 through 1988
Article
Full-text available
  • Sep 1991
To describe the epidemiology of recent unintentional carbon monoxide poisoning deaths in the United States. Descriptive analysis of carbon monoxide-related deaths in the United States from 1979 through 1988, based on death certificate reports compiled by the National Center for Health Statistics. All US deaths, 1979 through 1988. We reviewed data from 56,133 death certificates that contained codes implicating carbon monoxide as a contributing cause of death. Of these, 25,889 were suicides, 210 were homicides, 15,523 were associated with severe burns or house fires, and 11,547 were classified as unintentional. The number of unintentional deaths decreased steadily by about 63 deaths per year, from 1513 in 1979 to 878 in 1988. The highest death rates occurred in winter and among males, blacks, the elderly, and residents of northern states. Motor vehicle exhaust gas caused 6552 (57%) of the unintentional deaths; 5432 (83%) of these were associated with stationary automobiles. The rate of unintentional death from carbon monoxide poisoning is decreasing. This may be attributable to improvements in automobile pollution control systems and improved safety of cooking and heating appliances. Prevention programs should target young drivers, males, and the elderly.
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Carbon Monoxide Poisoning – A Public Health Perspective
Article
  • May 2000
  • TOXICOLOGY
Carbon monoxide (CO) may be the cause of more than one-half of the fatal poisonings reported in many countries; fatal cases also are grossly under-reported or misdiagnosed by medical professionals. Therefore, the precise number of individuals who have suffered from CO intoxication is not known. The health effects associated with exposure to CO range from the more subtle cardiovascular and neurobehavioral effects at low concentrations to unconsciousness and death after acute or chronic exposure to higher concentrations of CO. The morbidity and mortality resulting from the latter exposures are described briefly to complete the picture of CO exposure in present-day society. The symptoms, signs, and prognosis of acute CO poisoning correlate poorly with the level of carboxyhemoglobin (COHb) measured at the time of hospital admission; however, because CO poisoning is a diagnosis frequently overlooked, the importance of measuring COHb in suspicious settings cannot be overstated. The early symptoms (headache, dizziness, weakness, nausea, confusion, disorientation, and visual disturbances) also have to be emphasized, especially if they recur with a regular periodicity or in the same environment. Complications occur frequently in CO poisoning. Immediate death is most likely cardiac in origin because myocardial tissues are most sensitive to the hypoxic effects of CO. Severe poisoning results in marked hypotension, lethal arrhythmias, and electrocardiographic changes. Pulmonary edema may occur. Neurological manifestation of acute CO poisoning includes disorientation, confusion, and coma. Perhaps the most insidious effect of CO poisoning is the development of delayed neuropsychiatric impairment within 2–28 days after poisoning and the slow resolution of neurobehavioral consequences. Carbon monoxide poisoning during pregnancy results in high risk for the mother by increasing the short-term complication rate and for the fetus by causing fetal death, developmental disorders, and chronic cerebral lesions. In conclusion, CO poisoning occurs frequently; has severe consequences, including immediate death; involves complications and late sequelae; and often is overlooked. Efforts in prevention and in public and medical education should be encouraged.
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Adaptation of Saccharomyces cerevisiae to saline stress through laboratory evolution
Article
  • Mar 2011
  • J EVOLUTION BIOL
Most laboratory evolution studies that characterize evolutionary adaptation genomically focus on genetically simple traits that can be altered by one or few mutations. Such traits are important, but they are few compared with complex, polygenic traits influenced by many genes. We know much less about complex traits, and about the changes that occur in the genome and in gene expression during their evolutionary adaptation. Salt stress tolerance is such a trait. It is especially attractive for evolutionary studies, because the physiological response to salt stress is well-characterized on the molecular and transcriptome level. This provides a unique opportunity to compare evolutionary adaptation and physiological adaptation to salt stress. The yeast Saccharomyces cerevisiae is a good model system to study salt stress tolerance, because it contains several highly conserved pathways that mediate the salt stress response. We evolved three replicate lines of yeast under continuous salt (NaCl) stress for 300 generations. All three lines evolved faster growth rate in high salt conditions than their ancestor. In these lines, we studied gene expression changes through microarray analysis and genetic changes through next generation population sequencing. We found two principal kinds of gene expression changes, changes in basal expression (82 genes) and changes in regulation (62 genes). The genes that change their expression involve several well-known physiological stress-response genes, including CTT1, MSN4 and HLR1. Next generation sequencing revealed only one high-frequency single-nucleotide change, in the gene MOT2, that caused increased fitness when introduced into the ancestral strain. Analysis of DNA content per cell revealed ploidy increases in all the three lines. Our observations suggest that evolutionary adaptation of yeast to salt stress is associated with genome size increase and modest expression changes in several genes.
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Determination of total hemoglobin in forensic blood samples with special reference to carboxyhemoglobin analysis
Article
  • Dec 1990
  • FORENSIC SCI INT
For the determination of total hemoglobin (Hb) in blood containing elevated carboxyhemoglobin (COHb), a newly developed reagent containing a 100-fold concentration of ferricyanide (20 g/l) and a 2-fold concentration of Sterox SE was compared with a standard reagent (0.2 g/l ferricyanide), the reagent of van Kampen and Zijlstra, using forensic blood samples and experimentally heated blood samples. There were no significant differences between the spectra of hemiglobincyanide (HiCN) solution produced with our reagent and the van Kampen and Zijlstra reagent using experimentally heated blood samples. Although the spectra of HiCN changed gradually with increased heating time and with the passage of time after mixing, the absorbance at 540 nm (A540) did not change until at least 120 min for both the reagents. When forensic blood samples containing elevated COHb were mixed with the van Kampen and Zijlstra reagent, total-Hb concentrations determined 5 min after mixing were 10-20% higher than those determined after 180 min. The overestimates of total Hb determined after 5 min resulted in comparable underestimates of percentage saturation of COHb (COHb%) when COHb% was obtained from the ratio of COHb content, determined by gas chromatogrpahy, to total-Hb concentration in blood. However, there was an extremely good correlation between the values of total Hb in forensic blood samples determined with the van Kampen and Zijlstra reagent after 180 min and those determined with our reagent after 5 min. From the results obtained, our reagent proved to be suitable for the determination of total Hb in forensic science practice.
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Carbon monoxide poisoning: A Review epidemiology, pathophysiology, clinical findings, and treatment options including hyperbaric oxygen therapy
Article
  • Feb 1989
  • J Toxicol Clin Toxicol
Carbon monoxide (CO) poisoning is the leading cause of poisoning deaths (accidental and intentional) in the United States. While confirmation of CO poisoning is easily obtained via assessment of carboxyhemoglobin (COHgb) levels, evaluation of the severity of intoxication is both difficult and inconsistent. Acute intoxication most commonly results in neurologic dysfunction and/or myocardial injury. Delayed neurologic sequelae are observed in approximately 10% of patients. New information from clinical observations and animal research has prompted a re-evaluation of the clinical assessment of the severity of CO intoxication and its resultant pathophysiology. Patients at the extremes of age (the very young and the elderly), those with pre-existing cardiovascular and/or pulmonary disease, as well as pregnancy are at increased risk. Once the diagnosis of CO poisoning has been established, treatment with 100% O2 is indicated. Based on the body of clinical, basic and scientific information currently available, patients who manifest signs of serious intoxication (i.e., unconsciousness or altered neurologic function, cardiac or hemodynamic instability) should be considered candidates for hyperbaric oxygen therapy (HBO) in addition to other appropriate supportive and intensive care. Any patient who has suffered an interval of unconsciousness, regardless of the patient's clinical exam on arrival, warrants HBO therapy. Treatment plans based on any specific COHgb level are not well founded.
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