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Effects of Carbon Monoxide and On Human Health

Thomas NA and Jaiswal A* Research Article Department of Epidemiology and Public Health, Central University of Tamil Nadu, Thiruvarur, Volume 5 Issue 3 Tamil Nadu, Received Date: March 29, 2021

Published Date: May 06, 2021 Ajeet Jaiswal, Department of Epidemiology and Public Health, Cen- *Corresponding author: DOI: 10.23880/phoa-16000182 tral University of Tamil Nadu, India, Email: [email protected]

Abstract

Carbon monoxide and Cyanide are most familiar . Fire accidents act as main source for both poisonings. Carbon monoxide poisoning is formed from incomplete combustion of carbon compounds. Cyanide is readily available chemical and widely used in many industries like jewelry, paper, textiles. It is also used as weapon by terrorists. The methodology used in this paper is the review of secondary data sources available on the subject from library, internet, PubMed. Works done by

and cyanide poisoning. Both poisonings have almost similar kind of effects on human body and the effect of poisoning on body several experts in the field was collected and interpreted. This review aims at detailed study on effects of carbon monoxide varies according to the dose. The review highlights that there is a need of effective and accurate for both poisonings. The preventive measures can reduce the number and lethality from the exposures and psychiatric referral is essential for patients with intentional poisoning.

Keywords: Carbon Monoxide; Cyanide; Carboxyheamoglobin; Oxyheamoglobin; Hydroxycobalamine; HBOT;

Abbreviation: MPO: Myeloperoxidase; ROS: Reactive The common sources of the are improper working Species. vehicles, generators, stoves, improper gas appliances. It can Introduction of heating appliances, fires, improper ventilation of motor Carbon monoxide poisoning and Cyanide poisoning cause chronic and acute poisonings [5]. are the two most known types of intoxication. Both can be of CO poisoning. The fatality rate is 0.5 to 1 per 1000000 occurred individually as well as together. Presences of both persons.In United Almost States 50% there of the are fatal approximately poisonings 40000 are due cases to carbon monoxide. It is seen as a major reason for death in andpoisonings Roman areperiods seen we in are fire aware accidents on dangerous [1]. These effects types of high in three quarters of burnt patients, which indicates intoxications can be accidental or intentional [2]. Since Greek fire accidents [2]. The carboxyl heamoglobin levels are seen monoxide poisoning goes undiagnosed in most burnt cases carbon monoxide. It was used for executions earlier [3]. It is a high probability of carbon monoxide poisoning [4]. Carbon gas without color, taste and smell [4]. Incomplete combustion of carbon substances causes carbon monoxide poisoning [5]. [6]. In Britain CO poisoning occur by central heating fault

Effects of Carbon Monoxide and Cyanide Poisoning On Human Health Public H Open Acc 2 Public Health Open Access

require large amount of resources to recover from the attack

whereHistory as in U.Sshows the mainthat reasonin 1857 is Claudethrough Bernard exhaust foundfumes [3].out Both the mother and fetus are affected by cyanide poisoning that carboxyl heamoglobin is formed in CO poisoning by [10]. Cyanide exposure is highly lethal to pregnant women. reversible displacement of oxygen from heamoglobin. In 1926 another fact on hypoxia was revealed, it was that one[6]. poisoning As both indirectly carbon monoxidereduce other poisoning also. Physicians and cyanide should poisoning can be formed in fire accidents, the treatment for but also due to poor tissue uptake of oxygen. In the years 1960-70shypoxia is coalnot onlygas was caused converted by difficulty to Carbon in oxygen monoxide transport free take a special care to find out such poisonings in fire victims natural gases. It reduced the number of poisonings. Similarly to avoidMethodology undiagnosed conditions [6]. the poisoning from car exhausts was reduced by use of The present study is based on secondary resources available on the topic Carbon monoxide and cyanide catalyticCarbon converters monoxide [3]. poisoning is seen severe in pregnant poisoning. Data are collected from library, PubMed and women. Due to carbon monoxide poisoning maternal internet sites concerned using the search terms carbon monoxide poisoning, cyanide poisoning, hyperbaric . The search was done up to November 5 2020. Works Likemortality carbon is monoxide between 19-24%,Cyanide is while also a fetal dangerous mortality chemical. is 36- 67%. It is the third most cause of accidental deaths in U.S [6]. analysis and interpretation are done. done by several experts in the field are selected and further hydrogenCyanide poisoning cyanide. In is 1800 creating it was more extracted morbidity from now . [6]. In Results and Discussion Cyanide1786, cyanide exists inwas various first isolated forms. It from can bePrussian a gas as blue Hydrogen dye as Cyanide and it can be a , or sodium Carbon Monoxide Poisoning

a pale blue or colorless liquid, while in high temperature it Etiology: In carbon monoxide poisoning, heamoglobin cyanide [7]. In low temperature looks like binds to CO. Heamoglobin binds to carbon monoxide with an naturally found in , lima beans, almonds, and become gas with bitter smell [8]. Cyanide can be leftwardaffinity 240 shift times of oxygen-heamoglobin greater than oxygen dissociation [5]. This association curve of manyof apricots, industries , like peaches paper, textiles,[8]. They plastics, are cyanogenic electroplating, foods result in formation of carboxyheamoglobin [2]. It causes the photographic[9]. It is also solutions, involved inmetal cigarette cleaning. smoking. It is utilized It is usedin gold in in heamoglobin. This stabilized form is known as R state. It industry to separate gold from its ore. Similar to carbon oxyheamoglobin [3]. The binding of CO forms stabilization increases affinity for oxygen in other sites of heamoglobin. It monoxide, fire accidents results in cyanide poisonings also causereduces myocardial the release infarction of oxygen and [4]. . Carbon monoxide Both of shows these [8]. According to toxic exposure surveillance system, greater affinity to myoglobin compared to heamoglobin and in the period of 1993-2003 there were 3165 cyanide poisonings.35% of burnt patients have high levels of cyanide finallySimilarly result in carbon cellular monoxide hypoxia [3]. binds to ferrous of content in their blood, showing probability of cyanide Cytochrome oxidase of mitochondria and stop oxidative phosphorylation. It causes decrease in Adenosine both for murders and homicides. For murder attempts triphosphate production or the energy production of body melamine,poisonings polyurethane, [7]. Cyanide ispoly used acrilonitrile, for intentional hydrogen poisonings, cyanide between components of and form pose threat mainly to international food and water supplies. [10]. The shuffling of electrons continues to take place Jonestownare used [9]. massacre It is also usedis the by most terrorists known to poseincident threats. of usingThey cyanide as a weapon. More than 900 deaths occurred by Pathophysiology:superoxides, which Carboncan cause monoxide cell, damage enters [4]. into the body drinking cyanide containing liquid. Osama Bin Ladan and mainly through . It enters the lungs and diffuses to alveolar membranes and then into heamoglobin of blood

aISIS genocidal also make agent threats (CDC). by Drinkingcyanide poisonings water was [10].contaminated In World more when compared to transfusion of similar War 2 hydrogen cyanide was used by Germans as , as concentration[6]. Studies shows of carbon that inhalation monoxide of carbonexposed monoxide RBC. In casecauses of terrorist weapon as it is rapid in action, readily available, non smokers the carboxyheamoglobin levels greater than doesby industrial not require waste any containing special knowledge [9]. to use. It acts And as it an is ideal able 2% and for smokers a level greater than 10% is enough to

to cause mass and difficulties to society. After all it produce symptoms [4]. The carboxyheamoglobin level in Thomas NA and Jaiswal A. Effects of Carbon Monoxide and Cyanide Poisoning On Human Copyright© Thomas NA and Jaiswal A. Health. Public H Open Acc 2021, 5(3): 000182. 3 Public Health Open Access

blood of poisoned patient is directly correlated with clinical necrosis, acute renal failure, parkinsonism. Young adults express peripheral neuropathy also Psychiatric effects like irritability, depression and neuropsychological defects like manifestationThe presence [3]. of excess carbon monoxide can activate impairment to attention, short term memories are also platelets by displacing NO from heamproteins in platelet. These NO react with super oxides and form peroxynitrate are rarely affected. Muscle necrosis is caused by the increase inexpressed creatine [14,15].phosphokinase. Body organs Chronic like exposures kidney, , in pregnantpancreas ladies cause growth retardation, fetal distress, death of fetus Theseand inhibit activated function platelets of stimulate mitochondria neutrophils [4]. Thus in blood carbon to releasemonoxide myeloperoxidase poisoning increase (MPO). the Theactivation release of of platelets MPO results [11]. Diagnosis[3]. and Treatment: The diagnosis of carbon It again causes the formation of Xanthine oxidase which monoxide poisoning should be based on clinical triad, which generatesin inflammatory reactive effects oxygen by activatingspecies (ROS). more neutrophilsThus both MPO[12]. assesses consistent symptoms, history of recent exposure, and ROS catalyze lipid peroxidation and increase the myelin increased carboxyheamoglobin levels. Of these carboxy content in body. This myelin increases the lymphocyte But recent studies shows that normal levels of carboxy heamoglobin can’tlevels be act taken as confirmation as absence offor carbon the suspect monoxide [4]. responses and activates microglia of brain [4]. Finally all theseCarbon process monoxide leads to neurological poisoning andcauses cardiac inactivation injuries [12]. of used for diagnosis fetus, but the differentiation between Calcium ATPase in plasma membrane and cause large wavelengthpoisoning [4].of carboxy Pulse CO heamoglobin oximetry measurementand oxyheamoglobin is also

intracellular lipases and proteases are activated by decrease screening test that can be used, but smoking and use ininflux ATP of production, calcium , which which causes results the in depolarization brain injury. The of is difficult. Carbon monoxide breath analyzer is a simple mitochondrial membranes and can cause death of the of patientsThere are confound no available the result [3]. for the poisoning. 100% normobaric oxygen therapy and hyper baric oxygen therapy person [4]. Carbon monoxide exposure can increase carbon are used and found effective. Both methods remove the ofmonoxide heamoxygenases, production which in body is dependent [13]. The brainon heam systolic content heam of carbon monoxide from heamoglobin by increasing partial levels are increased by CO exposure [4]. It induces activation pressure of oxygen, which in turn increase the dissociation tissues and increase the effects of poisoning. body [13]. Then the heamoxygenase enzyme form CO from Toxico Kinetics: According to World Health Organization, a rate [16]. Normobaric oxygen therapy decreases the half life long term exposure greater than 6ppm of carbon monoxide into 74 minutes while HBOT decreases the half life into 20 neurominutes. cognitive HBOT showsdysfunction. a reversal It is effect recommended on inflammation for serious and is 320 minutes in a standard room with 21% of oxygen. dysfunction of mitochondria [4]. It is highly effective against Whileis toxic in to 1000% human ofbeings oxygen [4]. the The half half life life reduces of carbon to monoxide less than 90 minutes. In hyperbaric oxygen condition of 3 ATM the half casesOther of acute than poisonings these, some[17]. other methods are used. life of CO again reduces to 23 minutes so hyperbaric oxygen Application of high concentration of oxygen with carbon therapy is used for reducing the effects of carbon monoxide dioxide is used as CO poisoning cause decrease in carbon dioxide level in body. So this method increases ventilation from carbon dioxide. Similarly normocapnic hyperpnea, Clinicalpoisoning [2].Manifestations: The extracorporeal membrane oxygenation, photo dynamic vary with concentration and duration of exposure. Low blood illuminations are used as optional methods. The study concentration of toxicant causes both cardiovascular and of Roderique and collegues claims that hydroxycobalamine neurobehavioral effects. Acute and lengthy exposure leads and ascorbic can be used to convert CO into carbon to coma and death, the starting of chronic poisoning can be dioxide. Cyclo dextrin encapsulated porphyrin complex are

clinical manifestations are , nausea, weakness, lethargy.mistaken asLethargy flu depression, can lead food to poisoning misdiagnosis [3]. The of commonchronic also Thefound survivors helpful byhave Kitagshi to compromise and colleagues with [4]. quality of life

symptoms like , hypertension, central nervous case of intentional poisoning they are referred to psychiatric symptoms,fatigue syndrome abdominal [14]. pain, Acute , CO poisoning paresis, convulsions, also show counseling.with low cognitive Follow upperformance, of the patient depression, is recommended stress [18]. within In

, erythrocytosis, hyperglycemia, muscle depression, neurocognitive impairments and myocardial unconsciousness, myocardial ischemia, arterial fibrillation, 4-8 weeks after exposure. Special care should be given to

Thomas NA and Jaiswal A. Effects of Carbon Monoxide and Cyanide Poisoning On Human Copyright© Thomas NA and Jaiswal A. Health. Public H Open Acc 2021, 5(3): 000182. 4 Public Health Open Access

lethal dose of cyanide is 50 mg, an exposure greater than 50 mg cause death of individuals in 5-15 minutes. It will take Preventioninfarction [2]. Measures: detectors are installed in home. It should be on same level as fuel burning appliance.To The find alarm out should CO poisoning be kept in CO a dizziness,at least 1-4 mild hours, confusion; if we are abdominal consuming pain small and quantities high dose of place, which is heard from all rooms. It minimizes the risk of symptomscyanide [19]. are The hyperventilation, low dose symptoms tachycardia, are headache, , vomiting, respiratory arrest, hypotension, dyspnea, , coma be done to make awareness on people about incidents on homeexposure and during workplaces. sleep The[5]. Publicvisible healthexample campaigns of the campaign should and high concentration of oxygen levels in venous can cause is shown by U.S through their “invisible killer campaign”. and can cause death [10]. Increased lactate levels in blood The use of catalytic converters reduces the exposure from in coma 2 clinical features are important. They are absence ofsepsis, myocardial and bradycardia.infarction, liver Cyanide failure inhibits[10]. For oxidative patients industry also. Physicians, engineers, gas industries should be phosphorylation and thereby oxygen transport. So a fully wellautomobiles aware of [4]. the Public issue. educationProper ventilation should be should provided be done by gas in oxygenated heamoglobin will be present and cyanosis is

houses [3]. The person should be removed from the exposure Diagnosisabsent in them and [19].Treatment: The toxic effect of poisoning is immediatelyCyanide to Poisoning prevent complications [2]. directly related to quantity of cyanide in body. The diagnostic

Etiology: Cyanide is readily available and widely used urine, saliva. But analysis of blood is taken as reliable. The chemical. It is well known for its toxic effects. Exposure to reliabilitymethods of include oral swab quantification depends on ofthe cyanidequantity of in cyanide blood, cyanide can be occurred through contaminated air, water, in saliva at the time of swab collection. Whereas in case of . Exposure through inhalation depends on urine, smoking increase cyanide concentration in urine respiratory condition of individuals. Oral exposure results in food, soil [8] is not available. The diagnosis can be toxidrome, which is symptomand due to based filtration analysis of kidney of exposure. the actual It helps content to avoid of cyanide delay Pathophysiology:continued absorption Inhalation of toxicant of cyanide[10]. gas is having more toxicant effects than ingestion. Cyanide diffuses into blood in treatmentThe treatment by waiting methods laboratory are administrationconfirmation [10]. of 100% between cyanide anion and undissociated form of HCN. oxygen and decontamination methods like using activated HCNafter formexposure can easily[7]. After cross absorption cell membrane CN maintain compare equilibrium to other charcoal, gastric lavage. The effective treatment is providing forms.HCN also inhibit enzymes like succinic dehydrogenase, antidote intravenously or intraosseous. It should be mutase, and cytochrome oxidase of electron transport chain. done without delay. Intravenous administration requires Cyanide binds with ferric ion of cytochrome a3 in electron skill. Treatment for cyanide poisoning can be divided transport chain of mitochondria and inhibits oxidative into 3. First one is methamoglobin generators and nitric phosphorylation and thereby aerobic respiration. Thus oxide donors. It includes sodium , , and anaerobic increases and it results in academia dimethyl aminophenol. They create hypotension and and hyper lactemia. Potassium cyanide and change to hydrogen cyanide in stomach acidic conditions [10]. Use of can cause Sodiumcerebral haemorrhage is a category [20]. The C drug second for pregnant group is women. sulfur Toxic[10]. Cyanide Kinetics: is a hepato toxic and neuro toxic chemical [6]. Itdonors. create Itprotection includes for sodium fetus by sulfate creating and a glutathionegradient towards [10]. to express signs and symptoms of the poisoning. The body The concentration of 40 mol/L is enough hydroxycobalamine, ethylene diamine tetra- acetate The enzyme named help in this. It is found mother [6]. The third group is directly binding agents, like particularlycontains a specialin liver and detoxification muscle. Rhodanese mechanism convert for cyanide.cyanide to . Thiocyanate is soluble in water, so it is Hydroxycobalamine[10]. Hydroxycobalamine convert is cyanidean expensive into cyanocobalamine antidote. It should or excreted through urine. Thiosulfate acts as a sulfur donor in vitaminbe given B12 intravenous and it is excretedwithin 10-15 through minutes urine. of But exposure it can cause [21].

Clinicalthis mechanism Manifestations: [7]. In exposures through kidney injury [6]. Cobalt EDTA creates a cobaltocyanide and symptoms are expressed within seconds. But in oral ingestion reduces toxic effects [22]. In case of intentional poisonings of it will take hours to express the symptoms. Preventionthey should beMeasures: referred toAs psychiatricbreathing cause counseling high toxic [7]. effects Symptoms vary with concentration of poison in body. The avoid situations that lead to inhalation of the ,

Thomas NA and Jaiswal A. Effects of Carbon Monoxide and Cyanide Poisoning On Human Copyright© Thomas NA and Jaiswal A. Health. Public H Open Acc 2021, 5(3): 000182. 5 Public Health Open Access

especially in labs. Leave the area of exposure as soon as possible. Remove the clothing and discard the exposed is the effective treatment for carbon monoxide poisonings, clothes. Wash the exposed body parts with soap and water. whilesymptoms hydroxycobalamine expressed in both is the [7]. effective Hyperbaric antidote oxygen for therapycyanide Avoid touching contaminated areas, clothes, jewelry. Avoid mouth to mouth resuscitation as it cause risk to the person poisonings can be reduced by taking effective preventive measures.poisonings [6]. The morbidity and mortality from these

who provide CPR [8]. Provide education to public and References workersDiscussion about such possibilities [7]. 1. Breen PH, Isserles SA, Westley J, Roizen MF, Taitelman Carbon monoxide and cyanide are most common poisonings. Carbon monoxide poisonings are common in poisoning: a place for treatment. Anesth Analg 671-677.UZ (1995) Combined carbon monoxide and cyanide before responding to it. For example carbon monoxide 80(4): poisoningfire accidents causes [2]. deathIt sometimes of person causes in sleep death before of individuals affected 2. Hanley ME, Patel PH (2020) Carbon Monoxide Toxicity.

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