{"id":43,"date":"2019-03-06T04:31:21","date_gmt":"2019-03-06T04:31:21","guid":{"rendered":"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/?post_type=chapter&#038;p=43"},"modified":"2019-04-25T05:49:22","modified_gmt":"2019-04-25T05:49:22","slug":"carbon-monoxide-toxicity","status":"publish","type":"chapter","link":"https:\/\/ebooks.inflibnet.ac.in\/esp15\/chapter\/carbon-monoxide-toxicity\/","title":{"rendered":"Carbon Monoxide Toxicity"},"content":{"raw":"<div><span style=\"float: right\"><a href=\"https:\/\/youtu.be\/dWsQaGh5pwU\" target=\"_blank\" rel=\"noopener\"><img src=\"http:\/\/epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/2018\/11\/download.png\" alt=\"epgp books\" width=\"75px\" height=\"75px;\" \/><\/a>\r\n<\/span><\/div>\r\n\r\n<strong>TABLES OF CONTENTS<\/strong>\r\n<ol>\r\n \t<li><strong>Learning Outcomes<\/strong><\/li>\r\n<\/ol>\r\n<ol start=\"2\">\r\n \t<li><strong>Introduction<\/strong><\/li>\r\n<\/ol>\r\n<ol start=\"3\">\r\n \t<li><strong>CO occurrence in the body<\/strong><\/li>\r\n<\/ol>\r\n<strong>\u00a0 \u00a0 \u00a0 \u00a03.1 Endogenous route<\/strong>\r\n\r\n&nbsp;\r\n\r\n<strong>\u00a0 \u00a03.2 Exogenous route<\/strong>\r\n<ol start=\"4\">\r\n \t<li><strong>Exogenous Carbon Monoxide (CO) Formation<\/strong><\/li>\r\n<\/ol>\r\n<ol start=\"5\">\r\n \t<li><strong>Sources of Human Exposure to CO<\/strong><\/li>\r\n<\/ol>\r\n<ol start=\"6\">\r\n \t<li><strong>Mechanism of Action and Toxicological Effects of Carbon Monoxide (CO)<\/strong><\/li>\r\n<\/ol>\r\n<ol start=\"7\">\r\n \t<li><strong>References<\/strong><\/li>\r\n<\/ol>\r\n&nbsp;\r\n<ol>\r\n \t<li><strong>Learning Outcomes<\/strong><\/li>\r\n<\/ol>\r\n<ul>\r\n \t<li style=\"text-align: justify\">After going through this module, you shall be able to:<\/li>\r\n \t<li style=\"text-align: justify\">To know about carbon monoxide and its routes of occurrence in the body. To gain knowledge about\u00a0 \u00a0 \u00a0 \u00a0 \u00a0 Exogenous Carbon Monoxide (CO) Formation.<\/li>\r\n \t<li style=\"text-align: justify\">To understand about the Mechanism of Action and Toxicological Effects of Carbon Monoxide (CO).<\/li>\r\n \t<li style=\"text-align: justify\">To know about human health effects at different Carboxyhemoglobin (COHb) levels.<\/li>\r\n<\/ul>\r\n<ol start=\"2\">\r\n \t<li><strong> Introduction<\/strong><\/li>\r\n<\/ol>\r\n<p style=\"text-align: justify\">Carbon monoxide is a colorless, odorless, tasteless, nonirritant and ubiquitous asphyxiating gas produced by the incomplete combustion of hydrocarbons (solid, liquid and gaseous carbon containing fuels). CO is 96.5% as heavy as air and is not soluble in water. CO is a Criteria Air Pollutant as listed by US-EPA. It is usually found in high concentrations in the urban atmosphere. No other gaseous air pollutant with such a toxic potential as CO exists at such high concentrations in the urban environment. Historically, CO asphyxiation has been well documented since the ancient Roman time. The early exposures began from the use of firewood and then coal for domestic heating.<\/p>\r\n<strong><em>*Criteria Air Pollutants <\/em><\/strong>is used to describe \"a group of very common pollutants regulated by EPA on the basis of criteria (information on health and\/or environmental effects of pollution)\".\r\n\r\n<strong>3.CO occurrence in the body<\/strong>\r\n\r\n&nbsp;\r\n\r\nCO occurrence in the body occurs through two routes: Endogenous and Exogenous\r\n<p style=\"text-align: justify\">3.1. <strong>Endogenous route:<\/strong> Endogenously CO is produced by mainly hemoglobin catabolism (enzymatic heme degradation by HO) and minute amounts can also be produced as a byproduct of iron-catalyzed lipid peroxidation. The bulk of heme catabolism occurs in the reticuloendothelial system of the spleen and liver, hence the endogenous CO production. Endogeneous CO production accounts for less than 1% COHb levels of blood. At these physiologic levels CO may serve as a neurotransmitter or modulate other neurotransmitters and hormones. The functions of CO at these levels include neurotransmission, vasodilation, antiproliferation effects of smooth muscle, inhibition of platelet aggregation, and anti-inflammatory agent.<\/p>\r\n3.2. <strong>Exogenous route:<\/strong> Exogenous uptake from ambient air by lungs.\r\n\r\n<img class=\"aligncenter size-full wp-image-44\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-4.jpg\" alt=\"\" width=\"407\" height=\"154\" \/>\r\n<p style=\"text-align: center\"><strong>Fig. 1. Routs of Carbon Monoxide (CO) in the body<\/strong><\/p>\r\n\r\n<ol start=\"4\">\r\n \t<li><strong> Exogenous Carbon Monoxide (CO) Formation<\/strong><\/li>\r\n<\/ol>\r\nExogenous carbon monoxide (CO) formation usually occurs through one of the following three processes:\r\n<p style=\"text-align: justify\"><strong>1.Incomplete combustion of carbon \/ carbon\u2014containing compounds: <\/strong>When available oxygen is less than the amount required for complete combustion (i.e. insufficient supply of oxygen), or when there is poor mixing of fuel and air, carbon monoxide (CO) is formed instead of carbon dioxide (CO2 is the end product of complete combustion):<\/p>\r\n<img class=\"aligncenter wp-image-51\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-9.jpg\" alt=\"\" width=\"713\" height=\"61\" \/>Reactions between CO<strong>2<\/strong><strong> and carbon-containing materials at elevated temperatures: <\/strong>CO is also produced when CO2 reacts with carbon containing materials at elevated temperatures, commonly in many industrial devices, e.g. in blast furnaces.\r\n<p style=\"text-align: justify\"><img class=\"aligncenter size-full wp-image-52\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-10.jpg\" alt=\"\" width=\"568\" height=\"33\" \/>The CO produced in this way is necessary in certain industrial applications, as in the blast furnace of smelter, where CO acts as a reducing agent in the production of iron from Fe2O3 ores . However, some CO may escape into the atmosphere.<img class=\"aligncenter size-full wp-image-53\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-11.jpg\" alt=\"\" width=\"550\" height=\"26\" \/><strong>3.Dissociation of carbon dioxide (CO<\/strong><strong>2<\/strong><strong>) at high temperature: <\/strong>Dissociation of CO2 is favored by high temperature. Carbon dioxide (CO2) dissociates into CO and O at high temperature, as shown below in Eq.<\/p>\r\n<img class=\"aligncenter size-full wp-image-54\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-12.jpg\" alt=\"\" width=\"574\" height=\"71\" \/>\r\n\r\n<img class=\"aligncenter size-full wp-image-55\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-13.jpg\" alt=\"\" width=\"614\" height=\"369\" \/>\r\n<ol start=\"5\">\r\n \t<li><strong>Sources of Human Exposure to CO<\/strong><\/li>\r\n<\/ol>\r\n<p style=\"text-align: justify\">CO is an odorless and poisonous gas, which can neither be smelled nor seen and can kill a person in minutes if the concentration of the gas is high enough. Carbon monoxide is a common cause of accidental poisoning. Exposure to CO comes mainly from following sources:<\/p>\r\n<p style=\"text-align: justify\"><strong>1.CO in the surrounding ambient environment mainly from exhaust gases: <\/strong>Whenever any combustible fuel (e.g. gas, oil, kerosene, wood, or cahrcoal) is burned, CO is produced<strong>.<\/strong> CO in the ambient environment is emitted from exhaust gases from automobile and industrial machinery. With the emergence of automobiles propelled by an internal combustion engine, the CO emitted from the exhaust pipe has become the major source for human exposure.<\/p>\r\n<p style=\"text-align: justify\"><strong>2.Accidental intoxication: <\/strong>Through housefires (&gt;50,000 ppm CO), and home environmental problems such as defective furnaces, charcoal burning in poorly vented houses, or garages connected to living quarters, and space heaters in campers. The numerous fatal cases of CO poisoning that occur each year are almost always the result of improperly vented heating devices in the indoor areas. CO is\u00a0also<span style=\"text-align: initial;font-size: 1em\"> produced from explosives used in surface blasting. CO produced can travel through soil and get accumulated in confined spaces, creating a hazard for workers. Inside air in homes in the vicinity of a blast site may also acquire elevated CO levels.<\/span><\/p>\r\n<p style=\"text-align: justify\"><strong>3.Occupational exposure<\/strong>: Serious problems exist with occupational exposure to increased ambient CO for firefighters (&gt;10,000 ppm CO), traffic police, toll booth attendants, smelter workers, coal miners, coke ovens and transportation mechanics.<\/p>\r\n<p style=\"text-align: justify\"><strong>4.Cigarette smoking: <\/strong>Smokers have higher carboxyhemoglobin (COHb) levels than nonsmokers (Table 1). Particularly in the less developed countries, with a large percentage of the population smoking, nonsmokers are subjected to inhalation of CO from cigarette smoke in confined spaces. A cigarette smoker is exposed to 400\u2013500 ppm CO, resulting in COHb level of 3\u20138%, which may increase to 15% in a heavy smoker (Raub et al., 2000) in comparison to COHb of 1\u20133% in nonsmokers. In <em>hookah (<\/em>waterpipe) smoking, the exposure to CO from the combustion of charcoal is 10 fold greater than that of a cigarette smoking.<\/p>\r\n<p style=\"text-align: justify\"><img class=\"aligncenter size-full wp-image-56\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-14.jpg\" alt=\"\" width=\"659\" height=\"342\" \/><\/p>\r\n<p style=\"text-align: justify\"><strong style=\"font-size: 1em\">6.Mechanism of Action <\/strong><span style=\"font-size: 1em\">and<\/span><strong style=\"font-size: 1em\"> Toxicological Effects <\/strong><span style=\"font-size: 1em\">of Carbon Monoxide (CO)<\/span><\/p>\r\n<p style=\"text-align: justify\">A constant supply of O2 is needed for normal physiological functions in the body. O2 is carried to body tissue by hemoglobin (Hb). Each hemoglobin has four sites (heme) for binding with oxygen. Hemoglobin picks up O2 in the lungs, forming a complex called oxyhemoglobin Hb(O2)4 .<img class=\"aligncenter size-full wp-image-57\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-15.jpg\" alt=\"\" width=\"483\" height=\"51\" \/><\/p>\r\n<p style=\"text-align: justify\">Hb(O2)4 releases the O2 bound to it, to be used by body tissues. Hb then returns to the lungs for a new supply of O2. CO is toxic because it interferes with O2 delivery to the body's organs and tissues. CO gas binds avidly to Fe(II) in hemoglobin (Hb), forming carboxyhemoglobin, HbCO or COHb:<\/p>\r\n<img class=\"aligncenter size-full wp-image-58\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-16.jpg\" alt=\"\" width=\"602\" height=\"64\" \/>\r\n<p style=\"text-align: justify\">The chemical affinity of CO for combining with Hb is much greater ( 200 times) than that of O2. In presence of CO oxyhemoglobin readily releases the O2 bound and picks up CO to form carboxyhemoglobin. Since, a binding site on an Hb molecule cannot be occupied by both CO and O2 at the same time, substantial quantity of Hb preferentially ties up with CO forming carboxyhemoglobin. After CO binds with one site of hemoglobin molecule, the hemoglobin tetramer bound O2 with greater affinity, which makes it more difficult for the hemoglobin molecule to unload and deliver oxygen to the body's organs. Consequently, CO not only decreases the oxygen-carrying capacity of hemoglobin molecule (Hb) but also affects the release of oxygen to the body tissues, leading to tissue hypoxia thus severely impairing body functions specially of the heart and central nervous system (CNS).<\/p>\r\n<p style=\"text-align: justify\">The chemical reaction (8) is written with a double arrow denoting that this is reversible. Although, an increase in oxygen concentrations can shift the equilibrium in Equation (8) to the left, recovery of Hb is slow, while the asphyxiating effect of putting Hb out of business is rapid. The normal or background level of blood HbCO is about 0.5%. The CO is derived from both the CO in ambient air and the CO produced by the body during catabolism of heme (a component of Hb).<\/p>\r\nThe equilibrium percentage of HbCO in the bloodstream of a person continually exposed to an ambient air CO concentration of less than 100 ppm can be calculated from the following equation:\r\n\r\nPercent COHb in blood = 0.16 X (CO concentration in the air in ppm) + 0.5\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 (9)\r\n<p style=\"text-align: justify\">Health effects varying from impairment in awareness and judgement, headache, nausea, collapse and coma to death may be expected to occur based on COHb levels. Inhaled CO aggravates coronary heart diseases, as well as circulatory, lung, and respiratory diseases, due to reduced oxygen carrying capacity of the blood and increased demand on the heart and lungs. Demonstrated health effects associated with COHb levels are summarized in Table 2.<\/p>\r\n<img class=\"aligncenter size-full wp-image-60\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-17.jpg\" alt=\"\" width=\"668\" height=\"472\" \/>\r\n\r\n<strong> \u00a0 \u00a0 \u00a0 References: Bleecker (2015); Landis et al. (2011)<\/strong>\r\n<p style=\"text-align: justify\">Carbon monoxide also inhibits function of alveolar macrophages. This can lead to weakening tissue defenses against airborne bacterial infection. Maternal CO poisoning during pregnancy has been shown to cause fetal death because of lack of O2 in the fetal circulatory system. Carbon monoxide poisoning causing unconsciousness for 30 minutes to 5 hours does not do permanent damage to the mother but can cause brain damage, mental deficiency, or death to the fetus. Severity of damage is related to the month of pregnancy, the fetus being particularly vulnerable shortly before birth.<\/p>\r\n<p style=\"text-align: justify\">CO poisoning can be cured by exposing the affected person to oxygen, where the reverse reaction occurs. The half-life of COHb is 4-6 hours at rest at room air, which can be shortened to 60 to 90 minutes if 100% oxygen is given using a face mask. Since, more than 2 hours at 100% oxygen can cause pulmonary oxygen toxicity, the oxygen concentration should be reduced to 60% at 2 hours.<\/p>\r\n<img class=\"aligncenter size-full wp-image-61\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-18.jpg\" alt=\"\" width=\"232\" height=\"29\" \/>As mentioned previously, CO competes with O2 for binding of hemoglobin, but in addition, it also binds with other proteins, such as myoglobin, cytochrome P-450 and cytochrome c oxidase. Carbon monoxide also impairs the facilitated diffusion of O2 to the mitochondria, shifting the oxyhemoglobin dissociation curve to the left. Alteration of the oxyhemoglobin dissociation curve by COHb occurs in such a manner that O2 is released to tissues with great difficulty and at a lower O2 tension.\r\n\r\n<table>\r\n<tbody>\r\n<tr>\r\n<td><strong>you can view video on Carbon Monoxide Toxicity<\/strong><\/td>\r\n<td><a href=\"https:\/\/youtu.be\/dWsQaGh5pwU\" target=\"_blank\" rel=\"noopener\"><img class=\"alignnone wp-image-120\" src=\"http:\/\/epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/2018\/11\/download.png\" alt=\"\" width=\"36\" height=\"36\" \/><\/a><\/td>\r\n<\/tr>\r\n<\/tbody>\r\n<\/table>\r\n\r\n<strong>References<\/strong>\r\n<ol>\r\n \t<li style=\"text-align: justify\">Bleecker M. L. (2015) C<em>arbon monoxide intoxication.<\/em> In Lotti M. and Bleecker M.L. (Eds) <em>Handbook of Clinical Neurology<\/em>, Vol. 131 (3rd series) <em>Occupational Neurology<\/em> \u00a9 2015 Elsevier. Pp. 191-203.<\/li>\r\n \t<li style=\"text-align: justify\">Landis W.G., Sofield R.M., Yu M-H (2011).<em> Inorganic gaseous pollutants. In Introduction to Environmental <\/em>toxicology: <em>Molecular Substructures to Ecological Landscapes<\/em>, CRC Press. pp. 237-254<\/li>\r\n \t<li style=\"text-align: justify\">Piantadosi C. A. (2002) <em>Biological Chemistry of Carbon Monoxide. Antioxidants &amp; Redox Signaling<\/em> 4(2): 259-270<\/li>\r\n \t<li style=\"text-align: justify\">Raub J, Mathieu-Nolf M, Hampson N et al. (2000). <em>Carbon monoxide poisoning \u2013 a public health perspective. Toxicology<\/em> 145: 1\u201314.<\/li>\r\n<\/ol>\r\n&nbsp;\r\n\r\n&nbsp;","rendered":"<div><span style=\"float: right\"><a href=\"https:\/\/youtu.be\/dWsQaGh5pwU\" target=\"_blank\" rel=\"noopener\"><img decoding=\"async\" src=\"http:\/\/epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/2018\/11\/download.png\" alt=\"epgp books\" width=\"75px\" height=\"75px;\" \/><\/a><br \/>\n<\/span><\/div>\n<p><strong>TABLES OF CONTENTS<\/strong><\/p>\n<ol>\n<li><strong>Learning Outcomes<\/strong><\/li>\n<\/ol>\n<ol start=\"2\">\n<li><strong>Introduction<\/strong><\/li>\n<\/ol>\n<ol start=\"3\">\n<li><strong>CO occurrence in the body<\/strong><\/li>\n<\/ol>\n<p><strong>\u00a0 \u00a0 \u00a0 \u00a03.1 Endogenous route<\/strong><\/p>\n<p>&nbsp;<\/p>\n<p><strong>\u00a0 \u00a03.2 Exogenous route<\/strong><\/p>\n<ol start=\"4\">\n<li><strong>Exogenous Carbon Monoxide (CO) Formation<\/strong><\/li>\n<\/ol>\n<ol start=\"5\">\n<li><strong>Sources of Human Exposure to CO<\/strong><\/li>\n<\/ol>\n<ol start=\"6\">\n<li><strong>Mechanism of Action and Toxicological Effects of Carbon Monoxide (CO)<\/strong><\/li>\n<\/ol>\n<ol start=\"7\">\n<li><strong>References<\/strong><\/li>\n<\/ol>\n<p>&nbsp;<\/p>\n<ol>\n<li><strong>Learning Outcomes<\/strong><\/li>\n<\/ol>\n<ul>\n<li style=\"text-align: justify\">After going through this module, you shall be able to:<\/li>\n<li style=\"text-align: justify\">To know about carbon monoxide and its routes of occurrence in the body. To gain knowledge about\u00a0 \u00a0 \u00a0 \u00a0 \u00a0 Exogenous Carbon Monoxide (CO) Formation.<\/li>\n<li style=\"text-align: justify\">To understand about the Mechanism of Action and Toxicological Effects of Carbon Monoxide (CO).<\/li>\n<li style=\"text-align: justify\">To know about human health effects at different Carboxyhemoglobin (COHb) levels.<\/li>\n<\/ul>\n<ol start=\"2\">\n<li><strong> Introduction<\/strong><\/li>\n<\/ol>\n<p style=\"text-align: justify\">Carbon monoxide is a colorless, odorless, tasteless, nonirritant and ubiquitous asphyxiating gas produced by the incomplete combustion of hydrocarbons (solid, liquid and gaseous carbon containing fuels). CO is 96.5% as heavy as air and is not soluble in water. CO is a Criteria Air Pollutant as listed by US-EPA. It is usually found in high concentrations in the urban atmosphere. No other gaseous air pollutant with such a toxic potential as CO exists at such high concentrations in the urban environment. Historically, CO asphyxiation has been well documented since the ancient Roman time. The early exposures began from the use of firewood and then coal for domestic heating.<\/p>\n<p><strong><em>*Criteria Air Pollutants <\/em><\/strong>is used to describe &#8220;a group of very common pollutants regulated by EPA on the basis of criteria (information on health and\/or environmental effects of pollution)&#8221;.<\/p>\n<p><strong>3.CO occurrence in the body<\/strong><\/p>\n<p>&nbsp;<\/p>\n<p>CO occurrence in the body occurs through two routes: Endogenous and Exogenous<\/p>\n<p style=\"text-align: justify\">3.1. <strong>Endogenous route:<\/strong> Endogenously CO is produced by mainly hemoglobin catabolism (enzymatic heme degradation by HO) and minute amounts can also be produced as a byproduct of iron-catalyzed lipid peroxidation. The bulk of heme catabolism occurs in the reticuloendothelial system of the spleen and liver, hence the endogenous CO production. Endogeneous CO production accounts for less than 1% COHb levels of blood. At these physiologic levels CO may serve as a neurotransmitter or modulate other neurotransmitters and hormones. The functions of CO at these levels include neurotransmission, vasodilation, antiproliferation effects of smooth muscle, inhibition of platelet aggregation, and anti-inflammatory agent.<\/p>\n<p>3.2. <strong>Exogenous route:<\/strong> Exogenous uptake from ambient air by lungs.<\/p>\n<p><img loading=\"lazy\" decoding=\"async\" class=\"aligncenter size-full wp-image-44\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-4.jpg\" alt=\"\" width=\"407\" height=\"154\" srcset=\"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-4.jpg 407w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-4-300x114.jpg 300w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-4-65x25.jpg 65w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-4-225x85.jpg 225w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-4-350x132.jpg 350w\" sizes=\"auto, (max-width: 407px) 100vw, 407px\" \/><\/p>\n<p style=\"text-align: center\"><strong>Fig. 1. Routs of Carbon Monoxide (CO) in the body<\/strong><\/p>\n<ol start=\"4\">\n<li><strong> Exogenous Carbon Monoxide (CO) Formation<\/strong><\/li>\n<\/ol>\n<p>Exogenous carbon monoxide (CO) formation usually occurs through one of the following three processes:<\/p>\n<p style=\"text-align: justify\"><strong>1.Incomplete combustion of carbon \/ carbon\u2014containing compounds: <\/strong>When available oxygen is less than the amount required for complete combustion (i.e. insufficient supply of oxygen), or when there is poor mixing of fuel and air, carbon monoxide (CO) is formed instead of carbon dioxide (CO2 is the end product of complete combustion):<\/p>\n<p><img loading=\"lazy\" decoding=\"async\" class=\"aligncenter wp-image-51\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-9.jpg\" alt=\"\" width=\"713\" height=\"61\" srcset=\"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-9.jpg 655w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-9-300x26.jpg 300w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-9-65x6.jpg 65w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-9-225x19.jpg 225w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-9-350x30.jpg 350w\" sizes=\"auto, (max-width: 713px) 100vw, 713px\" \/>Reactions between CO<strong>2<\/strong><strong> and carbon-containing materials at elevated temperatures: <\/strong>CO is also produced when CO2 reacts with carbon containing materials at elevated temperatures, commonly in many industrial devices, e.g. in blast furnaces.<\/p>\n<p style=\"text-align: justify\"><img loading=\"lazy\" decoding=\"async\" class=\"aligncenter size-full wp-image-52\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-10.jpg\" alt=\"\" width=\"568\" height=\"33\" srcset=\"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-10.jpg 568w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-10-300x17.jpg 300w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-10-65x4.jpg 65w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-10-225x13.jpg 225w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-10-350x20.jpg 350w\" sizes=\"auto, (max-width: 568px) 100vw, 568px\" \/>The CO produced in this way is necessary in certain industrial applications, as in the blast furnace of smelter, where CO acts as a reducing agent in the production of iron from Fe2O3 ores . However, some CO may escape into the atmosphere.<img loading=\"lazy\" decoding=\"async\" class=\"aligncenter size-full wp-image-53\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-11.jpg\" alt=\"\" width=\"550\" height=\"26\" srcset=\"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-11.jpg 550w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-11-300x14.jpg 300w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-11-65x3.jpg 65w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-11-225x11.jpg 225w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-11-350x17.jpg 350w\" sizes=\"auto, (max-width: 550px) 100vw, 550px\" \/><strong>3.Dissociation of carbon dioxide (CO<\/strong><strong>2<\/strong><strong>) at high temperature: <\/strong>Dissociation of CO2 is favored by high temperature. Carbon dioxide (CO2) dissociates into CO and O at high temperature, as shown below in Eq.<\/p>\n<p><img loading=\"lazy\" decoding=\"async\" class=\"aligncenter size-full wp-image-54\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-12.jpg\" alt=\"\" width=\"574\" height=\"71\" srcset=\"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-12.jpg 574w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-12-300x37.jpg 300w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-12-65x8.jpg 65w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-12-225x28.jpg 225w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-12-350x43.jpg 350w\" sizes=\"auto, (max-width: 574px) 100vw, 574px\" \/><\/p>\n<p><img loading=\"lazy\" decoding=\"async\" class=\"aligncenter size-full wp-image-55\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-13.jpg\" alt=\"\" width=\"614\" height=\"369\" srcset=\"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-13.jpg 614w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-13-300x180.jpg 300w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-13-65x39.jpg 65w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-13-225x135.jpg 225w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-13-350x210.jpg 350w\" sizes=\"auto, (max-width: 614px) 100vw, 614px\" \/><\/p>\n<ol start=\"5\">\n<li><strong>Sources of Human Exposure to CO<\/strong><\/li>\n<\/ol>\n<p style=\"text-align: justify\">CO is an odorless and poisonous gas, which can neither be smelled nor seen and can kill a person in minutes if the concentration of the gas is high enough. Carbon monoxide is a common cause of accidental poisoning. Exposure to CO comes mainly from following sources:<\/p>\n<p style=\"text-align: justify\"><strong>1.CO in the surrounding ambient environment mainly from exhaust gases: <\/strong>Whenever any combustible fuel (e.g. gas, oil, kerosene, wood, or cahrcoal) is burned, CO is produced<strong>.<\/strong> CO in the ambient environment is emitted from exhaust gases from automobile and industrial machinery. With the emergence of automobiles propelled by an internal combustion engine, the CO emitted from the exhaust pipe has become the major source for human exposure.<\/p>\n<p style=\"text-align: justify\"><strong>2.Accidental intoxication: <\/strong>Through housefires (&gt;50,000 ppm CO), and home environmental problems such as defective furnaces, charcoal burning in poorly vented houses, or garages connected to living quarters, and space heaters in campers. The numerous fatal cases of CO poisoning that occur each year are almost always the result of improperly vented heating devices in the indoor areas. CO is\u00a0also<span style=\"text-align: initial;font-size: 1em\"> produced from explosives used in surface blasting. CO produced can travel through soil and get accumulated in confined spaces, creating a hazard for workers. Inside air in homes in the vicinity of a blast site may also acquire elevated CO levels.<\/span><\/p>\n<p style=\"text-align: justify\"><strong>3.Occupational exposure<\/strong>: Serious problems exist with occupational exposure to increased ambient CO for firefighters (&gt;10,000 ppm CO), traffic police, toll booth attendants, smelter workers, coal miners, coke ovens and transportation mechanics.<\/p>\n<p style=\"text-align: justify\"><strong>4.Cigarette smoking: <\/strong>Smokers have higher carboxyhemoglobin (COHb) levels than nonsmokers (Table 1). Particularly in the less developed countries, with a large percentage of the population smoking, nonsmokers are subjected to inhalation of CO from cigarette smoke in confined spaces. A cigarette smoker is exposed to 400\u2013500 ppm CO, resulting in COHb level of 3\u20138%, which may increase to 15% in a heavy smoker (Raub et al., 2000) in comparison to COHb of 1\u20133% in nonsmokers. In <em>hookah (<\/em>waterpipe) smoking, the exposure to CO from the combustion of charcoal is 10 fold greater than that of a cigarette smoking.<\/p>\n<p style=\"text-align: justify\"><img loading=\"lazy\" decoding=\"async\" class=\"aligncenter size-full wp-image-56\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-14.jpg\" alt=\"\" width=\"659\" height=\"342\" srcset=\"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-14.jpg 659w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-14-300x156.jpg 300w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-14-65x34.jpg 65w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-14-225x117.jpg 225w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-14-350x182.jpg 350w\" sizes=\"auto, (max-width: 659px) 100vw, 659px\" \/><\/p>\n<p style=\"text-align: justify\"><strong style=\"font-size: 1em\">6.Mechanism of Action <\/strong><span style=\"font-size: 1em\">and<\/span><strong style=\"font-size: 1em\"> Toxicological Effects <\/strong><span style=\"font-size: 1em\">of Carbon Monoxide (CO)<\/span><\/p>\n<p style=\"text-align: justify\">A constant supply of O2 is needed for normal physiological functions in the body. O2 is carried to body tissue by hemoglobin (Hb). Each hemoglobin has four sites (heme) for binding with oxygen. Hemoglobin picks up O2 in the lungs, forming a complex called oxyhemoglobin Hb(O2)4 .<img loading=\"lazy\" decoding=\"async\" class=\"aligncenter size-full wp-image-57\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-15.jpg\" alt=\"\" width=\"483\" height=\"51\" srcset=\"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-15.jpg 483w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-15-300x32.jpg 300w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-15-65x7.jpg 65w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-15-225x24.jpg 225w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-15-350x37.jpg 350w\" sizes=\"auto, (max-width: 483px) 100vw, 483px\" \/><\/p>\n<p style=\"text-align: justify\">Hb(O2)4 releases the O2 bound to it, to be used by body tissues. Hb then returns to the lungs for a new supply of O2. CO is toxic because it interferes with O2 delivery to the body&#8217;s organs and tissues. CO gas binds avidly to Fe(II) in hemoglobin (Hb), forming carboxyhemoglobin, HbCO or COHb:<\/p>\n<p><img loading=\"lazy\" decoding=\"async\" class=\"aligncenter size-full wp-image-58\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-16.jpg\" alt=\"\" width=\"602\" height=\"64\" srcset=\"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-16.jpg 602w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-16-300x32.jpg 300w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-16-65x7.jpg 65w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-16-225x24.jpg 225w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-16-350x37.jpg 350w\" sizes=\"auto, (max-width: 602px) 100vw, 602px\" \/><\/p>\n<p style=\"text-align: justify\">The chemical affinity of CO for combining with Hb is much greater ( 200 times) than that of O2. In presence of CO oxyhemoglobin readily releases the O2 bound and picks up CO to form carboxyhemoglobin. Since, a binding site on an Hb molecule cannot be occupied by both CO and O2 at the same time, substantial quantity of Hb preferentially ties up with CO forming carboxyhemoglobin. After CO binds with one site of hemoglobin molecule, the hemoglobin tetramer bound O2 with greater affinity, which makes it more difficult for the hemoglobin molecule to unload and deliver oxygen to the body&#8217;s organs. Consequently, CO not only decreases the oxygen-carrying capacity of hemoglobin molecule (Hb) but also affects the release of oxygen to the body tissues, leading to tissue hypoxia thus severely impairing body functions specially of the heart and central nervous system (CNS).<\/p>\n<p style=\"text-align: justify\">The chemical reaction (8) is written with a double arrow denoting that this is reversible. Although, an increase in oxygen concentrations can shift the equilibrium in Equation (8) to the left, recovery of Hb is slow, while the asphyxiating effect of putting Hb out of business is rapid. The normal or background level of blood HbCO is about 0.5%. The CO is derived from both the CO in ambient air and the CO produced by the body during catabolism of heme (a component of Hb).<\/p>\n<p>The equilibrium percentage of HbCO in the bloodstream of a person continually exposed to an ambient air CO concentration of less than 100 ppm can be calculated from the following equation:<\/p>\n<p>Percent COHb in blood = 0.16 X (CO concentration in the air in ppm) + 0.5\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 (9)<\/p>\n<p style=\"text-align: justify\">Health effects varying from impairment in awareness and judgement, headache, nausea, collapse and coma to death may be expected to occur based on COHb levels. Inhaled CO aggravates coronary heart diseases, as well as circulatory, lung, and respiratory diseases, due to reduced oxygen carrying capacity of the blood and increased demand on the heart and lungs. Demonstrated health effects associated with COHb levels are summarized in Table 2.<\/p>\n<p><img loading=\"lazy\" decoding=\"async\" class=\"aligncenter size-full wp-image-60\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-17.jpg\" alt=\"\" width=\"668\" height=\"472\" srcset=\"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-17.jpg 668w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-17-300x212.jpg 300w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-17-65x46.jpg 65w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-17-225x159.jpg 225w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-17-350x247.jpg 350w\" sizes=\"auto, (max-width: 668px) 100vw, 668px\" \/><\/p>\n<p><strong> \u00a0 \u00a0 \u00a0 References: Bleecker (2015); Landis et al. (2011)<\/strong><\/p>\n<p style=\"text-align: justify\">Carbon monoxide also inhibits function of alveolar macrophages. This can lead to weakening tissue defenses against airborne bacterial infection. Maternal CO poisoning during pregnancy has been shown to cause fetal death because of lack of O2 in the fetal circulatory system. Carbon monoxide poisoning causing unconsciousness for 30 minutes to 5 hours does not do permanent damage to the mother but can cause brain damage, mental deficiency, or death to the fetus. Severity of damage is related to the month of pregnancy, the fetus being particularly vulnerable shortly before birth.<\/p>\n<p style=\"text-align: justify\">CO poisoning can be cured by exposing the affected person to oxygen, where the reverse reaction occurs. The half-life of COHb is 4-6 hours at rest at room air, which can be shortened to 60 to 90 minutes if 100% oxygen is given using a face mask. Since, more than 2 hours at 100% oxygen can cause pulmonary oxygen toxicity, the oxygen concentration should be reduced to 60% at 2 hours.<\/p>\n<p><img loading=\"lazy\" decoding=\"async\" class=\"aligncenter size-full wp-image-61\" src=\"http:\/\/esp15.epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/sites\/160\/2019\/03\/3-18.jpg\" alt=\"\" width=\"232\" height=\"29\" srcset=\"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-18.jpg 232w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-18-65x8.jpg 65w, https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-content\/uploads\/sites\/160\/2019\/03\/3-18-225x28.jpg 225w\" sizes=\"auto, (max-width: 232px) 100vw, 232px\" \/>As mentioned previously, CO competes with O2 for binding of hemoglobin, but in addition, it also binds with other proteins, such as myoglobin, cytochrome P-450 and cytochrome c oxidase. Carbon monoxide also impairs the facilitated diffusion of O2 to the mitochondria, shifting the oxyhemoglobin dissociation curve to the left. Alteration of the oxyhemoglobin dissociation curve by COHb occurs in such a manner that O2 is released to tissues with great difficulty and at a lower O2 tension.<\/p>\n<table>\n<tbody>\n<tr>\n<td><strong>you can view video on Carbon Monoxide Toxicity<\/strong><\/td>\n<td><a href=\"https:\/\/youtu.be\/dWsQaGh5pwU\" target=\"_blank\" rel=\"noopener\"><img loading=\"lazy\" decoding=\"async\" class=\"alignnone wp-image-120\" src=\"http:\/\/epgpbooks.inflibnet.ac.in\/wp-content\/uploads\/2018\/11\/download.png\" alt=\"\" width=\"36\" height=\"36\" \/><\/a><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p><strong>References<\/strong><\/p>\n<ol>\n<li style=\"text-align: justify\">Bleecker M. L. (2015) C<em>arbon monoxide intoxication.<\/em> In Lotti M. and Bleecker M.L. (Eds) <em>Handbook of Clinical Neurology<\/em>, Vol. 131 (3rd series) <em>Occupational Neurology<\/em> \u00a9 2015 Elsevier. Pp. 191-203.<\/li>\n<li style=\"text-align: justify\">Landis W.G., Sofield R.M., Yu M-H (2011).<em> Inorganic gaseous pollutants. In Introduction to Environmental <\/em>toxicology: <em>Molecular Substructures to Ecological Landscapes<\/em>, CRC Press. pp. 237-254<\/li>\n<li style=\"text-align: justify\">Piantadosi C. A. (2002) <em>Biological Chemistry of Carbon Monoxide. Antioxidants &amp; Redox Signaling<\/em> 4(2): 259-270<\/li>\n<li style=\"text-align: justify\">Raub J, Mathieu-Nolf M, Hampson N et al. (2000). <em>Carbon monoxide poisoning \u2013 a public health perspective. Toxicology<\/em> 145: 1\u201314.<\/li>\n<\/ol>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n","protected":false},"author":3,"menu_order":3,"template":"","meta":{"_acf_changed":false,"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["dr-anju"],"pb_section_license":""},"chapter-type":[],"contributor":[58],"license":[],"class_list":["post-43","chapter","type-chapter","status-publish","hentry","contributor-dr-anju"],"part":3,"_links":{"self":[{"href":"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-json\/pressbooks\/v2\/chapters\/43","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-json\/wp\/v2\/users\/3"}],"version-history":[{"count":22,"href":"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-json\/pressbooks\/v2\/chapters\/43\/revisions"}],"predecessor-version":[{"id":726,"href":"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-json\/pressbooks\/v2\/chapters\/43\/revisions\/726"}],"part":[{"href":"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-json\/pressbooks\/v2\/parts\/3"}],"metadata":[{"href":"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-json\/pressbooks\/v2\/chapters\/43\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-json\/wp\/v2\/media?parent=43"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-json\/pressbooks\/v2\/chapter-type?post=43"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-json\/wp\/v2\/contributor?post=43"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/ebooks.inflibnet.ac.in\/esp15\/wp-json\/wp\/v2\/license?post=43"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}