Tikuisis (82) reviewed human carbon monoxide uptake and elimination in 1996. Smokers' polycythemia. Abstract. The issue of dosimetry is complex, but there exist physiologically based mathematical models to estimate many of the above variables and thus to predict tissue function. Toxic gas holds hints", "Molecular Gas Clumps from the Destruction of Icy Bodies in the Pictoris Debris Disk", "Comets (World Book Online Reference Center 125580)", "Pressure-Induced Polymerization of Carbon Monoxide: Disproportionation and Synthesis of an Energetic Lactonic Polymer", "New route to carbon-neutral fuels from carbon dioxide discovered by Stanford-DTU team - DTU", "Selective high-temperature CO 2 electrolysis enabled by oxidized carbon intermediates", "Role of Carbon Monoxide in HostGut Microbiome Communication", "Heme Oxygenase-1/Carbon Monoxide: From Basic Science to Therapeutic Applications", "Regulation of inflammation by the antioxidant haem oxygenase 1", "The therapeutic potential of carbon monoxide", "Biological signaling by carbon monoxide and carbon monoxide-releasing molecules", "Where is the Clinical Breakthrough of Heme Oxygenase-1 / Carbon Monoxide Therapeutics? [87], The technology was first given "generally recognized as safe" (GRAS) status by the U.S. Food and Drug Administration (FDA) in 2002 for use as a secondary packaging system, and does not require labeling. Within the cohort, 2813 (2.2%) were low in birth weight (between 1000 and 2499 grams). Thus, daily average concentrations of carbon monoxide and nitrogen dioxide exhibited the most consistent associations with emergency department visits for cardiac conditions. Many methods have been developed for carbon monoxide production.[64]. Carbon monoxide, with the chemical formula CO, is a colorless, odorless, and tasteless gas. Growth of the heart in health and disease. In: Penney DG, editor. The ability to avoid or flee danger could also be impaired by carbon-monoxide-induced limitations on exercise. Mayo Clinic does not endorse companies or products. It was discovered in the 1960s that CO can be endogenously produced in the body by heme oxygenase (HO) metabolism of heme to produce CO, iron, and biliverdin. Kleinman MT, et al. 103 (128) have recently been thoroughly reviewed by Helffenstein (97). Carbon monoxide (CO) is a colourless, non-irritant, odourless and tasteless toxic gas. (107), Ryan (108), Tvedt & Kjuus (109), Myers et al. Beef, sheep, and human sera, and beef plasma were saturated with the gas at 15, 20, 25, 30, and 37C. Bell ML, et al. Philadelphia, Pa.: Elsevier; 2018. https://www.clinicalkey.com. Benignus VA, et al. Jetter et al. Carbon monoxide is a relatively unreactive gas under ambient air conditions and is not absorbed by building materials or ventilation system filters. The outdoor air carbon monoxide concentration at the point of measurement may be significantly higher or lower than the concentration at the point of ventilation air intake. National Library of Medicine. CO is the leading cause of poisoning deaths in the United States and occurs when there is incomplete combustion of carbon-containing material such as coal, wood, natural gas . Accessed March 17, 2018. Carboxymyoglobin is more stable than the oxygenated form of myoglobin, oxymyoglobin, which can become oxidized to the brown pigment metmyoglobin. Recourse to these works is strongly encouraged. 68 August 2014 CO compoundshave shown efcacy animalmodels disease,including postoperative ileus, chronic colitis, necrotizing . Effect of low level carbon monoxide exposure on onset and duration of angina pectoris, a study in ten patients with ischemic heart disease. [Clinical observations regarding chronic coal-gas poisoning]. Benignus VA. A model to predict carboxyhemoglobin and pulmonary parameters after exposure to O, Summary of main evidence and decision-making in guideline formulation. At COHb levels of around 30%, the brain metabolism fell precipitously. Handbook of environmental data on organic chemicals. 0000035235 00000 n The cellular mechanisms described above from recent experimental studies may well be the avenues by which this health damage occurs. Thus, a separate guideline is recommended to address 24-hour exposures. It is combustible, may serve as a fuel source and can form explosive mixtures with air. Chapter 5.5 Carbon monoxide General description Carbon monoxide (CO) is one of the most common and widely distributed air pollutants. Penney DG. It was concluded that there is an association between change in short-term air pollution levels and the occurrence of asthma symptoms among children in Seattle. Smith & Landaw (117) reported that smokers develop polycythaemia. Exercise temperature plateau shifted by a moderate carbon monoxide poisoning. All four suffered transient loss of consciousness immediately prior to discovery of the problem. 630-08-0) Prevalence and Use With the single exception of CO 2 . Recurrent acute life-threatening events and lactic acidosis caused by chronic carbon monoxide poisoning in an infant. C6O26. It is established that many cases of carbon monoxide toxicity are misdiagnosed because the symptoms mimic other health problems. Penney (85) reviewed the effects of carbon monoxide exposure on developing animals and humans in 1996. [67] One method developed at DTU Energy uses a cerium oxide catalyst and does not have any issues of fouling of the catalyst.[68][69]. This, along with cardiomegaly, has been demonstrated numerous times following chronic carbon monoxide exposure in animals (118,119). Thom SR, et al. This has been known for some time, i.e. The most common symptoms they recorded were headache, nausea, dizziness and syncope. This assertion is borne out by Chambers et al. If we combine this information with your protected Endogenous carbon monoxide (CO) is an essential cell signaling molecule, which is closely related to numerous physiological and pathological processes. Carbon monoxide and physical work capacity. Indoor and outdoor levels of respirable particulates (PM10) and carbon monoxide (CO) in high-rise apartment buildings. Thus, hypothetically, any cardiac, vascular or pulmonary disease would have such an effect, as would other factors that limit the blood's ability to transport oxygen, such as anaemia. Acute elevation of blood carboxyhemoglobin to 6% impairs exercise performance and aggravates symptoms in patients with ischemic heart disease. In: Penney DG, editor. Statistically significant positive effects on increased congestive heart failure admissions on cool days were observed only for the carbon monoxide levels. This content does not have an Arabic version. Effects of ambient air pollution on non-elderly asthma hospital admissions in Seattle, Washington, 19871994. (156) followed the Los Angeles study with an investigation on birth weight in Boston, MA, Hartford, CT, Philadelphia, PA, Pittsburgh, PA, Springfield, IL and Washington, DC. This may take some time to load. We don't save this data. At the beginning of combustion, the pollutants released are dominated by particulate matter (elemental and organic carbon) but carbon monoxide dominates towards the end. Jensen LK, Klausen H, Elsnab C. Organic brain damage in garage workers after long-term exposure to diesel exhaust fumes. The solubility of carbon monoxide In various alcohols at pressures up to 4000 kPa has been measured by using a chromatographic technique to analyze equilibrated gas-ln-llquld mixtures from a pressure vessel. It is the simplest carbon oxide. This study provides evidence that exposure to higher levels of ambient contaminants, particularly carbon monoxide, increase the risk of hospital admissions for CVD. For the acute health effects, the literature search was conducted in the PubMed and Web of Science databases, searching the keywords carbon monoxide and health. Compromised brain function, in addition to being an adverse effect in itself, can contribute to sensory impairment that could result in failure to detect signs of danger or could impair decision-making capabilities, leading to an inability to respond appropriately to danger. 9F(`0 The solubility of H 2 has been measured as a function of pressure in ethanol + water and various solvents at (298 and 323) K. The results are compared with theoretical predictions for H 2 in different solvents and some mixtures and found to agree within 10% error, except for acetonitrile. In 2008, Hopkins (95) and Armstrong & Cunningham (96) reviewed the neurocognitive and affective outcomes of carbon monoxide poisoning in adults and children. Ischiropoulos et al. Health risk assessment of indoor air pollution in Finnish ice arenas. Electrocardiographic changes in healthy men during continuous low-level carbon monoxide exposure. This could be attributed to an actual small effect or to some small fraction of susceptible subjects having larger effects or to an inappropriate statistical model for the doseeffect curves. The standard free energy value is -257.2kJ. At 20%, COHb reduced the arterial oxygen content from about 19.8% to about 15.8% by volume. The duration was reduced as an inverse function of COHb level. Unfortunately, in the absence of adequate dosimetric information, and therefore dosimetric models, simulation by models is not possible. 2126 July 1996; pp. (143), in another study in Seattle, found a 30% increase in asthma in children for a 1.2-mg/m3 increment in carbon monoxide that lagged one day. Review/update the Ocular effects of chronic carbon monoxide exposure. Journal of the American Medical Association. This is an area requiring additional study, since at the present stage of knowledge the question cannot be resolved. Follow-up symptoms present two years after the carbon monoxide exposure included numbness in the extremities, restlessness, persistent headaches, irritability, confusion, difficulty in walking or moving the extremities, and memory loss. 0 +J Forbes WH, et al. [89][90][91], Carbon monoxide poisoning is the most common type of fatal air poisoning in many countries. Group A1 was exposed to 58291 mg/m3, Group A2 to 701595 mg/m3, Group B to < 23 mg/m3 and Group C to < 12 mg/m3 carbon monoxide in the course of their normal work. N1 is the number of cases for which air carbon monoxide concentration data are available. 2. Chaloulakou A, Mavroidis I, Duci A. Indoor and outdoor carbon monoxide concentration relationships at different microenvironments in the Athens area. Relationship between ambient air pollution and hospital admissions for cardiovascular disease in Kaohsiung, Taiwan. Tikuisis PF, et al. Studies concerning accidental or peak exposures are presented separately in Table 2.2. Effect of prolonged exposure to elevated carbon monoxide and carbon dioxide levels on red blood cell parameters during submarine patrols. [Changes in the visual field in cases of chronic coal-gas poisoning]. Akland GG, et al. This prevents oxygen from reaching your tissues and organs. June 30July 5, 2002; pp. Indoor and outdoor PM2.5 and CO in high- and low-density Guatemala villages. In ancient history, Hannibal executed Roman prisoners with coal fumes during the Second Punic War. The relative risk for a change from 1.2 mg/m3 to 3.5 mg/m3, the 25th and 75th percentiles of the exposure distribution, was 1.065. Geographical, spatial, and temporal distributions of multiple indoor air pollutants in four Chinese provinces. Journal of Exposure Analysis and Environmental Epidemiology. Maximal aerobic capacity at different levels of carboxyhemoglobin. (129) describe 30 people who developed warehouse workers' headache. >tlvz* Y/RQP6#SUea=Gpigl}an*Qv;qXx:=$IPJ@@ ()PJA;Pvh:JtLLLLLLLLEEvb=SL%E z:`Z3B=<3x*R==^u1%c'~ 6= Common symptoms include headache, lethargy/fatigue, nausea, dizziness and confusion. Horvath SM, et al. Air pollution and hospitalization for headache in Chile. The Ellingham diagram shows that CO formation is favored over CO2 in high temperatures. A multicompartment model of carboxyhemoglobin and carboxymyoglobin responses to inhalation of carbon monoxide. It has been suggested, based on physiological analysis and extrapolation, that brain function should not be reduced by more than 10% until COHb approaches around 18%. Davies DM, Smith DJ. Anthropogenic emissions are responsible for about two thirds of the carbon monoxide in the atmosphere and natural emissions account for the remaining one third. The gas mixture produced by this process is known as wood gas. Even though hypoxic stress may have been the only underlying mechanism at work, some nonetheless reported positive effects. 501505. Haldane J. Interestingly, the prevalence of depression was higher in patients with the less compared with the more severe poisoning at six months. 0000010499 00000 n "[94] The American Association of Poison Control Centers (AAPCC) reported 15,769 cases of carbon monoxide poisoning resulting in 39 deaths in 2007. Official websites use .gov Air pollution and daily mortality in three U.S. counties. d(ln(kH))/d(1/T) = Temperature dependence constant (K). Absorption and elimination of carbon monoxide by inactive young men. [78], Studies involving carbon monoxide have been conducted in many laboratories throughout the world for its anti-inflammatory and cytoprotective properties. Data compilation copyright endstream endobj 39 0 obj[58 0 R] endobj 40 0 obj<>stream The magnitude of a carbon monoxide effect would depend on the amount of oxygen available for metabolism in the tissue under consideration. Penney DG. The warning signs of carbon monoxide poisoning can be subtle. (120) studied the effects of carbon monoxide exposure on deaths of New York City bridge and tunnel employees over the period 19521981. 0000004649 00000 n There is a problem with The end result is lipid peroxidation of the brain, which starts during recovery from carbon monoxide poisoning. Kim D, et al. Both isn't really true: $\ce {CO}$ does not react under these conditions. Allred EN, et al. DOI: 10.1039/B401537A. Effects of air pollutants on acute stroke mortality. Y,o#PMR$JAwRd62!B-P i1pp'{\{g[[Cr34exw {TM;J"8`2xrp Naeher LP, et al. Values of carbon monoxide solubility In . Penney D, Benignus V, Kephalopoulos S, et al. xb```b``g`c`P/dd@ A GL``6 `apb[.nXY^[GzS4-5}{|W gBninY:{Y7@\((h 3cfR266 @h #} With laboratory carbon monoxide exposures of a few hours' duration, no symptoms were reported, even for COHb approaching 20%. Cookies are only used in the browser to improve user experience. Penney DG, Dunham E, Benjamin M. Chronic carbon monoxide exposure. 0000001496 00000 n Worn or poorly adjusted and maintained combustion devices (e.g., boilers, furnaces) can be significant sources, or if the flue is improperly sized, blocked, disconnected, or is leaking. Kirkpatrick J. Occult carbon monoxide poisoning. [The effects of occupational CO poisoning on the organs of smell, hearing and equilibrium]. Commun., 2004, 1070 https://www.atsdr.cdc.gov/mmg/mmg.asp?id=230&tid=42. To that end, there will be some discussion of epidemiological studies involving ultra-low-level carbon monoxide found in outside air. Combustion of high-grade fuels such as natural gas, butane or propane usually produces much less carbon monoxide, provided that sufficient air is supplied to ensure complete combustion. Please read Google Privacy & Terms for more information about how you can control adserving and the information collected. Ryan CM. The daily average carbon monoxide concentration was 3.2 mg/m3. This compensatory activity also occurs in neonates and fetuses (73,74). In the second study, a significantly increased risk of 1.06 (95% CI 1.021.09) was found for carbon monoxide, with a one-day lag. American Industrial Hygiene Association Journal. The boiling point of CO is -191.5 . family members or pets living in the same house) displaying similar symptoms? [56][57][63] Another method is heating an intimate mixture of powdered zinc metal and calcium carbonate, which releases CO and leaves behind zinc oxide and calcium oxide: Silver nitrate and iodoform also afford carbon monoxide: Finally, metal oxalate salts release CO upon heating, leaving a carbonate as byproduct: Thermal combustion is the most common source for carbon monoxide. Clearly, this was done for ethical reasons, but the possibility exists that higher exposures would have led to greater magnitudes of effect than for normal subjects. The solubility of carbon monoxide in 37 ionic liquids and in some organic solvents has been determined using high-pressure (13)C NMR spectroscopy and it was shown that the rate of the hydroformylation of 5-hexen-2-one does not correlate with the CO solubilty, as expected from the determined relative solubilities of CO compared to H (2). The amount of dissolved carbon monoxide in blood would seem to be highest for high-level carbon monoxide exposure. Komatsu et al. [79] These properties have the potential to be used to prevent the development of a series of pathological conditions including ischemia reperfusion injury, transplant rejection, atherosclerosis, severe sepsis, severe malaria, or autoimmunity. (b) Calculate G by two different methods. Khan K, Sharief N. Chronic carbon monoxide poisoning in children. In: Penney DG, editor. The amount of such dissolved carbon monoxide and the diffusion into various tissues has not been described or modelled. Carbon monoxide level was particularly found to have a stronger association with mortality than level of particulate matter. The guidelines section was formulated and agreed by the working group meeting in November 2009. It is naturally produced by many enzymatic and non-enzymatic pathways,[74] the best understood of which is the catabolic action of heme oxygenase on the heme derived from hemoproteins such as hemoglobin. xref Its molecular weight is 28.01 g/mol, melting point 205.1 C, boiling point (at 760 mmHg) 191.5 C (312.7 F), density 1.250 kg/m3 at 0 C and 1 atm and 1.145 kg/m3 at 25 C and 1 atm, and relative density (air = 1) 0.967 (1,2). in 2000 (89) and Hay in 2008 (90). Carbon monoxide (CO) is a stable oxide of carbon that is produced when there is partial oxidation of carbon-containing compounds. There was also a diminution of the sense of smell. Thyagarajan et al. Bruce EN, Bruce MC, Erupaka K. Prediction of the rate of uptake of carbon monoxide from blood by extravascular tissue. provided correct acknowledgement is given. (157) assessed the association between ambient air pollution and daily elementary school absenteeism in Washoe County, Nevada in the period 19961998. Yang CY, et al. Absence of symptoms with carboxyhemoglobin levels of 1623%. ;AP+ZMh.nc Carbon monoxide, in addition to being an environmental contaminant, is produced endogenously. This would potentially permit calculation of tissue dose for non-hypoxic tissue effects when the dosimetry models are developed. Stern FB, et al. The effect of prolonged exposure to carbon monoxide on human health. SOLUBILITY OF CARBON MONOXIDE AND HYDROGEN IN WATER AND SEA-WATER 69 Table 1. Methylene chloride, a solvent commonly found in paint and varnish removers, can break down (metabolize) into carbon monoxide when inhaled. Piatt JP, et al. White SR. Pediatric carbon monoxide poisoning. Aviation, Space, and Environmental Medicine. hY]T7+l;#J-}@Rlq2%-lQO["m- Y[r`kQ-h^*[IxT%}U-R{%nJQY1JI[-/59H3@R,Ko$Y,fHl@v`*\ 1 \!8$5@$k8Iz[5g. Carbon monoxide, which is generated in mammals during the degradation of heme by the enzyme heme oxygenase, is an important signaling mediator. K from, Temperature dependence parameter for Henry's Law constant. Levels of environmental carbon monoxide previously thought to be extremely low were shown to reduce birth weight in women exposed to carbon monoxide during the last trimester of pregnancy. Percent carboxyhemoglobin in resting humans exposed repeatedly to 1,500 and 7,500 ppm carbon monoxide. Carbon monoxide is a bioactive molecule which acts as a gaseous signaling molecule. To be sure, the percentage exercise reduction is greater for the angina patients than for the normal subjects, but this is simply due to the reduction in baseline exercise ability. in water at one atmosphere (101.325 kPa) and different temperatures are indicated in the diagrams below. Thus, the dosimetry for putative non-hypoxic effects of carbon monoxide exposure is not known. %PDF-1.6 % They concluded that carbon monoxide levels produced in vivo when humans are exposed to carbon monoxide can cause endothelial cells to liberate nitric oxide and derived oxidants, and that these products can adversely affect cell physiology. 1998-2023 Mayo Foundation for Medical Education and Research (MFMER). However, heart disease is a leading cause of sickness and death worldwide, and it is plausible that coronary artery disease would make patients more susceptible to cardiac failure from increased hypoxic cardiac stress (179), but there are no data to evaluate this hypothesis. Association between ambient carbon monoxide levels and hospitalizations for congestive heart failure in the elderly in 10 Canadian cities. [8], Carbon monoxide had been used for genocide during the Holocaust at some extermination camps, the most notable by gas vans in Chemno, and in the Action T4 "euthanasia" program.[99]. Colourless, odourless, tasteless and toxic gas, Except where otherwise noted, data are given for materials in their, Pages displaying short descriptions of redirect targets. 0000007445 00000 n When too much carbon monoxide is in the air, your body replaces the oxygen in your red blood cells with carbon monoxide. It is very less soluble in water. In: Zak R, editor. Published and reliable data for solubilities of synthesis gas, CO or H 2 in the above-mentioned systems is rather limited. 9 9BNCN!!Si)4$79'[4hp88,p88,Ah03].LL{=ttaAAOB= :4h0(`0 Effect of carbon monoxide on oxygen transport during exercise. During periods of rush hour traffic in 1968, carbon monoxide concentrations in tunnel toll booths were as high as 76192 mg/m3. Lee SC, Wang B. Characteristics of emissions of air pollutants from burning of incense in a large environmental chamber. The difference is that the cardiac impairment has simply reduced the baseline exercise ability. Infants living within 50 metres of a highway had an increased risk of 6%; those living in an area with higher exposure to wood smoke had an increase of 8% in their risk of bronchiolitis. Cognitive and affective outcomes of more severe compared to less severe carbon monoxide poisoning. Quantitative PET scan findings in carbon monoxide poisoning. This is clear from inspection of the data because the zero COHb point, had it been included in the fitting, would have been plotted well below the intercept of the fitted curve. Evidence for various cellular mechanisms not requiring hypoxic stress has recently appeared. This is an inverse measure in the sense that, as tissue oxygen increases towards the normal, function improves. National Center for Biotechnology Information. It mixes freely with air in any proportion and moves with air via bulk transport. Therefore, a third damaging mechanism of carbon monoxide exposure appears to be through its action on the immune system. Journal of the American College of Cardiology. A survey study of public perceptions about carbon monoxide. Mean ages of four groups broken out of the cohort was approximately 32 years (no significant difference). Cerebral circulatory response to carbon monoxide and hypoxic hypoxia in the lamb. See also http://www.coheadquarters.com/coacute.mech1.htm. U.S. Consumer Product Safety Commission. C. the catalyst is easily replaced during regular maintenance. Institut des Sciences et Ingnerie Chimiques (ISIC), Ecole Polytechnique Fdrale de Lausanne, EPFL-BCH, CH-1015 Lausanne, Switzerland The studies are listed by continent. COHb is widely used as a biomarker for carbon monoxide exposure. The original Hildebrand solubility parameter () is derived from the Cohesive Energy Density (CED) [4,5] V U 2 CED vap U vap is the energy of evaporation or the cohesive energy and V the molar volume. shall not be liable for any damage that may result from Furthermore, smoking at increased elevation dramatically increases the extent of the polycythaemia. Thus, recent studies suggest that the intracellular uptake of carbon monoxide could be a major cause of neurological damage (i.e. Carbon monoxide enters the body via inhalation and is diffused across the alveolar membrane with nearly the same ease as oxygen (O2). Walker (130) states that the incidence of chronic carbon monoxide exposure in Great Britain is officially 200 per year, while at the same time 250 000 gas appliances are condemned annually. Carbon monoxide and the nervous system. [75] Following the first report that carbon monoxide is a normal neurotransmitter in 1993,[8] carbon monoxide has received significant clinical attention as a biological regulator. (111) on chronic carbon monoxide poisoning have been reviewed by Penney (76). Carbon monoxide poisoning. Excluded were infants born before 37 or after 44 weeks of gestation, those weighing below 1000 or above 5500 grams at birth, those for whom fewer than 10 days of carbon monoxide measurements were available during the last trimester, and those whose mothers suffered from hypertension, diabetes or uterine bleeding during pregnancy. These studies were, however, not replicable in any case where such replication was attempted. Evidence exists that non-hypoxic events are responsible for impairments that sometimes develop several days after reduction of COHb due to high-level acute carbon monoxide exposure. Hong YC, et al. d(A C^ For example, the highest frequency of complaints in reports included headache, poor hearing, chest pain, lassitude, fatigue and forgetfulness. Annals of the New York Academy of Sciences. Two studies examining cardiovascular events and long-term exposure to carbon monoxide at ultra-low levels (i.e. Exposure to carbon monoxide may be particularly dangerous for: Depending on the degree and length of exposure, carbon monoxide poisoning can cause: Simple precautions can help prevent carbon monoxide poisoning: Keep your fuel-burning appliances and engines properly vented. The final dose for carbon-monoxide-induced hypoxic effects is thus seen to be some measure of tissue oxygenation. Longo LD. Kaye and T.H. Thus for non-hypoxic effects, it is frequently necessary to use less general evidence from empirical environmental data to make estimates of critical exposures. An implication of the above analysis is that if, owing to some pre-existing cardiovascular or pulmonary disease, the compensatory increase in blood flow were impaired, small increases in COHb could produce larger decreases in tissue oxygen and thus larger behavioural effects. Cerebral oxygenation of the fetus, newborn and adult. It results from incomplete oxidation of carbon in combustion. McGrath JJ. The formation of carboxymyoglobin also acts as another sink for carbon monoxide. (164) postulated that carbon monoxide poisoning causes adduct formation between myelin basic protein (MBP) and malonylaldehyde, a reactive product of lipid peroxidation, resulting in an immunological cascade. Some common man-made releases of Carbon Monoxide are from fumes of vehicles, engines . It results from incomplete oxidation of carbon in combustion. White (86) reviewed carbon monoxide poisoning in children in 2000. Neurocognitive and affective sequelae of carbon monoxide poisoning. )jHN)k01m-%4IQ2YUp.E Hydrogen (H 2) 288.15 1.510 10-5 A = -48. . For chronic exposures to carbon monoxide, red cell volume increases or plasma volume decreases (70), thus increasing the amount of oxygen that can be delivered. [66] Above 800C, CO is the predominant product: Another source is "water gas", a mixture of hydrogen and carbon monoxide produced via the endothermic reaction of steam and carbon: Other similar "synthesis gases" can be obtained from natural gas and other fuels.