Carbon Monoxide

Part III Toxicology Report

Carbon monoxide is one of the most abundant and extensively distributed air pollutants in the environment, present in almost every type of smoke produced by different fires. Exposure to carbon monoxide (CO) is poisonous and can lead to acute cardiovascular complications and neurological problems. This toxicology report explores CO’s chemical background, sources and environmental transport pathways, exposure mechanism, and health effects, and control mechanisms for the emissions.

1. Chemical Background

The toxin of interest, in this case, is Carbon Monoxide (CO). CO exists as an (odorless and colorless)  gas under room temperature and can be converted into a liquid at the boiling point of the temperature of -312.7°F (-191.5°C) and to solid under a freezing point temperature of -337°F (-205°C). Carbon monoxide is slightly lighter than air by 3%, with a density of 1.250 g/L at 32°F (0°C) and 760 mm Hg pressure. Carbon monoxide exists as a compound of carbon and oxygen. It is made up of carbon atoms bonded to oxygen atoms. CO belongs to the class of inorganic non-metallic compounds, where the largest atom of the compound belongs to the class of “other non-metals” (Goudarzi et al. 2014). 

Carbon monoxide is often referred to as a “silent killer” because of its odorless, invisibility, and tasteless, making the toxic gas the most unseen danger in the homes (Goudarzi et al. 2014). Indoor, CO concentrations in homes and workplaces with unvented or faulty combustion equipment, backdrafts, and downdrafts have been measured over 100 ppm and are likely to result in larger COHb levels than 10% after 8-hours of exposure (Raub, Mathieu-Nolf, Hampson, & Thom, 2000). Methods for testing carbon monoxide are through the use of a portable carbon monoxide meter or indoor air quality test. Indoor air quality test is considered as the most accurate test for CO. It uses an “electronic portable toxic multi-gas monitor,” which can be calibrated to detect CO gas from nearly 0 ppm and increments as smaller as 1ppm (Abelsohn, Alan, et al. 2002), making it the best.

• Source Context

Package of CO (carbon monoxide) is used in industries for various applications, such as metal fabrication. Historically CO gas has been applied in fuel-gas mixture with hydrogen and other gases for domestic and industrial heating. CO is widely used today to manufacture different chemicals such as esters, acids, and alcohol. CO also generates and regenerate catalysts, including nickel carbonyl, to reduce ores and metal carbonyl manufacturing.

Carbon monoxide is produced due to incomplete combustion of fuels such as oil, gas, coal and wood, which are sources of full use in many households. Running cars, burning charcoal, and cigarette smoking and generates carbon monoxide gas. Exposure to the dangerous level of CO can either be both indoor and outdoor. CO concentrations are the highest adjacent traffic congestion areas, near exhaust gases generated by internal combustion engines, in poorly ventilated areas such as tunnels and parking garages, and from industrial combustion zones (Raub, Mathieu-Nolf, Hampson, & Thom, 2000).

• Environmental Transport and Fate

Carbon monoxide is regarded as the most abundant and extensively distributed air pollutant in the environment. The gas is present in almost every type of smoke produced by different types of fires. The emission of CO in urban atmospheres exceeds all other forms of pollutants combined, excluding carbon dioxide (CO2) (Longo, Lawrence 1977). Nearly all forms of CO emissions are due to human technology, with about 90% of the total carbon monoxide emitted emanating from the combustion of fossil fuels resulting from motor vehicle emissions and industrial combustions. Some CO is also generated from natural sources such as seedling germination and higher plant growth, while others from cigarette smoking, burning coal, and wood (Arvola, Jouko, et al. 2011). The tonnage of carbon monoxide emitted continues to rise with the increased consumption of fossil fuels.

The CO released from combustion are dispersed and accumulates in various environmental compartments such as vegetation, soils, indoor dust, and come into contact with human and animals through complex transport pathways in the environment, including windborne particles, diffusion, deposition, evaporation, inhalation, ingestion of food and water, direct contact, among many other forms (Coburn, Ronald 1970).  Some CO particles released from industrial incineration facilities contribute largely to environmental compartments on a local scale within a 10 km radius (Levy, Richard,2015) and can travel to longer distances of more than 100 kilometers.

• Exposure Mechanisms

Carbon monoxide exposure and poisoning mechanisms are primarily through inhalation of CO gas from the air or contact with a contaminated environment. Where the CO present in the air is excess, the body automatically replaces the oxygen found in the red blood cells with CO gas particles, preventing oxygen from reading the body tissues (Weaver 1999). The levels of exposure vary. For instance, places and times of the day characterized by higher vehicular traffic result in a high level of exposure to CO compared to when traffic is low.

Other CO exposure mechanisms include tobacco smoking for smokers and non-smokers, gas appliances, and burning stoves. Poorly vented generators at home during an emergency power outage, gas, and charcoal grills have all been proven to generate dangerous levels of CO. CO released into the environment can stay for two months before converted into carbon dioxide through reaction with other air particles. Contact with excess levels of CO leads to the formation of a stable form of the gas called carboxyhemoglobin in the red blood cell, reducing the hemoglobin’s ability to release oxygen to oxygen destined to other oxygen-binding organs (Kalay, Nihat, et al. 2007). The effect is suffocation and even death in severe cases.

• Health Effects

Inhalation of CO can affect or poison almost every organ in the body. The method of CO poisoning is tissue hypoxia, as the binding affinity of carbon monoxide to hemoglobin is about 200-240 times that of oxygen. Therefore, the presence of an excess of CO in the bloodstream diminishes the hemoglobin’s oxygen carrying capacity and impairs oxygen release to the body tissues (Goudarzi et al. 2014).

High levels of CO inhalation for a long period increases the risk of heart diseases. The high demand for oxygen by the central nervous and cardiovascular systems makes them be highly affected by excess CO in the bloodstream. Carbon monoxide-related cardiovascular dysfunction includes myocardial infarctions, left-ventricular dysfunction, cardiogenic shock, transient myocardial stunning, and sudden death (Horowitz, Kaplan, & Sarpel 1987). Study shows that carbon monoxide’s cardiotoxicity causes a dual effect, which directly impacts the myocardium and myoglobin. CO binds with the myoglobin and affects oxygen reservoirs and subsequent oxygen release (Goudarzi et al. 2014). The binding of the CO to the cytochrome interrupts electron-transport chain and oxidase in the mitochondria, resulting in anaerobic respiration and formation of free radicles. Inflammation, relaxation of vascular smooth muscles, and thrombotic tendency are other effects of CO that can injure the cardiovascular system (Fruzsina & Johnson 2003).

Acute carbon monoxide poisoning can translate into severe long-standing neurological problems, resulting in disturbances in memory, cognition, language, and mood or behavior change (Chambers et al. 2008). CO can cause neurotoxicity to the brain or generate neuroprotection according to the context, concentration, and duration of exposure (Fechter, Laurence, 1987). Common notable signs of exposure to mild CO levels can cause short-term health effects such as dizziness, headache, nausea, and vomiting.

• Strategies To Assess Risk And Control Outcomes

Catalytic conversion of CO to carbon dioxide CO2 and the installation of CO detectors are the most commonly used method for reducing the impact of CO and protecting human health from its impacts (Ran, Nurmagambetov, & Sircar 2018).  Oxidation of poisonous carbon monoxide to nonpoisonous carbon dioxide at ambient conditions has proven critical for conservation in several applications and is also advocated by agencies such as the U.S. Environmental protection agency.

The overall responsibility for the control of CO and other poisonous gas emissions lies with the U.S. Environmental Protection Agency. However, because of special requirements, states such as California have special regulatory agencies called the Air Resource Board to regulate emissions. The U.S. has emphasized on evaporative emission control since 1971, with all the vehicle manufacturers required to produce closed fuel systems to reduce direct CO emissions to the atmosphere. Alternative fuel automobiles and machines, including the production of hybrid cars and pure electric propulsions (Ran, Nurmagambetov, & Sircar 2018), are also considered to reduce the toxic gas emissions environment.

Conclusion

Carbon monoxide is one of the most abundant and extensively distributed air pollutants. The gas is known as a silent killer for its odorless, invisibility, and tasteless nature. CO is present in almost all combustion running cars, burning charcoal, cigarette smoking, and getting into our body systems through inhalation. Exposure to excess CO causes cardiovascular and neurological complications. Hence there need to reduce its levels in the atmosphere. Catalytic conversion of CO to carbon dioxide CO2 is among the methods used to reduce CO emissions.

References

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Arvola, Jouko, et al. “Combining steel and chemical production to reduce CO 2 emissions.” Low Carbon Economy 2.03 (2011): 115.

Chambers, Chelsea A., et al. “Cognitive and affective outcomes of more severe compared to less severe carbon monoxide poisoning.” Brain Injury 22.5 (2008): 387-395.

Coburn, Ronald F. “The carbon monoxide body stores.” Annals of the New York Academy of Sciences 174.1 (1970): 11-22.

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Goudarzi, Gholamreza, et al. “Cardiovascular deaths related to Carbon Monoxide Exposure in Ahvaz, Iran.” Iranian Journal of Health, Safety and Environment 1.3 (2014): 126-131.

Horowitz, A. L., R. Kaplan, and G. Sarpel. “Carbon monoxide toxicity: MR imaging in the brain.” Radiology 162.3 (1987): 787-788.

Johnson, Fruzsina K., and Robert A. Johnson. “Carbon monoxide promotes endothelium-dependent constriction of isolated gracilis muscle arterioles.” American Journal of Physiology-Regulatory, Integrative, and Comparative Physiology 285.3 (2003): R536-R541.

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Longo, Lawrence D. “The biological effects of carbon monoxide on the pregnant woman, fetus, and newborn infant.” American journal of obstetrics and gynecology 129.1 (1977): 69-103.

Ran, T., Nurmagambetov, T., & Sircar, K. (2018). Economic implications of unintentional carbon monoxide poisoning in the United States and the cost and benefit of CO detectors. The American Journal of Emergency Medicine, 36(3), 414-419.

Raub, J. A., Mathieu-Nolf, M., Hampson, N. B., & Thom, S. R. (2000). Carbon monoxide poisoning—a public health perspective. Toxicology, 145(1), 1-14.

Weaver, Lindell K. “Carbon monoxide poisoning.” Critical care clinics 15.2 (1999): 297-317. Wegiel, Barbara, Douglas W. Hanto, and Leo E. Otterbein. “The social network of carbon