Carbon monoxide (CO)

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Carbon monoxide (CO) is a tasteless, colorless, odorless gas, and therefore, gives no warning of its presence under any circumstances. Exposure to CO is a potential hazard whenever incomplete combustion occurs. Any source of combustion or industrial process consuming carbon-based fuel may create a source of carbon monoxide release. Certain industries are recognized to be particular hazardous with relation to carbon monoxide:

- iron and steel foundries;

- petroleum-refining plants;

- kraft paper pulp mills;

- sintering mills and facilities for the manufacture of formaldehyde and coke.

These sources are known to produce large amounts of carbon monoxide. The greatest danger actually lies in such processes as welding, garage work, and forklift truck operations. The amount of carbon monoxide produced usually does not create problems. However, CO poisoning may strike without warning if either the source of carbon monoxide increases for some reason or ventilation is decreased.[1]

CO exposure continues to be the leading cause of deaths by accidental poisoning in the United States and is responsible for more worldwide deaths by poisoning than any other substance. An estimated 500 to 2,100 people die accidentally each year in the United States secondary to CO poisoning.

Route of exposure: inhalation

Mechanism of toxicity

The exact mechanism by which CO causes injury is still largely unknown, although several theories have been explored. In the mid 1800s, Claude Bernard hypothesized that the deleterious effects of CO exposure were due to the poison’s great affinity for hemoglobin. The mechanism of carbon monoxide toxicity is primarily throughhypoxia. When inhaled, CO is absorbed through the lungs, whereit binds with haemoglobin to form COHb. As its affinity forHb is 234 times greater than that of oxygen, the amount of oxygenin the blood becomes greatly reduced, causing a hypoxic state.Furthermore, once CO is bound, it alters the dissociation curveof oxyhaemoglobin, thus reducing the rate at which oxygen isreleased to the cells. Tissues with a greater requirement foroxygen, such as the brain and heart, are more severely affectedby hypoxia. This binding causes a leftward shift of the oxygen hemoglobin saturation curve, making less oxygen available for the tissues and resulting in hypoxia. The hypoxia is further amplified by decreased cardiac function, which in turn leads to increasingly poor perfusion. As less oxygen is available to the tissues, more hypoxia results and, therefore, more grave symptoms and outcomes of CO exposure might be expected. The problem is that serum COHb levels do not directly correlate with severity of symptoms, particularly neurologic injuries. The exact reason why COHb levels cannot predict outcomes in patients who may have been exposed to CO is unknown, but this phenomenon may be related to a time lag between the person’s exposure and subsequent admission to a medical facility for evaluation. Given these findings, scientists have conducted numerous studies in search of a secondary means of cellular injury due to CO exposure. While no clear consensus has been reached thus far, several theories have been investigated, including impairment of cellular respiration, free radical formation (peroxidation), and initiation of inflammatory cascade.[2]

While hypoxia can account for some of the effects of CO exposure,it is not consistent with certain observations. In many cases,symptoms persist or even appear after COHb levels have returnedto normal. These delayed neuropsychological sequelae can appear2–40 days after exposure. They include symptoms seen duringexposure, such as lethargy, headaches, and concentration problems,as well as other symptoms, such as amnestic syndromes, dementia,psychosis, and Parkinsonism. These cannot be explained by hypoxiaalone, as one would expect an improvement of symptoms once thehypoxic stress is removed. Another indication that a toxicmechanism besides hypoxia might be involved is that there isno clear correlation between COHb levels and the effects onhealth. Levels of COHb do not always correspond to the intensityof symptoms and cannot be used to reliably predict the patient’soutcome.[3]

Infants, elderly, pregnant women, patients with coronary artery disease, anemia, and lung disease are at greatest risk of toxicity from exposure to CO.[4] Diagnosis may be suggested by the circumstances that caused the patient to seek medical attention. Exposure to a known source of carbon monoxide, such as being in a closed garage or being overcome by smoke inhalation, is a primary diagnostic clue.( Zenz, C)

Target organs: central nerve system, cardiovascular system

Brain damage can consist of infarction of the cerebral cortex, degenerative changes, formation of cysts, gliosis, paravascular infiltration, loss of myelin, softening of white matter. The basal ganglia show the most severe damage, with loss of cells and demyelination. (Zenz, C)

Symptoms include general malaise, headache, nausea, dyspnea, vomiting, and alteration in mental status. One of the most common manifestations of both acute and chronic CO exposure is headache, although no typical characteristic or location of headache associated with CO exposure has been identified. Other symptoms are vague and varied and may include dizziness, fatigue, visual changes, memory and concentration deficits, and shortness of breath. Less frequently, patients may present with pulmonary, cardiovascular, or GI complaints. Severe exposure may cause coma, seizures, arrhythmias, and death. Symptoms of anoxia may be prominent without cyanosis due to the cherry-red color of carboxyhemoglobin.

Symptoms of carbon monoxide exposure

Central nervous system: amnesia, confusion, difficulty concentrating, dizziness, loss of consciousness, Parkinsonism.

Constitutional: fatigue, personality changes, seizures, weakness.

Gastrointestinal: abdominal cramps, diarrhea, nausea, vomiting

Pulmonary/cardiovascular: angina, palpitations, shortness of breath. ( Dawn Colomb-Lippa)

Symptoms of delayed neurologic deterioration after CO exposure: apathy, apraxia, memory deficits, Parkinsonism, psychomotor retardation. ( Dawn Colomb-Lippa)

In acute poisoning severity of symptoms is related to level of COHb in the blood. Non-exposed individuals typically have carboxihemoglobin levels below 5%, the level can be as high as 10% in an active smoker. A blood level greater than 5% in a symptomatic patient may indicate chronic CO toxicity and requires further evaluation:

Ø < 5% COHb – no signs and symptoms;

Ø 5-10% - may exacerbate angina in patients with heart disease;

Ø 10-20% - mild headache, breathlessness on exertion;

Ø 20-30% - throbbing headache, irritability, mental changes, fatigue;

Ø 30-40% - severe headache, weakness, nausea, dizziness, visual problems, confusion;

Ø 40-50% - increased confusion, hallucinations, severe ataxia, rapid breathing;

Ø 50-60% - syncope or coma with convulsions, tachycardia with weak pulse;

Ø 60-70% - deep coma, incontinence of urine and feces;

Ø 70-80% - profound coma, depressed respiration, absent reflexes;

Ø 80% - rapid death from respiratory arrest.[5]

Chronic exposure to low levels of carbon monoxide can cause vague symptoms that are easily mistaken for other common illnesses. Patients may be diagnosed with a variety of conditions including chronic fatigue syndrome, depression and influenza. Carbon monoxide exposure should be considered in the differential diagnosis of patients who present with chronic symptoms of headache, fatigue, dizziness, nausea and mental confusion, especially when these symptoms onset during the winter heating season. If the exposure is ongoing, these symptoms can become chronic and may lead to more serious health problems.

CO is a well known cardiovascular toxin, even low levels of carboxyhemoglobin exacerbate myocardial ischemia in subjects with coronary artery disease.[6] A study conducted in Seoul tests the hypothesis that patients with congestive heart failure are more susceptible to the effects of air pollution (including CO). Cardiac cause of death was considerably increased by the effect of CO. (Kwon, Ho-Jang) Another study tests the effects of air pollution on the heart. CO has also been implicated as a cause of adverse cardiovascular effect.[7]Carbon monoxide poisoning is one of the few recognized causes of reversible sensorineural hearing loss, though it may also lead to a permanent deficit.[8]

Carbon monoxide leads to chemical potentiation of noise-induced hearing loss.[9]

The fetus is extremely susceptible to the effects of CO and the gas readily crosses the placenta. Prenatal exposures can cause congenital malformations, low birth weight, and permanent brain damage, resulting in mental retardation, hypotonia, areflexia, basal ganglia damage, microcephaly and seizure disorders. ( Knobeloch L)

Maternal exposure to air pollutants, including carbon monoxide, is associated with adverse pregnancy outcomes. A major research focus has been to investigate the effects of air pollution on birth weight, low birth weight (LBW; < 2,500 g), and intrauterine growth retardation (IUGR). Ambient CO levels in the first trimester were independently associated with lower birth weight and IUGR in term infants through the mechanism of reduced fetal growth.[10]Another study also indicates that low birth weight was relatedto higher levels of exposure to carbon monoxide inthe first trimester. A 1 ppm increase in carbon monoxide exposure was associatedwith a 23.1 g weight reduction.[11]

Dictionary

Sintering is a method for making objects from powder, by heating the material (below its melting point) whereby the particles bond to each other. Sintering is traditionally used for manufacturing ceramic objects and some kinds of pottery.

The Kraft process (also known as Kraft pulping or sulfate process) is used in production of paper pulp and involves the use of caustic sodium hydroxide and sodium sulfide to extract the lignin from the wood fiber in large pressure vessels called digesters. The process's name is derived from German kraft, meaning strong; both capitalized and lowercase names (Kraft process and kraft process) appear in the literature. It was developed by Carl Dahl in 1884 and now is used for about 80% of production volume of paper.

Kraft-thick brown paper: tough, usually brown paper made from chemically treated wood pulp. Use: bags, wrapping paper.

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