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• [Health status of female workers of oil-processing enterprises]
• A multicenter, prospective study of fetal outcome following accidental carbon monoxide poisoning in pregnancy.
• Additivity of carbon monoxide and protein deficiency on neonatal mortality in mice.
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Example Content from MEDITEXT for 630-08-0:


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ACUTE EXPOSURE INFORMATION

  1. SOURCES: Odorless, colorless gas produced by the incomplete combustion of any carbon containing substance. Common sources include household fires, home furnaces, stoves and water heaters, and vehicle exhaust. Another potential source is methylene chloride (often used as a paint stripper or degreaser) that is absorbed through inhalation, ingestion, or dermal contact and is subsequently metabolized by the liver to carbon monoxide.
  1. PHARMACOLOGY: Binds to hemoglobin with an affinity approximately 250 times greater than that of oxygen.
  1. TOXICOLOGY: Impairs oxygen delivery, producing cellular hypoxia and ischemia.
  1. EPIDEMIOLOGY: Common poisoning; one of the leading toxicologic causes of death.
  1. WITH POISONING/EXPOSURE
    1. MILD TO MODERATE TOXICITY: Headache, nausea, dizziness, vomiting, weakness, and confusion are often reported, with headache being the most common.
    1. SEVERE TOXICITY: Coma, syncope, seizures, cardiac dysrhythmias, myocardial ischemia, and death result from more severe poisonings and reflect damage to the organ systems (brain and heart) with the highest oxygen demand. Delayed neurocognitive effects, which include dementia, amnestic syndromes, psychosis, parkinsonism, chorea, apraxia, neuropathies, difficulty concentrating, and personality changes, can occur from 2 to 40 days following the initial exposure. Unfortunately, there are no good predictive markers for who will develop neurocognitive sequelae, including the initial carboxyhemoglobin level or the severity of the initial poisoning.
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