Clinical effects—The principal signs of CO intoxication are those of hypoxia. They progress in the following sequence: (1) psychomotor impairment; (2) headache and tightness in the temporal area; (3) confusion and loss of visual acuity;
TABLE 56–1 Examples of permissible exposure limit values (PELs) of some common air pollutants and solvents in parts per million (ppm).1 1These exposure limits can be found at http://www.osha.gov, 1910.1000, Tables Z-1 and Z-2. The OSHA standards are updated frequently and readers are referred to the website for the most current information.
2PELs are 8-hour TWA (time-weighted average) values for a normal 8-hour workday to which workers may be repeatedly exposed without adverse effects.
(4) tachycardia, tachypnea, syncope, and coma; and (5) deep coma, convulsions, shock, and respiratory failure. There is great variability in individual responses to carboxyhemoglobin concentration. Carboxyhemoglobin levels below 15% may produce headache and malaise; at 25% many workers complain of headache, fatigue, decreased attention span, and loss of fine motor coordination. Collapse and syncope may appear at around 40%; and with levels above 60%, death may ensue as a result of irreversible damage to the brain and myocardium. The clinical effects may be aggravated by heavy labor, high altitudes, and high ambient temperatures. CO intoxication is usually thought of as a form of acute toxicity. There is evidence that chronic exposure to low CO levels may lead to adverse cardiac effects, neurologic disturbance, and emotional disorders. The developing fetus is quite susceptible to the effects of CO exposure. Exposure of a pregnant woman to elevated CO levels at critical periods of fetal development may cause fetal death or serious and irreversible but survivable birth defects.
3. Treatment—Patients who have been exposed to CO must be removed from the exposure source immediately. Respiration must be maintained and high flow and concentration of oxygen—the specific antagonist to CO—should be administered promptly. If respiratory failure is present, mechanical ventilation is required, High concentrations of oxygen may be toxic and may contribute to the development of acute respiratory distress syndrome. Therefore, patients should be treated with high concentrations only for a short period. With room air at 1 atm, the elimination half-time of CO is about 320 minutes; with 100% oxygen, the half-time is about 80 minutes; and with hyperbaric oxygen (2–3 atm), the half-time can be reduced to about 20 minutes. Although some controversy exists about hyperbaric oxygen for CO poisoning, it may be used if it is readily available. It is particularly recommended for the management of pregnant women exposed to CO. Hypothermic therapy to reduce metabolic demand of the brain has also been useful. Cerebral edema that results from CO poisoning does not seem to respond to either mannitol or steroid therapy and may be persistent. Progressive recovery from treated CO poisoning, even of a severe degree can be complete but some patients manifest neuropsychological and motor dysfunction for a long time after recovery from acute CO poisoning.
Sulfur dioxide (SO2) is a colorless irritant gas generated primarily by the combustion of sulfur-containing fossil fuels. The current OSHA PEL (Table 56–1) is given on the OSHA website (see http://www.osha.gov, Standard Number 1910.1000, Table Z-1).
1.