Carbon Monoxide

Properties of the chemical

Carbon monoxide (CO) is an odorless, tasteless and colorless gas that is produced when there is incomplete combustion of carbon-containing fuels such as coal, petroleum peat and natural gas. Automobile exhaust accounts for more than half of all man-made carbon monoxide. Carbon monoxide is produced in industrial processes involving carbon-containing fuels and is found in homes with malfunctioning water heaters, furnaces or other appliances that use natural gas. Cigarette smoke may contain as much as 5 percent carbon monoxide, and secondhand smoke contains as much as 4.5 percent carbon monoxide.

Uses of the chemical

Carbon monoxide is a reducing agent in blast furnaces and is used in the purification of metals, as well as in the production of acetic acid, formic acid, methyl formate, N, N-Dimethylformamide, acrylic acid, propanoic acid and phosgene. A large variety of chemicals, ranging from saturated hydrocarbons to oxygenated compounds such as methanol, are produced using carbon monoxide.

Absorption, Distribution, Metabolism and Excretion (ADME)

Carbon monoxide is absorbed through the lungs, and the concentration of carboxyhemoglobin will depend on the concentrations of inspired carbon monoxide, the duration of exposure, degree of pulmonary ventilation and the concentration of carboxyhemoglobin originally present. In addition to its reaction with hemoglobin, carbon monoxide combines with myoglobin, cytochromes and metalloenzymes such as cytochrome c oxidase and cytochrome P-450. The binding of carbon monoxide to hemoglobin produces carboxyhemoglobin and decreases the oxygen-carrying capacity of blood. This appears to be the principal mechanism of action underlying the induction of toxic effects of low-level carbon monoxide exposures. The precise mechanisms by which toxic effects are induced are not fully understood but likely include the induction of a hypoxic state in many tissues of diverse organ systems. COHb if fully dissociable, and, once acute exposure is terminated, the carbon monoxide will be excreted through the lungs. Only a very small amount of carbon monoxide is oxidized into carbon dioxide.

Clinical effects of acute exposure

  • Ocular exposures: Low concentrations of bromine vapor produce irritation of the eye with lacrimation. Photophobia and blepharospasm are seen in higher concentrations. 
  • Dermal exposures: Both the liquid and vapor forms are extremely irritating to the skin. There is no immediate visible skin reaction with contact. Any delay in treatment before the initial signs of injury become apparent often results in more extensive damage. The most common local effects are blister formation, a brownish discoloration of the skin and slow-healing ulcers.
  • Inhalation exposures: Inhalation symptoms progress from coughing, choking, dyspnea and wheezing to either immediate or delayed bronchoconstriction. Other symptoms include the development of laryngeal spasm, glottal edema, asthma and tracheobronchitis. With increased parenchymal penetration, it is likely there will be peribronchiolar abscesses, pulmonary infiltrates consistent with chemical pneumonitis, bronchiolitis and pulmonary edema. Severe respiratory symptoms may be delayed for several hours after exposure.  
  • Ingestion exposures: Although ingestion is unlikely, a brownish discoloration of the tongue and buccal mucosa may occur and be accompanied by the characteristic bromine breath odor.

In-field treatment prior to arrival at a healthcare facility

  • Ocular exposures: Irrigate the eye(s) with copious amounts of tepid water for at least 15 minutes.
  • Dermal exposures: Remove contaminated clothing, and thoroughly wash the affected area with copious amounts of water for 20 minutes.
  • Inhalation exposures: Remove the patient from the source of bromine contamination. Supply oxygen if available. 
  • Ingestion exposures: Rinse out mouth with large amounts of water. Small amounts of water – 240 ml for adults or 120 ml for children – should be ingested to dilute the chemical.

Special note to first responders:

  • Wear a positive-pressure Self-Contained Breathing Apparatus (SCBA).
  • Wear chemical protective clothing that is specifically recommended by the manufacturer.

Treatment of exposures in a health care facility

  • Ocular exposures: Initiate or continue eye irrigation using 0.9 percent saline solution. If irritation, pain, swelling, lacrimation or photophobia persists, further medical evaluation is recommended.
  • Dermal exposures: Remove contaminated clothing, and thoroughly wash the affected area in a shower of water for 20 minutes. Since the effects may be delayed, close observation for blistering and discoloration of the skin is required for the next 24 hours.
  • Inhalation exposures: Begin respiratory support based on patient symptoms. Maintain an adequate airway,  oxygen and inhaled beta adrenergic agonist as needed. The delayed onset of severe respiratory symptoms justifies hospitalization for 24 hours. Initial chest x-ray and spirometry are recommended. Repeat chest radiograph and spirometry are recommended to determine the progression or resolution of residual effects. The course and prognosis of a bromine exposure depends on the concentration and duration of the exposure. Effects may vary from mild irritation of the mucous membranes to severe damage of the skin and lung parenchyma. Death is secondary to severe hypoxemia with metabolic acidosis due to acute obstructive ventilatory impairment.
  • Ingestion exposures: Irrigate the oral mucosa with copious amounts of water. Give the patient small amounts of water – 240 ml for adults or 120 ml for children. Look for brownish discoloration of the tongue and buccal mucosa. Observe the patient for blistering for 24 hours.

For more poison prevention and first aid information, call the Poison Control Center toll-free,

Downloadable .pdf on Bromine.