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Epidemiologic Notes and Reports Carbon Monoxide Poisoning -- Weld County, Colorado, 1993

In March 1993, the Colorado Department of Public Health and Environment (CDPHE) was notified that six family members residing in a home in Weld County had suffered carbon monoxide (CO) poisoning; five of the persons died. An investigation indicated that the source of CO had been a van parked in the garage of the home; the van had been left running, and the exhaust fumes leaked into the home. This report summarizes the investigation of this incident.

On March 10, 1993, at 7:32 p.m., emergency personnel in Weld County received an inactivity alert from the heart monitor of an outpatient. On arrival at the patient's home, they found the six family members (three adults and three children) to be dead or unconscious. Four persons (a 77-year-old woman who was wearing the heart monitor, two other adults aged 29 and 30 years, and one 8-year-old child) were pronounced dead at the scene. The decedents were found on the first floor of the house, in upstairs bedrooms, and in the basement; on autopsy, carboxyhemoglobin (COHb) levels of the decedents ranged from 72% to 78%. Two other children (aged 12 and 11 years) were found unconscious in the basement. Although their initial COHb levels were similar, clinical features of the two patients were distinctly different.

Patient 1. On discovery, the 12-year-old boy was in electromechanical dissociation but was successfully resuscitated. On physical examination in the emergency department, he was flaccid with intermittent decerebrate posturing, had no spontaneous breathing, and was unresponsive to pain. The pH of an arterial blood sample was 7.01 and the COHb level, 16%. CO poisoning was diagnosed. After his metabolic status was stabilized, hyperbaric oxygen (HBO) therapy was initiated. Following the first course of treatment, the patient became hypotensive and required vasopressor therapy; cardiac evaluation revealed diminished cardiac function. On March 11, an electroencephalogram (EEG) revealed seizure activity, and a computed tomography (CT) scan of the brain showed diffuse cerebral edema with hypodense anoxic white matter. On March 15, the patient died.

Patient 2. On discovery, the 11-year-old boy was comatose. At the hospital, he had an initial COHb level of 12% and had stable cardiovascular function but remained comatose and required ventilatory support; CO poisoning was diagnosed. During the first week of hospitalization, he also received HBO therapy. Neurologic examination demonstrated decorticate posturing and mixed reflexes. EEGs revealed diffuse slowing; a CT scan showed moderate cerebral edema with white matter involvement and petechial hemorrhages of the cortex, basal ganglia, and thalami. He remained comatose but ventilatory support was not required. At the beginning of the fourth week, he began to regain consciousness and to respond to voice commands; an EEG showed improved electrical activity. He subsequently was transferred to a pediatric rehabilitation program, improved, and, during January 1994, returned to school and resumed routine daily activities.

Investigation. A police investigation suggested that a van parked in the garage of the family home had been left running after the family had returned from an outing the previous night, approximately 24 hours before discovery. The garage adjoined the family room on the first level of the tri-level home. When emergency personnel arrived at the home, they found the door between the garage and the house was closed.

Approximately 2 hours after discovery of the family, environmental sampling by the gas company detected CO levels ranging from 17 to 64 parts per million (ppm) throughout the house; a sample from inside the van measured 448 ppm CO. These measurements were taken after emergency personnel had opened the garage door and several windows in the house. The furnace and hot water heater were inspected; exhaust vents on both appliances had been installed properly, and there were no indications of high CO output. Reported by: M Cook, MS, L Miller, MD, Injury Epidemiology; R Hoffman, MD, State Epidemiologist, Colorado Dept of Public Health and Environment; B Clem, MD, Presbyterian/St. Luke's Medical Center, Denver; Greeley Police Dept. Air Pollution and Respiratory Health Br, Div of Environmental Hazards and Health Effects, National Center for Environmental Health, CDC.

Editorial Note

Editorial Note: Since 1985, CDPHE has conducted surveillance for fatal and nonfatal unintentional CO poisoning. Although CO poisoning is preventable, during 1986-1991, a total of 174 fatal and 779 nonfatal unintentional CO poisonings were reported in Colorado. Nationally, approximately 590 deaths occur annually from unintentional CO poisoning (1). Fatal CO poisoning occurring in the household setting could be prevented if occupants could become alerted to the presence of the gas before concentrations reached toxic levels. The deaths described in this report resulted from inhalation of exhaust that leaked into the home from the adjoining garage where a van had been left running.

CO is an insidious poison that is a naturally occurring byproduct of the incomplete combustion of fuels. Because CO is colorless, tasteless, odorless, and nonirritating, its presence usually is not detected. CO is a component of exhaust and smoke (including cigarette smoke), and accumulation of CO may be associated with any combus-tion process occurring indoors (e.g., home heating, cooking, or a running vehicle or gasoline-powered tool) -- particularly when ventilation is inadequate (2,3).

CO induces toxic effects by tightly binding to hemoglobin to form COHb and reducing the oxygen-carrying capacity of the blood. Other potential mechanisms of toxicity include binding to cytochrome oxidase in the mitochondria, thereby interfering with cellular respiration (4), and inducement of cardiovascular compromise and consequent endothelial disruption (5). Because CO can induce toxicity by more than one pathway, COHb levels indicate exposure to CO but do not correlate consistently with symptoms or prognosis. Therefore, treatment and prognosis of CO poisoning are based on the clinical status of the patient at presentation rather than on COHb levels.

Diagnosis of CO poisoning is problematic because early symptoms of CO exposure are nonspecific (e.g., headache, dizziness, weakness, nausea, visual disturbances, and confusion) (4,6) and may be mistaken for symptoms of acute, self-limited illnesses (e.g., upper respiratory tract infection and food poisoning). At least three factors are associated with COHb levels and symptoms: 1) the concentration of CO in the environment; 2) the duration of exposure; and 3) the interval between exposure and clinical assessment (as illustrated by the cases described in this report). In general, however, exposure to CO concentrations of 80-140 ppm for 1-2 hours can result in COHb concentrations of 3%-6% (normal concentration: less than 2% for nonsmokers, 5%-9% for smokers); this concentration may be associated with decreased exercise tolerance and, in persons who are at risk, may precipitate angina attacks and cardiac arrhythmias (7). Clinical manifestations associated with CO concentrations of 105-205 ppm and COHb levels of 10%-20% include headache, nausea, and mental impairment. Manifestations associated with COHb levels of 30%-60% include more profound central nervous system effects, coma, and death (8). Treatment of CO poisoning requires termination of exposure and initiation of therapy with 100% oxygen; HBO therapy has been recommended for patients with neurologic or cardiac symptoms, pregnant women, and children when higher cortical function cannot be measured (4,9).

As a result of unintentional CO poisoning incidents in Colorado, CDPHE and the U.S. Consumer Product Safety Commission (CPSC) held a press conference on October 1, 1993 (the beginning of the winter heating season) to emphasize the occurrence of CO poisonings in Colorado, provide strategies to prevent such injuries, and discuss and demonstrate the use of CO detectors. Because a high proportion of unintentional deaths from CO poisoning are associated with exposure in the household setting, CPSC has proposed national mandatory installation of CO detectors in all new residential construction beginning in 1995 and has recommended installation of these devices in all existing homes. Additional information about residential CO detectors that meet Underwriter's Laboratory standards (UL 2034) is available from the CPSC Product Safety Hotline, telephone (800) 638-2772 or (301) 504-0220.


  1. Cobb N, Etzel RA. Unintentional carbon monoxide-related deaths in the United States, 1979 through 1988. JAMA 1991;266:659-63.

  2. CDC. Carbon monoxide levels during indoor sporting events -- Cincinnati, 1992-1993. MMWR 1994;43:21-3.

  3. CDC. Carbon monoxide levels in indoor tractor-pull events -- Manitoba, Canada. MMWR 1990;39:743-5.

  4. Thom SR, Keim LW. Carbon monoxide poisoning: a review. Clin Toxicol 1989;27:141-56.

  5. Okeda T, Funata N, Higashino F, Takano T, Yokoyama K. Comparative study on pathogenesis of selective cerebral lesions in carbon monoxide poisoning and nitrogen hypoxia in cats. Acta Neuropathol 1982;56:265-72.

  6. Meredith T, Vale A. Carbon monoxide poisoning. Br Med J 1988;296:77-8.

  7. US Environmental Protection Agency. Air quality criteria for carbon monoxide. Washington, DC: US Environmental Protection Agency, Office of Research and Development, 1991; publication no. EPA-600/8-90/045F.

  8. Llano A, Raffin T. Management of carbon monoxide poisoning. Chest 1990;97:165-9.

  9. Viccellio P, ed. Handbook of medical toxicology. Boston: Little, Brown, and Company, 1993.

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