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International Notes Carbon Monoxide Levels in Indoor Tractor-Pull Events -- Manitoba, Canada

Carbon monoxide (CO) and other noxious gases produced by internal combustion devices are health hazards in enclosed spaces. In facilities such as underground garages and indoor arenas, CO is a particular concern because of its rapid toxic effects and potentially high concentrations. In February and November 1988, the City of Winnipeg Health Department (WHD), Manitoba, Canada, conducted surveys of two tractor-pull events in an indoor 15,000-seat arena to determine levels of CO. During the November event, an attempt was made to mitigate CO levels. This report summarizes findings from the two surveys.

A "tractor" is a truck or other vehicle modified to look like a farm tractor (e.g., large rear wheels and smaller front wheels) and powered by a variety of units (e.g., aircraft turbines and supercharged car engines). During a typical "pull," approximately 12 tractors compete in pulling a 40- to 50-ton sled across a 75-m (82-yd)-long dirt surface in the fastest time. A tractor-pull event lasts approximately 2 hrs and involves 25 individual pulls.

Previous monitoring of CO in the arena's seating area during full-occupancy hockey games indicated CO levels of 0-10 ppm; an ice-edger and an ice-resurfacing machine, both of which emit CO, were used several times each during each game. The WHD's recommended indoor guideline levels are 33 ppm for a 1-hr exposure and 18 ppm for an 8-hr exposure.

To measure CO levels during the tractor-pull events, certified public health inspectors used a Gastech CO-82 Carbon Monoxide Detector* to record levels before the events and at half hour intervals during the events at 25 seating locations at varying heights within the arena.

At the February event, measurements indicated an average level of 68 ppm at the start (8 p.m.) of the first of 25 pulls; however, several tractors had been running their engines before the first pull. By 10:30 p.m. (the end of the competition), the CO level had increased to 262 ppm. In general, CO levels were uniform throughout the seating area. During this event, however, the ventilation system had not been operating at full capacity, tractors had been allowed to run their engines before the event, and large doors to the arena's ground floor had been closed.

During the November event, measures to decrease CO levels included reducing the number of pulls to 24, expanding the event by 2 hrs to permit decay in the CO level, and opening ventilating louvres in the arena roof. WHD inspectors used the same measuring apparatus to take readings at the same locations as in the February event. CO levels at the beginning of the event averaged 77.5 ppm and increased to 435.7 ppm by the event's close.

This evaluation indicated that the control measures were not effective in reducing CO levels. Participants did not want to retrofit their tractors with pollution-control devices because this would decrease the horsepower of the tractors. Therefore, WDH officials required that appropriate ventilation improvements be implemented before further tractor-pull events could be permitted in the arena. However, because one evaluation concluded that the costs to implement the ventilation improvements were prohibitive, a tractor pull scheduled for February 1989 was cancelled, and no further such events are to be held in the arena. Adapted from: Canada Diseases Weekly Report 1990;16-17:79-81, as reported by: G Solkoski, Director, Environmental Health Div, City of Winnipeg Health Dept, Manitoba. Div of Environmental Hazards and Health Effects, Center for Environmental Health and Injury Control, CDC.

Editorial Note

Editorial Note: Because CO poisoning is frequently not suspected in persons suffering from CO intoxication, morbidity from CO poisoning is difficult to estimate. Unintentional poisoning has resulted from exposure to high levels of CO from automobiles, ice-resurfacing machines, fork lifts, recreational vehicles, and kerosene heaters and other fuel-burning household devices (1-3). Current Environmental Protection Agency outdoor air quality standards permit 9 ppm CO as an 8-hr average and 35 ppm as a maximum 1-hr level (4). In the United States, there are no indoor air standards for CO. Japan has established a guideline of 10 ppm (5).

Because adverse effects have occurred in healthy persons who continuously breathe CO levels of 15 ppm (6) (and because susceptible persons may experience toxicity at lower levels), the levels attained in the Winnipeg arena during the tractor-pull events represented a potential health hazard to both participants and observers. However, the City of Winnipeg Ambulance Department, which provides staff and equipment for all major sporting events, did not report any incidents of CO intoxication during the tractor-pull events.

CO is a colorless, odorless, nonirritating gas produced by incomplete combustion of fuels and present in all exhaust and smoke, including cigarette smoke. CO is toxic because 1) it avidly binds to hemoglobin to form carboxyhemoglobin (COHb), which reduces the oxygen-carrying capacity of blood, and 2) it inhibits cytochrome oxidase within mitochondria, thereby poisoning cellular respiration. The latter effect is increased in cases in which tissue hypoxia already exists and in cases of chronic CO intoxication (1). The risk for toxicity is proportionate to metabolic rate, exercise, prolonged exposure, and high altitude. Populations at risk for CO poisoning include the elderly, the poor (during the winter heating season), pregnant women (because of risk to the fetus), and persons with heart disease, lung disease, or anemia.

Symptoms of mild to moderate CO poisoning are nonspecific; the most commonly reported symptoms are headache, dizziness, weakness, nausea, confusion, shortness of breath, and visual problems (7). In addition, CO exposure can cause or exacerbate cardiac abnormalities (e.g., angina), and low COHb levels can cause complex ventricular arrhythmias (8). Occult CO poisoning should be suspected when these symptoms occur in two or more persons who have a history of sharing enclosed quarters (9). A blood COHb level greater than 2% in nonsmokers or greater than 10% in smokers confirms CO exposure; levels of greater than or equal to 30% are commonly associated with severe symptoms and may result in neuropsychiatric sequelae. Because COHb levels may not reflect tissue levels, they should be interpreted cautiously--especially in cases of chronic CO intoxication. Home or worksite measurement of ambient CO levels may be necessary to establish the diagnosis in cases of chronic low-level exposure.

Treatment in milder cases consists of 100% oxygen; hyperbaric oxygen should be used to treat moderate to severe intoxication (COHb greater than 40%), particularly in pregnant women or when evidence exists of neurologic changes or cardiac arrhythmias (1,10). Preventive measures include regular automobile maintenance; routine cleaning and adequate venting of gas-fired stoves, furnaces, and appliances; and adequate ventilation and pollution controls during indoor events such as tractor pulls.


  1. Thom SR, Keim LW. Carbon monoxide poisoning: a review. Clin

Tox 1989;27:141-56.

2. CDC. Carbon monoxide exposures at an ice skating rink--Colorado. MMWR 1986;35:435-6,441.

3. CDC. Carbon monoxide poisoning in a garment-manufacturing plant--North Carolina. MMWR 1987;36:543-5.

4. National Air Pollution Control Administration. Air quality criteria for carbon monoxide. Washington, DC: US Department of Health, Education, and Welfare, Public Health Service, Environmental Health Service, 1970; publication no. AP-62.

5. Walsh PJ, Dudney CS, Copenhaver ED, eds. Indoor air quality. Boca Raton, Florida: CRC Press, 1984:66.

6. Davies LM, Smith DJ. Electrocardiographic changes in healthy men during continuous low-level carbon monoxide exposure. Environ Res 1980;21:197-206.

7. Burney RE, Wu SC, Nemiroff MJ. Mass carbon monoxide poisoning: clinical effects and results of treatment in 184 victims. Ann Emerg Med 1982;11:394-9.

8. Sheps DS, Herbst MC, Hinderliter AL, et al. Production of arrhythmias by elevated carboxyhemoglobin in patients with coronary artery disease. Ann Intern Med 1990;113: 343-51.

9. Heckerling PS, Leikin JB, Maturen A. Occult carbon monoxide poisoning: validation of a prediction model. Am J Med 1988;84:251-6. 10. Broome JR, Skrine H, Pearson RR. Carbon monoxide poisoning: forgotten not gone! Br J Hosp Med 1988;39:298-305. *Use of trade names is for identification only and does not imply endorsement by the Public Health Service or the U.S. Department of Health and Human Services.

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