November 2002
INTOXICATING SPORT
Back to contents

EHJ November 2002, pages 328-330

A joint investigation into an accident at a go-kart racing stadium, which resulted in a number of staff and customers suffering from carbon monoxide toxicity, throws up some interesting results

Go-kart racing was introduced to this country by American servicemen, based in the UK during the Second World War, and has gradually expanded in popularity since. In its early years, karting was expensive and less accessible to the general public, but over the last 20 years or so, indoor circuits that supply karts for hire have sprung up in or near nearly every major town in the country, revolutionising the sport.

But, last year an incident at a local go-karting stadium led to a number of people suffering carbon monoxide intoxication, and a joint investigation by the local authority and the district consultant in communicable disease control was immediately launched.

On Saturday 3 November 2001, three separate parties (60 people in total) attended karting sessions at an indoor stadium, for a period of around four hours. The management at the stadium provided the group with a fleet of 10 new propane-powered karts which had not been driven together on the track before, and subsequently there were problems with the gas karts stalling. The company, which had been operating from the premises for over nine years, had previously used petrol-powered karts.

Within two hours of the sessions commencing, eight members of the group began to feel unwell with headache, lethargy, nausea and disorientation, although the management team was not informed of any ill effects to members of the public or staff until 4pm. At this time, a decision was made to change back to the petrol-powered karts, and the new propane-powered karts have not been used for public sessions since then.

Following the incident, statements were obtained from all members of staff on duty during the session. Six of the seven on duty experienced headaches and one became dizzy and collapsed. However, only two actually informed the duty manager.

Once the session had ended and the group dispersed, two hours later, eight individuals were still experiencing symptoms and felt unwell. They each attended the accident and emergency departments of their local hospitals, between five to seven hours after leaving the stadium. On examination they all had clinical signs consistent with carbon monoxide (CO) toxicity. This was confirmed in four individuals who were blood tested for carboxyhaemoglobin (COHb). The individuals were discharged following observation and appropriate oxygen therapy.

Patient CHOb (%) Symptons Smoker
Patient 1 6.9 Headache, lethargy No
Patient 2 15 Headache, nausea, lethargy, sore eyes Yes
Patient 3 7.7 Headache, nausea, lethargy No
Patient 4 7.0 Headache Yes
Patient 5 N/M Headache, disorientation Yes
Patient 6 N/M Headache, nausea Yes
Patient 7 N/M Headache, nausea, dizziness,
muscle aching
Yes
Patient 8 N/M Headache, dizziness Yes

Table 1: Blood COHb levels of those individuals with symptons

Table 1 shows the blood COHb levels of those people that reported symptoms. It is important to note that these concentrations were at least five hours post exposure and that no medical treatment had been given prior to this time. The half-life of CO when breathing air is approximately five hours. Normal COHb levels due to endogenous CO production are 0.4-0.7 per cent; in non-smokers in urban areas this may be raised to 1-2 per cent as a result of environmental exposure; smokers may have a COHb level of 5-6 per cent.

Carbon monoxide (CO) intoxication is a common form of unintentional poisoning. CO is a colourless, odourless, tasteless gas which combines reversibly with haemoglobin (Hb) with an affinity 200-300 times greater than oxygen to form carbohaemoglobin (COHb). The clinical features of CO poisoning are diverse and the severity of poisoning depends on the concentration of CO in the inspired air, length of exposure and the general health of the exposed person.1

Assuming a simple kinetic model, then it is reasonable to suggest that the levels were approximately double at the cessation of exposure. Patient 2, though a smoker, had a concentration of 15 per cent on presentation (at least five hours post exposure), which would indicate that his potential COHb might have been as high as 30 per cent during exposure.

The signs, symptoms and prognosis of acute CO poisoning correlate poorly with the degree of COHb measured on arrival at hospital. Exposure to CO concentrations of 80-140 ppm for 1-2 hours can result in blood COHb levels of 3-6 per cent; this concentration may be associated with decreased exercise tolerance and, in persons who are otherwise at risk, can precipitate angina pectoris and cardiac arrhythmias.2

Clinical manifestations associated with CO concentrations of 105-205 ppm and COHb levels of 10-20 per cent include headache, nausea, mild exertional dyspnoea, and mental impairment. Coma, convulsions, and cardiorespiratory arrest may occur if COHb exceeds 60 per cent.

The incident in question occurred coincident with the use of new propane-powered karts. These were taken out of use immediately, but the actual CO concentration in the stadium at the time is unknown because no measurements were taken. Subsequently, measurements were taken at the same track during a race meeting involving petrol-powered karts, and it was found that the CO concentrations were more than double the occupational exposure standard (OES) of 30 ppm, in spite of the fact that the karts were fitted with catalytic converters, unlike the propane powered karts.

The local authority was instrumental in the subsequent investigation. An improvement notice was initially served, to require a COSHH assessment of exhaust fumes from the go-karts. Further to the results of this COSHH assessment, four improvement notices were served in order to:

  • improve the ventilation;
  • carry out CO monitoring of the employees;
  • keep records of air monitoring; and
  • provide information to employees and other people on the premises.

On the recommendations of the COSHH report, short-term measures were put into effect, namely:

  • the fire and shutter doors were required to be open during meetings;
  • the roof fans were to be kept running for half an hour after racing finishes; and
  • the marshals rotated during eight-hour shifts.

These measures were checked during a number of visits to the premises during the investigation. The company concerned has co-operated throughout the investigation and is complying with the improvement notices.

Since 1999, the chemical incident response service (London) has been involved with two other similar incidents. The first involved 11 patients with COHb levels ranging from 12-20 per cent, following a two-hour exposure. Symptoms included headache, nausea, and two patients collapsed. Five were admitted overnight and discharged well the next day. The second incident involved 10 employees from a new indoor arena.

It appears that the number of reports of CO toxicity from go-karting arenas may be increasing. It is also likely that small incidents affecting only one or two individuals may have gone previously unreported. The risk of such incidents in future could be much reduced if some simple precautions are followed:

  • the concentrations of the exhaust gases, and in particular CO, can be calculated from emission data from the engine suppliers, ventilation data from the building, and operational data such as the number of karts in use;
  • this investigation showed the importance of checking the actual ventilation performance, and not merely assuming that the design specification is being met. It should be checked on commissioning, annually, and after any repair;
  • the CO concentration in the exhaust can be reduced from about 4.5 per cent to 1 per cent by fitting and maintaining catalytic converters. These should be mandatory at all indoor tracks;
  • the CO concentration should be monitored with CO meters which are of low cost; and
  • as business proprietors, managers of go-karting arenas have a legal requirement to undertake a risk assessment on their premises. It is especially important this is revised when any changes are introduced, such as structural alterations to the arena or the type or quantity of karts. Unfortunately, the published guidance from the Health and Safety Executive is very poor in this area, and the need for a COSHH assessment of exposure is buried in an appendix.3

References

  1. Meredith T, Vale A, (1988) "Carbon monoxide poisoning", BMJ 296: 77-78
  2. Hampson NB, 1996. "Carbon monoxide poisoning at an indoor ice arena and bingo hall - Seattle, 1996". MMWR 45(13): 265-267
  3. HSG 200 Go-karts. Guidance for safe operation and use. HSE Books, 2000

Authors

  • Elaine Higgins, senior environmental health officer, Rochford District Council;
  • Amelia Cummins, consultant in communicable disease control, Essex Health Protection Team;
  • Henrietta Harrison, information scientist, Chemical Incident Response Service and
  • Danny Gazzi, occupational hygienist, Industrial Health Control.

For further details e-mail: elaine.higgins@rochford.gov.uk or amelia.cummins@sessex-ha.nthames.nhs.uk