Carbon monoxide (CO) is a colourless, odourless and tasteless gas that is a product of the incomplete combustion of solid, liquid and gaseous carbon-based fuels. These include wood, coal, petrol, diesel, LPG, CNG, kerosene and oil.
Sources of carbon monoxide concentrations in ambient air in New Zealand are typically motor vehicle emissions and domestic home heating in most urban areas. Concentrations of carbon monoxide in the indoor environment from indoor sources can also pose a major health threat. High concentrations of CO indoors can occur as a result of emissions from non-vented gas cookers and heaters. Other common indoor sources of CO include solid fuel burning and smoking.
Carbon monoxide impacts on health by reducing the oxygen carrying capacity of the blood. This occurs because CO binds more readily to haemoglobin than does oxygen and results in the formation of carboxyhaemoglobin (COHb), which leaves less haemoglobin available for transferring oxygen around the body.
The ambient air quality guideline values (Ministry for the Environment, 2002) for CO are:
These revised guideline values for CO are the same as those adopted in 1994 (Ministry for the Environment, 1994). The aim of the guideline values is to prevent exposure to levels of ambient CO that would result in blood COHb levels greater than 2.5%, at any level of physical activity.
Carbon monoxide concentrations have been measured in many urban centres of New Zealand. In most locations, concentrations are within the guideline values at ambient air quality monitoring sites. The main exception is Christchurch, where the eight-hour average guideline value is sometimes exceeded during the winter months at the central St Albans ambient air quality monitoring site. CO concentrations have also exceeded the ambient air quality guideline values at a number of 'traffic peak' sites that are primarily in Auckland, Wellington and Christchurch.
The proportion of the relative populations likely to be affected by guideline value exceedences at the 'traffic peak' monitoring sites is less than for the ambient 'residential neighbourhood' sites. This is because the elevated concentrations of CO will be localised at the roadside and will disperse with increasing distance from the source. Thus exposure to elevated concentrations will depend on proximity to the road. Those most likely to be affected by roadside CO concentrations include shop workers and those residing in other dwellings located near to high-density traffic areas, and drivers.
The formation of COHb reduces the amount of haemoglobin available for the transportation of oxygen around the body. This can impact on the brain, nervous tissues, heart muscle and other specialised tissues that require large amounts of oxygen to function. As a result of oxygen deprivation, these organs and tissues may suffer temporary or permanent damage.
Those most susceptible to the health effects of ambient air exposure to CO include those with ischaemic heart disease, other forms of cardiac disease including cyanotic heart disease, hypoxaemic lung disease, cerebrovascular disease, peripheral vascular disease, those with anaemia and haemoglobin abnormalities, children, and developing foeti.
Dennison (2002) provides a comprehensive summary of the literature on health effects of carbon monoxide. This indicates the results of toxicological studies and the consequent evaluation of the lowest observed adverse effect levels (LOAEL) and no observed adverse effect levels (NOAEL) (Table 2.1) as well as recent epidemiological studies, which suggest that effects may occur at concentrations lower than indicated by toxicology. The latter suggest that health effects of CO concentrations may occur at concentrations lower than measured in many urban areas in New Zealand (Table 2.2).
Table 2-1: Adverse health effects from exposure to carbon monoxide
View adverse health effects from exposure to carbon monoxide (large table)
Table 2-2: Summary of epidemiological studies for carbon monoxide
View summary of epidemiological studies for carbon monoxide (large table)
Table 2.3 gives an indication of approximate COHb blood levels (percentage) associated with the 99.9 percentile eight-hour average CO concentrations measured in each urban area in New Zealand. This is based on information presented in Dennison et al., (2002) which indicates that the relationship between CO and haemoglobin is linear at CO concentrations of up to 250mg/m3 at sea level, and that COHb% at equilibrium can be reasonably approximated by the following relationship when exposure is continuous:
COHb% = CO(mg/m3) x 0.16
(equation presented in Dennison et al., 2002 as adapted from Bascom et al., 1996).
Table 2-3: Estimate COHb% based on 99.9 percentile eight-hour average CO concentrations measured in urban centres of New Zealand
A comparison of the estimated COHb% levels associated with exposure to CO concentrations at the 99.9 percentile level in each monitoring site suggests that CO concentrations in some areas of New Zealand could have impacts on health. In the areas of Christchurch (St Albans), Wellington (Civic Centre and Huia Pool), and Auckland (Queen Street), exposure to CO concentrations could have resulted in a significant decrease in work capacity in healthy adults, a decreased exercise capacity at the onset of angina and an increased duration of angina in people with ischaemic heart disease. Similarly, prolonged exposure to concentrations measured at these sites and other sites such as those measured at Dominion Road and Khyber Pass in Auckland could impact on the developing foetus resulting in reduced birth weight in non-smokers.
The degree of these impacts, however, will depend on the extent of exposure. In areas such as Christchurch (St Albans), the monitoring is likely to reflect concentrations to which a reasonable proportion of the population is exposed for a reasonable duration. In comparison, elevated concentrations at some of the traffic peak sites may be limited to an area close to the roadside. The population exposed and the duration of the exposure could therefore be limited.
While results of the epidemiological studies presented in Table 2.2 suggest that health effects of CO may occur at COHb levels lower than 2.5%, Dennison et al (2002) concludes that there is still some question as to whether these effects are due to CO or whether CO is acting as an indicator for pollution from combustion sources. Consequently no additional calculations of the potential impact of CO based on these relationships have been carried out.