Short-term exposure to ozone irritates the airways and reduces lung function. The effects from long-term exposure are less well known.
Ground level ozone is a particularly reactive gas consisting of three oxygen atoms joined together. It is formed by chemical reactions between other pollutants. In particular, it originates due to the action of ultra-violet light in the reaction of oxides of nitrogen with carbon compounds (volatile organic compounds or VOCs). These reactions take place over periods of several hours or even days.
Ozone levels tend to be higher in the countryside than in cities, and greater in summer than winter. Some ozone travels over large distances as a transboundary pollutant.
On the other hand, it accumulates as a component of photochemical smog. This can occur over large areas, for example across north west Europe or in cities in spells of prolonged dry sunny weather. The photo-chemical smog reported from Los Angeles in the early 1950s contained high concentrations of ozone and related compounds and high concentrations of particles. This smog was acutely irritating to the eyes.
Ozone levels fluctuate markedly with time and are highest when there is hot bright weather. Short-term ozone peaks at ground level are associated with increased hospital admissions. In exposure chamber experiments, human subjects experience lung inflammation at ozone concentrations below those which habitually occur outdoors in the UK.
In outside air, an eight hour-running average of 70 micrograms per cubic metre (µg/m3) ozone is typical. The EU target value to protect human health is 120 µg/m3 (averaging period of maximum daily eight-hour mean) not to be exceeded on more than 25 days per calendar year, averaged over three years.
The EU requires that the public be informed when hourly levels are above an 'information threshold' of 180 µg/m3 or an 'alert threshold' of 240 µg/m3. Visit the Defra website [external link] for more information on EU air Quality legislation.
Exposure to high concentrations of ozone produces irritation of the eyes and narrowing of the airways
There is a wide variation in individuals' sensitivity to the effects of ozone. Those suffering from asthma are not necessarily more sensitive to ozone than other people but as they may already have some impairment of lung function, a further reduction caused by ozone may produce more significant effects than a similar reduction in those with normal lung function. Many air pollutants cause narrowing of the airways: this can be monitored by means of lung function tests.
Unlike the health effects of sulphur dioxide the effects of exposure to ozone do not appear immediately after exposure begins: they build up over several hours. Measurements of ozone concentrations are averaged over 8 hours, as this most closely represents the exposures likely to be harmful to human health.
During a pollution episode (a period of abnormally high air pollution) high levels of ozone may worsen asthma or trigger asthma attacks. Some non-asthmatic individuals might also experience discomfort when breathing, particularly if they are exercising vigorously outdoors. The mechanism underlying this effect is not well understood: the effect is not seen with other gases that cause narrowing of the airways.
Epidemiological studies have also suggested that ozone contributes to cardiovascular disease probably through its pro-inflammatory effects on the lung.
Ozone's respiratory irritation formed the endpoint upon which the Expert Panel on Air Quality Standards (EPAQS) set as the ozone Air Quality Standard in 1994. Chamber studies revealed that ozone was an irritant gas to both healthy individuals and those with lung disease. It is a powerful oxidant that reacts to cause epithelial cell damage and inflammation, driven in large part by an influx of neutrophil leukocytes. Naturally occurring antioxidants generated by the lung offer some protection against these effects.
Since the EPAQS 1994 report, there has been increasing epidemiological evidence that short-term exposure to ozone has important adverse effects on asthmatics, with evidence for increased demands on the National Health Service.
The main findings are that
• exacerbations of asthma can occur at lower atmospheric concentrations than previously appreciated,
• additive interactions occur with other factors, such as pollen allergen exposure and other pollutants, which also stimulate exacerbations of asthma
• there are specific genetic variations that influence the inflammatory and irritant responses to ozone.
There is also accumulating evidence that asthmatic airways respond more severely to ozone exposure, i.e. have more of an inflammatory response than those of allergic but non asthmatic subjects.
A recently observed effect on the lungs of ozone is its capacity to slow airway growth and therefore result in reduced baseline lung function in children who are repeatedly exposed to high concentrations. This effect is unlikely to be relevant to ozone levels generally encountered in the UK.
In addition to asthma, ozone episodes are associated with increased respiratory morbidity in older people, especially those with pre-existent chronic obstructive lung disease and the genetic variant of emphysema, alpha-1 antitrypsin deficiency.
The majority of adverse health effects (morbidity) attributable to short-term ozone exposure are respiratory in nature. However, there is mounting evidence that this pollutant is also associated with heart attacks (myocardial infarction) and cardiac arrhythmias in the older population.
Epidemiological studies suggest that ozone contributes to cardiovascular disease probably through its pro-inflammatory effects on the lung.
Extract from COMEAP's Review of the UK Air Quality Index (2011)
The effects on health of short-term exposure to ozone have been studied using time-series methods
A range of effects have been reported including an increase in risk of death from heart disease and an increase in numbers of admissions to hospital for treatment of heart and lung disorders.
Peak eight hour average concentrations of ozone have been studied and these form the basis for the work we have done to quantify the effects of ozone on health in the UK. Read more about Epidemiological studies in air pollution.
Calculating numbers of deaths and hospital admissions due to short-term exposure to ozone
Deaths (all causes)
Respiratory hospital admissions
+ 3.0% per 50 µg/m3 increase in ozone
8 hour mean
+ 3.5% per 50 µg/m3 increase in ozone
8 hour mean
Table 1 Estimates of Coefficients to quantify the health effects of short-term exposure to ozone COMEAP 1998
Subsequently, in 2005, The World Health Organisation proposed that effects of ozone short-term exposure to ozone be quantified only where 8-hr daily average ozone exceeds 35ppb (70 µg/m3) (WHO, 2006). This was as a precaution, to avoid over-estimating effects, because there was a lack of evidence about whether or not there was an effect on mortality of ozone at lower concentrations. There is however no evidence of a population threshold or ‘safe level’.
The Health effects of Climate Change in the UK 2012 report by the Health Protection Agency (now known as Public Health England) published calculations for short-term exposure to ozone and the effects on health. These were quantified using no threshold and thresholds of 70 µg/m3 and 100 µg/m3 for health effects.
Read more about thresholds
The possible effects of long-term exposure to ozone are not well understood and so far COMEAP has not made any recommendations
There is some evidence that summertime ozone, at concentrations higher than about 50 µg/m3 1-hour peak, is associated with increased risk of respiratory mortality (Jerrett et al., 2009). There is also some evidence for an effect of long-term exposure to ozone on lung-function growth in children and these effects increase the plausibility of an effect of long-term exposure to ozone on mortality.
The Health effects of Climate Change in the UK 2012 [external link]