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Posted: June 28, 2005

Science of Sport: Air Pollution

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Along with the highly publicised concerns about whether the 2004 Athens Olympic facilities would be completed in time, the various national Olympic organisations were also preoccupied with the environmental challenges that confronted competitors. Everyone knew it was going to be hot but, as the Games drew closer, the full implications of holding them in one of Europe’s most polluted cities finally dawned on everyone(1).

Despite the sterling efforts of the Greek organising committee to reduce air pollution levels in time, many predicted that athletes would be affected by breathing problems on an unprecedented scale, while those with asthma would suffer potentially catastrophic exacerbation of their condition.

The Greek authorities strenuously dened these risks, claiming that competing in Athens was likely to be no more injurious to health than, say, in London. Maybe they are right – time will tell. Meanwhile, what this debate highlights is the growing concern over the impact of air pollution on the health of city-dwellers, especially those who exercise.

For those of us who live and exercise in the city, the potential health risks of breathing a cocktail of air pollutants are a very real concern. Links between high levels of air pollution and lung disease(2), cardiovascular disease(3) and even cancer(4) are being established in the medical literature. For example, elevated levels of air pollution are closely associated with both an increased prevalence of asthma(5) and an increased incidence of acute exacerbation in all patients with cardiorespiratory illness(2,6).

A study presented at the American Heart Association’s meeting in 2003 identified significant associations between cardiovascular disease deaths and a number of air pollutant concentrations(3), and it is estimated that pollution causes 19 premature deaths per 100,000 of population across Europe(1).

Although these mortality data refer to patients with pre-existing disease, they highlight the serious implications of exposure to air pollution. In addition, the accumulating evidence of an association between exposure to air pollution and the development of debilitating and potentially life-threatening illness should give all of us cause for concern.

Although it is now well established that breathing polluted air has a negative impact upon health, there is no direct evidence about the longterm health implications of exercising in a polluted environment. Common sense would suggest that if your lungs are exposed to 10 times the quantity of air during exercise than at rest, this must be equivalent to increasing exposure duration 10- fold; in other words, a one-hour exercise exposure is similar to a 10-hour resting exposure.

To add insult to injury, when you exercise you switch from nasal to oral breathing, which allows air to bypass your body’s natural defence against inhaled particles – the elaborate filtering system that lies between your nose and the back of your throat.

To top it all, during exercise we inhale more deeply and rapidly than usual, which means that particles and other pollutants are carried to the deepest reaches of the lungs. Scary stuff!

So what air pollutants should we be concerned about, and how can city-dwellers find out about the daily risks of exercising outdoors?

Most TV and radio weather reports now provide information about air pollution (eg www.bbc.co.uk/weather), especially in the summer months when ‘photochemical smog’ becomes a problem. In addition, in the UK local information is available on Teletext, the internet (www.airquality.co.uk), or via freephone (0800 556677). Pollution levels are given a numerical indicator and banded to provide information about associated health risks, as follows:

  • Low (1-3) – effects unlikely to be noticed, even by those who are sensitive to air pollution;
  • Moderate (4-6) – sensitive people may notice mild effects but these are unlikely to need action;
  • High (7-9) – sensitive people may notice significant effects and may need to take action;
  • Very high (10) – effects on sensitive people, described for high pollution, may worsen.

In the developed world, air pollutants come principally from vehicle exhaust emissions and are highest in urban areas (with one exception – ozone is frequently highest in rural areas around cities, as it is a very mobile gas). The level of pollution on any given day and in any given city is determined by a combination of factors, not just the volume of vehicle traffic.

For example, cities like Athens have relatively high levels of air pollution because of local meteorology, topography and infrastructure. Athens is an industrialised, highly populated Mediterranean coastal city surrounded by mountains. In the summer, photochemical smog forms during the day in the strong sunlight and is confined by the surrounding mountains. At night, the direction of the sea breeze that had held the smog over the city reverses, and the smog cloud is drawn out to sea. However, the next day the sea breeze brings the smog back over the city, where its concentration is increased further by the daily dose of traffic fumes.

Other notorious smog hotspots are Bangkok, Beijing, London, Los Angeles, Mexico City, New Delhi, New York, Paris, Santiago de Chile, Sao Paulo, Sydney, and Vancouver. As we all know, the 2008 Olympics will be hosted by Beijing. Furthermore, London, Paris and New York are all front-runners to host the 2012 Games, so the issue of air pollution and Olympic competition venues looks set to run and run.

Not all vehicle emissions are harmful, but there are six that carry a health and/or performance impairment risk:

  • carbon monoxide (CO)
  • nitrogen dioxide (NO2)
  • ozone (O3)
  • particulate matter (PM10)
  • sulphur dioxide (SO2)
  • volatile organic compounds (VOC).

Implications of chronic exposure

The full implications of chronic exposure to the cocktail of pollutants that city-dwellers breathe in every day are largely unknown, although some links have been made, as described above. Circumstantial evidence of a long-term health risk is strong for VOCs such as benzopyrene, which is a well-known carcinogen. VOCs contribute to the blue-brown haze associated with photochemical smog and also cause eye and respiratory tract irritation.

In terms of immediate detrimental influences to breathing and the oxygen transport system, high levels of carbon monoxide (CO) are associated with a decrease in the oxygen carrying capacity of the blood and a reduced maximal oxygen uptake and lactate threshold. Levels of CO are declining as more and more cars are fitted with catalytic converters, but there are peaks around congested roads, and concentrations are highest inside slow-moving cars, which has implications for athletes travelling to competitions by car.

The problem of PM10

Air pollution information also reports on air concentrations of particles less than 10 microns in size, so-called PM10. PM10 is a concern because it can be deposited in the deeper reaches of the lungs, and levels peak during smogs and at roadsides. The combination of PM10, sulphur dioxide and water vapour forms sulphuric acidcoated particles that deposit deep inside the lung with fairly obvious consequences (irritation and asthma-like symptoms). The particles themselves are made up of a variety of compounds, including carcinogenic hydrocarbons and lead.

The deep, rapid breathing of exercise may enhance deposition of PM10 in the lungs, placing exercisers at increased risk. An increased risk of lung cancer has been demonstrated in Oslo residents whose homes were in the more polluted areas of the city(4), but the full implications of exposure to PM10 is currently unknown.

Nitrogen dioxide (NO2) and sulphur dioxide (SO2) are both very soluble gases that convert to nitric and sulphuric acid when they make contact with the moist lining of the mouth and lungs. They cause soreness of the nasopharynx and lungs, coughing and breathlessness, as well as inducing symptoms of asthma in both healthy people and asthmatics. Fortunately, concentrations of both gases are usually fairly low and these symptoms are very rare.

Unfortunately, the same cannot be said for ozone (O3), which is good news in the stratosphere, where it filters out UV radiation, but very bad news at ground level (the troposphere). O3 is formed by the action of strong sunlight on other atmospheric pollutants (principally VOC and NO2), so concentrations are highest during summer. Because O3 is very mobile, the highest concentrations are often found in the rural areas around cities. As with NO2 and SO2, O3 induces asthma-like symptoms and lung inflammation. In addition to irritating the lungs directly, O3 also acts on the nervous system to inhibit breathing, making it difficult and painful to take deep breaths; it has been suggested that this may be part of a protective reflex to minimise the lungs’ exposure to the irritant.

Research has shown that responsiveness to O3 is a function of concentration, exposure duration, and level of ventilation(7), which means its effects are magnified by exercise. There also appears to be large inter-individual variation in responsiveness to O3, with some people showing large decrements in their lung function, while others show little or no ill effect(8,9).

The effects of exposure to ambient outdoor concentrations of O3 were studied in a group of amateur cyclists during a summer competitive season in the eastern Netherlands(10). The authors noted a significant relationship between ambient O3 concentration and the cyclists’ post-exercise lung function as well as wheeze, chest tightness and shortness of breath (worst when O3 was highest). These relationships persisted when the observations at concentrations above 60 parts per billion (ppb) were excluded, suggesting that a detrimental influence remained, even on days when O3 concentration would be deemed ‘moderate’.

Ozone for asthmatics

Because of their pre-existing lung inflammation, asthmatics have been assumed to have a greater responsiveness to O3 than people with normal lung function(11). Interestingly, though, recent evidence suggests that this may not be the case(12), and that asthma severity does not predict responsiveness(13). However, there is evidence that lung inflammation in response to O3 exposure may be more severe in asthmatics(14), which might have serious long-term implications as well as leading to acute exacerbation of their condition(12).

It has also been demonstrated that O3 exposure exacerbates responsiveness of asthmatics to other respiratory irritants, such as SO2, which suggests it may be misleading to consider the detrimental effects of single pollutant challenges in laboratory studies(15).

Because O3 triggers an inflammatory response within the lung, it has been suggested that supplementing the lungs’ natural antioxidant capacity might increase their ability to withstand the oxidative stresses imposed by O3 inhalation. In two studies from the same group in the Netherlands, competitive cyclists supplemented with antioxidant vitamins (approx 100mg vitamin E + 500mg vitamin C) had their lung function assessed before and after training or competition(16,17).

Supplementation was found to significantly attenuate the O3-induced decrements in lung function in both studies. These data are further supported by a study on street workers in Mexico City, who also demonstrated attenuated lung function impairment when placed on a similar supplementation regimen(18).

So far, we’ve considered only the health-related implications of exposure to O3, but there is also ample evidence that O3 impairs exercise performance(19). Recent unpublished research from Napier University in Scotland suggests that running time trial performance (8k) is impaired by around 1% while breathing an O3 concentration of 100ppb, which is typical for a major city at the height of summer. The athletes in the study also suffered impaired lung function, coughing and breathing difficulties after the exercise bout. However, when antioxidant supplements were taken before a second time trial conducted with 100ppb O3, performance was restored to the control level.

While a 1% decrement in time trial performance may not seem too bad, it would have a potentially disastrous impact on a worldclass athlete competing in a major event. And, although levels of O3 are typically low to moderate in the UK, during last summer’s heat wave, they reached record levels in major cities such as London (125ppb).

By now, you’re probably wondering whether its just too risky to exercise at all in what we used to think of as the ‘fresh air’. However, life is about managing risk; yes, you could damage your health by running along that dual carriageway, or cycling to work, but you could also be hit by a dozy driver. The solution is to be sensible about when and where you exercise and remember that air quality is poorest in urban areas, especially around heavily used and congested roads (although O3 is the exception).

To minimise your risk without ruining your enjoyment of what remains a healthy activity, follow this advice:
Don’t exercise…
…during rush hour;
…in close proximity to a congested road;
…in obvious smog;
…when there is a combination of high vehicle emissions and strong sunlight.

Don’t travel to a competition in a poorly ventilated car through congested areas (CO concentrations are highest inside cars).

Do:

  • check the pollution forecasts;
  • be particularly cautious if you have asthma. Use your inhaler before exercising and consult your GP if your symptoms worsen, as you may need a change of medication;
  • consider taking antioxidant vitamin supplements (100mg vitamin E + 500mg vitamin C);
  • consider using a personal air filtration device (but be careful to check the manufacturer’s claims against independent reports; not all masks perform as well as manufacturers would have you believe.

Alison McConnell

References

  1. www.apheis. net
  2. Monaldi Arch Chest Dis 57 (3-4), 156- 60, 2002
  3. www.americanheart.org/presenter.jhtml?identifier=3016889
  4. Thorax 58 (12), 1071-6, 2003
  5. Respiration 71(1):51-9, 2004
  6. Indian J Chest Dis Allied Sci 44 (1), 13- 9, 2002
  7. Am J Respir Crit Care Med 156 (3 Pt 1), 715-22, 1997
  8. Arch Environ Health 46 (3), 145- 149, 1991
  9. Am J Respir Crit Care Med 151 (1), 33-40,1995
  10. Am J Respir Crit Care Med 150 (4), 962-6, 1994
  11. Environ Health Perspect 103 Suppl 2, 103-5, 1995
  12. Mol Aspects Med 21 (1-2), 1-48, 2000
  13. Eur Respir J 11 (3), 686-93, 1998
  14. Res Rep Health Eff Inst 78, 1-37, discussion 81-99, 1997
  15. Am Rev Respir Dis 141 (2), 377-80, 1990
  16. Occup Environ Med 55 (1), 13-7, 1998
  17. Am J Epidemiol 149 (4), 306-14, 1999
  18. Am J Respir Crit Care Med 2002 Sep 1; 166 (5), 703-9
  19. J Appl Physiol 61 (3), 960-6, 1986

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