Posted: June 28, 2005
Science of Sport: Air Pollution
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
- www.apheis. net
- Monaldi Arch Chest Dis 57 (3-4), 156- 60, 2002
- www.americanheart.org/presenter.jhtml?identifier=3016889
- Thorax 58 (12), 1071-6, 2003
- Respiration 71(1):51-9, 2004
- Indian J Chest Dis Allied Sci 44 (1), 13- 9, 2002
- Am J Respir Crit Care Med 156 (3 Pt 1), 715-22, 1997
- Arch Environ Health 46 (3), 145- 149, 1991
- Am J Respir Crit Care Med 151 (1), 33-40,1995
- Am J Respir Crit Care Med 150 (4), 962-6, 1994
- Environ Health Perspect 103 Suppl 2, 103-5, 1995
- Mol Aspects Med 21 (1-2), 1-48, 2000
- Eur Respir J 11 (3), 686-93, 1998
- Res Rep Health Eff Inst 78, 1-37, discussion 81-99, 1997
- Am Rev Respir Dis 141 (2), 377-80, 1990
- Occup Environ Med 55 (1), 13-7, 1998
- Am J Epidemiol 149 (4), 306-14, 1999
- Am J Respir Crit Care Med 2002 Sep 1; 166 (5), 703-9
- J Appl Physiol 61 (3), 960-6, 1986
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