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On asthma and allergies
[21-Jun-2004]
‘The enormous increase in asthma prevalence in the Western world over the past 30 years cannot be explained by changes in ambient air pollution.’
Stephen Holgate
MRC clinical professor of immunopharmacology
We are in the midst of an epidemic of allergic disease in 2004.

The UK is at the top of the league table for asthma in 13-14 year olds with almost one third reporting symptoms in the past 12 months. These alarming figures are paralleled by allergic rhinitis, eczema, food allergy, drug allergy and life-threatening anaphylaxis. According to recent UK data, one in 70 children is allergic to peanuts, an allergy that has trebled in the past four years; hospital admission for anaphylaxis has increased sevenfold in the past decade.

It is frequently stated that at least for asthma these disturbing trends are caused by air pollution. While outdoor pollutants such as ozone and particulates (especially from diesel vehicles) can make asthma worse by increasing airway inflammation in a sensitive group of people, evidence for their role in creating new asthma in previously unaffected individuals is highly controversial. Some recent facts are:

  1. Diesel particulates increase the formation of the allergic antibody (IgE) and can also increase sensitisation to commonly encountered allergens in the air.

  2. In children, ozone, particulates and possibly NO2 exposure that are mostly derived from traffic pollutants are associated with a small but detectable reduction in lung growth in children.

  3. Exposure to pollutants increases the expression of bronchitis in children.

  4. Air pollution increases the effects of respiratory virus infection in asthmatic children.

  5. Variation in genes that either protect from or augment the damaging effects of pollutants on the lung are being identified.

  6. In non-human primates, exposure to ozone at levels encountered in air pollution episodes produces structural changes in the lung favouring an asthmatic state, especially when there is a simultaneous exposure to allergens, for example from dust mites.

  7. There are a few longitudinal population-based studies which suggest that a small increase in asthma could be caused by pollution - for example, ozone in California, oxides of nitrogen and particles in Japan and derivatives of chlorine in swimming pools, as well as increased reporting of asthma symptoms in those close to busy roads.

The enormous increase in asthma prevalence over the past three decades seen in the UK and elsewhere in the Western world cannot be explained by changes in ambient air pollution. While it is not possible to rule out in its entirety a contribution played by outdoor air pollution as an inducer of new asthma, available evidence points to no or at most minimal effects. Countries such as New Zealand, Australia and Canada, which have some of the best air quality in the world, are only a little behind the UK in their high asthma and allergy prevalence.

Lifestyle differences are far more likely to be responsible for the increase in allergy. These include:

  1. Increase in allergen exposure (for example, to dust mites, moulds, pet allergens) in 'tight' centrally heated houses, and exposure to new allergens, such as latex and household medicines.

  2. Allergy favours the higher social classes and small families.

  3. Allergy is greater in urban versus rural environments, with considerably less allergy occurring in children raised on livestock farms.

  4. There is reduced allergy in developing countries but in all cases this is increasing as they adopt a number of Western habits, including housing and diet.

  5. There is less allergy in those with previous infections such as measles, hepatitis A, B and C, Toxoplasmosis and Helicobacter pylori; when individuals are infected with parasites such as round worm or hookworm; or in children attending day care centres from infancy where they are exposed to respiratory infections.

  6. There is less allergy in children exposed to anthroposophical factors (for example, Steiner schools).

Taken together these findings suggest that early life exposure to micro-organisms or their products, whether inhaled or ingested, are important in protecting against allergy by stimulating special 'toll' or 'pattern recognition' receptor on immune cells, directing our early immune response towards greater protection against allergy.

This 'hygiene hypothesis' is attractive in connecting the Western dominance and rising trends of allergy with changing behaviour, but most of the studies listed above fit better for allergy than for asthma. Thus, while allergy contributes to asthma, in itself it is insufficient to cause chronic asthma. So what other factors could be involved?

A strong focus is being directed to diet and obesity, as two factors that have changed dramatically in Western society over the past 30 years - there has been a reduction in fruit/vegetable and associated anti-oxidant intake, and there is also more overeating, with attendant changes to hormones linked to both weight gain and the immune response, such as leptin. Other possibilities include environmental influences on the developing baby in the uterus. Maternal tobacco smoking in pregnancy is a clear predisposing factor for the development of asthma and allergy in the offspring.

However, rather than assessing these effects of air pollution at a population level, what we need are studies taking into account vulnerable subgroups either subjected to high pollutant exposures or those genetically susceptible. Understanding how pollutants interact with the developing and as well as the fully developed lung in children has advanced considerably in recent years. In the developing lung and in early childhood the protective metabolic pathways against pollutants are immature, making this period one of increased vulnerability.

A shift in the size and chemical composition of outdoor air pollution related to increased use of diesel-powered vehicles is also a cause for concern, despite the green image portrayed for diesel in relation to CO2 emission and global warming. The ability of ultrafine particles to penetrate deep in the lung and then into the tissue itself exposes mechanisms of enhancing respiratory disease not previously conceived. Because we know so little about the effects of these on human health there is an urgent need to undertake further research on the short- and long-term effects of these highly reactive ultrafine particles on human lungs. In animals, the toxicity of this ultrafine fraction is directly related to surface area which is orders of magnitude greater than with traditional suspended particulate.

To conclude, it is likely that both asthma and allergy have increased to epidemic proportions in the UK for multiple reasons, linked to lifestyle changes over the past 30 years. There is recent evidence that in the UK the high prevalence figures for asthma have plateaued, but this is not true of other allergic conditions like nut and latex allergy.

While there are factors driving asthma that are not involved in the causation of allergy and vice versa, the two when combined conspire to reveal asthma symptoms in those genetically at risk. Air pollution may contribute, but available evidence to date suggests that if this is the case, the effect is small.

Stephen Holgate is Medical Research Council clinical professor of immunopharmacology, based at the University of Southampton.

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The head-to-head
Stephen Holgate
University of Southampton
Mike Pilling
Distributed Institute for Atmospheric Composition
Bjorn Lomborg
author of The Skeptical Environmentalist
Tony Juniper
Friends of the Earth
Jennie Bristow
spiked
Robert Maynard
UK Dept. of Health
Austin Williams
Future Cities Project
Frank Murray
Murdoch University
Mark Jackson
University of Exeter
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UK Air Pollution Information System

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Encyclopedia of the Atmospheric Environment
Manchester Metropolitan University


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