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Diesel Particles In Air Slow Kids' Lung Development

An Austrian study covering almost 900 schoolchildren, whose results are published in the latest issue of the European Respiratory Journal (ERJ) shows that exposure to particulate matter such as that emitted during diesel combustion impacts adversely on respiratory pathway development in children.

The article's authors estimate that 35,000 avoidable asthma attacks are caused by this effect every year in Austria alone.

It was already known that air pollution in general, especially the solid particles emitted by diesel engines and domestic heating, were harmful to the lungs and caused increased levels of hospitalization for respiratory and cardiac problems, more frequent asthma attacks and higher death rates.

Dutch, American and Austrian teams have shown, for example, that sharp increases in the level of particles with a diameter of 10 microns or less (PM10) had an immediate impact on lung function.

There was much less evidence regarding the impact of such pollution on children's lung growth and thus, indirectly, on their future lung function.

Dr. Thomas Frischer and his team from the University of Vienna Children's Hospital in Vienna set out to overcome that gap by examining how, over a long period, such solid particle pollution could affect children's lung growth.

For their study, they took eight sites selected previously by the Governmental Air Pollution Surveillance Agency of Lower Austria, situated at between 161 and 738 meters above sea level.

Industrial sites and those next to very busy roads were deliberately excluded, as were those for which the data on solid particle levels were lacking. Five of the sites were in rural locations.

The children were registered at schools selected for each site by the local authorities. A total of 975 children between the ages of eight and eleven were thus included in the Frischer study and 860 eventually underwent all of the planned investigations.

Each child's respiratory function was examined twice a year, in spring and early autumn, for a three-year period.

At the same time, their parents were questioned about their smoking habits, their child's respiratory symptoms and all allergic reactions (these were also tested by means of two skin tests to measure sensitivity to seven common aeroallergens).

In parallel to these clinical data, air temperature and sulfur dioxide, nitrogen dioxide and ozone levels were continuously measured, while levels of solid particles with a diameter of 10 microns or less (PM10) were measured every fortnight.

The intervals between the two annual examinations of lung function thus corresponded to two periods of pollution (summer and winter).

The data published in this month's ERJ show that while ozone levels peaked in summer and concentrations of sulfur dioxide and nitrogen dioxide were higher in winter, particle concentrations varied between 10.6 and 30.4 micrograms per cubic meter according to region, with summer and winter averages of 17.36 and 21.03 micrograms per cubic meter respectively.

This level of solid particles in the air had a very clear adverse impact during the three summers of the study, particularly on two key parameters used to measure lung function growth in children.

The first is the well known peak expiratory flow (PEF), which could be expected to increase every year as the child's major airways broadened. Following the elimination of potential influence by different variables, it became clear that an increase in solid particle pollution of 10 micrograms per cubic meter held back PEF increase by 84 millimeters per year.

Naturally, the impact of solid particles was greater in summer, when children tend to enjoy games and other activities in the open air. Fortunately, though, particle concentrations were at their lowest during the summer season.

The second lung function parameter used by the Frischer team was what specialists call mid expiratory flow (MEF25-75), which reflects the growth of the small airways.

This was also adversely affected by summer PM10 levels, as demonstrated by the ERJ figures. Following adjustment, it was found that an increase in solid particle levels of 10 micrograms per cubic meter held back MEF25-75 growth by 329 ml/sec per year of exposure.

These damaging effects of particle pollution clearly compound those of nitrogen dioxide and ozone.

Dr. Frischer emphasizes in the article that, while the slowing of lung function growth caused by particle pollution is obviously too weak to have acute consequences, it can have significant long-term consequences for those exposed as children.

Above all, these disturbances can cause respiratory problems in subjects already suffering from reduced lung function.

Frischer estimates, based on other studies done elsewhere, that particle exposure leads to some 35,000 asthma attacks every year in Austria alone.

Moreover, a reduction of lung growth is a significant risk factor for accelerated lung function decline. This, in turn, can provoke the early development of chronic obstructive pulmonary disease (COPD).

"These results are all the more alarming because these children have already been exposed to this pollution for some eight years. Our data should encourage government bodies to take more interest in the chronic as well as the short-term effects of air pollution," Frischer adds.

It is true that air pollution standards are based only on acute effects. "What's more", he adds, "our results show that regulations need to be developed specifically to limit solid particle exposure."

Such measures can be expected to be difficult to implement. Yet they will certainly contribute to minimizing the many cardiovascular and respiratory effects of exposure to diesel gas, to which no age group is immune, according to the article.

[Contact: Prof. Thomas Frischer]

10-May-2002

 

 

 

 

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