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There is convincing scientific evidence showing that ambient particulate matter (PM) is related to both short and long term health effects. Increased mortality and hospitalisation for cardiopulmonary causes have been noted in several studies evaluating the effects of PM10 or PM2.5 (PM <10 or 2.5 μm in diameter).1 However, urban air pollution consists of a complex mixture of gases and particulate agents that vary over time and through space, depending on its sources, distance and meteorological conditions.2 Much of the scientific interest has been devoted to the toxicology of the ultrafine fraction of airborne particles (<0.1 μm).3 These particles are usually emitted from combustion sources (eg, gasoline or diesel powered engines) or are formed from chemical conversion of gases in the atmosphere. They are relatively short lived and combine into larger particles between 0.1 and about 1 μm in diameter (accumulation mode). These particles tend to penetrate deeper in the alveolar part of the lung and have a larger surface area than larger sized particles, eliciting greater potential interaction with human tissues and a stronger inflammatory reaction. The epidemiological evidence linking ultrafine particles with respiratory health effects is still limited and controversial. In the current issue of Thorax, Halonen and colleagues4 provide new and compelling evidence on the respiratory effects of particles of various sizes that will certainly stimulate further research (see page 635).
Different sized particles were measured daily in Helsinki over a period of 7 years, and a source apportionment method was applied to separate the PM2.5 fraction from four sources (traffic, long range transport, soil and road dust, and coal/oil combustion). Daily counts of asthma emergency room visits among children, and asthma/chronic obstructive pulmonary disease (COPD) emergency room visits among adults and the elderly were collected. After careful control for time varying confounding factors, ultrafine particles, CO and NO2 were strongly associated with asthma in children with a delay of 3–5 days. In contrast, asthma and COPD in the elderly were clearly associated with larger particles (accumulation mode, PM2.5, coarse particles), and CO and NO2 at immediate lag (same day). Traffic related particles had a strong delayed effect on children’s emergency room visits for asthma whereas traffic related and long range transported particles had an immediate effect on asthma/COPD visits of the elderly.
There are several strengths of the paper: a new approach to study the effect of air pollution that combines specificity in the exposure assessment (daily measurements with a differential mobility particle sizer), consideration of the pollution sources and specificity in the age groups corresponding to different respiratory conditions. The authors also give interesting indications for understanding the toxicology of particulate matter. Two aspects need to be discussed in light of the differences between asthma and COPD regarding their baseline obstructive and inflammatory characteristics: the timing of the effects that characterise the response to air pollutants in patients with asthma and in COPD patients, and the difference in the size of the particles eliciting the effects.
Childhood asthma is characterised by reversible airflow obstruction, bronchial hyperresponsiveness and an underlying inflammation. The study by Halonen and colleagues4 stresses the delayed role of ultrafine particles on this condition. There are other epidemiological observations with similar findings. Two time series studies on emergency room visits or hospitalisations for childhood asthma in the USA5 and Copenhagen6 support the delayed effect of ultrafine particles. The delayed effects found in these studies, including the Finnish investigation, apparently are at odds with recent results from a field study in London where patients with asthma walking on Oxford Street had an immediate decline in lung function in response to fine and ultrafine particles from diesel traffic, higher that those walking in Hyde Park.7 A study by Delfino and colleagues8 indicated an immediate increase in exhaled nitric oxide (an established biomarker of airway inflammation) in children with asthma in relation to elemental carbon and other indicators of traffic related air pollution.
As Halonen and colleagues4 are aware, there are probably several reasons for the differences between studies that show an immediate effect on inflammation and lung function in patients with asthma and studies indicating a delayed effect on emergency room visits: there is a large underlying population distribution of asthma sensitivity and severity, asthma medication (inhaled bronchodilators and corticosteroids) may reverse the symptoms of air pollution and finally behavioural reasons may play a role, as not all families immediately recognise the severity of their child’s symptoms. Nevertheless, a real lag time is likely between exposure to ultrafine particles and acute respiratory symptoms requiring emergency care because inflammatory events in the lungs develop over a range of hours to days. In addition, ultrafine particles may increase bronchial reactivity, secondary to airway inflammation, which may subsequently trigger symptoms after exposure to a variety of other environmental exposures.9
Unlike asthma, COPD is associated with irreversible airways obstruction and chronic airways inflammation with increasing frequency and severity of exacerbations.10 Fine and large particles may act as inflammatory agents with an abrupt increase in airways resistance, and worsen expiratory flow limitation and dynamic hyperinflation. The declining clinical status may require prompt emergency care for more severe forms of the disease, especially when it is accompanied by cardiac dysfunction. Moreover, systemic inflammation in response to the oxidative stress induced by PM exposure has been suggested in patients with COPD11 ,12 that may be responsible for acute cardiovascular morbidity. It is not surprising then that several studies have found an acute effect of PM10 or PM2.5 on COPD emergency room visits or hospital care,13–16 although in some cases an effect was not found17 or a delayed lag was detected.18
As in most time series studies that measure daily variations in different air pollutants, fixed monitoring stations represent daily variations in overall population exposure. However, a differential exposure misclassification for different pollutants or size fractions may influence the results when the effects are compared. For example, vehicular traffic constitutes the most significant source of ultrafine particles near roads and the variability in exposure can be much higher than in background areas. Although Halonen and colleagues4 indicate a reassuringly high correlation between outdoor and indoor concentrations of ultrafine particles, these results need confirmation in other areas with different environmental and urban conditions.
The possibility of generalising the findings from this study to other urban contexts is limited because of the varying nature of the pollutant mix generated from traffic. Other areas in Europe tend to have a much higher proportion of diesel powered vehicles than Nordic countries. As has been already suggested,19 evaluating the health effects of particle size alone is difficult as it is not independent of its chemical composition. The different chemical compounds of PM (eg, transition metals) may contribute differently to the PM induced health effects. There is a need for a large data set that should include the size of the particles, their sources and their chemical composition. Although the study in Helsinki offers an important insight in this direction, it is a “one city” study and the results should be replicated in different contexts. Therefore, we are only approaching an understanding of the problem. What Europe clearly needs is a multi-city study, similar to the APHEA in the 1990s,20 to evaluate the short term health effects of particles of different size, their sources and compositions.21 The health data and ability to perform such studies are readily available, but time series of concentration levels of size fractions, chemical compositions and inventory of source contribution are not. While a large PM specialisation programme is ongoing in the USA,22 Europe is lagging behind.
The European Union has recently approved the new annual limit for PM2.5 (25 μg/m3) and a revision of the PM2.5 standard is foreseen for 2013. The EU conclusions have been controversial,23 as adverse health effects have been detected at a much lower level of fine particles, as in the Helsinki study. There are 5 years to develop an approach that characterises sizes, properties and sources of PM, and evaluate health effects while combining epidemiological, toxicological and clinical data.
Competing interests: None.