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Gases from fossil fuel combustion: a danger to infants?
  1. J Grigg
  1. Correspondence to:
    Dr J Grigg
    Division of Child Health, Department of Infection, Immunology and Inflammation, University of Leicester, PO Box 65, Leicester LE2 7LX, UK; jg33le.ac.uk

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Commentary on the paper by Klonoff-Cohen et al (see page 750)

The combustion of fossil fuels generates a complex mixture of gases, particles and chemicals, many of which have the potential to impair human health.1 In older adults, epidemiological studies have consistently shown increased cardiovascular mortality associated with increased levels of air pollution.2 There is also concern, acknowledged by regulatory authorities, that very young children represent another vulnerable population. Many of the factors that could increase the vulnerability of young children to air pollution remain speculative. One known variable is that infants have a higher minute ventilation relative to lung surface area.3 Thus for the same pollutant concentration, infants’ airways will receive a higher exposure than adults. However, paediatric mortality associated with air pollution has not, until recently, been regarded as a major issue. The paper by Klonoff-Cohen and colleagues4 in this issue is therefore of particular interest. In this case-control study the authors found that monthly sudden infant death syndrome (SIDS) counts tracked with monthly averaged outdoor nitrogen dioxide (NO2) concentrations, and that high levels of NO2 over the preceding 24 hours was a significant risk factor for SIDS. Effects were also observed for carbon monoxide (CO), but these were less consistent.

NO2 is not the most potent gaseous oxidant, and causes less airway inflammation than ozone.5 Recent research has therefore focused primarily on other pollutants. However, all combustion processes in air directly produce oxides of nitrogen (for example, NO2 and NOx). NO2 is also formed when nitrogen oxide (NO), emitted from vehicle exhausts, reacts with atmospheric ozone. Thus winter NO2 peaks are associated with low wind speeds and temperature inversions, whereas summer NO2 peaks are associated with ozone peaks during hot sunny days. In the UK, half of NO2 emissions are from road transport, and emissions have fallen from 2744 kt in 1990 to 1728 kt in 2000. Widespread exceedences of the 40 μg/m3 annual mean limit remain, and are projected to continue over the next decade.6 A causal relation between NO2 and SIDS would therefore be an important stimulus for NO2 reduction strategies. However, as Klonoff-Cohen and colleagues4 acknowledge, there are some important limitations to their data. First, individual exposure was at best approximate, with concentrations in some cases extrapolated for monitoring stations several kilometres from the home. Nerriere and colleagues7 compared personal NO2 exposure with extrapolated levels from central monitoring stations, and concluded that ambient NO2 concentrations should be used “with caution” in assessing individual exposure—rightly pointing out that a major source of NO2 is gas cooking. Second, the association between NO2 and SIDS may be confounded by correlated pollutants such as inhaled particles,8 or an unrecognised social variable with a high spatial correlation with outdoor NO2. Indeed, concomitant emissions of NO2 and CO from vehicle exhausts9 may account for the association between CO and SIDS. Third there is no biological explanation for a mechanism of interaction between NO2 and SIDS, although in the past uncertainty about mechanisms has not been a barrier to successful SIDS reduction interventions.10 One possible explanation is that NO2 alters the pulmonary immunological response to trivial viral infections—an interaction that has been reported for asthmatic children.11 Nevertheless, Klonoff-Cohen and colleagues’ study,4 whose findings are compatible with a recent Canadian report which found a significant association between daily rates of SIDS and increased NO2 (and SO2) on the previous day,12 should help to refocus researchers’ attention on gaseous pollutants, and young children as an important vulnerable age group. The methodological issues of research in this age group are challenging,12 but newly developed computer models which calculate gaseous emissions and their dispersion at the spatial level of individual households,13 may allow reanalysis of pre-existing birth cohort datasets. Until more data become available, no specific recommendations can be given to parents who are concerned about reducing the risk of SIDS. Wide variations in NO2 occur within small spatial areas, and both avoiding exposure and living a normal life is virtually impossible. It may well be that regulators concerned about the potential health impact of NO2 on young infants should not concentrate on this single pollutant, but aim to reduce all combustion products emitted within suburban areas. However, when developing exposure reduction policies, data on the association between NO2 and SIDS will be important in any health impact analysis.

Commentary on the paper by Klonoff-Cohen et al (see page 750)

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  • Competing interests: none

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