Children are most sensitive to modern air pollution

Max Wallis

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This debate got a poor send-off from the Commissioning Editor, Jennie Bristow when she sidelined the science by declaring concern is ‘driven less by pollutants in the atmosphere than by a broader cultural unease’ and then attacked the science-based children-and-health statements of the World Health Organisation (WHO).

Her declaring ‘air pollution has improved dramatically over the past 50 years’ was mistaken. Vehicle and particularly diesel fumes worsened in the last two decades; we’ve tackled the sulphur and lead, and are making headway on visible particles and NOx, but are not yet trying to abate the most dangerous ultrafine particles. Outside urban areas, we’re experiencing the highest ever levels of ozone (summertime smog). Current abatement plans (for the NOx and VOC precursors) for this Europe-wide pollutant are officially inadequate so Norman Baker is right to stress the problem.

‘Air pollution kills babies’ was the title of a 1999 Editorial in the journal Epidemiology. Though the message is slow to penetrate in the UK, evidence since 1999 has built up the case that outdoor air pollution is causally associated with infant mortality and adverse pregnancy outcomes.

Scientists did think in the ’90s that infant mortality increases with particulate levels only in exceptional places (Sao Paulo; Mexico; Czech Republic) but an international team led by Reinhard Kaiser (of Basel) has now found the same in a study of 23 US metropolitan areas. They found not only increased infant mortality from respiratory disease (normal weight babies) at higher levels of PM10 (24 per cent increase for PM10 in excess of a baseline) but also lesser increases in sudden infant death syndrome and in all-cause mortality.

Beate Ritz et al. (UCLA) find increased birth defects in California correlating with PM, while Liu et al. (Canada) find retarded foetal development correlates with increased NO2 and CO in Vancouver. Kaiser and co-authors conclude ‘air pollution-related infant mortality is a major public health problem’.

Jennie Bristow also derides the WHO figures of up to 13,000 deaths from air pollution of European 1-4 year olds, supposing without evidence that existing respiratory conditions are aggravated (ie, the excuse of early ‘harvesting’ of weaklings. It’s likely that there are actually more numerous deaths and they are accompanied by non-fatal birth defects, and early development of respiratory conditions in far greater numbers. Infant lungs are now shown to be far more susceptible to air toxins than are adult lungs.

The study by Rob McConnell et al. ‘Asthma in exercising children exposed to ozone’ (Lancet 2002; 359:386-91) has been cited in this debate by Austin Williams. It hit the headlines in 2002 for its evidence that, contrary to conventional wisdom, ozone is involved in the development of new onset asthma. This was sufficient for the north American authorities to caution on children taking part in vigorous sport during pollution episodes, but the UK authorities were unmoved. Stephen Holgate’s personal assessment should not determine the UK’s stance; the issue confronts us – when is evidence sufficient to give cautionary advice under the precautionary principle and should this be determined by an open participative process (whether or not COMEAP changes its past judgement)?

The WHO Children’s Environment and Health Action Plan for Europe (CEHAPE) adopted by the Budapest Ministerial conference in June is important because it accepts that children’s health is more sensitive and vulnerable to environmental factors. We can no longer assume children are represented by healthy adults, but need to set air pollution standards protective of children.

The UK’s health and air quality ministers did attend at Budapest and our Health Protection Agency is to take the CEHAPE (“see-happi”) plan forward. Let’s hope a child-centred approach will change the official culture of denial.

Max Wallis, UK

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