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Sizing up the evidence

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Vehicle exhausts—major contributors to polluted air—are detrimental to children's health, as epidemiological and experimental evidence reviewed by Grigg in Archives of Disease in Childhood shows.

Diesel exhaust particles—a carbon core plus any number of adsorbed high molecular weight substances—are the primary particles in polluted air. Particulate matter (PM), comprising coarse, ≤10 μm (PM10); fine, ≤2.5 μm (PM2.5); and ultrafine, ≤ 0.1 μm (UF) particles, are inhaled and the smallest penetrate to the alveoli. Vehicle exhausts and other fuel emissions produce fine and ultrafine particles, and the more technically advanced engines can generate more ultrafine particles.

According to large epidemiological studies total infant mortality is associated with exposure to PM10. Short term effects on lung function are considered small in healthy children but greater with underlying respiratory disease, and these may be underestimated because of confounders and imprecise measures of individual exposure. Studies of children living by roads—affording a better indication of individual exposure—conflict owing to insufficient control of confounders and because GPs not paediatricians see most children with respiratory health problems. Experimental data show that cytokines and proinflammatory mediators are induced in lung cells by diesel exhaust particles in vitro, and in children the ultrafine component reaches alveolar macrophages.


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Electron micrograph of diesel particles from a vehicle exhaust pipe, showing carbonaceous ultrafine particles singly and in aggregates. Bar=100nm.

A prospective birth cohort study with optimum measures of individual exposure and respiratory function would establish whether PM10 causes disease as well as worsening it.

Once the size of the effects and the most toxic fraction are known, unravelling how these particles cause harm will be possible and, maybe, whether they initiate asthma.

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