The neurological effects of air pollution in children

Environmental exposures in utero and during early life may permanently change the body's structure, physiology and metabolism, and lead to diseases in adult life 1. Infants are particularly vulnerable because of their rapid growth and cell differentiation, immaturity of metabolic pathways and development of vital organ systems. The central nervous system has unprotected barriers and a broad time window of conformation, leading to a long period of vulnerability in the developmental process and to susceptibility to any environmental insult 2. Research conducted among a limited series of pollutants (including lead, mercury and polycyclic aromatic hydrocarbons (PAH)) shows that early-life exposure to chemicals at current environmental levels can be neurotoxic years or even decades after exposure 3.

Traffic-related air pollution, basically urban outdoor pollution, is a global public health problem 4. Cardiorespiratory effects and mechanisms have been fully investigated 5. In contrast, little is known regarding neurological effects, with only some preliminary evidence. In rats, ultrafine carbon particles have been found in the olfactory bulb and the cerebrum and cerebellum after inhalation exposure 6; this finding has been reproduced more recently with manganese particles directly translocated to the olfactory nerve from the nose to the brain 7. In one study, dogs living in a highly polluted region in Mexico City (Mexico) had an increase in brain inflammation compared with animals living in a less polluted area 8. The brain tissue of animals from Mexico City had higher levels of nuclear factor-{kappa}B activation and nitric oxide production, as well as the principal pro-inflammatory cytokines interleukin (IL)-1 and tumour necrosis factor (TNF)-{alpha}, compared with the animals from the nonpolluted area 9. In a study on human autopsies in Mexico City, exposure to severe air pollution has been associated with increased levels of cyclooxygenase (COX)-2 and accumulation of the 42-amino-acid form of β-amyloid, a cause of neuronal dysfunction 10.

There are two small studies in children from the general population exposed to urban air. The first study related PAH in particulate form, as collected with individual pumps during two consecutive days in 181 pregnant women from New York City (NY, USA), to mental health measured at age 3 yrs in their offspring 11. The short measurement of the exposure (only 2 days), their narrow variability (only low and high levels), and the poor specificity of PAH (the principal source is smoking) resulted in preliminary research that is not very conclusive. The second study related average air pollution exposure during childhood (carbon particles at home address derived by spatial modelling) to intelligence at age 9 yrs in 202 children from Boston (MA, USA) 12. The study, however, followed only 20% of those recruited and did not measure prospectively the variations in air pollution or the time-activity patterns of the participants. The two studies adjusted for potential confounders, such as socio-economic conditions or internal doses of lead, but failed to adjust for other factors, such as noise. Overall, these two studies were the first to translate into humans the evidence suggested in animal studies, but their deficiencies in size and design call for larger and more detailed research.