Eur Respir J 2008; 32: 535–537

DOI: 10.1183/09031936.00073708
CopyrightßERS Journals Ltd 2008

EDITORIAL

The neurological effects of air pollution in children

J. Sunyer*,#,"

nvironmental exposures in utero and during early life consecutive days in 181 pregnant women from New York City

E may permanently change the body’s structure, physiol-

ogy and metabolism, and lead to diseases in adult life [1].
Infants are particularly vulnerable because of their rapid growth
(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
and cell differentiation, immaturity of metabolic pathways and the poor specificity of PAH (the principal source is smoking)
development of vital organ systems. The central nervous system resulted in preliminary research that is not very conclusive. The
has unprotected barriers and a broad time window of conforma- second study related average air pollution exposure during
tion, leading to a long period of vulnerability in the developmental childhood (carbon particles at home address derived by spatial
process and to susceptibility to any environmental insult [2]. modelling) to intelligence at age 9 yrs in 202 children from
Research conducted among a limited series of pollutants (includ- Boston (MA, USA) [12]. The study, however, followed only 20%
ing lead, mercury and polycyclic aromatic hydrocarbons (PAH)) of those recruited and did not measure prospectively the
shows that early-life exposure to chemicals at current environ- variations in air pollution or the time-activity patterns of the
mental levels can be neurotoxic years or even decades after participants. The two studies adjusted for potential confoun-
exposure [3]. ders, such as socio-economic conditions or internal doses of
lead, but failed to adjust for other factors, such as noise. Overall,
Traffic-related air pollution, basically urban outdoor pollution, these two studies were the first to translate into humans the
is a global public health problem [4]. Cardiorespiratory effects evidence suggested in animal studies, but their deficiencies in
and mechanisms have been fully investigated [5]. In contrast, size and design call for larger and more detailed research.
little is known regarding neurological effects, with only some
preliminary evidence. In rats, ultrafine carbon particles have THE LUNG AND THE UNDERLYING MECHANISMS
been found in the olfactory bulb and the cerebrum and Oxidative stress, changes in autonomous function and progres-
cerebellum after inhalation exposure [6]; this finding has been sion of atherosclerosis have been hypothesised to be mechanisms
reproduced more recently with manganese particles directly of the neurological effect of urban air pollution in humans at any
translocated to the olfactory nerve from the nose to the brain [7]. age [13]. Among them, inflammation secondary to oxidative
In one study, dogs living in a highly polluted region in Mexico stress appears to be the major suspected culprit for delay in
City (Mexico) had an increase in brain inflammation compared conformation and maturation during developmental steps. Even
with animals living in a less polluted area [8]. The brain tissue of though most of the available research about the inflammatory
animals from Mexico City had higher levels of nuclear factor-kB effects of air pollution refers to the lungs, there is evidence that
activation and nitric oxide production, as well as the principal the oxidative stress and inflammation induced by particles
pro-inflammatory cytokines interleukin (IL)-1 and tumour translates systemically beyond the lungs [14]. For example, we
necrosis factor (TNF)-a, compared with the animals from the found in an international longitudinal study of 1,003 adult
nonpolluted area [9]. In a study on human autopsies in Mexico subjects that particle count increased markers of systemic
City, exposure to severe air pollution has been associated with inflammation (IL-6 and fibrinogen peripheral levels) [15].
increased levels of cyclooxygenase (COX)-2 and accumulation
of the 42-amino-acid form of b-amyloid, a cause of neuronal The major underlying hypothesis is that chronic respiratory
dysfunction [10]. tract inflammation may lead to brain inflammation by altering
levels of circulating cytokines, such as TNF-a and IL-1. These
There are two small studies in children from the general cytokines have the ability to upregulate COX-2, a potent active
population exposed to urban air. The first study related PAH in mediator of inflammation, in capillary brain endothelium [16].
particulate form, as collected with individual pumps during two Changes in brain cytokine and chemokine expression in mice
have been directly linked to intranasal exposure to ultrafine
carbon [17]. Carbon particles themselves generally adsorb
*Centre for Environmental Epidemiological Research (CREAL), #Municipal Institute of Medical transition metals (including antimony, barium, copper, iron
Research (IMIM), Universitat Pompeu Fabra, Barcelona, and "El Centro de Investigación Biomédica and zinc) emitted from traffic exhaust and also from tyres and
en Red de Epidemiologı́a y Salud Pública (CIBERESP), Spain. brake wear. These metals, which are mainly generated by
SUPPORT STATEMENT: J. Sunyer has received funds for research from the European Union, the traffic in the current urban atmospheres [18], have been shown
government of Spain and Catalonia, and La Caixa Fundation. to induce oxidative stress in the lung [16].
STATEMENT OF INTEREST: None declared. An alternative hypothetical mechanism of the neurological
CORRESPONDENCE: J. Sunyer, CREAL-IMIM, Dr Aiguader 88, 08003 Barcelona, Spain. Fax: 34
933160575. E-mail: jsunyer@imim.es
effect of air pollution is based on the observation that ultrafine
particles containing metals translocate directly to the brain, c
EUROPEAN RESPIRATORY JOURNAL VOLUME 32 NUMBER 3 535
NEUROLOGICAL AIR POLLUTION EFFECTS IN CHILDREN J. SUNYER

without entering the lung [7]. Changes in cognitive function in individual exposure to air pollutants and antioxidants, and of
children have been shown to be associated with relatively low the genetic contribution) to further investigate the suspicion that
internal doses of lead [19] and mercury [3]. In addition to being our urban air is neurotoxic for our children.
linked to cognitive deficits in children, lead has been related to
a diversity of behavioural problems (reading problems, school
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