Alzheimer’s Risk Gene May Aggravate Neurological Air Pollution Effects in Children

Summary: According to researchers, children who carry the APOE4 gene and who are exposed to air pollution have higher behavior problem scores and their attention capacity was slower to develop.


There is growing evidence that exposure to air pollution adversely affects cognitive and behavioural development in children. However, the mechanisms underlying this association are, as yet, unknown. Now, the findings of a new study from the Barcelona Institute for Global Health (ISGlobal), an institute supported by the “la Caixa” Banking Foundation, suggest that the ε4 variant of the APOE gene may play a significant role in this process. The study has been published in the journal Environmental Health Perspectives.

Previous studies carried out within the framework of the BREATHE project have linked childhood exposure to air pollution with diminished cognitive development, increased behavioural problems, and even structural differences in the brains of the children studied.

In the new study, which analysed data from over 1,600 children attending 39 schools in Barcelona, scientists observed that the association between exposure to traffic-related pollution and adverse effects on neurodevelopment was more marked in the children who carried the ε4 allele of the APOE gene. Carriers of this genetic variant had higher behaviour problem scores and their attention capacity developed more slowly. Moreover, the volume of the caudate nucleus, an anatomical brain structure, tended to be smaller in that population.

“These findings suggest that children who carry this allele could be more vulnerable to the detrimental effects that air pollution has on important aspects of their neurodevelopment,” explained Silvia Alemany, ISGlobal researcher and lead author of the study

Neurodegenerative Diseases

“Systemic inflammation and oxidative stress are two of the most well-established mechanisms underlying the adverse health effects of air pollution. Interestingly, both these mechanisms are also involved in the pathogenesis of dementia. In fact, research has demonstrated an association between exposure to air pollution and cognitive impairment in older people. All these considerations, and the fact that APOE ε4 is the most important known genetic risk factor for Alzheimer’s disease, led us to wonder whether the allele might also have a relationship with the adverse effects air pollution has on brain function in children,” says Silvia Alemany.

Participants at the BREATHE project in Barcelona (Spain) take computerised tests. image is credited to Barcelona Institute for Global Health (ISGlobal).

Genetic data were available for all of the participants. Tests were carried out to evaluate cognitive functions, behavioural problems and possible symptoms of attention deficit hyperactivity disorder. Traffic-related air pollution levels were calculated on the basis of actual measurements. Magnetic resonance imaging data were available for 163 of the study participants.

“More research will be needed in other populations to replicate these results and we need to establish whether this possible genetic vulnerability also applies to exposure to air pollution during earlier stages of development, for example, in the prenatal period,” warns ISGlobal researcher Jordi Sunyer, director of the BREATHE project. “In any case, once again the findings are clear: it is essential to implement measures to reduce traffic in the urban environment and, particularly, in places where children are present, such as the areas around schools.”.

About this neuroscience research article

Funding: European Research Council, Generalitat de Catalunya, La Caixa Foundation, Instituto de Salud Carlos III, Spanish Ministry of Economy and Finance funded this study.

Source: Pau Rubio – ISGLOBAL
Publisher: Organized by
Image Source: image is credited to Barcelona Institute for Global Health (ISGlobal).
Original Research: Open access research for “Traffic-Related Air Pollution, APOE ε4 Status, and Neurodevelopmental Outcomes among School Children Enrolled in the BREATHE Project (Catalonia, Spain)” by Silvia Alemany, Natàlia Vilor-Tejedor, Raquel García-Esteban, Mariona Bustamante, Payam Dadvand, Mikel Esnaola, Marion Mortamais, Joan Forns, Barend L. van Drooge, Mar Álvarez-Pedrerol, Joan O. Grimalt, Ioar Rivas, Xavier Querol, Jesus Pujol, and Jordi Sunyer in Environmental Health Perspectives. Published August 2 2018.

Cite This Article

[cbtabs][cbtab title=”MLA”]ISGLOBAL”Alzheimer’s Risk Gene May Aggravate Neurological Air Pollution Effects in Children.” NeuroscienceNews. NeuroscienceNews, 6 September 2018.
<>.[/cbtab][cbtab title=”APA”]ISGLOBAL(2018, September 6). Alzheimer’s Risk Gene May Aggravate Neurological Air Pollution Effects in Children. NeuroscienceNews. Retrieved September 6, 2018 from[/cbtab][cbtab title=”Chicago”]ISGLOBAL”Alzheimer’s Risk Gene May Aggravate Neurological Air Pollution Effects in Children.” (accessed September 6, 2018).[/cbtab][/cbtabs]


Traffic-Related Air Pollution, APOE ε4 Status, and Neurodevelopmental Outcomes among School Children Enrolled in the BREATHE Project (Catalonia, Spain)

Traffic-related air pollution is emerging as a risk factor for Alzheimer’s disease (AD) and impaired brain development. Individual differences in vulnerability to air pollution may involve the ε4 allele of Apolipoprotein E (APOE) gene, the primary genetic risk factor for AD.

We analyzed whether the association between traffic air pollution and neurodevelopmental outcomes is modified by APOEε4 status in children.

Data on parent-reported behavior problems (total difficulties scores, Strengths and Difficulties Questionnaire), teacher-reported attention-deficit hyperactivity disorder (ADHD) symptom scores, cognitive performance trajectories (computerized tests of inattentiveness and working memory repeated 2–4 times during January 2012–March 2013), and APOE genotypes were obtained for 1,667 children age 7–11 y attending 39 schools in or near Barcelona. Basal ganglia volume (putamen, caudate, and globus pallidum) was measured in 163 of the children by MRI (October 2012–April 2014.) Average annual outdoor polycyclic aromatic hydrocarbons (PAHs), elemental carbon (EC), and nitrogen dioxide (NO2) concentrations were estimated based on measurements at each school (two 1-wk campaigns conducted 6 months apart in 2012).

APOEε4 allele carriers had significantly higher behavior problem scores than noncarriers, and adverse associations with PAHs and NO2 were stronger or limited to ε4 carriers for behavior problem scores (P-interaction 0.03 and 0.04), caudate volume (P-interaction 0.04 and 0.03), and inattentiveness trajectories (P-interaction 0.15 and 0.08, respectively). Patterns of associations with the same outcomes were similar for EC.

PAHs, EC, and NO2 were associated with higher behavior problem scores, smaller reductions in inattentiveness over time, and smaller caudate volume in APOEε4 allele carriers in our study population, and corresponding associations were weak or absent among ε4 noncarriers. These findings support a potential role of APOE in biological mechanisms that may contribute to associations between air pollution and neurobehavioral outcomes in children.

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