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Article by: Katherine Lawless

Air pollution and cognitive dysfunction: uncovering the TRAP

2019-07-12

When you are on your morning commute to work, whether you drive or ride the bus, you might not realize that you are exposed to traffic-related air pollution (TRAP). When people think of air pollution, factory emissions are the first that come to mind. However, the most contributing factor to air pollution happens to be right in your neighbourhood: vehicles.[1],[2]

Traffic emissions have a high correlation of elemental carbon (EC), equivalent to black carbon, and nitrogen dioxide (NO2), as well as PAHs (polycyclic aromatic hydrocarbons) which are known to be released by emission such as gasoline.[2]

The TRAP effect

Exposure to TRAP has a detrimental effect on cognitive and behavioral development outcomes in children. Prenatal exposure to PAHs has been associated with cognitive developmental delays in children by age 3 and decreased intelligence by age 5. PAHs have also been characterized with symptoms of anxiety, depression, and attention problems from ages 6 to 7. Other studies have also found that there is a worse cognitive performance among those exposed to high levels of NO2 near their schools. TRAP has also been associated with cognitive impairment with the elderly.[2]

TRAP and the link to APOE ε4

APOE is a protein, encoded by the APOE gene, that is a major lipid transporter expressed in the brain and is involved in the mechanism of neurogenesis plasticity and neural repair. Calderon-Garciduenas et al. discovered that children who carried the APOE ε4 allele, which has been commonly associated with Alzheimer’s disease, inhibited the children’s ability to achieve and consolidate cognitive and behavioural function when exposed to air pollution.[1],[2]

According to Alemany S et al. ε4 carriers (25% of the population) are less efficient than non-carriers in transporting cholesterol and lipids, which are important for maintaining synaptic integrity and plasticity. ε4 carriers also have enhanced Alzheimer’s disease and are more vulnerable to neuroinflammation and oxidative stress induced by air pollution exposure.[2]

Recent discoveries:

  • Schikowski et al (2015): Exposure to air pollution was associated with decreased performance in neuropsychological tasks among the ε4 carriers. [3]
  • Cacciottolo et al (2017): Female carriers of the ε4 allele were shown to have stronger associations to TRAP and dementia risk compared to the other allele types of APOE. [4]

A group in Spain wanted to extend these findings by examining the relationship between neurodevelopmental outcomes, APOE ε4, and TRAP in school children in Barcelona.[1]

The BREATHE Project

In Barcelona, Spain, Alemany S et al. launched the BREATHE project to study the TRAP effects on the neurodevelopment of a cohort of primary school children from schools in areas that have a high correlation of EC and NO2 levels, due to high traffic emissions. They collected 1667 Oragene•DNA saliva samples for genotyping. As a result of the analysis, they found 384 children to be ε4 carriers.[2]

They selected 39 primary schools to maximize the contrast in TRAP levels. They measured the exposure to outdoor PAHs, EC, and NO2 at each school. Starting in 2012, they analyzed the behavioural outcomes based on behavioural problem scores and attention deficit-hyperactivity disorder (ADHD) symptoms. They assessed cognitive function including attentiveness and working memory trajectories by having the children complete a number of tests. They also assessed the children’s brain function by performing a series of Magnetic Resonance Imaging (MRI).[2]

Results

Alemany S et al. discovered that school TRAP exposures were associated with significantly worse behaviour problems and smaller reductions in attentiveness over time among the APOE ε4 carriers. Differences between carriers and non-carriers on the ADHD and working memory scores were non-significant and had only borderline effects with NO2 and PAHs, however, a previous study (Wisdom et al.) with a large adult cohort found that those who are APOE ε4 carriers had poorer memory tests than the non-carriers.[5]

Therefore, they found that associations between TRAP and some neurodevelopmental outcomes were stronger among APOE ε4 carriers than among non-carriers.

Since traffic emissions are the main source of PAHS, EC, and NO2, the BREATHE project hopes that their findings are replicated to ensure that traffic emissions are regulated and reduced all over the world. Protecting environment conditions are needed for optimal neurodevelopment during childhood, as it could have consequences for health later in life.

Oragene·DNA self-collection kits were used in the above research studies for genetic analysis. If you are interested in trying saliva samples for your own project, click on the free kits request button or email info@dnagenotek.com.

Request free trial kits of any DNA Genotek saliva kit

References:

[1] Claderon-Garciduenas L et al. Early alzheimer’s and parkinson’s disease pathology in urban children: friend versus foe responses – it is time to face the evidence. Biomed Res Int. 1-16 PMID: 23509683. (2013).

[2] Alemany S et al. Traffic-related air pollution, APOE e4 status, and Neurodevelopmental outcomes among school children enrolled in the BREATHE project. Env Health Perspectives. 126(8):087001 (2018).

[3] Schikowski T et al. Association of air pollution with cognitive functions and its modifications by APOE gene variants in elderly women. Environ Res. 142; 10-16 (2015).

[4] Cacciottolo M et al. Particulate air pollutants, APOE alleles and their contributions to cognitive impairment in older women and to amyloidogenesis in experimental models. Transl Psychiatry. 7(1):e1002 (2017).

[5] Widsom NM et al. The effects of apolipoprotein E on non-impaired cognitive functioning: a meta-analysis. Neurobiol Aging.  32(1):63-74 (2011).

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