I live in Los Angeles and it’s unfortunate, but true, that the brown cloud of smog hanging over our city is as much an icon of LA as the Hollywood hills. My morning bike commute is spent sucking on the tailpipes of my fellow Angelenos, and it turns out this doesn’t just make me cranky. A recent article published in Neurotoxicology suggests that those of us who live in urban environments are much more likely to experience cognitive decline with age. The culprit? Air pollution.
While air pollution is generally thought of as a modern problem, humans have evolved to handle polluted air from sources such as forest fires and volcanic eruptions. Coughing removes large particles from the lung, while macrophages, a type of immune cell, are responsible for engulfing and degrading small particles. However, some particles are so small that they can penetrate the lung wall, and gaseous forms of air pollution, such as ozone, easily cross the lung wall just like oxygen or carbon dioxide.
The brain is connected to the vascular system, so toxins able to penetrate the lung wall end up in the blood, having potential access to brain tissue. Due to the immense importance of the brain, the body has developed a unique way of protecting it from toxins: the blood brain barrier (BBB). The BBB acts as a checkpoint for the brain; anything that enters the brain cavity must pass through the BBB first and, in general, the BBB does an excellent job.
In order for any component of air pollution to access the brain it must pass through the BBB. It can do this by either by being so small it goes undetected or by mimicking a ‘safe’ chemical that the BBB normally allows to pass through. Additionally, the integrity of the BBB can be compromised by toxin exposure or even aging itself, which in turn allows more potential toxins to access the brain. For instance, one study in mice demonstrated that prolonged exposure to air pollution can cause a decrease in tight junction proteins that hold cells of the BBB tightly together and increases in ‘matrix metalloproteinases,’ which are able to breakdown the exterior of the cell. This effectively causes a breach in the BBB, shaking the security system of the brain and thereby allowing previously unauthorized molecules to enter the brain milieu.
The recent article by Gatto et al. in Neurotoxicology focuses on how three particular components of air pollution, ozone, nitrous dioxide and PM2.5 (particulate matter with a diameter of less than 2.5 microns), may be linked to cognitive decline. The ability of some of these chemicals to create free radicals and activate inflammatory pathways may explain their link to decreased brain functioning. Alternatively, air pollution could damage the brain indirectly. For instance, it is well documented that air pollution can lead to an increase in heart attacks and the clogging of heart arteries (atherosclerosis). If the heart valves are clogged and cannot pump as much blood, then the brain could suffer from reduced oxygenation (oxidative stress), which could in turn lead to poor cellular function and/or death.
In summary, growing evidence in animal models and now in human epidemiological studies suggests that prolonged exposure to certain air pollution components may lead to cognitive decline. While the molecular mechanisms behind this link are still unclear, it is likely that oxidative stress and inflammation play a key role in causing the brain cell dysfunction and/or death responsible for cognitive deficits.
Escrito por Ciara Martin.
Gatto N.M., Henderson V.W., Hodis H.N., St. John J.A., Lurmann F., Chen J.C. & Mack W.J. (2014). Components of air pollution and cognitive function in middle-aged and older adults in Los Angeles, NeuroToxicology, 40 1-7. DOI: 10.1016/j.neuro.2013.09.004
Oppenheim H.A., Lucero J., Guyot A.C., Herbert L.M., McDonald J.D., Mabondzo A. & Lund A.K. (2013). Exposure to vehicle emissions results in altered blood brain barrier permeability and expression of matrix metalloproteinases and tight junction proteins in mice, Particle and Fibre Toxicology, 10 (1) 62. DOI: 10.1186/1743-8977-10-62