When we talk about our obesigenic (obesity-promoting) environment, the first things that usually come to mind are our overall highly processed, poor nutritional value, fast access, supersized food supply, and our communities and societies which are mostly built in a way that promote inactivity.  In addition to these obvious contributors, there is also a lot of data gathering on environmental pollutants: not only chemicals that we eat and drink – but also pollutants in the very air we breathe.


A recent review discusses how pollution in the air promotes inflammation and damage to many parts of our bodies, resulting in promotion of obesity.


The offender discussed in this review is fine airborne particulate matter (let’s call it FAPM for short): tiny particles of organic and inorganic material that floats around in our atmosphere.  These consist of carbon rich nuclei glopped together with polycyclic aromatic hydrocarbons, endotoxins, and transition metals.


Pause.  EEEeeew.   Yep, we are breathing the stuff.


The smallest FAPM can get right into our bloodstream from our lungs, and are then internalized into our body tissues. White blood cells also deliver FAPMs from our lungs to our body tissues.


Here are some of the mechanisms by which FAPMs promote obesity (dig into the article for much more detail):

  • Inside our cells, FAPMs trigger production of reactive oxygen species, which activate inflammatory pathways. 
  • FAPM triggers inflammation in the appetite regulation center of the brain (called the hypothalamus) by a number of mechanisms, which disrupts the healthy hunger/fullness appetite signals which drives weight gain.
  • FAPM exposure increases gut permeability (leakiness), allowing the migration of substances produced by our gut bacteria into our systems.  This triggers inflammation and metabolic dysfunction in white adipose tissue, and stimulates energy-burning brown fat to convert to white fat.  Toxins generated by FAPM in the airways (eg oxidized lipids, reactive oxygen species, and pro inflammatory chemicals) also travel to our fat tissue to cause dysfunction in our fat tissues.
  • FAPM increases cortisol levels, which promotes adiposity.
  • FAPM increases oxidative stress and inflammation in fat tissue, and induces dysfunction and a reduced number of mitochondria (energy burning organelles) in our fat cells. This mitochondrial dysfunction impairs glucose and lipid oxidation, stimulating triglyceride storage and enlargement of fat cells.
  • FAPM can affect thyroid function, which is an important regulator of our metabolism.  Chronic exposure to FAPM is associated with lower thyroid hormone levels, which would translate to lower resting metabolism (ie lower resting energy burn).
  • FAPMs interfere with skeletal muscle health, having detrimental effects on muscle mass and physical performance, especially amongst the elderly.  The same themes come out here (inflammation, mitochondrial dysfunction, etc), but in addition, FAPM has been shown to increase sedentary behavior, which of course does not promote good mucle health.


With the above mechanisms at play, it is not a surprise that people exposed to high FAPM are more likely to have abdominal obesity, nor that chronic inhalation of FAPM triggers insulin resistance, metabolic syndrome, and diabetes in humans. 


So what can we do about the risk of obesity and metabolic dysfunction imposed on us by… breathing?? (beyond the obvious need to reduce air pollution globally, or moving to a place with cleaner air)


As noted by the authors, lifestyle interventions can reduce whole-body inflammation (eg physical activity).  They also discuss very early rodent data looking at antioxidant and anti-inflammatory compounds and supplements, with a long way to go in studying these possibilities.  The authors question whether exercising in highly polluted areas could possibly outweigh the health benefits – now isn’t that a Catch22 – more data is clearly needed to answer these pressing questions.


PS – Many readers are likely wondering whether forest fire smoke could have an adverse impact on metabolic health and obesity risk.  As forest fire smoke has historically been episodic and short-lived, to my knowledge, this has not (yet) been evaluated.


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