Air pollution’s hidden cost: Study finds links to metabolic dysfunction and type 2 diabetes

Air pollution may significantly worsen insulin resistance and metabolic disorders like type 2 diabetes. 

Research suggests that PM2.5 exposure impairs brown adipose tissue function, disrupting its ability to regulate metabolism.

The impairment is linked to epigenetic changes driven by the enzymes HDAC9 and KDM2B in brown fat cells, which alter gene regulation.

New research suggests air pollution may significantly accelerate the development of metabolic disorders like insulin resistance and type 2 diabetes, in addition to harming the lungs and heart.

In the study, mice were exposed to concentrated tiny particles in the air to demonstrate how long-term exposure to fine air pollutants can affect the body’s ability to regulate blood sugar and maintain healthy metabolism.

The study focused on a specific type of pollution known as PM2.5 (fine particulate matter), which are airborne particles smaller than 2.5 micrometers that are often inhaled deeply into the lungs.

“Our findings help explain how environmental pollutants like PM2.5 contribute to the development of insulin resistance and metabolic disease, and they point to potential new targets for prevention or treatment,” says Francesco Paneni, professor at the Center for Translational and Experimental Cardiology of the University of Zurich and the University Hospital Zurich, Switzerland.

Altered brown adipose tissue

In a lab setup designed to closely mimic chronic urban air exposure in humans, researchers exposed laboratory mice to either filtered air or concentrated PM2.5 for six hours a day, five days a week, over a period of 24 weeks.

The researchers paid close attention to brown adipose tissue, a type of fat that helps the body generate heat and burn calories, making it essential in balancing energy and glucose metabolism.

The study focused on a specific type of pollution known as PM2.5, which are airborne particles smaller than 2.5 micrometers that are often inhaled deeply into the lungs.After five months, the mice that had inhaled PM2.5 showed signs of disrupted metabolism, including impaired insulin sensitivity. Examinations revealed that the function of their brown fat cells had been “significantly altered.”

“In particular, we found that the expression of important genes in brown adipose tissue — which regulate its ability to produce heat, process lipids, and handle oxidative stress — was disturbed,” explains Paneni.

“These changes were accompanied by increased fat accumulation and signs of tissue damage and fibrosis within the tissue.”

Two enzymes drive epigenetic changes

The researchers discovered that air pollution had triggered significant changes in the regulation of DNA in brown fat cells.

These included modified DNA methylation patterns and changes in how accessible certain genes were for being turned on or off, in a process called chromatin remodeling.

Without altering the genetic code itself, these epigenetic changes impact how cells function by regulating gene activity.

The study authors identify two enzymes as the main drivers of this process: HDAC9 and KDM2B. These are responsible for modifying histones, the proteins that DNA wraps around.

In mice exposed to PM2.5, the researchers found these histones bound to specific regions of the DNA in brown fat cells, which reduced key chemical tags, or methyl groups, that normally promote gene activity.

“When these enzymes were experimentally suppressed, brown fat function improved, whereas increasing their activity led to further declines in metabolism,” notes Paneni.

A recent observational study supports that consuming fruits may reduce the harmful effects of air pollution on lung function. Women who consumed four or more portions of fruit daily showed less decline in lung health than those who consumed less. The paper identifies that fruits’ antioxidant and anti-inflammatory properties play a role in this protective effect.