An international study revealed that long-term exposure to fine particulate air pollution impairs metabolic health by disrupting the normal function of brown fat in the body.

Recent research indicates that air pollution affects not only the lungs and heart but also the metabolic system, being associated with increased risks of disorders such as type 2 diabetes and insulin resistance.

In this context, Francesco Paneni, professor at the Center for Translational and Experimental Cardiology at the University of Zurich and Zurich University Hospital, led a research study to highlight this link between air pollution and metabolic disorders (including diseases like obesity).

The researchers exposed laboratory mice to fine particles of type PM2.5 – particles smaller than 2.5 micrometers that can be inhaled deep into the lungs – for six hours daily, five days a week, over 24 weeks, simulating chronic urban pollution exposure.

After about five months, the exposed mice showed clear metabolic disturbances, including impaired insulin sensitivity and deterioration of brown fat function, the tissue responsible for generating heat, burning calories, and maintaining energy balance in the body.

Molecular analyses showed that exposure to PM2.5 particles led to dysregulation of gene expression within brown fat cells, disrupting genes responsible for heat production, fat metabolism, and oxidative stress management. There was also increased fat accumulation and signs of tissue damage and fibrosis.

These disturbances were found to result from epigenetic changes including DNA methylation modifications and chromatin remodeling (the material that makes up chromosomes inside the cell nucleus), affecting gene activation or repression without altering the genetic code itself.

The researchers identified two key enzymes involved in this process, HDAC9 and KDM2B, which modify histone proteins around which DNA is wrapped. Analysis showed that increased activity of these enzymes was linked to decreased chemical marks that promote normal gene expression in brown fat cells.

Paneni said, “When we experimentally inhibited the activity of these two enzymes, brown fat function significantly improved, while their activation led to further metabolic deterioration.”

The study’s results confirm that fine particulate air pollution poses a direct risk to the body’s metabolic balance, not only through inflammation or oxidative stress but also by altering how genes are regulated within cells.

Paneni concluded, “These findings help us better understand how environmental pollutants like PM2.5 contribute to the development of metabolic diseases and point to new potential targets for prevention and treatment.”

The study was published in the journal JCI Insight.