Even low levels of traffic air pollution can damage the liver, new study shows

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Researchers found significant changes in liver function in mice exposed to traffic-derived air pollution. (Photo credit: Семен Саливанчук)

Long-term exposure to even small amounts of air pollution from vehicles promotes abnormal changes in the liver—potentially increasing the risk of fatty liver disease, according to new research in mice.

Mice exposed to fine particulate matter (PM2.5, or tiny pollutant particles of 2.5 micrometers or less)  for 12 weeks showed inflammation in the liver, more fat buildup, and changes in certain fat-related molecules, according to the study, published Jan. 27 [2025] in the Journal of Environmental Sciences. The researchers also found an increase in liver immune cells (macrophages), suggesting that the liver had been damaged and was trying to repair itself.

“Previous research has shown that exposure to heavily polluted air is associated with liver disorders, however this study reveals even low levels can cause harm. It suggests there is no safe level of exposure to traffic-derived air pollution,” says Professor Hui Chen from the University of Technology Sydney (UTS), who co-authored the study with international expert Professor Jacob George, director of the Storr Liver Centre

“We think of air pollution as being harmful to people’s lungs, but it has a broader impact on health including on the liver.”

Fatty liver disease is a condition where too much fat builds up in the liver. The most common liver disease worldwide, it can lead to inflammation (hepatitis), scarring (fibrosis or cirrhosis), and an increased risk of cancer and liver failure.

There are two main types: one caused by drinking too much alcohol (alcohol-associated fatty liver disease) and another called metabolic dysfunction-associated steatotic fatty liver disease (MASLD), formerly known as nonalcoholic fatty liver disease.

Pollutants enter the lungs, blood

Obesity and type 2 diabetes increase the risk of developing MASLD. Large studies have also shown that air pollution may be linked to a higher risk of serious conditions such as dangerous blood clots, respiratory diseases, preterm birth and low birth weight, and liver diseases like MAFLD because PM2.5 (fine particulate matter, or tiny particles of 2.5 micrometers or less) can get into the lungs and enter the bloodstream. 

Sources of fine particulate matter are widespread, including combustion sources such as motor vehicle exhaust, smoke from forest fires, and coal-fired power plants that can disperse pollutants over large distances, contaminating land and water. People with heart or lung diseases, children, older adults, minority populations, and low socioeconomic status populations are the most likely to be affected by air pollution, according to the EPA.

People who live within about 50 to 500 yards of busy roads are continuously exposed to fine particulate matter. For this study, the researchers exposed five-week-old male mice to a 10-microgram dose of PM2.5 collected from a major road in Sydney, Australia. Indications of inflammation, scarring, and changes to liver fats and sugars, were measured at four, eight, and 12 weeks.

The liver is critical for metabolism, the researchers note. It clears toxins, regulates blood sugar, produces bile, and processes essential vitamins and proteins, among many other functions. Prolonged exposure to PM2.5  appeared to trigger inflammation and oxidative stress after eight weeks, as well as:

The researchers also discovered changes in 64 specific proteins in the liver, many linked to conditions like fatty liver disease, immune system dysfunction, and processes associated with cancer.  

“The effect was cumulative. At four weeks we didn’t see much change, but by eight weeks there was disruption to the normal metabolic function of the liver and by 12 weeks we could see significant changes,” says first author Dr Min Feng, a medical doctor and PhD candidate in the UTS Faculty of Science.

Liver works harder but still accumulates fat

A large-scale protein (proteomics) analysis also showed that the PPAR pathway, which deals with extra fat, was activated as a way for the liver to adapt, the researchers say. However, these changes didn’t stop the liver from producing and storing too much fat. 

At the same time, the study showed a decrease in overall fat mass with long-term low-dose PM2.5 exposure, which the researchers say might mean that fat is moving around the body.

They also say liver weight changed during the study. At four weeks, it decreased, which might mean that PM2.5 caused sudden liver injury. At eight weeks, however, liver weight increased, possibly because the liver was trying to repair itself by growing new cells and accumulating fat. 

By 12 weeks, there was less fat around the kidneys. This could be because of fat being moved to the liver and other organs, due to PM2.5 disrupting how the body handles fat, the researchers say.

They note several limitations of the study. The proteomics analysis did not identify specific pathways that explain why PM2.5 exposure increased liver fat (TG) and its building blocks. Instead, it only showed changes in markers related to making proteins, repairing DNA, and breaking down proteins. 

The researchers say they also studied only male mice because males are more likely to develop fatty liver and seem more sensitive to PM2.5 effects on the liver.

To minimize exposure to traffic-derived air pollution, experts suggest avoiding peak-hour traffic, taking less congested routes when walking or cycling, and considering wearing a mask. Also, keep car windows closed with air recirculation mode on while driving in heavy traffic, and consider using an air filter at home.

Reference

Feng M, Padula MP, Asaad SA, et al. Prolonged exposure to low-dose traffic-derived PM2.5 causes fatty liver disorder in mice. Journal of Environmental Sciences. Published online January 2025. doi:10.1016/j.jes.2025.01.025