Low-level traffic air pollution linked to liver damage and fatty liver disease

Long-term exposure to low levels of traffic-related air pollution harms the liver and may raise the risk of metabolic-associated fatty liver disease, a new study in mice suggests.

Fatty liver, also called hepatic steatosis, is the most common liver disease worldwide, and occurs when excess fat builds up in liver cells. It can lead to inflammation, scarring (cirrhosis), and an increased risk of cancer and liver failure.

“We think of air pollution as being harmful to people’s lungs, but it has a broader impact on health including on the liver,” said lead author Professor Hui Chen from the University of Technology Sydney (UTS).

“The liver is critical for metabolism. It clears toxins, regulates blood sugar, and produces essential vitamins and proteins, among many other functions. If the liver isn't functioning properly, it can leave people feeling tired and unwell due to disrupted metabolism,” said Professor Chen.

“When we inhale air pollution, the very tiny particles known as PM2.5 enter the bloodstream through the lungs. The liver, which filters toxins from the blood, then accumulates these substances, which can include heavy metals such as arsenic, lead, nickel and zinc.”

World-leading liver specialist Professor Jacob George, Director of the Storr Liver Centre at The Westmead Institute for Medical Research, studies the causes of liver diseases and cancer, and is a co-author on the study.

“Around one in three Australian adults has fatty liver disease, and it is more common in those who are overweight or have diabetes,” said Professor George.

“Lifestyle factors such as a bad diet, lack of exercise and excessive alcohol contribute to the development of fatty liver, however this research suggests that your environment, particularly exposure to traffic air pollution, may also be a contributing factor,” said Professor Chen.

The study, Prolonged exposure to low-dose traffic-derived PM2.5 causes fatty liver disorder in mice, was recently published in the Journal of Environmental Sciences.

The researchers exposed mice to a dose (10 micrograms daily of traffic-derived PM2.5 particles) that reflects typical human exposure in Sydney, collected from a major road in Sydney. 

Signs of inflammation and fibrosis, or scarring, as well as changes to liver sugars and fats, were measured at four, eight and 12 weeks.

“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,” said first author Dr Min Feng, a medical doctor and PhD candidate in the UTS Faculty of Science.

Exposure to air pollution particles caused more immune cells to gather in the liver and it increased inflammation. It also led to more scar tissue forming.

The liver's fat processing went up, and potentially harmful fats like triglycerides, diacylglycerols, and ceramides also increased. At the same time, the liver stored less sugar for energy.

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

“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,” said Professor Chen.

“To minimise exposure to traffic-derived air pollution, avoid peak hour traffic, take less congested routes when walking or cycling or consider wearing a mask, and keep car windows closed with air recirculation mode on while driving in heavy traffic,” she said.