Traffic pollution may increase risk of fatty liver disease: Mouse study
Findings suggest air pollution is independent risk factor for disease
Long-term exposure to air pollution from traffic, even at relatively low concentrations, may increase the risk of fatty liver disease, according to a new study done in mice.
This association was seen “even in the absence of classical risk factors, such as processed/fast food consumption,” the researchers wrote.
The team, from the University of Technology Sydney (UTS) in Australia, noted that these findings emphasize that “prolonged exposure to low-dose [traffic pollution] can be an independent risk factor for fatty liver disease.”
Hui Chen, MD, PhD, the study’s senior author and a professor at UTS, noted that “previous research has shown that exposure to heavily polluted air is associated with liver disorders.”
Now, “this study reveals even low levels can cause harm,” Chen said in a university press release. “It suggests there is no safe level of exposure to traffic-derived air pollution.”
The study, “Prolonged exposure to low-dose traffic-derived PM2.5 causes fatty liver disorder in mice,” was published in the Journal of Environmental Sciences.
Investigating short-term and prolonged traffic pollution exposure
It’s well-established that air pollution can have negative effects on health. One type of air pollution molecule associated with traffic and shown to cause damage is fine particulate matter of 2.5 micrometers or less, known as PM2.5. It’s 30 times smaller than a strand of human air.
“When we inhale air pollution, the very tiny particles known as PM2.5 enter the bloodstream through the lungs,” Chen said. “The liver, which filters toxins from the blood, then accumulates these substances, which can include heavy metals such as arsenic, lead, nickel and zinc.”
Previous studies have indicated that exposure to heavy air pollution may cause liver damage and increase the risk of various liver diseases, including fatty liver disease, which is marked by fat accumulation in the liver. Over time, this fat buildup can cause liver inflammation and scarring, known as fibrosis, which eventually may lead to permanent liver scarring, called cirrhosis, and liver failure.
According to Jacob George, PhD, a liver specialist and the director of the Storr Liver Centre at the Westmead Institute for Medical Research in Australia, “around one in three Australian adults has fatty liver disease, and it is more common in those who are overweight or have diabetes.”
To date, however, there’s been little investigation into the effects on the liver of low-level traffic-derived PM2.5, according to the researchers.
To learn more, the team investigated the impact of PM2.5 exposure on liver health in mice. Their focus was threefold: looking at short-term exposure — over a four-week period — sub-chronic exposure, over eight weeks, and prolonged exposure, spanning 12 weeks or nearly three months.
The researchers specifically used a PM2.5 dose in mice, as it corresponds with the dose to which people in Australia are most likely to be exposed. The team checked for changes in liver inflammation, fibrosis, fatty molecules, and sugars.
Although the health impact, especially in the short term, may not appear as serious as that due to living in heavily polluted air, the long-term impact cannot be ignored. … PM [particulate matter] emissions from road traffic form the major source of pollution in urban areas.
“PM [particulate matter] emissions from road traffic form the major source of pollution in urban areas,” the researchers wrote, adding that “chronic low-level exposure to such PMs applies to individuals residing within 50 to 500 meters [about 164 to 1,640 feet] of major roads.” For reference, 164 feet is about 55 yards.
“Although the health impact, especially in the short term, may not appear as serious as that due to living in heavily polluted air, the long-term impact cannot be ignored,” the team wrote.
Mice showed ‘all hallmarks of fatty liver disease at 12 weeks’
After 12 weeks of exposure to low-level PM2.5, the animals’ livers showed increased fat accumulation and fibrosis, high counts of inflammatory immune cells, and high levels of inflammatory and fibrosis-related molecules, the results showed. In turn, levels of the sugar molecule glycogen — which plays a role in energy production in the body — were reduced after prolonged exposure to PM2.5.
“Livers from PM2.5-exposed mice exhibited all hallmarks of fatty liver disease at 12 weeks,” the researchers wrote.
Min Feng, MD, the study’s first author and a PhD candidate in the UTS Faculty of Science, noted that “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,” Feng said.
Importantly, according to the researchers, the mice showed signs of fatty liver even though their diet was unchanged.
Chen noted that lifestyle factors — such as a poor diet, a lack of exercise, and greater alcohol consumption — are known to 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,” Chen said.
Researcher makes suggestions for reducing traffic pollution exposure
Chen made suggestions for steps humans can take to curb their exposure to traffic pollution.
“To [minimize] 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,” Chen said.
He added: “We think of air pollution as being harmful to people’s lungs, but it has a broader impact on health including on the liver.”
Overall, the team stressed a need for additional research into the mechanisms by which air pollution leads to liver damage.
As one limitation of this study, the team noted that, because research has suggested that males are more susceptible to fatty liver disease, only male mice were used in the experiments. Thus, the researchers stressed that further research is needed to see if these same findings hold in females.
“Future studies should identify the key molecular regulator(s) underlying the abnormal [fat] accumulation in the liver in order to suggest novel targets for developing potential intervention strategies,” the scientists wrote.
About the Author
