Long-term exposure to sulfur dioxide in air seen to raise risk of IPF
Disease 7.5 times more likely with lengthy exposure, high genetic susceptability
Long-term exposure to even low levels of sulfur dioxide (SO2), an air pollutant with a strong odor, may place people at a higher risk of developing idiopathic pulmonary fibrosis (IPF), a study in over 400,000 U.K. residents found.
The association’s strength grew as genetic susceptibility to the disease and length of exposure rose. Compared with people with a low genetic risk and low SO2 exposure, those with a high genetic risk and high exposure were about 7.5 times more likely to develop IPF.
“These findings have important implications for developing policies aimed at enhancing air quality and reducing ambient SO2 exposure, particularly for people with a high genetic risk,” the researchers wrote.
The study, “Low-level ambient sulfur dioxide exposure and genetic susceptibility associated with incidence of idiopathic pulmonary fibrosis: A national prospective cohort study,” was published in Chemosphere.
Sulfur dioxide, pollutant tied to fossil fuels, possibly important IPF cause
In pulmonary fibrosis, lung tissues become scarred and thickens over time, making it harder to breathe and get enough oxygen into the bloodstream. When the disease’s cause is unknown, it’s called idiopathic.
Certain factors, such as environmental exposure to harmful substances, may make it more likely for someone to develop this disease, which also can be affected by changes in one or many genes.
Air pollution is a well-known environmental risk factor for many respiratory conditions. In people with IPF, breathing polluted air can increase the risk of an acute exacerbation, which happens when a triggering event results in a sudden worsening of symptoms.
SO2 is a colorless gas that comes primarily from burning the fossil fuels used in vehicles and in many industries and agriculture. Exposure to SO2 can irritate the eyes, nose, and throat. When inhaled in high levels, sulfur dioxide can cause lung damage.
Exposure to high SO2 levels has resulted in pulmonary fibrosis in some people. But whether low exposure to the gas, even at concentrations lower than current air quality guidelines, increases the risk of developing IPF is unknown.
Researchers in China examined data covering 402,042 people who participated in the UK Biobank, a large database of health information from volunteers in England, Wales, and Scotland.
Participants’ mean age was 56.4, and just over half (53.3%) were women. After a median of 11.8 years, 2,562 (0.64%) had been diagnosed with IPF. At the time of diagnosis, their mean age was 70.4, and many (68.8%) were previous or current smokers.
Exposure to sulfur dioxide was estimated based on SO2 levels in the air where each person lived. Resulted showed that people who developed the disease were exposed to significantly higher levels of SO2 than those who did not (2.53 vs. 2.25 micrograms, or mcg, per cubic meter of air).
Even small increases in SO2 exposure led to significant increases in IPF risk. For each increase in SO2 exposure by 1 mcg per cubic meter of air, the risk of developing IPF increased by about 67%, after accounting for potentially confounding factors, such as age, sex, smoking status, and body weight.
“The study suggests that long-term exposure to ambient SO2, even at concentrations lower than current air quality guidelines set by the [World] Health Organization and European Union, may be an important risk factor for IPF,” the researchers wrote.
WHO, EU guidelines for SO2 exposure may be inadequate for health
Air quality guidelines set by the World Health Organization (WHO) limit the daily SO2 exposure levels to 40 mcg per cubic meter of air. European Union standards set the limit at 125 mcg per cubic meter of air.
Researchers also looked at each person’s genetic information to calculate a polygenic risk score for IPF, a measure of how likely someone is to develop a disease based on their genetic makeup.
As would be expected, data showed that more patients who went on to develop IPF had a high polygenic risk score, or a high genetic risk, than those who did not develop the disease (38.6% vs. 20.2%). Statistical analyses taking confounding factors into account also showed that people with a high genetic score had a 3.78 times higher risk of IPF.
“Genetic predisposition to IPF may also increase the risk of incident IPF,” the researchers wrote.
When accounting for both exposure to SO2 and polygenic risk score, the researchers found an additive interaction — meaning the two factors together increased the risk of IPF more than the sum of either factor alone. In total, the risk of developing IPF was 7.48 times higher for those with high exposure and a high genetic risk than for those with low exposure and low genetic risk.
“To our knowledge, the current study is the first to assess potential gene-environment interactions between gene risk and ambient SO2 for the development of IPF,” the team wrote. “Notably, the associations between ambient SO2 and IPF were more pronounced among participants with high genetic risk.”
These findings have important implications for developing better and stricter air quality control policies, which may help to protect people from developing lung diseases such as IPF, the researchers concluded.