Even low levels of air pollution impacts gene expression

Summary: Exposure to low levels of air pollution over a decade led to changes in gene expression associated with morbidity and mortality in the longer term.

Source: Monash University

New data from a landmark study done by Monash University researchers in Australia raises significant concerns that even short-term exposure to low level air pollution can affect gene expression, leaving us at risk of other diseases such as cancer, cardiovascular and respiratory diseases.

It has long been known that exposure to air pollution, including the widespread smoke events in the US and Europe, can lead to short term health problems such as respiratory distress. It is also known that longer-term exposure to air pollutants leads to oxidative stress and issues like an increased risk of cardiovascular disease.

Research, published in the journal Environment International, provides the first evidence that exposure to even very low levels of air pollution can change gene expression that are the hallmark of diseases such as cancer.

Research from Associate Professor Yuming Guo from the Monash School of Public Health and Preventive Medicine, and colleagues at Nagasaki University in Japan and Cambridge University in the UK, studied blood samples from 266 pairs of twins (192 identical and 74 non identical) as well as 165 parents in Brisbane over periods from 2005 to 2010. The volunteers are part of the Brisbane System Genetics Study.

The periods when the blood samples were taken were matched to data from seven air quality monitoring stations around Brisbane at that time, to measure the levels of exposure to PM2.5 (the main particulate matter in smoke) and sulphur dioxide (the main gaseous pollutant).

The researchers studied expression in six genes associated with oxidative stress and inflammation, which have long been considered important features of disease processes initiated by pollutants.

This shows a smokey skyline
The researchers studied expression in six genes associated with oxidative stress and inflammation, which have long been considered important features of disease processes initiated by pollutants. The image is in the public domain.

The researchers found that even the low levels of air pollution experienced in Brisbane over the decade of the study led to change of gene expression associated with morbidity and mortality in the longer term.

The latest study is further evidence that exposure to air pollutants, even at low levels, has long term health consequences, which has real life implications for the current COVID pandemic. according to Associate Professor Guo. “This is the first evidence as to how exactly exposure to low level of air pollution actually alters our gene expression which in turn impacts out health,” he said.

“Combined with the global consequences of COVID 19 and its impact on respiratory health there is even a greater need to be conscious of limiting our exposure to air pollution.”

About this neuroscience research article

Source:
Monash University
Media Contacts:
Tania Ewing – Monash University
Image Source:
The image is in the public domain.

Original Research: Closed access
“Candidate gene expression in response to low-level air pollution”. Lina Madaniyazi, Shanshan Li, Shuai Li, Yuming Guo.
Environment International doi:10.1016/j.envint.2020.105610.

Abstract

Candidate gene expression in response to low-level air pollution

Background
Epidemiological studies have linked air pollutants to adverse health effects even at low exposure levels, but limited evidence is available on its associations with gene expression levels.

Aim

To investigate associations between air pollutants and gene expression levels.

Methods
We collected data from Brisbane System Genetics Study (BSGS) — a family-based system genetics study. Expression levels of candidate genes were obtained for whole blood from 266 pairs of twins (192 monozygotic and 74 dizygotic pairs) and 165 parents. Data on individual phenotypes were also obtained, including age, sex, Body Mass Index and exposure to smoke. Daily data on mean temperature and air pollutants, including particulate matter with aerodynamic diameter ≤2.5 μm (PM2.5), ozone (O3), nitrogen dioxide (NO2) and sulfur dioxide (SO2), were collected from seven monitoring stations for the day when the blood samples were collected. The association between each air pollutant and expression level of each gene was analyzed by using generalized linear models with adjustment for temperature and individual phenotypes, and its difference between monozygotic and dizygotic twins was investigated.

Results
The mean value for daily concentration of air pollutants were 5.9 µg/m3 for PM2.5, 16.3 ppb for O3, 6.5 ppb for NO2, and 1.4 ppb for SO2, respectively. All air pollutants’ levels in Brisbane during our study period were well under the National Air Quality Standard Air pollutant levels. We observed positive associations (false discovery rate [) among twins between PM2.5 and expression levels of HSPA8 and SOD1 and also between SO2 and AHR expression level. Negative associations were observed between SO2 and 11 genes among twins, including AHR, DUSP1, GEMIN4, GPX1, KLF2, PTGS2, TLR4, TNF, TNFRSF1B, TXNRD1, and XBP1, with most of them found at lag 0–7 days (FDR < 0.1). Furthermore, the association between SO2 and DUSP1 expression level was stronger among monozygotic twins than dizygotic twins (FDR < 0.1). We did not find strong evidence linking air pollutants to gene expression levels among parents.

Conclusion
Our findings require confirmation but suggest potential associations of expression levels at several genes with air pollutants at low exposure level and an individual’s genetic background modifies the association between SO2 and DUSP1 gene, which may help bridge the gap of epidemiological studies with both in vivo and in vitro toxicological experiments and provide some insights into the role of nature-nurture of an individual in gene expression response to air pollutants.

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