Summary: A decade-long study found that even low-level air pollution can alter gene expression linked to long-term disease risk, including cancer and cardiovascular and respiratory conditions.
Source: Monash University
New findings from researchers at Monash University raise important concerns: brief or low-level exposure to air pollution can change gene expression in ways associated with chronic disease and increased mortality.
Air pollution is already known to provoke immediate respiratory symptoms and, with longer exposure, to contribute to oxidative stress and cardiovascular problems. The new research extends this knowledge by showing that even relatively low concentrations of pollutants can alter the activity of genes involved in inflammation and cellular stress—changes that are characteristic of disease processes such as cancer and heart disease.
Published in the journal Environment International, the study examined blood samples collected between 2005 and 2010 from participants in the Brisbane System Genetics Study. The team — led by Associate Professor Yuming Guo of the Monash School of Public Health and Preventive Medicine, with collaborators at Nagasaki University and Cambridge University — analyzed samples from 266 twin pairs (192 identical and 74 fraternal) and 165 parents to explore how short-term exposure to particulate and gaseous pollutants affected gene expression.
Researchers matched the timing of each blood sample to air quality readings from seven monitoring stations in the Brisbane area. They focused on PM2.5 (fine particulate matter commonly present in smoke) and sulfur dioxide (SO2), and measured expression of six candidate genes known to be involved in oxidative stress and inflammation—key pathways in pollutant-related disease.
The study found that even the modest pollution levels recorded in Brisbane during the study period were associated with measurable changes in gene expression. Notably, exposure to PM2.5 correlated with higher expression of HSPA8 and SOD1, while SO2 exposure showed both positive and negative associations across multiple genes. Several negative associations between SO2 and genes involved in immune and stress responses (including AHR, DUSP1, GEMIN4, GPX1, KLF2, PTGS2, TLR4, TNF, TNFRSF1B, TXNRD1, and XBP1) were observed, particularly within a week after exposure.
Importantly, the research detected differences in these associations between monozygotic and dizygotic twins, suggesting that genetic background modifies how an individual’s gene expression responds to pollutant exposure. For example, the link between SO2 and DUSP1 expression appeared stronger among identical twins, implying a role for inherited factors in determining sensitivity to air pollution.
Average daily pollutant levels over the study were relatively low—about 5.9 µg/m3 for PM2.5, 16.3 ppb for ozone (O3), 6.5 ppb for nitrogen dioxide (NO2), and 1.4 ppb for SO2—values that met national air quality standards. Despite these low concentrations, associations with gene expression were still detectable in the twin cohort. The researchers did not find similarly strong associations among the parent participants.
Associate Professor Guo emphasized the broader public health implications: these findings provide concrete biological evidence that even low-level pollutant exposure can alter molecular pathways tied to chronic disease risk. In the context of the COVID-19 pandemic—which affects respiratory health globally—reducing air pollution exposure remains particularly relevant, as compromised respiratory and immune systems may worsen disease outcomes.
About the study
The research used whole-blood gene expression data from the Brisbane System Genetics Study. Investigators adjusted analyses for individual characteristics such as age, sex, body mass index, and smoking exposure, as well as daily temperature. Daily pollutant concentrations were taken from monitoring stations matching the date each blood sample was collected. Statistical models assessed associations between each pollutant (PM2.5, O3, NO2, SO2) and the expression of selected genes, and compared effects in monozygotic versus dizygotic twins.
Key conclusions
While the results require replication, they suggest that low-level air pollution can influence the expression of genes involved in inflammation and oxidative stress. The findings also point to an interaction between environmental exposures and genetic background in shaping molecular responses. This research helps connect epidemiological observations with biological mechanisms and underscores the importance of minimizing air pollution exposure to protect long-term health.
About this research
Source: Monash University
Media contact: Tania Ewing – Monash University
Image source: Public domain
Original research: “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.
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