Keywords
1. DNA Methylation and Air Pollution
2. Particulate Matter PM2.5 Health Effects
3. Non-smoking Population Epigenetics
4. AHRR Gene Environmental Impacts
5. Taiwan Air Quality Research
In a groundbreaking study published in Clinical Epigenetics, researchers have uncovered significant changes in DNA methylation associated with exposure to fine particulate matter (PM2.5) in the blood DNA of non-smoking Taiwanese adults. The study focused on a specific gene known as the aryl hydrocarbon receptor repressor (AHRR), particularly the cg05575921 site, which is linked with smoking and lung cancer. However, the exposure source in this study was not tobacco smoke but rather ambient air pollution.
DOI: 10.1186/s13148-019-0662-9
Background on DNA Methylation and AHRR
DNA methylation is a process which typically acts to repress gene expression and can have profound implications for health, influencing cancer, metabolic, neurological, and autoimmune disorders (Moore et al., 2013; Jin & Liu, 2018). The AHRR gene, pivotal for this study, regulates the filtration of toxins by binding environmental pollutants such as tobacco smoke, mediating the deleterious effects via the mechanism of DNA methylation (Jones, 2012; Reynolds et al., 2015).
Study Methodology and Participant Selection
The robust study, helmed by Tantoh Disline Manli and colleagues from Chung Shan Medical University and collaborating institutions, leveraged data from the extensive Taiwan Biobank dataset (2008-2015). The study’s stringent inclusion criteria led researchers to analyze 708 non-smoking participants between the ages of 30-70. Specifically, the team examined the patterns of blood DNA methylation at AHRR cg05575921 in relation to PM2.5 exposure, a major component of air pollution known for its association with various negative health outcomes (van der Zee et al., 2016).
The Impact of PM2.5 on AHRR Methylation
High-resolution data indicated that participants living in areas with elevated PM2.5 levels exhibited significant hypomethylation at the AHRR cg05575921 site compared with those in lower PM2.5 areas. This hypomethylation has been previously associated with increased gene expression, potentially spelling health consequences for individuals exposed to air pollution, even in the absence of active or passive smoking (Gao et al., 2017).
Implications for Public Health
The findings thrust air pollution into the spotlight once more, reinforcing the narrative that even non-smokers can suffer genetic changes typically associated with smoking. This suggests that policy implementation for reducing air pollution could have far-reaching health benefits. Moreover, lung cancer, commonly associated with smoking, could also be influenced by PM2.5 through the same biological pathways (Ambatipudi et al., 2016).
Regional Differences in Air Quality
Taiwan’s struggle with air pollution is not uniform across the island. Urban and industrial regions typically report higher PM2.5 levels (Chen et al., 1999), emphasizing the need for targeted air quality interventions. The study’s comparative approach across different residential areas underlines the direct impact that residential environments can have on individual health profiles.
The Future of Air Pollution and Epigenetics Research
While this research marks a significant step in understanding the epigenetic consequences of air pollution, there remains much to uncover. For instance, the extent to which these methylation changes at the AHRR gene site correlate with actual disease manifestation remains an open question (Ma & Li, 2017).
Ethical and Data Transparency
The study was conducted with ethical approval from the Chung Shan Medical University Institutional Review Board (CS2-17070), although the details of informed consent, given the use of biobank data, were not explicitly mentioned in the source material. The authors declared no competing interests, maintaining the integrity of the research outcomes.
Conclusion
Non-smoking individuals are not immune to the adverse effects of smoking-related gene methylation changes, implicating air pollution as a public health concern that transcends direct tobacco exposure. The cg05575921 site of the AHRR gene provides a measurable biomarker that reflects an individual’s air quality exposure, potentially serving as a valuable tool for public health surveillance and intervention.
References
1. Moore, L. D., Le, T., & Fan, G. (2013). DNA methylation and its basic function. Neuropsychopharmacology, 38, 23. doi: 10.1038/npp.2012.112.
2. Jin, Z., & Liu, Y. (2018). DNA methylation in human diseases. Genes & Diseases, 5(1), 1–8. doi: 10.1016/j.gendis.2018.01.002.
3. Jones, P. A. (2012). Functions of DNA methylation: islands, start sites, gene bodies and beyond. Nature Reviews Genetics, 13, 484. doi: 10.1038/nrg3230.
4. Bojesen, S. E., Timpson, N., Relton, C., Smith, G. D., & Nordestgaard, B. G. (2017). AHRR (cg05575921) hypomethylation marks smoking behaviour, morbidity, and mortality. Thorax, 72(7), 646–653. doi: 10.1136/thoraxjnl-2016-208789.
5. Gao, X., Zhang, Y., Saum, K.-U., Schöttker, B., Breitling, L. P., & Brenner, H. (2017). Tobacco smoking and smoking-related DNA methylation are associated with the development of frailty among older adults. Epigenetics, 12(2), 149–156. doi: 10.1080/15592294.2016.1271855.