Air pollution is not only a significant threat to our environment, but also to our health. Ranging from vehicles to industrial facilities, common sources of air pollution are all around us. These pollutants are linked to serious health issues, such as respiratory disease, impaired lung function, asthma, cancer, chronic bronchitis, and increased morbidity. According to the WHO, outdoor air pollution was estimated to cause 3.7 million premature deaths worldwide in 2012. It’s most abundant in urban areas in Southeast Asia and the Eastern Mediterranean region, where pollution levels can be as much as 10 times higher than the WHO recommended level. Previous research has uncovered an association between inhaling diesel exhaust fumes and notable epigenetic changes – which affected around 400 genes – and new research continues to uncover an underlying epigenetic connection to toxin exposure. In a study published in Environmental Toxicology and Pharmacology, researchers at Zhejiang University discovered a link between traffic-related air pollution (TRAP) and an increase in an epigenetic mark found on histone proteins.
The epigenetic modification they investigated is known as histone acetylation, specifically at histone H3 lysine 9 (H3K9). This particular mark is known to lead to transcriptionally active chromatin, impacting gene expression, DNA repair, and cell differentiation and proliferation, among other cellular processes. Histone acetylation, a popular histone modification studied in the field of epigenetics, is defined as the addition of an acetyl group to histone proteins at lysine residues on histone tails.
In the study, rats were housed in cages and exposed to three levels of traffic-related air pollution – high, moderate, and low – at various locations in Zhejiang, China during both spring and autumn. The researchers looked at particulate matter of various sizes (PM2.5 and PM10) and nitrogen dioxide (NO2), and measured these air pollutants once every hour. In order to test whether a dose-response relationship existed between TRAP exposure and H3K9 acetylation, the team assessed the levels of this histone modification at 4 hours and after 7 days. Histones were extracted from peripheral blood mononuclear cells (PBMCs) and lung tissues using EpiGentek’s EpiQuik Total Histone Extraction Kit immediately following the exposure.
Then, to quantify levels of global acetyl histone H3K9, the researchers used an ELISA-like, colorimetric assay. The EpiQuik Global Acetyl Histone H3K9 Quantification Kit (Colorimetric) enabled them to calculate the precise amounts of H3K9 acetylation at varying exposure levels. Overall, they found that rats exposed to TRAP for 7 days at both high and low exposure sites demonstrated a dose dependent increase of H3K9 acetylation levels.
In addition, the rats exposed to high amounts of TRAP for 7 days had significantly higher levels of H3K9 acetylation than those exposed to moderate amounts. However, they didn’t see any changes in histone acetylation in the rats after 4 hours.
But could this histone modification occur over an even longer period of time? We aren’t usually exposed to traffic-related air pollution for just a few days or hours. It’s more likely that we would come in contact with TRAP for our entire lives, for instance, while we’re stuck in traffic or even walking around town. In order to explore whether prolonged exposure to high levels of TRAP had a significant impact on this epigenetic mark, the researchers assessed H3K9 acetylation levels after an additional 14 and 28 days during both seasons. They found that, overall, the levels of this particular mark were still significantly higher compared to the control group, but there was no statistically significant difference between the rats exposed for 7, 14, or 28 days (Fig. 1).
The research team also investigated whether or not there was a relationship between a few components of air pollution – particulate matter and nitrogen dioxide – and this mark. The team reported that when the rats were exposed for 7 days, PM2.5 and PM10 levels were positively associated with H3K9 acetylation levels in both lung tissues and PBMCs. There was no relationship found, however, in regard to NO2 levels.
The scientists believe that this study, which is the first to report the effects of TRAP on H3K9 acetylation in both PCMBs and lung tissues, helps elucidate the epigenetic changes caused by air pollution exposure and could be used as a tool for understanding the connection between pollutants and lung disorders. Because air pollution continues to rise, it is crucial to understand the impact inhaling these particles may have on our epigenetic signature and our health.
Source: Dinga R., Jina Y., Liua, X., Zhub, Z., Zhanga, Y., Wanga, T., Xu, Y. (2016). H3K9 acetylation change patterns in rats after exposure to traffic-related air pollution. Environmental Toxicology and Pharmacology, 42: 170-175.
