Exposure to Airborne Particulate Matter is Associated with Methylation Pattern in the Asthma Pathway

Abstract

Background: Asthma exacerbation and other respiratory symptoms are associated with exposure to air pollution. Since environment affects gene methylation, it is hypothesized that asthmatic responses to pollution are mediated through methylation. Materials & methods: We study the possibility that airborne particulate matter affects gene methylation in the asthma pathway. We measured methylation array data in clinic visits of 141 subjects from the Normative Aging Study. Black carbon and sulfate measures from a central monitoring site were recorded and 30-day averages were calculated for each clinic visit. Gene-specific methylation scores were calculated for the genes in the asthma pathway, and the association between the methylation in the asthma pathway and the pollution measures was analyzed using sparse Canonical Correlation Analysis. Results: The analysis found that exposures to black carbon and sulfate were significantly associated with the methylation pattern in the asthma pathway (p-values 0.05 and 0.02, accordingly). Specific genes that contributed to this association were identified. Conclusion: These results suggest that the effect of air pollution on asthmatic and respiratory responses may be mediated through gene methylation.

KEYWORDS::

• black carbon
• epigenetics
• gene-specific methylation scores
• pathway analysis
• sulfate

Disclaimer

This publication was made possible by USEPA grant RD 83479801. Its contents are solely the responsibility of the grantee and do not necessarily represent the official views of USEPA. Furthermore, USEPA does not endorse the purchase of any commercial products or services mentioned in the publication.

Financial & competing interests disclosure

This work was supported by the National Institute of Environmental Health Sciences (ES00002 and R01ES015172 to A Baccarelli and J Schwartz, and R00ES017744 to A Maity) and the National Cancer Institute (R37-CA076404 and P01-CA134294 to T Sofer, A Maity and X Lin). This publication was made possible by USEPA grant RD 83479801. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Ethical conduct of research

The authors state that they have obtained appropriate institutional review board approval or have followed the principles outlined in the Declaration of Helsinki for all human or animal experimental investigations. In addition, for investigations involving human subjects, informed consent has been obtained from the participants involved.

Notes

Data taken from [101].

Additional information

Funding

This work was supported by the National Institute of Environmental Health Sciences (ES00002 and R01ES015172 to A Baccarelli and J Schwartz, and R00ES017744 to A Maity) and the National Cancer Institute (R37-CA076404 and P01-CA134294 to T Sofer, A Maity and X Lin). This publication was made possible by USEPA grant RD 83479801. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.