Objective: The main objective of this pilot study was to gather preliminary information about how telomere length (TL) varies in relation to exposure to polycyclic aromatic hydrocarbons (PAHs) in children living in a highly polluted city.
Methods: We conducted a cross-sectional study of children living in Fresno, California (n = 14). Subjects with and without asthma were selected based on their annual average PAH level in the 12-months prior to their blood draw. We measured relative telomere length from peripheral blood mononuclear cells (PBMC).
Results: We found an inverse linear relationship between average PAH level and TL (R2 = 0.69), as well as between age and TL (R2 = 0.21). Asthmatics had shorter mean telomere length than non-asthmatics (TLasthmatic = 1.13, TLnon-asthmatic = 1.29).
Conclusions: These preliminary findings suggest that exposure to ambient PAH may play a role in telomere shortening.
Become familiar with previous evidence suggesting that telomere length may be a biomarker of air pollution-induced cytotoxicity.
Summarize the new findings on the association between polycyclic aromatic hydrocarbon (PAH) exposure and telomere length in adolescents, including those with asthma.
Discuss the implications for recommendations and policies to mitigate the health and respiratory effects of traffic-related air pollution.
Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, Berkeley (Ms Lee, Dr Noth, Dr Hammond, Dr Eisen, Dr Balmes); Division of Immunology and Allergy, School of Medicine, Stanford University, Stanford (Dr Nadeau); Department of Biochemistry and Biophysics (Dr Lin); Division of Occupational and Environmental Medicine, School of Medicine (Dr Balmes), University of California, San Francisco, San Francisco, California.
Address correspondence to: John R. Balmes, MD, Division of Environmental Health Sciences, School of Public Health, University of California, 50 University Hall, Berkeley, CA 94720 (firstname.lastname@example.org).
Funding sources: Funding for this research was provided by the Global Health Research Foundation and a NIEHS grant (R01 HL081521 and R01 ES020926), the California Air Resources Board (contract nos. 99-322, 99-323, and 01-346 ), the US EPA (PO no. 2A-0540-NASX ), and the Mickey Leland National Urban Air Toxics Research Center ( RFA 2005-01). This work was also performed as part of the University of California, Berkeley/Stanford Children's Environmental Health Center, pre-Center funded (2010 to 2014) by NIEHS 1P20ES018173 and EPA RD-83459601. This publication was made possible by CDC/NIOSH T42 OH008429-13. Its contents are solely the responsibility of the grantee and do not necessarily represent the official views of the US EPA. Further, the US EPA does not endorse the purchase of any commercial products or services mentioned in the publication.
Author Contributions: Conceived the study, analyzed the data, and was the primary author of the paper: EL. Provided intellectual input and contributed to the writing of the paper: JB, EE, KH. Telomere length measurement and interpreting results: JL. Designed the study and provided PBMC samples: KN, MP. Provided PAH exposure data, edited, and reviewed the paper: KH, BN. The authors declare that they have no conflicting interest.
Authors Balmes, Lee, Noth, Hammond, Eisen, have no relationships/conditions/circumstances that present potential conflict of interest. Co-authors Kari Nadeau and Jue Lin have not completed the forms.
The JOEM editorial board and planners have no financial interest related to this research.