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Published on: May 20, 2018
Associations of Annual Ambient Fine Particulate Matter Mass and Components with Mitochondrial DNA Abundance
Cheng Peng1, Akin Cayir, Marco Sanchez-Guerra
1From the aChanning Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; bVocational Health College, Canakkale Onsekiz Mart University, Çanakkale, Turkey; cDepartment of Developmental Neurobiology, National Institute of Perinatology, Mexico City, Mexico; dDepartment of Environmental Health, Harvard T. H. Chan School of Public Health, Boston, MA; eDepartment of Statistics, Colorado State University, Fort Collins, CO; fDepartment of Environmental Health Sciences, Columbia Mailman School of Public Health, New York, NY; gDepartment of Biostatistics, Harvard School of Public Health, Boston, MA; and hNormative Aging Study, Veterans Affairs Boston Healthcare System and the Department of Medicine, Boston University School of Medicine, Boston, MA.
Background:
Fine particulate matter (PM2.5) represents a mixture of components with potentially different toxicities. However, little is known about the relative effects of PM2.5 mass and PM2.5 components on mitochondrial DNA (mtDNA) abundance, which may lie on the pathway of PM2.5-associated disease.
Methods:
We studied 646 elderly male participants in the Normative Aging Study from Greater Boston to investigate associations of long-term exposure to PM2.5 mass and PM2.5 components with mtDNA abundance. We estimated concentrations of pollutants for the 365-day preceding examination at each participant's address using spatial- and temporal-resolved chemical transport models. We measured blood mtDNA abundance using RT-PCR. We applied a shrinkage and selection method (adaptive LASSO) to identify components most predictive of mtDNA abundance, and fit multipollutant linear mixed-effects models with subject-specific intercept to estimate the relative effects of individual PM component.
Results:
MtDNA abundance was negatively associated with PM2.5 mass in the previous year and-after adjusting for PM2.5 mass-several PM2.5 components, including organic carbon, sulfate (marginally), and nitrate. In multipollutant models including as independent variables PM2.5 mass and PM2.5 components selected by LASSO, nitrate was associated with mtDNA abundance. An SD increase in annual PM2.5-associated nitrate was associated with a 0.12 SD (95% confidence intervals [CI] = -0.18, -0.07) decrease in mtDNA abundance. Analyses restricted to PM2.5 annual concentration below the current 1-year U.S. Environmental Protection Agency standard produced similar results.
Conclusions:
Long-term exposures to PM2.5-associated nitrate were related to decreased mtDNA abundance independent of PM2.5 mass. Mass alone may not fully capture the potential of PM2.5 to oxidize the mitochondrial genome.See video abstract at, http://links.lww.com/EDE/B274.
Insights
Fine particulate matter (PM2.5) exposure, especially from nitrate, is linked to lower mitochondrial DNA (mtDNA) abundance in elderly men. This suggests PM2.5 components, not just mass, impact cellular health and disease pathways.
Area of Science:
- Environmental Health
- Toxicology
- Molecular Biology
Background:
- Fine particulate matter (PM2.5) is a complex mixture with varying toxicities.
- The impact of PM2.5 components on mitochondrial DNA (mtDNA) abundance is not well understood.
- mtDNA abundance may be a key factor in PM2.5-associated diseases.
Purpose of the Study:
- To investigate the association between long-term exposure to PM2.5 mass and its components with mtDNA abundance.
- To identify specific PM2.5 components that affect mtDNA abundance.
- To estimate the relative effects of PM2.5 components on mtDNA abundance.
Main Methods:
- Study included 646 elderly male participants from the Normative Aging Study.
- Pollutant concentrations were estimated using chemical transport models for the 365 days preceding examination.
- Blood mtDNA abundance was measured using RT-PCR, and adaptive LASSO was used for component selection.
Main Results:
- Negative association found between PM2.5 mass and mtDNA abundance.
- Organic carbon and nitrate were associated with decreased mtDNA abundance after adjusting for PM2.5 mass.
- An increase in PM2.5-associated nitrate correlated with a decrease in mtDNA abundance.
Conclusions:
- Long-term exposure to PM2.5-associated nitrate independently reduces mtDNA abundance.
- PM2.5 mass alone may not fully represent its potential to damage the mitochondrial genome.
- Findings highlight the importance of specific PM2.5 components in environmental health research.
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