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Transcriptome-wide analyses indicate mitochondrial responses to particulate air pollution exposure.

ABSTRACT: Due to their lack of repair capacity mitochondria are critical targets for environmental toxicants. We studied genes and pathways reflecting mitochondrial responses to short- and medium-term PM10 exposure.Whole genome gene expression was measured in peripheral blood of 98 adults (49% women). We performed linear regression analyses stratified by sex and adjusted for individual and temporal characteristics to investigate alterations in gene expression induced by short-term (week before blood sampling) and medium-term (month before blood sampling) PM10 exposure. Overrepresentation analyses (ConsensusPathDB) were performed to identify enriched mitochondrial associated pathways and gene ontology sets. Thirteen Human MitoCarta genes were measured by means of quantitative real-time polymerase chain reaction (qPCR) along with mitochondrial DNA (mtDNA) content in an independent validation cohort (n = 169, 55.6% women).Overrepresentation analyses revealed significant pathways (p-value <0.05) related to mitochondrial genome maintenance and apoptosis for short-term exposure and to the electron transport chain (ETC) for medium-term exposure in women. For men, medium-term PM10 exposure was associated with the Tri Carbonic Acid cycle. In an independent study population, we validated several ETC genes, including UQCRH and COX7C (q-value <0.05), and some genes crucial for the maintenance of the mitochondrial genome, including LONP1 (q-value: 0.07) and POLG (q-value: 0.04) in women.In this exploratory study, we identified mitochondrial genes and pathways associated with particulate air pollution indicating upregulation of energy producing pathways as a potential mechanism to compensate for PM-induced mitochondrial damage.

SUBMITTER: Winckelmans E

PROVIDER: S-EPMC5563023 | biostudies-other | 2017 Aug

REPOSITORIES: biostudies-other

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Project description:Chronic exposure to particulate air pollution may accelerate cognitive decline in older adults, although data on this association are limited. Our objective was to examine long-term exposure to particulate matter (PM) air pollution, both coarse ([PM 2.5-10 ?m in diameter [PM(2.5-10)]) and fine (PM <2.5 ?m in diameter [PM(2.5)]), in relation to cognitive decline.The study population comprised the Nurses' Health Study Cognitive Cohort, which included 19,409 US women aged 70 to 81 years. We used geographic information system-based spatiotemporal smoothing models to estimate recent (1 month) and long-term (7-14 years) exposures to PM(2.5-10), and PM(2.5) preceding baseline cognitive testing (1995-2001) of participants residing in the contiguous United States. We used generalized estimating equation regression to estimate differences in the rate of cognitive decline across levels of PM(2.5-10) and PM(2.5) exposures. The main outcome measure was cognition, via validated telephone assessments, administered 3 times at approximately 2-year intervals, including tests of general cognition, verbal memory, category fluency, working memory, and attention.Higher levels of long-term exposure to both PM(2.5-10) and PM(2.5) were associated with significantly faster cognitive decline. Two-year decline on a global score was 0.020 (95% CI, -0.032 to -0.008) standard units worse per 10 ?g/m(3) increment in PM(2.5-10) exposure and 0.018 (95% CI, -0.035 to -0.002) units worse per 10 ?g/m(3) increment in PM(2.5) exposure. These differences in cognitive trajectory were similar to those between women in our cohort who were approximately 2 years apart in age, indicating that the effect of a 10-?g/m(3) increment in long-term PM exposure is cognitively equivalent to aging by approximately 2 years.Long-term exposure to PM(2.5-10) and PM(2.5) at levels typically experienced by many individuals in the United States is associated with significantly worse cognitive decline in older women.

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Transcriptome-wide analyses indicate mitochondrial responses to particulate air pollution exposure.

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