ArticlePloS one2013
Mitochondrial genetic background modifies the relationship between traffic-related air pollution exposure and systemic biomarkers of inflammation.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Health effects of ultrafine particles: a systematic literature review update of epidemiological evidence.International journal of public health · 2019Pooled it
- PMAntioxidants (Basel, Switzerland) · 2026Article
- Air pollution exposure associated with decline rates in skeletal muscle mass and grip strength and increase rate in body fat in elderly: a 5-year follow-up study.Environmental health and preventive medicine · 2025Article
- Assessing community health risks from exposure to ultrafine particles containing transition metals in the Greater Houston Area.The Science of the total environment · 2024Article
- Coarse Particulate Matter and Markers of Inflammation and Coagulation in the Multi-Ethnic Study of Atherosclerosis (MESA) Population: A Repeat Measures Analysis.Environmental health perspectives · 2024Article
- The Impact of Fine Particulate Matter 2.5 on the Cardiovascular System: A Review of the Invisible Killer.Nanomaterials (Basel, Switzerland) · 2022Review
- Prenatal particulate matter exposure and mitochondrial mutational load at the maternal-fetal interface: Effect modification by genetic ancestry.Mitochondrion · 2022Article
- Effect of Silymarin Supplementation in Lung and Liver Histological Modifications during Exercise Training in a Rodent Model.Journal of functional morphology and kinesiology · 2021Article
- Associations Between Maternal Lifetime Stress and Placental Mitochondrial DNA Mutations in an Urban Multiethnic Cohort.Biological psychiatry · 2021Article
- Accelerated epigenetic age as a biomarker of cardiovascular sensitivity to traffic-related air pollution.Aging · 2020Article
- Cardiovascular adaptations to particle inhalation exposure: molecular mechanisms of the toxicology.American journal of physiology. Heart and circulatory physiology · 2020Review
- Synthesis of Harvard Environmental Protection Agency (EPA) Center studies on traffic-related particulate pollution and cardiovascular outcomes in the Greater Boston Area.Journal of the Air & Waste Management Association (1995) · 2019Article
- A review of gene-by-air pollution interactions for cardiovascular disease, risk factors, and biomarkers.Human genetics · 2019Review
- A Muscarinic Antagonist Reduces Airway Inflammation and Bronchoconstriction Induced by Ambient Particulate Matter in a Mouse Model of Asthma.International journal of environmental research and public health · 2018Article
- p66Shc Mediates Mitochondrial Dysfunction Dependent on PKC Activation in Airway Epithelial Cells Induced by Cigarette Smoke.Oxidative medicine and cellular longevity · 2018Article
- Impacts of the Mitochondrial Genome on the Relationship of Long-Term Ambient Fine Particle Exposure with Blood DNA Methylation Age.Environmental science & technology · 2017Article
- Mitochondrial Function in Allergic Disease.Current allergy and asthma reports · 2017Review
- Article
- MicroRNA-1228(*) inhibit apoptosis in A549 cells exposed to fine particulate matter.Environmental science and pollution research international · 2016Article
- Update on the Mechanisms of Pulmonary Inflammation and Oxidative Imbalance Induced by Exercise.Oxidative medicine and cellular longevity · 2016Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundMitochondria are the main source of reactive oxygen species (ROS). Human mitochondrial haplogroups are linked to differences in ROS production and oxidative-stress induced inflammation that may influence disease pathogenesis, including coronary artery disease (CAD). We previously showed that traffic-related air pollutants were associated with biomarkers of systemic inflammation in a cohort panel of subjects with CAD in the Los Angeles air basin.
objectiveWe tested whether air pollutant exposure-associated inflammation was stronger in mitochondrial haplogroup H than U (high versus low ROS production) in this panel (38 subjects and 417 observations).
methodsInflammation biomarkers were measured weekly in each subject (≤ 12 weeks), including interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), C-reactive protein, interleukin-6 soluble receptor and tumor necrosis factor-soluble receptor II. We determined haplogroup by restriction fragment length polymorphism analysis. Air pollutants included nitrogen oxides (NOx), carbon monoxide (CO), organic carbon, elemental and black carbon (EC, BC); and particulate matter mass, three size fractions (<0.25 µm, 0.25-2.5 µm, and 2.5-10 µm in aerodynamic diameter). Particulate matter extracts were analyzed for organic compounds, including polycyclic aromatic hydrocarbons (PAH), and in vitro oxidative potential of aqueous extracts. Associations between exposures and biomarkers, stratified by haplogroup, were analyzed by mixed-effects models.
resultsIL-6 and TNF-α were associated with traffic-related air pollutants (BC, CO, NOx and PAH), and with mass and oxidative potential of quasi-ultrafine particles <0.25 µm. These associations were stronger for haplogroup H than haplogroup U.
conclusionsResults suggest that mitochondrial haplogroup U is a novel protective factor for air pollution-related systemic inflammation in this small group of subjects.
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