Ozone effects on blood biomarkers of systemic inflammation, oxidative stress, endothelial function, and thrombosis: The Multicenter Ozone Study in oldEr Subjects (MOSES)
Autoři:
John R. Balmes aff001; Mehrdad Arjomandi aff001; Philip A. Bromberg aff004; Maria G. Costantini aff006; Nicholas Dagincourt aff007; Milan J. Hazucha aff004; Danielle Hollenbeck-Pringle aff008; David Q. Rich aff009; Paul Stark aff007; Mark W. Frampton aff010
Působiště autorů:
Department of Medicine, University of California at San Francisco, San Francisco, CA, United States of America
aff001; Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA, United States of America
aff002; San Francisco Veterans Affairs Medical Center, San Francisco, CA, United States of America
aff003; Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, NC, United States of America
aff004; Center for Environmental Medicine, Asthma and Lung Biology, University of North Carolina, Chapel Hill, NC, United States of America
aff005; Health Effects Institute, Boston, MA, United States of America
aff006; New England Research Institute, Watertown, MA, United States of America
aff007; Alpert Medical School, Brown University, Providence, RI, United States of America
aff008; Department of Public Health Sciences, University of Rochester Medical Center, Rochester, NY, United States of America
aff009; Department of Medicine, University of Rochester Medical Center, Rochester, NY, United States of America
aff010; Department of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, United States of America
aff011
Vyšlo v časopise:
PLoS ONE 14(9)
Kategorie:
Research Article
prolekare.web.journal.doi_sk:
https://doi.org/10.1371/journal.pone.0222601
Souhrn
The evidence that exposure to ozone air pollution causes acute cardiovascular effects is mixed. We postulated that exposure to ambient levels of ozone would increase blood markers of systemic inflammation, prothrombotic state, oxidative stress, and vascular dysfunction in healthy older subjects, and that absence of the glutathione S-transferase Mu 1 (GSTM1) gene would confer increased susceptibility. This double-blind, randomized, crossover study of 87 healthy volunteers 55–70 years of age was conducted at three sites using a common protocol. Subjects were exposed for 3 h in random order to 0 parts per billion (ppb) (filtered air), 70 ppb, and 120 ppb ozone, alternating 15 min of moderate exercise and rest. Blood was obtained the day before, approximately 4 h after, and approximately 22 h after each exposure. Linear mixed effect and logistic regression models evaluated the impact of exposure to ozone on pre-specified primary and secondary outcomes. The definition of statistical significance was p<0.01. There were no effects of ozone on the three primary markers of systemic inflammation and a prothrombotic state: C-reactive protein, monocyte-platelet conjugates, and microparticle-associated tissue factor activity. However, among the secondary endpoints, endothelin-1, a potent vasoconstrictor, increased from pre- to post-exposure with ozone concentration (120 vs 0 ppb: 0.07 pg/mL, 95% confidence interval [CI] 0.01, 0.14; 70 vs 0 ppb: -0.03 pg/mL, CI -0.09, 0.04; p = 0.008). Nitrotyrosine, a marker of oxidative and nitrosative stress, decreased with increasing ozone concentrations, with marginal significance (120 vs 0 ppb: -41.5, CI -70.1, -12.8; 70 vs 0 ppb: -14.2, CI -42.7, 14.2; p = 0.017). GSTM1 status did not modify the effect of ozone exposure on any of the outcomes. These findings from healthy older adults fail to identify any mechanistic basis for the epidemiologically described cardiovascular effects of exposure to ozone. The findings, however, may not be applicable to adults with cardiovascular disease.
Klíčová slova:
Inflammation – Blood – Biomarkers – Oxidative stress – Platelets – Platelet activation – Ozone – Fibrinogen
Zdroje
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