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Accelerated aging and altered subclinical response to ozone exposure in young, healthy adults.
Weston, William C; Bind, Marie Abèle; Cascio, Wayne E; Devlin, Robert B; Diaz-Sanchez, David; Ward-Caviness, Cavin K.
Afiliación
  • Weston WC; Center for Public Health and Environmental Assessment, US Environmental Protection Agency, Chapel Hill, NC 27514, USA.
  • Bind MA; US Department of Energy, Oak Ridge Institute for Science and Education, Oak Ridge, TN 37830, USA.
  • Cascio WE; Biostatistics Center, Massachusetts General Hospital, Boston, MA 02114, USA.
  • Devlin RB; Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.
  • Diaz-Sanchez D; Center for Public Health and Environmental Assessment, US Environmental Protection Agency, Chapel Hill, NC 27514, USA.
  • Ward-Caviness CK; Center for Public Health and Environmental Assessment, US Environmental Protection Agency, Chapel Hill, NC 27514, USA.
Environ Epigenet ; 10(1): dvae007, 2024.
Article en En | MEDLINE | ID: mdl-38846065
ABSTRACT
Ozone exposure induces a myriad of adverse cardiopulmonary outcomes in humans. Although advanced age and chronic disease are factors that may exacerbate a person's negative response to ozone exposure, there are no molecular biomarkers of susceptibility. Here, we examine whether epigenetic age acceleration (EAA) is associated with responsiveness to short-term ozone exposure. Using data from a crossover-controlled exposure study (n = 17), we examined whether EAA, as measured in lung epithelial cells collected 24 h after clean air exposure, modifies the observed effect of ozone on autonomic function, cardiac electrophysiology, hemostasis, pulmonary function, and inflammation. EAA was assessed in lung epithelial cells extracted from bronchoalveolar lavage fluids, using the pan-tissue aging clock. We used two analytic approaches (i) median regression to estimate the association between EAA and the estimated risk difference for subclinical responses to ozone and (ii) a block randomization approach to estimate EAA's effect modification of subclinical responses. For both approaches, we calculated Fisher-exact P-values, allowing us to bypass large sample size assumptions. In median regression analyses, accelerated epigenetic age modified associations between ozone and heart rate-corrected QT interval (QTc) ([Formula see text]= 0.12, P-value = 0.007) and between ozone and C-reactive protein ([Formula see text] = -0.18, P = 0.069). During block randomization, the directions of association remained consistent for QTc and C-reactive protein; however, the P-values weakened. Block randomization also revealed that responsiveness of plasminogen activator inhibitor-1 (PAI-1) to ozone exposure was modified by accelerated epigenetic aging (PAI-1 difference between accelerated aging-defined block groups = -0.54, P-value = 0.039). In conclusion, EAA is a potential biomarker for individuals with increased susceptibility to ozone exposure even among young, healthy adults.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Environ Epigenet Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Environ Epigenet Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido