3/30/2023 0 Comments Detectx cortisolUrinary DNA oxidation marker 8-hydroxy-deoxy-guanosine increased 14% (6.4%, 21%) 1-hr post exposure to copper urinary neural marker vanillylmandelic acid increased 29% (3%, 54%) 1-hr post exposure to aluminum and urinary cortisol increased 88% (0.9%, 176%) 1-hr post exposure to vanadium. For example, the blood inflammatory marker vascular endothelia growth factor (VEGF) increased 5.3% (95% confidence interval: 0.3%, 10.2%) 1-hr post exposure to nickel the traumatic brain injury marker ubiquitin C-terminal hydrolase L1 (UCHL1) increased 11% (1.2%, 21%) and 14% (0.3%, 29%) 1-hr and 21-hr post exposure to barium, respectively and the systemic stress marker cortisol increased 1.5% (0%, 2.9%) and 1.5% (0.5%, 2.8%) 1-hr and 21-hr post exposure to silver, respectively. Exposure to various metals (silver, aluminum, barium, copper, iron, potassium, lithium, nickel, tin, and/or vanadium) was significantly associated with increased levels of various blood or urinary biomarkers. ![]() ![]() Results for metals were expressed as change (%) from daily pre-exposure biomarker levels after exposure to a metal at a level equivalent to the mean concentration. For example, UCHL1 increased 9.4% (1.8%, 17%) in blood 21-h post exposure to ascorbate-related OP, while urinary malondialdehyde increased 19% (3.6%, 35%) and 8-hydroxy-deoxy-guanosine increased 24% (2.9%, 48%) 21-h post exposure to ascorbate- and glutathione-related OP, respectively.ConclusionOur results from this exploratory study suggest that metal constituents and OP in ambient PM may influence biomarker levels associated with systemic inflammation, oxidative stress, perturbations of neural function, and systemic physiological stress. Exposure to ascorbate- or glutathione-related OP was significantly associated with increased inflammatory and neural biomarkers including interleukin-6, VEGF, UCHL1, and S100 calcium-binding protein B in blood, and malondialdehyde and 8-hydroxy-deoxy-guanosine in urine. Results for OP were expressed as change (%) from daily pre-exposure biomarker levels after exposure to ascorbate-related OP at a level equivalent to the mean concentration, or for exposure to glutathione-related OP at a level above the limit of detection. Urinary DNA oxidation marker 8‑hydroxy‑deoxy‑guanosine increased 14% (6.4%, 21%) 1-h post exposure to copper urinary neural marker vanillylmandelic acid increased 29% (3%, 54%) 1-h post exposure to aluminum and urinary cortisol increased 88% (0.9%, 176%) 1-h post exposure to vanadium. For example, the blood inflammatory marker vascular endothelia growth factor (VEGF) increased 5.3% (95% confidence interval: 0.3%, 10.2%) 1-h post exposure to nickel the traumatic brain injury marker ubiquitin C-terminal hydrolase L1 (UCHL1) increased 11% (1.2%, 21%) and 14% (0.3%, 29%) 1-h and 21-h post exposure to barium, respectively and the systemic stress marker cortisol increased 1.5% (0%, 2.9%) and 1.5% (0.5%, 2.8%) 1-h and 21-h post exposure to silver, respectively. ![]() We used mixed-regression models to analyze associations adjusting for PM size and mass concentration.ResultsResults for metals were expressed as change (%) from daily pre-exposure biomarker levels after exposure to a metal at a level equivalent to the mean concentration. Blood and urine samples were collected pre-exposure, and 1-h and 21-h post exposure for assessment of biomarkers. ![]() Metal concentrations and OP (measured by ascorbate and glutathione depletion in synthetic airway fluid) in PM were analyzed. Exposures lasted 130 min, separated by ≥2 weeks. In this exploratory study, we examined the effects of metals and oxidative potential (OP) in urban PM on biomarkers of systemic inflammation, oxidative stress and neural function.MethodsFifty-three healthy non-smoking volunteers (mean age 28 years, twenty-eight females) were exposed to coarse (2.5-10 μm, mean 213 μg/m3), fine (0.15-2.5 μm, 238 μg/m3), and/or ultrafine concentrated ambient PM (3). BackgroundOxidative stress and inflammation are considered to be important pathways leading to particulate matter (PM)-associated disease.
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