Metals and oxidative potential in urban particulate matter influence systemic inflammatory and neural biomarkers: A controlled exposure study

Abstract

Background: Oxidative stress and inflammation are considered to be important pathways leading to particulate matter (PM)-associated disease. 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. Methods: Fifty-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 (<0.3 μm, 136 μg/m3). Exposures lasted 130 minutes, separated by ≥2 weeks. Metal concentrations and OP (measured by ascorbate and glutathione depletion in synthetic airway fluid) in PM were analyzed. Blood and urine samples were collected pre-exposure, and 1-hour and 21-hour post exposure for assessment of biomarkers. We used mixed-regression models to analyze associations adjusting for PM size and mass concentration. Results: 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. 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. 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. Urinary 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. 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. 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. For example, UCHL1 increased 9.4% (1.8%, 17%) in blood 21-hr 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-hr post exposure to ascorbate- and glutathione-related OP, respectively. Conclusion: Our results from this exploratory study suggest that metal constituents and OP in ambient PM may influence biomark...

Biomonitoring of Metals in Children Living in an Urban Area and Close to Waste Incinerators

“…In a study assessing the short-term oxidative potential of urban particulate matter in adult nonsmoking volunteers, several metals present in coarse, fine, and ultrafine PM (including Ba, Cu, Ni, and V) were significantly associated with increased levels of biomarkers of systemic inflammation, oxidative stress, and neural function. Ba, in particular, induced a significant increment (+11% at 1 h, +14% at 21 h postexposure) of L1(UCHL1) (traumatic brain injury marker ubiquitin C-terminal hydrolase L1); Cu exposure increased (+14% at 1 h) levels of the DNA oxidation marker 8-hydroxy-deoxy-guanosine; urinary cortisol increased by 88% after exposure to V, and the blood inflammatory marker VEGF (vascular endothelia growth factor) increased by 5.3% 1 h after Ni exposure [80].…”

Oxidative Potential Versus Biological Effects: A Review on the Relevance of Cell-Free/Abiotic Assays as Predictors of Toxicity from Airborne Particulate Matter

“…In total 58 studies were identified exploring both the OP and biological effects of PM and/or combustion particles in cells, animals or humans [27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80,81,82,83,84]. Among these were three cases of multiple studies based on the same particle samples and measurements of OP: Two studies on in vitro and in vivo effects of a set of wood smoke and PM samples [45,46], and six studies from a series of PM exposures of human volunteers under the RAPTES (Risk of Airborne Particles: A Toxicological–Epidemiological Hybrid Study) project [67,68,69,70,71,72], and three epidemiolo...…”

Metal Ion Release from Fine Particulate Matter Sampled in the Po Valley to an Aqueous Solution Mimicking Fog Water: Kinetics and Solubility

“…Metal ions, non-metallic anions, and their inorganic derivatives (oxides, salts, etc. ) are among the PM constituents (Brito et al, 2018;Meng et al, 2013;Popoola et al, 2018) which are considered to be co-responsible for PM toxicity, likely because of the oxidative stress which several chemical species may induce in cellular tissues (Meng et al, 2013;Liu et al, 2018;Yang et al, 2019). If PM is in contact with environmental or physiological solutions, the substances contained in the particles may be released, thus becoming bio-accessible and potentially toxic to living organisms and human tissues.…”