1.
Blood Plasma's Protective Ability against the Degradation of S-Nitrosoglutathione under the Influence of Air-Pollution-Derived Metal Ions in Patients with Exacerbation of Heart Failure and Coronary Artery Disease.
Wądołek, A, Drwiła, D, Oszajca, M, Stochel, G, Konduracka, E, Brindell, M
International journal of molecular sciences. 2021;(19)
Abstract
One of the consequences of long-term exposure to air pollutants is increased mortality and deterioration of life parameters, especially among people diagnosed with cardiovascular diseases (CVD) or impaired respiratory system. Aqueous soluble inorganic components of airborne particulate matter containing redox-active transition metal ions affect the stability of S-nitrosothiols and disrupt the balance in the homeostasis of nitric oxide. Blood plasma's protective ability against the decomposition of S-nitrosoglutathione (GSNO) under the influence of aqueous PM extract among patients with exacerbation of heart failure and coronary artery disease was studied and compared with a group of healthy volunteers. In the environment of CVD patients' plasma, NO release from GSNO was facilitated compared to the plasma of healthy controls, and the addition of ascorbic acid boosted this process. Model studies with albumin revealed that the amount of free thiol groups is one of the crucial factors in GSNO decomposition. The correlation between the concentration of NO released and -SH level in blood plasma supports this conclusion. Complementary studies on gamma-glutamyltranspeptidase activity and ICP-MS multielement analysis of CVD patients' plasma samples in comparison to a healthy control group provide broader insights into the mechanism of cardiovascular risk development induced by air pollution.
2.
Plasma nitrite is an indicator of acute changes in ambient air pollutant concentrations.
Gandhi, SK, Rich, DQ, Ohman-Strickland, PA, Kipen, HM, Gow, A
Inhalation toxicology. 2014;(7):426-34
-
-
Free full text
-
Abstract
CONTEXT Endothelial dysfunction has been suggested as a potential mechanism by which ambient air pollution may cause acute cardiovascular events. Recently, plasma nitrite has been developed as a marker of endothelial dysfunction. OBJECTIVES We examined the changes in plasma nitrite concentration associated with increases in ambient air pollutant concentrations in the previous 7 d. MATERIALS AND METHODS We linked up to three measurements of plasma nitrite concentrations obtained from 49 students to 24-h average concentrations of five criteria air pollutants [particle mass < 2.5 µm in aerodynamic diameter (PM(2.5)), carbon monoxide (CO), sulfur dioxide (SO₂), nitrogen dioxide (NO₂), and ozone (O₃)] measured at two monitoring sites closest to Rutgers University campus (6-15 miles) in New Jersey during the years 2006-2009. We examined the change in plasma nitrite associated with each interquartile-range (IQR) increase in pollutant concentration in the previous 24 h and six preceding 24- h periods, using linear mixed models. RESULTS IQR increases in mean PM(2.5) (7.0 µg/m³) and CO (161.7 parts per billion) concentrations in the first 24 h before the plasma nitrite measurement were associated with increased plasma nitrite concentrations (PM(2.5): 15.5 nanomolar; 95% confidence interval (CI): 2.4, 28.5; CO: 15.6 nanomolar; 95% CI: 2.4, 28.9). Increased plasma nitrite associated with IQR increases in O₃ and SO₂ concentrations over longer lags were observed. DISCUSSION AND CONCLUSION Rapid increases in plasma nitrite following exposure to ambient air pollutants support the hypothesis that ambient air pollution is associated with inducible nitric oxide synthase-mediated systemic inflammation in humans.
3.
[Particles in the outside air increase the risk of cardiovascular diseases].
Peters, A, ,
Gesundheitswesen (Bundesverband der Arzte des Offentlichen Gesundheitsdienstes (Germany)). 2005;:S79-85
Abstract
Evidence accumulated during the mid-1990 s that ambient particulate air pollution aerosol particles may not only exacerbate respiratory diseases but also be a risk factor for cardiovascular disease exacerbation. The aim of the studies described here was to assess the impact of the 1985 smog episode on the risk factor profile in the randomly selected population-based sample of the MONICA survey 1984/85 (S1). During a 13-day period in January 1985 sulphur dioxide concentrations increased four times and concentrations of total suspended atmospheric particles doubled. The impact of this time period on plasma viscosity, plasma C-reactive protein concentrations, heart rate and blood pressure was investigated. Regression models were used to assess these associations adjusting for individual risk factors such as gender, age, body mass index, serum total cholesterol and HDL-cholesterol, smoking, physical activity and medication for cardiovascular diseases and for weather conditions during the survey period. An increase in plasma viscosity, C-reactive protein and heart rate was estimated during the air pollution episode. There was also an increase in blood pressure, but this appeared to be attributable to the weather conditions during the air pollution episode. All the four outcomes were associated with the sulphur dioxide concentrations and the total suspended particle concentrations during the survey. These results indicate that ambient air pollution, particularly ambient particulate air pollution may induce systemic inflammation and modulate the autonomic function of the heart. These pathomechanisms may contribute to the observed associations between ambient air pollution concentrations and cardiovascular disease exacerbation such as hospitalisation and mortality due to cardiovascular diseases.