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Arterial stiffening is associated with increased cardiovascular risk. Whether exposure to relatively high levels of air pollution is associated with arterial stiffening is unclear. We aimed to assess the association between exposure to major air pollutants and arterial stiffening. PubMed, SCOPUS and Web of Science databases (through 31 January 2017) were searched using a combination of terms related to exposure to gaseous [nitrogen dioxide (NO2), nitrogen oxides (NOx) and sulphur dioxide (SO2)] or particulate matter pollutants (PM2.5, PM10 and PM10-2.5), arterial stiffness (pulse wave velocity) and reflected waves (augmentation index, augmentation pressure). Pertinent information were extracted from selected studies. In this systematic review were included 8 studies with available data on air pollution and arterial stiffness/reflected waves parameters (8 studies explored the effects of exposure to particulate matter pollutants, 3 studies the effects of exposure to gaseous pollutants); seven of them reported increased arterial stiffness/reflected waves after exposure to air pollution (6 of 8 studies after particulate matter pollutants; 2 of 3 studies after gaseous pollutants). Arterial stiffness and reflected waves were increased in the majority of the studies after both short- and long-term exposure to air pollutants. In conclusion, available evidence supports an association of main air pollutants with increased arterial stiffness and reflected waves. This finding may have implications for population-based strategies for the reduction of arterial stiffness, a vascular biomarker and an intermediate endpoint for cardiovascular disease. [ABSTRACT FROM AUTHOR]

Heavy metals are extensively used in agriculture and industrial applications such as production of pesticides, batteries, alloys, and textile dyes. Prolonged, intensive or excessive exposure can induce related systemic disorders. Kidney is a target organ in heavy metal toxicity for its capacity to filter, reabsorb and concentrate divalent ions. The extent and the expression of renal damage depends on the species of metals, the dose, and the time of exposure. Almost always acute kidney impairment differs from chronic renal failure in its mechanism and in the magnitude of the outcomes. As a result, clinical features and treatment algorithm are also different. Heavy metals in plasma exist in an ionized form, that is toxic and leads to acute toxicity and a bound, inert form when metal is conjugated with metallothionein and are then delivered to the liver and possible causing the kidney chronic damage. Treatment regimens include chelation therapy, supportive care, decontamination procedures and renal replacement therapies. This review adds specific considerations to kidney impairment due to the most common heavy metal exposures and its treatment. [ABSTRACT FROM AUTHOR]

Osteoporosis and cardiovascular disease are worldwide public health issues. Recent evidence indicates a possible role of the canonical Wnt/β-catenin signalling pathway as a common mediator between these two diseases. The aim of the present study was to investigate the relationship between serum concentrations of sclerostin and Dkk1, two extracellular inhibitors of Wnt/β-catenin signalling, with carotid intima-media thickness (CIMT) and with arterial stiffness, evaluated by measuring the pulse wave velocity (PWV) in an ambulatory population of adults. To this aim, 67 subjects were recruited in the 'Atherosclerosis and osteoporosis: identification of common pathogenetic factors' investigation. Serum sclerostin levels correlated positively with CIMT (r=0.314, p=0.03) and inversely with the augmentation index, a marker of arterial stiffness (r=-0.286, p<0.05), whereas Dkk1 did not. Moreover, in a multivariate linear regression model, sclerostin [β -0.1472; p=0.0023; standard error (SE)=0.04620] was an independent predictor of PWV in the study subjects. Our study shows that, following adjustment for confounders, sclerostin is an independent predictor of arterial stiffness in an ambulatory population, whereas Dkk1 is not. [ABSTRACT FROM AUTHOR]