[Using the Mini-Mental State Examination (MMSE) for preliminary assessment of cognitive impairment in subjects exposed to air pollution with particulate matter]. / Utilizzo del Mini-Mental State Examination (MMSE) per la valutazione preliminare del deterioramento cognitivo in soggetti esposti a particolato atmosferico.

Epidemiologic and clinical studies have linked elevated concentrations of particulate matter to adverse health effects. In particular, has been demonstrated an association between UFPs exposure and occurrence of acute respiratory infections, lung cancer, chronic chronic obstructive pulmonary diseases and cardiovascular diseases. Recently, the exposure to particulate air pollution has been linked to cognitive decline. In this work, we used the Mini-Mental State Examination (MMSE) in a preliminary assessment of cognitive function in individuals who have lived and carried out work in heavily urbanized areas, where ambient levels of particulate air pollution were frequently above the standard of the law. The results showed the presence of mild-moderate cognitive impairment in 39.4% of the subjects examined compared to the control group.

Apoptotic and proinflammatory effect of combustion-generated organic nanoparticles in endothelial cells.

Air pollution exposure in industrialized cities is associated with an increased risk of morbidity and mortality attributed to cardiovascular diseases. Combustion exhausts emitted from motor vehicles and industries represent a major source of nanoparticles in the atmosphere. Flame-generated organic carbon nanoparticles (OC NPs) provide interesting model nanoparticles that simulate fresh combustion emissions near roadways or combustion sources. These model nanoparticles can be produced by controlling flame operating conditions and used to test possible toxicological mechanisms responsible for the observed health effects. OC NPs were used to investigate their possible effect on endothelial cells (EC) growth and production of proinflammatory lipid mediators. Results indicated a dose and time-dependent reduction in cell viability following incubation of EC with OC NPs for 24 and 48h. Fluorescence-activated cell sorting revealed that EC treated with OC NPs showed a cell proliferation index significantly lower than that of control cells and an increased apoptotic cell death. The annexin assay confirmed the increased apoptotic cell death. Moreover, OC NPs also induced a time-dependent increase of proinflammatory lysophospholipid production. These results, establishing that OC NPs induce EC proinflammatory lysophosholipid production and apoptotic cell death, provide the first evidence of the detrimental effect of OC NPs on EC.