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In epidemiological studies associations have been observed consistently and coherently between ambient concentrations of particulate matter and morbidity and mortality. With improvement of measurement techniques, the effects became clearer when smaller particle sizes were considered. Therefore, it seems worthwhile to look at the smallest size fraction available today, namely ultrafine particles (UPs, diameter below 0.1 μm) and to compare their health effects with those of fine particles (FPs, diameter below 2.5 μm). However, there are only few studies available which allow such a comparison.

Four panel studies with asthma patients have been performed in Germany and Finland. A decrease of peak expiratory flow and an increase of daily symptoms and medication use was found for elevated daily particle concentrations, and in three of these studies it was strongest for UPs. One large study on daily mortality is available from Germany. It showed comparable effects of fine and ultrafine particles in all size classes considered. However, FPs showed more immediate effects while UPs showed more delayed effects with a lag of four days between particulate concentrations and mortality. Furthermore, immediate effects were clearer in respiratory cases, whereas delayed effects were clearer in cardiovascular cases.

In total, the limited body of studies suggests that there are health effects, due to both UPs and FPs, which might be independent from each other. If this is confirmed in further investigations, it might have important implications for monitoring and regulation, which until now does not exist for UPs. Data from Germany show that FPs cannot be used as indicator for UPs: the time trends for FPs decreased, while UPs was stable and the smallest size fraction of UPs has continually increased since 1991/92.

Zinc status, inflammation, and genetic determinants are prominent mechanisms in the pathogenesis of atherosclerosis (AT) and its compliances (cardiovascular diseases). In this review, we report the possible impact of zinc on AT development as well as the role played by a significant genetic determinant involved in inflammation, such as interleukin-6 (IL-6). Genetic polymorphism of IL-6 may affect a different inflammatory response as well as zinc turnover, predisposing to AT. Indeed, zinc deficiency is suggested as a risk factor for AT with advancing aging. The increment of dysfunctional proteins involved in zinc homeostasis, i.e. metallothioneins (MT), caused by persistent inflammation and oxidative stress may further contribute to zinc deficiency and consequently to the development of AT. A zinc supplementation may be useful to achieve healthy aging and, as such, to prevent AT, but it is necessary to consider the individual genetic background (especially when referred to IL-6 and MT polymorphisms) for the success of zinc intervention. Therefore, a zinc genomic approach may offer a reasonable hope for understanding the impact of zinc on molecular processes that maintain health and prevent the development of AT.