Regarding short-term usage, the studied e-cigarettes generate smaller changes in lung function but similar nicotinergic impact to tobacco cigarettes. Future research should target the health effects of long-term e-cigarette usage, including the effects of nicotine dosage.

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Rationale: The acute effect of secondhand smoke (SHS) on lung function and the duration of system disruption remain unknown. Objectives: To assess the SHS effects and their duration on lung function and inflammatory markers. Methods: In a randomized single-blind crossover experiment data were obtained from 16 (8 women) nonsmoking adults at baseline and at 0, 1, and 3 hours after a 1-hour SHS exposure set at bar/ restaurant SHS levels. Measurements and Main Results: Serum and urine cotinine, lung function, and cytokines IL-4, IL-5, IL-6, tumor necrosis factor (TNF)-a, and IFN-g. At 0 hours most lung function parameters were significantly reduced (indicative: FEV 1 , 4.3 6 0.4 vs. 3.8 6 0.3 L; FEV 1 /FVC, 0.9 6 0.1 vs. 0.8 6 0.1; P , 0.05) but at 3 hours they were at baseline levels. In contrast, cotinine (serum, 8.9 6 3.2 vs. 35.5 6 10.2 ngÁml 21 ), IL-4 (41.3 6 5.8 vs. 44.2 6 4.5 pgÁml 21 ), IL-5 (36.1 6 3.2 vs. 60.1 6 7.0 pgÁml 21 ), IL-6 (2.5 6 0.3 vs. 7.6 6 1.4 pgÁml 21 ) and IFN-g (0.3 6 0.2 vs. 0.6 6 0.2 IUÁml 21 ) at 3 hours were higher than at baseline (P , 0.05). IL-4 and TNF-a increased only in men, whereas IL-5, IL-6, and IFN-g were different between sexes after exposure (P , 0.05). Regression analyses revealed inverse associations of FEV 1 and FEV 1 /FVC ratio with IL-5 (P , 0.05) in men and with IL-5 (P 5 0.01), IL-6 (P , 0.001), IFN-g (P 5 0.034) and serum cotinine (P , 0.001) in women. Conclusions: We conclude that 1 hour of SHS exposure at bar/ restaurant levels is accompanied by significant decrements on lung function and marked increases in inflammatory cytokines, particularly in men. More importantly, whereas most smoke-induced effects on lung function appear to recede within 60 minutes, inflammatory cytokines remain elevated for at least 3 hours after exposure to SHS. Keywords: passive smoking; cotinine; respiration; inflammatory markersIn the 10 minutes you will spend reading this article, 111 people will die somewhere in the world from tobacco-induced illnesses.* Fourteen of them have never smoked. † An overwhelming amount of evidence has emerged over the past decades on the adverse health effects of secondhand smoke (SHS) (1-5). Nevertheless, more than 126 million American and 130 million Chinese adult nonsmokers suffer daily SHS exposure, whereas global estimates include 700 million children and 50 million pregnant women (1). Latest reports show that, despite current measures, the prevalence rates of smoking are increasing (2, 3), while the tobacco industry predicts a global expansion of the tobacco epidemic in the near future (3). Moreover, arguments are being expressed that only chronic exposures to SHS represent a health risk and that there is no scientific basis for claims that brief, acute, transient SHS exposures represent a significant acute health hazard in nonsmokers (6). This is, in part, because our knowledge on the effects of SHS is based predominantly on longitudinal epidemiological studies, whereas experimental studies assessing the acute and short-term effects of SHS are sca...

Coffee is one of the most popular and widely consumed beverages worldwide due to its pleasant taste and aroma. A number of studies have been performed to elucidate the possible beneficial effects of coffee consumption on human health and have shown that coffee exhibits potent antioxidant activity, which may be attributed mainly to its polyphenolic content. However, there is also evidence to suggest that coffee roasting (the procedure which turns green coffee beans to the dark, roasted ones from which the beverage derives) may alter the polyphenolic profile of the beans (e.g., via the Maillard reaction) and, concomitantly, their antioxidant activity. In the present study, the antioxidant activity of 13 coffee varieties was examined in both green and roasted coffee bean extracts using 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2′-azinobis-(3-eth-ylbenzothiazoline-6-sulfonic acid) (ABTS•+) radical scavenging assays. In addition, 5 selected varieties were also examined for their protective effects against peroxyl and hydroxyl radical-induced DNA strand cleavage. Finally, C2C12 murine myoblasts were treated with non-cytotoxic concentrations of the most potent extract in order to examine its effects on the cellular redox status by measuring the glutathione (GSH) and reactive oxygen species (ROS) levels by flow cytometry. Our results revealed that, in 8 out of the 13 coffee varieties, roasting increased free radical scavenging activity as shown by DPPH and ABTS•+ assays. Moreover, we found that when one coffee variety was roasted for different amounts of time, the increase in the antioxidant activity depended on the roasting time. By contrast, in 5 varieties, roasting reduced the antioxidant activity. Similar differences between the roasted and green beans were also observed in the free radical-induced DNA strand cleavage assay. The observed differences in the antioxidant activity between the different coffee varieties may be attributed to their varying polyphenolic content and composition, as well as to the different molecules produced during roasting. In addition, in the cell culture assay, the tested coffee extract led to increased GSH levels in a dose-dependent manner, indicating the enhancement of cellular antioxidant mechanisms.