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SignificanceElectronic cigarettes, also known as e-cigarettes, are devices designed to imitate regular cigarettes and deliver nicotine via inhalation without combusting tobacco. They are purported to deliver nicotine without other toxicants and to be a safer alternative to regular cigarettes. However, little toxicity testing has been performed to evaluate the chemical nature of vapour generated from e-cigarettes. The aim of this study was to screen e-cigarette vapours for content of four groups of potentially toxic and carcinogenic compounds: carbonyls, volatile organic compounds, nitrosamines and heavy metals.Materials and methodsVapours were generated from 12 brands of e-cigarettes and the reference product, the medicinal nicotine inhaler, in controlled conditions using a modified smoking machine. The selected toxic compounds were extracted from vapours into a solid or liquid phase and analysed with chromatographic and spectroscopy methods.ResultsWe found that the e-cigarette vapours contained some toxic substances. The levels of the toxicants were 9-450 times lower than in cigarette smoke and were, in many cases, comparable with trace amounts found in the reference product.ConclusionsOur findings are consistent with the idea that substituting tobacco cigarettes with e-cigarettes may substantially reduce exposure to selected tobacco-specific toxicants. E-cigarettes as a harm reduction strategy among smokers unwilling to quit, warrants further study. (To view this abstract in Polish and German, please see the supplementary files online.).

Recent evidence suggests that e-cigarette users tend to change their puffing behaviors when using e-liquids with reduced nicotine concentrations by taking longer and more frequent puffs. Using puffing regimens modelled on puffing topography data from 19 experienced e-cigarette users who switched between 18 and 6 mg/mL e-liquids with and without power adjustments, differences in daily exposure to carbonyl compounds and estimated changes in cancer risk were assessed by production of aerosols generated using a smoking machine and analyzed using gas and liquid chromatography. Significant differences across conditions were found for formaldehyde and acetaldehyde (p < 0.01). Switching from a higher to a lower nicotine concentration was associated with greater exposure regardless of whether power settings were fixed or adjustable which is likely due to increased liquid consumption under lower nicotine concentration settings. Daily exposure for formaldehyde and acetaldehyde was higher for 17/19 participants when using low (6 mg/mL) compared with high (18 mg/mL) nicotine e-liquid concentration when power was fixed. When power adjustments were permitted, formaldehyde and acetaldehyde levels were higher respectively for 16/19 and 14/19 participants with the use of 6 compared with 18 mg/mL nicotine e-liquid. [ABSTRACT FROM AUTHOR]

Polycyclic aromatic hydrocarbons (PAHs) and their nitrated derivatives are responsible for mutagenic activation of ambient air. The aim of the study was the assessment of exposure for PAHs and nitro-PAHs in the urbanized region in Poland in comparison with the non-urbanized region and assessment of seasonal variation of PAHs and nitro-PAHs. Concentrations of 12 PAHs, 8 nitrated PAHs in total suspended particulate matter in air of urban and suburban (reference samples-mountain region) region in Poland during four seasons have been shown. The method of solvent extraction of particulate matter, fractionation organic extract and HPLC and GC/MS analysis were applied. The concentrations of PAHs and nitro-PAHs were 10–100 times lower in reference samples than concentrations of PAHs and nitro-PAHs in urban region in summer. The concentrations of PAHs and nitro-PAHs were highest in winter. The exposure profiles of PAHs and nitro-PAHs in four seasons have been shown. The correlation factor between concentrations of PAHs and nitro-PAHs was found. Important influence of ambient air temperature for PAHs and nitro-PAHs concentrations was shown. Obtained results suggest that the coal combustion in Polish households was the main source of PAHs and their nitro derivatives contaminations. Emission from transport sources is a secondary source of air pollution in urban areas. [ABSTRACT FROM AUTHOR]

OBJECTIVES: Changes in enzymatic antioxidant activity are frequently observed in workers occupationally exposed to lead. Few studies have investigated the influence of lead on the non-enzymatic antioxidant system. The aim of our study was to assess the influence of occupational exposure to lead on the plasma concentration of two hydrophobic forms of vitamin E: [alpha]-tocopherol and [gamma]-tocopherol. METHODS: A sample of 401 healthy men, aged 19-62, participated in the study. In total, 340 of these subjects were employed at the Mine and Metallurgical Plant in southern Poland. The workers who were occupationally exposed to lead were divided into quartiles (groups of 85 subjects). The lead concentrations in the blood of the subjects in the control group and in the lead exposure quartiles correspond to the following ranges: 10-72 [mu]g/l (control group); 82-206 [mu]g/l (Q1); 209-308 [mu]g/l (Q2); 308-394 [mu]g/l (Q3) and 395-644 [mu]g/l (Q4), respectively. RESULTS: Significant differences were observed only for the plasma concentration of [gamma]-tocopherol, which differed between the control group and Q1 (by 24.1%, p=0.0368), between Q1 and Q3 (by -18.8%, p=0.0115) and between Q1 and Q4 (by -25.7%, p=0.0002). Multiple linear regression analysis showed that the statistically significant, predictive properties of the [gamma]-tocopherol plasma concentration were as follows: triglycerides ([beta]=0.440)> age ([beta]=0.131)> whole cholesterol ([beta]=0.117)> blood lead concentration ([beta]=-0.108). For [alpha]-tocopherol, significant prognostic properties were triglycerides and total cholesterol ([beta]=0.485 and [beta]=0.399, respectively). CONCLUSIONS: Occupational exposure to lead is strongly correlated with the concentration of [gamma]-tocopherol but not [alpha]-tocopherol. [ABSTRACT FROM AUTHOR]

Background: Tobacco smoking is one of the most important risk factors for cardiovascular disease (CVD) and few biomarkers have been linked to the increased risk of CVD and tobacco smoking. Tobacco smoke has been shown to elevate the plasma levels of asymmetric dimethylarginine (ADMA), a metabolite of L-arginine and an endogenous inhibitor of endothelial nitric oxide synthase. The other potential biomarker that has not been studied to date is L-homoarginine, a homolog of L-arginine. The aim of this study was to evaluate the effects of cigarette smoking on L-homoarginine and other CVD biomarkers., Methods and Results: In a cross-sectional study of 231 healthy male volunteers, we measured plasma levels of L-homoarginine, L-arginine, and ADMA using the HPLC method. In smokers, we found that plasma L-homoarginine levels were 16.7% lower compared with nonsmokers after adjusting for age, body mass index, plasma creatinine, and metal blood levels (P<0.05). Plasma ADMA levels were only 6.0% higher in smokers when compared with the levels found in nonsmokers (P>0.05)., Conclusions: Our results suggest that, in contrast to ADMA, there is a strong association between exposure to tobacco smoke and plasma L-homoarginine levels. Further research in this field is needed to explain the mechanisms of the relationship of low L-homoarginine levels, smoking, and cardiovascular health.