Vapors from EC contain toxic and carcinogenic carbonyl compounds. Both solvent and battery output voltage significantly affect levels of carbonyl compounds in EC vapors. High-voltage EC may expose users to high levels of carbonyl compounds.

Many non-cigarette tobacco products, including e-cigarettes, contain various flavorings, such as fruit flavours. Although many flavorings used in e-cigarettes are generally recognized as safe when used in food products, concerns have been raised about the potential inhalation toxicity of these chemicals. Benzaldehyde, which is a key ingredient in natural fruit flavors, has been shown to cause irritation of respiratory airways in animal and occupational exposure studies. Given the potential inhalation toxicity of this compound, we measured benzaldehyde in aerosol generated in a laboratory setting from flavored e-cigarettes purchased online and detected benzaldehyde in 108 out of 145 products. The highest levels of benzaldehyde were detected in cherry flavored products. The benzaldehyde doses inhaled with 30 puffs from flavored e-cigarettes were often higher than doses inhaled from a conventional cigarette. Levels in cherry flavored products were over 1000 times lower than doses inhaled in the workplace. While e-cigarettes seem to be a promising harm reduction tool for smokers, findings indicate that using these products could result in repeated inhalation of benzaldehyde, with long-term users risking regular exposure to the substance. Given the uncertainty surrounding adverse health effects stemming from long-term inhalation of flavoring ingredients such as benzaldehyde, clinicians need to be aware of this emerging risk and ask their patients about use of flavored e-cigarettes.

The influence of fatty acid methyl esters (FAME) and hydrotreated vegetable oil (HVO) diesel blends on the exhaust emissions from a passenger car was examined. The impact of FAME for the cold urban phase (UDC) was increased CO and HC emissions, probably due to blend physical properties promoting incomplete combustion. The HVO blend caused the lowest CO and HC emissions for the UDC. NOx emissions did not change significantly with the fuel used, however the UDC was characterized by lower NOx emission for FAME blends. Particle emissions were highest with standard diesel. Emissions of carbonyl compounds increased as fuel biodiesel content increased, especially during the UDC. HVO in diesel fuel decreased carbonyl emissions. Formaldehyde and acetaldehyde were the most abundant carbonyl compounds in the exhaust gas. Total particle-bound PAH emissions were variable, the emission of heavier PAHs increased with blend biodiesel content. The HVO blend increased emission of lighter PAHs. Nitro-PAHs were identified only during the UDC and not for all blends; the highest emissions were measured for pure diesel. The results showed that emission of nitro-PAHs may be decreased to a greater extent by using biodiesel than using a HVO blend.

These findings support the hypothesis that occupational exposure to lead can promote atherosclerosis, particularly in highly exposed individuals.

1254SOBCZAK A et al. Circulation JournalOfficial Journal of the Japanese Circulation Society http://www. j-circ.or.jp useful biomarker for detecting individuals in the early stages of kidney dysfunction and for determining their risk for developing CVD. 7 To date, most experimental and epidemiological studies have focused on the effect of tobacco smoke on ADMA levels only. The first study of the influence of tobacco smoke on ADMA levels was performed using animal models and demonstrated an increase in ADMA concentrations in the endothelial cells of rabbits after prolonged exposure to nicotine. 8 Jiang et al 9 observed a significant increase in ADMA concentrations in rat plasma following a 4-week administration of nicotine in doses of 5 mg · kg −1 · day −1 , and they suggested that nicotine models the metabolic pathway of ADMA in cells by activating the alpha7 nicotinic acetylcholine receptor. However, studies based on the culture of human endothelium-derived EAhy 926 cells produced divergent results. Incubation of cells within 48 h with condensate of tobacco smoke at concentrations of 1.0 and 10.0 mg/L n the past decade, there has been increased interest in new markers of cardiovascular diseases (CVDs). These new markers of CVD risk include 2 metabolites of L-arginine: asymmetric and symmetric dimethylarginine (ADMA and SDMA, respectively). The toxic effect of tobacco smoke is multidirectional, but the mechanism of its action is not completely clear. 1-5 One mechanism may be explained by the adverse effect of tobacco smoke on the concentration of newly discovered cardiovascular risk factors, including ADMA and SDMA, which are metabolites of L-arginine. Increased plasma concentration of ADMA, which is an endogenous inhibitor of endothelial nitric oxide (NO) synthase, is a strong and independent predictor of morbidity and overall mortality of CVD in healthy women and the general population, as well as in patients with kidney insufficiency, ischemic heart disease, peripheral vascular disease, chronic heart failure, idiopathic pulmonary hypertension, and diabetes. 6 SDMA does not inhibit NO synthase, but may be a 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.