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The microbiological composition of tobacco products was studied using culture and chemical analysis (of tobacco leaves) or chemical analysis only (tobacco and tobacco smoke). The chemical analyses utilized gas chromatography-tandem mass spectrometry for determining 3-hydroxy fatty acids, muramic acid, and ergosterol as markers of respectively lipopolysaccharide (LPS), peptidoglycan, and fungal biomass. Mesophilic bacteria dominated in both fresh and cured tobacco leaves; a range of additional bacteria and fungi were also found albeit in minor amounts. The peptidoglycan and LPS concentrations were approximately the same in tobacco leaves as in cigarette tobacco. The concentrations of the measured microbial components were much lower in some cigarettes locally produced in China, Korea, and Vietnam than in cigarettes of international brands purchased in the same countries, and the concentrations in the smoke were in general agreement with the concentrations in cigarette tobacco. No differences in microbial load in tobacco of "light" and "full flavor" cigarettes were seen. Storing cigarettes at high humidity resulted in elevated levels of fungi in the cigarette tobacco leading to increased ergosterol concentrations in the smoke. The fact that tobacco smoke is a bioaerosol may help to explain the high prevalence of respiratory disorders among smokers and non-smokers exposed to second hand smoke since the same symptoms are also commonly associated with exposure to bioaerosols.

Exposure to environmental tobacco smoke (ETS) is an important worldwide public health issue. The present study demonstrates that cigarette smoke can be a major source of endotoxin (lipopolysaccharide, LPS) in indoor environments. Gas-chromatography/mass-spectrometry was used to determine 3-hydroxy fatty acids as markers of endotoxin in air-borne house dust in homes of smokers and non-smokers. Air concentrations of endotoxin were 4-63 times higher in rooms of smoking students than in identical rooms of non-smoking students. The fact that cigarette smoke contains large amounts of endotoxin may partly explain the high prevalence of respiratory disorders among smokers and may also draw attention to a hitherto neglected risk factor of ETS.

Mycotoxins are toxic, secondary metabolites frequently produced by molds in water-damaged indoor environments. We studied the prevalence of selected, potent mycotoxins and levels of fungal biomass in samples collected from water-damaged indoor environments in Sweden during a 1-year period. One hundred samples of building materials, 18 samples of settled dust, and 37 samples of cultured dust were analyzed for: (a) mycoflora by microscopy and culture; (b) fungal chemical marker ergosterol and hydrolysis products of macrocyclic trichothecenes and trichodermin (verrucarol and trichodermol) by gas chromatography-tandem mass spectrometry; and (c) sterigmatocystin, gliotoxin, aflatoxin B(1), and satratoxin G and H by high performance liquid chromatography-tandem mass spectrometry. Sixty-six percent of the analyzed building materials samples, 11% of the settled dust samples, and 51% of the cultured dust samples were positive for at least one of the studied mycotoxins. In addition, except in the case of gliotoxin, mycotoxin-positive building material samples contained 2-6 times more ergosterol than mycotoxin-negative samples. We show that (a) molds growing on a range of different materials indoors in water-damaged buildings generally produce mycotoxins, and (b) mycotoxin-containing particles in mold-contaminated environments may settle on surfaces above floor level. The mass spectrometry methods used in this study are valuable tools in further research to survey mycotoxin exposure and investigate potential links with health effects.

Practical ImplicationsIn the aftermath of natural disasters like hurricane Katrina water-damages on infrastructure and public and private property are often associated with health risks for remediation workers and returning residents. In the case of New Orleans evaluations of health hazards, health studies, and assessments of bioaerosol have been conducted previously. However, until now mycotoxins have not been addressed. Our study shows, for the first time, the presence of mycotoxins in dust collected in houses in New Orleans mold-contaminated because of the hurricane Katrina. The results may highlight the potential health threats posed by mold aerosols in post-disaster inhabited areas.

Cigarette smoke exposure is a strong risk factor for cardiovascular and respiratory diseases. However, the knowledge about how cigarette smoke induces damage to vasculature and airway is limited. The present study was designed to examine the effects of cigarette smoke particles extracted by heptane (heptane-soluble smoke particles, HSP), by water (watersoluble smoke particles, WSP) and by DMSO (DMSO-soluble smoke particles, DSP), which represent lipophilic, hydrophilic and ambiphoteric constituents from the cigarette smoke, respectively. Human aortic smooth muscle cell (HASMC) proliferation was assessed in cell culture. Rat resistance artery and airway contractile responses to serotonin, U46619, phenylephrine, noradrenaline, acetylcholine, des-Arg 9 -bradykinin, bradykinin, sarafotoxin 6c and endothelin-1 were monitored by a sensitive myograph system. Immunocytochemistry and cell-based phosphoELISA assay were used to demonstrate activation of extracellular signal-regulated kinases 1 ⁄ 2 (ERK1 ⁄ 2). For the first time, our results demonstrate that although all the three extracts promote HASMC proliferation, the HSP and DSP effects occur earlier. HSP and DSP, but not WSP, increase the contractile responses to sarafotoxin 6c, U46619 or bradykinin in rat mesenteric artery and ⁄ or in bronchi. ERK1 ⁄ 2 is activated by HSP and DSP in HASMCs and inhibition of ERK1 ⁄ 2 abrogated the smoke extracts-induced HASMC proliferation, while blockage of nicotinic receptors had no effects, suggesting that the toxic effects of the smoke extracts occur via activation of intracellular ERK1 ⁄ 2 signalling, but not nicotinic receptors.Exposure to cigarette smoke is strongly associated with cardiovascular diseases like atherosclerosis, coronary heart disease, stroke, myocardial infarction, aortic aneurysm and peripheral vascular disease [1,2]. In airways, cigarette smoke, via direct smoking or second-hand inhalation, exacerbates chronic obstructive pulmonary disease (COPD), chronic bronchitis and asthma and also causes lung cancer. An estimated 1.6 million cardiovascular deaths worldwide are attributable to smoking [3] and about 73% of the COPD mortality is related to cigarette smoke exposure [4]. However, our knowledge about how cigarette smoke induces cardiovascular and airway diseases is very limited.Cigarette smoke contains over 4000 different compounds. Among them, 158 chemical constituents of smoke are identified to be toxic hazards. Of the 17 non-cancer compounds, based on a non-cancer risk index, 15 individual chemical constituents contribute to the respiratory irritation and the cardiovascular dysfunction [5]. Previously, we have revealed that DMSO-soluble smoke particles (DSP), but not nicotine or water-soluble cigarette smoke particles (WSP), induce dysfunctions of vascular smooth muscle cells [6] suggesting that it is the lipid-soluble particles from cigarette smoke that are responsible for the toxic effects. Furthermore, DSP exerts a direct toxic effect on vascular endothelial cells and reduces endothelium-depende...

A gas chromatographic procedure was developed to determine the relative amounts of D-and L-arabinitol in urine. Samples were filtered, diluted, purified through extractions, evaporated, and treated with trifluoroacetic anhydride; the arabinitol derivatives thus obtained were separated on a chiral stationary phase and registered

Determination of D-arabinitol/L-arabinitol ratios (referred to as D/L-arabinitol ratios) in urine as a tool for the diagnosis of invasive candidiasis was investigated in a prospective study comprising 100 children with cancer. The analyses were made by gas chromatography. Positive D/L-arabinitol ratios were found for 10 of 10 children with confirmed invasive candidiasis, 12 of 23 patients undergoing empiric antifungal chemotherapy, and 4 of 67 children not receiving antifungal treatment. D/L-Arabinitol ratios were positive 3 to 31 days (median, 12 days) before the first culture-positive blood sample was drawn or empiric therapy was initiated. The regular monitoring of D/L-arabinitol ratios in urine holds great promise as a sensitive method for diagnosing invasive candidiasis in immunocompromised children with cancer. Moreover, it may be possible to use an early rise in D/L-arabinitol ratios as a basis for the institution of antifungal chemotherapy and as a means of avoiding unnecessary treatment with potentially toxic antifungal agents.