Sidestream Cigarette Smoke Research Articles

Pulmonary response of mice to a sequential exposure of side-stream cigarette smoke and multi-walled carbon nanotubes

Due to their unique properties, nano-sized carbon materials are predicted to have numerous applications in industry, but significant evidence exists to suggest their potential to cause toxicity. To determine if pre-exposure to side-stream cigarette smoke (SSCS) influences their toxicity, we examined the pulmonary response of smoke-exposed mice to multi-walled carbon nanotubes (MWCNT). Female A/J mice were exposed to SSCS in a whole body exposure chamber at approximately 40 mg/m3 for 4 weeks (6 h/d, 5 d/wk) and challenged with a single dose of MWCNT (40 µg) by the pharyngeal aspiration technique. A total of four groups were compared: air/phosphate buffered saline (PBS)-control, SSCS/PBS, air/MWCNT, and SSCS/MWCNT. At days 1 and 3 post-MWCNT treatment, lung tissues and bronchoalveolar lavage fluid (BALF) were collected and analyzed. In comparison with controls, significantly higher levels of total BAL cells were obtained from mice exposed to SSCS and MWCNT alone or combination. Influx of polymorphonuclear leukocytes (PMN) into BALF greatly increased in MWCNT alone and SSCS/MWCNT groups at both days 1 and 3 compared with controls. However, pre-exposure to SSCS significantly suppressed PMN response to MWCNT on day 1 but not day 3. Total BALF protein, lactate dehydrogenase, and mucin were significantly elevated in MWCNT and SSCS/MWCNT groups but not in the SSCS group, except mucin at day 3, when compared with controls. These results demonstrate that MWCNT markedly increases pulmonary toxicity in mice and SSCS pre-exposure plays a minor role in modulating MWCNT-induced lung toxicity at the concentrations and time points selected in the present study.

Short term exposure to cigarette smoke on general activity and anxiety

OBJECTIVE: Sidestream cigarette smoke differs from mainstream smoke because it presents more intense effects. We aimed to evaluate the performance of rats exposed to short term sidestream cigarette smoke during open field and elevated plus-maze tests. METHOD: Cigarette exposure was carried out during 5 days. The rats were exposed to the cigarette smoke during one hour. Elevated plus-maze and open field tests were applied according to previous studies. During the open field test we measured the time spent stopped, raising and the number of times that the rat intercepted each cross (locomotion). We examined the number of entries in the open and closed arms and the time spent in the closed and open arms during elevated plus-maze test. RESULTS: Control group presented significantly higher values regarding locomotion and raising during the open field test. No difference was noted between the groups regarding the elevated plus-maze test. CONCLUSION: Sidestream cigarette smoke exposure for short term on rats affects their performance during the open field test.

The influence of nitrogen dioxide on the determination of hydrogen cyanide in mainstream and sidestream cigarette smoke and the improvement of the determination method by continuous flow analyzer

Hydrogen cyanide is a well-known toxic component in cigarette smoke. Accurate determination of hydrogen cyanide is of great significance to assess the risk of cigarettes to public health.

Human health risk associated with exposure to toxic elements in mainstream and sidestream cigarette smoke

Toxic particulate elements present in cigarette smoke pose health threats to the life of smokers due to direct inhalation and at the same time increase health risks to non-smokers present in the vicinity of smokers because of their exposure. This study conducted a series of experiments using a controlled experimental chamber, equipped with simulated smoking conditions for characterization of particulate trace elements in mainstream and sidestream cigarette smoke. Four popular commercial cigarette brands available in Singapore market were used in this study. The target elements for extraction and analysis were Al, As, B, Ba, Be, Bi, Ca, Cd, Co, Cr, Cs, Cu, Fe, Ga, Hg, K, Li, Mg, Mn, Na, Ni, Pb, Rb, Se, Sn, Sr, Te, Tl and Zn of both water-soluble and total constituents. The human health risk assessment results showed that the sidestream smoke had higher concentrations of toxic elements than those in the mainstream smoke. However, risk assessment analysis revealed that the sidestream smoke resulted in less human health risks compared to the mainstream smoke due to the influence of dilution of particulate emissions in sidestream smoke prior to inhalation exposure experienced by non-smokers. The cumulative non-cancer and cancer risks of toxic elements varied from 2.0 to 3.1 and from 398.4×10−6 to 626.1×10−6 due to inhalation of cigarette smoke by an active smoker. In the case of non-smokers, the risks were estimated under three possible cases of exposure. The cumulative cancer risks under three different cases were greater than the permissible limits. Therefore, it could be concluded that the toxic particulate elements present in cigarette smoke have significant carcinogenic and non-carcinogenic health effects due to inhalation exposure in the environment.

Impaired transcriptional response of the murine heart to cigarette smoke in the setting of high fat diet and obesity.

Smoking and obesity are each well-established risk factors for cardiovascular heart disease, which together impose earlier onset and greater severity of disease. To identify early signaling events in the response of the heart to cigarette smoke exposure within the setting of obesity, we exposed normal weight and high fat diet-induced obese (DIO) C57BL/6 mice to repeated inhaled doses of mainstream (MS) or sidestream (SS) cigarette smoke administered over a two week period, monitoring effects on both cardiac and pulmonary transcriptomes. MS smoke (250 μg wet total particulate matter (WTPM)/L, 5 h/day) exposures elicited robust cellular and molecular inflammatory responses in the lung with 1466 differentially expressed pulmonary genes (p < 0.01) in normal weight animals and a much-attenuated response (463 genes) in the hearts of the same animals. In contrast, exposures to SS smoke (85 μg WTPM/L) with a CO concentration equivalent to that of MS smoke (~250 CO ppm) induced a weak pulmonary response (328 genes) but an extensive cardiac response (1590 genes). SS smoke and to a lesser extent MS smoke preferentially elicited hypoxia- and stress-responsive genes as well as genes predicting early changes of vascular smooth muscle and endothelium, precursors of cardiovascular disease. The most sensitive smoke-induced cardiac transcriptional changes of normal weight mice were largely absent in DIO mice after smoke exposure, while genes involved in fatty acid utilization were unaffected. At the same time, smoke exposure suppressed multiple proteome maintenance genes induced in the hearts of DIO mice. Together, these results underscore the sensitivity of the heart to SS smoke and reveal adaptive responses in healthy individuals that are absent in the setting of high fat diet and obesity.

Cardiovascular Responses Induced by Catalase Inhibitior into the Fourth Cerebral Ventricle Is Changed in Wistar Rats Exposed to Sidestream Cigarette Smoke

This experimental study aimed to evaluate the effects of central catalase inhibition on cardiovascular responses in rats exposed to sidestream cigarette smoke (SSCS) for 3 weeks. A total of 20 males Wistar rats (320-370g) were implanted with a stainless steel guide cannula into the fourth cerebral ventricle (4(th)V). Femoral artery and vein were cannulated for mean arterial pressure (MAP) and heart rate (HR) measurement and drug infusion, respectively. Rats were exposed to SSCS for three weeks, 180 minutes per day, 5 days/week [carbon monoxide (CO): 100-300 ppm)]. Baroreflex was tested with one pressor dose of phenylephrine (PHE, 8 μg/kg, bolus) and one depressor dose of sodium nitroprusside (SNP, 50 μg/kg, bolus). Cardiovascular responses were evaluated before and 15 minutes after 3-amino-1, 2, 4-triazole (ATZ, catalase inhibitor, 0.001g/100μL) injection into the 4(th) V. Vehicle treatment into the 4(th) V did not change cardiovascular responses. Central catalase inhibition increased tachycardic peak, attenuated bradycardic peak and reduced HR range at 15 minutes, increased MAP at 5, 15 and 30 min and increased HR at 5 and 15 min. In rats exposed to SSCS, central ATZ increased basal MAP after 5 min and increased HR at 5, 15 and 30 minutes, respectively, and attenuated bradycardic peak at 15 minutes. This study suggests that brain oxidative stress caused by SSCS influences autonomic regulation of the cardiovascular system.

Effects of the administration of a catalase inhibitor into the fourth cerebral ventricle on cardiovascular responses in spontaneously hypertensive rats exposed to sidestream cigarette smoke

OBJECTIVE:Previous studies have demonstrated a relationship between brain oxidative stress and cardiovascular regulation. We evaluated the effects of central catalase inhibition on cardiovascular responses in spontaneously hypertensive rats exposed to sidestream cigarette smoke.METHODS:Male Wistar Kyoto (WKY) rats and spontaneously hypertensive rats (SH) (16 weeks old) were implanted with a stainless steel guide cannula leading into the fourth cerebral ventricle (4th V). The femoral artery and vein were cannulated for arterial pressure and heart rate measurement and drug infusion, respectively. The rats were exposed to sidestream cigarette smoke for 180 minutes/day, 5 days/week for 3 weeks (CO: 100-300 ppm). The baroreflex was tested using a pressor dose of phenylephrine (8 μg/kg, bolus) and a depressor dose of sodium nitroprusside (50 μg/kg, bolus). Cardiovascular responses were evaluated before and 5, 15, 30 and 60 minutes after injection of a catalase inhibitor (3-amino-1,2,4-triazole, 0.001 g/100 μL) into the 4th V.RESULTS:Vehicle administration into the 4th V did not affect the cardiovascular response, whereas administration of the central catalase inhibitor increased the basal HR and attenuated the bradycardic peak (p<0.05) to a greater extent in WKY rats exposed to sidestream cigarette smoke than in WKY rats exposed to fresh air. However, in spontaneously hypertensive rats, the effect of the catalase inhibitor treatment was stronger in the fresh air condition (p<0.05).CONCLUSION:Administration of a catalase inhibitor into the 4th V combined with exposure to sidestream cigarette smoke has a stronger effect in WKY rats than in SH rats.

Thirdhand cigarette smoke in an experimental chamber: evidence of surface deposition of nicotine, nitrosamines and polycyclic aromatic hydrocarbons and de novo formation of NNK

BackgroundA growing body of evidence shows that secondhand cigarette smoke undergoes numerous chemical changes after it is released into the air: it can adsorb to indoor surfaces, desorb back into...

Cigarette smoke induces methylation of the tumor suppressor gene NISCH

We have previously identified a putative tumor suppressor gene, NISCH, whose promoter is methylated in lung tumor tissue as well as in plasma obtained from lung cancer patients. NISCH was observed to be more frequently methylated in smoker lung cancer patients than in non-smoker lung cancer patients. Here, we investigated the effect of tobacco smoke exposure on methylation of the NISCH gene. We tested methylation of NISCH after oral keratinocytes were exposed to mainstream and side stream cigarette smoke extract in culture. Methylation of the promoter region of the NISCH gene was also evaluated in plasma obtained from lifetime non-smokers and light smokers (< 20 pack/year), with and without lung tumors, and heavy smokers (20+ pack/year) without disease. Promoter methylation of NISCH was tested by quantitative fluorogenic real-time PCR in all samples. Promoter methylation of NISCH occurred after exposure to mainstream tobacco smoke as well as to side stream tobacco smoke in normal oral keratinocyte cell lines. NISCH methylation was also detected in 68% of high-risk, heavy smokers without detectable tumors. Interestingly, in light smokers, NISCH methylation was present in 69% of patients with lung cancer and absent in those without disease. Our pilot study indicates that tobacco smoke induces methylation changes in the NISCH gene promoter before any detectable cancer. Methylation of the NISCH gene was also found in lung cancer patients’ plasma samples. After confirming these findings in longitudinally collected plasma samples from high-risk populations (such as heavy smokers), examining patients for hypermethylation of the NISCH gene may aid in identifying those who should undergo additional screening for lung cancer.

Sidestream cigarette smoke and cardiac autonomic regulation

BackgroundThe literature has already demonstrated that cigarette influences the cardiovascular system. In this study, we performed a literature review in order to investigate the relationship between sidestream cigarette smoke (SSCS) and cardiac autonomic regulation.MethodsSearches were performed on Medline, SciELO, Lilacs and Cochrane databases using the crossing between the key-words: “cigarette smoking”, “autonomic nervous system”, “air pollution” and “heart rate variability”.ResultsThe selected studies indicated that SSCS exposure affects the sympathetic and parasympathetic responses to changes in arterial blood pressure. Moreover, heart rate responses to environmental tobacco smoke are increased in smokers compared to non-smokers. The mechanism involved on this process suggest increased oxidative stress in brainstem areas that regulate the cardiovascular system.ConclusionFurther studies are necessary to add new elements in the literature to improve new therapies to treat cardiovascular disorders in subjects exposed to sidestream cigarette smoke.

Review Article: Prevalence and Health Effects of Water Pipe (Shisha) Tobacco Smoking

Every day approximately 100 million people smoke water pipe. The trend is increasing in Arabic countries, in Europe and the USA especially in adolescents. Studies revealed that the tobacco smoke from water pipe, depending on the used tobacco and charcoal, contains higher concentrations of nicotine, carbon monoxide, carboxy hemoglobin,heavy metals, carcinogens and fine dust particles compared to cigarette smoke. According to studies, water pipe tobacco smoking was significantly associated with lung cancer, chronic lung diseases, periodontal diseases and low birth-weight. Similar to cigarette smoking, water pipe tobacco smoking causes a severe health risk by environmental tobacco smoke, because the side-stream smoke of the water pipe contains higher concentrations of polycyclic aromatic hydrocarbons, aldehydes and carbon monoxide compared to the side-stream smoke of cigarettes.

Sidestream Smoke Exposure Increases the Susceptibility of Airway Epithelia to Adenoviral Infection

BackgroundAlthough significant epidemiological evidence indicates that cigarette smoke exposure increases the incidence and severity of viral infection, the molecular mechanisms behind the increased susceptibility of the respiratory tract to viral pathogens are unclear. Adenoviruses are non-enveloped DNA viruses and important causative agents of acute respiratory disease. The Coxsackievirus and adenovirus receptor (CAR) is the primary receptor for many adenoviruses. We hypothesized that cigarette smoke exposure increases epithelial susceptibility to adenovirus infection by increasing the abundance of apical CAR.Methodology and FindingsCultured human airway epithelial cells (CaLu-3) were used as a model to investigate the effect of sidestream cigarette smoke (SSS), mainstream cigarette smoke (MSS), or control air exposure on the susceptibility of polarized respiratory epithelia to adenoviral infection. Using a Cultex air-liquid interface exposure system, we have discovered novel differences in epithelial susceptibility between SSS and MSS exposures. SSS exposure upregulates an eight-exon isoform of CAR and increases adenoviral entry from the apical surface whilst MSS exposure is similar to control air exposure. Additionally, the level of cellular glycogen synthase kinase 3β (GSK3β) is downregulated by SSS exposure and treatment with a specific GSK3β inhibitor recapitulates the effects of SSS exposure on CAR expression and viral infection.ConclusionsThis is the first time that SSS exposure has been shown to directly enhance the susceptibility of a polarized epithelium to infection by a common respiratory viral pathogen. This work provides a novel understanding of the impact of SSS on the burden of respiratory viral infections and may lead to new strategies to alter viral infections. Moreover, since GSK3β inhibitors are under intense clinical investigation as therapeutics for a diverse range of diseases, studies such as these might provide insight to extend the use of clinically relevant therapeutics and increase the understanding of potential side effects.

An improved high performance liquid chromatography-fluorescence detection method for the analysis of major phenolic compounds in cigarette smoke and smokeless tobacco products

An improved HPLC method has been developed for the determination of major phenolic compounds in cigarette smoke. A novel reversed phase column with a pentafluorophenylpropyl (PFP) ligand in the stationary phase was chosen to separate the positional isomers (p-, m-, and o-cresols). Methanol instead of acetonitrile was used as the organic mobile phase component to improve the separation of the isomers and cope with the crisis of global acetonitrile shortage in 2009. A shorter analytical column with smaller particle size was used to further increase separation efficiency and reduces solvent consumption. These improvements have led to a new HPLC method that is simpler and faster than the GC–MS method and more sensitive, selective and efficient than the widely used traditional HPLC method. The limit of detection (LOD) and limit of quantification (LOQ) of this method are at the ng/mL level for most of the phenols with good linearity (R2≥0.999) and precision (RSD<15%). The method has been validated using reference tobacco products. The mainstream and sidestream cigarette smoke yields of phenolic compounds obtained by this method are comparable to those obtained by traditional HPLC method with the advantage that p-, m-, and o-cresols can be determined and reported separately by the new method. The method can also be applied for analysis of phenols in smokeless tobacco product.

Determination of Benzo(a)Pyrene in Cigarette Smoke

Inder order to determine Benzopyrene (BaP) in Mainstream and Sidestream Smoke, a Solid phase extraction (SPE) cartridge was used to isolate the BaP fraction from the total particulate matter of mainstream cigarette smoke and sidestream cigarette smoke and the BaP were measured by RP-HPLC with ultraviolet detection. The result showed that the recovery rate of BaP extracted is 94.5%, compared with the relative standard of 6.95%. The yields of BaP in mainstream smoke for Virginia cigarette are higher than those for blended cigarettes. The yields of BaP in sidestream smoke are much higher than those in mainstream smoke. The proposed method involves an solid phase extract and HPLC-UV analysis procedure. With this method, the BaP yields in mainstream and sidestream cigarette smoke can be measured fast, easily and precisely using readily available apparatus and instruments.

Atherogenic and pulmonary responses of ApoE- and LDL receptor-deficient mice to sidestream cigarette smoke

Plasma lipoproteins play important roles in the development and progression of atherosclerosis. Two widely used mouse models of experimental atherosclerosis, apolipoprotein E-deficient (ApoE −/−) and LDL receptor-deficient (LDLr −/−) mice, have major differences in lipoprotein characteristics. These include differences in lipoprotein cholesterol distribution, lipoprotein compositions, apoliporoteins distribution, and susceptibility to oxidation. In the present study, we compared pulmonary and cardiovascular responses of ApoE −/− and LDLr −/− mice to sidestream cigarette smoke (SSCS) exposure to determine if strain differences influence their predisposition to SSCS-mediated promotion of atherosclerosis. Female ApoE −/− and LDLr −/− mice were maintained on a saturated fat enriched diet and exposed to SSCS in whole body exposure chambers for 15 weeks (4h/day, 5 days/week). At terminations, the levels of pulmonary injury markers in bronchoalveolar lavage (BAL) fluids from 6 mice per group and atherosclerotic lesion formation in 14 mice per group were analyzed. Total BAL cells and polymorphonuclear leukocytes were not significantly altered by SSCS exposure in both mouse models. Total protein, LDH, and cytokine concentrations in cell-free BAL fluids were also not significantly affected by chronic SSCS exposure in either mouse strain. SSCS significantly reduced surfactant protein D levels in both strains to a similar extent. However, SSCS exposure increased significantly the percent atherosclerotic lesion areas covering aortic intimal surfaces of ApoE −/− (control-25.3±1.52 vs. SSCS-31.9±2.02, p=0.012) as well as in LDLr −/− (control-30.97±1.1 vs. SSCS-36.61±1.7, p=0.028) mice. In contrast, the serum cholesterol concentrations of SSCS-exposed ApoE −/− mice were similar to that of controls (control-1255±85 vs. SSCS-1190±61mg/dl, p=0.552) but increased significantly in SSCS-exposed LDLr −/− mice (control-998±114 vs. SSCS-1577±142mg/dl, p=0.008). These results showing different effects of identical SSCS exposure on plasma cholesterol concentrations in these two mouse models suggest a role of multiple mechanisms in SSCS-induced atherosclerosis.

Control of Smoke‐Induced Proliferation and Migration of Human Breast Cancer Cells by PK11195, a Translocator Protein (TSPO) Antagonist

Cigarette smoking is linked to breast cancer, particularly in young women. However, the exact mechanism is unknown. We have recently established that TSPO is an important biomarker for breast cancer; its expression is increased with an increase in aggressiveness of cancer. The present study investigates whether exposure of mainstream (MS) as well as Sidestream (SS) cigarette smoke induces TSPO‐mediated cell proliferation and migration in a variety of human breast cancer epithelial cell lines and if so whether PK11195, a TSPO antagonist can counteract these effects. Human breast cancer cell lines (MCF10, MCF 12A and MCF 12F) were grown in DMEM/F‐12 and exposed to either MS or SS smoke generated from 1R3F cigarettes in a THRI MS‐SS smoke exposure machine using the modified version of CULTEX cell culture smoke exposure system. A sham control (SH) group was also used where cells were exposed to the same environmental condition without smoke exposure. Induction of cell proliferation and migration was observed at low doses of smoke whereas cellular apoptosis was observed at high doses in all cell lines regardless of MS and SS exposure. A combination of immunohistochemical, Western blot and receptor binding studies revealed an over‐expression of TSPO in all cell lines by both MS and SS smoke. Furthermore, both MS and SS smoke caused a higher level of TSPO in nuclei associated with an increase in nuclear cholesterol transport. The proliferation and migration was controlled when treated with PK11195, suggesting a therapeutic potential of PK11195 in controlling smoke induced breast cancer development. ( Supported by FAMRI Clinical Innovator Award # 062415).

Sidestream cigarette smoke effects on cardiovascular responses in conscious rats: involvement of oxidative stress in the fourth cerebral ventricle

BackgroundCigarette exposure increases brain oxidative stress. The literature showed that increased brain oxidative stress affects cardiovascular regulation. However, no previous study investigated the involvement of brain oxidative stress in animals exposed to cigarette and its relationship with cardiovascular regulation. We aimed to evaluate the effects of central catalase inhibition on baroreflex and cardiovascular responses in rats exposed to sidestream cigarette smoke (SSCS).MethodsWe evaluated males Wistar rats (320-370 g), which were implanted with a stainless steel guide cannula into the fourth cerebral ventricle (4th V). Femoral artery and vein were cannulated for mean arterial pressure (MAP) and heart rate (HR) measurement and drug infusion, respectively. Rats were exposed to SSCS during three weeks, 180 minutes, 5 days/week (CO: 100-300 ppm). Baroreflex was tested with a pressor dose of phenylephrine (PHE, 8 μg/kg, bolus) to induce bradycardic reflex and a depressor dose of sodium nitroprusside (SNP, 50 μg/kg, bolus) to induce tachycardic reflex. Cardiovascular responses were evaluated before, 5, 15, 30 and 60 minutes after 3-amino-1,2,4-triazole (ATZ, catalase inhibitor, 0.001 g/100 μL) injection into the 4th V.ResultsCentral catalase inhibition increased basal HR in the control group during the first 5 minutes. SSCS exposure increased basal HR and attenuated bradycardic peak during the first 15 minutes.ConclusionWe suggest that SSCS exposure affects cardiovascular regulation through its influence on catalase activity.

Enhanced effects of cigarette smoke extract on inflammatory cytokine expression in IL-1β-activated human mast cells were inhibited by Baicalein via regulation of the NF-κB pathway

BackgroundHuman mast cells are capable of a wide variety of inflammatory responses and play a vital role in the pathogenesis of inflammatory diseases such as allergy, asthma, and atherosclerosis. We have reported that cigarette smoke extract (CSE) significantly increased IL-6 and IL-8 production in IL-1β-activated human mast cell line (HMC-1). Baicalein (BAI) has anti-inflammatory properties and inhibits IL-1β- and TNF-α-induced inflammatory cytokine production from HMC-1. The goal of the present study was to examine the effect of BAI on IL-6 and IL-8 production from CSE-treated and IL-1β-activated HMC-1.MethodsMain-stream (Ms) and Side-stream (Ss) cigarette smoke were collected onto fiber filters and extracted in RPMI-1640 medium. Two ml of HMC-1 at 1 × 106 cells/mL were cultured with CSE in the presence or absence of IL-1β (10 ng/mL) for 24 hrs. A group of HMC-1 cells stimulated with both IL-1β (10 ng/ml) and CSE was also treated with BAI. The expression of IL-6 and IL-8 was assessed by ELISA and RT-PCR. NF-κB activation was measured by electrophoretic mobility shift assay (EMSA) and IκBα degradation by Western blot.ResultsBoth Ms and Ss CSE significantly increased IL-6 and IL-8 production (p < 0.001) in IL-1β-activated HMC-1. CSE increased NF-κB activation and decreased cytoplasmic IκBα proteins in IL-1β-activated HMC-1. BAI (1.8 to 30 μM) significantly inhibited production of IL-6 and IL-8 in a dose-dependent manner in IL-1β-activated HMC-1 with the optimal inhibition concentration at 30 μM, which also significantly inhibited the enhancing effect of CSE on IL-6 and IL-8 production in IL-1β-activated HMC-1. BAI inhibited NF-κB activation and increased cytoplasmic IκBα proteins in CSE-treated and IL-1β-activated HMC-1.ConclusionsOur results showed that CSE significantly increased inflammatory cytokines IL-6 and IL-8 production in IL-1β-activated HMC-1. It may partially explain why cigarette smoke contributes to lung and cardiovascular diseases. BAI inhibited the production of inflammatory cytokines through inhibition of NF-κB activation and IκBα phosphorylation and degradation. This inhibitory effect of BAI on the expression of inflammatory cytokines induced by CSE suggests its usefulness in the development of novel anti-inflammatory therapies.

Concentration of Reactive Oxygen Species (ROS) in Mainstream and Sidestream Cigarette Smoke

Reactive oxygen species (ROS) have been related to adverse health effects in recent years. Previous studies have reported ROS concentrations in mainstream smoke, but the reports have shown considerable variability and conclusions. There have been no prior measurements on sidestream smoke. In this study, the amounts of gas-phase and particle-bound ROS in tobacco smoke were determined using 2′,7′-dichlorodihydrofluorescin diacetate (DCFH-DA) as the fluorescent probe with hydrogen peroxide as the standard. Both research and commercially available cigarettes were tested using mainstream and sidestream smoke generated by a Single Cigarette Smoking Machine. For mainstream smoke from regular and light cigarettes, the total quantities of ROS were 120–150 nmol and 90–110 nmol, respectively. For sidestream smoke, the values were 60–90 nmol and 30–70 nmol for regular and light cigarettes, respectively. The effects of the cigarette filter on the emissions were to reduce the particle mass and particle-phase ROS in the mainstream smoke. Copyright 2012 American Association for Aerosol Research

Microbiological components in mainstream and sidestream cigarette smoke

BackgroundResearch has shown that tobacco smoke contains substances of microbiological origin such as ergosterol (a fungal membrane lipid) and lipopolysaccharide (LPS) (in the outer membrane of Gram-negative bacteria). The aim of the present study was to compare the amounts of ergosterol and LPS in the tobacco and mainstream (MS) and sidestream (SS) smoke of some popular US cigarettes.MethodsWe measured LPS 3-hydroxy fatty acids and fungal biomass biomarker ergosterol in the tobacco and smoke from cigarettes of 11 popular brands purchased in the US. University of Kentucky reference cigarettes were also included for comparison.ResultsThe cigarette tobacco of the different brands contained 6.88-16.17 (mean 10.64) pmol LPS and 8.27-21.00 (mean 14.05) ng ergosterol/mg. There was a direct correlation between the amounts of ergosterol and LPS in cigarette tobacco and in MS smoke collected using continuous suction; the MS smoke contained 3.65-8.23% (ergosterol) and 10.02-20.13% (LPS) of the amounts in the tobacco. Corresponding percentages were 0.30-0.82% (ergosterol) and 0.42-1.10% (LPS) for SS smoke collected without any ongoing suction, and 2.18% and 2.56% for MS smoke collected from eight two-second puffs.ConclusionsTobacco smoke is a bioaerosol likely to contain a wide range of potentially harmful bacterial and fungal components.