Cigarette tar accelerates atherosclerosis progression via RIPK3-dependent necroptosis mediated by endoplasmic reticulum stress in vascular smooth muscle cells.

BACKGROUND: Tar is the main toxic of cigarettes, and its effect on atherosclerosis progression and the underlying mechanisms remain largely unknown. Vascular smooth muscle cells (VSMCs) play a key role in atherogenesis and plaque vulnerability. The present study sought to investigate the mechanism of atherosclerosis progression through tar-induced VSMC necroptosis, a recently described form of necrosis. METHODS: The effect of tar on atherosclerosis progression and VSMC necroptosis was examined in ApoE-/- mice and cultured VSMCs. The role of necroptosis in tar-induced plaque development was evaluated in RIPK3-deletion mice (ApoE-/-RIPK3-/-). The key proteins of necroptosis in carotid plaques of smokers and non-smokers were also examined. Quantitative proteomics of mice aortas was conducted to further investigate the underlying mechanism. Pharmacological approaches were then applied to modulate the expression of targets to verify the regulatory process of tar-induced necroptosis. RESULTS: Tar administration led to increased atherosclerotic plaque area and reduced collagen and VSMCs in ApoE-/- mice. The expression of RIPK1、RIPK3、and MLKL in VSMCs of plaques were all increased in tar-exposed mice and smokers. RIPK3 deletion protected against VSMC loss and plaque progression stimulated by tar. In mechanistic studies, quantitative proteomics analysis of ApoE-/- mice aortas suggested that tar triggered endoplasmic reticulum (ER) stress. PERK-eIF2α-CHOP axis was activated in tar-treated VSMCs and atherosclerotic plaque. Inhibition of ER stress using 4PBA significantly reduced plaque progression and VSMC necroptosis. Further study revealed that ER stress resulted in calcium (Ca2+) release into mitochondria and cytoplasm. Elevated Ca2+ levels lead to mitochondrial dysfunction and excessive reactive oxygen species (ROS) production, which consequently promote RIPK3-dependent necroptosis. In addition, Ca2+/calmodulin-dependent protein kinase II (CaMKII) activated by cytosolic Ca2+ overload binds to RIPK3, accounting for necroptosis. CONCLUSION: The findings revealed that cigarette tar promoted atherosclerosis progression by inducing RIPK3-dependent VSMC necroptosis and identified novel avenues of ER stress and Ca2+ overload.

Updated view of tars for psoriasis: what have we learned over the last decade?

Tars are one of the most effective, unknown, and oldest therapies for psoriasis. They include coal tar (CT) and biomass-derived products. These treatments, particularly the CT, have proven to be cost-effective with long remission times compared to other systemic or topical treatments. However, they have hardly evolved in recent years, as they are not well-embraced by clinicians or patients because of concerns regarding cosmesis and safety. This review summarizes current knowledge about the chemical characterization, mechanism of action, toxicity, and clinical studies supporting the use of tars for psoriasis over the last decade. Trends within these above aspects are reviewed, and avenues of research are identified. CT is rich in polycyclic aromatic hydrocarbons, whereas biomass-derived tars are rich in phenols. While the activation of the aryl hydrocarbon receptor is involved in the antipsoriatic effect of CT, the mechanism of action of biomass-derived products remains to be elucidated. No conclusive evidence exists about the risk of cancer in psoriasis patients under CT treatment. Large, randomized, double-blind, controlled clinical trials are necessary to promote the inclusion of tars as part of modern therapies for psoriasis.

Characterization of tars from recycling of PHA bioplastic and synthetic plastics using fast pyrolysis.

The aim of this study was to investigate the pyrolysis products of polyhydroxyalkanoates (PHAs), polyethylene terephthalate (PET), carbon fiber reinforced composite (CFRC), and block co-polymers (PS-b-P2VP and PS-b-P4VP). The studied PHA samples were produced at temperatures of 15 and 50 oC (PHA15 and PHA50), and commercially obtained from GlasPort Bio (PHAc). Initially, PHA samples were analyzed by nuclear magnetic resonance (NMR) spectroscopy and size exclusion chromatography (SEC) to determine the molecular weight, and structure of the polymers. Thermal techniques such as thermogravimetry (TG) and differential scanning calorimetry (DSC) analyses were performed for PHA, CFRC, and block co-polymers to investigate the degradation temperature range and thermal stability of samples. Fast pyrolysis (500 oC, ∼102 °C s-1) experiments were conducted for all samples in a wire mesh reactor to investigate tar products and char yields. The tar compositions were investigated by gas chromatography-mass spectrometry (GC-MS), and statistical modeling was performed. The char yields of block co-polymers and PHA samples (<2 wt. %) were unequivocally less than that of the PET sample (~10.7 wt. %). All PHA compounds contained a large fraction of ethyl cyclopropane carboxylate (~ 38-58 %), whereas PAH15 and PHA50 additionally showed a large quantity of 2-butenoic acid (~8-12 %). The PHAc sample indicated the presence of considerably high amount of methyl ester (~15 %), butyl citrate (~12.9 %), and tributyl ester (~17 %). The compositional analyses of the liquid fraction of the PET and block co-polymers have shown carcinogenic and toxic properties. Pyrolysis removed matrices in the CRFC composites which is an indication of potential recovery of the original fibers.

Knockdown of mitochondrial threonyl-tRNA synthetase 2 inhibits lung adenocarcinoma cell proliferation and induces apoptosis.

Lung cancer is a significant global burden. Aminoacyl-tRNA synthetases (aaRSs) can be reliably identified by the occurrence and improvement of tumors. Threonyl-tRNA synthetase (TARS) and mitochondrial threonyl-tRNA synthetase 2 (TARS2) are both aaRSs. Many studies have shown that TARS are involved in tumor angiogenesis and metastasis. However, TARS2 has not yet been reported in tumors. This study explored the role of TARS2 in the proliferation and apoptosis of lung adenocarcinoma (LUAD). TARS2 expression in lung adenocarcinoma and non-cancerous lung tissues was detected via immunohistochemistry. Cell proliferation was detected using MTS, clone formation, and EdU staining assays. Flow cytometry was used to detect cell cycle, mitochondria reactive oxygen species (mROS) production, and apoptosis. Mitochondrial membrane potential (MMP ΔΨm) was detected using JC-1 fluorescent probes. Cell cycle, apoptosis-related pathway, and mitochondrial DNA (mtDNA) -encoded protein expression was detected via Western blotting. Finally, the effect of TARS2 on tumor growth was examined using a xenotransplanted tumor model in nude mice. We found that TARS2 was highly expressed in lung adenocarcinoma tissues and associated with poor overall survival (OS). Mechanistic analysis showed that knockdown of TARS2 inhibited proliferation through the retinoblastoma protein (RB) pathway and promoted mROS-induced apoptosis. Knockdown of TARS2 inhibits tumor growth in a xenotransplanted tumor model. TARS2 plays an important role in LUAD cell proliferation and apoptosis and may be a new therapeutic target.

Survivorship of 4,748 Contemporary Total Ankle Replacements from the French Discharge Records Database.

BACKGROUND: Studies of survivorship of primary total ankle replacements (TARs) beyond 5 years have shown varying results among early and modern designs. National cohorts give valuable insights about TAR outcomes, revision risk factors, and specific designs. The purpose of this study was to investigate implant survivorship and risk factors for revision of contemporary TARs using our national database. METHODS: This observational study included patients identified in the national PMSI (Programme médicalisé des systèmes d'information) database as having undergone TAR from 2010 to 2019. Demographics, discharge data, concomitant procedures, and type of implant were extracted. Kaplan-Meier estimations were performed to determine time to revision using metal component revision for implant failure and revision for deep infection as end points. Weighted Cox models were used for risk factor analysis, including risks of early revision (within the first 2 years). The adjusted hazard ratios (HRadj) were reported with 95% confidence intervals. RESULTS: A cohort of 4,748 patients was extracted. The mean age at surgery was 63 years; 43% of the patients were female. The mean follow-up was 5 years (range, 1 to 10 years). Revisions were noted in 817 cases (17%), including 734 with metal component revision and 83 with revision due to deep infection. The 1-year, 2-year, 5-year, and 10-year survivorship free of metal component revision was 95%, 90%, 84%, and 78%, respectively. Younger age, implants derived from second-generation designs, and an institutional volume of ≤10 TARs per year were found to be independent predictors of revision for any cause. In addition to the above factors (except for implant generation), male sex and concomitant osteotomies and/or fusion were found to be significant predictors for any early revision. CONCLUSIONS: The 10-year survivorship free of metal component revision after TAR was 78%, which was consistent with other national registries. Revisions were associated with young age, associated arthritis or deformities requiring concomitant fusion or osteotomy, and implants derived from second-generation designs. Institutions where >10 procedures were performed per year were associated with better TAR survivorship. LEVEL OF EVIDENCE: Therapeutic Level IV. See Instructions for Authors for a complete description of levels of evidence.

Comparison of Mainstream Smoke Yields between Linear and Rotary Smoking Machines and Evaluation of "Super Pad" Extraction for Linear Smoking Machines.

Two-tail t test statistical analyses of International Organization for Standardization nonintense and Canadian Intense mainstream smoke yields of total particulate matter, tar, nicotine, and carbon monoxide from cigarettes show that mean quantities are generally higher for a linear smoking machine at a 95% confidence level but a rotary smoking machine has better precision. A novel "super pad" analysis concept combines four smaller filter pads from a linear smoking machine, resulting in increased mean constituent yields and reduced variability. Although measurement variability is still greater than that of rotary machines, super padding may be useful to reduce the variance caused by linear smoking machines.

Impact of chronic smoking on traumatic brain microvascular injury: An in vitro study.

Traumatic brain injury (TBI) is a major reason of cerebrovascular and neurological damage. Premorbid conditions such as tobacco smoking (TS) can worsen post-TBI injuries by promoting vascular endothelial impairments. Indeed, TS-induced oxidative stress (OS) and inflammation can hamper the blood-brain barrier (BBB) endothelium. This study evaluated the subsequence of chronic TS exposure on BBB endothelial cells in an established in vitro model of traumatic cell injury. Experiments were conducted on confluent TS-exposed mouse brain microvascular endothelial cells (mBMEC-P5) following scratch injury. The expression of BBB integrity-associated tight junction (TJ) proteins was assessed by immunofluorescence imaging (IF), Western blotting (WB) and quantitative RT-PCR. We evaluated reactive oxygen species (ROS) generation, the nuclear factor 2-related (Nrf2) with its downstream effectors and several inflammatory markers. Thrombomodulin expression was used to assess the endothelial haemostatic response to injury and TS exposure. Our results show that TS significantly decreased Nrf2, thrombomodulin and TJ expression in the BBB endothelium injury models while increased OS and inflammation compared to parallel TS-free cultures. These data suggest that chronic TS exposure exacerbates traumatic endothelial injury and abrogates the protective antioxidative cell responses. The downstream effect was a more significant decline of BBB endothelial viability, which could aggravate subsequent neurological impairments.

Toxicity of Water- and Organic-Soluble Wood Tar Fractions from Biomass Burning in Lung Epithelial Cells.

Widespread smoke from wildfires and biomass burning contributes to air pollution and the deterioration of air quality and human health. A common and major emission of biomass burning, often found in collected smoke particles, is spherical wood tar particles, also known as "tar balls". However, the toxicity of wood tar particles and the mechanisms that govern their health impacts and the impact of their complicated chemical matrix are not fully elucidated. To address these questions, we generated wood tar material from wood pyrolysis and isolated two main subfractions: water-soluble and organic-soluble fractions. The chemical characteristics as well as the cytotoxicity, oxidative damage, and DNA damage mechanisms were investigated after exposure of A549 and BEAS-2B lung epithelial cells to wood tar. Our results suggest that both wood tar subfractions reduce cell viability in exposed lung cells; however, these fractions have different modes of action that are related to their physicochemical properties. Exposure to the water-soluble wood tar fraction increased total reactive oxygen species production in the cells, decreased mitochondrial membrane potential (MMP), and induced oxidative damage and cell death, probably through apoptosis. Exposure to the organic-soluble fraction increased superoxide anion production, with a sharp decrease in MMP. DNA damage is a significant process that may explain the course of toxicity of the organic-soluble fraction. For both subfractions, exposure caused cell cycle alterations in the G2/M phase that were induced by upregulation of p21 and p16. Collectively, both subfractions of wood tar are toxic. The water-soluble fraction contains chemicals (such as phenolic compounds) that induce a strong oxidative stress response and penetrate living cells more easily. The organic-soluble fraction contained more polycyclic aromatic hydrocarbons (PAHs) and oxygenated PAHs and induced genotoxic processes, such as DNA damage.

Cumulative cigarette tar exposure and lung cancer risk among Japanese smokers.

OBJECTIVE: Tar concentration in cigarette brands is chronologically decreasing in the USA and Japan. However, studies investigating lung cancer risk with cumulative tar exposure in Western and Asian countries are insufficient. To investigate the risk of lung cancer with cumulative cigarette tar exposure, we conducted a case-control study among Japanese current smokers. METHODS: This study used data from the US-Japan lung cancer joint study in 1993-1998. A total of 282 subjects with histologically confirmed lung cancer and 162 hospital and 227 community controls were included in the study, and two control groups were combined. The information regarding tar concentration was obtained from the published documents and additional estimation using the equation of regression. Cumulative tar concentration was calculated by multiplying the annual value of brand-specific tar concentration by years of smoking. The odds ratios and 95% confidence intervals for lung cancer with cumulative tar exposure were estimated using a logistic model. RESULTS: The odds ratios for lung cancer with both lower (1-59.8 × 105 mg) and higher (>59.8 × 105 mg) total cumulative tar exposure were statistically significant (3.81, 2.23-6.50 and 11.64, 6.56-20.67, respectively) with increasing trend (P < 0.001). The stratification analysis showed higher odds ratios in subjects with higher cumulative tar exposure regardless of inhalation, duration of smoking filtered cigarettes and histological type. CONCLUSIONS: This study showed that cumulative tar exposure is a dose-dependent indicator for lung cancer risk, and low-tar exposure was still associated with increased cancer risk.

Risk evaluation of environmentally persistent free radicals in airborne particulate matter and influence of atmospheric factors.

Environmentally persistent free radicals (EPFRs) was considered unrecognized composition of air pollutants and might help explain the long-standing medical mystery of why non-smokers develop tobacco-related diseases like lung cancer. EPFRs in airborne fine particulate matter (PM2.5) can induce oxidative and DNA damage when inhaled. We assessed the inhalation risk of EPFRs in PM2.5 and factors influencing this risk in Beijing as a large city with frequent haze events. The average concentration of EPFRs in PM2.5 was 6.00 × 1017 spins/m3 in spring, autumn, and winter; lower concentrations were recorded in the summer. To estimate the daily inhalation risk of EPFRs in PM2.5, we used the equivalent EPFRs in cigarette tar. The average daily inhalation exposure of EPFRs in PM2.5 was estimated to be the equivalent of 33.1 cigarette tar EPFRs per day (range: 0.53-226.9) during both haze and non-haze days. The major factors influencing EPFR concentrations in the atmosphere were precipitation and humidity, which reduced airborne concentrations. Levels of PM2.5 and carbon monoxide were positively correlated with EPFR concentrations. The health risks of inhaling airborne EPFRs could be significant and should be recognized and quantified.

Survey of characteristics of exposure to mainstream cigarette smoke using discarded cigarette butts from Korean smokers.

Evaluating the characteristics of exposure to mainstream cigarette smoke is an essential field in tobacco research because of the large risk burden among smokers. Detailed evaluation of the complex factors pertaining to the exposure of smokers to mainstream cigarette smoke was attempted by analysis of discarded cigarette butts. A total of 5475 samples of discarded cigarette butts was collected to investigate the exposure characteristics in relation to Korean smokers. The basic physico-chemical characteristics of cigarettes, including the filter length, filter type, menthol addition, and nicotine and tar content, were determined and the manufacturer and cigarette size were identified. The tobacco-burned percentage (TBP)) and tar staining were used as physical markers, and actual human exposure to cigarette smoke was determined using the part filter method. Multiple linear regression analyses and generalized ordinal logistic regression analysis were conducted to identify the relationship between the socio-demographic factors and the physico-chemical characteristics of the cigarettes themselves and the exposure characteristics. Significant associations were observed between the TBP and age group, occupational group, manufacturer, tar staining, ISO tar content, and filter length. Increased odds of smoking with a heavier tar stain among Korean smokers were associated with blue collar workers vs. other workers, manufacturer B vs. other manufacturers, recess filter vs. other filter types, ISO tar content, and TBP. Finally, significant associations between the log-transformed human-smoked tar and nicotine yields and occupational group, the TBP, tar staining, and physico-chemical properties of cigarettes were found and were used to propose models for predicting the actual exposure to tar and nicotine. The proposed models account for 60-61% and 47-49% of the variance of human exposure to tar and nicotine, respectively. This analysis of discarded cigarette butts revealed that various factors, including socio-demographic factors such as age group and occupational group, as well as the physico-chemical properties of cigarette products such as the filter type and length, cigarette size, ISO tar and nicotine content, and mentholation, affect the characteristics of exposure of Korean smokers to mainstream cigarette smoke.

Can Removing Tar Information From Cigarette Packages Reduce Smokers' Misconceptions About Low-Tar Cigarettes? An Experiment From One of the World's Lowest Tar Yield Markets, South Korea.

INTRODUCTION: Despite regulations that forbid cigarette packages from displaying messages such as "mild," "low-tar," and "light," many smokers still have misperceptions about "light" or "low-tar" cigarettes. One reason may be that tar amount displays continue to be permitted. This study examines whether removing tar delivery information from packaging reduces consumer misperceptions about "low-tar" cigarettes. METHODS: An online experiment was conducted in South Korea among 531 smokers who were randomly assigned to one of two conditions: with and without tar information on cigarette packages. Participants evaluated which type of cigarette was mildest, least harmful, easiest for nonsmokers to start smoking, and easiest for smokers to quit. RESULTS: Ten out of 12 chi-square tests showed that people judged the lowest reported tar delivery cigarette to be the mildest (p < .01), least harmful (p < .05), easiest to start (p < .05), and easiest to quit (p < .05)-less so in the "no-tar" condition than the "tar" condition. A higher level of misbeliefs about supposed low-tar cigarettes were found in the "tar" condition compared to the "no-tar" condition for all three brands (t = 5.85, 4.07, 3.82, respectively, p < .001). Regression analyses showed that the "no-tar" condition negatively predicted the level of misbeliefs after controlling for demographic and smoking-related variables (B [SE] = -.72 (.12), -.50 (.12), -.48 (.13), respectively, p < .001). CONCLUSIONS: Banning reported tar deliveries from cigarette packages is likely to reduce smokers' misconceptions about "low-tar" cigarettes. When reported tar deliveries are absent, smokers have inconsistent judgments about differently packaged cigarettes. IMPLICATIONS: When cigarette packages depict lower reported tar number deliveries, participants erroneously perceive them to be less harmful than packages displaying higher tar numbers. These misperceptions of harm may prompt smokers who might otherwise attempt to quit smoking to instead consume cigarettes with lower tar deliveries due to the mistaken belief that they will reduce their risk.

The educational gap in tar and nicotine content in purchases of cigarettes: An observational study using large-scale representative survey data from Japan.

The intensity of tobacco use is commonly measured by the number of cigarettes, which is inaccurate because it masks the heterogeneity and substances contained in tobacco. Unlike existing studies, this study adopted the tar and nicotine content of purchased cigarettes as proxies for smoking intensity and elicited socioeconomic disparities from the participants regarding tobacco use. Using a nationally representative consumer panel survey of Japan from 2010 to 2014, we found that socioeconomic disparities in smoking are more pronounced when tar and nicotine content in cigarettes is considered. University graduates purchased 26% fewer cigarettes, and 40% less tar or nicotine than their secondary school-educated counterparts. Low education groups purchased more tar-rich cigarettes, which cost less than low-tar cigarettes. The public health recommendations for reducing socioeconomic health inequalities might be understated because they are drawn from evidence based on the number of cigarettes smoked.

Cade oil poisoning: about a case.

Throughout Morocco, cade oil is used in folk medicine for many purposes, in particular for atopic dermatosis. It is also used as a wormer. Cade oil poisoning of newborns and infants thus often has an iatrogenic origin, resulting especially from the ingestion of a significant amount or from a prolonged and extensive cutaneous application. Thus, this oil, used for therapeutic purposes, is responsible for a non-negligible number of cases of poisoning, some fatal. We report a case of poisoning after cutaneous application of cade oil in a 2-month-old infant. The outcome was fatal. This report calls attention to the real possibility of this event and emphasizes the interest of preventing it by promoting information to families in Morocco.

Facile Preparation of Dual-Shell Novel Covalent-Organic Framework Functionalized Magnetic Nanospheres Used for the Simultaneous Determination of Fourteen Trace Heterocyclic Aromatic Amines in Nonsmokers and Smokers of Cigarettes with Different Tar Yields Based on UPLC-MS/MS.

The facile preparation, characterization, and application of novel dual-shell TpBD (a kind of covalent-organic framework) coated magnetic nanospheres as sorbents for simple, fast, and high selectivity capture of 14 heterocyclic aromatic amines (HAAs) are reported. Quantum chemistry theory calculations were conducted to directly and quantifiably describe the multiple interactions, including π-π, hydrogen bonding, cation-π, static electricity, and ion-exchange, between TpBD and heterocyclic aromatic amines. The excellent adsorption capacity of TpBD coated magnetic nanospheres was further evaluated by extraction of 14 HAAs from nonsmokers' and smokers' urine samples. Under the optimized conditions, the magnetic solid phase extraction process can be completed with high recovery ranging from 95.4% to 129.3%. After being washed with acetonitrile and water successively, the collected sorbents can be easily recycled and reused five times without any significant difference in performance. Coupled with the ultra performance liquid chromatography-tandem mass spectrometer detection, the exposure level of HAAs in nonsmokers and smokers smoking cigarettes with different tar yields were successfully explored. And, this implied that the robust method based on the versatile TpBD coated dual-shell magnetic nanospheres sorbents represents a great potential application in the analysis of disease markers and body fluids.

Tar, nicotine and carbon monoxide yield of UK cigarettes and the risk of non-muscle-invasive and muscle-invasive bladder cancer.

Cigarette smoking is a major risk factor for bladder cancer (BC); however, the impact of cigarette content remains unclear. This study aims to investigate tar, nicotine and carbon monoxide (TNCO) yields of different filtered cigarettes in relation to BC risk. From the Bladder Cancer Prognosis Programme 575 non-muscle-invasive bladder cancer (NMIBC) cases, 139 muscle-invasive bladder cancer (MIBC) cases and 130 BC-free controls with retrospective data on smoking behaviour and cigarette brand were identified. Independently measured TNCO yields of cigarettes sold in the UK were obtained through the UK Department of Health and merged with the Bladder Cancer Prognosis Programme dataset to estimate the daily intake of TNCO. BC risk increased by TNCO intake category for NMIBC cases (P <0.050 in all multivariate models), but only for the daily intake of tar for MIBC cases (P=0.046) in multivariate models. No difference in risk was observed between smokers of low-tar/low-nicotine and high-tar/high-nicotine cigarettes compared with never smokers, either for NMIBC (P=0.544) or MIBC (P=0.449). High daily intake of TNCO additionally increases the risk of both NMIBC and MIBC compared with low daily intake. However, as there is no difference in BC risk between low-tar/low-nicotine and high-tar/high-nicotine cigarette smokers, it remains unclear whether smoking behaviour or TNCO yield of cigarettes explains this association.

ß-Carotene Supplementation and Lung Cancer Incidence in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study: The Role of Tar and Nicotine.

INTRODUCTION: The Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study demonstrated that ß-carotene supplementation increases lung cancer incidence in smokers. Further, cigarettes with higher tar and nicotine content are associated with a higher risk of lung cancer. However, no studies have examined whether the increased risk associated with ß-carotene supplementation in smokers varies by the tar or nicotine content of cigarettes. METHODS: The ATBC Study was a randomized, double-blind intervention trial conducted in southwest Finland. A total of 29 133 male smokers, aged 50-69 years, were enrolled and randomly assigned to one of four groups (α-tocopherol, ß-carotene, both, or placebo). Cox proportional hazards models were used to estimate the hazard ratio (HR) and 95% confidence intervals (CI) of lung cancer risk by ß-carotene trial assignment stratified by a priori categories of cigarette tar and nicotine content. RESULTS: The ß-carotene supplementation group had significantly higher risk of developing lung cancer in all categories of tar content (yes vs. no ß-carotene supplementation-ultralight cigarettes [≤7 mg tar]: HR = 1.31, 95% CI = 0.91 to 1.89; nonfiltered cigarettes [≥21 mg tar]: HR = 1.22, 95% CI = 0.91 to 1.64; p for interaction = .91). Similarly, there was no interaction with nicotine content (yes vs. no ß-carotene supplementation-ventilated cigarettes [≤0.8 µg nicotine]: HR = 1.23, 95% CI = 0.98 to 1.54; nonfiltered cigarettes [≥1.3 µg nicotine]: HR = 1.22, 95% CI = 0.91 to 1.64; p for interaction = .83). CONCLUSION: These findings support the conclusion that supplementation with ß-carotene increases the risk of lung cancer in smokers regardless of the tar or nicotine content of cigarettes smoked. Our data suggest that all smokers should continue to avoid ß-carotene supplementation. IMPLICATIONS: Previous studies demonstrated that ß-carotene supplementation increases risk of lung cancer in smokers. This study moves the field forward by examining the potential for modification of risk of lung cancer with different levels of tar and nicotine in cigarettes smoked, as interaction with carcinogens in these components of cigarette smoke is hypothesized to be the mechanism by which ß-carotene increases risk. Our study provides evidence that the increased risk of lung cancer in smokers who take ß-carotene supplements is not dependent upon the tar or nicotine level of cigarettes smoked and suggests that all smokers should continue to avoid ß-carotene supplementation.

Gas reforming and tar decomposition performance of nickel oxide (NiO)/SBA-15 catalyst in gasification of woody biomass.

In the gasification of biomass, it is necessary to limit the amount of by-product tar and increase the yields of hydrogen (H2) and carbon monoxide (CO) (syngas). Therefore, we conducted gasification and reforming experiments on woody biomass using an electric tubular furnace, to evaluate the gas reforming and tar decomposition performance of a NiO/SBA-15 catalyst. As a result, we found that this catalyst is effective for H2 production. It is believed that the increase in H2 volume due to the catalyst occurs through a steam reforming reaction involving hydrocarbons, including methane (CH4), and the water-gas shift reaction. With respect to the influence of the gasifying agent on the reforming effect of the catalyst, the amount of generated carbon dioxide (CO2) and hydrogen (H2) increases because the shift reaction is promoted by supplying steam. On the other hand, it was inferred that the shift reaction rarely occurred because it approaches equilibrium by supplying O2. Furthermore, it is suggested that light aromatic hydrocarbons are decomposed by the catalyst. Implications: The mesoporous silica catalyst NiO/SBA-15 was highly effective for H2 production and decomposition of light aromatic compounds in the gasification of woody biomass. In the catalyst reaction, supplying steam promoted H2 production. From thermodynamic analysis and discussion, it was also inferred that supplying O2 might prevent the water gas shift reaction. The results are useful for designing a process needed for rich H2 production and gas refining process for further use of syngas.

Analytical Determination of Nicotine and Tar Levels in Various Dokha and Shisha Tobacco Products.

In the Middle East, there is no precise data and literature on tobacco-based products, such as dokha and shisha. The proposed study aims to quantify the levels of nicotine and tar in different kinds of dokha and shisha products that are sold in the local marketplace. The amount of nicotine in dokha and shisha products can be quantitatively determined using a combination of the "kissling" and "silicotungstic acid" method proposed by Robert M. Chapin. The tar residue from the smoke sample was collected on a glass wool placed before the stopcock (tap) of a separatory funnel as the smoke passes through the inlet of an electronically controlled vacuum pump. The nicotine levels in dokha and shisha samples ranged from 23.83 to 52.80 mg/g and 0.80 to 20.52 mg/g, respectively. The nicotine level varies between different tobacco products. It varies from 0.5 to 19.5 mg/g in cigarettes, from 10.3 to 23.1 mg/g in snuff tobacco, from 11 to 18 mg/g in electronic cigarettes and from 2.9 to 16.6 mg/g in chewing tobacco. The tar levels in the dokha and shisha samples ranged from 21.6 to 45.02 mg/g and 1.68 to 11.87 mg/g, respectively. Smokers are at a high risk of getting lung cancer, chronic obstructive pulmonary disease, emphysema and coronary artery disease owing to the high levels of nicotine and tar present in dokha and shisha tobacco products. These findings contradict the widespread belief among teenagers that dokha and shisha tobacco products are safer alternatives to cigarettes.

Cigarette Filter Ventilation and Smoking Protocol Influence Aldehyde Smoke Yields.

The WHO study group on tobacco product regulation (TobReg) advised regulating and lowering toxicant levels in cigarette smoke. Aldehydes are one of the chemical classes on the TobReg smoke toxicants priority list. To provide insight in factors determining aldehyde yields, the levels of 12 aldehydes in mainstream cigarette smoke of 11 Dutch brands were quantified. Variations in smoking behavior and cigarette design affecting human exposure to aldehydes were studied by using four different machine testing protocols. Machine smoking was based on the International Standardization Organization (ISO) and Health Canada Intense (HCI) regime, both with and without taping the filter vents. The 11 cigarette brands differed in (i) design and blend characteristics; (ii) tar, nicotine, and carbon monoxide (TNCO) levels; (iii) popularity; and (iv) manufacturer. Cigarette smoke was trapped on a Cambridge filter pad and carboxen cartridge. After being dissolved in methanol/CS2 and derivatization with DNPH, the aldehyde yields were determined using HPLC-DAD. Using an intense smoking regime (increased puff volume, shorter puff interval) significantly increased aldehyde yields, following the pattern: ISO < ISO-taped < HCI-untaped < HCI. For all of the regimes, acetaldehyde and acrolein yields were strongly correlated ( r = 0.804). The difference in TNCO and aldehyde levels between regular and highly ventilated low-TNCO cigarettes (as measured using ISO) diminished when smoking intensely; this effect is stronger when combined with taping filter vents. The highly ventilated low-TNCO brands showed six times more aldehyde production per mg nicotine for the intense smoking regimes. In conclusion, acetaldehyde and acrolein can be used as representatives for the class of volatile aldehydes for the different brands and smoking regimes. The aldehyde-to-nicotine ratio increased when highly ventilated cigarettes were smoked intensely, similar to real smokers. Thus, a smoker of highly ventilated low-TNCO cigarettes has an increased potential for higher aldehyde exposures compared to a smoker of regular cigarettes.