Measuring the Impact of Cigarette Smoke on the UPR

2011 ◽  
pp. 147-164 ◽  
Author(s):  
Hong Zhao ◽  
Jin Yang ◽  
Lin Shan ◽  
Ellen D. Jorgensen
Keyword(s):  
Cigarette Smoke ◽  
The Impact

scholarly journals A 7-month inhalation toxicology study in C57BL/6 mice demonstrates reduced pulmonary inflammation and emphysematous changes following smoking cessation or switching to e-vapor products

2021 ◽  
Vol 5 ◽  
pp. 239784732199587
Author(s):  
Ashutosh Kumar ◽  
Ulrike Kogel ◽  
Marja Talikka ◽  
Celine Merg ◽  
Emmanuel Guedj ◽  
...  
Keyword(s):  
Smoking Cessation ◽  
Cigarette Smoke ◽  
Pulmonary Inflammation ◽  
Clinical Signs ◽  
Inhalation Study ◽  
Toxicology Study ◽  
Nasal Tissue ◽  
Product Switching ◽  
The Impact

Cigarette smoking causes serious diseases, including lung cancer, atherosclerotic coronary artery disease, peripheral vascular disease, chronic bronchitis, and emphysema. While cessation remains the most effective approach to minimize smoking-related disease, alternative non-combustible tobacco-derived nicotine-containing products may reduce disease risks among those unable or unwilling to quit. E-vapor aerosols typically contain significantly lower levels of smoke-related harmful and potentially harmful constituents; however, health risks of long-term inhalation exposures are unknown. We designed a 7-month inhalation study in C57BL/6 mice to evaluate long-term respiratory toxicity of e-vapor aerosols compared to cigarette smoke and to assess the impact of smoking cessation (Cessation group) or switching to an e-vapor product (Switching group) after 3 months of exposure to 3R4F cigarette smoke (CS). There were no significant changes in in-life observations (body weights, clinical signs) in e-vapor groups compared to the Sham Control. The 3R4F CS group showed reduced respiratory function during exposure and had lower body weight and showed transient signs of distress post-exposure. Following 7 months of exposure, e-vapor aerosols resulted in no or minimal increase in pulmonary inflammation, while exposure to 3R4F CS led to impairment of lung function and caused marked lung inflammation and emphysematous changes. Biological changes observed in the Switching group were similar to the Cessation group. 3R4F CS exposure dysregulated the lung and nasal tissue transcriptome, while these molecular effects were substantially lower in the e-vapor group. Results from this study demonstrate that in comparison with 3R4F CS, e-vapor aerosols induce substantially lower biological responses including pulmonary inflammation and emphysematous changes, and that complete switching from CS to e-vapor products significantly reduces biological changes associated with CS in C57BL/6 mice.

Maternal Oxidative Stress, Placental Morphometry, and Fetal Growth in Diabetic Rats Exposed to Cigarette Smoke

2018 ◽  
Vol 26 (9) ◽  
pp. 1287-1293 ◽  
Author(s):  
Yuri K. Sinzato ◽  
Estela M. Bevilacqua ◽  
Gustavo T. Volpato ◽  
Rogelio E. Hernandez-Pando ◽  
Marilza V. C. Rudge ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Fetal Growth ◽  
Fetal Development ◽  
Oxidative Stress Biomarkers ◽  
Junctional Zone ◽  
Pregnant Rats ◽  
Stress Biomarkers ◽  
Vascular Walls ◽  
The Impact

The diabetic syndrome affects pregnancy, contributing to placental functional and structural disruptions and impaired fetal development, with many reports indicating tobacco-associated morbidity and perinatal mortality. In our study, an experimental rat model of diabetes and cigarette smoke exposure in pregnant rats was used to determine the impact of the combination of diabetes and exposure to cigarette smoke during pregnancy on maternal oxidative stress biomarkers and placental and fetal development. Diabetes was induced by streptozotocin, and dams were exposed to cigarette smoke by mainstream smoke generated by a mechanical smoking device and delivered into a chamber. Four groups of dams were studied: nondiabetic (C, control) and diabetic (D) exposed to filtered air and nondiabetic (CS) and diabetic (DS) exposed to cigarette smoke prior to and during pregnancy. Maternal oxidative stress biomarkers, placental morphology, and fetal growth were determined close to term. The combination of diabetes and cigarette smoke resulted in elevated maternal blood glucose levels and increased number of small fetuses. Placentas from the DS group showed increased junctional zone and decreased labyrinthine area. The morphological alterations were characterized by extensive vascular congestion, thickness, and hyalinization of the vascular walls, numerous decidual cells with abundant glycogen, and macrophages with cytoplasmic inclusions of hemosiderin. Additionally, they showed increased glycogen accumulation and junctional zone structural derangement with ectopic giant cells. No alterations were observed in maternal oxidative stress status. Thus, our result suggests that diabetes makes pregnant rats more susceptible to the adverse effects of exposure to cigarette smoke on placental morphometry and fetal growth.

scholarly journals The Evolving E-cigarette: Comparative Chemical Analyses of E-cigarette Vapor and Cigarette Smoke

2020 ◽  
Vol 2 ◽  
Author(s):  
Anthony Cunningham ◽  
Kevin McAdam ◽  
Jesse Thissen ◽  
Helena Digard
Keyword(s):  
Thermal Decomposition ◽  
Thermal Degradation ◽  
Benzoic Acid ◽  
Cigarette Smoke ◽  
Iron Alloy ◽  
Decomposition Products ◽  
Nickel Iron ◽  
Degradation Reactions ◽  
Nickel Iron Alloy ◽  
The Impact

Background: E-cigarette designs, materials, and ingredients are continually evolving, with cotton wicks and diverse coil materials emerging as the popular components of atomisers. Another recent development is the use of nicotine salts in e-liquids to replicate the form of nicotine found in cigarette smoke, which may help cigarette smokers to transition to e-cigarettes. However, scientific understanding of the impact of such innovations on e-cigarette aerosol chemistry is limited.Methods: To address these knowledge gaps, we have conducted a comparative study analyzing relevant toxicant emissions from five e-cigarettes varying in wick, atomiser coil, and benzoic acid content and two tobacco cigarettes, quantifying 97 aerosol constituents and 84 smoke compounds, respectively. Our focus was the potential for benzoic acid in e-liquids and cotton wicks to form aerosol toxicants through thermal degradation reactions, and the potential for nickel–iron alloy coils to catalyze degradation of aerosol formers. In addition, we analyzed e-cigarette emissions for 19 flavor compounds, thermal decomposition products, and e-liquid contaminants that the FDA has recently proposed adding to the established list of Harmful and Potentially Harmful Constituents (HPHCs) in tobacco products.Results: Analyses for benzene and phenol showed no evidence of the thermal decomposition of benzoic acid in the e-cigarettes tested. Measurements of cotton decomposition products, such as carbonyls, hydrocarbons, aromatics, and PAHs, further indicated that cotton wicks can be used without thermal degradation in suitable e-cigarette designs. No evidence was found for enhanced thermal decomposition of propylene glycol or glycerol by the nickel–iron coil. Sixteen of the 19 FDA-proposed compounds were not detected in the e-cigarettes. Comparing toxicant emissions from e-cigarettes and tobacco cigarettes showed that levels of the nine WHO TobReg priority cigarette smoke toxicants were more than 99% lower in the aerosols from each of five e-cigarettes as compared with the commercial and reference cigarettes.Conclusions: Despite continuing evolution in design, components and ingredients, e-cigarettes continue to offer significantly lower toxicant exposure alternatives to cigarette smoking.

Insights from a multi-year program designed to test the impact of ingredients on mainstream cigarette smoke toxicity

2011 ◽  
Vol 23 (sup1) ◽  
pp. 172-183 ◽  
Author(s):  
Charles L. Gaworski ◽  
Karl A. Wagner ◽  
Michael J. Morton ◽  
Michael J. Oldham
Keyword(s):  
Cigarette Smoke ◽  
Smoke Toxicity ◽  
The Impact ◽  
Mainstream Cigarette Smoke

scholarly journals Exposure of cigarette smoke aggravates noise induced kidney damage

2020 ◽  
Vol 10 (2) ◽  
pp. e12-e12
Author(s):  
Jamshid Alizadeh ◽  
Zohre Jaffarzadeh ◽  
Kambiz Ahmadi Angali ◽  
Massumeh Ahmadizadeh
Keyword(s):  
Oxidative Stress ◽  
Renal Function ◽  
Cigarette Smoke ◽  
Noise Exposure ◽  
Health Hazard ◽  
Male Rats ◽  
Sodium Pentobarbital ◽  
Biochemical Tests ◽  
Sound Exposure ◽  
The Impact

Introduction: Noise is defined as an interfering and unwanted sound. Exposure to noise induces health problems in humans and animals. Cigarette smoke (CS) has also been known to cause serious problems in health hazard and leads to many kinds of diseases. However, the effects of these agents on the kidney are poorly studied. Objectives: The current study purposes to investigate the impact of noise and/or CS on rat’s kidney Materials and Methods: Four groups of six Wistar adult male rats were used. They randomly were divided into four groups of rats. The first group was used as control. The second group was exposed to noise. The third group was exposed to cigarette smoking and the fourth group was exposed to both noise and CS. The experiments were repeated for two weeks (five days per week). Twenty-four hours after last exposure, the animals were killed by sodium pentobarbital overdose. Renal function was evaluated by the determination of blood urea nitrogen (BUN) and creatinine levels. Oxidative stress was estimated by glutathione (GSH) and malondialdehyde (MDA) assays. Results: The concentrations of BUN and creatinine remarkably raised (P ≤ 0.05) in all groups compared to those in control rats. However, elevations of the biochemical tests were more predominant in rats exposed to combined noise and CS. Elevation of MDA was observed in all exposed rats, while it was more pronounced in the animals exposed to the combined noise and CS when compared to control, CS or noise exposure rats alone. The level of GSH decreased in all exposed groups. It was more obvious in rats exposed to the combined noise and CS when compared to those of control and exposure rats to noise or CS separately. Conclusion: Exposure to noise or CS impaired renal function. Generation of oxidative stress at least in part may be responsible for their nephrotoxicity. Our findings demonstrated CS aggravated noise induced impairment of renal function.

scholarly journals Discriminating Spontaneous From Cigarette Smoke and THS 2.2 Aerosol Exposure-Related Proliferative Lung Lesions in A/J Mice by Using Gene Expression and Mutation Spectrum Data

2021 ◽  
Vol 3 ◽  
Author(s):  
Yang Xiang ◽  
Karsta Luettich ◽  
Florian Martin ◽  
James N. D. Battey ◽  
Keyur Trivedi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cigarette Smoke ◽  
Human Lung ◽  
Gene Signature ◽  
Lung Tumors ◽  
Tumor Classification ◽  
Spontaneous Tumors ◽  
Data Set ◽  
Inhalation Study ◽  
The Impact

Mice, especially A/J mice, have been widely employed to elucidate the underlying mechanisms of lung tumor formation and progression and to derive human-relevant modes of action. Cigarette smoke (CS) exposure induces tumors in the lungs; but, non-exposed A/J mice will also develop lung tumors spontaneously with age, which raises the question of discriminating CS-related lung tumors from spontaneous ones. However, the challenge is that spontaneous tumors are histologically indistinguishable from the tumors occurring in CS-exposed mice. We conducted an 18-month inhalation study in A/J mice to assess the impact of lifetime exposure to Tobacco Heating System (THS) 2.2 aerosol relative to exposure to 3R4F cigarette smoke (CS) on toxicity and carcinogenicity endpoints. To tackle the above challenge, a 13-gene gene signature was developed based on an independent A/J mouse CS exposure study, following by a one-class classifier development based on the current study. Identifying gene signature in one data set and building classifier in another data set addresses the feature/gene selection bias which is a well-known problem in literature. Applied to data from this study, this gene signature classifier distinguished tumors in CS-exposed animals from spontaneous tumors. Lung tumors from THS 2.2 aerosol-exposed mice were significantly different from those of CS-exposed mice but not from spontaneous tumors. The signature was also applied to human lung adenocarcinoma gene expression data (from The Cancer Genome Atlas) and discriminated cancers in never-smokers from those in ever-smokers, suggesting translatability of our signature genes from mice to humans. A possible application of this gene signature is to discriminate lung cancer patients who may benefit from specific treatments (i.e., EGFR tyrosine kinase inhibitors). Mutational spectra from a subset of samples were also utilized for tumor classification, yielding similar results. “Landscaping” the molecular features of A/J mouse lung tumors highlighted, for the first time, a number of events that are also known to play a role in human lung tumorigenesis, such as Lrp1b mutation and Ros1 overexpression. This study shows that omics and computational tools provide useful means of tumor classification where histopathological evaluation alone may be unsatisfactory to distinguish between age- and exposure-related lung tumors.

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