Smoking is recognized as a significant risk factor for numerous disorders, including cardiovascular diseases, respiratory conditions, and various forms of cancer. While the exact pathogenic mechanisms continue to be explored, the induction of oxidative stress via the production of excess reactive oxygen species (ROS) is widely accepted as a primary molecular event that predisposes individuals to these smoking-related ailments. This review focused on how cigarette smoke (CS) promotes ROS formation rather than the pathophysiological repercussions of ROS and oxidative stress. A comprehensive analysis of existing studies revealed the following key ways through which CS imposes ROS burden on biological systems: (1) ROS, as well as radicals, are intrinsically present in CS, (2) CS constituents generate ROS through chemical reactions with biomolecules, (3) CS stimulates cellular ROS sources to enhance production, and (4) CS disrupts the antioxidant system, aggravating the ROS generation and its functions. While the evidence supporting these mechanisms is chiefly based on in vitro and animal studies, the direct clinical relevance remains to be fully elucidated. Nevertheless, this understanding is fundamental for deciphering molecular events leading to oxidative stress and for developing intervention strategies to counter CS-induced oxidative stress.

Through the Mas receptor, angiotensin-(1-7) [Ang-(1-7)] has been shown to have a key role in the development of lung inflammation. This systematic review (SR) sought to identify the relationship between lung damage brought on by exposure to cigarette smoke (CS) and the ACE2-Ang-(1-7)-Mas pathway. In this investigation, relevant keywords were used to search PubMed (MEDLINE), Scopus (Elsevier), and Institute for Scientific Information (ISI) Web of Science up to December 2022. Nine studies were chosen because they satisfied the inclusion/exclusion criteria. The majority of research concluded that exposure to CS increased the risk of lung damage. Smoking cigarettes is the main cause of COPD because it causes massive amounts of reactive oxygen and nitrogen species to enter the lungs, which stimulate the production of inflammatory cytokines like IL-1 β, IL-6, and TNF-α, as well as the invasion of inflammatory cells like neutrophils and macrophages. These findings support the renin-angiotensin system\'s (RAS) involvement in the pathophysiology of smoking-induced damage. Additionally, via stimulating pro-inflammatory mediators, aberrant RAS activity has been linked to lung damage. Lung inflammation\'s etiology has been shown to be significantly influenced by the protective known RAS arm ACE2-Ang-(1-7)-Mas. In conclusion, these are important for informing policymakers to pass legislation limiting the use of smoking and other tobacco to prevent their harmful effects.

Cigarette smoke is a classic risk factor for many diseases. The microbiota has been recently indicated as a new, major player in human health. Its deregulation-dysbiosis-is considered a new risk factor for several illnesses. Some studies highlight a cross-interaction between these two risk factors-smoke and dysbiosis-that may explain the pathogenesis of some diseases. We searched the keywords \"smoking OR smoke AND microbiota\" in the title of articles on PubMed®, UptoDate®, and Cochrane®. We included articles published in English over the last 25 years. We collected approximately 70 articles, grouped into four topics: oral cavity, airways, gut, and other organs. Smoke may impair microbiota homeostasis through the same harmful mechanisms exerted on the host cells. Surprisingly, dysbiosis and its consequences affect not only those organs that are in direct contact with the smoke, such as the oral cavity or the airways, but also involve distant organs, such as the gut, heart, vessels, and genitourinary tract. These observations yield a deeper insight into the mechanisms implicated in the pathogenesis of smoke-related diseases, suggesting a role of dysbiosis. We speculate that modulation of the microbiota may help prevent and treat some of these illnesses.

BACKGROUND: Maternal exposure to cigarette smoke in pregnancy may play a role in the development of testicular cancer in offspring. An updated and comprehensive systematic review of the available evidence is needed.
OBJECTIVE: To identify and evaluate current evidence on maternal exposure to cigarette smoke during pregnancy and testicular cancer in offspring.
METHODS: A systematic search of English peer-reviewed original literature in PubMed through a block search approach. Publications were considered if assessing maternal exposure to cigarette smoke and the risk of testicular cancer in offspring.
RESULTS: Among the 636 identified records, 14 publications were eligible for review and 10 for meta-analysis. Quality assessment of the publications was conducted. Most included publications were case-control studies (n = 11, 79%), while the remaining were ecological studies (n = 3, 21%). Completeness of reporting was high, but more than half were considered subject to potential bias. The trend synthesis showed that half (n = 7) of the included publications demonstrated a higher risk of testicular cancer in the sons of mothers exposed to cigarette smoke during pregnancy. The meta-analysis generated an overall summary risk estimate of 1.00 (95% CI: 0.88; 1.15) (n = 10 publications), with a lower risk for seminoma (0.79, 95% CI: 0.59; 1.04) and nonseminoma (0.96, 95% CI: 0.74; 1.26) (n = 4 publications).
CONCLUSIONS: This systematic review did not provide evidence of an association between maternal exposure to cigarette smoke and risk of testicular cancer in offspring. An overall positive trend was suggested, but it had low statistical precision. The methodological limitations across publications encourage further research based on valid exposure data.

Chronic obstructive pulmonary disease (COPD), as the third leading cause of death among adults, is a significant public health problem around the world. However, about 75% of smokers do not develop the disease despite the severe smoking burden. COPD is a heterogeneous disease, and several phenotypes, with differences in their clinical picture and response to treatment, have been distinguished. Metabolomic studies provide information on metabolic pathways, and therefore are a promising tool for understanding disease etiopathogenesis and the development of effective causal treatment. The aim of this systematic review was to analyze the metabolome of the respiratory epithelial lining fluid of patients with COPD, compared to healthy volunteers, refractory smokers, and subjects with other lung diseases. We included observational human studies. Sphingolipids, phosphatidylethanolamines, and sphingomyelins distinguished COPD from non-smokers; volatile organic compounds, lipids, and amino acids distinguished COPD from smokers without the disease. Five volatile organic compounds were correlated with eosinophilia and four were associated with a phenotype with frequent exacerbations. Fatty acids and ornithine metabolism were correlated with the severity of COPD. Metabolomics, by searching for biomarkers and distinguishing metabolic pathways, can allow us to understand the pathophysiology of COPD and the development of its phenotypes.

The bioactive chemicals in cigarette smoke (CS) and e-cigarette vapor (EV) may affect pathogenic bacteria in the nasopharyngeal microflora, which may have implications on the pathophysiology of respiratory infections in cigarette smokers and e-cigarette users. In this systematic review, we seek to synthesize the research evidence supporting this hypothesis. To address the central research question, \"what is known from the published, peer-reviewed literature about the effects of cigarette smoke or e-cigarette vapor exposure on the physiology of human pathogenic bacteria?\", we screened the PubMed®, Web of ScienceTM, and ScienceDirect databases for reports examining the virulence characteristics and gene expression in human pathogenic bacteria exposed to either CS or EV. The principal conclusion from our analysis is that exposure to either CS or EV induces the virulence of respiratory pathogenic bacteria in a strain-dependent manner, which may in turn facilitate respiratory infections in cigarette smokers and e-cigarette users. In addition, we present evidence that nicotine and reactive oxygen species are the main chemicals responsible for CS/EV-mediated alterations in bacterial physiology. We note limitations that this review does not examine reports describing the alterations in host respiratory physiology or nasopharyngeal dysbiosis caused by CS/EV exposure. Future research to determine whether CS/EV-mediated augmentation of bacterial virulence indeed plays a role in human respiratory tract infections is warranted.

Chronic obstructive pulmonary disease (COPD) is an increasing and major global health problem. COPD is also the third leading cause of death worldwide. Oxidative stress (OS) takes place when various reactive species and free radicals swamp the availability of antioxidants. Reactive nitrogen species, reactive oxygen species (ROS), and their counterpart antioxidants are important for host defense and physiological signaling pathways, and the development and progression of inflammation. During the disturbance of their normal steady states, imbalances between antioxidants and oxidants might induce pathological mechanisms that can further result in many non-respiratory and respiratory diseases including COPD. ROS might be either endogenously produced in response to various infectious pathogens including fungi, viruses, or bacteria, or exogenously generated from several inhaled particulate or gaseous agents including some occupational dust, cigarette smoke (CS), and air pollutants. Therefore, targeting systemic and local OS with therapeutic agents such as small molecules that can increase endogenous antioxidants or regulate the redox/antioxidants system can be an effective approach in treating COPD. Various thiol-based antioxidants including fudosteine, erdosteine, carbocysteine, and N-acetyl-L-cysteine have the capacity to increase thiol content in the lungs. Many synthetic molecules including inhibitors/blockers of protein carbonylation and lipid peroxidation, catalytic antioxidants including superoxide dismutase mimetics, and spin trapping agents can effectively modulate CS-induced OS and its resulting cellular alterations. Several clinical and pre-clinical studies have demonstrated that these antioxidants have the capacity to decrease OS and affect the expressions of several pro-inflammatory genes and genes that are involved with redox and glutathione biosynthesis. In this article, we have summarized the role of OS in COPD pathogenesis. Furthermore, we have particularly focused on the therapeutic potential of numerous chemicals, particularly antioxidants in the treatment of COPD.

Halitosis is a health condition which counts cigarette smoking (CS) among its major risk factors. Cigarette smoke can cause an imbalance in the oral bacterial community, leading to several oral diseases and conditions, including intraoral halitosis. Although the best approach to decrease smoking-related health risks is quitting smoking, this is not feasible for many smokers. Switching to potentially reduced-risk products, like electronic vapor products (EVP) or heated tobacco products (HTP), may help improve the conditions associated with CS. To date, there have been few systematic studies on the effects of CS on halitosis and none have assessed the effects of EVP and HTP use. Self-assessment studies have shown large limitations owing to the lack of reliability in the participants\' judgment. This has compelled the scientific community to develop a strategy for meaningful assessment of these new products in comparison with cigarettes. Here, we compiled a review of the existing literature on CS and halitosis and propose a 3-layer approach that combines the use of the most advanced breath analysis techniques and multi-omics analysis to define the interactions between oral bacterial species and their role in halitosis both in vitro and in vivo. Such an approach will allow us to compare the effects of different nicotine-delivery products on oral bacteria and quantify their impact on halitosis. Defining the impact of alternative nicotine-delivery products on intraoral halitosis and its associated bacteria will help the scientific community advance a step further toward understanding the safety of these products and their potentiall risks for consumers.

Smoking during pregnancy is hazardous to both the mother and the foetus, according to a substantial amount of recorded data. Exposure to nicotine and other compounds in cigarette smoke increases the risk of sudden infant death syndrome (SIDS) by two to five times during pregnancy. Serotonergic abnormalities have been discovered in SIDS infants in the zone of the medulla oblongata, which is known to control cardio-respiratory function. SIDS establishes a connection between depression, learning difficulties and behavioural disorders. Prenatal nicotine intake during the second trimester affects the dopaminergic neurological system, making the foetal brain more susceptible to nicotine and developing ADHD symptoms not just in a foetus but in adolescents also. Prenatal nicotine exposure alters the neurological route of neurotransmitters, acetylcholine and dopamine. Nicotine enhances neuronal activity in adults but desensitizes these processes in babies and young children exposed prenatally. The impact of a neurotoxin like nicotine is determined by the amount and duration of exposure. Continued exposure throughout pregnancy will influence a wide range of activities in the neurodevelopment, whereas exposure confined to a single stage of pregnancy may only affect the processes that are forming at that stage. To decrease the effect of nicotine on neonates due to maternal smoking strategies like nicotine replacement therapy (NRT), folic acid treatment and other behavioural treatments have been studied. Hence, this review focuses on the impact of exposure to nicotine on neonates, which results in various neurological consequences and smoking cessation therapies.

The aim of the present study was to compare concentrations of IgG, IgA, IgM and IgD in both serum and saliva samples from smoking and non-smoking individuals using a protein microarray assay. The findings were also compared to previous studies. Serum and saliva were collected from 48 smoking male individuals and 48 age-matched never-smoker male individuals. The protein microarray assays for detection of human IgG, IgM, IgA and IgD were established and optimized using Ig class-specific affinity-purified goat anti-human Ig-Fc capture antibodies and horseradish peroxidase (HRP)-conjugated goat anti-human Ig-Fc detection antibodies. The Ig class specificity of the microarray assays was verified, and the optimal dilutions of serum and saliva samples were determined for quantification of Ig levels against standard curves. We found that smoking is associated with reduced IgG concentrations and enhanced IgA concentrations in both serum and saliva. By contrast, smoking differentially affected IgM concentrations-causing increased concentrations in serum, but decreased concentrations in saliva. Smoking was associated with decreased IgD concentrations in serum and did not have a significant effect on the very low IgD concentrations in saliva. Thus, cigarette smoking differentially affects the levels of Ig classes systemically and in the oral mucosa. Although there is variation between the results of different published studies, there is a consensus that smokers have significantly reduced levels of IgG in both serum and saliva. A functional antibody deficiency associated with smoking may compromise the body\'s response to infection and result in a predisposition to the development of autoimmunity.