RESUMEN
This cross-sectional study used data from Brazil's National Student Health Survey (PeNSE), from 2015 and 2019, to compare consumption of tobacco products among adolescent students in Brazil and identify associated factors. The study variables were current cigarette smoking, use of other tobacco products and use of any tobacco product. Pearson's Chi-square test was used to ascertain associations between the variables; bivariate and multivariate analyses were performed using logistic regression. Cigarette smoking remained stable between 2015 (6.6%) and 2019 (6.8%), but use of any tobacco product increased (from 10.6% in 2015 to 14.8% in 2019), involving particularly hookahs (7.8%) and e-cigarettes (2.8%). Cigarette smoking was greater among adolescents aged 16 and 17, whose skin colour was black or brown, who missed classes without permission, who reported having no friends, displayed other risk factors, such as drinking alcoholic beverages, or who were passive smokers. The prevalence of smoking has increased over the years and is associated with sociodemographic aspects and other health risk behaviour, highlighting the need for lifelong health promotion actions.
O estudo objetiva comparar o consumo de diferentes produtos do tabaco entre os escolares adolescentes no Brasil em 2015 e 2019 e identificar os fatores associados ao seu uso. Estudo transversal com dados da Pesquisa Nacional de Saúde do Escolar (PeNSE) de 2015 e 2019. Variáveis: uso atual de cigarro, uso de outros produtos do tabaco e uso de qualquer produto do tabaco. Foi usado o teste do Qui-quadrado de Pearson para verificar associação entre as variáveis, realizada análise bivariada e a multivariada por meio da regressão logística. O uso de cigarros se manteve estável entre 2015 (6,6%) e 2019 (6,8%). Mas houve aumento do uso de qualquer produto do tabaco (de 10,6% em 2015 para 14,8% em 2019), sendo o narguilé o mais frequente (7,8%) seguido do cigarro eletrônico (2,8%). O uso de cigarro foi mais elevado entre os adolescentes de 16 e 17 anos, com cor da pele preta e parda, que faltaram as aulas sem autorização, entre aqueles que relataram não ter amigos, que apresentavam outros fatores de risco como consumir bebidas alcoólicas e que eram fumantes passivos. A prevalência de tabagismo aumentou ao longo dos anos e foi associada com aspectos sociodemográficos e a outros comportamentos de risco à saúde, o que alerta para a necessidade de ações de promoção da saúde ao longo do ciclo de vida.
Asunto(s)
Fumar Cigarrillos , Encuestas Epidemiológicas , Estudiantes , Uso de Tabaco , Humanos , Brasil/epidemiología , Adolescente , Estudios Transversales , Femenino , Masculino , Estudiantes/estadística & datos numéricos , Prevalencia , Fumar Cigarrillos/epidemiología , Factores de Riesgo , Uso de Tabaco/epidemiología , Conductas de Riesgo para la Salud , Sistemas Electrónicos de Liberación de Nicotina/estadística & datos numéricos , Consumo de Bebidas Alcohólicas/epidemiología , Fumar/epidemiología , Modelos LogísticosRESUMEN
Globally, there are around 1.3 billion cigarette consumers, indicating it to be the second highest risk factor for early death and morbidity. Meanwhile, psychological therapy offers tools based on its different models and techniques, which can contribute to smoking cessation. In this context, this study gathers scientific evidence to identify psychological therapies that can be used to reduce cigarette consumption. A systematic review of controlled clinical studies was conducted, implementing the PRISMA methodology. Search queries were performed with terms extracted from MESH (Medical Subject Headings) and DECS (Descriptors in Health Sciences). Subsequently, the search was queried in the scientific databases of Medline/PubMed, Cochrane, Scopus, Science Direct, ProQuest, and PsycNet, with subsequent verification of methodological quality using the Joanna Briggs Institute checklists. The selected documents revealed that cognitive behavioral therapy prevails due to its use and effectiveness in seven publications (25%). The cognitive approach with mindfulness therapy is found in 4 publications (14%), the transtheoretical model with motivational therapy in 4 publications (14%), brief psychological therapy in 3 publications (10%), and the remaining 10 documents (37%) correspond with others. Intervention studies refer to cognitive behavioral therapy as the most used in reducing cigarette consumption; in terms of the duration of abstinence, scientific evidence shows beneficial effects with short-term reduction.
Asunto(s)
Fumar Cigarrillos , Cese del Hábito de Fumar , Humanos , Cese del Hábito de Fumar/psicología , Cese del Hábito de Fumar/métodos , Fumar Cigarrillos/psicología , Terapia Cognitivo-Conductual , Psicoterapia/métodosRESUMEN
OBJECTIVE: To analyze the effect of hookah and cigarettes on the oral mucosa of smokers through the use of exfoliative cytology. STUDY DESIGN: Smear samples were collected by exfoliative cytology from the tongue of 33 hookah smokers, 22 cigarette smokers, and 30 non-smokers. The selected analyses include micronuclei (MN), metanuclear anomalies, epithelial maturation, and cytomorphology (nuclear area [NA], cytoplasmic area [CA], and NA/CA ratio). RESULTS: The largest differences observed for MN and metanuclear anomalies were between cigarette smokers and the control group (notably 1 MN P = .04; total cells with MN P = .039; total MN P = .042; karyorrhexis and binucleation, P = .0001). The hookah group, compared with the control group, showed the greatest differences for karyolysis (P = .0023), binucleation (P = .0003), and broken egg (P = .008). Significant differences were found between the smokers and the control groups regarding changes in the superficial cell without nucleus, perinuclear halo, vacuolization, color change, mucus, and keratohyalin granules. There was a significant increase in the NA and NA/CA ratio in the smoker groups. CONCLUSION: This study showed that a combined analysis of exfoliative cytology associated with other diagnostic methods is a useful tool for studying oral carcinogenesis. Hookah and cigarettes showed similar effects in terms of displaying substantial cytogenetic and cytotoxic damage.
Asunto(s)
Pruebas de Micronúcleos , Mucosa Bucal , Humanos , Mucosa Bucal/patología , Mucosa Bucal/citología , Masculino , Femenino , Adulto , Persona de Mediana Edad , Micronúcleos con Defecto Cromosómico , Fumar/efectos adversos , Citodiagnóstico/métodos , Fumar Cigarrillos/efectos adversos , Estudios de Casos y ControlesRESUMEN
OBJECTIVE: To assess the impact of tobacco control regulations and policy implementation on smoking cessation tendencies in cigarette users born between 1982 and 1991 in Chile. DESIGN: Longitudinal cross-sectional study. SETTING: National level. PARTICIPANTS: Data from the National Survey of Drug Consumption (Service of Prevention and Rehabilitation for Drug and Alcohol Consumption). A pseudo-cohort of smokers born between 1982 and 1991 (N=17 905) was tracked from 2002 to 2016. PRIMARY AND SECONDARY OUTCOMES MEASURES: Primary outcome was the tendency to cease smoking conceptualised as the report of using cigarettes 1 month or more ago relative to using cigarettes in the last 30 days. The main exposure variable was the Tobacco Policy Index-tracking tobacco policy changes over time. Logistic regression, controlling for various factors, was applied. RESULTS: Models suggested a 14% increase in the smoking cessation tendency of individuals using cigarettes 1 month or more ago relative to those using cigarettes in the last 30 days (OR 1.14, CI 95% CI 1.10 to 1.19) for each point increment in the Tobacco Policy index. CONCLUSIONS: Our study contributes to documenting a positive impact of the implementation of interventions considered in the MPOWER strategy in the progression of smoking cessation tendencies in smokers born between 1982 and 1991 in Chile.
Asunto(s)
Cese del Hábito de Fumar , Humanos , Chile/epidemiología , Cese del Hábito de Fumar/estadística & datos numéricos , Estudios Transversales , Masculino , Estudios Longitudinales , Femenino , Adulto , Persona de Mediana Edad , Adulto Joven , Adolescente , Fumar Cigarrillos/epidemiología , Política de Salud , Modelos Logísticos , Productos de Tabaco/legislación & jurisprudencia , Control del TabacoRESUMEN
With highly active antiretroviral therapy, HIV infection has become a treatable chronic disease. However, modifiable risk factors such as cigarette smoking continue to impact the morbidity and mortality of people with HIV (PWH). We assessed the prevalence and factors associated with cigarette smoking and motivation to quit among PWH in Western Jamaica. A cross-sectional study was conducted in which 392 adults seeking HIV care at health facilities in Western Jamaica completed an interviewer-administered questionnaire. Current smoking prevalence among participants was 17.4%. Current smoking was significantly associated with being male (OR = 2.99), non-Christian/non-Rastafarian (OR = 2.34), living or working with another smoker (aOR =1.86), being moderate to severely depressed (OR = 3.24), having an alcohol drinking problem (OR = 1.84), and never being asked by a healthcare provider if they smoked (OR = 3.24). Among the PWH who currently smoke, 36.7% are moderately to highly dependent on nicotine. One-third of people who smoke (33.8%) started smoking for the first time after HIV diagnosis, while 66.2% initiated smoking before; 88% were willing to quit smoking. These findings provide baseline information for designing and implementing a comprehensive smoking cessation program that considers the needs of PWH in Jamaica, with the potential of becoming a replicable model for other HIV-specialized healthcare settings in the Caribbean.
Asunto(s)
Fumar Cigarrillos , Infecciones por VIH , Humanos , Jamaica/epidemiología , Masculino , Femenino , Estudios Transversales , Adulto , Infecciones por VIH/epidemiología , Infecciones por VIH/psicología , Prevalencia , Fumar Cigarrillos/epidemiología , Fumar Cigarrillos/psicología , Factores de Riesgo , Persona de Mediana Edad , Encuestas y Cuestionarios , Cese del Hábito de Fumar/psicología , Cese del Hábito de Fumar/estadística & datos numéricos , Motivación , Adulto Joven , Fumar/epidemiología , Fumar/psicologíaRESUMEN
BACKGROUND: The increase in the use of psychoactive substances, alcohol and cigarettes in young people has become a public health problem. The identification of factors that increase or reduce the risk of exposure to these substances and the possible relationship between them is essential for planning strategies with a risk approach; hence the reason for this study. The objective was to establish the profile of use of psychoactive substances, alcohol and cigarettes and the factors associated with such use in nursing students of a higher education institution. METHODS: Quantitative, observational, analytical cross-sectional study. RESULTS: We included 310 students from 1â¯st to 9th semester of a Nursing programme from a private higher education institution in Bogotá. The prevalence of psychoactive substance use in the last year was 2.96% (95%CI, 1.36-5.54), with marijuana being the substance most used (55.55%). The prevalence of alcohol and cigarette use during the last 12 months was estimated at 86.64% (95%CI, 83.24-91.0) and 12.16% (95%CI, 8.43-15.88) respectively. A statistically significant association was found between the use of these substances: alcohol use was associated with cigarette use (ORâ¯=â¯3.22; Pâ¯=â¯0.006) and smoking was associated with psychoactive substance use (ORâ¯=â¯15.4; Pâ¯<â¯0.001). CONCLUSIONS: Alcohol use increases the likelihood of smoking cigarettes, and this in turn increases the likelihood of psychoactive substance use, in this university population.
Asunto(s)
Consumo de Bebidas Alcohólicas , Psicotrópicos , Estudiantes de Enfermería , Trastornos Relacionados con Sustancias , Humanos , Estudios Transversales , Estudiantes de Enfermería/estadística & datos numéricos , Masculino , Femenino , Adulto Joven , Prevalencia , Psicotrópicos/administración & dosificación , Consumo de Bebidas Alcohólicas/epidemiología , Trastornos Relacionados con Sustancias/epidemiología , Adulto , Colombia/epidemiología , Adolescente , Fumar/epidemiología , Factores de Riesgo , Fumar Cigarrillos/epidemiologíaRESUMEN
INTRODUCTION: This study evaluated the effects of cigarette smoke inhalation (CSI) on apical periodontitis (AP) induced in rats by histometric, immunohistochemical, and microtomographic analysis. METHODS: A total of 32 male Wistar rats were divided into 4 experimental groups (n = 8): control, CSI, AP, and CSI + AP. Rats in the CSI and CSI + AP groups inhaled cigarette smoke by remaining inside a smoking chamber for 8 minutes 3 times a day for 50 days. After 20 days of smoke inhalation, rats in the AP and CSI + AP groups had the pulp of their first right lower molar exposed to induce AP. Blood was collected on day 50 to evaluate nicotine and serum cotinine levels. The animals' mandibles were removed for histologic processing to evaluate bone resorption by histometric, immunohistochemical (receptor activator of nuclear factor kappa B ligand/osteoprotegerin), and microtomographic analysis. The Student t test was applied. RESULTS: Histometric analysis showed a larger area of bone resorption (P < .05) and microtomographic analysis found greater resorption volume (P < .001) for the CSI + AP group compared with the AP group. The CSI + AP group presented a high RANKL immunostaining pattern compared with the AP group (P < .001). CONCLUSIONS: CSI increased bone resorption caused by AP.
Asunto(s)
Resorción Ósea , Fumar Cigarrillos , Periodontitis Periapical , Ratas , Masculino , Animales , Ratas Wistar , Resorción Ósea/diagnóstico por imagen , Resorción Ósea/patología , Periodontitis Periapical/diagnóstico por imagenAsunto(s)
Humanos , Masculino , Femenino , Tabaquismo/tratamiento farmacológico , Cese del Hábito de Fumar , Fumar Cigarrillos/tratamiento farmacológico , Agentes para el Cese del Hábito de Fumar/administración & dosificación , Alcaloides de Quinolizidina/administración & dosificación , Síndrome de Abstinencia a Sustancias/prevención & control , Ensayos Clínicos Controlados Aleatorios como Asunto , Receptores Nicotínicos/efectos de los fármacos , Resultado del Tratamiento , Agentes para el Cese del Hábito de Fumar/efectos adversos , Duración de la Terapia , Alcaloides de Quinolizidina/efectos adversos , Nicotina/antagonistas & inhibidoresRESUMEN
Introducción: La leucoplasia es la lesión potencialmente maligna más común de la mucosa bucal; el consumo de tabaco es el principal factor etiológico; se presentan distintos grados de displasia epitelial. Su estudio permite conocer mejor las manifestaciones clínicas e histopatológicas de esta enfermedad. Objetivo: Caracterizar clínica e histopatológicamente la leucoplasia homogénea bucal en pacientes fumadores de tabaco. Métodos: Se realizó un estudio descriptivo y transversal. El universo estuvo compuesto por 75 pacientes fumadores de tabaco y cigarros, atendidos en la consulta estomatológica del Policlínico de Especialidades del Hospital Clínico-Quirúrgico Saturnino Lora Torres de Santiago de Cuba. Mediante el examen clínico e histopatológico se diagnosticó leucoplasia homogénea bucal. Para la recolección del dato primario se confeccionó un modelo con las siguientes variables: grupo de edad, sexo, diagnóstico clínico, tiempo en el hábito de fumar, localización anatómica y estudio histopatológico de la enfermedad. Resultados: En la casuística prevaleció el sexo masculino (58,6 por ciento) y el grupo etario de 60 años y más (41,3 por ciento); la hiperparaqueratosis (64,0 por ciento), el infiltrado inflamatorio crónico ligero (60,0 por ciento) y la displasia epitelial leve (73,3 por ciento) fueron las alteraciones hísticas más comunes en fumadores con 21 y más años. La hipercromasia del núcleo (100,0 por ciento) y el pleomorfismo nuclear (96,80 por ciento) resultaron los cambios celulares más prominentes. Las alteraciones de los clavos interpapilares (92,0 por ciento), la hiperplasia del estrato basal (88,9 por ciento) y la pérdida de la polaridad (87,3 por ciento) resultaron los signos displásicos tisulares más significativos en la leucoplasia bucal y la mucosa de carrillo (40,0 por ciento) el sitio anatómico de mayor ocurrencia de lesiones. Conclusiones: Todos los pacientes fumadores de tabaco y cigarro presentaron, clínicamente, lesiones leucoplásicas bucales, confirmadas por el estudio histopatológico; el sexo masculino y el grupo de 60 y más años son los de mayor afectación. La hiperparaqueratosis, el infiltrado inflamatorio crónico ligero y la displasia epitelial leve fueron los de mayor predominio; la hipercromasia del núcleo y el pleomorfismo nuclear fueron los cambios celulares más prominentes. En el tejido displásico epitelial prevalecieron las alteraciones de los clavos interpapilares, la hiperplasia del estrato basal y la pérdida de la polaridad y el sitio más afectado, la mucosa de carrillo(AU)
Introduction: Leukoplakia is the most common potentially malignant lesion of the buccal mucosa; tobacco use is the main etiological factor; different degrees of epithelial dysplasia are present. Its study allows a better understanding of the clinical and histopathological manifestations of this disease. Objective: To clinically and histopathologically characterize homogeneous buccal leukoplakia in patients who smoke tobacco. Methods: A descriptive and cross-sectional study was performed. The universe was composed of 75 patients who smoked tobacco and cigars, attended in the stomatological consultation of the Specialties Polyclinic of the Clinical-Surgical Hospital Saturnino Lora Torres of Santiago de Cuba. By means of clinical and histopathological examination, homogeneous buccal leukoplakia was diagnosed. For the collection of the primary data, a model was made with the following variables: age group, sex, clinical diagnosis, time in smoking habit, anatomical location and histopathological study of the disease. Results: Male sex (58.6 percent)) and age group 60 years and older (41.3 percent) prevailed in the casuistry; hyperkeratosis (64.0 percent)), mild chronic inflammatory infiltrate (60.0 percent)) and mild epithelial dysplasia (73.3 percent)) were the most common histopathological alterations in smokers aged 21 years and older. Hyperchromasia of the nucleus (100.0 percent)) and nuclear pleomorphism (96.80 percent)) were the most prominent cellular changes. Interpapillary nail alterations (92.0 percent)), stratum basale hyperplasia (88.9 percent)) and loss of polarity (87.3 percent)) resulted the most significant tissue dysplastic signs in buccal leukoplakia and cheek mucosa (40.0 percent)) the anatomical site of highest occurrence of lesions. Conclusions: All tobacco and cigarette smoking patients presented, clinically, buccal leukoplastic lesions, confirmed by histopathological study; male sex and the 60 and older age group are the most affected. Hyperparapokeratosis, mild chronic inflammatory infiltrate and mild epithelial dysplasia were the most predominant; hyperchromasia of the nucleus and nuclear pleomorphism were the most prominent cellular changes. In the epithelial dysplastic tissue, interpapillary nail alterations, hyperplasia of the stratum basale and loss of polarity prevailed and the most affected site, the cheek mucosa(AU)
Asunto(s)
Humanos , Masculino , Persona de Mediana Edad , Leucoplasia Bucal , Diagnóstico Clínico , Fumar Cigarrillos , Fumadores , Estudios TransversalesRESUMEN
This study aimed to explore the pathways that can influence cigarette smoking among adolescents. This population-based cohort followed a random sample of 12-year-old adolescents from southern Brazil for 6 years. Regular cigarette smoking was assessed through a self-reported question, previously used in the Brazilian National Survey of Scholar Health. We also gathered data on bullying, dental caries at baseline, incidence of caries, sex, friend network, and Sense of Coherence (SOC). Socioeconomic and demographic characteristics were also collected. Structural equation modeling was used to evaluate the pathways. Of the 1,134 adolescents examined at baseline, 768 were re-evaluated (67.7% retention rate). The prevalence of smoking was 37.6%. This prevalence was directly affected by low SOC (SC: -0.14, p < 0.01), low household income (SC: -0.12, p < 0.01), and male sex (SC: 0.15, p < 0.01). Presence of dental caries at baseline indirectly influenced the occurrence of dental bullying at follow-up via the incidence of dental caries (SC: 0.01, p < 0.05). Dental bullying indirectly influenced cigarettes consumption via SOC (SC: 0.62, p < 0.05). Friend network also indirectly influenced the consumption of cigarettes via SOC (SC: 0.32, p < 0.05). Psychosocial factors influence adolescent cigarette consumption through its higher direct and indirect effects (via bullying). In addition, behavioral, sociodemographic, and clinical factors also influence the occurrence of smoking.
Asunto(s)
Acoso Escolar , Fumar Cigarrillos , Caries Dental , Enfermedades de la Boca , Humanos , Masculino , Adolescente , Niño , Salud Bucal , Caries Dental/epidemiología , Caries Dental/etiología , Caries Dental/psicología , Análisis de Clases Latentes , Brasil/epidemiologíaRESUMEN
Objective: To assess the prevalence of current cigarette smoking among transgender women in Argentina, and to examine the unique associations of current cigarette smoking with demographic and psychosocial factors. Methods: This study is a secondary data analysis of the TransCITAR - a prospective cohort study of transgender individuals living in Buenos Aires, Argentina - baseline data. The baseline survey collected information on sociodemographic characteristics, perceived health status, depressive symptoms, suicide attempts, current cigarette smoking, alcohol use disorder, and substance use. Participants were also asked about lifetime experiences of physical and sexual violence perpetrated by partners, clients and/or the police, and experiences of gender identity stigma in the past year from healthcare workers and the police. Lastly, participants were asked if they had ever been arrested. Fisher's exact test was used to compare proportions in categorical variables and student t-test was used for continuous variables. Significant associations with current cigarette smoking were tested in a logistic regression model adjusted for all significant associations. Results: A total of 41.7% of participants (n = 393) reported current cigarette smoking. Compared to their non-smoking counterparts, participants who reported current cigarette smoking (1) had completed less education, (2) were more likely to be born in Argentina, (3) more likely to had migrated to Buenos Aires from other parts of the country, (4) more likely to report a history of sex work, (5) more likely to perceive their health as excellent, (6) more likely to screen positive for hazardous alcohol drinking, (7) more likely to report any substance and cocaine use in the past year, (8) more likely to experience gender identity stigma from the police in the past year, and (9) more likely to being arrested in their lifetime (all p's < 0.05). After controlling for all significant associations, education level of less than high school (AOR = 1.79, 95% CI 1.02-2.12), hazardous drinking (AOR = 2.65, 95% CI 1.30-5.37), and any substance use in the last year (AOR = 2.14, 95% CI 1.16-3.94) were positively and independently associated with current cigarette smoking. Conclusion: Among transgender women in Argentina, current cigarette smoking was more than double the rate for cisgender women. Current cigarette smoking was associated with education, hazardous drinking, and any drug use. These results will inform future smoking cessation interventions among transgender women in Argentina.
Asunto(s)
Fumar Cigarrillos , Trastornos Relacionados con Sustancias , Personas Transgénero , Humanos , Masculino , Femenino , Personas Transgénero/psicología , Fumar Cigarrillos/epidemiología , Prevalencia , Argentina/epidemiología , Estudios Prospectivos , Identidad de Género , Trastornos Relacionados con Sustancias/epidemiologíaRESUMEN
OBJECTIVE: To evaluate the effects of cigarette smoke inhalation on the immune-inflammatory profile of experimental apical periodontitis in rats. METHODOLOGY: In total, 32 male Wistar rats were divided into four groups (n = 8): AP-induced apical periodontitis; S-cigarette smoke inhalation; APS-induced AP and cigarette smoke inhalation; and C (control)-neither AP nor cigarette smoke inhalation. To induce cigarette smoke inhalation, the animals were kept in a chamber filled with tobacco smoke for 8 min thrice a day for 50 days. AP was induced 20 days after inhalation initiation by exposing their coronary pulp to their oral environment for 30 days. After animals were euthanized, their right hemimaxillae were removed for histopathological, semi-quantitative and immunohistochemical (F4/80, CD206 and iNOS) analyses. RESULTS: Quantitative data showed a moderate number of inflammatory infiltrates in AP and an intense number in APS (p < .05). Comparing F4/80+ cells showed no statistically significant differences among groups, but we found more CD206+ cells in AP than in C and S (p > .05). INOS+ immunostaining showed a significant increase in AP and APS, when compared with C and S (p < .05). APS had more iNOS+ cells than AP (p < .05). CONCLUSION: Cigarette smoke inhalation worsened AP, leading to a predominantly pro- inflammatory profile in our experimental model.
Asunto(s)
Fumar Cigarrillos , Periodontitis Periapical , Ratas , Masculino , Animales , Ratas Wistar , Periodontitis Periapical/patologíaRESUMEN
Even though epidemiological studies suggest that tobacco smoking and high-risk human papillomavirus (HR-HPV) infection are mutually exclusive risk factors for developing head and neck cancer (HNC), a portion of subjects who develop this heterogeneous group of cancers are both HPV-positive and smokers. Both carcinogenic factors are associated with increased oxidative stress (OS) and DNA damage. It has been suggested that superoxide dismutase 2 (SOD2) can be independently regulated by cigarette smoke and HPV, increasing adaptation to OS and tumor progression. In this study, we analyzed SOD2 levels and DNA damage in oral cells ectopically expressing HPV16 E6/E7 oncoproteins and exposed to cigarette smoke condensate (CSC). Additionally, we analyzed SOD2 transcripts in The Cancer Genome Atlas (TCGA) Head and Neck Cancer Database. We found that oral cells expressing HPV16 E6/E7 oncoproteins exposed to CSC synergistically increased SOD2 levels and DNA damage. Additionally, the SOD2 regulation by E6, occurs in an Akt1 and ATM-independent manner. This study suggests that HPV and cigarette smoke interaction in HNC promotes SOD2 alterations, leading to increased DNA damage and, in turn, contributing to development of a different clinical entity.
Asunto(s)
Fumar Cigarrillos , Neoplasias de Cabeza y Cuello , Proteínas Oncogénicas Virales , Infecciones por Papillomavirus , Humanos , Virus del Papiloma Humano , Papillomavirus Humano 16/metabolismo , Infecciones por Papillomavirus/complicaciones , Proteínas E7 de Papillomavirus/genética , Proteínas E7 de Papillomavirus/metabolismo , Proteínas Oncogénicas Virales/genética , Proteínas Oncogénicas Virales/metabolismo , Daño del ADN , Neoplasias de Cabeza y Cuello/complicacionesRESUMEN
SUMMARY: A great deal of attention of air pollution on respiratory health is increasing, particularly in relation to haze days. It is that exposure to cigarette smoke augments the toxicity of common air contaminants, thereby increasing the complexity of respiratory diseases. Although there are various mechanisms involved to respiratory diseases caused or worsen by cigarette smoking, in which the role of AQPs in the lung with regard to fluid homeostasis still remains elusive. In this paper, we copied the rat models based on smoke generator, and investigated the morphological changes of mucosa and related functions depending on the balance of lining liquid of alveoli via AQPs expression. Compared with normal group, weak labelling of AQP1 and AQP5 protein abundance were clearly detected in the corresponding part of smoke exposure groups compared with normal group. Hence, it is suggested that the contribution of AQPs in the lung is diminished, thereby causing perturbed balancing between resorptive and secretory fluid homeostasis under cigarette smoking.
Cada vez se presta más atención a la contaminación del aire en la salud respiratoria, particularmente, en relación con los días de neblina. En consecuencia la exposición al humo del cigarrillo aumenta la toxicidad de los contaminantes comunes del aire, lo que además aumenta la complejidad de las enfermedades respiratorias. Aunque existen varios mecanismos involucrados en las enfermedades respiratorias causadas o empeoradas por el tabaquismo, en las que el papel de las AQP en el pulmón respecto a la homeostasis de líquidos sigue siendo difícil de alcanzar. En este artículo, copiamos los modelos de rata basados en el generador de humo e investigamos los cambios morfológicos de la mucosa y las funciones relacionadas según el equilibrio del líquido de revestimiento de los alvéolos a través de la expresión de AQP. En comparación con el grupo normal, se detectó claramente un etiquetado débil de la abundancia de proteínas AQP1 y AQP5 en la parte correspondiente de los grupos de exposición al humo en comparación con el grupo control. Por lo tanto, se sugiere que la contribución de las AQP en el pulmón está disminuida, provocando así un equilibrio perturbado entre la homeostasis del líquido secretor y de reabsorción bajo el hábito de fumar cigarrillos.
Asunto(s)
Animales , Ratas , Sistema Respiratorio/patología , Fumar Cigarrillos/efectos adversos , Sistema Respiratorio/efectos de los fármacos , Líquidos Corporales/metabolismo , Inmunohistoquímica , Microscopía Electrónica , Ratas Sprague-Dawley , Acuaporinas/metabolismo , Homeostasis , Pulmón/efectos de los fármacos , Pulmón/patologíaRESUMEN
AIM: The aim of this study was to evaluate the effects of cigarette smoke inhalation (CSI) on inflammation, pro-inflammatory mediators and haematological parameters in rats with induced apical periodontitis (AP). METHODOLOGY: Thirty-two 3-month-old male Wistar rats were divided into four experimental groups (n = 8): C-Control; S-rats with CSI; AP-rats with AP; and SAP-rats with CSI + AP. Animals in groups S and SAP inhaled cigarette smoke by remaining inside a smoking chamber for 8 min, three times daily, for 50 days. After 20 days of smoke inhalation, animals in AP and SAP groups had the pulps of the lower right first molar exposed to oral environment for 30 days to induce AP. In these subsequent 30 days, animals in group S and SAP continued with CSI. On Day 50, animals were euthanized and mandibles were histologically processed to assess inflammatory infiltrate, immunohistochemical interleukins (IL-1ß, IL-6 and TNF-α), and blood samples collected for laboratory analysis. The Mann-Whitney test was performed for non-parametric data and the pairwise analyses of Student's t-test for parametric data, with a significance level of p < .050. RESULTS: Inflammatory infiltrate was moderate in AP group and more severe in the SAP (p = .010). The interleukins IL-6, IL-1ß and TNF-α were higher in SAP group (p < .001) when compared to the AP group. A greater number of red blood cells (p = .010), haemoglobin (p = .007) and neutrophils (p = .014) were observed in the SAP group in comparison with the AP group. CONCLUSION: Cigarette smoke inhalation induced a more severe inflammatory infiltrate, with increased levels of pro-inflammatory cytokines and changes in haematological parameters in rats with induced AP. Thus, CSI aggravated AP, exacerbating the inflammatory response.
Asunto(s)
Fumar Cigarrillos , Periodontitis Periapical , Ratas , Masculino , Animales , Ratas Wistar , Interleucina-6 , Factor de Necrosis Tumoral alfa , Periodontitis Periapical/patologíaRESUMEN
Individuals with chronic obstructive pulmonary disease (COPD) are more susceptible to exacerbation crisis triggered by secondary lung infections due to the dysfunction of antiviral signaling, principally via suppression of IFN-γ. Although the probiotic is known for controlling pulmonary inflammation in COPD, the influence of the Lactobacillus rhamnosus (Lr) on antiviral signaling in bronchial epithelium exposed to cigarette smoke extract (CSE) and viruses, remains unknown. Thus, the present study investigated the Lr effect on the antiviral signaling and the secretion of inflammatory mediators from bronchial epithelial cells (16HBE cells) exposed to CSE and SARS-CoV-2. The 16HBE cells were cultured, treated with Lr, stimulated with CSE, and infected with SARS-CoV-2. The cellular viability was evaluated using the MTT assay and cytotoxicity measured by lactate dehydrogenase (LDH) activity. The viral load, TLR2, TLR3, TLR4, TLR7, TLR8, MAVS, MyD88, and TRIF were quantified using specific PCR. The pro-inflammatory mediators were measured by a multiplex biometric immunoassay, and angiotensin converting enzyme 2 (ACE2) activity, NF-κB, RIG-I, MAD5, and IRF3 were measured using specific ELISA kits. Lr decreased viral load, ACE2, pro-inflammatory mediators, TLR2, TLR4, NF-κB, TLR3, TLR7, and TLR8 as well as TRIF and MyD88 expression in CSE and SARS-CoV-2 -exposed 16HBE cells. Otherwise, RIG-I, MAD5, IRF3, IFN-γ, and the MAVS expression were restored in 16HBE cells exposed to CSE and SARS-CoV-2 and treated with Lr. Lr induces antiviral signaling associated to IFN-γ secreting viral sensors and attenuates cytokine storm associated to NF-κB in bronchial epithelial cells, supporting its emerging role in prevention of COPD exacerbation.
Asunto(s)
COVID-19 , Fumar Cigarrillos , Lacticaseibacillus rhamnosus , Enfermedad Pulmonar Obstructiva Crónica , Humanos , SARS-CoV-2/metabolismo , FN-kappa B/genética , FN-kappa B/metabolismo , Enzima Convertidora de Angiotensina 2/metabolismo , Fumar Cigarrillos/efectos adversos , Receptor Toll-Like 4/metabolismo , Receptor Toll-Like 2 , Factor 88 de Diferenciación Mieloide/metabolismo , Receptor Toll-Like 3/metabolismo , Receptor Toll-Like 7/metabolismo , Receptor Toll-Like 8/metabolismo , COVID-19/metabolismo , Células Epiteliales/metabolismo , Enfermedad Pulmonar Obstructiva Crónica/metabolismo , Citocinas/metabolismo , Mediadores de Inflamación/metabolismo , Antivirales/metabolismo , Proteínas Adaptadoras del Transporte Vesicular/metabolismoRESUMEN
ABSTRACT Objective: To identify the tobacco effect on flexural properties and the microhardness of three acrylic resins. Material and Methods: Three resins were tested: two thermo-polymerizable acrylic resins (RMB 20 and BMS 014) and one autopolymerized acrylic resin. The 3-point bending and microhardness tests were carried out with a universal tensile-compression machine and a micro-Vickers hardness tester. The acrylic resin specimens have been exposed for 21 days to cigarette smoke in a smoking room. Their mechanical strength was compared to unexposed samples. Statistical analysis was performed using the data processing software SPSS Statistics 21.0. Results: The flexural properties of the resins were affected by cigarette smoke only in the case of Major Base 20® (drop in strength with p= 0.02; 0.6; 0.7 and in elastic modulus with p= 0.86; 0.74 and 0.85 for Major Base 20®, BMS 014® and Major Repair®). The cigarette smoke affected significantly microhardness for all groups (p<0.001). Conclusion: Cigarette smoking does not affect the flexural properties of the acrylic resin (BMS 014® and Major Repair® unlike Major Base 20®), but it does reduce the microhardness.
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Dentaduras , Fumar Cigarrillos/efectos adversos , Resistencia Flexional , Propiedades de Superficie , Análisis de VarianzaRESUMEN
Paracoccidioidomycosis (PCM) may present as an acute/subacute clinical form, characterized by a progressive disease arising from the airborne initial infection, or, most often, as an asymptomatic or subclinical infection that may manifest later during an individual's life, the chronic form. Epidemiological studies show the existence of a strong association between smoking and the development of the chronic form. Current evidence demonstrates that cigarette smoke (CS) has immunosuppressive properties that could be implicated in the increasing susceptibility to the chronic form of PCM. To address this issue, we developed a murine model of a non-progressive pulmonary form of PCM that was exposed to CS at a magnitude that mimicked a moderate smoker. The chronic CS exposure started after 2 weeks and lasted up until 20 weeks post-infection, with the aim of mimicking human natural history, since it is estimated that individuals from endemic areas are infected early in life. The control group consisted of infected but not CS-exposed mice. We assessed the lung fungal burden (colony forming units [CFU]) and the area affected by the granulomatous inflammatory response, fungal dissemination to spleen and liver, and, by immunohistochemistry, the presence of CD4 and CD8 lymphocytes, CD68 and MAC-2 macrophages, and IFN-γ, IL-10 and TNF expressing cells within the granulomatous response. We detected a CS effect as early as 2 weeks after exposure (four weeks post-infection) when the lung CFU of exposed animals was significantly higher than in their non-exposed counterparts. At 12 weeks, the CS-exposed animals presented a more severe disease, as witnessed by the persistent higher lung fungal load (although it did not reach statistical significance [ p = 0.054]), greater dissemination to other organs, greater affected area of the lung, decreased IFN-γ/IL-10 ratio, and higher TNF expression within the granulomas, compared with CS-non-exposed mice. The number of CD4 and CD8 lymphocytes infiltrating the granulomas was similar between both mice groups, but there was a decrease in the number of MAC-2+ macrophages. No difference was noted in the CD68+ macrophage number. However, the follow-up in week 20 showed that the immunological effects of exposure to CS ceased, with both CS and NCS mice showing the same infectious features, i.e., a trend for resolution of the infection. In conclusion, we show that chronic CS-exposure alters the course of the disease in an experimental model of subclinical pulmonary PCM, confirming the epidemiological link between CS-exposure and the chronic form of PCM. However, we also show that this effect is transitory, being detected between 4- and 12-weeks post-infection but not thereafter. The possible immune mechanisms that mediate this effect and the reasons for its transitory effect are discussed.
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Fumar Cigarrillos , Paracoccidioidomicosis , Humanos , Ratones , Animales , Paracoccidioidomicosis/microbiología , Interleucina-10 , Modelos Animales de Enfermedad , Fumar Cigarrillos/efectos adversos , Progresión de la Enfermedad , Granuloma , Ratones Endogámicos C57BLRESUMEN
Cigarette smoking throughout life causes serious health issues in the lungs. The electronic cigarette (E-Cig) use increased, since it was first introduced in the world. This research work compared the short-term exposure consequences to e-cigarette vapor and cigarette smoke in male mice. Forty-five C57BL/6 mice were randomized into control (C) in an ambient air exposition cigarette smoke (CS) and aerosol electronic cigarette (EC), both were exposed to 120 puffs, 3 times/day during five days. Then, in the experimental protocol, the euthanized mice had their tissues removed for analysis. Our study showed that CS and EC resulted in higher cell influx into the airways, and an increase in macrophage counts in CS (209.25 ± 7.41) and EC (220.32 ± 8.15) when compared to C (108.40 ± 4.49) (p < 0.0001). The CS (1.92 ± 0.23) displayed a higher pulmonary lipid peroxidation as opposed to C (0.93 ± 0.06) and EC (1.23 ± 0.17) (p < 0.05). The EC (282.30 ± 25.68) and CS (368.50 ± 38.05) promoted increased levels of interleukin 17 when compared to C (177.20 ± 10.49) (p < 0.05). The EC developed shifts in lung histoarchitecture, characterized by a higher volume density in the alveolar air space (60.21; 55.00-65.83) related to C (51.25; 18.75-68.75) and CS (50.26; 43.75-62.08) (p =0.002). The EC (185.6 ± 9.01) presented a higher respiratory rate related to CS (133.6 ± 10.2) (p < 0.002). Therefore, our findings demonstrated that the short-term exposure to e-cig promoted more acute inflammation comparing to cigarette smoke in the ventilatory parameters of the animals.
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Fumar Cigarrillos , Cigarrillo Electrónico a Vapor , Sistemas Electrónicos de Liberación de Nicotina , Aerosoles , Animales , Modelos Animales de Enfermedad , Interleucina-17 , Pulmón , Masculino , Ratones , Ratones Endogámicos C57BL , NicotianaRESUMEN
AIM: To analyze the consumption of oxygen and to quantify the mitochondrial respiratory chain proteins (OXPHOS) in the gastrocnemius muscle of rats exposed to cigarette smoke and/or RT practitioners. MAIN METHODS: Wistar rats were divided into groups: Control (C), Smoker (S), Exercise (E) and Exercise Smoker (ES). Groups F and ES were exposed to the smoke of 4 cigarettes for 30 min, 2× a day, 5× a week, for 16 weeks. Groups E and ES performed four climbs with progressive load, 1× per day, 5× per week, for 16 weeks. The gastrocnemius muscle was collected for analysis of OXPHOS content and oxygen consumption. Groups S (vs. C) and ES (vs. C and E) showed lower body weight gain when observing the evolution curve. KEY FINDINGS: The S rats showed a reduction in the NDUFB8 proteins of complex 1, SDHB of complex 2, MTC01 of complex 4 and ATP5A of complex 5 (ATP Synthase) compared to Group C. Additionally, S rats also showed increased consumption of O2 in Basal, Leak, Complex I and I/II combined measures compared to the other groups, suggesting that the activity of the mitochondria of these animals increased in terms of coupling and uncoupling parameters. SIGNIFICANCE: Our data suggest that exposure to cigarette smoke for 16 weeks is capable of causing impairment of mitochondrial function with reduced expression of respiratory chain proteins in skeletal muscle. However, the RT was effective in preventing impairment of mitochondrial function in the skeletal muscle of rats exposed to secondary cigarette smoke.