RESUMO
Objetivo: Caracterizar a população asmática pediátrica e avaliar as repercussões do tabagismo passivo nos sintomas da asma na infância. Métodos: A amostra é composta de 384 pacientes, entre 2 e 14 anos, com diagnóstico de asma, acompanhados no ambulatório de pneumologia pediátrica do Hospital de Clínicas da Universidade Federal do Paraná. A avaliação ocorreu por meio de uma ficha de dados, aplicada em forma de entrevista aos responsáveis ou à criança participante. Resultados: A exposição ao tabagismo passivo esteve presente em 55% das crianças. Aglomeração domiciliar, menor renda familiar, menor nível de escolaridade materna e paterna foram vistos significativamente no grupo exposto. A população exposta mostrou maior frequência de asma classificada como moderada, maior uso de corticoide inalatório e maior frequência de sintomas diurnos (presentes pelo menos uma vez na semana em 60% dos pacientes). Conclusão: Foi alta a prevalência de crianças asmáticas expostas ao tabagismo passivo. Condição socioeconômica baixa foi confirmada no grupo exposto. Asma de gravidade moderada, maior uso de corticoides inalados e maior frequência de sintomas diurnos foram vistos no grupo de expostos. Este estudo confirma a necessidade imediata de adoção de medidas efetivas no combate ao tabagismo passivo como estratégia imprescindível para o controle da asma na infância.
Objective: To characterize the pediatric asthmatic population and to evaluate the repercussions of passive smoking on childhood asthma symptoms. Methods: The sample consisted of 384 patients, aged 2 to 14 years, diagnosed with asthma, who were followed up at the pediatric pulmonology outpatient clinic of the Hospital de Clínicas of the Federal University of Paraná. The evaluation was carried out by means of a data sheet, administered in the form of an interview to the legal guardians or to the participating child. Results: Exposure to passive smoking was present in 55% of the children. Household agglomeration, lower family income, and lower level of maternal and paternal schooling were seen in the exposed group. The exposed population showed a higher frequency of asthma classified as moderate, greater use of inhaled corticosteroids, and greater frequency of diurnal symptoms (present at least once a week in 60% of patients). Conclusion: The prevalence of asthmatic children exposed to passive smoking was high. Low socioeconomic condition was confirmed in the exposed group. Asthma of moderate severity, greater use of inhaled corticosteroids, and greater frequency of diurnal symptoms were seen in the exposed group. This study confirms the immediate need to adopt effective measures to combat passive smoking as an essential strategy for the control of childhood asthma.
Assuntos
Humanos , Pré-Escolar , Criança , Adolescente , Asma , Poluição por Fumaça de Tabaco , Pacientes , Sinais e Sintomas , Família , Aglomeração , Prevalência , Estudos Transversais , Corticosteroides , Escolaridade , RendaRESUMO
Exposure to environmental tobacco smoke (ETS) is associated with high morbidity and mortality, mainly in childhood. Our aim was to evaluate the effects of postnatal ETS exposure in the brain 2-deoxy-2-[18F]-fluoro-D-glucose (18F-FDG) uptake of mice by positron emission tomography (PET) neuroimaging in a longitudinal study. C57BL/6J mice were exposed to ETS that was generated from 3R4F cigarettes from postnatal day 3 (P3) to P14. PET analyses were performed in male and female mice during infancy (P15), adolescence (P35), and adulthood (P65). We observed that ETS exposure decreased 18F-FDG uptake in the whole brain, both left and right hemispheres, and frontal cortex in both male and female infant mice, while female infant mice exposed to ETS showed decreased 18F-FDG uptake in the cerebellum. In addition, all mice showed reduced 18F-FDG uptake in infancy, compared to adulthood in all analyzed VOIs. In adulthood, ETS exposure during the early postnatal period decreased brain 18F-FDG uptake in adult male mice in the cortex, striatum, hippocampus, cingulate cortex, and thalamus when compared to control group. ETS induced an increase in 18F-FDG uptake in adult female mice when compared to control group in the brainstem and cingulate cortex. Moreover, male ETS-exposed animals showed decreased 18F-FDG uptake when compared to female ETS-exposed in the whole brain, brainstem, cortex, left amygdala, striatum, hippocampus, cingulate cortex, basal forebrain and septum, thalamus, hypothalamus, and midbrain. The present study shows that several brain regions are vulnerable to ETS exposure during the early postnatal period and these effects on 18F-FDG uptake are observed even a long time after the last exposure. This study corroborates our previous findings, strengthening the idea that exposure to tobacco smoke in a critical period interferes with brain development of mice from late infancy to early adulthood.
Assuntos
Anti-Hipertensivos , Poluição por Fumaça de Tabaco , Criança , Cognição , Humanos , HipertensãoRESUMO
El estrés oxidativo ha sido considerado por muchos investigadores como la principal causa de daño tisular generado por el consumo de alcohol en combinación con nicotina. Sin embargo, se desconoce si existe una potenciación de la inducción de Hsps como respuesta al daño celular en el caso de fumadores involuntarios que consumen etanol, y si los sistemas de citoprotección endógena, específicamente la proteína anti-estrés Hsp70, tienen alguna participación. En tal sentido, en este trabajo se determinó la presencia de las Hsp70 y su correspondencia con la respuesta subcelular cardiaca en el estrés tóxico individual y combinado de etanol y exposición pasiva al humo del cigarrillo (EPHC) en ratas. Se utilizaron 60 ratas hembras Sprague-Dawley (80- 100gr), divididas aleatoriamente en cuatro grupos: grupo control; grupo etanol (2 g/kg p.c. 50%, vía oral); grupo humo (exposición pasiva al humo de 8 cigarrillos) y grupo combinado (etanol-humo). Los tratamientos se suministraron diariamente en dosis única, durante 15 días continuos. Seguidamente, posterior al sacrificio de los animales se tomaron muestras de la pared ventricular izquierda del corazón para el estudio bioquímico y subcelular. Los resultados mostraron un paralelismo entre la mayor acumulación de Hsp70 y el menor daño subcelular en el tejido cardiaco. El tratamiento combinado de alcohol y EPHC promovió la respuesta al estrés en el corazón, a través de un proceso de coinducción, resultando en mayor acumulación de Hsp70. Se sugiere un papel cardioprotector de las Hsp70.
Many researchers have considered oxidative stress as the main cause of tisular damage induced by alcohol and nicotine together. Oxidative stress is associated to the induction of stress proteins. However, in the case of passive smoke, it is unknown whether the stress proteins are induced and what kind of role they could have. In this regard, this work determined Hsp70 and their relationship to subcellular heart response in individual and combined ethanol and passive smoke cigarette exposition in rats. 60 female Sprague-Dawley (80-100g) rats, were randomized into four group: control; ethanol (2 g/kg c.w. 50%, oral route); passive smoke of 8 cigarettes and ethanol/smoke group. Single dose daily treatment was given during 15 days. Once therats were killed, samples for biochemical and subcellular analysis were made from left ventricular wall. Results showed a strong relationship between bigger accumulation of Hsp70 and smaller cardiac cellular damage. Ethanol plus passive smoke treatment promoted the stress response by co-induction and an increased Hsp70 accumulation was induced. It is suggested a cardiac protective role for Hsp70.