Astaxanthin attenuates cigarette smoke-induced small airway remodeling via the AKT1 signaling pathway.

BACKGROUND: Astaxanthin (AXT) is a keto-carotenoid with a variety of biological functions, including antioxidant and antifibrotic effects. Small airway remodeling is the main pathology of chronic obstructive pulmonary disease (COPD) and is caused by epithelial-to-mesenchymal transition (EMT) and fibroblast differentiation and proliferation. Effective therapies are still lacking. This study aimed to investigate the role of AXT in small airway remodeling in COPD and its underlying mechanisms. METHODS: First, the model of COPD mice was established by cigarette smoke (CS) exposure combined with intraperitoneal injection of cigarette smoke extract (CSE). The effects of AXT on the morphology of CS combined with CSE -induced emphysema, EMT, and small airway remodeling by using Hematoxylin-eosin (H&E) staining, immunohistochemical staining, and western blot. In addition, in vitro experiments, the effects of AXT on CSE induced-EMT and fibroblast function were further explored. Next, to explore the specific mechanisms underlying the protective effects of AXT in COPD, potential targets of AXT in COPD were analyzed using network pharmacology. Finally, the possible mechanism was verified through molecular docking and in vitro experiments. RESULTS: AXT alleviated pulmonary emphysema, EMT, and small airway remodeling in a CS combined with CSE -induced mouse model. In addition, AXT inhibited the EMT process in airway cells and the differentiation and proliferation of fibroblasts. Mechanistically, AXT inhibited myofibroblast activation by directly binding to and suppressing the phosphorylation of AKT1. Therefore, our results show that AXT protects against small airway remodeling by inhibiting AKT1. CONCLUSIONS: The present study identified and illustrated a new food function of AXT, indicating that AXT could be used in the therapy of COPD-induced small airway remodeling.

El cigarrillo: dispositivo de ingeniería perfecto, pero no seguro. Es basura / The cigarette: a perfect, but not safe, engineering device. It is garbage

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Perception of the Quality of Life of Tobacco Growers Exposed to Pesticides: Emphasis on Health, Hearing, and Working Conditions

Abstract Introduction Tobacco farming exposes workers to various health risks due to the high application of pesticides needed to control pests, weeds and fungal diseases that prevent the tobacco plant growth. Objective To analyze the perception of the quality of life of tobacco growers exposed to pesticides, with emphasis on general health, hearing, and working conditions. Method This is a descriptive, cross-sectional study using a quantitative approach with farmers from southern Brazil. Data were collected from November of 2012 to November of 2014. For data collection, we opted for the 36-item short form health survey (SF-36) questionnaire, and a questionnaire with closed questions about health, hearing and working conditions. We evaluated a total of 78 subjects; the study group, made up of 40 tobacco farmers exposed to pesticides, and a control group of 38 participants without occupational exposure to pesticides. Both groups are residents of the same municipality, and users of the federal public health system. Results The results showed that tobacco growers had lower quality of life scores compared with the control group. Significant differences were observed in the areas of pain and general health. There were correlations between physical elements and chronic diseases; hearing complaints and a lack of personal protective equipment use, occupation and hearing complaints, as well as general health and hearing complaints. Conclusion Tobacco farming is a risky activity for general and hearing health, and it can impact the quality of life of those working in this field. (AU)

Papel de las sustancias tóxicas en la muerte súbita cardiaca / The role of toxic substances in sudden cardiac death

El consumo de sustancias tóxicas constituye un factor de riesgo significativo para la muerte súbita cardiaca. Los tóxicos con mayor relevancia son las drogas ilegales (especialmente la cocaína), el alcohol y el tabaco, y en menor medida, las sustancias dopantes. Diversos medicamentos también incrementan el riesgo de muerte súbita cardiaca. En el presente artículo se hace una revisión sobre el mecanismo de acción y la patología inducida por estos tóxicos; se ofrece información epidemiológica, se destaca la trascendencia de una investigación forense protocolizada y se discuten las implicaciones de la patología forense en la prevención. La posibilidad de consumo de drogas de abuso debería ser tenida en cuenta en toda muerte súbita cardiaca de un adolescente, joven o adulto de edad mediana, principalmente en varones. En deportistas sería conveniente descartar el uso de sustancias dopantes; y en pacientes que toman psicofármacos valorar su influencia en el fallecimiento, aún con niveles terapéuticos (AU)

The use of toxic substances is a main risk factor for sudden cardiac death. The most relevant toxic substances are the illegal drugs (especially cocaine), ethanol, tobacco, and doping substances. Additionally, several therapeutic drugs are able to increase the risk for sudden cardiac death. The aim of the present paper is to review the mechanism of action and the main pathological problems induced by toxic substances. Moreover, we provide epidemiological information, underlie the importance of a standardised forensic investigation, and discuss the role of forensic pathology in the prevention of this phenomenon. The possibility of consumption of any drug of abuse should be considered in any case of sudden cardiac death in adolescents, young, or middle-age patients, especially in men. In athletes the use of doping substances should be ruled-out. In patients under psychopharmacological treatment, the putative influence of these drugs should be borne in mind (AU)

O impacto dos aditivos do tabaco na toxicidade da fumaça do cigarro: uma avaliação crítica dos estudos patrocinados pela indústria do fumo / El impacto de los aditivos del tabaco en la toxicidad del humo del cigarrillo: una evaluación crítica de los estudios de la industria del tabaco / The impact of tobacco additives on cigarette smoke toxicity: a critical appraisal of tobacco industry studies

Resumo: A produção de cigarros envolve uma série de substâncias e materiais além do próprio tabaco, do papel e do filtro. Os aditivos do tabaco incluem conservantes, flavorizantes, intensificadores, umectantes, açúcares e compostos de amônio. Embora as empresas produtoras de tabaco aleguem que os aditivos não aumentam a toxicidade da fumaça e não tornam os cigarros mais atraentes ou viciantes, tais alegações são contestadas por pesquisadores independentes. Os autores realizaram uma revisão dos estudos sobre os efeitos dos aditivos sobre a composição química e toxicidade da fumaça. Os aditivos elevam os níveis de formaldeído e causam pequenas alterações nos níveis de outros analitos medidos na fumaça. Estudos toxicológicos (testes de mutagenicidade e de citotoxicidade em células de mamíferos, estudos da exposição por 90 dias por via inalatória em ratos e ensaios do micronúcleo em células da medula óssea) indicaram que os aditivos do tabaco não aumentam a toxicidade da fumaça. Entretanto, é conhecido que os estudos em roedores falham em predizer o potencial carcinogênico da fumaça do cigarro, e os testes realizados tiveram poder estatístico insuficiente para detectar diferenças pequenas, porém relevantes do ponto de vista toxicológico, entre cigarros experimentais (com aditivos) e controles (sem aditivos). Em conclusão, esta revisão da literatura mostrou que o impacto dos aditivos na toxicidade da fumaça do tabaco ainda permanece por ser esclarecido.

Resumen: La producción de cigarrillos involucra un número de sustancias y materiales diferentes al tabaco en sí, papel y filtro. Los aditivos del tabaco incluyen aromas artificiales, potenciadores del sabor, humectantes, azúcares, y compuestos de amonio. A pesar de que las compañías sostienen que los aditivos del tabaco no aumentan la toxicidad del humo y no hacen los cigarrillos más atractivos y adictivos, estas afirmaciones son cuestionadas por investigadores independientes. Este trabajo ha revisado los estudios sobre los efectos de los aditivos del tabaco en la química del humo y su toxicidad. Los aditivos del tabaco conllevan niveles más altos de formaldehído y otros cambios menores en los análisis realizados del humo. Estudios toxicológicos (tests de mutagenicidad en bacterias y citotoxicidad en mamíferos, ensayos de inhalación en ratas 90 días y células del micronúcleo de la médula ósea) mostraron que los aditivos del tabaco no aumentaron la toxicidad del humo. Los ensayos de roedores, sin embargo, no predijeron adecuadamente la carcinogenicidad del humo del tabaco, y no eran claramente suficientes para dar a conocer, sin embargo, las pequeñas, pero toxicológicamente relevantes, diferencias entre el test (con/aditivos del tabaco) y control (sin/aditivos del tabaco) en cigarrillos. Esta revisión de la literatura nos lleva a la conclusión de que el impacto dañino de los aditivos del tabaco en el humo continúa estando poco claro.

Abstract: Cigarette production involves a number of substances and materials other than just tobacco, paper and a filter. Tobacco additives include flavorings, enhancers, humectants, sugars, and ammonium compounds. Although companies maintain that tobacco additives do not enhance smoke toxicity and do not make cigarettes more attractive or addictive, these claims are questioned by independent researchers. This study reviewed the studies on the effects of tobacco additives on smoke chemistry and toxicity. Tobacco additives lead to higher levels of formaldehyde and minor changes in other smoke analytes. Toxicological studies (bacterial mutagenicity and mammalian cytoxicity tests, rat 90 days inhalation studies and bone-marrow cell micronucleus assays) found that tobacco additives did not enhance smoke toxicity. Rodent assays, however, poorly predicted carcinogenicity of tobacco smoke, and were clearly underpowered to disclose small albeit toxicologically relevant differences between test (with tobacco additives) and control (without tobacco additives) cigarettes. This literature review led to the conclusion that the impact of tobacco additives on tobacco smoke harmfulness remains unclear.

Diferencias entre hombres y mujeres en la tendencia temporal de la mortalidad por cáncer de pulmón en España (1980-2013) / Differences between Men and Women in Time Trends in Lung Cancer Mortality in Spain (1980-2013)

Introducción: El principal factor de riesgo del cáncer de pulmón es el tabaco, cuyo consumo varía según la edad y el sexo. El objetivo de este trabajo es describir la tendencia de la mortalidad por cáncer de pulmón por sexo y edad desde 1980 hasta 2013 en España. Métodos: Se utilizaron los datos de mortalidad por cáncer de pulmón (código 162 para la novena revisión de la Clasificación Internacional de Enfermedades y códigos C33 y C34 para la décima revisión) y los datos de población proporcionados por el Instituto Nacional de Estadística. Se calcularon las tasas de mortalidad bruta, truncada, ajustada por edad y específicas por edad y se estimó el cambio porcentual anual (CPA) mediante un modelo de regresión joinpoint. Resultados: La tasa ajustada por edad aumentó significativamente de 1980 a 1991 entre hombres (CPA = 3,12%) y descendió significativamente desde 2001 hasta 2013 (CPA = − ;1,53%), con un patrón similar observado para tasas específicas según grupos de edad. Entre mujeres, la tasa ajustada por edad aumentó desde 1989 (CPA de 1989 a 1997 = 1,82%), con un aumento más pronunciado desde 1997 hasta el final del estudio en 2013 (CPA = 4,41%). Conclusiones: Las tendencias divergentes en la prevalencia de tabaco podrían explicar el aumento de la mortalidad por cáncer de pulmón entre las mujeres españolas desde los inicios de los años noventa. Se deberían implementar políticas de salud pública enfocadas a ayudar a la reducción del consumo de tabaco entre las mujeres fumadoras, y detener el aumento de la mortalidad por cáncer de pulmón

Introduction: The main risk factor for lung cancer is smoking, a habit that varies according to age and sex. The objective of this study was to explore trends in lung cancer mortality by sex and age from 1980 to 2013 in Spain. Methods: We used lung cancer mortality (International Classification of Diseases code 162 for the 9th edition, and codes C33 and C34 for 10th edition) and population data from the Spanish National Statistics Institute. Crude, truncated, age-adjusted mortality and age-specific mortality rates were assessed through joinpoint regression to estimate the annual percent change (APC). Results: Age-adjusted mortality rate significantly increased from 1980 to 1991 among men (APC = 3.12%) and significantly decreased between 2001 and 2013 (APC = − 1.53%), a similar pattern was observed in age-specific rates. Among women, age-adjusted mortality rate increased from 1989 (APC 1989-1997 = 1.82%), with the greatest increase observed from 1997 until the end of the study in 2013 (APC = 4.41%). Conclusions: Diverging trends in the prevalence of smoking could explain the increase in the rate of lung cancer-related mortality among Spanish women since the early 1990s. Public health policies should be implemented to reduce tobacco consumption in women and halt the increase in lung cancer mortality

ETAP: una escala de tabaquismo para la atención primaria de salud / ETAP: a smoking scale for Primary Health Care

OBJETIVO: Obtener una escala de exposición al tabaco para abordar la deshabituación. DISEÑO: Seguimiento de una cohorte. Validación de una escala. Emplazamiento: Unidad de investigación de atención primaria. Tenerife. PARTICIPANTES: Seis mil setecientos veintinueve participantes de la cohorte «CDC de Canarias». MÉTODOS: Se construyó una escala bajo la hipótesis de que el tiempo de exposición al tabaco es el factor clave para expresar riego acumulado; su validez discriminante fue probada sobre casos prevalentes de infarto agudo de miocardio (IAM) (n = 171) y se obtuvo su mejor punto de corte para cribado preventivo. Se comprobó su validez predictiva con casos incidentes de IAM (n = 46), comparándose el poder predictivo con factores (hipertensión, diabetes, dislipemia) clásicos de riesgo de IAM, incluido el índice años a paquete diario (APD). RESULTADOS: La escala obtenida fue la suma del triple de años que se había fumado, más los expuestos al tabaco en casa y en el trabajo. La frecuencia de IAM aumentó con los valores de la escala, siendo el valor 20 años de exposición el mejor punto de corte para la actuación preventiva puesto que presentó adecuados valores predictivos para el IAM incidente. La escala superó a APD en la predicción del IAM y compitió con los marcadores y factores de riesgo conocidos. CONCLUSIÓN: La escala propuesta permite una medición válida de exposición al tabaco y proporciona un criterio útil y sencillo que puede ayudar a promover una disposición al cambio y realizar una prevención oportuna. Aún requiere probar su validez tomando como referente otros problemas asociados al tabaco

OBJECTIVE: To obtain a scale of tobacco exposure to address smoking cessation. DESIGN: Follow-up of a cohort. Scale validation. SETTING: Primary Care Research Unit. Tenerife. PARTICIPANTS: A total of 6729 participants from the 'CDC de Canarias' cohort. METHODS: A scale was constructed under the assumption that the time of exposure to tobacco is the key factor to express accumulated risk. Discriminant validity was tested on prevalent cases of acute myocardial infarction (AMI; n = 171), and its best cut-off for preventive screening was obtained. Its predictive validity was tested with incident cases of AMI (n = 46), comparing the predictive power with markers (age, sex) and classic risk factors of AMI (hypertension, diabetes, dyslipidaemia), including the pack-years index (PYI). RESULTS: The scale obtained was the sum of three times the years that they had smoked plus years exposed to smoking at home and at work. The frequency of AMI increased with the values of the scale, with the value 20 years of exposure being the most appropriate cut-off for preventive action, as it provided adequate predictive values for incident AMI. The scale surpassed PYI in predicting AMI, and competed with the known markers and risk factors. CONCLUSION: The proposed scale allows a valid measurement of exposure to smoking and provides a useful and simple approach that can help promote a willingness to change, as well as prevention. It still needs to demonstrate its validity, taking as reference other problems associated with smoking

Año SEPAR 2015-16: EPOC y tabaco. ¿Qué podemos esperar? / SEPAR Year 2015-16: COPD and Smoking. What Awaits?

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La pipa de agua / No disponible

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Lesão pulmonar aguda induzida pela administração endovenosa de extrato da fumaça do cigarro / Acute lung injury induced by the intravenous administration of cigarette smoke extract

OBJETIVO: Investigar os efeitos agudos da administração endovenosa de extrato da fumaça do cigarro (EFC) em parâmetros funcionais respiratórios, inflamatórios e histológicos em ratos e comparar esse potencial modelo de lesão pulmonar aguda (LPA) com aquele com o uso de ácido oleico (AO). MÉTODOS: Foram estudados 72 ratos Wistar machos divididos em quatro grupos: tratados somente com soro fisiológico (SF; grupo controle); tratados com EFC e SF (grupo EFC); tratados com SF e AO (grupo AO); e tratados com EFC e AO (grupo EFC/AO). RESULTADOS: As médias de complacência foram significantemente menores nos grupos AO e EFC/AO (2,12 ± 1,13 mL/cmH2O e 1,82 ± 0,77 mL/cmH2O, respectivamente) do que no controle (3,67 ± 1,38 mL/cmH2O). A proporção de neutrófilos e a atividade das metaloproteinases 2 e 9 em lavado broncoalveolar foram significantemente maiores nos grupos AO e EFC/AO que no controle. O acometimento pulmonar avaliado por morfometria foi significantemente maior nos grupos AO e EFC/AO (72,9 ± 13,8% e 77,6 ± 18,0%, respectivamente) do que nos grupos controle e EFC (8,7 ± 4,1% e 32,7 ± 13,1%, respectivamente), e esse acometimento foi significantemente maior no grupo EFC que no grupo controle. CONCLUSÕES: A administração endovenosa de EFC, nas doses e tempos deste estudo, associou-se à LPA mínima. O EFC não potencializou a LPA induzida por AO. Estudos adicionais são necessários para esclarecer o papel potencial desse modelo como método de estudo dos mecanismos de agressão pulmonar pelo tabaco.

OBJECTIVE: To investigate the acute effects of intravenous administration of cigarette smoke extract (CSE) on histological, inflammatory, and respiratory function parameters in rats, as well as to compare this potential acute lung injury (ALI) model with that with the use of oleic acid (OA). METHODS: We studied 72 Wistar rats, divided into four groups: control (those injected intravenously with saline); CSE (those injected intravenously with CSE and saline); OA (those injected intravenously with saline and OA); and CSE/OA (those injected intravenously with CSE and OA). RESULTS: Mean lung compliance was significantly lower in the OA and CSE/OA groups (2.12 ± 1.13 mL/cmH2O and 1.82 ± 0.77 mL/cmH2O, respectively) than in the control group (3.67 ± 1.38 mL/cmH2O). In bronchoalveolar lavage fluid, the proportion of neutrophils was significantly higher in the OA and CSE/OA groups than in the control group, as was the activity of metalloproteinases 2 and 9. Pulmonary involvement, as assessed by morphometry, was significantly more severe in the OA and CSE/OA groups (72.9 ± 13.8% and 77.6 ± 18.0%, respectively) than in the control and CSE groups (8.7 ± 4.1% and 32.7 ± 13.1%, respectively), and that involvement was significantly more severe in the CSE group than in the control group. CONCLUSIONS: The intravenous administration of CSE, at the doses and timing employed in this study, was associated with minimal ALI. The use of CSE did not potentiate OA-induced ALI. Additional studies are needed in order to clarify the potential role of this model as a method for studying the mechanisms of smoking-induced lung injury.

Lung morphology and growth of rats exposed to tobacco smoke and alcohol / Estudo morfológico dos pulmões e crescimento de ratos expostos à fumaça do cigarro e ao álcool

PURPOSE: Investigate the morphological effects of chronic exposure to tobacco smoke inhalation and alcohol consumption on the lungs and on the growth of rats. METHODS: Sixty male Wistar rats were divided into four groups: control, tobacco, alcohol, tobacco + alcohol, for a period of study 260 days. Morphological analysis was conducted by optical and electron microscopy. Rat growth was investigated by measuring the snout-anus length, body mass index and body weight. RESULTS: The three groups exposed to the drugs presented lower growth and lower weight than the control group. The percentages of alveolitis, bronchiolitis and the mean alveolar diameter were greater, particularly in the groups exposed to tobacco smoke, but were not significantly different from the control group. Electron microscopy revealed more intense apoptotic and degenerative lesions in the smoking group, while degenerative lesions in the lamellar bodies were more intense with the association of both drugs. CONCLUSIONS: This experimental model showed morphological alterations observed by electron microscopy, principally due to tobacco smoke exposure. Alcohol and tobacco hindered the growth of rats, such that tobacco showed a greater effect on body length and alcohol on body weight.

OBJETIVO: Investigar os efeitos morfológicos da exposição crônica à inalação de fumaça do tabaco e o do consumo de álcool nos pulmões e no crescimento de ratos. MÉTODOS: Sessenta ratos Wistar machos foram distribuídos em quatro grupos: controle, tabaco, álcool e tabaco + álcool, e acompanhados por um período de 260 dias. No final do periodo foi realizada análise morfológica dos pulmões por microscopia óptica e eletrônica. O crescimento dos ratos foi investigado através da medição do comprimento focinho-ânus, peso corporal e índice de massa corporal. RESULTADOS: Os três grupos expostos às drogas apresentaram peso e comprimento significativamente menores que os do grupo controle. As percentagens de bronquiolite e alveolite, e o diâmetro alveolar médio foram maiores nos grupos expostos à fumaça do tabaco, mas sem significancia estatística quando comparadas ao grupo controle. A microscopia eletrônica revelou apoptose mais intensa e lesões degenerativas no grupo de fumantes, enquanto lesões degenerativas nos corpos lamelares foram mais intensas com a associação de ambas as drogas. CONCLUSÕES: Este modelo experimental mostrou alterações morfológicas observadas por microscopia eletrônica, principalmente devido à exposição ao tabaco. Tanto o alcool como o tabaco prejudicaram o crescimento dos animais, o tabaco mostrando um efeito maior sobre o comprimento e o álcool sobre o peso corporal.

In vitro assessment of reproductive toxicity of cigarette smoke and deleterious consequences of maternal exposure to its constituents

Cigarette smoke is known to be a serious health risk factor and considered reproductively toxic. In the current study, we investigated whether constituents of cigarette smoke, pyrazine, 2-ethylpyridine, and 3-ethylpyridine, adversely affect reproductive functioning such as oocyte maturation and sperm capacitation. Our findings indicated that three smoke components were involved in retardation of oocyte maturation in a dose-dependent manner and the lowest-observed-adverse-effect level (LOAEL) was determined to be 10-10M. However, individual smoke components administrated at the LOAEL did not attenuate oocyte maturation, demonstrating that all three toxicants were equally required for the observed growth impairment. When exposed to all three components at 10-10M during in vitro capacitation, murine sperm lost forward progression and were unable to show adequate hyperactivation, which is indicative of the incompletion of the capacitation process. Only sperm administrated with 3-ethylpyridine alone showed significant reduction in capacitation status, suggesting the chemical is the one responsible for disrupting sperm capacitation. Taken together, this is the first report that documents the effect of cigarette smoke components on oocyte maturation and sperm capacitation. The present findings demonstrate the adverse effects of smoke constituents of mammalian reproduction and the differences in sensitivity to smoke components between male and female gametes. Since both processes take place in the female reproductive system, our data provide new insights into deleterious consequences of maternal exposure to cigarette smoke.

Efeitos da fumaça de cigarro sobre a osteogênese e a resistência mecânica óssea em ratos / Effects of cigarette smoke on osteogenesis and bone mechanical resistance in rats

This paper reports a study of the effects of exposure to cigarette smoke on osteogenesis and the mechanical strength of bone in rats. Twelve male rats were separated into two groups (n=6): CT (control) and CI (cigarette). All the animals had free access to rat chow and water throughout the experiment. Group CI was exposed to the smoke of 6 cigarettes/day for 12 weeks. After 6 weeks of exposure to cigarette smoke, a defect was produced on the parietal bone and dense hydroxyapatite (DHA) ceramic bodies were implanted into cavities made surgically in the tibia of the animals, in each group. After surgery, the CT and CI groups returned to normal experimental conditions and, at the end of 12 weeks, they were euthanized, and their tibiae and parietal bones removed for histological processing, while the femurs were subjected to biomechanical tests in a MTS TestStar II three-point flexion module. Consumption of solid and liquid diet was satisfactory in both groups, all animals gaining weight throughout the experiment. CI animals showed a smaller volume of newly formed bone in the parietal defect (8.l9±0.2) and around the DHA implant in the tibia (33±0.5) than the rats in the CT group (14.4±0.5 and 39±1 respectively). The maximum force needed to break the femur was smaller in CI (119±3.2) than in CT (140±6.5). The results of this study led to the conclusion that exposure to cigarette smoke interfered with osteogenesis in the bone defect and around the DHA implant and reduced the maximum force required to completely break the femur, revealing that bone fragility can be caused by tobacco smoke.

O presente estudo teve como objetivo avaliar os efeitos da exposição à fumaça de cigarro sobre a osteogênese e a resistência mecânica do osso em ratos. Foram utilizados doze ratos machos, divididos em dois grupos (n=6): grupo CT (controle) e grupo CI (cigarro). Durante 12 semanas, os animais do grupo CI foram expostos à fumaça de seis cigarros/dia. Após seis semanas de exposição à fumaça de cigarro, uma falha óssea de 5mm foi produzida no osso parietal e corpos cerâmicos de hidroxiapatita densa (HAD) foram implantados em cavidade produzida cirurgicamente na tíbia dos animais do grupo CI e CT. Após as cirurgias, os animais retornaram aos protocolos experimentais e, ao término de doze semanas de experimentação, foram eutanasiados, as tíbias e os ossos parietais foram coletados para processamento histológico e os fêmures encaminhados para ensaio biomecânico em um módulo MTS TestStar II®. A exposição à fumaça do cigarro não interferiu no ganho de peso dos animais e os consumos de dieta líquida e sólida foram satisfatórios entre os grupos. Os animais do grupo CI apresentaram menor volume de osso neoformado na falha óssea (8,9±0,2) produzida no osso parietal e ao redor do implante de HAD na tíbia (33±0,5). A força máxima necessária para romper o fêmur dos animais foi menor no grupo CI (119±3,2) do que no grupo CT (140±6,5). Com bases nos resultados obtidos no presente trabalho, pôde-se concluir que a exposição à fumaça do cigarro interferiu na osteogênese da falha óssea e ao redor do implante de HAD, diminuiu a força máxima necessária para a ruptura completa dos fêmures e demonstrando a fragilidade óssea causada pelo hábito tabagista.

Avances en salud respiratoria 2010: la visión a través del área de tabaquismo / Advances in respiratory health 2010: the perspective from the Smoking and Health Section

El área de tabaquismo de la Sociedad Española de Neumología y Cirugía Torácica (SEPAR) se ha mostrado muyactiva a lo largo del año 2010 en cuanto a la realización de trabajos de investigación. Muchos de ellos hanculminado en la publicación de interesantes artículos. En este artículo se comentan y analizan los principalestrabajos de investigación clínica y básica que han sido llevados a cabo por los diferentes miembros del área detabaquismo de la SEPAR.Se revisan las diferentes disciplinas incluidas en el tema tabaquismo: diagnóstico y tratamiento, epidemiología,genética, bibliometría y enfermedades relacionadas con el consumo del tabaco(AU)

The Smoking and Health Section of the Spanish Society of Pneumology and Thoracic Surgery has been highlyactive in research throughout 2010. Many of the research studies performed have led to interestingpublications. The present article analyzes the main clinical and basic research articles published by thedistinct members of the Society’s Smoking and Health Section.The various disciplines included under the heading of smoking are reviewed: diagnosis and treatment,epidemiology, genetics, bibliometry and tobacco-related diseases(AU)

Exposição ocupacional e ambiental a agrotóxicos e nicotina na cultura de fumo do município de Arapiraca, AL / Occupational and Environmental Exposure to Pesticides and Nicotine in Tobacco Culture of the Municipality of Arapiraca / AL

No Brasil, o cultivo do tabaco é associado a graves problemas de saúde entre os agricultores, e que podem evoluir para um quadro de depressão e suicídio. A exposição de trabalhadores rurais a agrotóxicos em culturas de tabaco é, na maioria das vezes, tratada como um evento isolado, desconsiderando-se a exposição concomitante a outras substâncias, como a nicotina, presente nas folhas de tabaco. O presente trabalho tem como objetivo analisar as exposições ocupacionais e ambientais a agrotóxicos e nicotina na cultura de tabaco do município de Arapiraca, AL, com ênfase nos efeitos dessas exposições sobre a atividade da enzima acetilcolinesterase (AChE). A partir do conhecimento do processo de trabalho local, um grupo de 72 fumicultores do município foram avaliados com relação exposição a agrotóxicos organofosforados (OP) e carbamatos e à nicotina nos períodos de cultivo e entre-safra do tabaco. A exposição a agentes anticolinesterásicos foi avaliada através da análise da atividade da AChE eritrocitária, enquanto a exposição à nicotina foi avaliada através dos níveis plasmáticos de cotinina. Um grupo composto por 45 indivíduos foi utilizado como controle na comparação da atividade da AChE. Complementarmente, avaliou-se o efeito in vitro da exposição à nicotina e a OP sobre a atividade da AChE. A análise dos resultados mostrou que, nos testes in vitro, a nicotina somente inibiu a AChE em concentrações iguais ou superiores a 0,5mM. A nicotina não apresentou efeito aditivo nas inibições da AChE por etil paroxon in vitro. (...) Seis indivíduos não fumantes apresentaram valores de cotinina entre 50 e 200 ng/mL, caracterizando uma exposição ocupacional a nicotina. A análise dos resultados in vivo mostrou que os níveis de cotinina plasmático apresentado pelos agricultores não têm correlação com a atividade da AChE. Isto aponta para a possibilidade da não ocorrência de um efeito aditivo da exposição à nicotina e agrotóxicos sobre a atividade da AChE, fator que pode ser utilizado para um diagnóstico diferencial entre a exposição a agrotóxicos e à nicotina entre trabalhadores da cultura fumageira.

Pulmonary toxicity of chronic exposure to tobacco and biomass smoke in rats

OBJECTIVE: The objective of this study was to examine the separate and combined effects of tobacco and biomass smoke exposure on pulmonary histopathology in rats. INTRODUCTION: In addition to smoking, indoor pollution in developing countries contributes to the development of respiratory diseases. METHODS: Twenty-eight adult rats were divided into four groups as follows: control group (Group I, no exposure to tobacco or biomass smoke), exposed to tobacco smoke (Group II), exposed to biomass smoke (Group III), and combined exposure to tobacco and biomass smoke (Group IV). After six months the rats in all four groups were sacrificed. Lung tissue samples were examined under light microscopy. The severity of pathological changes was scored. RESULTS: Group II differed from Group I in all histopathological alterations except intraparenchymal vascular thrombosis. There was no statistically significant difference in histopathological changes between the subjects exposed exclusively to tobacco smoke (Group II) and those with combined exposure to tobacco and biomass smoke (Group IV). The histopathological changes observed in Group IV were found to be more severe than those in subjects exposed exclusively to biomass smoke (Group III). DISCUSSION: Chronic exposure to tobacco and biomass smoke caused an increase in severity and types of lung injury. CONCLUSION: Exposure to cigarette smoke caused serious damage to the respiratory system, particularly with concomitant exposure to biomass smoke.

Modelo de cámara inhaladora para los estudios controlados sobre la toxicidad del humo del tabaco en los roedores / An Inhalation Chamber Model for Controlled Studies of Tobacco Smoke Toxicity in Rodents

Introducción: El tabaquismo constituye un grave problema de salud pública en todo el mundo. Los modelos animales actúan como un paso intermedio entre los estudios de laboratorio y los estudios en seres humanos. Los modelos aplicados son difíciles de reproducir debido al uso de diferentes tipos de cámaras inhaladoras y principalmente por la falta de una monitorización constante de la concentración del humo del tabaco.ObjetivoDesarrollar una cámara inhaladora para ratas (con la exposición exclusiva del hocico) en la que pueda mantenerse y monitorizarse constantemente la cantidad de monóxido de carbono (CO).Material y métodosSe expusieron ratas Wistar macho, de 250g de peso, a 50 partes por millón de CO producido por el humo del tabaco de un cigarrillo sin filtro. Los animales se sometieron a una exposición de 2h y, acto seguido, fueron sacrificados a las 0, a las 4, a las 24 y a las 48h. El grupo de control se dejó libre dentro de pequeñas cámaras perpendiculares y solo recibió 5l/min de aire comprimido.ResultadosEl modelo fue capaz de aumentar la concentración de carboxihemoglobina inmediatamente después del término de la exposición (p<0,001), observándose una disminución desde las 2h en adelante comparado con la concentración del grupo de control. La concentración plasmática de cotinina aumentó inmediatamente después de la exposición y todavía se detectó a las 2 y a las 4h (p<0,05).ConclusiónConcluimos que este sistema de cámara inhaladora puede mantener una concentración controlada de CO en un modelo en el que se expone a pequeños animales a la inhalación de humo de cigarrillos, lo que permite estudios adecuadamente controlados, al igual que investigaciones sobre otros gases tóxicos y contaminantes ambientales(AU)

Introduction: Smoking is a serious worldwide public health problem. Animal models act as a bridge between laboratory and human studies. The models applied are difficult to reproduce because of the use of different types of inhalation chambers and mainly because of the lack of continuous monitoring of smoke concentration.ObjectiveTo develop an inhalation chamber for rats (with only the nose exposed) in which the amount of carbon monoxide (CO) can be maintained and monitored constantly.Material and methodsMale Wistar rats weighing 250g were exposed to 50ppm CO produced by the smoke from a filter-free cigarette. The animals were submitted to a single 2-h exposure and then sacrificed at 0, 4, 24 and 48h. The control group was left restrained inside the small perpendicular chambers, receiving only 5L/min of compressed air.ResultsThe model was able to increase HbCO levels immediately after the end of exposure (p<0.001), with a decrease being observed from 2h onwards when compared to the levels of the control group. Plasma cotinine increased immediately after exposure, and showed still detectable levels at 2 and 4h (p<0.05).ConclusionWe conclude that the presented inhalation chamber system is able to maintain a controlled CO concentration in a model in which small animals are exposed to the inhalation of cigarette smoke, permitting well-controlled studies, as well as investigations involving other toxic gases and air pollutants(AU)

Impacto de la Ley del tabaco en el lugar de trabajo: estudio de seguimiento de una cohorte de trabajadores en España 2005–07 / Impact of the Tobacco Law on the workplace: a follow up study of a cohort of workers in Spain 2005–2007

ObjetivoEs describir los cambios producidos, por la Ley del tabaco en su consurno, en fumadores trabajadores activos.DiseñoEstudio de seguimiento, post-intevención, de una cohorte de usuarios.EmplazamientoCentros de salud de Valencia y Mallorca.ParticipantesUsuarios que acuden a los centros de salud.IntervencionesEl trabajo de campo consistió en la captación y cumplirnentación, para cada paciente, de una hoja de recogida de datos.Mediciones principalesLas variables que se recogieron fueron sexo, edad, lugar de trabajo, nivel educativo, número de trabajadores de la empresa, número de cigarrillos fumados. Se le indicó, que al día siguiente contara los cigarrillos fumados durante todo el día, diferenciando si había sido en horario laboral o fuera de él. Si fue en el trabajo informó si había sido dentro del lugar de trabajo o fuera. Al día siguiente se le llamó por teléfono para que nos indicara el número de cigarrillos fumados. Se repitió esta llamada a los seis y dieciocho meses.ResultadosSe ha reducido la prevalencia en un 9% al mes, y el número de cigarrillos fumados en el lugar de trabajo. Las variables relacionadas con cumplir la ley fueron el nivel educativo, el sexo del trabajador y el tamaño de la empresa.ConclusionesLa entrada en vigor de la Ley del tabaco ha sido efectiva(AU)

Objective: The aim of this study is to describe the changes caused by the Law on Tobacco and its consumption in workers who are active smokers.DesignA post-intervention follow up study of a cohort of users.SettingHealth Centres in Valencia and Majorca.ParticipantsUsers who attended health centres.InterventionThe field work consisted of each patient filling in a case report form with the requested information.Main measurementsThe variables collected were, sex, place of work, education level, number of workers in the company, number of cigarettes smoked. They were told that on the following day they had to count the cigarettes smoked throughout the day, noting whether they had been smoked during or outside working hours. If they smoked during working hours, they reported whether it was inside or outside the workplace. On the following day they were telephoned to let us know the number of cigarettes smoked. This telephone call was repeated at six months and eighteen months.ResultsSmoking prevalence and the number of cigarettes smoked in the workplace has been reduced by 9% per month. The variables associated with compliance with the law were education level, the sex of the worker, and the size of the company.ConclusionsThe coming into force of the Tobacco Law has been effective(AU)