RESUMO
BACKGROUND: We investigated the net changes in prevalence of symptoms of asthma and rhinitis over 10 years in a cohort of young by baseline sensitization status. METHODS: One thousand one hundred ninety three Chilean adults subjects aged 22-28 living in a semi-rural area of central Chile answered a lifestyle and the European Community Respiratory Health Survey (ECRHS) questionnaires. Bronchial hyper-responsiveness (BHR) and skin prick test (SPT) to eight allergens were measured at baseline in 2001. Ten years later, 772 participants completed the questionnaires again. Estimates of adjusted net changes in prevalence of symptoms by sensitization status at baseline and association between sensitization status at baseline and respiratory symptoms ten years later were assessed. RESULTS: A quarter of the participants were sensitized to at least one allergen in 2001. Prevalence of wheeze had a net change per year of -0.37 % (95 % Confidence Interval -0.71 to 0.02 %; p = 0.067). Self-reported nasal allergies in the last 12 months increased by 0.83 % per year (95 % CI 0.49 to 1.17 %; p < 0.001). Those sensitized to either cat fur (OR 1.76; CI 1.01 to 3.05), cockroach, (OR 2.09; 1.13 to 3.86) blend of grass and pollens (1.78; 95 % CI 1.08 to 2.92), or weeds (OR 1.77; 95 % CI 1.01 to 3.12) in 2001 were more likely to have wheeze in the last 12 months 10 years later. CONCLUSION: Symptoms of asthma remained stable or slightly changed over 10 years in adults, whilst rhinitis and nasal allergies greatly increased. Being sensitized to at least one allergen is a risk factor for persistent symptoms of asthma and rhinitis, but not for determining net changes of symptoms over time. The underlying causes for the contrasting trends between asthma and nasal allergy are unknown.
Assuntos
Asma/epidemiologia , Sons Respiratórios/etiologia , Rinite Alérgica Sazonal/epidemiologia , Adulto , Alérgenos/imunologia , Animais , Gatos , Chile/epidemiologia , Baratas/imunologia , Cães , Feminino , Humanos , Imunoglobulina E/sangue , Modelos Logísticos , Masculino , Pólen/imunologia , Estudos Prospectivos , Testes Cutâneos , Adulto JovemRESUMO
Chronic obstructive pulmonary disease (COPD) mortality and morbidity have increased significantly worldwide in recent decades. Although cigarette smoke is still considered the main risk factor for the development of the disease, estimates suggest that between 25% and 33% of COPD patients are non-smokers. Among the factors that may increase the risk of developing COPD, biomass smoke has been proposed as one of the most important, affecting especially women and children in developing countries. Despite the epidemiological evidence linking exposure to biomass smoke with adverse health effects, the specific cellular and molecular mechanisms by which this pollutant can be harmful for the respiratory and cardiovascular systems remain unclear. In this article we review the main pathogenic mechanisms proposed to date that make biomass smoke one of the major risk factors for COPD.
Assuntos
Biomassa , Doença Pulmonar Obstrutiva Crônica/etiologia , Lesão por Inalação de Fumaça/complicações , Fumaça/efeitos adversos , Adulto , Poluentes Atmosféricos/efeitos adversos , Poluição do Ar em Ambientes Fechados/efeitos adversos , Animais , Criança , Culinária , Citocinas/metabolismo , Exposição Ambiental , Feminino , Gases/efeitos adversos , Calefação , Humanos , Inflamassomos/efeitos dos fármacos , Inflamação/etiologia , Mediadores da Inflamação/metabolismo , Masculino , Camundongos , Estresse Oxidativo , Material Particulado/efeitos adversos , Gravidez , Efeitos Tardios da Exposição Pré-Natal , População Rural , Canais de Potencial de Receptor Transitório/efeitos dos fármacosRESUMO
La evidencia científica ha puesto de manifiesto que la exposición a humo de tabaco ambiental (HTA) es un problema de salud pública a nivel mundial. Las campañas a nivel internacional y nacional tienen por objetivo disminuir el consumo de tabaco y con ello la exposición en la población general. Uno de los grupos más vulnerables a los efectos de la exposición a HTA son los niños, dado que tienen un sistema inmunitario y respiratorio en desarrollo y a que ventilan más aire por unidad de masa corporal por lo que pueden inhalar una mayor dosis efectiva de contaminantes por kg de peso. Ellos forman parte de los denominados fumadores pasivos cuya principal fuente de exposición es el consumo de tabaco en el hogar. En este grupo la exposición a HTA se ha relacionado con aumento de infecciones respiratorias bajas, inducción y exacerbación de asma, otitis media y bajo peso al nacer. Este artículo resume la evidencia sobre los daños a nivel respiratorio que provoca la exposición a HTA en la infancia y señala las ventajas de su control.
Assuntos
Humanos , Criança , Saúde da Criança , Poluição por Fumaça de Tabaco/efeitos adversos , Doenças Respiratórias/induzido quimicamente , Poluição do Ar em Ambientes Fechados/efeitos adversos , Suscetibilidade a Doenças , Doenças Respiratórias/epidemiologia , Prevalência , RespiraçãoRESUMO
OBJECTIVES: We assessed the effects of indoor risk factors, including smoking, on different types of cough and on cough and wheeze in combination. METHODS: Our sample was composed of 1232 men and women residing in a semirural area of Chile. We used a standardized questionnaire, sensitization to 8 allergens, and bronchial hyperresponsiveness to methacholine to assess cough and wheeze characteristics. Information was gathered on dampness, mold, ventilation, heating, housing quality, smoking, and environmental tobacco smoke exposure. RESULTS: Most exposures were associated with cough alone or cough in combination with wheeze. Smoking, past smoking, and environmental tobacco smoke exposure were strongly associated with dry cough and wheeze. The use of coal for heating was associated with dry cough. Leaks, mold, and lack of kitchen ventilation were associated with cough and wheeze. Nocturnal cough and productive cough were associated with specific types of sensitization, but dry cough was not. Productive cough was associated with hyperresponsiveness to methacholine. CONCLUSIONS: Several different types of indoor exposures, including environmental tobacco smoke exposure, are important contributors to morbidity associated with cough and wheeze. A vigorous preventive strategy designed to lower exposures to indoor risk factors would lower rates of respiratory morbidity.
Assuntos
Alérgenos , Hiper-Reatividade Brônquica/etiologia , Tosse/etiologia , Exposição Ambiental/efeitos adversos , Sons Respiratórios , Fumar/efeitos adversos , Adolescente , Adulto , Fatores Etários , Hiper-Reatividade Brônquica/epidemiologia , Chile/epidemiologia , Tosse/epidemiologia , Feminino , Humanos , Entrevistas como Assunto , Masculino , Fatores de Risco , Inquéritos e QuestionáriosRESUMO
BACKGROUND: Smoking is the main risk factor for Chronic Obstructive Pulmonary Disease (COPD), an important cause of morbidity and mortality. AIM: To estimate smoking attributable risk and population attributable risk in COPD patients attended in Public Health Services of Santiago. MATERIALS AND METHODS: A case control study matched by sex and age was carried out. Crude and adjusted attributable risks as well as population attributable risk were estimated, controlled by potential confounders and by interaction variables. RESULTS: Mean ages for cases and controls were 68 and 67 years respectively. When compared to the control group, COPD patients had a higher smoking prevalence (at least 100 cigarettes in their life span: 89.7% vs 60.3%; p <0.01). Among COPD patients, heavy smokers proportion was 4 times higher than in controls, they smoked for more years (43 vs 31; p <0.01) and more cigarettes per day (18 vs 5; p <0.01). Adjusted attributable risk was 87% (95% Confidence Interval (CI): 63.7-94.8). If a patient smoked at least 100 cigarettes in his/her life span and this risk was 92.7% (CI: 82.4-96.9) for heavy smokers. Projecting this index to Santiago inhabitants, about 87,000 individuals older than 40 years would be suffering COPD due to smoking. CONCLUSIONS: This article confirms the strong association between smoking and COPD. Attributable risks are high and significant, even when they are adjusted by confounding variables. Women had a higher risk than men, at lower levels of tobacco consumption.
Assuntos
Serviços de Saúde/economia , Doença Pulmonar Obstrutiva Crônica/etiologia , Fumar/efeitos adversos , Adulto , Estudos de Casos e Controles , Chile/epidemiologia , Custos e Análise de Custo , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Razão de Chances , Prevalência , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Fatores de Risco , Distribuição por Sexo , Fumar/epidemiologia , Poluição por Fumaça de Tabaco/economia , Poluição por Fumaça de Tabaco/estatística & dados numéricosRESUMO
Asthma epidemiology relies heavily on standardized questionnaires, but little is known about the understanding of asthma symptoms among adults in the community. In 2004, the authors assessed the level of agreement between responses to a standardized questionnaire and responses to a questionnaire completed by participants after viewing a demonstration of asthma symptoms. The study involved 601 young adults from Chile. The field-workers were trained to explain and demonstrate the asthma symptoms to the participants. The symptoms were wheeze, waking at night with breathlessness, breathlessness following exercise, and waking with cough. The kappa statistic did not exceed 0.4, and the recorded prevalence of asthma symptoms following the demonstration was 30-60% lower than that for the standardized questionnaire. Using bronchial responsiveness as the proxy gold standard, the positive likelihood ratios for wheeze and waking short of breath were higher following symptom demonstration. The low agreement between the standardized questionnaire and the postdemonstration questionnaire and the likelihood ratios' closeness to 1 for the standardized questionnaire decreases the authors' confidence in the appropriateness of this tool for estimating the prevalence of asthma in the community. For etiologic studies of asthma, it may contribute to the lack of consistency between different studies analyzing the same etiologic exposures.
Assuntos
Asma/diagnóstico , Educação em Saúde , Conhecimentos, Atitudes e Prática em Saúde , Inquéritos e Questionários , Adulto , Asma/epidemiologia , Asma/fisiopatologia , Chile/epidemiologia , Tosse/etiologia , Dispneia/etiologia , Feminino , Humanos , Masculino , Sons Respiratórios/etiologia , População Rural , Gravação em VídeoRESUMO
To study the effect of ozone in a chronically damaged lung, we used a bleomycin (BLM) induced pulmonary fibrosis model. Both endotracheal instillation of BLM and O3 exposure both produce lung inflammation and fibrosis. Oxidative stress would be a common mechanism of damage for both BLM and O3. Our aim was to assess lung injury induced by 5 and 60 days of intermittent exposure to 0.25 ppm O3 in rats with bleomycin-induced pulmonary fibrosis. Thirty-day-old Sprague Dawley rats were endotracheally instilled with BLM (1 U/100 g body weight) and, 30 days later, exposed to 0.25 ppm 03 (0.25 ppm 4 h per day, 5 days a week). Histopatology controls were instilled with saline and breathing room air. Histopathological evaluation of lungs was done 5 and 60 days after O3 exposure. BLM-induced lung damage did not change after 60 days of intermittent O3 exposure. Five days of O3 exposure increased the mean score of BLM-induced pulmonary inflammation and fibrosis (p=0.06). Frequency of bronchopneumonia increased from 1/7 to 6/6 (p <0.001), suggesting that a short-term exposure to O3 in a previously damaged lung might be a risk factor for developing further lung injury.
Assuntos
Broncopneumonia/induzido quimicamente , Pulmão/efeitos dos fármacos , Ozônio/toxicidade , Fibrose Pulmonar/induzido quimicamente , Animais , Bleomicina , Broncopneumonia/patologia , Modelos Animais de Doenças , Sinergismo Farmacológico , Pulmão/patologia , Fibrose Pulmonar/patologia , Ratos , Ratos Sprague-Dawley , Fatores de TempoRESUMO
To study the effect of ozone in a chronically damaged lung, we used a bleomycin (BLM) induced pulmonary fibrosis model. Both endotracheal instillation of BLM and O3 exposure both produce lung inflammation and fibrosis. Oxidative stress would be a common mechanism of damage for both BLM and O3. Our aim was to assess lung injury induced by 5 and 60 days of intermittent exposure to 0.25 ppm O3 in rats with bleomycin-induced pulmonary fibrosis. Thirty-day-old Sprague Dawley rats were endotracheally instilled with BLM (1 U/100 g body weight) and, 30 days later, exposed to 0.25 ppm O3 (0.25 ppm 4 h per day, 5 days a week). Histopatology controls were instilled with saline and breathing room air. Histopathological evaluation of lungs was done 5 and 60 days after O3 exposure. BLM-induced lung damage did not change after 60 days of intermittent O3 exposure. Five days of O3 exposure increased the mean score of BLM-induced pulmonary inflammation and fibrosis (p=0.06). Frequency of bronchopneumonia increased from 1/7 to 6/6 (p <0.001), suggesting that a short-term exposure to O3 in a previously damaged lung might be a risk factor for developing further lung injury.
Assuntos
Animais , Recém-Nascido , Ratos , Pneumopatias/induzido quimicamente , Ozônio/efeitos da radiação , Ozônio/toxicidade , Modelos Animais , Ratos Sprague-DawleyRESUMO
BACKGROUND: Recent evidence implicates fine particulate matter (PM2.5), principally from vehicular exhaust, as a major cause of increased mortality and morbidity. However, there are limited data on the impact of PM2.5 on infant respiratory illnesses. METHODS: We conducted a cohort study of 504 infants recruited at 4 months of age from primary health care units in southeastern Santiago, Chile. Project physicians followed infants through the first year of life via monthly check-ups and by appointments on demand. We obtained data for fine particulate matter, sulfur dioxide (SO2), and nitrogen dioxide (NO2) from the governmental monitoring network. RESULTS: The most frequent diagnosis during follow-up was wheezing bronchitis, occurring 19.5 times per 100 infants per month. After adjusting for sex, socioeconomic level, family history of asthma, minimum temperature, and number of older siblings, we found that an increase of 10 microg/m of PM2.5 24-hour average was related to a 5% increase (95% confidence interval 0-9%) in the risk for wheezing bronchitis (1-day lag). This association was present for different lags, with a maximum observed for a 9-day lag (9%; 6-12%). No consistent association was detected with NO2 or SO2 ambient levels. Lower socioeconomic status and having older siblings were also associated with the risk of wheezing bronchitis. The association of PM2.5 and wheezing bronchitis was stronger among infants with a family history of asthma than among infants without. CONCLUSIONS: Air pollution in the form of fine particulates, mostly from vehicular exhaust, may adversely affect infants' respiratory health with potential for chronic effects later in life.
Assuntos
Bronquite/etiologia , Exposição Ambiental/efeitos adversos , Sons Respiratórios/etiologia , Poluição por Fumaça de Tabaco/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar em Ambientes Fechados/análise , Bronquite/epidemiologia , Chile/epidemiologia , Estudos de Coortes , Feminino , Humanos , Lactente , Masculino , Análise Multivariada , Tamanho da Partícula , Fatores de Risco , Fatores Socioeconômicos , Poluição por Fumaça de Tabaco/análiseRESUMO
This study was conducted to relate blood lead levels in infants to changes in lead emissions in Santiago, Chile, a heavily polluted setting where leaded gasoline began to be replaced with unleaded gasoline in 1993. Over an 18-mo period, 422 infants had blood lead levels, cotinine, and iron status determined at 12 mo. Blood lead levels fell at an average rate of 0.5 microg/dl every 2 mo, from 8.3 to 5.9 microg/dl, as the city experienced a net fall of 30% in the quantity of leaded gasoline sold. Time progression, car ownership, serum cotinine, and type of housing were significantly associated with a blood lead level > or = 10 microg/dl. In this study, the authors demonstrated that infant blood lead levels, even if relatively low, can drop very rapidly in conjunction with decreases in environmental lead exposure.
Assuntos
Carcinógenos/química , Exposição Ambiental , Gasolina , Chumbo/sangue , Emissões de Veículos/análise , Chile/epidemiologia , Cotinina/sangue , Feminino , Seguimentos , Humanos , Lactente , Ferro/sangue , Masculino , Veículos Automotores/economia , Propriedade , Pobreza , Política Pública , Fatores de Tempo , População UrbanaRESUMO
A survey was addressed to 57 editors of Chilean biomedical journals, on how to attract more and better manuscripts to their journals. Thirty seven editors (65%) answered this survey. According to them the main motivation of Medical Societies for editing their own journals is to improve information acquisition. To communicate an experience, followed by getting credits in their curriculum vitae, were considered by the editors as the main motivations of authors to submit papers. The most frequent deficiencies of manuscripts received are: disorganization in their presentation and bad adherence to journal's requirements for submitting manuscripts. An improvement in the relationship between author-editor-reviewer was mentioned by most of the editors, as the mechanism to be used to enhance the quality of the manuscripts. Only 14 editors (38%) agree in that there is a decrease in the number of original papers submitted. This decrease was attributed by most of them, to a high pressure for publishing in journals with the highest impact factor. Suggestions on how to improve the Chilean biomedical journals included: a) to professionalize editorial work and to increase meticulousness when reviewing manuscripts; b) to increase the recognition of articles published in Chilean biomedical journals, when applying for academic promotions or research grants and c) to create a "national impact factor".
Assuntos
Publicações Periódicas como Assunto/normas , Chile , Humanos , Inquéritos e QuestionáriosRESUMO
Santiago de Chile has a high level of air pollutiom with ozone (O3), carbon monoxide (CO) and particles equal of smaller than 16 mum (PM(10)) usually exceeding the accepted standards. This situation should be noxious for the exposed population and particularly -in the case of O3 and PM(10-) for the respiratory system. However, such an effect is rather difficult to demonstrate and it depends on the type of population under study.
Assuntos
Humanos , Lactente , Criança , Poluição do Ar/efeitos adversos , Sistema Respiratório/fisiopatologia , Doenças Respiratórias/etiologia , Bronquite/etiologia , Broncopneumonia/etiologia , Chile , Pneumonia/etiologia , Fatores de RiscoRESUMO
Enrique Egaña-Barahona. Born Santiago, Chile, 10 March 1912. Deceased Santiago, Chile, 23 November 1997. MD, University of Chile, 1936. Rockefeller Foundation Fellow at Harvard University Medical School, 1940-1944. Professor of Pathophysiology, 1963; Director, Institute of Experimental Medicine, Faculty of Medicine, University of Chile. Author of a Textbook on General Pathophysiology (1963) and of many scientific articles in Chilean and American medical journals. Strong supporter of evidence-based medicine as well as of medical education by envolving students in short research projects.
Assuntos
Humanos , História do Século XX , Patologia , Fisiologia , Sistema Nervoso Central , Medicina Baseada em Evidências , RetratoRESUMO
Estudios previos han demostrado que la instilación endotraquial de bleomicina en la rata produce edema e inflamación al cabo de 24H y cierto grado de fibrosis luego de 15 días. El objetivo de este trabajo fue evaluar el daño pulmonar inducido a largo plazo (3,7,14,30 y 60 días)por la instilación endotraqueal de 1U de bleomicina por 100g de peso a fin de relacionar las alteraciones del lavado broncoalveolar (LBA) conla histopatología pulmonar. La serie control consistió en ratas instiladas con NaCl 0,9 por ciento vía endotraqueal y sometidas a similares procedimientos. En el LBA se practicó recuento celular y determinaciones de proteínas, fosfolípidos, fosfatasa alcalina gama glutamiltranspeptidasa (GGT). Se observó aumento significativo (p<0,05)de la realción peso pulmonar/peso corporal en las ratas tratadas con bleomicina la histología reveló daño pulmonar temprano (3 a 7 días):aumento de neutrófilos y eosinófilos y hemorragia intra-alveolar. En días ulteriores (14 a 60 días) se observó pérdida de la arquitectura, proliferación de neumocitos tipo II y fibrosis pulmonar. En el LBA de las ratas tratadas con bleomicina se observó aumento significativo (p<0,05)en realción a la serie de control en las siguientes variables: células (3 y 14 días), proteínas (3-7 y 30 días), fosfolípidos, fosfatasa alcalina y GGT (7-14 y 30 días). En el daño pulmonar pr bleomicina existiría relación entre el grado de inflamación de la fase exudativa y las alteraciones del LBA. La determinación de fosfatasa alcalina y GGT en el LBA podría ser potencialmente útil en el seguimiento del daño pulmonar por bleomicina
Assuntos
Animais , Ratos , Bleomicina/efeitos adversos , Líquido da Lavagem Broncoalveolar/fisiopatologia , Pneumopatias/patologia , Pulmão , Edema Pulmonar/induzido quimicamente , Fibrose Pulmonar/induzido quimicamenteAssuntos
Coelhos , Animais , Masculino , Epoprostenol/análogos & derivados , Epoprostenol/farmacologia , Ácidos Graxos não Esterificados/farmacologia , Leucotrienos/fisiologia , Pulmão/fisiologia , Tromboxano A2/farmacologia , Epoprostenol/administração & dosagem , Hemodinâmica/efeitos dos fármacos , Infusões Intravenosas , Pulmão/efeitos dos fármacosRESUMO
Se exploró la actividad de gama-glutamil transpeptidasa (GGT) en el lavado broncoalveolar (LBA) como posible indicador de daño tisular en la reexpansión pulmonar de un neumotórax experimental unilateral. Seis conejos adultos sedados con Ketamina y Acetilpromazina, se sometieron a neumotórax inyectando 20 ml de N2/kg en el espacio pleural derecho. Diariamente se repuso el N2 reabsorvido y al tercer día se reexpandió el pulmón aplicando -100 mm de Hg durante 2 h. Se extrajo y separó los pulmones y se practicó LBA con 9 ml de NaCl 0,9% /g x 5 veces a 4 grados Celcius. Previo recuento celular total el LBA se centrifugó 2 veces a 140 g por 10 minutos determinándose proteínas totales y actividad de GGT en el "pellet". Se encontró un aumento significativo tanto de células (p = 0,02) como de proteínas (p < 0,02) y de la actividad de GGT (p < 0,007) en el LBA del pulmón reexpandido comparado con el pulmón contralateral (prueba "t" de student para muestras pareadas). La actividad de GGT se correlacionó lineal r = 0,8 y significativamente p < 0,005; análisis de varianza) con el contenido de proteínas del LBA. Los resultados sugieren que el aumento de GGT en el LBA sería un indicador del daño pulmonar difuso provocado por la reexpansión
Assuntos
Coelhos , Animais , Líquido da Lavagem Broncoalveolar/análise , gama-Glutamiltransferase/enzimologia , Pneumotórax , Pulmão/fisiopatologiaRESUMO
La infusión intravenosa de ácidos grasos libres (AGL) en conejos producem edema pulmonar por aumento de la permeabilidad, reacción inflamatoria y aumento del surfactante alveolar. Con el objetivo de definir el rol del anión super-óxido (O2-) en el daño pulmonar difuso producido por EGL, se evaluó el efecto de la superóxido dismutasa (SOD). Se estudiaron 4 series de conejos que recibieron: a) AGL (n = 6): 10 mg AGL/Kg/min.i.v. durante 15 minutos. b) Vehículo de AGL (n=5)i.v. durante 15 y 25 minutos AGL + SOD (mg/Kg i.v. durante 15 y 25 minutos respectivamente (n = 6); d) Vehículo + SOD durante 15 y 25 minutos respectivamente (n = 7). Al cabo de 96 horas los conejos fueron sacrificados, determinándose en el lavado bronquioalveolar: proteínas, fosfatidilcolina disaturada (DPPC) y el recuento celular. Hubo un aumento significativo de DPPC del recuento de células en todas las seires en comparación a la serie vehículo (b). SOD no modificó las alteraciones inducidas por AGL, aunque "per se" aumentó la DPPC y el recuento de células en el LBA. La histología pulmonar mostró edema perivascular e intra-alveolar en los animales inyectados con AGL. Estas alteraciones fueron francamente disminuidas por la SOD. Estos resultados sugieren que el O2- tendria un rol sólo secundario en el daño pulmonar difuso por AGL, ya que SOD protegió solo parcialmente al pulmón de este daño