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SUMMARY: The study explores the relationship between chronic exposure to fine particulate matter (PM2.5), sourced from wood smoke, and the histological structure and endocrine function of the uterus in nulliparous adult rats. It assesses potential structural changes in the uterus that could impact reproductive health, viewing PM2.5 exposure as a possible risk factor. A controlled experiment was conducted in a city known for high air pollution levels, exposing rats to filtered and unfiltered air conditions, thus mimicking human PM2.5 exposure. Histological findings indicated a significant increase in collagen density and uterine wall thickness in PM2.5 exposed subjects, suggesting a reproductive function risk. However, no significant differences were observed in progesterone and estradiol hormone levels, pointing to the complex relationship between PM2.5 exposure and its endocrine impact, and emphasizing the need for further studies for a deeper understanding. This work highlights the importance of thoroughly investigating the long-term effects of PM2.5 pollution on reproductive health, underlining the significance of considering environmental exposure as a critical factor in reproductive health research.
El estudio explora la relación entre la exposición crónica a partículas finas (PM2,5), procedentes del humo de leña, y la estructura histológica y la función endocrina del útero en ratas adultas nulíparas. Evalúa posibles cambios estructurales en el útero que podrían afectar la salud reproductiva, considerando la exposición a PM2,5 como un posible factor de riesgo. Se llevó a cabo un experimento controlado en una ciudad conocida por sus altos niveles de contaminación del aire, exponiendo ratas a condiciones de aire filtrado y sin filtrar, imitando así la exposición humana a PM2,5. Los hallazgos histológicos indicaron un aumento significativo en la densidad del colágeno y el grosor de la pared uterina en sujetos expuestos a PM2,5, lo que sugiere un riesgo para la función reproductiva. Sin embargo, no se observaron diferencias significativas en los niveles de las hormonas progesterona y estradiol, lo que apunta a la compleja relación entre la exposición a PM2,5 y su impacto endocrino, y enfatiza la necesidad de realizar más estudios para una comprensión más profunda. Este trabajo destaca la importancia de investigar a fondo los efectos a largo plazo de la contaminación por PM2,5 en la salud reproductiva, subrayando la importancia de considerar la exposición ambiental como un factor crítico en la investigación de la salud reproductiva.
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Animales , Femenino , Ratas , Humo/efectos adversos , Útero/efectos de los fármacos , Madera , Ratas Sprague-Dawley , Contaminantes Atmosféricos/toxicidad , Contaminación del Aire , Material Particulado/toxicidad , Genitales Femeninos/efectos de los fármacosRESUMEN
Introduction: There is a need to better understand the etiotypes of chronic obstructive pulmonary disease (COPD) beyond the tobacco-smoke (TS-COPD). Wood smoke COPD (WS-COPD) is characterized by greater airway compromise, milder emphysema, and slower rate of lung function decline than TS-COPD. However, it is unclear if these two etiotypes of COPD have differences in sputum biomarker concentrations. Objective was to compare sputum levels of selected sputum biomarkers between WS-COPD and TS-COPD, and healthy controls. Methods: Eighty-eight women (69±12 years) were recruited and classified into: WS-COPD (n=31), TS-COPD (n=29) and controls (n=28). Using ELISA, we determined induced sputum levels of metalloproteinase 9 (MMP-9), chemokine ligand 5 (CCL5), interleukin-8 (IL-8), chemokine ligand 16 (CCL16/HCC-4) and vascular endothelial growth factor (VEGF-1). Differences were analyzed by Kruskal-Wallis and Mann-Whitney-U tests and correlation between airflow limitation and biomarkers by Spearman's test. Results: At similar degree of airflow obstruction, anthropometrics and medications use, the level of sputum CCL5 was higher in TS-COPD than WS-COPD (p=0.03) without differences in MMP-9, IL-8, CCL16/HCC-4, and VEGF-1. Women with WS-COPD and TS-COPD showed significantly higher sputum levels of MMP-9, IL-8 and CCL5 compared with controls (p<0.001). FEV1% predicted correlated negatively with levels of MMP-9 (rho:-0.26; P=0.016), CCL5 (rho:-0.37; P=0.001), IL-8 (rho:-0.42; P<0.001) and VEGF (rho:-0.22; P=0.04). Conclusion: While sputum concentrations of MMP-9, IL-8, and CCL5 were higher in COPD women compared with controls, women with TS-COPD had higher levels of CCL5 compared with those with WS-COPD. Whether this finding relates to differences in pathobiological pathways remains to be determined.
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Carcinoma Hepatocelular , Neoplasias Hepáticas , Enfermedad Pulmonar Obstructiva Crónica , Contaminación por Humo de Tabaco , Humanos , Femenino , Enfermedad Pulmonar Obstructiva Crónica/diagnóstico , Enfermedad Pulmonar Obstructiva Crónica/etiología , Enfermedad Pulmonar Obstructiva Crónica/metabolismo , Interleucina-8/metabolismo , Esputo/metabolismo , Factor A de Crecimiento Endotelial Vascular/metabolismo , Madera , Metaloproteinasa 9 de la Matriz/metabolismo , Carcinoma Hepatocelular/metabolismo , Ligandos , Neoplasias Hepáticas/metabolismo , Humo/efectos adversos , Biomarcadores/metabolismo , Quimiocinas/metabolismo , Productos de TabacoRESUMEN
Biomass burning is common in much of the world, and in some areas, residential wood-burning has increased. However, air pollution resulting from biomass burning is an important public health problem. A sampling campaign was carried out between May 2017 and July 2018 in over 64 sites in four sessions, to develop a spatio-temporal land use regression (LUR) model for fine particulate matter (PM) and wood-burning tracers levoglucosan and soluble potassium (Ksol) in a city heavily impacted by wood-burning. The mean (sd) was 46.5 (37.4) µg m-3 for PM2.5, 0.607 (0.538) µg m-3 for levoglucosan, and 0.635 (0.489) µg m-3 for Ksol. LUR models for PM2.5, levoglucosan, and Ksol had a satisfactory performance (LOSOCV R2), explaining 88.8%, 87.4%, and 87.3% of the total variance, respectively. All models included sociodemographic predictors consistent with the pattern of use of wood-burning in homes. The models were applied to predict concentrations surfaces and to estimate exposures for an epidemiological study.
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Contaminantes Atmosféricos , Material Particulado , Material Particulado/análisis , Contaminantes Atmosféricos/análisis , Madera/química , Chile , Monitoreo del Ambiente/métodosRESUMEN
BACKGROUND: The role of wood smoke (WS) exposure in the etiology of chronic obstructive pulmonary disease (COPD), lung cancer (LC), and mortality remains elusive in adults from countries with low ambient levels of combustion-emitted particulate matter. This study aims to delineate the impact of WS exposure on lung health and mortality in adults age 40 and older who ever smoked. METHODS: We assessed health impact of self-reported "ever WS exposure for over a year" in the Lovelace Smokers Cohort using both objective measures (i.e., lung function decline, LC incidence, and deaths) and two health related quality-of-life questionnaires (i.e., lung disease-specific St. George's Respiratory Questionnaire [SGRQ] and the generic 36-item short-form health survey). RESULTS: Compared to subjects without WS exposure, subjects with WS exposure had a more rapid decline of FEV1 (- 4.3 ml/s, P = 0.025) and FEV1/FVC ratio (- 0.093%, P = 0.015), but not of FVC (- 2.4 ml, P = 0.30). Age modified the impacts of WS exposure on lung function decline. WS exposure impaired all health domains with the increase in SGRQ scores exceeding the minimal clinically important difference. WS exposure increased hazard for incidence of LC and death of all-cause, cardiopulmonary diseases, and cancers by > 50% and shortened the lifespan by 3.5 year. We found no evidence for differential misclassification or confounding from socioeconomic status for the health effects of WS exposure. CONCLUSIONS: We identified epidemiological evidence supporting WS exposure as an independent etiological factor for the development of COPD through accelerating lung function decline in an obstructive pattern. Time-to-event analyses of LC incidence and cancer-specific mortality provide human evidence supporting the carcinogenicity of WS exposure.
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Enfermedad Pulmonar Obstructiva Crónica , Calidad de Vida , Adulto , Envejecimiento , Humanos , Pulmón , Enfermedad Pulmonar Obstructiva Crónica/diagnóstico , Enfermedad Pulmonar Obstructiva Crónica/epidemiología , Enfermedad Pulmonar Obstructiva Crónica/etiología , Humo/efectos adversos , Fumadores , Madera/efectos adversosRESUMEN
Exposure to air pollutants in wildfire smoke and indoor pollution causes lung diseases. Short-term exposure to wood smoke (WS) is partially known to alter the expression of human matrix metalloproteinases (MMPs), inflammatory cytokines, and tissue inhibitors of metalloproteinases (TIMPs). Accordingly, we investigated the effect of exposing guinea pigs to WS for two and four three-hour periods on different days. The daily content of particles reported by indoor pollution was produced by 60 g of pinewood. We analyzed the cell profile and collagen content in bronchoalveolar lavages (BAL). The mRNA expression of pro-inflammatory cytokines, MMPs, and TIMPs was studied in lung tissue. Cytokines and gelatinolytic activity were analyzed in BAL and serum. The results showed that total cells, macrophages, neutrophils, and collagen increased in BAL, whereas neutrophils and lymphocytes decreased. TGF-ß1, TNF-α, IFN-γ, IL-1ß, IL-6, IL-8, MMP-2, MMP-9, TIMP-1, and TIMP-2 were upregulated in lungs, downregulating IL-12. TNF-α, IFN-γ, TGF-ß1, IL-1ß, IL-6, and IL-8 were increased in BAL and serum, decreasing IL-12. Gelatinase activity was increased in serum. Thus, guinea pigs exposed to short-term domestic doses of WS overexpressed pro-inflammatory cytokines, MMPs, and TIMPs. These results are similar to ECM remodeling and pulmonary and systemic inflammation reported in humans.
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Wood smoke (WS) contains many harmful compounds, including polycyclic aromatic hydrocarbons (PAHs). WS induces inflammation in the airways and lungs and can lead to the development of various acute and chronic respiratory diseases. Pulmonary fibroblasts are the main cells involved in the remodeling of the extracellular matrix (ECM) during the WS-induced inflammatory response. Although fibroblasts remain in a low proliferation state under physiological conditions, they actively participate in ECM remodeling during the inflammatory response in pathophysiological states. Consequently, we used normal human lung fibroblasts (NHLFs) to assess the potential effects of the PAHs-containing wood smoke extract (WSE) on the growth rate, total collagen synthesis, and the expression levels of collagen I and III, matrix metalloproteinase (MMP)-1, MMP-2, MMP-9, tissue inhibitor of metalloproteinase (TIMP)-1, TIMP-2, and the transforming growth factor (TGF)-ß1. We also assessed MMPs activity. The results showed that WSE induced a trimodal behavior in the growth rate curves in NHLFs; the growth rate increased with 0.5-1 % WSE and decreased with 2.5% WSE, without causing cell damage; 5-20% WSE inhibited the growth and induced cell damage. After 3 hours of exposure, 2.5% WSE induced an increase in total collagen synthesis and upregulation of TGF-ß1, collagen I and III, MMP-1, TIMP-1, and TIMP-2 expression. However, MMP-2 expression was downregulated and MMP-9 was not expressed. The gelatinase activity of MMP-2 was also increased. These results suggest that WSE affects the ECM remodeling in NHLFs and indicate the potential involvement of PAHs in this process.
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Matriz Extracelular/efectos de los fármacos , Fibroblastos/efectos de los fármacos , Inflamación/inducido químicamente , Inflamación/fisiopatología , Enfermedades Pulmonares/inducido químicamente , Extractos Vegetales/efectos adversos , Humo/efectos adversos , Proliferación Celular/efectos de los fármacos , Humanos , Magnoliopsida/química , Madera/químicaRESUMEN
SUMMARY: Exposure to air pollution and its pollutants has been associated with important effects on human health since the first years of life, thus it has been seen that exposure to tobacco smoke and wood smoke is directly related to cardiovascular and pulmonary diseases, respiratory and cancers. However, exposure to air pollution during fetal development and its effects on brain structure and function during early childhood and adolescence have been little studied. In this review we have analyzed the literature on prenatal exposure to tobacco and wood smoke and its relationship with hypothalamic development and cognition in the first years of life.The molecular, morphological and physiological aspects of the relationship between pre- and postnatal exposure to tobacco and wood smoke with neural developmental, cognitive and behavioral problems during early childhood and adolescence have not yet been fully clarified. The information available in the scientific literature based on antecedents obtained from epidemiological studies has been negatively affected by confounding variables and great methodological challenges that make it impossible to affirm an exact causal relationship with certainty.
RESUMEN: La exposición a la contaminación del aire se ha asociado con importantes efectos en la salud humana desde los primeros años de vida. Estudios han demostrado con certeza que la exposición al humo de tabaco y humo de leña está directamente relacionada con enfermedades cardiovasculares, pulmonares, respiratorias y cánceres. Sin embargo, la exposición a la contaminación del aire durante el desarrollo fetal y sus efectos a posteriori sobre la estructura y función del cerebro durante la primera infancia y la adolescencia son aún desconocidos. En esta revisión analizamos la literatura sobre la exposición prenatal al tabaco y al humo de leña y su relación con el desarrollo hipotalámico y la cognición en los primeros años de vida. Los aspectos moleculares, morfológicos y fisiológicos de la asociación entre la exposición pre y postnatal al humo de tabaco o al humo de leña con problemas del desarrollo neurológico normal, cognitivos y de comportamiento durante la primera infancia y la adolescencia aún no se han aclarado completamente. La información disponible en la literatura científica basada en antecedentes obtenidos de estudios epidemiológicos ha sido afectada negativamente por variables de confusión y grandes desafíos metodológicos que hacen imposible afirmar una relación directa y causal exacta con certeza.
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Humanos , Femenino , Embarazo , Niño , Adolescente , Contaminación por Humo de Tabaco/efectos adversos , Cognición/efectos de los fármacos , Exposición por Inhalación/efectos adversos , Material Particulado/efectos adversos , Hipotálamo/efectos de los fármacos , Efectos Tardíos de la Exposición Prenatal , Humo , MaderaRESUMEN
SUMMARY: Residential heating with wood is an important source of ambient air pollution. Evidence links air pollution to serious health effects such as respiratory and cardiovascular mortality and morbidity. We hypothesized that prenatal exposure to wood smoke pollution causes morphological changes in the development of the rat lung, leading to altered lung structure and function during later life. We presumed that analysis of the fetal lung stereology provides novel insights into the underlying processes mediating particulate matter associated developmental changes and damage. The objective of the study was to investigate the effects of exposure during gestational period to wood smoke pollution on lung fetal morphology. To test this, pregnant rats were exposed during pregestational and gestational periods to wood smoke pollution. Complete lungs samples were obtained from 24 fetus from healthy female G3 rats subjected to cesarean at 19 days post-fecundation. The lungs were prepared for histological and stereological analysis. The volume fraction of terminal bronchioles VV [tb, lung] and volume fraction of parenchyma VV [par, lung], surface density of terminal bronchioles SV [tb, lung] as well as numerical density of bronchiolar exocrinocytes NA [ec,lung] were calculated by light microscopy. Statistical analysis detected significant differences between groups in volume density VV [tb, lung; %] (p=0.0012) and surface density SV [tb, lung; mm2/mm3] (p<0.0001) of the terminal bronchioles. However, it did not show differences between groups in the stereological parameter volume density VV [par, lung; %] (p=0.0838) and numerical density of bronchiolar exocrinocytes NA [ec,lung; nº/mm2] (p=0.0705). The analysis of the evidence obtained indicates that exposure to environmental pollution was affects lung maturation, and particularly the proportion and area of terminal bronchioles in the fetal lung. In conclusion, maternal exposure to wood smoke pollution during pregnancy was associated with a decrease in the lower conducting airways of lungs, which, according to urban pollution studies, could be related to early childhood lower respiratory illness. The public health implications of this study are that reducing or avoiding exposure to wood smoke is important before and during pregnancy.
RESUMEN: La calefacción residencial con leña es una fuente importante de contaminación ambiental. La evidencia vincula la contaminación del aire con graves efectos sobre la salud, como la mortalidad y la morbilidad respiratoria y cardiovascular. Hipotetizamos que la exposición prenatal a la contaminación por humo de leña causa cambios en el desarrollo del pulmón de rata, lo que conduce a una morfo-función pulmonar alteradas durante la vida posterior, creemos que el análisis de la estereología pulmonar fetal proporcionará nuevos conocimientos sobre los procesos subyacentes que median esos cambios. El objetivo del estudio fue investigar los efectos de la exposición prenatal a la contaminación ambiental por humo de leña sobre la morfología pulmonar fetal. Ratas preñadas fueron expuestas durante los períodos pregestacional y gestacional a la contaminación por humo de leña. En fetos de 19 días post-fecundación fue obtenido el pulmón para análisis histológico y estereológico. Fue determinado la fracción de volumen de bronquiolos terminales VV [tb, pulmón], fracción de volumen del parénquima VV [par, pulmón], densidad superficial de los bronquiolos terminales SV [tb, pulmón] así como la densidad numérica de exocrinocitos NA [ec, pulmón]. El análisis estadístico detectó diferencias significativas entre grupos en la densidad de volumen V [tb, pulmón; %] (p=0,0012) y densidad superficial SV [tb, pulmón; mm2/mm3] (p<0,0001) de los bronquiolos terminales. Sin embargo, no demostró diferencias entre grupos en la densidad de volumen VV [par, pulmón; %] (p=0,0838) y numérica de exocrinocitos bronquiolares NA [ec, pulmón; nº / mm ] (p=0,0705). El análisis de la evidencia obtenida indica que la exposición a la contaminación ambiental afectó la maduración pulmonar, y particularmente la proporción y área de bronquiolos terminales en el pulmón fetal. En conclusión, la exposición materna a la contaminación por humo de leña durante la gestación se asoció a una disminución de las vías respiratorias conductoras de aire en pulmón, lo que, según estudios de contaminación urbana, podría estar relacionado con enfermedades de las vías respiratorias inferiores en la primera infancia. Las implicaciones para la salud pública de este estudio son que reducir o evitar la exposición al humo de leña es importante previo y durante la gestación. Por otro lado, la contaminación por humo de leña tiene un gran impacto en la salud pública que, en teoría, es posible prevenir.
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Animales , Femenino , Embarazo , Ratas , Contaminantes Atmosféricos/toxicidad , Contaminación del Aire/efectos adversos , Pulmón/efectos de los fármacos , Humo/efectos adversos , Madera , Análisis de Varianza , Exposición Materna/efectos adversos , Modelos Animales de Enfermedad , Exposición a Riesgos Ambientales , Material Particulado/toxicidad , Feto/efectos de los fármacos , Calefacción , Pulmón/patologíaRESUMEN
SUMMARY: Studies in humans showed that prenatal exposure to urban air pollution (AP) influences fetal development, and increases the incidence of adverse pregnancy outcomes and some diseases in postnatal life. However, most of these were performed in environments where the main source of environmental particulate matters (PM) emission is diesel combustion by motor vehicles and industries, thereby ignoring the effects produced by wood smoke pollution. We hypothesized that morphological changes in the placenta could contribute to the reduction in fetal size associated with different periods of exposure to AP produced by wood smoke pollution prior to and during pregnancy. The objective of the study was to investigate the quantitative effects of long-term exposure to environmental levels of wood smoke pollution on the macroscopic and microscopic morphology of the placenta in rats. To test this, pregnant rats were exposed during pregestational and gestational periods to wood smoke pollution in indoor and outdoor environments. At 19 days of gestation, the placentas were obtained by caesarean and were prepared for histological, planimetric and stereological analysis. The volume and proportions of the placental compartments were estimated. In addition, stereological estimators in fetal capillaries were calculated in the labyrinth region. Crown rump length, fetus weight and litter weight were influenced by pregestational and gestational exposure periods. Exposure to wood smoke pollution during pregestational period has significant effect on the volume of the placenta, and consequently on fetal height. In conclusion, this study demonstrated that long-term outdoor exposure to wood smoke pollution from residential heating affects fetal health, decreasing the absolute volume of the entire placenta and the placental interface between the mother and fetus, decreasing the total volume of blood vessels present in the labyrinth region ofthe placenta and affecting the size of the fetus.
RESUMEN: Estudios en humanos demostraron que la exposición prenatal a la polución del aire urbano influye en el desarrollo fetal y aumenta la incidencia de resultados adversos de la gestación y algunas enfermedades postnatales. Sin embargo, la mayoría de ellos fueron realizados en entornos donde la principal fuente de emisión de material particulado, fue la combustión de petróleo por vehículos a motor e industrias, ignorando los efectos producidos por el humo de leña producido por la calefacción intradomiciliaria. Hipotetizamos respecto a que los cambios de la placenta contribuirían a la disminución del tamaño fetal relacionado a los períodos de exposición al humo de leña durante los periodos pregestacional y gestacional. El objetivo del estudio fue investigar los efectos cuantitativos de la exposición al humo de leña sobre la morfología macroscópica y microscópica en placenta de ratas. Para probar esto, ratas preñadas fueron expuestas durante los períodos pregestacional y gestacional a la contaminación por humo de leña en ambientes interiores y exteriores. A los 19 días de gestación, las placentas fueron obtenidas por cesárea y fueron preparadas para un análisis histológico, planimétrico y estereológico. Fue estimado el volumen absoluto y las proporciones de los compartimentos placentarios. Además, fueron calculados estimadores estereológicos en capilares fetales del laberinto y trofoblasto. La longitud, el peso del feto y el peso de la camada fueron influenciados por los períodos de exposición pregestacional y gestacional. La exposición a la contaminación por humo de leñá durante el período pregestacional tuvo un efecto significativo en el volumen de la placenta y, en consecuencia, en la altura del feto. En conclusión, este estudio demostró que la exposición a largo plazo al humo de leña afecta la salud del feto, disminuyendo el volumen absoluto de la placenta, además, afecta la interfaz placentaria entre la madre y feto, disminuyendo el volumen total de vasos sanguíneos presentes en la región del laberinto placentario y por consecuente afectando el tamaño del feto.
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Animales , Femenino , Embarazo , Ratas , Placenta/efectos de los fármacos , Humo/efectos adversos , Contaminantes Atmosféricos/toxicidad , Feto/efectos de los fármacos , Madera , Ratas Sprague-Dawley , Exposición Materna/efectos adversos , /efectos adversos , Tamaño Corporal , Desarrollo Fetal/efectos de los fármacos , Contaminación Ambiental/efectos adversos , Material ParticuladoRESUMEN
BACKGROUND: Household air pollution (HAP) is one of the most important environmental risk factors worldwide associated with chronic respiratory diseases. OBJECTIVES: The present study focused on respiratory health in a population with high wood smoke exposure in Nicaragua. METHODS: We employed a cross-sectional study with 213 participants. Data on the prevalence of chronic bronchitis (chronic bronchitis), chronic obstructive pulmonary disease (COPD) and asthma, including respiratory scores and pulmonary function tests, were documented. The role of risk factors for chronic bronchitis was analyzed. RESULTS: We found a high prevalence of chronic airway diseases in the population exposed to wood smoke. A higher prevalence of chronic bronchitis was found in persons serving as primary cooks in households. Further confounding factors for chronic bronchitis included age, a prior diagnosis of asthma, inhalational allergies and lower socioeconomic status. Respiratory scores were elevated in individuals with chronic bronchitis. CONCLUSIONS: This is one of the first studies in a wood smoke-exposed population in Nicaragua showing a high prevalence of chronic bronchitis and COPD with an emphasis on the analysis of personal and environmental risk factors. Further studies are needed to address which combination of interventions is most efficient for ameliorating respiratory health hazards. PARTICIPANT CONSENT: Obtained. ETHICS APPROVAL: The study protocol was approved by the Ethics Committee of the University of Luebeck, Germany (reference number 12-214), and by the Ethics Committee of the Department of Medical Sciences at National Autonomous University of Nicaragua, Managua, Nicaragua. COMPETING INTERESTS: The authors declare no competing financial interests.
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Lung cancer (LC), the leading cause of cancer-related deaths worldwide, is a complex and highly heterogeneous disease. Additional to its biological complexity, LC patients are often confronted with a high degree of stigma, mostly from the association of the disease with tobacco. Nonetheless, a proportion of LC patients are never-smokers, a population which we are beginning to comprehensively explore. Several risk factors have been linked to LC in never-smokers. Studies have consistently shown that radon exposure and domestic fuel smoke increase LC risk. Additionally, infections such as Mycobacterium tuberculosis, and Human Papilloma Virus are also risk factors. Other less conclusive associations include inflammatory diseases such as asthma and sarcoidosis. Moreover, we are now aware that molecular characteristics of LC vary widely according to smoking history, with important therapeutic implications. This review comprehensively assesses the current knowledge in terms of risk factors and disease characteristics in the never-smoker lung cancer population.
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Exposición a Riesgos Ambientales/efectos adversos , Contaminación por Humo de Tabaco/efectos adversos , Humanos , Neoplasias Pulmonares/etiología , Neoplasias Pulmonares/patología , Radón/efectos adversos , Factores de Riesgo , Fumar TabacoRESUMEN
BACKGROUND: The usefulness of C-reactive protein (CRP) as a non-specific marker of inflammation during pregnancy and lactation is unclear in impoverished populations where co-existing infections and vitamin deficiencies are common. METHODS: This cross-sectional study in Panama recruited 120 pregnant and 99 lactating Ngäbe-Buglé women from 14 communities in rural Panama. Obstetric history, indoor wood smoke exposure, fieldwork, BMI, vitamins A, B12, D, and folic acid, and inflammation markers (CRP, neutrophil/lymphocyte ratio (NLR), plateletcrit and cytokines) were measured. Multiple regressions explored both associations of CRP with other inflammatory markers and associations of CRP and elevated CRP based on trimester-specific cut-offs with maternal factors, infections and vitamin deficiencies. RESULTS: CRP was higher in pregnancy (51.4 ± 4.7 nmol/L) than lactation (27.8 ± 3.5 nmol/L) and was elevated above trimester specific cut-offs in 21% of pregnant and 30% of lactating women. Vitamin deficiencies were common (vitamin A 29.6%; vitamin D 68.5%; vitamin B12 68%; folic acid 25.5%) and over 50% of women had two or more concurrent deficiencies as well as multiple infections. Multiple regression models highlighted differences in variables associated with CRP between pregnancy and lactation. In pregnancy, CRP was positively associated with greater indoor wood smoke exposure, caries and hookworm and negatively associated with Ascaris and vaginal Lactobacillus and Bacteroides/Gardnerella scores. Consistent with this, greater wood smoke exposure, caries as well as higher diplococcal infection score increased the odds of trimester-elevated CRP concentrations whereas longer gestational age lowered the likelihood of a trimester-elevated CRP. During lactation, folic acid deficiency was associated with higher CRP whereas parity, number of eosinophils and Mobiluncus score were associated with lower CRP. Also, a higher BMI and Trichomonas vaginalis score increased the likelihood of an elevated CRP whereas higher parity and number of eosinophils were associated with lower likelihood of an elevated CRP. CONCLUSIONS: Infections both raise and lower CRP concentrations in pregnant and lactating mothers. Only folic acid deficiency during lactation was associated with higher CRP concentrations. Caution is required when interpreting CRP concentrations in pregnant and lactating women who have co-existing nutrient deficiencies and multiple infections.
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Avitaminosis/epidemiología , Proteína C-Reactiva/metabolismo , Enfermedades Transmisibles/epidemiología , Adolescente , Adulto , Avitaminosis/etiología , Enfermedades Transmisibles/etiología , Estudios Transversales , Femenino , Humanos , Indígenas Centroamericanos/estadística & datos numéricos , Lactancia , Panamá/epidemiología , Embarazo , Adulto JovenRESUMEN
BACKGROUND: Tobacco-smoke is the major etiological factor related to lung cancer. However, other important factor is chronic wood smoke exposure (WSE). Approximately 30 % of lung cancer patients in Mexico have a history of WSE, and present different clinical, pathological and molecular characteristics compared to tobacco related lung cancer, including differences in mutational profiles. There are several molecular alterations identified in WSE associated lung cancer, however most studies have focused on the analysis of changes in several pathogenesis related proteins. METHODS: Our group evaluated gene expression profiles of primary lung adenocarcinoma, from patients with history of WSE or tobacco exposure. Differential expression between these two groups were studied through gene expression microarrays. RESULTS: Results of the gene expression profiling revealed 57 statistically significant genes (p < 0.01). The associated biological functional pathways included: lipid metabolism, biochemistry of small molecules, molecular transport, cell morphology, function and maintenance. A highlight of our analysis is that three of the main functional networks represent 37 differentially expressed genes out of the 57 found. These hubs are related with ubiquitin C, GABA(A) receptor-associated like protein; and the PI3K/AKT and MEK/ERK signaling pathways. CONCLUSION: Our results reflect the intrinsic biology that sustains the development of adenocarcinoma related to WSE and show that there is a different gene expression profile of WSE associated lung adenocarcinoma compared to tobacco exposure, suggesting that they arise through different carcinogenic mechanisms, which may explain the clinical and mutation profile divergences between both lung adenocarcinomas.
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Adenocarcinoma/metabolismo , Neoplasias Pulmonares/metabolismo , Proteínas de Neoplasias/metabolismo , Hollín/envenenamiento , Contaminación por Humo de Tabaco/efectos adversos , Madera/efectos adversos , Adenocarcinoma/etiología , Exposición a Riesgos Ambientales , Femenino , Regulación Neoplásica de la Expresión Génica , Humanos , Neoplasias Pulmonares/etiología , Masculino , México/epidemiología , Persona de Mediana Edad , Prevalencia , Factores de Riesgo , TranscriptomaRESUMEN
BACKGROUND: Malignant mesothelioma is a neoplasm of bad prognosis, it is linked with asbestos contact, but there are cases without this antecedent. OBJECTIVE: To investigate the relationship of asbestos exposition and other factors with malignant mesothelioma. METHODS: Retrospective analysis of histologic confirmed cases of malignant mesothelioma, neoplasic familiar history, tobacco smoking, exposure to wood smoke and to asbestos, were annotated in a paired case/control study 1: 1-3 with logistic regression model to identify risk factors for OR. RESULTS: 61 cases of malignant mesothelioma were confirmed by histopathologic study, 41 male and 20 female. Mean age was 56 years ± 13 years; 56 cases (91.8%) correspond to epithelial malignant mesothelioma, three sarcomatous (4.9%) one desmoplastic and one biphasic. One in eight (13.1%) had exposure to asbestos. Model of logistic regression with four variables: history of familiar cancer, tobacco smoking, wood smoke and asbestos exposition, the the last one with an OR= 3.083 and p > 0.05. No other variables found to be a risk factor for malignant mesothelioma. CONCLUSIONS: Exposure to asbestos is a risk factor for malignant mesothelioma, which is confirmed in this study, however it is important to extend the investigation of other possible causal factors of this disease.
Antecedentes: el mesotelioma maligno es un tumor de mal pronóstico relacionado con el contacto con asbesto; sin embargo, existen numerosos casos sin este antecedente. Objetivo: describir la relación entre la exposición al asbesto y otros factores con el mesotelioma maligno. Material y métodos: estudio retrospectivo de casos y controles pareado 1: 1-3 por edad y sexo de pacientes con diagnóstico de mesotelioma maligno. Se registraron: la exposición al asbesto, tabaco, humo de leña y antecedentes familiares de cáncer. Se empleó regresión logística para razones de momios (ORs). Resultados: se estudiaron 61 casos con mesotelioma maligno, 41 hombres y 20 mujeres. La edad promedio fue 56 ± 13 años; 56 casos fueron mesotelioma maligno epitelial (91.8%), tres sarcomatosos (4.9%), uno desmoplásico y uno bifásico. Sólo en 8 (13.1%) se identificó exposición al asbesto. En el modelo de regresión logística el asbesto tuvo una razón de momios de 3.083 p > 0.05. Ninguna otra variable resultó ser un factor de riesgo para mesotelioma maligno. Conclusiones: la exposición al asbesto es un factor de riesgo para mesotelioma maligno, lo que se confirma en este estudio; sin embargo, es importante ampliar la investigación de otros posibles factores causales de esta enfermedad.
Asunto(s)
Neoplasias Pulmonares/etiología , Mesotelioma/etiología , Neoplasias Pleurales/etiología , Adulto , Anciano , Amianto/efectos adversos , Exposición a Riesgos Ambientales , Femenino , Hospitales Generales/estadística & datos numéricos , Humanos , Neoplasias Pulmonares/diagnóstico por imagen , Neoplasias Pulmonares/patología , Masculino , Mesotelioma/diagnóstico por imagen , Mesotelioma/patología , Mesotelioma Maligno , Persona de Mediana Edad , Síndromes Neoplásicos Hereditarios/epidemiología , Enfermedades Profesionales/etiología , Enfermedades Profesionales/patología , Neoplasias Pleurales/diagnóstico por imagen , Neoplasias Pleurales/patología , Estudios Retrospectivos , Factores de Riesgo , Población Rural/estadística & datos numéricos , Humo/efectos adversos , Fumar/efectos adversos , Fumar/epidemiología , Nicotiana , Tomografía Computarizada por Rayos X , Población Urbana/estadística & datos numéricos , MaderaRESUMEN
PURPOSE: Chronic obstructive pulmonary disease (COPD) related to wood smoke exposure is characterized by important inflammation of the central and peripheral airways without significant emphysema. The objective of this study is to describe the bronchial hyperresponsiveness (BHR) level in women with COPD related to wood smoke exposure and to compare it with the BHR in women with COPD related to tobacco smoking. MATERIALS AND METHODS: TWO GROUPS OF WOMEN WITH STABLE COPD WERE STUDIED: (1) wood smoke exposed (WS-COPD); and (2) tobacco smoke exposed (TS-COPD). A methacholine challenge test (MCT) was performed in all patients according to American Thoracic Society criteria. BHR levels were compared using the methacholine concentration, which caused a 20% fall in the FEV1 (PC20). RESULTS: Thirty-one patients, 19 with WS-COPD and 12 with TS-COPD, were included. There were no significant differences between the groups in baseline FVC, FEV1, IC, FEF25-75, and FEF25-75/FVC. All 31 patients had a positive MCT (PC20<16 mg/mL) and the fall in the FEV1 and IC was similar in both groups. The severity of BHR was significantly higher in the WS-COPD patients (PC20: 0.39 mg/mL) than in the TS-COPD patients (PC20: 1.24 mg/mL) (P=0.028). The presence of cough, phlegm, and dyspnea during the test were similar in both groups. CONCLUSION: We found moderate to severe BHR in women with WS-COPD, which was more severe than in the TS-COPD women with similar age and airflow obstruction. This paper suggests that the structural and inflammatory changes induced by the chronic exposure to wood smoke, described in other studies, can explain the differences with TS-COPD patients. Future studies may clarify our understanding of the impact of BHR on COPD physiopathology, phenotypes, and treatment strategies.
Asunto(s)
Hiperreactividad Bronquial/fisiopatología , Enfermedad Pulmonar Obstructiva Crónica/fisiopatología , Humo/efectos adversos , Madera , Anciano , Anciano de 80 o más Años , Hiperreactividad Bronquial/etiología , Colombia , Estudios Transversales , Femenino , Humanos , Persona de Mediana Edad , Enfermedad Pulmonar Obstructiva Crónica/etiología , Pruebas de Función Respiratoria , Índice de Severidad de la Enfermedad , Contaminación por Humo de Tabaco/efectos adversosRESUMEN
La enfermedad pulmonar obstructiva crónica (EPOC) es una de las enfermedades más frecuentes a nivel mundial, cuya prevalencia está en aumento y representa una enormecarga de salud para la sociedad. En América Latina, las cifras estimadas de prevalencia varían entre el 7.8% y 19.7%. Si bien el humo de cigarrillo es el factor de riesgo más importante para el desarrollo de esta enfermedad, la exposición al humo de combustiblesde biomasa, especialmente leña, dentro del hogar, para cocinar y calefaccionar, es también una causa relevante aunque poco reconocida de EPOC en los países en vías de desarrollo. Teniendo en cuenta que la mitad de la población mundial, unos 3 mil millones de personas, utilizan combustibles de este tipo, el impacto que pudiera tener sobre la salud de la población expuesta, es un tema de especial consideración.
Chronic Obstructive Pulmonary Disease (COPD) is a leading cause of morbidity and mortality worldwide that is increasing and which represents a substantial economic and social burden. The prevalence of COPD in Latin America ranges from 7.8% to 19.7%.Although smoking tobacco is the leading cause in developing COPD, the use of biomass fuels for cooking or heating is also an important cause of this disease, particularly in developing countries. As half of the world population, around 3 thousand million people, use solid fuels, the impact that the use of such fuels could have on the health of theaffected population is an issue that deserves specific consideration.