Helicobacter pylori: Microorganismo patógeno o mutualista en poblaciones colombianas / Helicobacter pylori: Pathogenic or mutualistic microorganism in Colombian populations / Helicobacter pylori: microrganismo patógeno ou mutualista em populações Colombianas

Introducción: El riesgo de desarrollar cáncer gástrico varía entre continentes, países y regiones. A pesar de que existe una alta prevalencia de Helicobacter pylori su rol como patógeno o mutualista define el riesgo de cáncer gástrico en las regiones de Colombia. Objetivo: Discutir el rol de Helicobacter pylori en el riesgo de cáncer gástrico en Colombia. Materiales y métodos: Revisión de literatura mediante la búsqueda, en las bases de datos LILACS, SciELO, PubMed. Resultados: La coevolución del humano y de Helicobacter pylori; la virulencia de genes cagA, vacA; el tipo de respuesta inmune inflamatoria a Helicobacter pylori (Th1) o antinflamatoria (Th2) y la susceptibilidad humana a cáncer gástrico (IL1β, IL10), junto a la dieta y factores ambientales explican el papel de Helicobacter pylori como patógeno o mutualista asociado al riesgo de cáncer gástrico en Colombia. Conclusiones: Helicobacter pylori tiene un rol mutualista principalmente en poblaciones de bajo riesgo de cáncer gástrico (costas), no obstante, en poblaciones con alto riesgo de cáncer gástrico (andes), su papel como patógeno amerita la erradicación; única estrategia para mitigar la alta incidencia de este cáncer en Colombia.

Introduction: The risk to develop gastric cancer varies between continents, countries and regions. Although there is a high prevalence of Helicobater pylori, its role as either pathogen or mutualistic bacteria defines the risk of gastric cancer in Colombian regions. Objective: To discuss the role of Helicobacter pylori in the risk of gastric cancer in Colombia. Materials and methods: A literature review based on searching LILACS, SciELO, and PubMed databases. Results: Helicobacter pylori role as either a pathogen or mutualistic microorganism associated with gastric cancer risk in Colombia can be explained by analyzing elements such as: human and Helicobacter pylori coevolution; cagA and vacA gene virulence; inflammatory (Th1) or anti-inflammatory (Th2) responses induced by Helicobacter pylori; human susceptibility to gastric cancer (IL1β, IL10); diet; and environmental factors. Conclusions: Even though Helicobacter pylori has a mutualistic role in populations at low gastric cancer risk (coastal regions), its role as a pathogen in populations at higher risk (Andean regions) justifies its eradication as a key strategy to mitigate the incidence of this cancer in Colombia.

Introdução: O risco de desenvolver câncer gástrico varia entre continentes, países e regiões. Embora haja uma alta prevalência de Helicobacter pylori, seu papel como patógeno ou mutualista define o risco de câncer gástrico nas regiões da Colômbia. Objetivo: Discutir o papel do Helicobacter pylori no risco de câncer gástrico na Colômbia. Materiais e métodos: Revisão da literatura por meio da busca, nas bases de dados LILACS, SciELO e PubMed. Resultados: A coevolução de humanos e Helicobacter pylori; a virulência dos genes cagA, vacA; o tipo de resposta imune inflamatória ao Helicobacter pylori (Th1) ou anti-inflamatório (Th2) e a suscetibilidade humana ao câncer gástrico (IL1β, IL10), juntamente com a dieta e fatores ambientais explicam o papel do Helicobacter pylori como patógeno ou mutualista associado ao risco de câncer gástrico na Colômbia. Conclusões: Helicobacter pylori tem um papel mutualista principalmente em populações de baixo risco de câncer gástrico (litoral), porém, em populações com alto risco de câncer gástrico (andes), seu papel como patógeno justifica a erradicação; única estratégia para mitigar a alta incidência deste câncer na Colômbia.

Quantitative risk assessment of occupational exposure to PCDD/Fs in the waste incineration industry / 中华劳动卫生职业病杂志

Objective: To analyze the level of PCDD/Fs exposure of occupational workers in the waste incineration industry and explore the risk of occupational exposure. Methods: In September 2021, literature on environmental PCDD/Fs exposure in waste incineration plants published from the establishment of the database to February 10, 2021 was retrieved from CNKI database. A total of 1365 literatures were retrieved, and 7 met the criteria for inclusion. The US Environmental Protection Agency (EPA) inhalation risk model was used to assess and analyze carcinogenic and non-carcinogenic risks of PCDD/Fs exposure among occupational workers in the waste incineration industry. Results: A total of 86 sampling sites were included in incineration plants in 7 regions. The study of Wuhan area showed that the concentration of working environment near the waste incinerator in the same factory was the highest, followed by the rest and office area in the factory. The concentration of PCDD/Fs in waste incinerators was the highest in Southwest China (4880.00-24880.00 pg TEQ/m(3)), and the lowest in Shenzhen (0.02-0.44 pg TEQ/m(3)). According to the cancer risk assessment, with the increase of exposure years, the risk of cancer increased. The highest risk of cancer was found in the waste incineration plants in Southwest China. When the exposure period was 1 year, the risk was moderate (22.40×10(-6)-114.20×10(-6)). When the exposure time was more than 5 years, the risk of cancer was high. In Jinan, workers working near the incinerator had a moderate risk of cancer after five years of exposure. In Zhejiang, workers were at medium risk of cancer after exposure for more than 20 years. Workers in Wuhan, Shanghai, Zhejiang Province, Shenzhen and the Pearl River Delta were still at low risk of cancer after 40 years of occupational exposure. HQ>1 of workers working near the waste incinerators in Jinan, Zhejiang Province and Southwest China, and the qualitative evaluation results showed that the non-carcinogenic risk was unacceptable. Conclusion: There are great differences in PCDD/Fs of occupational exposure in waste incineration industry, and the occupational exposure exceeding the occupational exposure limit has higher carcinogenic and non carcinogenic risks.

Experimental carcinogenesis with 7, 12-dimethylbenz(a)anthrazene (DMBA) and its inhibition with isothi-ocyanates / Carcinogénesis experimental con 7, 12-dimetilbenzantraceno (DMBA) y su inhibición con isitiocianatos

Introduction: DMBA is a chemical carcinogen that induces carcinomas within a few weeks of its application. We developed an experimental model of carcinogenesis induced by DMBA dissolved in 0,5% paraffin oil (DMBA-PO), verifying the inhibitory effect of the carcinogenicity of phenyl isothiocyanate (PhITC), phenethyl (PhnITC) and benzyl isothiocyanate (BITC). Material and Methods: For this, 88 hamsters were distributed into three groups: one exposed to DMBA-PO (Group 1, n=12), three subgroups (n=12) exposed to PhITC, PhnITC, BITC and DMBA-PO (Group 2, n=36) and four control subgroups (n=10) that were not exposed to the carcinogen in which PO (paraffin oil) and isothiocyanates were applied (Group 3, n=40). Results: The experiment had a duration of 20 weeks, at the end of which the inhibitory effect was established by comparing the lesions developed in the groups that received isothiocyanates with the group that was only treated with DMBA-PO. The carcinogenic effect of DMBA-PO is 100% (35 carcinomas) and the inhibitory effect was 0, whereas in the presence of isothiocyanates the carcinogenic effect decreases, with an inhibitory effect of 86% for BITC (5 carcinomas) and 74% for PhITC (9 carcinomas). Conclusion: The inhibitory effect for PhnITC is 80% in relation to invasive OSCC (1 carcinoma).

Introducción: El DMBA es un carcinógeno químico que induce carcinomas a las pocas semanas de su aplicación. Desarrollamos un modelo experimental de carcinogénesis inducida por DMBA disuelto en aceite de parafina al 0,5% (DMBA-Ap) comprobando el efecto inhibidor de la carcinogénesis de los isotiocianatos fenil (PhITC), fenetil (PhnITC) y bencil isotiocianato (BITC). Material y Métodos: Para ello, se distribuyeron 88 hámsteres en 3 grupos: uno expuesto al DMBA-Ap (Grupo 1, n=12), tres subgrupos (n=12) expuestos a PhITC, PhnITC, BITC y DMBA-Ap (Grupo 2, n=36) y cuatro subgrupos controles (n=10), no expuestos al carcinógeno en el que se aplicaron Ap e isotiocianatos (Grupo 3, n=40). Resultados:El experimento tuvo una duración de 20 semanas, al final de la cual se establece de forma comparativa el efecto inhibidor comparando las lesiones desarrolladas en los grupos que recibieron isotiocianatos con respecto al grupo tratado sólo con DMBA-Ap. El efecto carcinógeno del DMBA-Ap es del 100% (35 carcinomas) y el efecto inhibidor 0, mientras que en presencia de isotiocianatos el efecto carcinógeno disminuye, con un efecto inhibidor del 86% para BITC (5 carcinomas) y del 74% para el PhITC (9 carcinomas). Conclusión:El efecto inhibidor del PhnITC es del 80% en relación con el COCE invasivo (1 carcinoma).

Helicobacter pylori: novedades, genes de virulencia y resistencia a los antibióticos en Colombia / Helicobacter pylori: novelties, virulence genes and antibiotic resistance in Colombia / Helicobacter pylori: novidades, genes de virulência e resistência aos antibióticos na Colômbia

Helicobacter pylori es un carcinógeno tipo I resistente a múltiples antibióticos y con alta prioridad en salud pública. La infección por este microorganismo está influenciada por una interacción compleja entre la genética del huésped, el entorno y múltiples factores de virulencia de la cepa infectante. Afecta al 50 % de la población mundial, provocando afecciones gastroduodenales graves, la mayoría de forma asintomática. El 20 % de los individuos con H. pylori pueden desarrollar a través del tiempo lesiones gástricas preneoplásicas y el 2 % de ellos un cáncer gástrico. Las manifestaciones clínicas gastrointestinales y extragastrointestinales están asociadas a su virulencia y a la respuesta del sistema inmunológico con la liberación de citosinas proinflamatorias, tales como TNF-alfa, IL-6, IL-10 e IL-8, causantes de inflamación aguda y crónica. Múltiples factores de virulencia han sido estudiados como el gen A asociado a la citotoxina (CagA) y la citotoxina vacuolante (VacA), los cuales juegan un rol importante en la aparición del cáncer gástrico. Dada la resistencia cada vez mayor a los antibióticos utilizados, las líneas de estudio en el futuro inmediato deben estar encaminadas en establecer la utilidad de los nuevos antibióticos y la determinación de profagos colombianos en todo el país. Esta revisión tiene como objetivo hacer una puesta al día sobre las características del H. pylori, los mecanismos patogénicos, genes de virulencia, su asociación con el mayor riesgo de cáncer gástrico, farmacorresistencia microbiana y su erradicación.

Helicobacter pylori is recognized as a class I carcinogen resistant to multiple antibiotics and with high priority in public health. The infection caused by this microorganism is influenced by a complex interaction between host genetics, environment, and multiple virulence factors of the infecting strain. It affects 50% of the world population, causing severe gastroduodenal conditions, most of them asymptomatic. Through time, 20% of individuals with H. pylori may develop preneoplastic gastric lesions and 2% of them develop gastric cancer. The gastrointestinal and extra-gastrointestinal clinical manifestations are associated with its virulence and the response of the immune system with the release of pro-inflammatory cytokines, such as TNF-alpha, IL-6, IL-10 and IL-8, which cause acute and chronic inflammation. Multiple virulence factors have been studied, such as cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA), which play an important role in the development of gastric cancer. Due to the increasing antibiotics resistance, the research in the immediate future should be aimed at establishing the usefulness of the new antibiotics and the determination of Colombian prophages throughout the country. This paper aims to update the characteristics of H. pylori, its pathogenic mechanisms, virulence genes, its association with the increased risk of gastric cancer, microbial drug resistance, and eradication.

Helicobacter pylorié um carcinógeno tipo I resistente a múltiplos antibióticos e com alta prioridade na saúde pública. A infecção por este microrganismo está influenciada por uma interação complexa entre a genética do hospede, o entorno e múltiplos fatores de virulência da cepa infectante. Afeta a 50% da população mundial, provocando afeções gastroduodenais graves, a maioria de forma assintomática. 20% dos indivíduos com H. pylori podem desenvolver através do tempo lesões gástricas pré-neoplásicas e 2% deles um câncer gástrico. As manifestações clínicas gastrointestinais e extragastrointestinais estão associadas à sua virulência e à resposta do sistema imunológico com a liberação de citocinas pró-inflamatórias, tais como TNF-alfa, IL-6, IL-10 e IL-8, causantes de inflamação aguda e crónica. Múltiplos fatores de virulência hão sido estudados como o gene. A associado à citotoxina (CagA) e a citotoxina vacuolante (VacA), os quais jogam um papel importante no aparecimento do câncer gástrico. Dada a resistência cada vez maior aos antibióticos utilizados, as linhas de estudo no futuro imediato devem estar encaminhadas em estabelecer a utilidade dos novos antibióticos e a determinaçãode profagos colombianos em todo o país. Esta revisão tem como objetivo fazer uma atualização sobre as características do H. pylori, os mecanismos patogénicos, genes de virulência, sua associação com o maior risco de câncer gástrico, farmacorresistência microbiana e sua erradicação.

Pollution characteristics, source analysis, and risk assessment of metal and metalloid in PM2.5 of Shijiazhuang city / 中华预防医学杂志

In 2020, the mass concentration of PM2.5 in Shijiazhuang urban area was(80.30±71.43)μg/m3. The Spearman correlation analysis between metals and metalloids showed that Sb with Cd, Pb, Ni, Se, Cd with Pb, Ni, Se, Pb with Ni, Se, Ni with Se, and Se with Tl were positively correlated, with a coefficient greater than 0.5. The main sources of metals and metalloids of PM2.5 were traffic emissions, fuel combustion, metal smelting and dust. The HQ values of Pb, Hg and Mn for each population were less than 1, with lower non-carcinogenic risk. The R values of carcinogenic risk of Ni and Cd in each population were less than 1×10-6, which could be acceptable risk level for the population. The R values of carcinogenic risk of As and Cr in different populations were between 1×10-6 and 1×10-4, with potential carcinogenic risk, particularly higher in adult males.

Carcinoma urotelial del tracto urinario superior: a propósito de un caso y revisión de la literatura / Upper urinary tract urothelial carcinoma: case report and review of the literature

El carcinoma urotelial (CU) del tracto urinario superior es infrecuente y representa solo del 5%-10% de todos los CU. Estas neoplasias crecen a partir del urotelio de los cálices renales hasta el tercio distal del uréter. Se reporta el caso de un paciente masculino de 68 años de edad quien presenta enfermedad actual de 3 meses de evolución caracterizada por dolor lumbar izquierdo, tipo cólico, de leve a moderada intensidad, el cual atenúa parcialmente con el uso de AINES, asociado a hematuria visible total de predominio nocturno. El uroanálisis mostró hematuria macroscópica y la citología urinaria evidenció atipias sugerentes de carcinoma. La TAC abdomino-pélvica contrastada evidenció un defecto de llenado en relación al cáliz inferior de riñón izquierdo y plastrón ganglionar paraaórtico izquierdo. Se practicó nefroureterectomía radical izquierda evidenciando tumor de 3 x 3 x 1 cm en relación a pelvis renal extensiva a cáliz inferior invadiendo parénquima renal. El estudio histopatológico mostró un carcinoma urotelial papilar infiltrativo de alto grado con márgenes sin lesiones y ganglios linfáticos con metástasis. El paciente evoluciona satisfactoriamente durante el período postoperatorio y actualmente recibe terapia adyuvante. A pesar de ser una patología poco frecuente, puede presentarse y el urólogo debe estar en capacidad para poder enfrentarla(AU)

Upper urinary tract urothelial carcinoma (UC) is infrequent and represents only 5%-10% of all UCs. These neoplasms grow from the urothelium of renal calyces to the distal third of the ureter. A case of UC of the upper urinary tract is reported in a 68-year-old male patient with a 3-month history of left lumbar mild to moderate pain, which partially mitigates with the use of NSAIDs associated with visible total predominantly nocturnal hematuria. Macroscopic hematuria was evident and urinary cytology reported carcinoma suggestive atypias. Contrasted CT of abdomen and pelvis showed filling defect in relation to lower calyx of the left kidney and left para-aortic ganglion plastron. Radical left nephroureterectomy was performed showing a 3 x 3 x 1 cm tumor in relation to the renal pelvis extending to the lower cavity and invading renal parenchyma. Histopathology showed high grade infiltrative papillary CU with margins without lesions and lymph nodes with metastasis. Patient evolves satisfactorily in the postoperative period and is currently in adjuvant therapy. Although this pathology is rare, it can occur and the urologist must be able to face it(AU)

Revisión: Factores asociados a cáncer colorrectal / Review: Associated factors with colorectal cancer

Resumen Introducción: El cáncer colorrectal (CCR) es la neoplasia de mayor frecuencia en vías digestivas, constituyendo del 9 al 10% de todos los cánceres en el mundo. Se considera que es multicausal, pues abarca factores intrínsecos del huésped como mutaciones genéticas, hormonales y condiciones inmunológicas; además de factores externos como dietas poco saludables, consumo de alcohol, obesidad, sedentarismo, tabaquismo y la exposición ambiental a carcinógenos. Las manifestaciones clínicas son poco específicas, razón por la cual el diagnóstico está enfocado en grupos de riesgo relacionados con la edad e historia familiar demostrada. Objetivo: Identificar los factores genéticos y de estilos de vida predisponentes al desarrollo de CCR. Metodología: Se realizó una búsqueda de la bibliografía respectiva en las bases de datos ScienceDirect, Google académico, Redalyc, Scielo, Proquest publicada durante el período 2004- 2019, mediante las palabras clave: Colorrectal cancer, risk factors, epidemiology, mortality, mutation, incidence. Resultados: Se observaron factores genéticos predisponentes entre un 20% a 25% de las personas con CCR asociados principalmente con la mutación de gen APC. En relación al cáncer esporádico, se identifica hasta en un 80% de los casos, relacionado con el consumo no controlado de alimentos como carnes rojas, embutidos, café, además de hábitos como el consumo de cigarrillo y alcohol conjuntamente con el estrés y comorbilidades como la obesidad y la diabetes. Conclusión: La multicausalidad del CCR está centrada en factores tanto internos como externos siendo de relevancia el seguimiento para personas genéticamente predispuestas y la implementación de estilos de vida saludables que reduzcan la mortalidad por esta causa.

Abstract Introduction: Colorectal cancer (CRC) is the most frequent neoplasm in the digestive tract; it constitutes 9 of 10% of all cancer cases in the world. This type of cancer is considered multicausal since it is associated with intrinsic and extrinsic factors. Among the internal factors, there are genetic, hormonal mutations, and immunological conditions. On the other hand, the external factors are composed of unhealthy diets, alcohol consumption, obesity, sedentary lifestyle, smoking habits, and environmental exposure to carcinogens. The clinical symptoms are not very specific; that is why the diagnosis is focused on risk groups related to age and proven family medical history. Objective: To identify genetic factors and lifestyle factors related to the development of Colorectal cancer (CRC). Methodology: A literature search was carried out in databases such as ScienceDirect, Google Scholar, Redalyc, Scielo, Proquest, in a range of time between 2004 and 2019. The keywords: colorectal cancer, risk factors, epidemiology, mortality, mutation, and incidence were used as helpers for the search. Results: Predisposing genetic factors were observed in about 20% to 25% of people with CRC associated primarily with the APC gene mutation. In terms of sporadic cancer, the results showed that 80% of the cases were related to the uncontrolled consumption of red meat, sausages, and coffee. Additionally, smoking and alcoholic behaviors, stress, and comorbidities, such as obesity and diabetes, were also the cause of the development of this issue. Conclusion: CRC could be caused by internal and external factors. Based on this, the people with a genetic predisposition to this issue should monitor themselves frequently and implement a healthy lifestyle that reduces the probability of suffering from this type of cancer.

Biomarkers of susceptibility and effect in car painters exposed to organic solvents / Biomarcadores de susceptibilidad y efecto en pintores de carros expuestos a solventes orgánicos

Abstract Introduction: Car painters are routinely exposed to organic solvents classified as carcinogenic and mutagenic substances. Objective: To characterize the population susceptibility and evaluate the genotoxic effects of exposure to organic solvents. Methods: A cross-sectional study comparing a group of car painters exposed to organic solvents with a non-exposed group. CYP2E1 polymorphisms and the presence of micronuclei in lymphocytes were determined. Results: One hundred twenty-two workers participated in the study: 62 who worked in car paint shops and were exposed to solvents, and 60 who were not exposed. There were statistically significant differences between the two groups regarding micronucleated cells and nucleoplasmic bridges frequencies (p=0.042 and p=0.046, respectively; exact likelihood ratio). Significant differences were found at the interaction between the CYP2E1 genotype c1c1 and occupational exposure to solvents, with higher frequencies of micronuclei (p= 0.013) and micronucleated cells (p= 0.015). However, when the frequencies of micronuclei, micronucleated cells and nucleoplasmic bridges in the exposure group were compared between the c1c1 and c2c2/c1c2 allele groups of the CYP2E1 polymorphism, statistically significant differences were found. Conclusions: This study confirms that when workers with CYP2E1 polymorphisms, specifically the c1c1 genotype, are exposed to organic solvents, they are more likely to have somatic cell mutations, a condition associated with increased susceptibility to diseases such as cancer

Resumen Introducción: Los pintores de vehículos automotores están rutinariamente expuestos a agentes como los solventes orgánicos, capaces de producir efectos mutágenos y carcinógenos. Objetivo: Caracterizar la susceptibilidad poblacional y evaluar los efectos genotóxicos debidos a la exposición a solventes orgánicos. Métodos: Estudio de corte transversal que comparó a un grupo de pintores de carros expuestos a solven tes orgánicos con un grupo de personas no expuestas. Fueron determinados tanto los polimorfismos de CYP2E1 como la presencia de micronúcleos en linfocitos. Resultados: Participaron 122 personas, 62 trabajadores de talleres de pintura de autos expuestos a solventes y 60 personas no expuestas. Con relación al cuestionario Q 16, 32% de los expuestos refirieron síntomas sugestivos de neurotoxicidad. Las frecuencias de células micronucleadas y de puentes nucleoplásmicos fueron significativamente mayores en los expuestos que en los no expuestos: p= 0.042 y p= 0.046, respectivamente, Razón de verosimilitud exacta). Fueron halladas diferencias significativas en la interacción de CYP2E1 (c1c1) y la exposición ocupacional a solventes, con mayores frecuencias de micronúcleos (p= 0.013) y de células micronucleadas (p= 0.015). Conclusiones: Este estudio reafirma que los trabajadores expuestos a solventes orgánicos con polimorfismos de CYP2E1, específicamente con genotipo c1c1, tienen mayor probabilidad de presentar mutaciones en las células somáticas, condición asociada con una mayor susceptibilidad a enfermedades como el cáncer

Lung cancer related to occupational exposure: an integrative review / Cáncer de pulmón relacionado con la exposición ocupacional: revisión integrativa / Câncer de pulmão relacionado à exposição ocupacional: revisão integrativa

ABSTRACT Objective: To identify in the literature the carcinogenic agents found in the work environment, the occupations and the risk for lung cancer. Method: A descriptive and analytical study of the Integrative Literature Review type was carried out in national and international databases from the last ten years in the period from 2009 to 2018, concerning 32 studies referring to association between carcinogenic substances to which the worker is exposed and lung cancer. Results: Nine (28.1%) publications originated in China and only one in Brazil. The most exposed workers were from the secondary sector, 50% being from industry and 6.2% from construction, mostly male. Asbestos and silica stood out among the carcinogenic substances most associated with lung cancer risk, accounting for 37.5% and 28.1%, respectively. Conclusions: The association between occupational exposure and the risk for lung cancer was characterized in this research by the substantial scientific evidence from the described studies that confirm this association.

RESUMEN Objetivo: Identificar en la literatura los agentes cancerígenos presentes en el entorno laboral, las ocupaciones y el riesgo de cáncer de pulmón. Método: Estudio descriptivo y analítico de una revisión integradora realizada en una base de datos nacional e internacional de los últimos diez años, entre 2009 y 2018, que comprende 32 estudios referidos a la vinculación entre el cáncer de pulmón y las sustancias cancerígenas de exposición ocupacional. Resultados: Nueve (28,1%) publicaciones tuvieron su origen en China y solo una en Brasil. Los trabajadores más expuestos pertenecían al sector secundario, el 50% a la industria y un 6,2% a la construcción, siendo en su mayoría hombres. El asbesto y la sílice se destacaron entre las sustancias cancerígenas más asociadas con el riesgo de cáncer de pulmón, con índices de 37,5% y el 28,1%, respectivamente. Conclusiones: La vinculación entre la exposición ocupacional y el riesgo de cáncer de pulmón se caracterizó en esta investigación por la evidencia científica sustancial de los estudios descriptos que confirman esta asociación.

RESUMO Objetivo: Identificar na literatura os agentes carcinogênicos presentes no ambiente ocupacional, as ocupações e o risco do câncer de pulmão. Método: Estudo descritivo e analítico de revisão integrativa realizada em base de dados nacionais e internacionais dos últimos dez anos, entre 2009 e 2018, compreendendo 32 estudos referentes à associação entre câncer de pulmão e substâncias carcinogênicas de exposição ocupacional. Resultados: Nove (28,1%) publicações originadas na China e apenas uma brasileira. Os trabalhadores mais expostos foram do setor secundário, sendo 50% da indústria e 6,2% da construção civil, em sua maioria do sexo masculino. O amianto e a sílica sobressaíram-se entre as substâncias carcinogênicas mais associadas ao risco de câncer de pulmão correspondendo a 37,5% e 28,1%, respectivamente. Conclusões: A associação entre a exposição ocupacional e o risco de câncer de pulmão ficou caracterizada nesta pesquisa pelas substanciais evidências científicas dos estudos descritos que confirmam essa associação.

Carcinógenos ambientales asociados a cáncer infantil / Environmental carcinogens associated with childhood cancer

Resumen Introducción: La Sociedad Americana de Cáncer indica que al año se diagnostican 163.300 casos de cáncer infantil en el mundo. En Colombia fueron reportadas 300 muertes por esta causa en menores de edad durante el año 2015. Actualmente, las principales asociaciones etiológicas de cáncer infantil son la radiación ionizante y exposición a pesticidas, convirtiéndose en una prioridad emergente en la agenda mundial de salud infantil. Objetivo: Identificar factores carcinogénicos asociados al incremento de riesgo en la aparición de cáncer infantil. Materiales y métodos: Se realizó una revisión de artículos científicos en inglés y español en la base de datos PubMed, ScienceDirect, SciELO, y publicaciones estadísticas de la Organización Mundial de la Salud, Asociación Americana de Cáncer y el Instituto Nacional de Cancerología de Colombia. Resultados: Se describieron diferentes factores carcinogénicos como radiación ionizante, agentes biológicos, patrones dietéticos, exposición a pesticidas, tabaco y asbesto, destacando su asociación en el desarrollo de cáncer infantil. Conclusión: El reconocimiento de los agentes carcinogénicos frecuentemente asociados con cáncer infantil, permite identificar el impacto de estos sobre la salud, y generar medidas preventivas más eficaces que puedan reducir la carga global de la enfermedad.

Abstract Introduction: The American Cancer Society indicates that each year 163,300 cases of childhood cancer are diagnosed worldwide. In Colombia, 300 deaths were reported from this cause in minors during 2015. Currently, the main etiological associations of childhood cancer are ionizing radiation and exposure to pesticides, making it an emerging priority in the global agenda for children's health. Objective: To identify carcinogenic factors associated with the increased risk in the onset of childhood cancer. Materials and methods: A review of scientific articles in English and Spanish was carried out in PubMed, ScienceDirect, SciELO, and statistical publications of the World Health Organization, American Cancer Association and the National Cancer Institute of Colombia. Results: Different carcinogenic factors were described as ionizing radiation, biological agents, dietary patterns, exposure to pesticides, tobacco and asbestos, highlighting their association in the development of childhood cancer. Conclusion: The recognition of the carcinogenic agents frequently associated with childhood cancer, allows the identification of their impact on health, and generates more effective preventive measures that can reduce the worldwide burden of the disease.

Effect of Arrabidaea chica extract against chemically induced breast cancer in animal model

Abstract Purpose: To examine the effects of Arrabidaa chica (Bignoniacea) extract, a native plant of the Amazon known as crajiru, on a 7,12-dimethyl-1,2-benzanthracene (DMBA)-induced breast cancer model in Wistar rats. Methods: We compared the response of breast cancer to the oral administration of A. chica extract (ACE) for 16 weeks, associated or not with vincristine. Groups: normal control; DMBA (50mg/kg v.o,) without treatment; DMBA+ACE (300 mg/kg); DMBA+vincristine. 500μg/kg injected i.p; DMBA+ACE+Vincristine 250μg/kg i.p. Imaging by microPET and fluorescence, biochemistry, oxidative stress, hematology and histopathology were used to validate the treatments. Results: All animals survived. A gradual weight gain in all groups was observed, with no significant difference (p>0.05). The oral administration of ACE and ACE+vincristine 50% significantly reduced breast tumors incidence examined with PET-18FDG and fluorescence (p<0.001). Significant reduction of serum transaminases, oxidative stress and hematological toxicity were observed in these groups. Antioxidant enzyme levels in breast tissue were significantly higher compared to the DMBA and DMBA+vincristine groups. Conclusion: These results demonstrate for the first time that ACE positively influences the treatment of DMBA-induced breast cancer in animal model, inducing a reduction in oxidative stress and chemotherapy toxicity, meaning that ACE may have clinical implication in further studies.

Pollution in the Americas: a leading cause of disease burden and an opportunity for cancer prevention / Contaminación en las Américas: causa principal de carga de la enfermedad y una oportunidad para prevención del cáncer

Abstract: Objective: Environmental and occupational agents are causes of cancer and disease worldwide while their control and the reduction of the associated disease burden remains complex. Materials and methods: This paper summarizes the current status of the burden of environmental and occupational causes of disease in the Americas based on presentations from a panel on environment, occupation and other environmental risk factors for cancer in the Americas, delivered in Panama, at the international conference Promoting Health Equity and Transnational Collaborations for the Prevention and Control of Cancer in the Americas. Results: Three case studies are presented to illustrate the impact of specific environmental and occupational agents and the challenge of control. Conclusions: There are still fully avoidable exposures to carcinogens, as well documented in the case of asbestos in Brazil. Thus, there are abundant targets for intervention to reduce cancer in the Americas.

Resumen: Objetivo: Los agentes ambientales y ocupacionales son causas de cáncer y enfermedades en todo el mundo, mientras que su control y reducción de la carga de enfermedad asociada siguen siendo puntos complejos. Material y métodos: Este documento resume el estado actual de la carga de las causas ambientales y ocupacionales de las enfermedades en las Américas a partir de las presentaciones de un panel sobre medio ambiente, ocupación y otros factores de riesgo ambientales para el cáncer en las Américas, realizado en Panamá, en la conferencia internacional Promoviendo la Equidad en Salud y las Colaboraciones Transnacionales para la Prevención y el Control del Cáncer en las Américas. Resultados: Se presentan tres estudios de caso para ilustrar el impacto de agentes ambientales y ocupacionales específicos y el desafío del control. Conclusiones: Todavía hay exposiciones totalmente evitables a los carcinógenos, como está bien documentado en el caso del asbesto en Brasil. Hay abundantes puntos estratégicos de intervención para reducir el cáncer en las Américas.

Mecanismo carcinogénico asociado a la exposición al Bisfenol A / Carcinogenic mechanism associated of Bisphenol A exposure

Resumen Introducción: El Bisfenol A (BPA) es un producto químico al que los seres humanos están expuestos ampliamente por la vía oral, inhalación y transdérmica. Justificación: Dada la importancia de la patología oncológica que puede estar asociada a exposición a este químico, resulta imprescindible comprender mejor sus posibles mecanismos de acción asociados a carcinogénesis. Objetivo General: Investigar el mecanismo carcinogénico asociado a la exposición a BPA. Resultados: Aunque la mayoría de las investigaciones se han orientado hacia el efecto disruptor endocrino, con la limitante que los estudios in vivo son realizados en animales, existen estudios recientes que muestran su posible efecto carcinogénico en tejidos humanos. Sin embargo, se requiere más investigación sobre el papel del BPA de dosis baja (como ocurre en condiciones ambientales normales) y su efecto en la regulación de los cambios globales de expresión génica y las alteraciones epigenéticas en las células, que permitan establecer vínculos con carcinogénesis; esta revisión demuestra que los estudios realizados hasta la fecha señalan varios factores que pueden estar involucrados, como efectos mutagénicos que incluyen cambios en la transcripción génica y enzimáticos que promueven la proliferación celular limitando la apoptosis y favorecen la angiogénesis y migración de células tumorales. Conclusión: Si bien en la actualidad se reconoce que la célula cancerígena adquiere características patológicas que le ayudan a sobrevivir en el organismo, estas características obedecen a mecanismos moleculares genéticos y epigéneticos, muchos de los cuales han sido descritos para el caso de la exposición humana al BPA.

Abstract Introduction: Bisphenol A (BPA) is a chemical to which humans are extensively exposed orally, inhaled and transdermally. Justification: Given the importance of the oncological pathology that may be associated with exposure to this chemical, it is essential to better understand its possible mechanisms of action associated with carcinogenesis. Objective: To investigate the carcinogenic mechanism associated with BPA exposure. Results: Although the majority of investigations have been oriented towards the endocrine disrupting effect, with the limitation that in vivo studies are carried out in animals, recent studies have shown that they can be carcinogenic in human tissues. However, more research is required on the role of low-dose BPA (as occurs under normal environmental conditions) and its effect on the regulation of global changes in gene expression and epigenetic alterations in cells, which allow establishing links with carcinogenesis; this review shows that the studies carried out to date point to several factors that may be involved, such as mutagenic effects that include changes in gene transcription and enzymes that promote cell proliferation, limiting apoptosis and promoting angiogenesis and migration of tumor cells. Conclusion: Although it is currently recognized that the cancer cell acquires pathological characteristics that help it to survive in the organism, these characteristics are due to genetic and epigenetic molecular mechanisms, many of which have been described for the case of human exposure to BPA.

To be or not to be a carcinogen; delving into the glyphosate classification controversy

The International Agency for Research on Cancer (IARC) placed the most widely used herbicide glyphosate (GLY) into the category 2A (probably carcinogenic to humans), a classification questioned by experts from academia and industry. This article critically appraised the epidemiological and experimental data that led the IARC working group (WG) to consider GLY a probable human carcinogen and the ensuing controversy. An association of GLY with non-Hodgkin lymphoma was suggested by some observational studies. A non-causal explanation for this weak association, however, cannot be excluded. Contrary to WG's view, long-term rodent assays yielded no convincing evidence that GLY is carcinogenic. The mechanistic evidence remains elusive as well. Bacterial reverse mutation tests (including tester strains sensitive to oxidative mutagens) were clearly negative, and so were rodent genotoxicity assays by oral route. Tests with mammalian cells in vitro yielded conflicting results at high (cytotoxic) concentrations of GLY-based formulations. Conflicting results were also obtained when high doses of GLY-based herbicides were administered to rodents by the intraperitoneal route. Such high doses are unlikely to be attained in realistic scenarios of exposure. Finally, the IARC classification is based on a conjectural hazard, and rational public health interventions must be based on estimated risks.

Gum arabic and red propolis protecteting colorectal preneoplastic lesions in a rat model of azoxymethane

Abstract Purpose: To evaluate red propolis, gum arabic and L-lysine activity on colorectal preneoplastic lesions induced by azoxymethane (AOM). Methods: The study featured 4 control groups (I-IV) and 4 experimental groups (V-VIII), totaling 48 rats. Once a week for 2 weeks, animals on control groups received saline, while animals in experimental groups received azoxymethane (15 mg/kg i.p.). The follow up along 16 weeks included daily oral gavage to administer water (I and V), L-lysine (150 mg/kg)(II and VI), própolis (100mg/5ml/kg)(III and VII), or gum arabic (5ml/kg)(IV and VIII). Was performed surgery on the animals in the end of this time in order to collect blood for biological assays (TBARS, GSH), followed by their sacrifice to tissue extract. Results: Oxidative stress (TBARS) and the number of aberrant crypt foci (ACF) in distal colon were lower using própolis (p<0.01 for both parameters). Gum arabic reduced preneoplastic lesions (ACF ≤ 4 crypts) on distal colon and on the entire colon (p<0.05). Conclusions: Red propolis reduced AOM-induced oxidative stress (TBARS) and total number of ACF in the distal colon. L-lysine neither protected against nor enhanced AOM-induced ACF. Gum arabic reduced the number of ACF.

Health effects of exposure to radon: implications of the radon bed mattress incident in Korea / 한국역학회지

Radon is a naturally occurring radioactive material formed by the slow decay of uranium and thorium found in the earth's crust or construction materials. Internal exposure to radon accounts for about half of the natural background radiation dose to which humans are exposed annually. Radon is a carcinogen and is the second leading cause of lung cancer following smoking. An association between radon and lung cancer has been consistently reported in epidemiological studies on mine workers and the general population with indoor radon exposure. However, associations have not been clearly established between radon and other diseases, such as leukemia and thyroid cancer. Radiation doses are assessed by applying specific dose conversion coefficients according to the source (e.g., radon or thoron) and form of exposure (e.g., internal or external). However, regardless of the source or form of exposure, the effects of a given estimated dose on human health are identical, assuming that individuals have the same sensitivity to radiation. Recently, radiation exceeding the annual dose limit of the general population (1 mSv/yr) was detected in bed mattresses produced by D company due to the use of a monazite-based anion powder containing uranium and thorium. This has sparked concerns about the health hazards for mattress users caused by radiation exposure. In light of this event, this study presents scientific information about the assessment of radon and thoron exposure and its human implications for human health, which have emerged as a recent topic of interest and debate in society.

Health effects of exposure to radon: implications of the radon bed mattress incident in Korea / 한국역학회지

Radon is a naturally occurring radioactive material formed by the slow decay of uranium and thorium found in the earth's crust or construction materials. Internal exposure to radon accounts for about half of the natural background radiation dose to which humans are exposed annually. Radon is a carcinogen and is the second leading cause of lung cancer following smoking. An association between radon and lung cancer has been consistently reported in epidemiological studies on mine workers and the general population with indoor radon exposure. However, associations have not been clearly established between radon and other diseases, such as leukemia and thyroid cancer. Radiation doses are assessed by applying specific dose conversion coefficients according to the source (e.g., radon or thoron) and form of exposure (e.g., internal or external). However, regardless of the source or form of exposure, the effects of a given estimated dose on human health are identical, assuming that individuals have the same sensitivity to radiation. Recently, radiation exceeding the annual dose limit of the general population (1 mSv/yr) was detected in bed mattresses produced by D company due to the use of a monazite-based anion powder containing uranium and thorium. This has sparked concerns about the health hazards for mattress users caused by radiation exposure. In light of this event, this study presents scientific information about the assessment of radon and thoron exposure and its human implications for human health, which have emerged as a recent topic of interest and debate in society.

Evaluation of Hazardous Chemicals with Material Safety Data Sheet and By-products of a Photoresist Used in the Semiconductor-Manufacturing Industry

BACKGROUND: The photolithography process in the semiconductor industry uses various chemicals with little information on their constitution. This study aimed to identify the chemical constituents of photoresist (PR) products and their by-products and to compare these constituents with material safety data sheets (MSDSs) and analytical results. METHODS: A total of 51 PRs with 48 MSDSs were collected. Analysis consisted of two parts: First, the constituents of the chemical products were identified and analyzed using MSDS data; second, for verification of the by-products of PR, volatile organic compounds were analyzed. The chemical constituents were categorized according to hazards. RESULTS: Forty-five of 48 products contained trade secrets in amounts ranging from 1 to 65%. A total of 238 ingredients with multiple counting (35 ingredients without multiple counting) were identified in the MSDS data, and 48.7% of ingredients were labeled as trade secrets under the Korea Occupational Safety and Health Act. The concordance rate between the MSDS data and the analytical result was 41.7%. The by-product analysis identified 129 chemicals classified according to Chemical Abstracts Service No., with 17 chemicals that are carcinogenic, mutagenic, and reprotoxic substances. Formaldehyde was found to be released from 12 of 21 products that use novolak resin. CONCLUSION: We confirmed that several PRs contain carcinogens, and some were not specified in the toxicological information in the MSDS. Hazardous chemicals, including benzene and formaldehyde, are released from PRs products as by-products. Therefore, it is necessary to establish a systematic management system for chemical compounds and the working environment.

Splicing isoform-specific functional genomic in cancer cells

Alternative splicing is a regulated process whereby one gene can generate multiple mRNA isoforms susceptible to be translated into protein isoforms of various functions. Several publications report the aberrant expression of splicing isoforms in cancer cells and tissues. However, in most cases, their function remains to be established. In this review article, I will discuss the molecular tool available to perform isoform-specific functional genomics, the methodologies to quantify their effectiveness and the resulting isoform-specific phenotype in human cancer cell lines (AU)