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1.
Chinese Journal of Preventive Medicine ; (12): 25-28, 2022.
Article in Chinese | WPRIM | ID: wpr-935245

ABSTRACT

The ex vivo biosensor assay is developed to assess the health effects and toxicological mechanism of environmental pollutants with internal environment homeostasis changes by integrating the in vivo exposure evaluation, in vitro outcomes analysis, and systematic environment component screening. This toxicology testing model combines the real-world exposure of people in the field and the study of molecular mechanism exploration in lab experiments to overcome the shortcomings of a single toxicology method. It provides a new technique and perspective for toxicity testing and risk assessment in mesoscale between macroscopic population study and microscopic mechanism exploration.


Subject(s)
Humans , Biosensing Techniques , Environmental Pollutants/toxicity , Risk Assessment , Toxicity Tests
2.
Braz. j. biol ; 81(2): 499-507, 2021. tab, graf, ilus
Article in English | LILACS, VETINDEX | ID: biblio-1153369

ABSTRACT

Increased agricultural production has been increased use of pesticides worldwide, which poses a threat to both human and environmental health. Recent studies suggest that several non-target organisms, from bees to mammals, show a wide variety of toxic effects of pesticides exposure, including impaired behavior, development and reproduction. Among mammals, bats are usually a neglected taxon among ecotoxicological studies, although they play important ecological and economical roles in forest ecosystems and agriculture through to seed dispersal and insect population control. Considering their wide variety of food habits, bats are exposed to environmental pollutants through food or water contamination, or through direct skin contact in their roosting areas. In order to better understand the risk posed by pesticides to bats populations, we compiled studies that investigated the main toxicological effects of pesticides in bats, aiming at contributing to discussion about the environmental risks associated with the use of pesticides.


O aumento da produção agrícola tem levado ao aumento do uso de pesticidas em todo o mundo, o que representa uma ameaça para a saúde humana e ambiental. Estudos recentes sugerem que vários organismos não-alvo, de abelhas a mamíferos, apresentam uma grande variedade de efeitos tóxicos após a exposição aos pesticidas a pesticidas, incluindo alterações de comportamento, no desenvolvimento e na reprodução. Entre os mamíferos, os morcegos geralmente são negligenciados entre os estudos ecotoxicológicos, embora desempenhem importantes papéis ecológicos e econômicos nos ecossistemas florestais e na agricultura por meio do controle de dispersão de sementes e de populações de insetos. Considerando sua ampla variedade de hábitos alimentares, eles estão expostos a poluentes ambientais através da contaminação de alimentos ou água, ou através do contato direto com a pele em suas áreas de descanso. Para entender melhor o risco que os agrotóxicos representam para as populações de morcegos, compilamos estudos que investigaram os principais efeitos toxicológicos de agrotóxicos em morcegos, visando à discussão sobre os riscos ambientais associados ao uso de agrotóxicos.


Subject(s)
Animals , Pesticides/toxicity , Pyrethrins/analysis , Chiroptera/physiology , Environmental Pollutants/toxicity , Insecticides, Organochlorine/analysis , Bees , Ecosystem , Agriculture , Bioaccumulation
3.
Biomedical and Environmental Sciences ; (12): 192-202, 2021.
Article in English | WPRIM | ID: wpr-878337

ABSTRACT

Objective@#To investigate involvement of the aryl hydrocarbon receptor (AhR) in the immunomodulatory effects of cadmium (Cd).@*Methods@#The effect of Cd on AhR activation ( @*Results@#Cd increased @*Conclusion@#AhR signaling is involved in the lung leukocyte proinflammatory cytokine response to Cd. The relevance of the AhR to the cytokine response to Cd provides new insight into the mechanisms of Cd immunotoxicity.


Subject(s)
Animals , Male , Rats , Basic Helix-Loop-Helix Transcription Factors/immunology , Cadmium/toxicity , Cytochrome P-450 CYP1A1/immunology , Cytochrome P-450 CYP1B1/immunology , Cytokines/immunology , Environmental Pollutants/toxicity , Receptors, Aryl Hydrocarbon/immunology
4.
Chinese Journal of Biotechnology ; (12): 3591-3603, 2021.
Article in Chinese | WPRIM | ID: wpr-921450

ABSTRACT

Wet detoxification has traditionally been seen as the most promising technology for treating chromium-contaminated sites. However, the addition of chemicals in the wet detoxification process not only increases the cost but also introduces extra pollutants. Moreover, the chromium-containing slag may be re-dissolved in the form of Cr(VI), and the increased concentration of Cr(VI) results in a serious "returning to yellow" phenomenon in the chromium-contaminated sites, causing undesirable secondary pollution. Microbial remediation is a promising technology to address the re-dissolution of chromium-containing slag after wet detoxification, and this article reviews the advances in this area. Firstly, the toxicity, current situation and conventional technologies for treating the chromium-containing slag were briefly summarized. The mechanisms of the inevitable re-dissolution of chromium-containing slag after wet detoxification were summarized. Three main mechanisms, namely bioreduction, biosorption and biomineralization, which are involved in the environmental-friendly and efficient microbial remediation technology, were reviewed. The variation of microbial species and the succession of microbial community during the bioremediation of chromium-contaminated sites were discussed. Finally, future research directions were prospected with the aim to develop long-term, stable and sustainable technologies for remediating the chromium-contaminated sites.


Subject(s)
Biodegradation, Environmental , Chromium/toxicity , Environmental Pollutants/toxicity
5.
Environmental Health and Preventive Medicine ; : 34-34, 2021.
Article in English | WPRIM | ID: wpr-880352

ABSTRACT

BACKGROUND@#Arsenic is a developmental neurotoxicant. It means that its neurotoxic effect could occur in offspring by maternal arsenic exposure. Our previous study showed that developmental arsenic exposure impaired social behavior and serotonergic system in C3H adult male mice. These effects might affect the next generation with no direct exposure to arsenic. This study aimed to detect the social behavior and related gene expression changes in F2 male mice born to gestationally arsenite-exposed F1 mice.@*METHODS@#Pregnant C3H/HeN mice (F0) were given free access to tap water (control mice) or tap water containing 85 ppm sodium arsenite from days 8 to 18 of gestation. Arsenite was not given to F1 or F2 mice. The F2 mice were generated by mating among control F1 males and females, and arsenite-F1 males and females at the age of 10 weeks. At 41 weeks and 74 weeks of age respectively, F2 males were used for the assessment of social behavior by a three-chamber social behavior apparatus. Histological features of the prefrontal cortex were studied by ordinary light microscope. Social behavior-related gene expressions were determined in the prefrontal cortex by real time RT-PCR method.@*RESULTS@#The arsenite-F2 male mice showed significantly poor sociability and social novelty preference in both 41-week-old group and 74-week-old group. There was no significant histological difference between the control mice and the arsenite-F2 mice. Regarding gene expression, serotonin receptor 5B (5-HT 5B) mRNA expression was significantly decreased (p < 0.05) in the arsenite-F2 male mice compared to the control F2 male mice in both groups. Brain-derived neurotrophic factor (BDNF) and dopamine receptor D1a (Drd1a) gene expressions were significantly decreased (p < 0.05) only in the arsenite-F2 male mice of the 74-week-old group. Heme oxygenase-1 (HO-1) gene expression was significantly increased (p < 0.001) in the arsenite-F2 male mice of both groups, but plasma 8-hydroxy-2'-deoxyguanosine (8-OHdG) and cyclooxygenase-2 (COX-2) gene expression were not significantly different. Interleukin-1β (IL-1β) mRNA expression was significantly increased only in 41-week-old arsenite-F2 mice.@*CONCLUSIONS@#These findings suggest that maternal arsenic exposure affects social behavior in F2 male mice via serotonergic system in the prefrontal cortex. In this study, COX-2 were not increased although oxidative stress marker (HO-1) was increased significantly in arsnite-F2 male mice.


Subject(s)
Animals , Female , Male , Mice , Pregnancy , Arsenic/toxicity , Arsenites/toxicity , Behavior, Animal/drug effects , Environmental Pollutants/toxicity , Gene Expression/drug effects , Genetic Markers , Maternal Exposure/adverse effects , Mice, Inbred C3H , Oxidative Stress/genetics , Prefrontal Cortex/drug effects , Prenatal Exposure Delayed Effects/psychology , Reverse Transcriptase Polymerase Chain Reaction , Serotonin/metabolism , Social Behavior , Sodium Compounds/toxicity
6.
Environmental Health and Preventive Medicine ; : 31-31, 2021.
Article in English | WPRIM | ID: wpr-880350

ABSTRACT

BACKGROUND@#The industrial revolution has resulted in increased synthesis and the introduction of a variety of compounds into the environment and their potentially hazardous effects have been observed in the biota. The present study was aimed to evaluate the potential endocrine-disrupting effects of chronic exposure to the low concentrations of bisphenol S (BPS) in male rats.@*METHODS@#Weaning male Sprague-Dawley rats (22 days old) were either exposed to water containing 0.1% ethanol for control or different concentrations of BPS (0.5, 5, and 50 μg/L) in drinking water for 48 weeks in the chronic exposure study. After completion of the experimental period, animals were dissected and different parameters (hormone concentrations, histology of testis and epididymis, oxidative stress and level of antioxidant enzymes in the testis, daily sperm production (DSP), and sperm parameters) were determined.@*RESULTS@#Results of the present study showed a significant alteration in the gonadosomatic index (GSI) and relative reproductive organ weights. Oxidative stress in the testis was significantly elevated while sperm motility, daily sperm production, and the number of sperm in epididymis were reduced. Plasma testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) concentrations were reduced and estradiol levels were high in the 50 μg/L-exposed group. Histological observations involved a significant reduction in the epithelial height of the testis along with disrupted spermatogenesis, an empty lumen of the seminiferous tubules, and the caput region of the epididymis.@*CONCLUSION@#These results suggest that exposure to 5 and 50 μg/L of BPS for the chronic duration started from an early age can induce structural changes in testicular tissue architecture and endocrine alterations in the male reproductive system which may lead to infertility in males.


Subject(s)
Animals , Male , Rats , Biomarkers , Endocrine Disruptors/toxicity , Environmental Exposure/adverse effects , Environmental Pollutants/toxicity , Hypothalamo-Hypophyseal System/physiopathology , Infertility, Male/physiopathology , Phenols/toxicity , Rats, Sprague-Dawley , Sulfones/toxicity , Testis/physiopathology , Toxicity Tests, Chronic
7.
Salud pública Méx ; 61(4): 417-426, Jul.-Aug. 2019. graf
Article in English | LILACS | ID: biblio-1099317

ABSTRACT

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.


Subject(s)
Humans , Disease/etiology , Occupational Exposure/adverse effects , Environmental Pollutants/toxicity , Occupational Diseases/etiology , Panama , Asbestos/toxicity , Americas , Brazil , Carcinogens/toxicity , Petroleum Pollution/adverse effects , Epidemiology , Risk Factors , Air Pollution, Indoor/adverse effects , Sex Distribution
8.
Rev. chil. pediatr ; 89(6): 761-765, dic. 2018.
Article in Spanish | LILACS | ID: biblio-978152

ABSTRACT

Resumen: En el presente articulo se revisan los mecanismos del imprinting epigenético mediante el cual se producen los efectos diferidos generados por la exposición prenatal o infantil temprana a agentes químicos contaminantes. Se revisaron las bases de datos Pubmed y Embase para identificar estudios publicados entre 2005 y 2018, junto a artículos considerados pioneros en este ámbito. Se incluyeron además, datos generados en nuestro Laboratorio. Como fuente de información secundaria se citan normas chilenas de concentraciones de algunos contaminantes en agua potable publicados por el Ministerio de Salud de Chile. Se describen cambios en la metilación de diversos genes causados por exposición prenatal o infantil temprana a algunos contaminantes ambientales relevantes en Chile: arsénico, plomo, ftalatos y fenoles, y se mencionan algunas de las enfermedades orgánicas y cambios neuroconductuales que se desarrollan más tarde en la vida como consecuencia de dichas exposi ciones. Se sugiere que un mayor conocimiento de los factores ambientales y una mejor educación de la población, permitirían una protección más adecuada de embarazadas y lactantes, en especial durante las ventanas de susceptibilidad y que los pediatras y obstetras, serían los profesionales mejor indicados para desarrollar estas acciones. Se sugiere además la necesidad de adecuar normas am bientales y aumentar la fiscalización de contaminantes y sus fuentes, para prevenir el deterioro de la salud de las futuras generaciones.


Abstract: This review explains the epigenetic imprinting mechanisms by which the delayed effects generated by prenatal or early childhood exposure to chemical pollutants are produced. Pubmed and Embase databases were reviewed to identify studies published between 2005 and 2018, along with articles considered pioneers in this field. We also included data generated in our Laboratory. As a source of secondary information, Chilean standards on concentrations of some pollutants in drinking water published by the Ministry of Health of Chile are cited. Changes are described in the methylation of diverse genes caused by prenatal or early childhood exposure to some relevant environmental po llutants in Chile such as arsenic, lead, phenols, and phthalates, and some of the organic diseases and neurobehavioral changes that occur later in life as a consequence of these exposures are mentioned. We suggest that a wider knowledge of environmental factors and better education of the population would allow a more adequate protection of pregnant women and infants especially during the win dows of susceptibility, and that pediatricians and obstetricians would be in the best position to deve lop these actions. We also suggest the need to adapt environmental standards and increase the control of pollutants and their sources to prevent health deterioration of future generations.


Subject(s)
Humans , Female , Pregnancy , Adult , Prenatal Exposure Delayed Effects/etiology , Maternal Exposure/adverse effects , Epigenesis, Genetic , Environmental Pollutants/toxicity , Prenatal Exposure Delayed Effects/genetics
9.
Salud colect ; 13(2): 225-237, abr.-jun. 2017.
Article in Spanish | LILACS | ID: biblio-903689

ABSTRACT

RESUMEN Este artículo analiza la percepción social de la exposición humana a los compuestos químicos, y los discursos y las prácticas sobre las fronteras corporales ante la contaminación interna. A partir de una investigación cualitativa e interdisciplinar en Cataluña, se exploran los significados sociales que se atribuyen a los peligros y riesgos ambientales y alimentarios de los compuestos químicos que afectan a la salud humana y el lugar que el cuerpo ocupa en la producción de estos discursos. Entre junio y noviembre de 2011 se realizaron 43 entrevistas semiestructuradas a trabajadores con alguna conciencia sobre contaminantes químicos, en las que se profundizó cómo estas personas (re)interpretan los diferentes discursos existentes sobre la contaminación interna, sus percepciones sobre la introducción de compuestos químicos en el cuerpo y los peligros que estas sustancias representan para la salud.


ABSTRACT This article analyses the social perception of human exposure to chemical compounds and discourses and practices regarding bodily boundaries when faced with internal contamination. Based on qualitative and interdisciplinary research carried out in Catalonia, the social meanings attributed to the environmental and food dangers and risks related to chemical compounds that affect human health, and the place that the body takes in the production of these discourses, were explored. In order to do so, between June and November 2011, 43 semi-structured interviews with workers with some awareness of chemical contaminants were carried out, emphasizing how these people (re)interpret the different existing discourses about internal contamination as well as their perceptions regarding the introduction of chemical compounds into the body and the dangers that these substances pose to health.


Subject(s)
Humans , Social Perception , Health Knowledge, Attitudes, Practice , Environmental Exposure/adverse effects , Environmental Pollutants/toxicity , Spain , Food Contamination , Risk , Qualitative Research
10.
Cienc. tecnol. salud ; 4(1): 79-86, 20170600. ilus
Article in Spanish | LILACS | ID: biblio-882840

ABSTRACT

Estimar el grado de remoción de contaminantes emergentes en el proceso de tratamiento de aguas residuales es de importancia para evaluar la efectividad de las técnicas empleadas en la actualidad. El triclosán (TCS) es un agente antimicrobiano sintético de amplio espectro, estudios recientes sugieren que presenta elevado potencial como interruptor endocrino. Se determinó la concentración de TCS en cuatro muestras de aguas residuales obtenidas en diferentes etapas del proceso de tratamiento de aguas en la Planta Piloto para el Tratamiento de Aguas Residuales Ingeniero Arturo Pazos Sosa (IAPS). Las muestras de agua fueron filtradas en membrana, tratadas por adición de TCS estándar y formación de un compuesto complejo coloreado amarillo-café cuya absorbancia a 475 nm fue registrada en un espectrofotómetro Cary® 50 UV-Vis. Se identificó la presencia de TCS en concentraciones por arriba de 200 µg/L en tres diferentes etapas del tratamiento de aguas residuales en la planta piloto IAPS lo que permitió concluir que el grado de remoción de TCS en esta planta de tratamiento de aguas osciló entre 31 y 95% dependiendo de la etapa de tratamiento, sin embargo el agua del efluente de la planta no puede considerarse como potable ya que la concentración de TCS determinada en este estudio sobrepasa por al menos un orden de magnitud de diez los niveles a los cuales no se han reportado efectos adversos hacia organismos vivos.


Estimating the degree of contaminants' removal during wastewater treatment is important to evaluate the effectiveness of the current treatment techniques. Triclosan (TCS) is a synthetic broad spectrum antimicrobial agent and recent investigations suggest that this compound has high potential as endocrine disruptor. The concentration of TCS was measured in four wastewater samples obtained at different processing steps at the Ingeniero Arturo Pazos Sosa (IAPS) pilot plant. The wastewater samples were treated by membrane filtration, standard addition of TCS and the subsequent formation of a brown-yellow colored complex, whose absorbance at 475nm was measured in a Cary 50® UV-Vis spectrophotometer. TCS was found at concentrations over 200 µg/L in three different phases of the wastewater treatment at the IAPS plant. In conclusion, the degree of TCS removal in this plant was between 31 and 95% depending on the treatment stage. However plant effluent cannot be considered potable since the TCS concentration found in this study is at least ten times higher than those at which adverse effects to living organisms have not been detected.


Subject(s)
Humans , Male , Female , Triclosan/analysis , Wastewater/toxicity , Water Purification , Contaminant Removal , Environmental Pollutants/toxicity , Endocrine Disruptors/analysis , Wastewater
11.
J. pediatr. (Rio J.) ; 93(2): 111-119, Mar.-Apr. 2017. graf
Article in English | LILACS | ID: biblio-841331

ABSTRACT

Abstract Objective: Autism spectrum disorders are lifelong and often devastating conditions that severely affect social functioning and self-sufficiency. The etiopathogenesis is presumably multifactorial, resulting from a very complex interaction between genetic and environmental factors. The dramatic increase in autism spectrum disorder prevalence observed during the last decades has led to placing more emphasis on the role of environmental factors in the etiopathogenesis. The objective of this narrative biomedical review was to summarize and discuss the results of the most recent and relevant studies about the environmental factors hypothetically involved in autism spectrum disorder etiopathogenesis. Sources: A search was performed in PubMed (United States National Library of Medicine) about the environmental factors hypothetically involved in the non-syndromic autism spectrum disorder etiopathogenesis, including: air pollutants, pesticides and other endocrine-disrupting chemicals, electromagnetic pollution, vaccinations, and diet modifications. Summary of the findings: While the association between air pollutants, pesticides and other endocrine-disrupting chemicals, and risk for autism spectrum disorder is receiving increasing confirmation, the hypothesis of a real causal relation between them needs further data. The possible pathogenic mechanisms by which environmental factors can lead to autism spectrum disorder in genetically predisposed individuals were summarized, giving particular emphasis to the increasingly important role of epigenetics. Conclusions: Future research should investigate whether there is a significant difference in the prevalence of autism spectrum disorder among nations with high and low levels of the various types of pollution. A very important goal of the research concerning the interactions between genetic and environmental factors in autism spectrum disorder etiopathogenesis is the identification of vulnerable populations, also in view of proper prevention.


Resumo Objetivo: Os transtornos do espectro autista (TEAs) são vitalícios e normalmente são doenças devastadoras que afetam gravemente o funcionamento social e a autossuficiência. A etiopatogenia é presumivelmente multifatorial, resultante de uma interação muito complexa entre fatores genéticos e ambientais. O aumento drástico na prevalência de TEAs observado nas últimas décadas levou à maior ênfase no papel dos fatores ambientais na etiopatogenia. O objetivo desta análise da narrativa biomédica foi resumir e discutir os resultados dos estudos mais recentes e relevantes sobre os fatores ambientais hipoteticamente envolvidos na etiopatogenia dos TEAs. Fontes: Foi feita uma pesquisa na Biblioteca Nacional de Medicina dos Estados Unidos (PubMed) sobre os fatores ambientais hipoteticamente envolvidos na etiopatogenia dos TEAs não sindrômicos, inclusive poluentes atmosféricos, pesticidas e outros desreguladores endócrinos, poluição eletromagnética, vacinas e alterações na dieta. Resumo dos achados: Embora a associação entre poluentes atmosféricos, pesticidas e outros desreguladores endócrinos e o risco de TEA tenha recebido cada vez mais confirmações, a hipótese de uma relação causal real entre eles ainda precisa de mais dados. Os possíveis mecanismos patogênicos por meio dos quais os fatores ambientais podem causar TEA em indivíduos geneticamente predispostos foram resumidos, com ênfase especial no papel cada vez mais importante da epigenética. Conclusões: Futuras pesquisas devem investigar se há uma diferença significativa na prevalência de TEA entre nações com níveis altos e baixos de vários tipos de poluição. Um objetivo muito importante da pesquisa a respeito das interações entre fatores genéticos e ambientais na etiopatogenia do TEA é a identificação de populações vulneráveis, também em virtude da prevenção adequada.


Subject(s)
Humans , Female , Pregnancy , Child , Autistic Disorder/etiology , Autistic Disorder/genetics , Environmental Pollutants/toxicity , Autism Spectrum Disorder/etiology , Autism Spectrum Disorder/genetics , Prenatal Exposure Delayed Effects , Risk Factors , Maternal Exposure/adverse effects , Genetic Predisposition to Disease
12.
J. pediatr. (Rio J.) ; 93(1): 17-27, Jan.-Feb. 2017. graf
Article in English | LILACS | ID: biblio-841319

ABSTRACT

Abstract: Objective: This study aims to identify the scientific evidence on the risks and effects of exposure to environmental contaminants in children during sensitive developmental periods. Data source: The search was performed in the Bireme database, using the terms: children's health, environmental exposure, health vulnerability, toxicity pathways and developmental disabilities in the LILACS, MEDLINE and SciELO systems. Data synthesis: Children differ from adults in their unique physiological and behavioral characteristics and the potential exposure to risks caused by several threats in the environment. Exposure to toxic agents is analyzed through toxicokinetic processes in the several systems and organs during the sensitive phases of child development. The caused effects are reflected in the increased prevalence of congenital malformations, diarrhea, asthma, cancer, endocrine and neurological disorders, among others, with negative impacts throughout adult life. Conclusion: To identify the causes and understand the mechanisms involved in the genesis of these diseases is a challenge for science, as there is still a lack of knowledge on children's susceptibility to many environmental contaminants. Prevention policies and more research on child environmental health, improving the recording and surveillance of environmental risks to children's health, should be an ongoing priority in the public health field.


Resumo: Objetivo: O presente estudo busca identificar as evidências científicas sobre os riscos e efeitos da exposição de contaminantes ambientais no organismo infantil durante os períodos sensíveis de seu desenvolvimento. Fonte de dados: As pesquisas foram feitas pelo banco de dados da Bireme, com os termos children's health, environmental exposure, health vulnerability, toxicity pathways e developmental disabilities nos sistemas Lilacs, Medline e SciELO. Síntese de dados: A criança difere do adulto por suas características singulares de ordem fisiológica, comportamental e do potencial de exposição a riscos frente às ameaças do ambiente. A exposição a agentes tóxicos é analisada por meio dos processos toxicocinéticos nos sistemas e órgãos durante as janelas sensíveis do desenvolvimento infantil. Os efeitos causados transparecem no aumento da prevalência de malformações congênitas, diarreia, asma, cânceres, distúrbios endócrinos e neurológicos, entre outros, com impactos negativos ao longo da vida adulta. Conclusão: Identificar as causas e compreender os mecanismos envolvidos na gênese desses agravos é um desafio que se impõe à ciência, visto que ainda há uma lacuna de conhecimento sobre a suscetibilidade infantil para muitos contaminantes ambientais. Políticas de prevenção e mais pesquisas em saúde ambiental infantil, que impulsionem o registro e a vigilância epidemiológica dos riscos ambientais à saúde da criança, devem ser uma prioridade contínua no campo da saúde pública.


Subject(s)
Humans , Child , Developmental Disabilities/etiology , Environmental Exposure/adverse effects , Environmental Pollutants/toxicity , Developmental Disabilities/classification , Developmental Disabilities/physiopathology , Child Welfare , Health Knowledge, Attitudes, Practice , Environmental Health
13.
Rev. panam. salud pública ; 40(3): 181-185, Sep. 2016.
Article in English | LILACS | ID: biblio-830720

ABSTRACT

ABSTRACT Climate change is a social justice as well as an environmental issue. The magnitude and pattern of changes in weather and climate variables are creating differential exposures, vulnerabilities, and health risks that increase stress on health systems while exacerbating existing and creating new health inequities. Examples from national and local health adaptation projects highlight that developing partnerships across sectors and levels are critical for building climate-resilient health systems and communities. Strengthening current and implementing new health interventions, such as using environmental information to develop early warning systems, can be effective in protecting the most vulnerable. However, not all projected risks of climate change can be avoided by climate policies and programs, so health system strengthening is also critical. Applying a health inequity lens can reduce current vulnerabilities while building resilience to longer-term climate change. Taking inequities into account is critical if societies are to effectively prepare for and manage the challenges ahead.


RESUMEN El cambio climático es un asunto no solo ambiental, sino también de justicia social. La magnitud y naturaleza de los cambios observados en las variables de tiempo meteorológico y clima están llevando a exposiciones, vulnerabilidades y riesgos de salud diferenciales que incrementan la sobrecarga de los sistemas de salud y exacerban las inequidades sanitarias existentes, a la vez que generan nuevas inequidades. Los proyectos nacionales y locales de adaptación al cambio climático para proteger la salud humana ponen de manifiesto que la creación de alianzas entre diferentes sectores y en distintos niveles es fundamental para lograr que haya sistemas de salud y comunidades capaces de recuperarse de los efectos del clima. El fortalecimiento de las intervenciones de salud en curso y la aplicación de nuevas intervenciones, tales como el uso de información de tipo ambiental para crear sistemas de alerta temprana, pueden ser eficaces para proteger a los grupos más vulnerables. Sin embargo, no todos los riesgos previstos en relación con el cambio climático pueden evitarse por medio de políticas y programas climáticos, de manera que el fortalecimiento de los sistemas de salud también es fundamental. La aplicación de una óptica de inequidad sanitaria puede reducir las vulnerabilidades actuales y al mismo tiempo crear capacidad de recuperación frente a los efectos del cambio climático a más largo plazo. Si las sociedades han de prepararse para los retos que se avecinan y hacerles frente de una manera eficaz, es imprescindible que se tengan en cuenta las inequidades.


Subject(s)
Carbon/toxicity , Environmental Pollutants/toxicity , Government Programs , National Health Programs , Vulnerable Populations
14.
Clinics ; 70(5): 350-355, 05/2015. tab, graf
Article in English | LILACS | ID: lil-748270

ABSTRACT

OBJECTIVE: Sacrococcygeal pilonidal sinus is common in young men and may recur over time after surgery. We investigated whether a factor exists that can aid in the determination of the preferred technique between the early Limberg flap and Karydakis flap techniques for treating recurrent pilonidal sinus. MATERIALS AND METHODS: This prospective and randomized study enrolled 71 patients with recurrent pilonidal sinus in whom the Limberg flap or Karydakis flap techniques were applied for reconstruction after excision. Patients were divided into two groups as follows: 37 patients were treated with the Limberg flap technique and 34 patients were treated with the Karydakis flap technique. Fluid collection, wound infection, flap edema, hematoma, partial wound separation, return to daily activities, pain score, complete healing time, painless seating and patient satisfaction were compared between the groups. ClinicalTrial.gov: NCT02287935. RESULTS: The development rates of total fluid collection, wound infection, flap edema, hematoma, and partial wound separation were 9.8%, 16%, 7%, 15% and 4.2%, respectively; total flap necrosis was not observed in any patient (p<0.001). During the average follow-up of 28 months, no patients (0%) developed recurrent disease. The two groups differed with respect to early surgical complications (p<0.001). CONCLUSION: In this study, use of the Limberg flap was associated with lower complication rates, shorter length of hospital stay, early return to work, low pain score, high patient satisfaction and better complete healing duration. Therefore, we recommend the Limberg flap for treatment of recurrent pilonidal sinus. .


Subject(s)
Animals , Male , Rats , Aryldialkylphosphatase/genetics , Environmental Pollutants/toxicity , Gene Expression Regulation, Enzymologic/drug effects , Liver/drug effects , Polychlorinated Biphenyls/toxicity , Antioxidants/metabolism , Aryldialkylphosphatase/blood , Cholesterol, HDL/blood , Cholesterol, LDL/blood , Dose-Response Relationship, Drug , Lipid Peroxidation/drug effects , Liver/enzymology , Malondialdehyde/metabolism , Rats, Sprague-Dawley , Thiobarbituric Acid Reactive Substances/metabolism
15.
Clinics ; 70(5): 346-349, 05/2015. tab, graf
Article in English | LILACS | ID: lil-748281

ABSTRACT

OBJECTIVE: This study sought to determine the serum aminotransferase levels of patients with predialysis chronic kidney disease and establish their relationships with serum creatinine levels and glomerular filtration rate. METHODS: Patients with chronic kidney disease were evaluated between September 2011 and May 2012. Aminotransferase and creatinine serum levels were measured using an automated kinetic method, and glomerular filtration rates were estimated using the Cockroft-Gault and Modification of Diet in Renal Disease formulas to classify patients into chronic kidney disease stages. RESULTS: Exactly 142 patients were evaluated (mean age: 64±16 years). The mean creatinine serum level and glomerular filtration rate were 3.3±1.2 mg/dL and 29.1±13 mL/min/1.73 m2, respectively. Patients were distributed according to their chronic kidney disease stages as follows: 3 (2.1%) patients were Stage 2; 54 (38%) were Stage 3; 70 (49.3%) were Stage 4; and 15 (10.5%) were Stage 5. The mean aspartate aminotransferase and alanine aminotransferase serum levels showed a reduction in proportion to the increase in creatinine levels (p=0.001 and p=0.05, respectively) and the decrease in glomerular filtration rate (p=0.007 and p=0.028, respectively). Alanine aminotransferase and aspartate aminotransferase serum levels tended to be higher among patients classified as stage 2 or 3 compared with those classified as stage 4 or 5 (p=0.08 and p=0.06, respectively). CONCLUSIONS: The aspartate aminotransferase and alanine aminotransferase serum levels of patients with predialysis chronic kidney disease decreased in proportion to the progression of the disease; they were negatively correlated with creatinine levels and directly correlated with glomerular filtration rate. .


Subject(s)
Humans , Male , Environmental Pollutants/toxicity , Foreskin/drug effects , Keratinocytes/drug effects , Polychlorinated Biphenyls/toxicity , Telomerase/metabolism , Telomere Shortening/drug effects , Cell Culture Techniques , Cell Line , Cell Cycle/drug effects , Cell Survival/drug effects , DNA , Dose-Response Relationship, Drug , Enzyme Activation , Foreskin/enzymology , Foreskin/ultrastructure , Keratinocytes/enzymology , Keratinocytes/ultrastructure , Oxidative Stress/drug effects , Superoxides/metabolism , Telomere Shortening/genetics
16.
Korean Journal of Radiology ; : 1142-1152, 2015.
Article in English | WPRIM | ID: wpr-163288

ABSTRACT

OBJECTIVE: This study evaluated the CT characteristics of pleural plaques in asbestos-exposed individuals and compared occupational versus environmental exposure groups. MATERIALS AND METHODS: This study enrolled 181 subjects with occupational exposure and 98 with environmental exposure from chrysotile asbestos mines, who had pleural plaques confirmed by a chest CT. The CT scans were analyzed for morphological characteristics, the number and distribution of pleural plaques and combined pulmonary fibrosis. Furthermore, the CT findings were compared between the occupational and environmental exposure groups. RESULTS: Concerning the 279 subjects, the pleural plaques were single in 2.2% and unilateral in 3.6%, and showed variable widths (range, 1-20 mm; mean, 5.4 +/- 2.7 mm) and lengths (5-310 mm; 72.6 +/- 54.8 mm). The chest wall was the most commonly involved (98.6%), with an upper predominance on the ventral side (upper, 77.8% vs. lower, 55.9%, p < 0.001) and a lower predominance on the dorsal side (upper, 74.9% vs. lower, 91.8%, p = 0.02). Diaphragmatic involvement (78.1%) showed a right-side predominance (right, 73.8% vs. left, 55.6%, p < 0.001), whereas mediastinal plaques (42.7%) were more frequent on the left (right, 17.6% vs. left, 39.4%, p < 0.001). The extent and maximum length of plaques, and presence and severity of combined asbestosis, were significantly higher in the occupational exposure group (p < 0.05). CONCLUSION: Pleural plaques in asbestos-exposed individuals are variable in number and size; and show a predominant distribution in the upper ventral and lower dorsal chest walls, right diaphragm, and left mediastinum. Asbestos mine workers have a higher extent of plaques and pulmonary fibrosis versus environmentally exposed individuals.


Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Asbestos, Serpentine/toxicity , Asbestosis/etiology , Asian People , Environmental Pollutants/toxicity , Mining , Occupational Exposure , Pleural Diseases/etiology , Republic of Korea , Tomography, X-Ray Computed
17.
Journal of Veterinary Science ; : 297-306, 2015.
Article in English | WPRIM | ID: wpr-66456

ABSTRACT

Exposure to cadmium (Cd) induces apoptosis in osteoblasts (OBs); however, little information is available regarding the specific mechanisms of Cd-induced primary rat OB apoptosis. In this study, Cd reduced cell viability, damaged cell membranes and induced apoptosis in OBs. We observed decreased mitochondrial transmembrane potentials, ultrastructure collapse, enhanced caspase-3 activity, and increased concentrations of cleaved PARP, cleaved caspase-9 and cleaved caspase-3 following Cd treatment. Cd also increased the phosphorylation of p38-mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinases (ERK)1/2 and c-jun N-terminal kinase (JNK) in OBs. Pretreatment with the caspase inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, ERK1/2 inhibitor (U0126), p38 inhibitor (SB203580) and JNK inhibitor (SP600125) abrogated Cd-induced cell apoptosis. Furthermore, Cd-treated OBs exhibited signs of oxidative stress protection, including increased antioxidant enzymes superoxide dismutase and glutathione reductase levels and decreased formation of reactive oxygen species. Taken together, the results of our study clarified that Cd has direct cytotoxic effects on OBs, which are mediated by caspase- and MAPK pathways in Cd-induced apoptosis of OBs.


Subject(s)
Animals , Rats , Apoptosis/drug effects , Cadmium/toxicity , Caspases/metabolism , Environmental Pollutants/toxicity , Osteoblasts/drug effects , Oxidative Stress/drug effects , Rats, Sprague-Dawley , p38 Mitogen-Activated Protein Kinases/metabolism
18.
Article in English | IMSEAR | ID: sea-153786

ABSTRACT

Wide spread use of Di-(2-ethylhexyl) phthalate (DEHP) has made it a ubiquitous contaminant in today’s environment, responsible for possible carcinogenic and endocrine disrupting effects. In the present investigation an integrative toxico-proteomic approach was made to study the estrogenic potential of DEHP. In vitro experiments carried out with DEHP (0.1-100 μM) induced proliferations (E-screen assay) in human estrogen receptors-α (ERα) positive MCF-7 and ERα negative MDA-MB-231 breast cancer cells irrespective of their ERα status. Further, DEHP suppressed tamoxifen (a potent anti-breast cancer drug) induced apoptosis in both cell types as shown by flowcytometric cell cycle analysis. Label-free quantitative proteomics analysis of the cell secretome of both the cell lines indicated a wide array of stress related, structural and receptor binding proteins that were affected due to DEHP exposure. The secretome of DEHP treated MCF-7 cells revealed the down regulation of lactotransferrin, an ERα responsive iron transport protein. The results indicated that toxicological effects of DEHP did not follow an ERα signaling pathway. However, the differential effects in MCF-7 and MDA-MB-231 cell lines indicate that ERα might have an indirect modulating effect on DEHP induced toxicity.


Subject(s)
Apoptosis/drug effects , Breast Neoplasms/pathology , Cell Cycle/drug effects , Cell Division/drug effects , Cell Line, Tumor/drug effects , Cell Line, Tumor/metabolism , Diethylhexyl Phthalate/toxicity , Environmental Pollutants/toxicity , Estrogen Receptor alpha/drug effects , Estrogen Receptor alpha/physiology , Estrogens , Female , Gene Expression Regulation, Neoplastic/drug effects , Humans , Lactoferrin/biosynthesis , Lactoferrin/genetics , Lactoferrin/metabolism , MCF-7 Cells/drug effects , MCF-7 Cells/metabolism , Mass Spectrometry/instrumentation , Microchemistry/instrumentation , Neoplasm Proteins/drug effects , Neoplasm Proteins/physiology , Neoplasm Proteins/metabolism , Neoplasms, Hormone-Dependent/pathology , Proteomics , Tamoxifen/antagonists & inhibitors , Tamoxifen/pharmacology
19.
Braz. j. microbiol ; 45(2): 573-583, Apr.-June 2014. ilus, graf, tab
Article in English | LILACS | ID: lil-723121

ABSTRACT

Chromium pollution is produced in connection with industrial processes like in tanneries. It has been suggested that bioremediation could be a good option for clean up. The stress effect of variable chromate levels, pHs and growth temperatures on biochemical parameters of two Cr(VI) reducing bacterial strains Pseudomonas aeruginosa Rb-1 and Ochrobactrum intermedium Rb-2 was investigated. Transmission electrone microscopy (TEM) was performed to study the intracellular distribution of Cr(VI). It was observed that initial stress of 1000 µgmL-1 caused significant enhancement of all studied biochemical parameters at pH 7.0 and growth temperature of 37 °C showing great bioremediation potential of the strains. Transmission electron microscopy revealed that the distribution of chromium precipitates was not uniform as they were distributed in the cytoplasm as well as found associated with the periplasm and outer membrane. Fourier transform infrared spectroscopy showed the possible involvement of carboxyl, amino, sulpohonate and hydroxyl groups present on the bacterial cell surface for the binding of Cr(VI) ions. Cr(VI) stress brought about changes in the distridution of these functional groups. It can be concluded that the investigated bacterial strains adjust well to Cr(VI) stress in terms of biochemical parameters and along that exhibited alteration in morphology.


Subject(s)
Chromium/metabolism , Ochrobactrum/metabolism , Pseudomonas aeruginosa/metabolism , Stress, Physiological , Chromium/toxicity , Cytoplasm/ultrastructure , Environmental Pollutants/metabolism , Environmental Pollutants/toxicity , Hydrogen-Ion Concentration , Microscopy, Electron, Transmission , Oxidation-Reduction , Ochrobactrum/drug effects , Ochrobactrum/radiation effects , Ochrobactrum/ultrastructure , Pseudomonas aeruginosa/drug effects , Pseudomonas aeruginosa/radiation effects , Pseudomonas aeruginosa/ultrastructure , Spectroscopy, Fourier Transform Infrared , Surface Properties , Temperature
20.
Journal of Veterinary Science ; : 485-493, 2014.
Article in English | WPRIM | ID: wpr-24552

ABSTRACT

Cadmium (Cd) is a well-known hepatotoxic environmental pollutant. We used rat hepatocytes as a model to study oxidative damage induced by Cd, effects on the antioxidant systems, and the role of N-acetylcysteine (NAC) in protecting cells against Cd toxicity. Hepatocytes were incubated for 12 and 24 h with Cd (2.5, 5, 10 microM). Results showed that Cd can induce cytotoxicity: 10 microM resulted in 36.2% mortality after 12 h and 47.8% after 24 h. Lactate dehydrogenase, aspartate aminotransferase, and alanine aminotransferase activities increased. Additionally, reactive oxygen species (ROS) generation increased in Cd-treated hepatocytes along with malondialdehyde levels. Glutathione concentrations significantly decreased after treatment with Cd for 12 h but increased after 24 h of Cd exposure. In contrast, glutathione peroxidase activity significantly increased after treatment with Cd for 12 h but decreased after 24 h. superoxide dismutase and catalase activities increased at 12 h and 24 h. glutathione S-transferase and glutathione reductase activities decreased, but not significantly. Rat hepatocytes incubated with NAC and Cd simultaneously had significantly increased viability and decreased Cd-induced ROS generation. Our results suggested that Cd induces ROS generation that leads to oxidative stress. Moreover, NAC protects rat hepatocytes from cytotoxicity associated with Cd.


Subject(s)
Animals , Rats , Acetylcysteine/metabolism , Antioxidants/metabolism , Cadmium/toxicity , Cell Survival/drug effects , Cells, Cultured , Environmental Pollutants/toxicity , Hepatocytes/drug effects , Oxidative Stress , Rats, Sprague-Dawley , Reactive Oxygen Species/metabolism
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