Causes of Leiomyosarcoma. OCCUPATIONAL and ENVIRONMENTAL EXPOSURESConsiderable evidence supports a relationship between occupational chemicals as vinyl chloride, phenoxyacetic acid herbicides, chlorphenols, dioxin, arsenical pesticides and medications, medicinal measures as Thorotrast exposure , immunosuppressive drugs, alkylating agents, androgen- anabolic steroids, and cutting oil exposure , and the development of soft tissue sarcoma. Statistical models identified different odds ratios across sarcoma subtypes for plywood exposure and exposure to wood and saw dust. Although exploratory, this analysis suggests that occupational risk factors for sarcoma are not uniform across subtypes. Fetch PMID: 1. 14. Fetch PMID: 1. 16. Fetch PMID: 9. 34. Fetch PMID: 1. 02. The franc also commonly distinguished as the French franc (FF), was a currency of France. Between 13, it was the name of coins worth 1 livre tournois and. Lena Dunham Reveals Huge New Tattoos After Latest Health Scare, Saying It Gives Her a Sense of 'Control'. The world of independent media, all in one place. Although bone and soft tissue sarcomas are not common, a significant number of patients who develop these tumors will die with metastatic disease. Part of the reason is that many of the patients have advanced disease at diagnosis. Identification of an etiologic agent should allow for diagnosis at an earlier stage. The role of various chemical agents in the development of sarcomas needs further definition, as the literature is replete with conflicting reports. Problems exist in that we are dealing with a variety of agents with different levels of exposure, possibly resulting in different types of neoplasms. Additionally, many of the agents in question are not pure substances, but frequently are contaminated with other potentially carcinogenic agents. Finally, the majority of studies reported are from different countries. Thus, there may be unidentified operative genetic and environmental factors.. Fetch PMID: 2. 66. PREVENTION AND ENVIRONMENTAL EXPOSUREEnvironmental causes probably account for well over half of all cancer cases. Most environmental risks are determined by lifestyle choices (smoking, diet, etc.), while the rest arise in community and workplace settings. The degree of cancer hazard posed by these voluntary and involuntary risks depends on the concentration or intensity of the carcinogen and the exposure dose a person received. In situations where high levels of carcinogens are present and where exposures are extensive, significant hazards may exist, but where concentrations are low and exposures limited, hazards are often negligible. When low- dose exposures persist over time they can represent significant public health hazards (for example, exposure to secondhand tobacco smoke). Various chemicals (for example, benzene, asbestos, vinyl chloride, arsenic, aflatoxin) show definite evidence of human carcinogenicity; others are considered probable human carcinogens based on evidence from animal experiments (for example, chloroform, dichlorodiphenyl- trichloroethane . Often in the past, direct evidence of human carcinogenicity has come from studies of workplace conditions involving sustained, high- dose exposures. Risks can be increased when particular exposures occur together (for example, asbestos exposure and cigarette smoking). Reference. Occupational Cancer Based on well- documented associations between occupational exposures and cancer, it is estimated that approximately 2. U. S. Each different type of cancer may have its own set of causes. Many factors play a role in the development of cancer. The importance of these factors is different for different types of cancer. A person's risk of developing a particular cancer is influenced by a combination of factors that interact in ways that are not fully understood. Some of the factors include: personal characteristics such as age, sex, and race family history of cancer diet and personal habits such as cigarette smoking and alcohol consumption, the presence of certain medical conditions, exposure to cancer- causing agents in the environment, and exposure to cancer- causing agents in the workplace. In many cases, these factors may act together or in sequence to cause cancer. NIOSH National Istitute of Occupational Safety and Health. The NIOSH Web site features many different types of databases and information resources. They are categorized here by Chemical; Injury, Illness & Hazards Data and Information; Publications; Respirators and other Personal Protective Equipment; Agriculture; and Construction. The most popular databases include the International Chemical Safety Cards, NIOSH Pocket Guide to Chemical Hazards, and NIOSHTIC- 2. NIOSH and cancer. National Institute for Occupational Safety and Health. NIOSH site. US Dept of Labour OSHA site. Occupational Safety and Health Administration. DEbBvgIjfrqYtwBi: Three years <a href=" http:// ">cost terbinafine 250 mg india. MSN Health and Fitness has fitness, nutrition and medical information for men and women that will help you get active, eat right and improve your overall wellbeing. OSHA site. Occupational and Environmental Epidemiology Branch,Cancer. Occupational Exposure Articles. Cancer Causes and Risks,from cancer. Hcg Diet Safe Chopsticks CumberlandFact Sheets. Artificial implants and soft tissue sarcomas. The carcinogenic potential of artificial implants has been of concern in recent years. This paper examines a possible association between artificial implants and soft tissue sarcomas. Fetch PMID: 7. 72. DIOXINExposure to Agent Orange and occurrence of soft- tissue sarcomas Agent Orange was the most common herbicide used in the Second Indochina War in the course of military operations in the former South Vietnam. Agent Orange is contaminated by the carcinogen 2,3,7,8- tetrachlorodibenzo- para- dioxin (TCDD) in mean concentrations of 2 mg/kg. After much dispute of a causal association between exposure to herbicides containing TCDD and occurrence of soft- tissue sarcoma .. Methodological problems are discussed which must be addressed in the epidemiologic evaluation of the outcome of soft tissue sarcoma. Other studies cited as well. Fetch PMID: 6. 52. Fetch PMID: 3. 30. Fetch PMID: 6. 74. Fetch PMID: 7. 47. Fetch PMID: 1. 47. Risk of soft tissue sarcomas and residence near incinerator of industrial wastes. To investigate the association between occurrence of soft tissue sarcomas (STS) in Mantua and residence near an incinerator of industrial wastes. CONCLUSION: The study shows a significant increase in risk of STS associated with residence within 2 km of an industrial waste incinerator; an aetiological role of 2,3,7,8- tetrachlorodibenzo- p- dioxin (TCDD) can be hypothesised. Fetch PMID: 1. 29. Fetch PMID: 1. 11. VINYL CHLORIDE and POLYMERIC MATERIALSExposure to polymeric materials in vascular soft- tissue sarcomas.. Since 1. 97. 4, several reports have appeared on a distinct relationship between the exposure to vinyl chloride monomers and angiosarcomas of the liver. Seven other patients showed exposure to several plastics or resins other than VC. Altogether, 1. 1 of 2. Moreover, it may be suspected from this analysis that polyvinyl chloride and its monomers are not the only polymeric materials that may contribute to an induction of angiosarcomas in humans. Repeated occupational histories have to be taken from the patients to achieve data of the greatest value, since there are many professional activities that do not primarily lead to the assumption of specific exposure to polymeric materials. In order to determine whether mutational patterns in target genes in vivo are characteristic of vinyl chloride .. Two alterations were found which could be attributed to a direct effect of vinyl chloride: .. In conclusion, there are no data so far indicating a real risk for humans to develop malignant tumors due to implanted meshes. Therefore we further propagate the implantation of meshes in hernia repair in adult patients. Fetch PMID: 1. 24. EPA site for radiation exposure. Radiation. Exposure to Tobacco Smoke. Tobacco Smoke. Environmental Exposures and Cancercancer. Environment. 2Majority of Cancers are Linked to the Environment. Environment. 3Breast Cancer and the Environment Studies supported by NCIEnvironment. HEAVY METAL EXPOSUREHeavy metals are metals like lead, arsenic, cadmium. The results have important implications for the medical management of Gulf War veterans who were wounded with DU fragments and who retain fragments in their soft tissues... After lifetime observation, the incidence of soft tissue sarcomas increased significantly .. These results indicate that DU fragments of sufficient size cause localized proliferative reactions and soft tissue sarcomas that can be detected with radiography in the muscles of rats. Fetch PMID: 1. 17. Arsenic exposure and carcinogenesis. Arsenic is well established as a human carcinogen.. Arsenic .. may act as a carcinogen through inhibition of DNA repair mechanisms, leading indirectly to increased mutations from other DNA damaging agents. Although our findings need verification in a larger study group, they are consistent with the hypothesis that inhibition of DNA repair capacity is a potential mechanism for the co- carcinogenic activity of arsenic. Arsenic. Occupational exposure to heavy metals: DNA damage induction and DNA repair inhibition prove co- exposures to cadmium, cobalt and lead as more dangerous than hitherto expected Co- exposure to cadmium, cobalt, lead and other heavy metals occurs in many occupational settings, such as pigment and batteries production, galvanization and recycling of electric tools. However, little is known about interactions between several heavy metals. In conclusion, the hazard due to cobalt exposure .. Co- exposure may cause genotoxic effects, even if the concentrations of individual heavy metals do not exceed TRK- values. In mammals, it exerts multiple toxic effects and has been classified as a human carcinogen by the International Agency for Research on Cancer. Cadmium affects cell proliferation, differentiation, apoptosis and other cellular activities. In this review multiple mechanisms are discussed, .. The inhibition of DNA repair processes by cadmium represents a mechanism by which cadmium enhances the genotoxicity of other agents and may contribute to the tumor initiation by this metal. The disruption of E- cadherin- mediated cell- cell adhesion by cadmium probably further stimulates the development of tumors. It becomes clear that there exist multiple mechanisms which contribute to the carcinogenicity of cadmium, ..
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