Relevant bibliographies by topics / Carcinogenics

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Carcinogenics'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 February 2022

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Journal articles on the topic "Carcinogenics"

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Yefi mova, N. V., I. V. Myl’nikova, M. V. Kuz’mina, L. G. Lisetskaya, and Ye Ye Loznevaya. "Carcinogenic risk assessment in population living in the ecologically problematic areas of Irkutsk region." Occupational Health and Industrial Ecology, no. 2 (March 14, 2019): 117–21. http://dx.doi.org/10.31089/1026-9428-2019-2-117-121.

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Irkutsk region is among territories of intense industrial development. Considerable part of the regional population is long exposed to chemical pollutants of environmental objects. Th e authors evaluated carcinogenic risk for the population of industrial centers and rural area. Findings are that maximal carcinogenic risk is carried by the urban population. Aggregated carcinogenic risk parameters evaluation proved inhalation to be a priority route of exposure. Irkutsk region appeared to have territories with high carcinogenic risk for public health. Among a list of chemicals in the ambient air are priority carcinogens: six-valent chromium and lead. The evidences necessitate measures on the risks minimization. Due to absent data on carcinogens content of drinkable water in some rural area, the necessity is to evaluate risk for the rural population by studies of drinkable water quality that does not match hygienic regulations, because oral one is a main route of carcinogens intake.
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Rakitskii, Valery N., Yuriy I. Stepkin, Oleg V. Klepikov, and Semyon A. Kurolap. "Assessment of carcinogenic risk caused by the impact of the environmental factors on urban population health." Hygiene and sanitation 100, no. 3 (April 16, 2021): 188–95. http://dx.doi.org/10.47470/0016-9900-2021-100-3-188-195.

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Introduction. The high level of environmental pollution in industrial cities, including carcinogens, causes an unacceptable risk to public health. In this regard, a quantitative risk assessment is required to develop preventive measures to reduce it. The aim of the study was to assess the carcinogenic risk to the health of the population of an industrialized city, caused by the probable presence of carcinogens in the ambient air, drinking water of the centralized water supply system, and the soil of the residential area. Material and research methods. The laboratory control of the content of carcinogens in environmental objects of the city of Voronezh for 2017-2020 was used as the reference data. The carcinogenic risk was assessed under the provisions of Guideline R. 2.1.10.1920-04 “Guidelines for assessing the risk to public health when exposed to chemicals that pollute the environment.” Results. Taking into account the regional peculiarities of the composition of pollutant emissions into the atmospheric air, 1,3-butadiene (source - production of synthetic rubber) should be classified as priority carcinogens requiring systematic monitoring and measures to reduce emissions and, accordingly, concentrations in the surface layer of atmospheric air and chromium6+ compounds (the main source is an aircraft plant), which contribute 69.9-75.7% and 21.7-26.9%, respectively, to the total values of the individual carcinogenic risk, which exceeds the maximum permissible level (1 • 10-4). The carcinogenic risk from exposure to drinking water pollutants (halogenated organic substances) and soil (under the scenario of accidental ingestion by preschool children) is below the maximum permissible risk (1 • 10-4). Conclusion. It is necessary to pay attention to increasing the sensitivity of the applied laboratory control methods, expanding the list of controlled carcinogenic pollutants, improving the monitoring system of carcinogens, and implementing measures to reduce the carcinogenic risk associated with atmospheric air pollution.
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Berezin, I. I., and G. A. Nikiforova. "About some aspects of sanitary and hygienic certification of carcinogenic enterprises." Russian Journal of Occupational Health and Industrial Ecology, no. 9 (March 19, 2020): 564–65. http://dx.doi.org/10.31089/1026-9428-2019-59-9-564-566.

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The actual problems of sanitary-hygienic certification of carcinogenic organizations are presented. The need to extend certification to all carcinogenic production, which will provide full information on the carcinogenic hazards of working conditions in order to eliminate the harmful effects of carcinogens.
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McDonald, AL, RJ Fielder, GE Diggle, DR Tennant, and CE Fisher. "Carcinogens in food: priorities for regulatory action." Human & Experimental Toxicology 15, no. 9 (September 1996): 739–46. http://dx.doi.org/10.1177/096032719601500904.

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A pragmatic possible approach to the prioritization of chemical carcinogens occurring as food contaminants is described, based on the carcinogenic risk to the popula tion. This should be of value in ensuring that resources for assessment and management of carcinogens in food are directed to the most important areas with regard to carcinogenic risk to the population. Key components of this approach are an assessment of the carcinogenic hazard to humans combined with estimations of intakes per person and of the proportion of the population exposed. These are used to derive an index referred to as the Population Carcinogenic Index. Concerning the hazard assessment expert judgement is used to place the chemical in one of five categories. The highest category is for chemical carcinogens that are believed to act by a genotoxic mechanism. It is recognised that such com pounds may vary enormously with respect to their potency and various approaches to ranking carcinogens on the basis of potency are reviewed. The approach adopted is to subdivide the genotoxic carcinogens category into high, medium and low potency based on the TD 50 value. Methods of estimating intakes and exposed populations are considered and an approach which groups these into broad categories is developed. The hazard and exposure assessments are then combined to derive the Population Carcinogenicity Index.
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MEDRADO-FARIA, MARCILIA DE A., JOSÉ WILSON R. DE ALMEIDA, DIRCE M. T. ZANETTA, and GILKA J. F. GATTÁS. "Nervous system cancer mortality in an industrialized area of Brazil 1980 - 1993." Arquivos de Neuro-Psiquiatria 58, no. 2B (June 2000): 412–17. http://dx.doi.org/10.1590/s0004-282x2000000300003.

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OBJECTIVES: The industrialization process and nervous system cancer (NSC) mortality in a urban region of Brazil. METHOD: From registries of the State System of Data Analysis Foundation (SEADE), 103 males deaths by NSC (ICD-9) in Baixada Santista (BS), from 1980 to 1993 were selected. Mortality ratios were calculated comparing the standardized mortality rate for ages over 10 years old (G1) and for the age group from 35 to 64 years old, in the industrialized and non-industrialized areas in three periods: 1980-1993, 1980-86, 1987-93. RESULTS: A statiscally significant high mortality was observed in the industrialized area, for ages over 10 in all periods and only from 1980 to 1993 for ages from 34 to 64. The highest mortality ratio occurred from 1980-86 for ages over 10 - 4.12 (CI 1.79-9.42). CONCLUSION: High mortality was probably related to the environmental and occupational exposure to many organic and inorganic chemical substances, considered carcinogenics, such as aliphatic and aromatic hydrocarbons, organochlorinated, formaldehyde, nitrogenated compounds and heavy metals, found in the port and industrial complex. We discuss the importance of case-control studies in characterizing the association of these and other risk factors in the determination of NSC.
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Klepikov, Oleg Vladimirovich, Yuriy Ivanovich Stepkin, Semen Aleksandrovich Kurolap, and Sergey Aleksandrovich Yeprintsev. "Organization of monitoring of carcinogens in the atmospheric air of the city and assessment of the health risk." Sanitarnyj vrač (Sanitary Doctor), no. 11 (November 1, 2020): 19–28. http://dx.doi.org/10.33920/med-08-2011-02.

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The aim of the study was to assess the carcinogenic risk to the health of the population of an industrialized city, caused by the probable presence of carcinogens in the ambient air. The results of laboratory control of the content of carcinogens in the atmospheric air of the city of Voronezh for 2017–2020 were used as the initial data. The carcinogenic risk was assessed in accordance with the provisions of Guideline R. 2.1.10.1920–04 «Guidelines for assessing the risk to public health when exposed to chemicals that pollute the environment.» Taking into account the regional peculiarities of the composition of pollutant emissions into the atmospheric air, 1,3-butadiene (source — production of synthetic rubber) should be classified as priority carcinogens requiring systematic monitoring and measures to reduce the volume of emissions and, accordingly, concentrations in the surface layer of atmospheric air and chromium 6+ compounds (the main source is an aircraft plant). These substances, depending on the territory (transport or industrial), contribute 69.9–75.7 % and 21.7–26.9 %, respectively, to the total values of the individual carcinogenic risk (from 4.27 × 10 –3 to 4.90 × 10 –3 for the adult population, from 3.38 × 10 –4 to 3.82 × 10 –4 for children 6 years old). For the rest of the laboratory controlled carcinogens (formaldehyde, lead, soot, styrene), the risks do not exceed the maximum permissible value. It was found that the territorial coverage of the urban area of Voronezh by monitoring the content of carcinogens in the atmospheric air (5 stationary and 5 route observation posts) and the number of laboratory-determined carcinogens (6 out of 18 taken into account in the projects of maximum permissible emissions of enterprises) is insufficient to obtain reliable information on the value carcinogenic risk to public health. To reduce the associated uncertainties in assessing the carcinogenic risk, further studies of the content of 8 carcinogens (1,3-butadiene, formaldehyde, lead, carbon black, chromium 6+, benzene, benz/a/pyrene, styrene) are planned at 13 additional control points of the urban area.
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Efimova, N. V., S. S. Khankharev, Vladimir R. Motorov, and E. V. Madeeva. "ASSESSMENT OF THE CARCINOGENIC RISK FOR THE POPULATION OF ULAN-UDE." Hygiene and sanitation 98, no. 1 (March 27, 2019): 90–93. http://dx.doi.org/10.18821/0016-9900-2019-98-1-90-93.

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Introduction. Oncological pathology has a high medical and social significance, so it is important to study the conditions of its formation. The aim of the study was to evaluate the cumulative carcinogenic risk for the population of the administrative center of the Republic of Buryatia (Ulan-Ude). Material and methods. The identification of the carcinogenic hazard caused by the entry of chemical ingredients into the ambient air was carried out in 2005-2015. The exposure assessment is based on long-term average annual concentrations of carcinogens in the air, drinking water, food. Indices of comparative carcinogenic hazard (HCR) and individual carcinogenic risk (ICR) are calculated. Results. The huge engineering enterprises are sources of several substances with carcinogenic effects (formaldehyde, chrome VI, cadmium, niсkel, epichlorohydrin, etc.).The individual carcinogenic risk for residents of Ulan-Ude is included in the range unacceptable for the general population. The main pathway for chemical agents to enter the body is inhalation (79%). The greatest contribution to the total individual carcinogenic risk on admission from the air was made by formaldehyde, chromium VI and Benz(a)pyrene. Priority carcinogens coming from drinking water and food are arsenic, cadmium, lead. Conclusion. Results of the assessment of individual carcinogenic risk in Ulan-Ude indicate an unacceptable level of the impact on the population. The assessment has a number of uncertainties, which determines the need to further improve the monitoring system for carcinogenic hazards.
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Abd Manan, Teh Sabariah, and Amirhossein Malakahmad. "Automated Detections of Carcinogenic Compounds in Estuaries: A Short Review." Applied Mechanics and Materials 699 (November 2014): 885–90. http://dx.doi.org/10.4028/www.scientific.net/amm.699.885.

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Cancer accounted around 13% of all deaths in 2008. About 70% of all cancer deaths occurred in low and middle income countries. Deaths from cancer worldwide are projected to continue to rise to over 13.1 million in 2030. Previous reports indicated that reservoir such as rivers and lakes contain various carcinogenic compounds. The carcinogens are being transported from the release points to the intake points. To avoid this phenomenon happen, the fast and accurate detection of carcinogens concentrations in water is crucial. This review presents automated detection methods of carcinogenic compounds in watercourses. Automated detections, particularly the application of sensors, have a relatively higher speed and sensitivity compared to chemical and biological approaches. However, sensors application limits on its functions. This review gives a description on the history of automated detections and various types of sensors such as automated optical sensor, submersible ultraviolet fluorometer sensor, photoelectrochemical sensor with the detection of DNA damage and trihalomethanes (THMs) sensor for detection of carcinogenic compounds. Sensors are varied according to specific types of carcinogens.
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Umemura, Takashi. "Possible Carcinogenic Mechanisms Underlying Renal Carcinogens in Food." Food Safety 2, no. 2 (2014): 17–30. http://dx.doi.org/10.14252/foodsafetyfscj.2014015.

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Pereira, Michael A. "Mouse Liver Tumor Data: Assessment of Carcinogenic Activity." Toxicology and Industrial Health 1, no. 4 (October 1985): 311–33. http://dx.doi.org/10.1177/074823378500100421.

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Significant numbers of chemicals have been shown to be carcinogenic in mouse liver although they do not exhibit carcinogenic activity in other organs or tissues of mice or rats. This review focuses on the reasons for the unique susceptibility of the mouse liver to these carcinogens and the extent to which the carcinogenic activity of a chemical in mouse liver can be used to predict carcinogenicity in humans. Many of these mouse liver carcinogens lack genotoxic activity and, as such, have been proposed to be tumor promoters. Two mechanisms that may explain the action of nongenotoxic carcinogens in mouse liver are reviewed. These are: (1) direct action on precursor cancer cells, either to accelerate their growth or to prevent their death and (2) the selective growth advantage, resulting from regenerative hyperplasia of precursor cancer cells in response to the necrosis of normal cells produced by hepatotoxins. Estimating human health risks on the basis of mouse liver tumor data is believed to differ for nongenotoxic and genotoxic carcinogens in two fundamental ways. The first involves intraspecies extrapolation and the second involves low-dose extrapolation. In conclusion, although mouse liver tumor data are seen to be of value in estimating human health hazard, it is important to distinguish between genotoxic and nongenotoxic mechanisms in applying such data. Further study of the biochemical and molecular mechanisms of chemical carcinogens is necessary to determine the relationship between their activity in mouse liver and their activity in humans.
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Dissertations / Theses on the topic "Carcinogenics"

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Pieroli, Dayse Aparecida. ""Análise quantitativa das regiões organizadoras nucleolares (NORs) em carcinomas epidermóides desenvolvidos em hamsters a partir do modelo DMBA-indução com agentes clareadores dentais"." Universidade de São Paulo, 2003. http://www.teses.usp.br/teses/disponiveis/23/23134/tde-22102003-110736/.

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RESUMO A grande prevalência de câncer bucal está relacionada à ação de agentes e de fatores físicos e químicos. As substâncias químicas têm grande importância na indução de cânceres em humanos. Existe grande preocupação em relação aos agentes clareadores à base de peróxido de carbamida a 10%, usados com freqüência na técnica de clareamento caseiro de dentes vitalizados. A preocupação deve-se ao potencial carcinogênico dessas substâncias. Com o efeito somatório sobre as células, toda e qualquer substância deve ser avaliada quanto ao seu potencial carcinogênico sobre a mucosa bucal. Com a intenção de avaliar a proliferação celular nos carcinomas epidermóides desenvolvidos no modelo DMBA-indução associado ao peróxido de carbamida 10%, utilizou-se um dos marcadores biológicos de proliferação celular, que é o método histoquímico pela técnica AgNOR. Foram avaliados quantitativamente os carcinomas epidermóides desenvolvidos no modelo DMBA-indução + peróxido de carbamida 10%, observando-se que: nos grupos I, II, III e VII, onde não houve proliferação celular compatível com alteração neoplásica, o número de ocorrências de NORs/núcleo foi menor que nos demais grupos; no grupo IV (DMBA), o número de ocorrência de NORs/núcleo foi menor que nos grupos V e VI (peróxido de carbamida 10% + DMBA). O número de ocorrência de NORs/núcleo foi maior nos grupos V (DMBA + Opalescence) e VI (DMBA + White & Brite), em que foram desenvolvidos carcinomas, caracterizando maior proliferação das células e maior grau de malignidade dos carcinomas epidermóides desenvolvidos. Tais conclusões evidenciaram que a proliferação celular nos grupos associados (clareadores + DMBA) foi mais intensa que no grupo do carcinógeno (DMBA), possivelmente pelo efeito promotor dos agentes clareadores. Observou-se uma ação promotora dos clareadores dentais à base de peróxido de carbamida 10% no modelo estudado, com capacidade para potencializar carcinógenos, levando a um possível desenvolvimento neoplásico.
SUMMARY Oral squamous cell carcinoma is the mouth most prevalent malignancy, accouting for more than 90% of all oral malignancies. It also known that the development of oral cancer has a strong relationship with chemical and physical action of some agents that are in daily contact with oral mucosa as drugs, food, alcohol, tobacco and environmental factors. Oral carcinogenesis has a cumulative effect upon cells, every substance with potential risk of evidencing this malignant process showed be evaluated. The concern is about carcinogenic potential this chemical bleaching agents in the proliferation cells. The bleaching agents containing 10% carbamide peroxide are often used for vital teeth home bleaching and there is the risk of tissue damage from ingestion of the substance and contact with the oral mucosa during the bleaching process. The current study involve the evaluation of the cell proliferation and squamous cell carcinomas development in DMBA induction-model + 10% carbamide peroxide using biologic markers in the detection of incipient cellular alterations with histochemical method AgNOR, to investigate the relationship between the number of interphase silver-stained nucleolar organizer regions (AgNORs). The numbers of the NORs can be related to proliferative activity and the degree of the developed malignancy tumours. The quantitative analysis of the number of the NORs in the group I (acetone), II (Opalescence), III (White & Brite) and VII (destiled water) showed no cells proliferation compatible with neoplasic alterations. The occurrence of the number per nucleus was less than in the others groups. The groups IV (carcinogen DMBA), V (DMBA + 10% carbamide peroxide - Opalescence), VI (DMBA + 10% carbamide peroxide - White & Brite) showed the development micro-invasive and invasive carcinomas. The occurrence of the number of the NORs/nucleus was greater in those three groups than in the groups without carcinomas. The groups V (DMBA + Opalescence) and VI (DMBA + White & Brite) developed a greater of the occurrence of the number of the NORs per nucleus than in the group IV (DMBA). In the groups V and VI with developed invasive carcinomas showed growth cells proliferation and increase in the rate of the malignancy in the squamous cells carcinomas developed. This showed an cell proliferation of the groups (DMBA + 10% carbamide peroxide) is more intensive than in the group IV, probably by promoter effect of the bleaching agents. It was concluded that the bleaching agents based on 10% carbamide peroxide used in this study model, has a enhance promoter action, with capacity for carcinogens pottentialy and developed neoplasic alterations.
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Guilhen, Ana Carolina Trindade. "Estudo das variantes alelicas da N-acetiltransferase 2 ( NAT2) em cancer de prostata e tireoide na população brasileira da região de Campinas." [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/310285.

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Orientador: Laura Sterian Ward
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
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Resumo: Os genes das N-acetiltransferases, que são polimórficos na população, codificam enzimas envolvidas na metabolização de drogas e de xenobióticos, como os provenientes do cozimento de carnes e do tabaco, e podem estar implicados no risco para o desenvolvimento de neoplasias. Para estudar o envolvimento dos genes NAT2 em tumores na população brasileira da região de Campinas, avaliamos seis polimorfismos (C282T; T481C; G590A; A803G; G857A; G191A) em câncer de tireóide e quatro (T481C; G590A; A803G e G857A) em câncer de próstata. Em um estudo de caso-controle, comparamos 126 indivíduos com câncer de próstata com 101 indivíduos controles com hiperplasia prostática benigna pareados para idade e condições de dieta e exposição ambiental; 139 indivíduos com câncer de tireóide (112 CP e 27CF) e 179 controles também adequadamente pareados. A análise foi feita pela extração de DNA com base no sangue periférico, PCR e restrição enzimática. Os polimorfismos T481C (76.24%) e A803G (59.41%) apareceram com maior freqüência entre os pacientes controles com hiperplasia prostática benigna do que nos com câncer da próstata (60.32% e 45.60%, p=0.0152 e 0.0186, respectivamente). Ao contrário, G857A foi mais freqüente entre os pacientes com câncer da próstata (18.4%) do que nos controles com hiperplasia prostática benigna (5.94%; p=0.0044). Assim, a presença do polimorfismo NAT2T481C reduziu o risco de câncer da próstata (OR=2.115; 95% C.I=1.155-3.872). Da mesma forma, a presença do polimorfismo NAT2A803G reduziu o risco de câncer da próstata (OR=1.973; 95%C.I=1.120-3.474; p=0.0186). Ao contrário, a presença do polimorfismo G857A aumentou o risco para câncer da próstata mais de quatro vezes (OR=4.095; 95%C.I=1.551-10.812). A presença de um fenótipo de acetilação lenta aumentou o risco para câncer de próstata em 24 vezes (OR=24.145;95%CI=1.416-411.63). Nos carcinomas da tireóide, observamos que mutações pontuais de tipo A803G apareceram com maior freqüência entre os casos de carcinomas (46.76%) do que nos controles (31.84%) (p=0.0069), enquanto que mutações pontuais de tipo G191A e C282T foram mais freqüentes nos controles (25,70% e 68.16% dos casos, respectivamente) do que nos casos (5,04% e 33,81%, respectivamente) (p=0,0001). Assim, a herança do polimorfismo A803G representou um risco de 1.8 vezes maior de desenvolver carcinoma diferenciado da tireóide (OR= 1.880; 95% IC= 1.189-2.973). Por outro lado, a herança dos polimorfismos G191A e C282T do gene NAT2 representou um fator de proteção de cerca de 80,6% contra o risco de desenvolver um carcinoma diferenciado da tireóide (OR=0.153; 95% IC=0.067-0.352 e OR=0.239; 95% IC=0.149-0.382, respectivamente). Em conclusão, nossos dados mostram que polimorfismos do gene NAT2 estão associados ao risco para o desenvolvimento tanto dos tumores de próstata quanto de tireóide, podendo vir a ser importantes marcadores de susceptibilidade para tais doenças em nossa população
Abstract: N-acetyltransferases (NAT), which are polymorphic in the population, metabolize important carcinogens such as different kinds of meat and tobacco products that have been directly implicated in the tumor initiation process. In order to investigate the role of NAT2 polymorphisms in the susceptibility to cancer in the Brazilian population from our region, we studied 6 polymorphisms (C282T; T481C; G590A; A803G; G857A; G191A) in differentiated thyroid cancer and 4 polymorphisms (T481C; G590A; A803G e G857A) in prostate cancer. We conducted a case-control prospective study comparing 126 prostate cancer to 101 benign prostatic hyperplasia patients paired for age, diet and environmental exposure; 139 thyroid cancer patients (112 papillary carcinomas and 27 follicular carcinomas) and 179 paired controls. Analyses were performed in DNA extracted from peripheral blood using the polymerase chain reaction-based restriction fragment length polymorphism method. We observed T481C (76.24%) and A803G (59.41%) polymorphisms with higher frequency among control patients than in prostate cancer cases (60.32% e 45.60%, p=0.0152 e 0.0186, respectively). On the contrary, G857A polymorphisms was more frequent among prostate cancer patients (18.4%) than in the benign hyperplasia control partients¿ group (5.94%; p=0.0044). Therefore, the presence of NAT2T481C polymorphism reduced the risk of prostate cancer (OR=2.115; 95% C.I=1.155-3.872). Likewise, the presence of NAT2A803G reduced the risk of prostate cancer (OR=1.973; 95%C.I=1.120-3.474; p=0.0186). On the contrary, the presence of G857A increased the risk for prostate cancer more than 4 times (OR=4.095; 95%C.I=1.551-10.812). The presence of a low acetylation phenotype increased the risk for prostate cancer more than 24 times (OR=24.145;95%CI=1.416-411.63). Regarding thyroid cancer, we observed that point mutations like A803G appears more frequently among thyroid carcinomas (46.76%) than in controls (31.84%) (p=0.0069), while G191A and C282T polymorphisms were more frequent among controls (25,70% and 68.16% of the cases, respectively) than among thyroid cancers (5,04% e 33,81%, respectively) (p=0,0001). Therefore, the inheritance of an A803G polymorphism represents an 1.8 times higher risk to thyroid cancer development (OR= 1.880; 95% IC= 1.189-2.973). On the other hand, the inheritance of G191A and C282T NAT2 polymorphisms represents a protection around 80,6% against the risk of thyroid cancer development (OR=0.153; 95% IC=0.067-0.352 and OR=0.239; 95% IC=0.149-0.382, respectively). In conclusion, our data demonstrate that NAT2 gene polymorphisms are associated to the risk to both prostate and thyroid cancer, suggesting they could become useful molecular markers of susceptibility to these tumors in our population
Mestrado
Clinica Medica
Mestre em Clinica Medica
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Yano, Claudia Lumy. "Estudos dos efeitos citotoxicos e de estresse oxidativo induzido pelo cloreto de cadmio associado ou não ao sulfato de zinco em celulas musculares esqueleticas e neoplasicas." [s.n.], 2006. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317755.

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Orientador: Maria Cristina Cintra Gomes Marcondes
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Metais pesados como o cádmio são considerados agentes tóxicos devido sua extensiva utilização nas indústrias e agropecuária e, como conseqüência, são amplamente dispersados no meio ambiente. No entanto, o cádmio tem sido foco, também, de inúmeras pesquisas relacionadas a exposição humana e suas conseqüências patológicas como o câncer. Estudos, claramente, caracterizam as relações de tumor de pulmão com a inalação do cádmio e mostram a possível participação deste metal tanto na iniciação quanto na progressão tumoral. Por outro lado, são raros os relatos da literatura envolvendo o mecanismo de ação do cádmio em tecido muscular, uma vez que já foi observado acúmulo desse metal em musculatura esquelética de animais. A administração do cloreto de cádmio, metal pesado designado como carcinogênico, em linhagem de células musculares esqueléticas C2C12 promoveu lesões consistentes com estresse oxidativo, observado pela diminuição da viabilidade celular, aumento da peroxidação de lipídios (conteúdo de malondialdeído) e conseqüente diminuição da enzima antioxidante glutationa transferase (GST). O estresse oxidativo, possivelmente, alterou a adesão celular e, conseqüentemente, houve retração dos miotúbulos, observada através de microscopia de luz e microscopia eletrônica de varredura (Capítulo I- Trabalho publicado no periódico Free Radical Biology & Medicine, 2005). A atenuação das lesões promovidas pelo cloreto de cádmio em linhagem de células C2C12 foi verificada com o pré-tratamento com o sulfato de zinco antecedendo o tratamento com cloreto de cádmio. Os efeitos protetores foram observados através da preservação da viabilidade celular, da GST, e diminuição do conteúdo de malondialdeído. A ação protetora foi verificada, também, na maior preservação da adesão celular, principalmente, contra as maiores concentrações de cádmio (Capítulo II- Trabalho a ser submetido ao periódico Free Radical Biology & Medicine). Por outro lado, a exposição crônica de células tumorais, linhagem de adenocarcinoma de cólon MAC13, ao cloreto de cádmio promoveu alterações morfológicas associadas ao aumento da atividade mitocondrial, interferência quanto à atividade lisossomal e diminuição da viabilidade celular, principalmente, na maior concentração de cádmio, após 24hs de exposição (Capítulo III- Trabalho a ser submetido ao periódico International Journal of Cancer)
Abstract: The heavy metals as cadmium are a toxic agent since it is extensively utilized in industry and can be amply distributed in environment. The cadmium is research focused as its pathological consequences in human exposure as it has been classified as carcinogenic agent. This fact is evident since the cadmium inhalation can be related to lung tumour and many studies show the possible participation of the cadmium on tumoral cells initiation and progression. However, few studies observed that cadmium can be accumulated in animal skeletal muscle cells and its action mechanisms are not completed known. The cadmium chloride exposure promoted oxidative stress and morphologic changes in C2C12 myotubes cell, in vitro, associated to decrease on cellular viability, high lipid peroxidation (increase on malondialdehyde content, MDA) and decrease on glutathione-S-transferase (GST) activity. The cadmium chloride produced chances on the cellular adhesion, integrity and retraction in C2C12 myotubes cells. These effects could be attenuated by zinc sulphate pre-treatment, which maintained the cellular viability, GST activity, reducing the MDA content. The zinc sulphate pre-treatment preserved the cellular adhesion, especially in high cadmium chloride concentration. Additionally, the tumoral cells (colon adenocarcinoma MAC 13) chronically exposed to cadmium chloride showed increase on the mitochondrial activity, and reduction on lysosomal and cellular viability, especially at high cadmium chloride concentration after 24h of treatment, probably indicating the tumoral cell changes
Doutorado
Biologia Celular
Doutor em Biologia Celular e Estrutural
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Dempsey, R. "The genetic toxicology of carcinogenic compounds." Thesis, Swansea University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.636437.

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This thesis involved the development of a range of assay systems for the detection of environmental mutagens and carcinogens. Initially a protocol was optimised for the induction of mitotic gene conversion in stationary-phase cultures of the yeast Saccharomyces cerevisiae, strain JD1 following exposure to compounds which require exogenous metabolic activation, which involved an initial incubation at 37oC for 2 hours followed by a 16 hour incubation at 28oC. This protocol was found to be effective for the detection of cyclophosphamide and sterigmatocystin. In two separate studies, the activities of a total of 14 different compounds were then investigated in yeast using this, and other protocols involving exponential-phase cultures. In the first study, benzidine and diaminoterphenyl were detected, although, despite being structural analogues, their metabolic requirements differed. Dimethylaminoazobenzene and cyanodimethylaniline could not be detected under any of the conditions examined. In the second of these studies 8 carcinogens and 2 non-carcinogens were examined. Only one of the carcinogens, Acrylonitrile, was detected. The inactivity of the other 7 carcinogens was considered to be due to their ineffectiveness at inducing mitotic gene conversion. A third study indicated that respiratory status of the yeast strain used, had both quantitative and qualitative effects on the detection of sterigmatocystin, benzidine and diaminoterphenyl. Further studies were performed on two additional assays, chromosomal aberration induction and mammalian cell transformation, as these endpoints had proved very successful for detecting chemicals which were not readily detected in assays for other genetic endpoints. BZD was found to induce chromosomal abberrations in peripheral human lymphocyte cultures, in the absence of S9, which was in contrast to the activity detected in the yeast system. It was suggested that this was due to metabolic competence of the human lymphocyte cells. Studies on the stepwise transformation of Syrian hamster dermal cells, led to the suggestion of a model for the occurrence of aneuploidy events during this process, and their fixation at completion of transformation. The significance of this with respect to the observed occurrence of aneuploidy with cancer is discussed.
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Lee, Chung-Wei Ph D. Massachusetts Institute of Technology. "Pathogenesis of the carcinogenic bacterium, Helicobacter pylori." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/39909.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Biological Engineering Division, 2007.
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Includes bibliographical references.
Gastric cancer is the second most common malignancy in the digestive system and the second leading cause of cancer-related death worldwide. Epidemiological data and experimental studies have identified several risk factors for gastric cancer, including Helicobacter pylori infection, low fruit and vegetable intake, N-nitrosoamine exposure, high salt diet, and smoking. Among these risk factors, H. pylori infection is the major cause of gastric cancer. Therefore, H. pylori has been classified as a type 1 (definite) carcinogen for gastric cancer by the World Health Organization (WHO) in 1994. H. pylori colonizes the human stomach and has been definitively linked to chronic gastritis. Infection in some: susceptible individuals results in serious gastric disease such as peptic ulcer or gastric cancer. The first aim of this thesis was to examine the role of different T cell subpopulations in H. pylori gastritis. Using a murine adoptive transfer model, adoptive transfer of wildtype (wt) effector T cells (TE) into H. pylori-infected lymphopenic Rag2-/- recipient mice resulted in H. pylori-associated corpus gastritis superimposed with non-specific gastroduodenitis. Cotransfer with TE and regulatory T cells (TR) from wt or IL10-/- mice reduced gastroduodenitis, but only wt TR cells reduced corpus gastritis.
(cont.) The second aim of this thesis was to evaluate the effect of vitamin C on H. pylori gastritis in vitamin C-deficient gulo-/- mice. It was found that a high vitamin C supplementation (3300 mg/L) in drinking water did not protect H. pylori gastritis, while a low vitamin C supplementation (33 mg/L) reduced the severity of H. pylori gastritis via an attenuated cellular immune response to H. pylori. The third aim of this thesis was to examine the role of DNA repair in H. pylori-associated gastric disease. We found that H. pylori-associated premalignant gastric atrophy was more severe in infected mice lacking DNA repair protein 3-alkyladenine DNA glycosylase or 06-methylguanine DNA methyltransferase in comparison to infected wt control mice. The forth aim of this thesis was to examine whether antimicrobial H. pylori eradication therapy could prevent gastric cancer development in INS-GAS mice, a model of gastric cancer. We found that antimicrobial H. pylori eradication therapy prevented the progression to gastric cancer in H. pylori-infected INS-GAS mice when treatment was instituted at an early stage of H. pylori infection.
(cont.) In conclusion, these studies provide further insight into the role of host immune responses in H. pylori pathogenesis. Additionally, information was garnered regarding the roles of vitamin C supplementation, DNA repair proteins, and H. pylori eradication therapy in H. pylori-associated gastric disease using genetically manipulated mice.
by Chung-Wei Lee.
Ph.D.
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Santos, José Miguel de Oliveira Dias Prudente dos. "Comparative effects of sediments contaminated by carcinogenic and non-carcinogenic PAHs in Dicentrarchus labrax: a semi-quantitative histopathological approach." Master's thesis, Faculdade de Ciências e Tecnologia, 2013. http://hdl.handle.net/10362/10771.

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Dissertação para obtenção do Grau de Mestre em Engenharia do Ambiente
Polycyclic Aromatic Hydrocarbons (PAHs) are considered priority pollutants due to their high risk to environmental and human health. Due to their hydrophobic character, in aquatic environments, these substances tend to adsorb to the particulate fraction and accumulate in the sediments. Despite their division into carcinogenic, potentially carcinogenic and non-carcinogenic to humans, little is known about the differences between modes of action of carcinogenic and non-carcinogenic PAHs in aquatic organisms. In order to understand the toxicity mechanisms of these two classes, laboratory assays were performed with juvenile basses (Dicentrarchus labrax) exposed to contaminated artificial sediments for 28 days. Sediment were spiked with environmentally-relevant concentrations of benzo[b]fluoranthene (a carcinogenic PAH) and phenanthrene (non-carcinogenic), either isolated or in mixture. Exposure effects were analysed through an indice-based semi-quantitative histopathological approach in hepatic tissue, due to the role of liver in the accumulation and detoxification of xenobiotics. Overall, significant alterations in the hepatic tissue were detected relatively to control tests, either for isolated or mixture assays, despite the low levels of exposure. Individuals exposed to benzo[b]fluoranthene presented higher severity and number of hepatic lesions compared to phenanthrene. Furthermore different toxicants caused different patterns of histopathological lesions and alterations. The results also show that histopathological condition indices of mixture-exposed individuals do not match the expected additive effects, suggesting a possible synergistic interaction effect between the contaminants. This work allows the conclusion that, albeit considered low, environmentally-relevant concentrations of PAHs in sediments may cause adverse effects in organisms, in this case, a demersal fish. On the other hand, results also suggest that a non-carcinogenic PAH may be responsible for considerable toxic effects, even in moderate concentrations. Altogether, requalifying risk assessment for these substances becomes of the upmost importance since PAHs (as other pollutants) are usually present in the environment in complex mixtures.
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Aquilina, Noel. "Evaluation of Human exposure to airborne carcinogenic compounds." Thesis, University of Birmingham, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.532265.

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Singh, Rajinder. "Are DNA adducts relevant markers of carcinogenic risk?" Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/30782.

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The formation of DNA adducts by the covalent binding of genotoxic chemicals to DNA and subsequent activation of proto-oncogenes is regarded as one of the initiating events in the process of carcinogenesis. An animal study was instigated using mice (SWR (high), Balb/c (intermediate) and C57BL/6J (low)) varying in their susceptibility to lung carcinogenesis, dosed with a single intraperitoneal injection of saline or /V-nitrosodiethylamine (NDEA) at 15 or 90 mg/kg body weight. Target (lung) and non-target tissues were removed 5h, 10h, 24h, 4d, 7d, 28d and 56d after dosing. Further groups of mice dosed with the same regime were left up to 18 months to allow for the development of tumours. Immunoslot-blot analysis was used for the determination of N-7 ethylguanine (N-7 EtG) and O6 ethylguanine (O6 EtG) adduct levels in the DNA from the tissues. Results from the high dose indicated a high tumour incidence, however there was no major significant difference in the levels or persistence of DNA adducts in target and non-target tissue of the three strains of mice. The relevance of these results is unclear since at this dose toxicity may have occurred resulting in cell death and induction of tumours by compensatory cell proliferation. No results were obtained for DNA adduct levels in the target tissue from the low dose group due to insufficient sensitivity of the immunoslot-blot method. The incidence of tumours in C57BL/6J mice was lower compared to the other two strains. These results do not allow decisive conclusions to be drawn concerning relationship between total levels of DNA adducts and differences in tumour susceptibility for the strains of mice. However the increased presence of DNA adducts in the target tissues (as exemplified by the C57BL/6J mice) significantly increased the likelihood of tumour development implying that DNA adducts are relevant markers for carcinogenic risk.
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Lian, Fuzhi. "The anti-carcinogenic effect of carotenoids against lung cancer /." Thesis, Connect to Dissertations & Theses @ Tufts University, 2006.

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Thesis (Ph.D.)--Tufts University, 2006.
Submitted to the School of Nutrition Science and Policy. Adviser: Xiang-Dong Wang. Includes bibliographical references. Access restricted to members of the Tufts University community. Also available via the World Wide Web;
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Frandsen, Henrik. "Food derived carcinogenic aminoimidazoazaarenes : bioactivation and DNA adduct formation /." København : Levnedsmiddelstyrelsen, 1996. http://hdl.handle.net/1800/452.

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Books on the topic "Carcinogenics"

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Castegnaro, Marcel, and Eric B. Sansone. Chemical Carcinogens. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71342-2.

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Mehrotra, N. K. Carcinogenic effects of pesticides. Lucknow, India: Industrial Toxicology Research Centre, 1990.

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Tinkler, J. J. B. Carcinogenic hazard of wood dusts. London: HMSO, 1986.

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Kellard, Brian. Hazardous substances: Carcinogens guide. Kingston upon Thames: Croner Publications, 1991.

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Chui, Connie K. F. Chemical carcinogens in food. Salford: University of Salford, 1992.

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9th report on carcinogens. 9th ed. [Research Triangle Park, N.C.]: U.S. Dept. of Health and Human Services, Public Health Service, National Toxicology Program, 2001.

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NATO Advanced Research Workshop on Endocrine Dirupters and Carcinogenic Risk Assessment (2001 Białystok, Poland). Endocrine disrupters and carcinogenic risk assessment. Amsterdam: IOS Press, 2002.

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Zia, Asif Iqbal, and Subhas Chandra Mukhopadhyay. Electrochemical Sensing: Carcinogens in Beverages. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32655-9.

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Shirachi, Donald Y. Carcinogenic effects of arsenic compounds in drinking water. Research Triangle Park, NC: U.S. Environmental Protection Agency, Health Effects Research Laboratory, 1987.

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Shirachi, Donald Y. Carcinogenic potential of arsenic compounds in drinking water. Research Triangle Park, NC: U.S. Environmental Protection Agency, Health Effects Research Laboratory, 1986.

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Book chapters on the topic "Carcinogenics"

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Mehlhorn, Heinz. "Carcinogenic Parasites." In Encyclopedia of Parasitology, 409–10. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_4723.

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Franzmann, Elizabeth. "Carcinogens." In Encyclopedia of Behavioral Medicine, 328–29. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_161.

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Franzmann, Elizabeth J. "Carcinogens." In Encyclopedia of Behavioral Medicine, 1–2. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-6439-6_161-2.

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Franzmann, Elizabeth J. "Carcinogens." In Encyclopedia of Behavioral Medicine, 367–69. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_161.

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Castegnaro, Marcel, and Eric B. Sansone. "Introduction." In Chemical Carcinogens, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71342-2_1.

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Castegnaro, Marcel, and Eric B. Sansone. "Hazards in Handling Chemical Carcinogens." In Chemical Carcinogens, 9–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71342-2_2.

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Castegnaro, Marcel, and Eric B. Sansone. "Methods for Disposal of Chemical Carcinogens and Spillage Treatment." In Chemical Carcinogens, 37–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71342-2_3.

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Berry, C. L. "Evaluating Carcinogenic Risks." In Nongenotoxic Carcinogenesis, 231–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-662-03022-6_13.

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Faguet, Guy. "Environmental Carcinogens." In The Conquest of Cancer, 69–79. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9165-6_4.

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Hemminki, K. "Environmental Carcinogens." In Handbook of Experimental Pharmacology, 33–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74775-5_2.

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Conference papers on the topic "Carcinogenics"

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Manabe, S., H. Yanagisawa, S. Ishikawa, Y. Kitagawa, K. Tohyama, S. Abe, and O. Wada. "TRYPTOPHAN PYROLYSIS PRODUCTS FOUND IN COOKED FOODS INHIBIT HUMAN PLATELET AGGREGATION BY INHIBITING CYCLOOXYGENASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643402.

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Humans are exposed to numerous toxic compounds in foods. During the past decade, several carcinogenic heterocyclic amines have been reported to be present in the cooked foods. Recently, we reported that some of the carcinogenic heterocyclic amines isolated from foods were present in human plasma. In order to know the effects of the carcinogens isolated from foods on the cell function, we investigated the effects of the carcinogenic heterocyclic amines including Trp-P-1(3-amino-l,4-dimethyl-5H-pyrido❘4,3-b❘indole) and Trp-P-2(3-amino-1-methyl-5H-pyrido❘4,3-b❘indole) on human platelet aggregation and polymorphonuclear leukocyte aggregation. Only tryptophan pyrolysis products, Trp-P-1 and Trp-P-2, had potent inhibitory effects on human platelet aggregation when platelets were preincubated with the carcinogens for 15 min. Other carcinogenic heterocyclic amines such as glutamic acid pyrolysates (Glu-P-1 and Glu-P-2) and 3H-imidazo ❘4,5-f❘quinoline-2-amines(IQ and MelQ) did show no effect on platelet aggregation even at 100 μM.The autoradiogram demonstrated that Tryptophan pyrolysis products, Trp-P-1 and Trp-P-2, dose-dependently inhibited the formation of HHT,PGD2,PGE2 and TXB2 induced by sodium arachidonate in human platelets labeled with ❘ 14c❘ arachidonic acid. Moreover, Trp-P-1 and Trp-P-2 did not show significant effects on leukocyte aggregation induced by sodium arachidonate (0.75mM) even at lOOnM. It is concluded that Trp-P-1 and Trp-P-2 isolated from cooked foodstuffs have potent inhibitory effects on the cyclo-oxygenase pathway of the platelet. Therefore, human platelet function might be affected with daily foods containing tryptophan pyrolysis products in vivo.
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Mosser, Mark F. "Progress on Environmentally Compliant Aluminum Ceramic Compressor Coatings." In ASME Turbo Expo 2004: Power for Land, Sea, and Air. ASMEDC, 2004. http://dx.doi.org/10.1115/gt2004-54294.

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During the last decade there has been an increasing emphasis on compliance to ever stricter environmental laws as well as compliance to regulations that have been designed to protect workers from exposure to toxic or otherwise harmful substances or processes. This world-wide emphasis has forced a continuing review of materials and processes used in the manufacture and protection of compressor materials from corrosion. Turbine compressors have been coated with silicone aluminum paint, diffused nickel cadmium and aluminum pigmented ceramic coatings that contain hexavalent chromium. These three processes utilize various chemicals including toxic substances, carcinogens and volatile organic compounds (VOC). All three of the coating processes need to be either made compliant or eliminated from use. This paper will review efforts that have been made to develop compliant aluminum ceramic compressor coating materials as applied to various steel and stainless steel substrates. In all cases the new materials that have been developed are free of toxic or carcinogenic materials. Test results will be compared to specification requirements for chrome containing compressor coatings in the area of physical properties including surface finish, thickness and adhesion. Additionally, environmental test data will be presented based on standard test methods that compare new compliant coatings with conventional chrome containing materials. Finally, process steps and conditions will be described for these new coatings.
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Y. A., Tunakova, Novikova S. V., Gabdrakhmanova G. N., and Fayzulin R. I. "Integral Assessment of Safety of Potable Waters in a Finishing Point of Consumption." In Environmental Engineering. VGTU Technika, 2017. http://dx.doi.org/10.3846/enviro.2017.056.

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The approach for integral assessment of potable waters with use of methods of the cluster analysis based on assessment of probability of intake of cations and anions of impurity with potable water and probabilities of carcinogenic and not carcinogenic changes in the state of health of the children’s population is offered.
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Ulzetueva, Irina, Bair Gomboev, Daba Zhamyanov, Valentin Batomunkuev, and Natalia Gomboeva. "ASSESSMENT OF CARCINOGENIC RISK OF DRINKING SURFACE WATER CONSUMPTION OF THE TRANSBOUNDARY BASIN OF THE SELENGA RIVER IN THE TERRITORY OF MONGOLIA." In GEOLINKS Conference Proceedings. Saima Consult Ltd, 2021. http://dx.doi.org/10.32008/geolinks2021/b1/v3/45.

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The assessment of the carcinogenic risk of the impact of drinking surface waters on the population health of the transboundary basin of the Selenga river in Mongolia is described in the article. We carried out expeditionary studies of the quality of drinking surface waters on the territory of four aimags, which represent different degrees of economic development and are completely included in the Selenga river basin: Khuvsgul, Arkhangai, Bulgan and Selenge. In this work, we used the methodology used by the US Environmental Protection Agency to quantify the carcinogenic risk of exposure to chemical compounds present in surface waters using the example of these aimags in Mongolia. The application of this methodology for risk assessment gives a great advantage over traditional methods of regulation. It has been established that on the territory of the Selenge aimag, the risk of developing a carcinogenic effect from the impact of priority pollutants on public health associated with the quality of drinking water is high and in the territory of Bulgan, Khuvsgul and Arkhangai aimags are medium, which requires state regulation of the risk and the development of appropriate standards.
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Dhineshkaarthi, K., S. K. Sathya Lakshmi Preeth, and R. Kumar. "MEMS cantilever based identification of carcinogenic MZN." In 2017 IEEE International Conference on Electrical, Instrumentation and Communication Engineering (ICEICE). IEEE, 2017. http://dx.doi.org/10.1109/iceice.2017.8191863.

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Hermans, Laurie. "1647b The european roadmap on carcinogens: let’s get smart about carcinogens at work." In 32nd Triennial Congress of the International Commission on Occupational Health (ICOH), Dublin, Ireland, 29th April to 4th May 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/oemed-2018-icohabstracts.648.

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Klotz, Kevin, Brian Klotz, and Bruce McMordie. "Eliminating Carcinogens in Compressor Coatings." In ASME Turbo Expo 2013: Turbine Technical Conference and Exposition. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/gt2013-94465.

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Introduced almost fifty years ago on steel compressor cases in J-79 engines, aluminum-ceramic coatings have come to play an essential role in protecting steel components in turbines and turbomachinery. The water-based “spray and bake” inorganic phosphate-base coatings are uniquely resistant to salt corrosion and heat, but pressure is growing to find an alternative to these materials. The slurries contain hexavalent chromium (Cr(VI)), a known carcinogen. In Europe, REACH initiatives restrict import and use of solutions containing hexavalent chromium. In the US, workplace exposure to Cr(VI) is limited to a mere 0.005 mg/m3 (5 micrograms) of Cr(VI) per person per 8 hour day and employers must monitor the health of those exposed even to such low levels. Aluminum-phosphate slurries clean up with water, but all effluent liquid must be captured and treated to remove Cr(VI). Solid waste that comes in contact with the slurry or rinse water must be segregated for proper disposal. Efforts to develop a safe, aluminum-phosphate coating without hexavalent chromium began in the early 1990s, but have met with limited success. Recently, a sacrificial, heat resistant aluminum-ceramic has been developed that contains no hazardous materials. This paper will review efforts to develop Cr-free Al-ceramic coatings and explain the promise of a new product that uses a different chemistry to produce an aluminum-ceramic coating that is protective, yet inherently non-hazardous.
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Sears, Cynthia L. "Abstract IA04: The carcinogenic potential of bacterial biofilms." In Abstracts: AACR Special Conference: Colorectal Cancer: From Initiation to Outcomes; September 17-20, 2016; Tampa, FL. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.crc16-ia04.

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Garg, R. K., Pardeep Kumar, R. S. Ram, and Zahid H. Zaidi. "Some carcinogenic polycyclic aromatic hydrocarbons by photoacoustic spectroscopy." In Photonics East '99, edited by Tuan Vo-Dinh and Robert L. Spellicy. SPIE, 1999. http://dx.doi.org/10.1117/12.372840.

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Ефимова, Н. В., Н. А. Судейкина, and В. Р. Моторов. "Individual carcinogenic risk for "end-to-end" engineering professions." In III International Scientific Forum "Health And Safety At The Workplace". Polikraft, 2019. http://dx.doi.org/10.31089/978-985-7153-76-3-2019-1-3-109-112.

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Reports on the topic "Carcinogenics"

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NMR Publicering. Emissions and air exposure of carcinogens and co-carcinogens in four Nordic countries. Nordisk Ministerråd, February 2014. http://dx.doi.org/10.6027/na2014-907.

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Broyde, S., and R. Shapiro. Interactions of carcinogens with DNA (deoxyribonucleic acid). Office of Scientific and Technical Information (OSTI), October 1989. http://dx.doi.org/10.2172/5477407.

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Cunningham, Albert R. Investigating the Mechanisms of Action and the Identification of Breast Carcinogens by Computational Analysis of Female Rodent Carcinogens. Fort Belvoir, VA: Defense Technical Information Center, August 2005. http://dx.doi.org/10.21236/ada443017.

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Cunningham, Albert R. Investigating the Mechanisms of Action and the Identification of Breast Carcinogens by Computational Analysis of Female Rodent Carcinogens. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada410270.

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Cunningham, Albert R. Investigating the Mechanism of Action and the Identification of Breast Carcinogens by Computational Analysis of Female Rodent Carcinogens. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada469150.

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Cunningham, Albert R. Investigating the Mechanisms of Action and the Identification of Breast Carcinogens by Computational Analysis of Female Rodent Carcinogens. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada425200.

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Perera, Frederica P. Biological Markers of Environmental Carcinogens in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 1998. http://dx.doi.org/10.21236/adb248851.

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Hattis, D. Pharmacokinetic/mechanism-based analysis of the carcinogenic risk of ethylene oxide. Office of Scientific and Technical Information (OSTI), August 1987. http://dx.doi.org/10.2172/7067804.

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Poet, Torka S., and Chuck Timchalk. Proposed Occupational Exposure Limits for Non-Carcinogenic Hanford Waste Tank Vapor Chemicals. Office of Scientific and Technical Information (OSTI), March 2006. http://dx.doi.org/10.2172/881941.

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Holland, J. M. Chronic Dermal Toxicity of Epoxy Resins I. Skin Carcinogenic Potency and General Toxicity. Office of Scientific and Technical Information (OSTI), January 2001. http://dx.doi.org/10.2172/777676.

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