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Dissertations / Theses on the topic 'Carcinogenics'

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Published: 4 June 2021
Last updated: 2 February 2022

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1

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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2

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
Made available in DSpace on 2018-08-07T13:30:36Z (GMT). No. of bitstreams: 1 Guilhen_AnaCarolinaTrindade_M.pdf: 1692988 bytes, checksum: 1868d3d53c2dafca822a331ec40cac6d (MD5) Previous issue date: 2006
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.
Leaf 187 blank.
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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Yoxall, Victoria R. "Interactions of tea with chemical carcinogens." Thesis, University of Surrey, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397201.

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Gill, Julie C. "An investigation of potential steroidal carcinogens." Thesis, Loughborough University, 1988. https://dspace.lboro.ac.uk/2134/11091.

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Various potential metabolites of steroids with alkylating properties were synthesised, with important cellular in order that their reaction constituents and their mutagenicity could be investigated by Dr. Grover of the Chester Beatty Research Institute. Promising compounds were also investigated by Dr. Traynor, of Loughborough University, as part of an ongoing project to find selectively toxic compounds to estrogen dependant tumours.
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Blakeborough, M. H. "Genotoxicity studies with potential large bowel carcinogens." Thesis, Liverpool John Moores University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234730.

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Brennan, Richard John. "Novel short-term tests for environmental carcinogens." Thesis, University of Warwick, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357499.

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Phillipson, Caroline Elizabeth. "The mechanism of activation of chemical carcinogens." Thesis, University of Surrey, 1986. http://epubs.surrey.ac.uk/847900/.

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Research has been carried out into the mechanisms of activation of chemical carcinogens, using the Ames mutagenicity test as an indication of this parameter. As the mixed-function oxidase system has been the major enzyme system investigated, initial studies were carried out to evaluate the specificity of assays for the two major forms of the terminal oxygenase, cytochromes P-450 and P-448. A combined use of inducers, inhibitors and purified enzymes confirmed the specificity of the ethoxyresorufin O-deethylation assay for cytochrome P-448, and further detailed studies emphasised the advantages of this activity over biphenyl 2-hydroxylase and aryl hydrocarbon hydroxylase. In addition, 9-hydroxyellipticine was found to be a specific inhibitor and inducer of cytochrome P-448, and provided a useful tool for both in vivo and in vitro investigations. Furthermore, a detailed study of the spectral interactions of substrates with cytochromes P-450 and P-448 indicated that these two cytochromes have distinctly different substrate binding sites, which could be related to their disparate metabolic specificities and contrasting roles in activation and detoxification of xenobiotics. The role of cytochromes P-450 and P-448, as well as other oxidative enzymes (i. e. the FAD-monooxygenase or Ziegler enzyme, and monoamine oxidase) in the activation of three major groups of carcinogens (nitrosamines, aromatic amines and polycyclic aromatic hydrocarbons) has been studied. An excellent positive correlation was observed between the activation of benzo(a)pyrene to mutagens and the O-deethylation of ethoxyresorufin, indicating that these are catalysed by the same form of cytochrome P-448. No similar clear-cut correlations could be obtained for dimethylnitrosamine and 2-acetylaminofluorene, and indeed, activation of dimethylnitrosamine could also not be related to its demethylation. In addition, a comprehensive study of species and sex differences in the activation of these three groups of carcinogens revealed that the rat (both male and female) was generally poor at activation, while in contrast, the hamster consistently provided a good activating system, especially in the case of the nitrosamines. Finally, preliminary studies have been carried out on the metabolic capacity of cytochrome P-450 in yeast and plant cells, and on the ability of iron-based chemical systems and haemoglobin to mimic the activity of cytochrome P-450. The cytochrome P-450 models were able to hydroxylate aniline and demethylate dimethylnitrosamine, while the yeast and plant preparations were most efficient at hydroxylating benzo(a)pyrene.
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Plná, Kamila. "Quantitative analysis of DNA adducts formed by some epoxides of industrial importance /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3869-5/.

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Shin, Vivian Yvonne, and 冼念慈. "A study on the carcinogenic mechanism of nicotine in gastric cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B30485976.

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18

Elwaer, Abdul-Hakim Rajab. "Novel strategies for trace determination of carcinogenic bromate in drinking waters." Thesis, University of Sheffield, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310870.

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Gudi, Girish Srinivas. "Evaluation of non-invasive biomarkers for carcinogenic exposure to cigarette smoke." Morgantown, W. Va. : [West Virginia University Libraries], 1999. http://etd.wvu.edu/templates/showETD.cfm?recnum=661.

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Thesis (M.S.)--West Virginia University, 1999.
Title from document title page. Document formatted into pages; contains xi, 107 p. : ill. (some col.) Includes abstract. Includes bibliographical references (p. 98-107).
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20

Arango, Tamayo Daniel Alejandro. "The Immune-modulatory and Anti-carcinogenic Mechanisms of the Flavonoid Apigenin." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1437511798.

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21

Bersaas, Audun Trygge Haugen. "MicroRNA, environmental carcinogens and risk of lung cancer." Thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for bioteknologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-12930.

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Lung cancer is the leading cause of cancer related deaths world wide. The major cause of lung cancer is tobacco smoking. Tobacco smoke contains many different carcinogens including polycyclic aromatic hydrocarbons (PAH), which are known to cause DNA damage and initiate tumourigenesis.The aryl hydrocarbon receptor (AHR) is a basic helix-loop-helix protein of the PER-ARNT-SIM (PAS) family of transcription factors, which is involved in many biological processes including development, cell cycle regulation, cell differentiation, cell-cell signalling, cellular growth, and circadian rhythms. Most of the known function of AHR, however, is regarding its role in transcriptional induction of xenobiotic metabolis- ing enzymes (XMEs). In the lung, PAHs bind and activate the AHR, leading to transcriptional induction of members of the cytochrome P450 (CYP) enzyme family that are involved in activation of pro-carcinogenic PAHs to carcinogenic metabolites.MicroRNAs (miRNAs), a group of short non-coding RNA molecules, mediate sequence specific silencing of messenger RNAs (mRNAs) and are important in regulation of gene expression. The deregula- tion of certain miRNAs has been observed in several types of cancer, including lung cancer. Like mRNAs, miRNAs belong to the class II type of genes, and transcription of these types of RNA can therefore be regulated by the same transcription factors.Little is known regarding the role of miRNAs in environmental toxicology. The aim of this thesis was to identify miRNAs regulated by the AHR, and consequently may be important in mediating toxicity of tobacco smoke carcinogens.Expression levels of 750 miRNAs in mouse lung of Ahr wild-type and knockout animals were pro- filed by RT-qPCR arrays. Fifteen miRNAs were found to be differentially expressed between the groups, of which only one was up-regulated. The biological pathways in which these miRNAs may be involved were studied by an bioinformatic approach. Four miRNAs from the mouse experiment, whose expression were most significantly divergent, together with three miRNAs previously reported to be regulated by the Ahr in murine cell lines, were studied in an RNA interference (RNAi) experiment in immortalised human lung epithelial cell lines. Two of these miRNAs, both selected from the literature, were found to have altered expression in AHR knockdown cells compared to control cells. Discrepancies between AHR regulated miRNAs identified in the in vivo and in vitro experiments were observed. Taken together this suggest a difference between effect of the AHR in vivo and in vitro, rather than differences between species.In conclusion, it was found that expression of several miRNAs possibly is regulated in an AHR- dependent manner in lung. Discrepancies between in vivo and in vitro experiments suggest that care must be taken when extrapolating miRNA expression data from cell culture studies to whole organs or organisms.
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22

Parland, William Keith. "Effects of chemical carcinogens on fish liver histology /." The Ohio State University, 1986. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487265143148098.

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23

Schoettler, Cameron J. "The carcinogenic profiles, trends, and cencer risks of regional smokeless tobacco products." Thesis, Boston University, 2013. https://hdl.handle.net/2144/12216.

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Thesis (M.A.)--Boston University
Smokeless tobacco products have existed for centuries and vary significantly across geographical regions. The constituents found in each smokeless tobacco product depends on many factors, including social customs, manufacturing regulations, and the availability of local raw ingredients. Unfortunately, tobacco products have been linked to cancer over the past several decades, particularly of the oral cavity. In this study, the carcinogenic profiles, relative risks of oral cancer, and usage trends for three unique smokeless tobacco regions (United States, Sweden, and India) will be evaluated in order to determine the relative safety for each product. In this paper, the chemical analysis of various products from United States, as well as Swedish snus and Indian gutkha were reviewed, to establish constituent profiles. The main carcinogens evaluated were the tobacco-specific n-nitrosamines; gutkha displayed the highest values of these ingredients, with snus displaying the lowest. Studies examining the relative risks for oral cancers associated with each of the three region’s smokeless tobacco products were assessed. Indian gutkha expressed the highest relative risk for developing oral cancers, and Swedish snus expressed the lowest (a very slight increased risk at that). To establish usage habits for each region-specific smokeless tobacco product, various epidemiological studies were analyzed and showed that gutkha was the most prevalently used product in its respective region, with Swedish snus only slightly trailing in use. Smokeless tobacco products were used the least in the United States. These studies concluded that the gutkha habits in India were the most damaging to the public health of the nation with regards to smokeless tobacco use, particularly due to the high prevalence of use and high relative risk of oral cancers. In a purely chemical sense, Swedish snus was less harmful than the counterparts often sold in the United States. Yet, with snus use significantly higher than smokeless tobacco use in the United States, it is thought that Sweden snus habits are more detrimental than those seen in the United States. However, smokeless tobacco is ultimately an unsafe practice in all three regions evaluated, and more should be done to remove carcinogens from the products and promote self-restraint for current users.
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24

MacGregor, James Orrock. "Some chemistry of muconaldehyde pertinent to the toxicology of benzene." Thesis, University of Newcastle Upon Tyne, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261267.

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25

Owens, Joanna. "Regulation of peroxisome proliferator-activated receptor-alpha (PPAR#alpha#)." Thesis, University of Surrey, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341337.

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26

Boyd, Gary William. "Cyclopenta[a]phenanthren-17-ones : structure/activity relationships." Thesis, University of Surrey, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334403.

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27

Gunaratnam, Mekala. "Cytotoxicity of hexavalent chromium in rat hepatocytes." Thesis, University of Strathclyde, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273813.

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28

Tsang, Ho-ching Felice. "Identification of ankyrin repeats and SOCS box protein 4 (ASB4) as oncogenic biomarker in liver cancer." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40738814.

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29

Wood, M. L. "Studies on the in vitro activation of chemical carcinogens." Thesis, University of York, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374198.

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30

Xie, Bin, and 謝彬. "Sex hormone-induced mammary carcinogensis [sic] in the noble rat." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31239523.

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31

Schellenberger, Mario [Verfasser], and Brunhilde [Akademischer Betreuer] Blömeke. "Immunoprophylactic approach against chemical carcinogensis / Mario Schellenberger ; Betreuer: Brunhilde Blömeke." Trier : Universität Trier, 2012. http://d-nb.info/119780630X/34.

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32

Johansson, Maria. "Influence of lipids and pro- and antioxidants on the yield of carcinogenic heterocyclic amines in cooked foods and model systems." Lund, Sweden : Dept. of Applied Nutrition and Food Chemistry, Lund Institute of Technology, Lund University, 1995. http://catalog.hathitrust.org/api/volumes/oclc/38206526.html.

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Bartlet-Jones, Michael. "Development of an immunoassay for addressing the question #Do 15,16-dihydrocyclopenta[a]phenanthren-17-one analogues exist in man?'." Thesis, University of Surrey, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240190.

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34

McDowall, Gordon David. "An investigation into the adaptive response to MNNG of Chinese hamster cells in vitro." Thesis, University of Bath, 1988. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.380897.

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35

Almora, Pinedo Yuan, Jorge Luis Arroyo-Acevedo, Oscar Herrera-Calderon, Cerrate Victor Manuel Chumpitaz, Quispe Renán Hañari, Jayo Johnny Aldo Tinco, Quino Cesar Franco, and Salvador Linder Figueroa. "Preventive effect of Oenothera rosea on N-methyl-N-nitrosourea- (NMU) induced gastric cancer in rats." Dove Medical Press Ltd, 2017. http://hdl.handle.net/10757/622967.

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Background: Currently, gastric cancer (GC) is considered a public health problem worldwide. Using medicinal plants for the prevention of chronic diseases such as cancer constitutes new alternatives in traditional medicine. Oenothera rosea (OR) could be an option, but it needs to be evaluated. Aim: The main objective of this study was to evaluate the protective effect of OR extract on N-methyl-N-nitrosourea (NMU)-induced GC in rats. Methods: In total, 80 male Holtzman rats were randomized into five groups. Group A received the saline solution (5mL/kg), group B received NMU 500 μg/kg (cancer inductor) by oral administration for 16 weeks, and groups C, D, and E were treated with OR extract (100, 200, and 300 mg/kg, respectively) and NMU in order to evaluate the preventive effect on cancer induced by NMU for 16 weeks. Blood and histological samples of stomachs were collected to determine histopathological, biochemical, and hematological parameters between different experimental groups. Results: Groups C, D, and E presented less histopathological changes such as anaplastic and hyperplastic cells, compared with group B. Hematological and biochemical parameters were recorded, and superoxide dismutase, malondialdehyde, and nitric oxide levels were statistically less than those of NMU group (P<0.05, P<0.01, and P<0.01). Conclusion: Considering the histopathological signs and the antioxidant activity in vivo as well as hematological and biochemical parameters of ethanolic extract of OR, we concluded that its administration in rats has a protective effect on GC, which is induced experimentally. This species could be studied in clinical trials for patients with GC in the future.
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36

Langford, Gillian A. "The relative mutagenic potencies of three carcinogenic compounds : a molecular dosimetry based assessment." Thesis, University of York, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.304261.

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37

McLuckie, Keith I. E. "The mutagenicity of the reaction of DNA with genotoxic carcinogens." Thesis, University of Leicester, 2003. http://hdl.handle.net/2381/7934.

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Mechanisms by which carcinogens induce mutations in human cells can be investigated using carcinogen exposed shuttle vector plasmids. In particular, the pSP189 plasmid can be treated with carcinogens in vitro and transfected into human fibroblasts. Following replication, where DNA repair or mutagenesis occurs, recovered plasmids can be screened in indicator bacteria for induced mutations in the supF gene. The aim of this study was to establish and utilise assays to investigate the mutagenicity of genotoxic agents. Specifically, two model reactive intermediates of the cancer drug tamoxifen, α-acetoxytamoxifen and 4-hydroxytamoxifen quinone methide (4-OHtamQM), along with binary treatments of BPDE with UVB or UVC radiation were assessed for their mutagenic potential in human cells. The quantitatively minor DNA adduct of tamoxifen formed by 4-OHtamQM is more mutagenic than the major tamoxifen adduct, formed by a-acetoxytamoxifen in Ad293 cells. The majority of mutations in α-acetoxytamoxifen treated plasmid were GC→TA transversions, while GC→AT transitions were predominant in 4-OHtamQM treated plasmid. Mutational hotspots were observed for both compounds. In GM04429 cells mutations induced by α-acetoxytamoxifen were mainly GC→TA, whereas in GM00637 fibroblasts GC→AT transitions were more common. Treatment of plasmid with BPDE preferentially induced GC→TA transversions whilst UVB and UVC induced GC→AT transitions. Binary treatments were more mutagenic than single treatments, with BPDE then UV being more mutagenic than UV then BPDE. This suggests a synergistic mechanism of activation of BPDE DNA adducts by UV radiation. In the final part of this work, a system for investigating the site-selectivity and consequences of mutagen reaction with DNA was developed. In the future this methodology can be used to detect mutations arising from specific DNA adducts inserted at known locations in important genes. This assay builds on the results provided by the standard supF assay and enables a more detailed investigation of the mechanisms involved in mutagenesis.
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38

Graham, Oliver William. "Understanding the potential mechanisms of action of dietary prostate carcinogens." Thesis, Imperial College London, 2017. http://hdl.handle.net/10044/1/61336.

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Prostate cancer is the most commonly diagnosed cancer in males in the UK, and while the precise aetiology of prostate cancer remains unknown, risk factors such as age and lifestyle have been identified. Consumption of a ‘western’ diet rich in well-done red meat has been implicated in the development of prostate cancer, due to the appreciable amounts of carcinogenic material found in these foods. Two common dietary carcinogens are benzo[a]pyrene (B[a]P) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), both of which have been identified as possible prostate mutagens. Another possible risk factor for prostate cancer is inflammation (a common condition in the prostate), specifically interleukin- 6 (IL-6) which is found elevated in the serum of prostate cancer patients. The underlying mechanisms behind the influence of dietary carcinogens and inflammation on the development of prostate cancer remain elusive, with limited knowledge about how inflammation may alter the modes of action of dietary carcinogens in the prostate. I hypothesised that IL-6 may alter the activation of B[a]P and PhIP, resulting in phenotypic alterations to prostate cells that are associated with cancer development. Using an in vitro, cell culture based model, the current project reported findings that both B[a]P and PhIP induce alterations in prostate cell migration while demonstrating genotoxic potential. Moreover, mixtures of B[a]P and PhIP induced significantly more genetic damage than either chemical in isolation, suggesting that interplay during simultaneous exposure in vivo may result in higher levels of DNA damage in the prostate. Further, PhIP-induced genotoxicity appeared to be a result of cytochrome P450-mediated production of reactive oxygen species. Finally, my data indicate that IL-6 increases B[a]P-mediated genetic damage, suggesting that activation of B[a]P in prostate cells may be altered by inflammatory cytokines such as IL-6, but more work is needed in order to verify this interaction. These novel findings must be explored in greater depth in order to fully understand how these factors interact in the prostate.
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39

Agurell, Eva. "Comparative studies of alkylating and N-heterocyclic compounds on different genetic endpoints with special emphasis on amplification of minisatellite sequences." Stockholm : Dept. of Genetic and Cellular Toxicology, Wallenberg Laboratory, Stockholm University, 1992. http://catalog.hathitrust.org/api/volumes/oclc/28206159.html.

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40

Haag, Grönlund Marie. "Liver tumour promoting effects by polychlorinated biphenyls /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3203-4/.

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41

曾可澄 and Ho-ching Felice Tsang. "Identification of ankyrin repeats and SOCS box protein 4 (ASB4) as oncogenic biomarker in liver cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40738814.

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42

Au, Chun-hei Victor, and 區晉熙. "The role of ankyrin repeats and SOCS box protein 4 (ASB4) in hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/196475.

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Hepatocellular carcinoma (HCC)is one of the commonly diagnosed cancers in the world. Most patients have poor prognosis due to late detection of disease. Ankyrin repeat and suppressor of cytokine signaling box protein 4(ASB4), as a member of the ASB family, possesses two domains, ankyrin repeat (AR) and suppressor of cytokine signaling (SOCS)box, which are responsible for recruiting the target proteins for proteasomal degradation. Previous study has demonstrated high expression level of ASB4 in metastatic HCC cells, implicating the properties of ASB4 in cancer invasiveness. With this hypothesis, various experiments were performed in this research project to elucidate the functional roles of ASB4 in HCC cells. The aim of this study is to characterize the roles of ASB4 in HCC by manipulating its expression level in HCC cell lines through gene knockdown and over-expression. Altering the level of ASB4 in HCC cells resulted in no significant effects on the cell proliferation rates. However, ASB4 was demonstrated to promote migration and invasion properties of HCC cells, as suppression of its level led to slower migration and made cells less invasive. Opposite effects on cell migration and invasion were observed when ASB4 was ectopically expressed. Regarding the regulatory mechanism of ASB4, miR-200a was demonstrated to be a negative regulator for ASB4. In summary, ASB4 is probably involved in the migration and invasion properties of HCC cells, and also, being regulated by miR-200a.
published_or_final_version
Surgery
Master
Master of Philosophy
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43

Watson, A. J. "Aflatoxin biosynthesis in Aspergillus." Thesis, University of East Anglia, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267259.

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Moret, Illana M. Merce. "Study of the effects of methapyrilene on fresh and cryopreserved rat hepatocytes." Thesis, University of Surrey, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318660.

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Dingley, Karen Hazel. "The application of immunoassay to the quantitation of aflatoxin B←1-DNA adducts." Thesis, University of York, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283428.

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Lynch, Peter Neil. "An investigation into the reactivity of nitrosobenzenes as carcinogenic metabolites of nitrobenzenes and anilines." Thesis, University of Newcastle Upon Tyne, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361594.

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47

Bryant, Matthew S. (Matthew Scott). "Estimation of human exposure to the carcinogenic aromatic amine 4-aminobiphenyl via hemoglobin dosimetry." Thesis, Massachusetts Institute of Technology, 1987. http://hdl.handle.net/1721.1/16491.

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48

Nishioka, Marcia G. "Identification of Carcinogenic Di-amines in the Indoor Environment from Common Urethane Polymer Products." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu148344608670484.

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49

Jilla, Abhinay. "Evaluation of Total Fume and Heavy Metal Emission Factors Applicable to Gas Metal Arc Welding." ScholarWorks@UNO, 2019. https://scholarworks.uno.edu/td/2612.

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Welding is a metal joining process widely used in many manufacturing facilities around the world. It involves the process of heating the base and filler metals to a high temperature that leads to the formation of fumes. Welding emissions consist of gaseous pollutants and micron and sub-micron particles consisting of different heavy metals. Health risks associated with exposures to weld fume is well recognized in the literature. This research evaluates emissions and emission factors applicable to gas metal arc welding (GMAW) on AH 36 (mild steel) and 316 L (stainless steel). Emission factors evaluated consisted, total fume, chromium, cobalt, lead, manganese, and nickel. A weld fume chamber is used to capture the welding fumes onto a filter and then further analyzed to quantify the total fume and heavy metal emissions. Critical operating parameters such as current, voltage, shielding gas, welding speed, and contact tube to work distance (CTWD) were considered while evaluating emissions and emission factors. The parameters with greater influence on emissions are selected, and then the heavy metal emissions are quantified by varying those parameters using inductively coupled plasma atomic emission spectrometry (ICP-AES) and portable XRF (X-Ray Fluorescence) analyzer. The heavy metal results from the ICP-AES and XRF are compared to explore the feasibility of using XRF analyzer in quantifying the heavy metals in welding fumes. Using the heavy metal emissions, the lifetime carcinogenic and non-carcinogenic risks are evaluated for the GMAW process. The mild steel (MS) and stainless steel (SS) statistical analysis results indicate current and voltage are most influencing parameters in generating the fumes in GMAW. This research found a significant linear relationship between ICP-AES and XRF heavy metal results. The lifetime carcinogenic and non-carcinogenic risks results indicate high potential health risks if not properly managed.
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Aragón, Aurora. "Dermal exposure to pesticides in Nicaragua : a qualitative and quantitative approach /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-588-7/.

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