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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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Revazova, Yulia A., and Nataliya A. Ilyushina. "On the issue of nongenotoxic cancerogenes." Toxicological Review 29, no. 4 (August 30, 2021): 51–55. http://dx.doi.org/10.36946/0869-7922-2021-29-4-51-55.
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Introduction. Chemical, physical or biological factors that can cause the formation and expansion of cancer cells are diverse in terms of both activity and mechanisms of action, which leads to the complexity of assessing the risk of developing malignant neoplasms. The aim. Discussion of the classification of carcinogens based on their ability to interact with DNA cell and possible mechanisms of genetic control of carcinogenesis processes induced by non-genotoxic carcinogens. Core content. The article draws attention to some controversial points related to the attribution of factors acting on the body to genotoxic or non-genotoxic carcinogens. The terminology used in the literature to describe genotoxic (mutagenic) and carcinogenic factors is presented. The mechanisms of action of non-genotoxic carcinogens are discussed. The important role of experts determining the danger to public health of factors with potential genotoxicity and carcinogenicity is noted. Conclusion. Non-genotoxic carcinogens are capable of inducing malignant growth through mechanisms not associated with direct damage to genetic structures in the cell. However, the realization of carcinogenic effects caused by such factors is determined by various mechanisms of genetic control.
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Adrianovsky, V. I., E. A. Kuzmina, N. V. Zlygosteva, A. P. Boyarsky, and G. Ya Lipatov. "A SYSTEM APPROACH TO CARCINOGENIC RISK ASSESSMENT AND MANAGEMENT FOR METALLURGICAL WORKERS EMPLOYED IN VARIOUS BLISTER COPPER PRODUCTION PROCESSES." Hygiene and sanitation 96, no. 12 (March 27, 2019): 1161–66. http://dx.doi.org/10.18821/0016-9900-2017-96-12-1161-1166.
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The paper presents results of the application of the system approach to carcinogenic risk assessment and management based on the identification carcinogens, prediction carcinogenic effects and rationale for targeted preventive and curative measures. Evidence from metallurgical shops where various blister copper production processes are used regardless of the existing smelting technologies shows the risk of cancer to be Federal Service for Surveillance on Consumer Rights Protection and Human Wellbeingeptable even when the working conditions are classified as permissible (class 2) in terms of chemical factors. The highest carcinogenic risk values are observed for occupations with workplaces characterized by a significant release of dust, arsenic being the main risk contributor. In cases of the blast furnace and reverberatory furnace smelting, carcinogenic risks for workers with a 25-year length of employment exceed the permissible level by 17.6 and 28.8 times, respectively, and in the case of bath smelting, carcinogenic risks exceed the permissible level by 5.1 times. The maximum length of employment for bath smelting shop workers amounts to 5.14 years, being by 1.42 and 0.89 years higher than that for the blast furnace and reverberatory furnace smelting shop workers, respectively. The observed cancer mortality rates exceed significantly the expected mortality rates for the tumor of all sites in cases of combined and respiratory cancers. The highest cancer mortality rates were recorded for batch loaders (60%) and smelter (40%) with the highest predicted carcinogenic risk values. Cancer-specific marker levels higher normal ones were detected in 73% of workers from the increased individual carcinogenic risk group. The proposed system approach to carcinogenic risk assessment and management will make it possible to try out components of the risk-based approach in the supervisory activities at industrial facilities with exposure to carcinogens, to establish the acceptable risk levels depending on the length of employment, identify the priority carcinogens; it will also allow indicating a rationale for additional testing for occupational carcinogenesis predictors as part of routine medical examination procedures and to develop preventive measures against key risk factors.
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Castaneda, Carlos A., Miluska Castillo, Iván Chavez, Fernando Barreda, Nancy Suarez, Jais Nieves, Luis A. Bernabe, et al. "Prevalence of Helicobacter pylori Infection, Its Virulent Genotypes, and Epstein-Barr Virus in Peruvian Patients With Chronic Gastritis and Gastric Cancer." Journal of Global Oncology, no. 5 (December 2019): 1–9. http://dx.doi.org/10.1200/jgo.19.00122.
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PURPOSE Helicobacter pylori (HP) and Epstein Barr virus (EBV) infections induce chronic gastritis (CG) and are accepted carcinogenics of gastric cancer (GC). Our objective for this study was to determine the prevalence of these agents and clinicopathological features of GC and CG associated with the infection. PATIENTS AND METHODS A single-center cohort of 375 Peruvian patients with GC and 165 control subjects with CG were analyzed. Evaluation of HP and EBV genes was performed through quantitative polymerase chain reaction. RESULTS Prevalence of HP was 62.9% in the whole population and 60.8% in the GC subset. The cagA gene was detected in 79.9%; vacAs1 and vacAm1 alleles in 41.6% and 60.7%, respectively; and concurrent expression of vacAs1 and vacAm1 in 30.4% of infected patients in the whole series. The prevalence of EBV was 14.1% in the whole population and was higher in GC ( P < .001). Coinfection of HP and EBV was found in 7.8% and was also higher in GC in univariate ( P < .001) and multivariate ( P = .011) analyses. Infection rates of HP and EBV were not associated with a geographic location in the whole series. Few clinicopathological features have been associated with infectious status. CONCLUSION Prevalence of HP infection and virulent strains are high in the Peruvian population. Infection by EBV was more frequent in patients with GC.
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Gottinger, H. W. "HAZARD: An Expert System for Risk Assessment of Environmental Chemicals." Methods of Information in Medicine 26, no. 01 (January 1987): 13–23. http://dx.doi.org/10.1055/s-0038-1635482.
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AbstractThe purpose of this paper is to report on an expert system in design that screens for potential hazards from environmental chemicals on the basis of structure-activity relationships in the study of chemical carcinogenesis, particularly with respect to analyzing the current state of known structural information about chemical carcinogens and predicting the possible carcinogenicity of untested chemicals. The structure-activity tree serves as an index of known chemical structure features associated with carcinogenic activity. The basic units of the tree are the principal recognized classes of chemical carcinogens that are subdivided into subclasses known as nodes according to specific structural features that may reflect differences in carcinogenic potential among chemicals in the class. An analysis of a computerized data base of known carcinogens (knowledge base) is proposed using the structure-activity tree in order to test the validity of the tree as a classification scheme (inference engine).
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Trosko, James E. "Reflections on the use of 10 IARC carcinogenic characteristics for an objective approach to identifying and organizing results from certain mechanistic studies." Toxicology Research and Application 1 (January 1, 2017): 239784731771083. http://dx.doi.org/10.1177/2397847317710837.
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To find a scientifically based method for evaluating mechanistic data related to risks to human beings, a new protocol for identifying, organizing, and summarizing mechanistic data for decision-making on cancer hazard identification was proposed by the International Agency for Research on Cancer and by an international working group of multidisciplinary experts. This Commentary examined the 10 key carcinogens’ characteristics proposed in the context of several paradigms assumed in the using of these 10 characteristics. These characteristics were assumed to represent a “carcinogen’s” mechanism of action but what was ignored were characteristics of the mechanisms of the “initiation,” “promotion,” and “progression” carcinogenic process. Challenges were made to the interpretation of genotoxicity data as well as from concepts and findings related to the promotion phase and the role of adult human stem cells. Reliance of interpretation of “genotoxicity” data (molecular-DNA lesions in DNA; induction of free radicals/oxidative stress markers; phenotypic surrogates of gene mutations), as well as from lesions in genomic versus mitochondrial DNA, or in the target cells for the carcinogenic process in either in vitro cultures or in vivo tissues, makes this “objective” use of the data questionable. A challenge to the “dedifferentiation” hypothesis of cancer was made. Because of an agent being misclassified as “genotoxic”—rather than an “epigenetic”—agent (which works by threshold levels; can be blocked; and must be present at critical times during development and at regular, sustained chronic exposures) could lead to unwise policy decisions.
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Katulskiy, Yury N. "About unification of indices of the possibility of disease occurrence in risk assessment methodology and the determination of the probability of non-carcinogenic effects in toxicological-hygienic, clinical and epidemiological studies and according to data about health-seeking behavior." Hygiene and sanitation 95, no. 10 (October 28, 2019): 998–1002. http://dx.doi.org/10.18821/0016-9900-2016-95-10-998-1002.
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In the methodology for the assessment of the risk the possibility of the disease occurrence under the impact of carcinogenic and non-carcinogenic substances is measured by different indices. This leads to the fact that within the single methodology there are used various scores for such similar index as the risk of the disease occurrence, as a result carcinogens and systemic toxicants happen to be inconsistent from this point of view. At the same time, unlike carcinogens risk indices for systemic toxicants do not allow to evaluate the number of possible diseases in the population during the corresponding period of time, because they contain no information about their probability. Obviously, from this point of view, the characteristics of carcinogenic risk have certain advantages. Therefore, noncarcinogenic risk should be assessed by the similar indices as carcinogenic ones. However, an obstacle to this is the fact that in toxicological-hygienic, clinical and epidemiological studies, according to the results of which there is determined the risk for systemic toxicants, the impact of non-lethal levels of the exposure is established not in separate individuals, as for carcinogens, but according to mean-group values of indices of the state of the body as the identification of the nonspecific effect under relatively non high doses (concentrations) in the single person is fairly difficult. Such data do not allow to estimate the probability of the break of the effect. Also the data concerning seeking for the medical help, considering repeated medical resource utilization due to protract diseases or afflictions occurring repeatedly in a person several times for the considered period of time fail to be the estimation of the probability for the disease occurrence. For the obtaining of the possibility of unification of the carcinogenic and non-carcinogenic indices of risk in the paper there are presented methods for the determination of the probability of non-carcinogenic effects in toxicological-hygienic, clinical and epidemiological studies, as well as according to statistical data on the seeking for the medical help, taking into account the repeated appeals of the protract or re-emerging diseases.
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Gold, L. S., T. H. Slone, and L. Bernstein. "Summary of carcinogenic potency and positivity for 492 rodent carcinogens in the carcinogenic potency database." Environmental Health Perspectives 79 (February 1989): 259–72. http://dx.doi.org/10.1289/ehp.8979259.
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Khudolei, Veniamin V. "Genes and enzymes of metabolic activation of xenobiotics in chemical carcinogenesis." Ecological genetics 1, no. 1 (January 15, 2003): 30–35. http://dx.doi.org/10.17816/ecogen1030-35.
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In the initial stage of chemical carcinogenesis the primary key event is metabolic activation of exogenic carcinogenic substances. The main enzymes of carcinogen's biotransformation (microsomal hydroxylation, reactions of conjugation) and genes which controlling the activity of these enzymes, has been characterized. The tissue(organ)specificity of expression of gene products (isoforms of su-perfamilies of CYPs and GSTs, family of NATs) as well as genetic polymorphism of enzymes involving into the biotransformation of carcinogenic xenobiotics were demonstrated
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Efimova, Natalya V., Natalya A. Sudeikina, Vladimir R. Motorov, Galina V. Kurenkova, and Elizaveta P. Lemeshevskaya. "Comparative assessment of the dynamics of individual carcinogenic risk for workers of the main professions of wagon repair production." Russian Journal of Occupational Health and Industrial Ecology, no. 5 (May 31, 2019): 260–65. http://dx.doi.org/10.31089/1026-9428-2019-59-5-260-265.
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Introduction.Part of the population working at carcinogenic enterprises is exposed to double exposure to carcinogens (in industrial and domestic conditions), however, studies to assess the total inhalation exposure is practically not carried out.The aim of the studyis hygienic assessment of the contribution of working environment factors to the formation of individual carcinogenic risk (ICR) for workers in the main professions in the car repair company, including the assessment of the predicted values of occupational risks in the dynamics of work experience.Materials and methods. There was the calculation of the levels of ICR for workers of the main professions in the wagon wheel, wagon meintenance, wagon assembly workshops. The assessment of exposure for workers is given on long-term average concentrations in the air of the working area and on average annual concentrations in the atmospheric air. When calculating the doses of toxicants in the air of the working area, «standard» parameters of pulmonary ventilation for an adult, body weight, work experience in contact with carcinogenic substances — from 1 to 30 years, the number of days in contact — 240, working time — 8 hours (in accordance with the duration of the working day) were used.Results.Workers of major occupations carcinogenic enterprise levels ICR differ in dozens of times. Calculation of ICR at 30-year work experience showed that in all studied main and auxiliary professions the total ICR was in the 4th range (more than 1,0·10–3). Unacceptable values for the predicted ICR for the professions of «painter», «locksmith-electrician», «impregnator», «mechanic of rolling stock» begin with a 5-year work experience, the least carcinogenic is the work of a tinker, whose risk reaches an unacceptable level after 20 years of the work experience. Among the most dangerous jobs should be attributed to the wagon assembly workshop. In contribution to the ICR the leading carcinogens are benzene, nickel, formaldehyde.Conclusions:The problems of monitoring carcinogens in the production environment, expert assessments to prove the professional genesis of malignant neoplasms were considered; it is noted that the rank number of carcinogenic professions of wagon repair production is as follows: painter, electrician, impregnator, mechanic of rolling stock.
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Loomis, Dana, Neela Guha, Amy L. Hall, and Kurt Straif. "Identifying occupational carcinogens: an update from the IARC Monographs." Occupational and Environmental Medicine 75, no. 8 (May 16, 2018): 593–603. http://dx.doi.org/10.1136/oemed-2017-104944.
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The recognition of occupational carcinogens is important for primary prevention, compensation and surveillance of exposed workers, as well as identifying causes of cancer in the general population. This study updates previously published lists of known occupational carcinogens while providing additional information on cancer type, exposure scenarios and routes, and discussing trends in the identification of carcinogens over time. Data were extracted from International Agency for Research on Cancer (IARC) Monographs covering the years 1971–2017, using specific criteria to ensure occupational relevance and provide high confidence in the causality of observed exposure-disease associations. Selected agents were substances, mixtures or types of radiation classified in IARC Group 1 with ‘sufficient evidence of carcinogenicity’ in humans from studies of exposed workers and evidence of occupational exposure documented in the pertinent monograph. The number of known occupational carcinogens has increased over time: 47 agents were identified as known occupational carcinogens in 2017 compared with 28 in 2004. These estimates are conservative and likely underestimate the number of carcinogenic agents present in workplaces. Exposure to these agents causes a wide range of cancers; cancers of the lung and other respiratory sites, followed by skin, account for the largest proportion. The dominant routes of exposure are inhalation and dermal contact. Important progress has been made in identifying occupational carcinogens; nevertheless, there is an ongoing need for research on the causes of work-related cancer. Most workplace exposures have not been evaluated for their carcinogenic potential due to inadequate epidemiologic evidence and a paucity of quantitative exposure data.
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Jongen, W. M. F., and F. O. Dorgelo. "Naturally occurring carcinogens and modulating factors in food of plant origin." Netherlands Journal of Agricultural Science 34, no. 3 (August 1, 1986): 395–404. http://dx.doi.org/10.18174/njas.v34i3.16793.
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The current state of knowledge concerning the process of carcinogenesis, including the role of initiators and promoters is discussed, and foods of plant origin which contain naturally occurring carcinogens and mutagens are highlighted. Carcinogens and promoters, anticarcinogens and endogenous formation of mutagens and carcinogens are also covered. The mutagenic activity in some foods of plant origin is tabulated and the role of plant breeding in introducing or deleting the carcinogenic or anticarcinogenic properties in these foods is discussed. It is suggested that future research will focus on tumour promotion. (Abstract retrieved from CAB Abstracts by CABI’s permission)
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Fukushima, Shoji, Min Gi, Masaki Fujioka, Anna Kakehashi, Hideki Wanibuchi, and Michiharu Matsumoto. "Quantitative Approaches to Assess Key Carcinogenic Events of Genotoxic Carcinogens." Toxicological Research 34, no. 4 (October 15, 2018): 291–96. http://dx.doi.org/10.5487/tr.2018.34.4.291.
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Tubiana, M. "The carcinogenic effect of exposure to low doses of carcinogens." Occupational and Environmental Medicine 49, no. 9 (September 1, 1992): 601–5. http://dx.doi.org/10.1136/oem.49.9.601.
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Farber, Emmanuel. "Hepatocarcinogenesis: How Do Peroxisome Proliferators Relate?" Journal of the American College of Toxicology 11, no. 3 (May 1992): 363–67. http://dx.doi.org/10.3109/10915819209141876.
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There is an increasing awareness that many peroxisome proliferators are being introduced into our environment and many of these have shown carcinogenic activity in some rodent species. The agents involved include drugs (e.g., hypolipdemic agents of several chemical structures including HMG CoA reductase inhibitors) and industrial chemicals. The neoplasms seen are mainly in the liver with a variable incidence in the pancreas. The association between peroxisome proliferation and neoplasms is impressive. Yet, there are several seemingly fundamental differences between carcinogenic peroxisome proliferators and mutagenic or genotoxic chemical carcinogens. Peroxisome proliferators in general are neither mutagenic nor genotoxic and do not induce precancerous hepatic lesions and liver cell cancer until they have reached the late stage. With many agents, it appears that a considerable degree of peroxisome proliferation must take place for them to be carcinogenic. One poorly documented speculation is that peroxisome proliferators induce cancer by acting mainly as promoters, presupposing that the animals being tested are “preinitiated,” a conclusion that is scientifically indefensible. This presentation covers a comparison between the key requirements for cancer development with genotoxic agents and those seen with peroxisome proliferators, and discusses the methylation of genes for selective enzymes of the resistance phenotype induced by mutagenic carcinogens.
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Hartwig, Andrea, Michael Arand, Bernd Epe, Sabine Guth, Gunnar Jahnke, Alfonso Lampen, Hans-Jörg Martus, et al. "Mode of action-based risk assessment of genotoxic carcinogens." Archives of Toxicology 94, no. 6 (June 2020): 1787–877. http://dx.doi.org/10.1007/s00204-020-02733-2.
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Abstract The risk assessment of chemical carcinogens is one major task in toxicology. Even though exposure has been mitigated effectively during the last decades, low levels of carcinogenic substances in food and at the workplace are still present and often not completely avoidable. The distinction between genotoxic and non-genotoxic carcinogens has traditionally been regarded as particularly relevant for risk assessment, with the assumption of the existence of no-effect concentrations (threshold levels) in case of the latter group. In contrast, genotoxic carcinogens, their metabolic precursors and DNA reactive metabolites are considered to represent risk factors at all concentrations since even one or a few DNA lesions may in principle result in mutations and, thus, increase tumour risk. Within the current document, an updated risk evaluation for genotoxic carcinogens is proposed, based on mechanistic knowledge regarding the substance (group) under investigation, and taking into account recent improvements in analytical techniques used to quantify DNA lesions and mutations as well as “omics” approaches. Furthermore, wherever possible and appropriate, special attention is given to the integration of background levels of the same or comparable DNA lesions. Within part A, fundamental considerations highlight the terms hazard and risk with respect to DNA reactivity of genotoxic agents, as compared to non-genotoxic agents. Also, current methodologies used in genetic toxicology as well as in dosimetry of exposure are described. Special focus is given on the elucidation of modes of action (MOA) and on the relation between DNA damage and cancer risk. Part B addresses specific examples of genotoxic carcinogens, including those humans are exposed to exogenously and endogenously, such as formaldehyde, acetaldehyde and the corresponding alcohols as well as some alkylating agents, ethylene oxide, and acrylamide, but also examples resulting from exogenous sources like aflatoxin B1, allylalkoxybenzenes, 2-amino-3,8-dimethylimidazo[4,5-f] quinoxaline (MeIQx), benzo[a]pyrene and pyrrolizidine alkaloids. Additionally, special attention is given to some carcinogenic metal compounds, which are considered indirect genotoxins, by accelerating mutagenicity via interactions with the cellular response to DNA damage even at low exposure conditions. Part C finally encompasses conclusions and perspectives, suggesting a refined strategy for the assessment of the carcinogenic risk associated with an exposure to genotoxic compounds and addressing research needs.
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Che, Xun, and Wei Dai. "Aryl Hydrocarbon Receptor: Its Regulation and Roles in Transformation and Tumorigenesis." Current Drug Targets 20, no. 6 (March 29, 2019): 625–34. http://dx.doi.org/10.2174/1389450120666181109092225.
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AhR is an environmental response gene that mediates cellular responses to a variety of xenobiotic compounds that frequently function as AhR ligands. Many AhR ligands are classified as carcinogens or pro-carcinogens. Thus, AhR itself acts as a major mediator of the carcinogenic effect of many xenobiotics in vivo. In this concise review, mechanisms by which AhR trans-activates downstream target gene expression, modulates immune responses, and mediates malignant transformation and tumor development are discussed. Moreover, activation of AhR by post-translational modifications and crosstalk with other transcription factors or signaling pathways are also summarized.
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Fukushima, Shoji, Min Wei, Anna Kakehashi, and Hideki Wanibuchi. "Threshold for Genotoxic Carcinogens: The Central Concern in Carcinogenic Risk Assessment." Genes and Environment 34, no. 4 (2012): 153–56. http://dx.doi.org/10.3123/jemsge.34.153.
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FUKUSHIMA, Shoji. "Medium-term Tests for Carcinogens and Carcinogenic Hazard Evaluation for Humans." Journal of Occupational Safety and Health 1, no. 2 (2008): 141–49. http://dx.doi.org/10.2486/josh.1.141.
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Farmer, P. B. "Carcinogen adducts: use in diagnosis and risk assessment." Clinical Chemistry 40, no. 7 (July 1, 1994): 1438–43. http://dx.doi.org/10.1093/clinchem/40.7.1438.
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Abstract Exposure to genotoxic carcinogens results in the formation of covalently bound adducts of the carcinogens with cellular nucleophilic molecules, including DNA and protein. Quantitative measurements of these adducts may be used to monitor exposure to these carcinogens. The analytical methods required to detect the adducts need to be of exceptional sensitivity and include 32P-postlabeling, immunoassay, and physicochemical techniques (e.g., mass spectrometry or fluorescence measurements). Owing to its accessibility and long lifetime, hemoglobin is also suitable for carcinogen adduct measurement, and techniques based on gas chromatography-mass spectrometry or immunoassay have been developed for this purpose. Although the measurement of adducts is now accepted as a valid means of monitoring exposure to carcinogens, the value of such measurements in indicating carcinogenic risk in humans is less certain. However, adduct concentrations, particularly at low doses of carcinogen, have in several instances been shown to correlate with tumorigenicity in animal experiments.
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LaMontagne, Anthony D., David C. Christiani, and Mary Lee Dunn. "Prevention of Work-Related Cancers." NEW SOLUTIONS: A Journal of Environmental and Occupational Health Policy 12, no. 2 (August 2002): 137–56. http://dx.doi.org/10.2190/7lhn-3cdr-9cqr-2vqv.
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Work-related cancers are highly preventable. The primary responsibility for prevention rests not with the workers who are affected by cancers, but with the manufacturers and distributors of carcinogenic substances and the companies who use them. U.S. public policies of strict product liability and the Occupational Safety and Health Act of 1970 address the issue of responsibility. Workers, health care providers, and others also have important roles that complement employers' preventive efforts. The range of prevention strategies available includes ones that should be applied to prevent potentially carcinogenic substances from being marketed and distributed; others that apply in the workplace where potential carcinogens are used; and public policy interventions aimed at ensuring universal implementation of pre-market and workplace prevention strategies. Work-related cancer remains a large problem, even though strategies exist to identify carcinogens and prevent and control on-the-job exposures. However, preventive efforts by government and the society have stalled and a continuing lack of toxicity information shows inadequate societal commitment. The principal barriers to prevention of work-related cancers are political and economic rather than scientific and medical.
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Parke, Dennis V., Costas Ioannides, and David F. V. Lewis. "The 1990 Pharmaceutical Manufacturers Association of Canada Keynote Lecture. The role of the cytochromes P450 in the detoxication and activation of drugs and other chemicals." Canadian Journal of Physiology and Pharmacology 69, no. 5 (May 1, 1991): 537–49. http://dx.doi.org/10.1139/y91-081.
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The roles of the cytochromes P450 are reviewed, with emphasis on their involvement in the detoxication of drugs and chemicals, the activation of carcinogens, and the toxicity of drugs. Cytochromes P450 have different characteristics. P450I mostly activates carcinogens and other chemicals by forming oxygenated reactive intermediates, which are also associated with the formation of neoantigens and immunotoxicity. P450IIE has a propensity to form oxygen radicals, which are cytotoxic and carcinogenic; other cytochromes generate oxygen radicals by futile cycling when activated by difficultly metabolized substrates. Novel procedures for the safety evaluation of chemicals are described; COMPACT is based on the computer graphic determination of the spatial conformation and electronic structure of chemicals to enable their activating cytochromes P450, and hence their toxicity, to be established; ENACT is based on quantifying the induction of individual cytochromes P450, since the extent of induction of P450I, and possibly other activating cytochromes, is directly related to the carcinogenic potential of the chemical.Key words: cytochromes P450, oxygen radicals, enzyme induction, drug metabolism, chemical toxicity.
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Qin, Chunhua, Amy G. Aslamkhan, Kara Pearson, Keith Q. Tanis, Alexei Podtelezhnikov, Erika Frank, Stephen Pacchione, Todd Pippert, Warren E. Glaab, and Frank D. Sistare. "AhR Activation in Pharmaceutical Development: Applying Liver Gene Expression Biomarker Thresholds to Identify Doses Associated With Tumorigenic Risks in Rats." Toxicological Sciences 171, no. 1 (May 25, 2019): 46–55. http://dx.doi.org/10.1093/toxsci/kfz125.
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Abstract Aryl hydrocarbon receptor (AhR) activation is associated with carcinogenicity of non-genotoxic AhR-activating carcinogens such as 2,3,7,8-tetrachlorodibenzodioxin (TCDD), and is often observed with drug candidate molecules in development and raises safety concerns. As downstream effectors of AhR signaling, the expression and activity of Cyp1a1 and Cyp1a2 genes are commonly monitored as evidence of AhR activation to inform carcinogenic risk of compounds in question. However, many marketed drugs and phytochemicals are reported to induce these Cyps modestly and are not associated with dioxin-like toxicity or carcinogenicity. We hypothesized that a threshold of AhR activation needs to be surpassed in a sustained manner in order for the dioxin-like toxicity to manifest, and a simple liver gene expression signature based on Cyp1a1 and Cyp1a2 from a short-term rat study could be used to assess AhR activation strength and differentiate tumorigenic dose levels from non-tumorigenic ones. To test this hypothesis, short-term studies were conducted in Wistar Han rats with 2 AhR-activating carcinogens (TCDD and PCB126) at minimally carcinogenic and noncarcinogenic dose levels, and 3 AhR-activating noncarcinogens (omeprazole, mexiletine, and canagliflozin) at the top doses used in their reported 2-year rat carcinogenicity studies. A threshold of AhR activation was identified in rat liver that separated a meaningful “tumorigenic-strength AhR signal” from a statistically significant AhR activation signal that was not associated with dioxin-like carcinogenicity. These studies also confirmed the importance of the sustainability of AhR activation for carcinogenic potential. A sustained activation of AhR above the threshold could thus be used in early pharmaceutical development to identify dose levels of drug candidates expected to exhibit dioxin-like carcinogenic potential.
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Serdiuk, A. M., I. O. Chernychenko, O. M. Lytvychenko, V. F. Babii, O. Ye Kondratenko, and D. O. Hlavachek. "Сarcinogenic substances in the atmospheric air of Dnipro city and risk to the population." Medicni perspektivi (Medical perspectives) 26, no. 1 (March 26, 2021): 226–31. http://dx.doi.org/10.26641/2307-0404.2021.1.228020.
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The objective – to study the dynamic changes for the health risk of the population of the industrial center in accordance with the state of atmospheric air pollution with carcinogenic compounds. The assessment of the state of atmospheric air pollution was carried out by us based on the results of physicochemical analysis of samples taken in places attached to the locations of stationary posts of state monitoring. The concentration of identified substances was determined by conventional methods: spectral-luminescent and gas chromatographic. Heavy metal concentrations were determined using data from the Central Geophysical Observatory of the Ministry of Emergency Situations. The calculation of the inhalation load of chemical carcinogens and the risks associated with them (non-carcinogenic and carcinogenic) was carried out in accordance with domestic guidelines. The assessment of dynamic changes in the nature of atmospheric air pollution with a complex of carcinogenic substances was made 5 of them are constantly recorded at levels exceeding hygienic standards. When compared with the reference concentrations, all compounds are characterized by high coefficients, indicating the likelihood of their effect on the body's immune system, respiratory organs, malformations, etc. A high individual carcinogenic risk of the effect of chromium VI and nitrosamines was determined. A total carcinogenic risk is formed at levels of 2.5 – 3.9×10-3, which should be considered as high; this requires development and implementation of preventive measures. On the territory of the industrial center, a high level of air pollution with increased carcinogenic and non-carcinogenic risk is stably registered.
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Pankov, V. A., N. V. Efimova, M. V. Kuleshova, and V. R. Motorov. "Carcinogenic risk assessment in aircraft construction workers." Occupational Health and Industrial Ecology, no. 2 (March 14, 2019): 122–26. http://dx.doi.org/10.31089/1026-9428-2019-2-122-126.
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Individual carcinogenic risk (ICR) was assessed in workers of main occupations in aircraft construction industry of East Siberia. Levels of ICR were evaluated for the main occupations workers during 1 to 30 years of service. Th e workers’ exposure was assessed according to longstanding average shift concentrations in the air of workplace, for the population — by average annual concentrations in the ambient air. To evaluate the risk not associated with occupation, the dose was taken for a period of 70 years life. Calculating dose of toxic chemicals in the air of workplace, the authors used “standard” parameters of pulmonary ventilation for adults, weight, days of exposure (240), working time (8 hours as a working day). Individual carcinogenic risk for Irkutsk population equaled 3.0E–04, in Ulan-Ude — 4.8E–04. Th e risk value for the general population is due to formaldehyde and chromium VI. Th e workers of main occupations in enterprises with carcinogenic jeopardy have ICR dozens of times higher than the general urban population. Considering a share in ICR, leading carcinogens for the aircraft construction enterprise workers are: formaldehyde — vulcanizers, chromium and nickel — for other occupations. ICR is considered as unacceptable for occupational groups in 5–15 years aft er starting work under hazardous conditions. Despite high level of ICR, the occupational control incompletely covers monitoring of carcinogens. Existing system of occupational studies fails to disclose etiologic role of occupational factors in occurrence of malignancies.
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Novotný, Ladislav, Anna Vachálková, and Alois Pískala. "Investigation of the Polarographic Properties and Potential Carcinogenity of Some Hydroxyurea Derivatives by DC Polarography." Collection of Czechoslovak Chemical Communications 61, no. 4 (1996): 656–62. http://dx.doi.org/10.1135/cccc19960656.
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Polarographic reduction was studied for a series of 7 urea derivatives and the results were used to assess their potential carcinogenity. The polarographic reduction was examined in absolutely anhydrous dimethylformamide by DC polarography. In the conditions applied, the majority of the compounds was reduced within a single two-electron step, only biuret and its formyl derivative were reduced in two one-electron steps. The potential carcinogenity of the substances was assessed based on the tg α value of the slope of dependence of the polarographic wave height on the concentration of α-lipoic acid added as a test substance. For hydroxyurea, which is the only substance in this series for which a carcinogenic activity has been demonstrated, the tg α parameter attained a value of 0.290. Still higher values were obtained for the formyl derivatives - formylbiuret (0.362) and 2-carbamoyl-1-formylguanidine (0.510). So high tg α values warn of a significant potential carcinogenity. The other substances studied exhibited considerably lower tg α values, indicating that their potential carcinogenity will be low.
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Marant Micallef, Claire, Kevin David Shield, Isabelle Baldi, Barbara Charbotel, Béatrice Fervers, Anabelle Gilg Soit Ilg, Pascal Guénel, et al. "Occupational exposures and cancer: a review of agents and relative risk estimates." Occupational and Environmental Medicine 75, no. 8 (May 7, 2018): 604–14. http://dx.doi.org/10.1136/oemed-2017-104858.
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ObjectivesThe contribution of occupational exposures to the cancer burden can be estimated using population-attributable fractions, which is of great importance for policy making. This paper reviews occupational carcinogens, and presents the most relevant risk relations to cancer in high-income countries using France as an example, to provide a framework for national estimation of cancer burden attributable to occupational exposure.MethodsOccupational exposures that should be included in cancer burden studies were evaluated using multiple criteria: classified as carcinogenic or probably carcinogenic by the International Agency for Research on Cancer (IARC) Monographs volumes 1–114, being a primary occupational exposure, historical and current presence of the exposure in France and the availability of exposure and risk relation data. Relative risk estimates were obtained from published systematic reviews and from the IARC Monographs.ResultsOf the 118 group 1 and 75 group 2A carcinogens, 37 exposures and 73 exposure-cancer site pairs were relevant. Lung cancer was associated with the most occupational carcinogenic exposures (namely, 18), followed by bladder cancer and non-Hodgkin’s lymphoma. Ionising radiation was associated with the highest number of cancer sites (namely, 20), followed by asbestos and working in the rubber manufacturing industry. Asbestos, bis(chloromethyl)ether, nickel and wood dust had the strongest effect on cancer, with relative risks above 5.ConclusionsA large number of occupational exposures continues to impact the burden of cancer in high-income countries such as France. Information on types of exposures, affected jobs, industries and cancer sites affected is key for prioritising policy and prevention initiatives.
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El-zaemey, Sonia, and Renee Carey. "O4A.3 Do shift workers have a different exposure to workplace carcinogens than non-shift workers?" Occupational and Environmental Medicine 76, Suppl 1 (April 2019): A32.3—A33. http://dx.doi.org/10.1136/oem-2019-epi.87.
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BackgroundThere is limited information on whether the prevalence of exposure to workplace carcinogens varies among shift workers and non-shift workers.MethodsThis analysis used data from the Australian Work Exposures Study-Cancer, a telephone survey which examined exposure to carcinogens in the workplace. Workers were classified as shift workers if they indicated that their usual roster ever included work between the hours of midnight and 5 am. Modified Poisson regression was used to estimate the adjusted prevalence ratios (aPRs) and 95% confidence internals (CIs).ResultsAmong the 5425 workers, 6.88% reported doing shiftwork. Overall, shift workers were more likely to be exposed to any carcinogen (aPR=1.16; 95% 1.06–1.26) and to multiple carcinogens (aPR=1.17; 95% 1.06–1.30) than non-shift workers.ConclusionsOur study shows that there are differences in exposure to carcinogenic agents among shift and non-shift workers, and so there is a need for prevention programs in order to reduce these discrepancies.
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Okamoto, Yoshinori, Hideto Jinno, Shinji Itoh, and Shinya Shibutani. "Less Carcinogenic Chlorinated Estrogens Applicable to Hormone Replacement Therapy." International Journal of Molecular Sciences 22, no. 13 (July 5, 2021): 7222. http://dx.doi.org/10.3390/ijms22137222.
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Human estrogens prescribed for hormone replacement therapy (HRT) are known to be potent carcinogens. To find safer estrogens, several chlorinated estrogens were synthesized and their carcinogenic potential were determined. A pellet containing either 2-chloro-17β-estradiol (2-ClE2) or 4-chloro-17β-estradiol (4-ClE2) was implanted subcutaneously for 52 weeks into August Copenhagen Irish (ACI) rats, a preferred animal model for human breast cancer. 17β-Estradiol (E2) frequently induced mammary tumors while both 2-ClE2 and 4-ClE2 did not. Their 17α-ethinyl forms, thought to be orally active estrogens, were also synthesized. Neither 2-chloro-17α-ethinylestradiol (2-ClEE2) nor 4-chloro-17α-ethinylestradiol (4-ClEE2) induced tumors. The less carcinogenic effects were supported by histological examination of mammary glands of ACI rats treated with the chlorinated estrogens. A chlorine atom positioned at the 2- or 4-position of E2 may prevent the metabolic activation, resulting in reducing the carcinogenicity. 2-ClE2 and 4-ClE2 administered subcutaneously and 2-ClEE2 and 4-ClEE2 given orally to ovariectomized rats all showed uterotrophic potency, albeit slightly weaker than that of E2. Our results indicate that less carcinogenic chlorinated estrogens retaining estrogenic potential could be safer alternatives to the carcinogenic estrogens now in use for HRT.
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Bazarova, Ekaterina L., Oleg F. Rosly, Anna A. Fedoruk, Natalya A. Roslaya, and Ilya S. Osherov. "Experience of individual carcinogenic risk evaluation in workers of metallurgic enterprise." Occupational Health and Industrial Ecology, no. 11 (February 18, 2019): 4–10. http://dx.doi.org/10.31089/1026-9428-2018-11-4-10.
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The predictive estimate of individual occupational carcinogenic risk for metallurgic enterprise workers with occupational exposure to chemical carcinogens helped to assign founders, blacksmiths, machine operators, nonferrous metals processing line operators, tool-makers, metal cutters, burners, grog operators to an increased risk group by probability of occupational cancer development. The retrospective epidemiologic study of chronic diseases prevalence and transitory disablement morbidity proved reliable increase of neoplasms occurrence under exposure to electromagnetic fields of personal computers — 1.5-fold, that to constant magnetic field — 1.2-fold; that to lead — 1.9-fold; that for increased body weight — 1.6-fold; that for hypodynamia — 1.2-fold; that for hypercholesterolemia — 1.3-fold; that for high blood pressure — 1.2-fold. The data obtained can serve as a basis of preventive strategy of carcinogenic risk minimization at an enterprise.
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Cunningham, Michael L. "Role of increased DNA replication in the carcinogenic risk of nonmutagenic chemical carcinogens." Mutation Research/Reviews in Genetic Toxicology 365, no. 1-3 (September 1996): 59–69. http://dx.doi.org/10.1016/s0165-1110(96)90012-3.
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Weston, A., D. K. Manchester, A. Povey, and C. C. Harris. "Detection of Carcinogen–Macromolecular Adducts in Humans." Journal of the American College of Toxicology 8, no. 5 (September 1989): 913–32. http://dx.doi.org/10.3109/10915818909018052.
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A major concern of molecular epidemiology is the identification of individuals at increased risk of cancer by obtaining evidence of high exposure to carcinogens that may lead to pathobiological lesions in target cells. DNA is considered to be a target for modification by mutagens and carcinogens; therefore, damage to DNA can be used as an internal, molecular dosimeter of carcinogen exposure. The reactive species of these carcinogens may bind either directly to DNA to form adducts or indirectly to cause secondary DNA lesions through free radicals and aldehydes. Highly sensitive and specific methods have been developed to measure DNA lesions and DNA repair products that are found in biological specimens from humans exposed to carcinogens in the environment. For example, DNA adducts have been measured in cells and tissues from people exposed environmentally to carcinogenic polycyclic aromatic hydrocarbons or alkylating agents. Antibodies recognizing carcinogen-DNA adducts have also been detected in human sera. Carcinogen-protein adducts are also being used as molecular dosimeters of carcinogen exposure. The advantages and limitations of the various methods used to measure carcinogen-macromolecular adducts are discussed here. The use of two or more complementary assays to obtain confirmatory results is recommended.
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Khlifi, Rim, Olfa Messaoud, Ahmed Rebai, and Amel Hamza-Chaffai. "Polymorphisms in the Human Cytochrome P450 and ArylamineN-Acetyltransferase: Susceptibility to Head and Neck Cancers." BioMed Research International 2013 (2013): 1–20. http://dx.doi.org/10.1155/2013/582768.
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The occurrence of head and neck cancer (HNC) is associated with smoking and alcohol drinking. Tobacco smoking exposes smokers to a series of carcinogenic chemicals. Cytochrome P450 enzymes (CYP450s), such asCYP1A1,CYP1B1, andCYP2D6, usually metabolize carcinogens to their inactive derivatives, but they occasionally convert the chemicals to more potent carcinogens. In addition, viaCYP450(CYP2E1) oxidase, alcohol is metabolized to acetaldehyde, a highly toxic compound, which plays an important role in carcinogenesis. Furthermore, twoN-acetyltransferase isozymes (NATs),NAT1andNAT2, are polymorphic and catalyze bothN-acetylation andO-acetylation of aromatic and heterocyclic amine carcinogens. Genetic polymorphisms are associated with a number of enzymes involved in the metabolism of carcinogens important in the induction of HNC. It has been suggested that such polymorphisms may be linked to cancer susceptibility. In this paper, we select four cytochromeP450enzymes (CYP1A1,CYP1BA1,CYP2D6, andCYP2E1), and twoN-acetyltransferase isozymes (NAT1andNAT2) in order to summarize and analyze findings from the literature related to HNC risk by focusing on (i) the interaction between these genes and the environment, (ii) the impact of genetic defect on protein activity and/or expression, and (iii) the eventual involvement of race in such associations.
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Tian, Hui, Xiujuan Liang, Yan Gong, Shimin Ma, Zhuang Kang, Qifa Sun, and Hongtao Jin. "Risk assessment of metals from shallow groundwater in Lianhuashan District, China." La Houille Blanche, no. 1 (February 2020): 5–15. http://dx.doi.org/10.1051/lhb/2019063.
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The present study was conducted to investigate trace metal (Fe, Mn, Cd, Pb, Zn, Cu, Al, As, Se, Hg, Sr, Ba, Li, Co, B, Ni, Ag, Mo and Cr) concentrations of drinking water samples in Lianhuashan District, China. Furthermore, the study aimed to ascertain carcinogenic and non-carcinogenic health risks of metals by ingestion and dermal absorption pathways to the local residents. Metal concentrations were compared with permissible limits set by the Chinese Standards, USEPA and WHO. The average concentrations of the analyzed elements are in the order of Fe > Sr > Mn > Al > Ba > Mo > Zn > B > Li > Pb > Cr > Ni > Cu > Ag > Co > As > Se > Cd > Hg. The results indicate that the concentrations of Cd, Zn, Cu, Ni, Se, Hg, Ba and Cr were lower than their respective permissible limits, whereas the concentrations of Fe, Mn, Pb, Al, As and Mo at some sampling sites exceeded the permissible limits. The total hazard index (HQtotal) of the metals (Cd, Zn, Cu, Al, Se, Hg, Sr, Ba, B, Ni, Ag, Cr) calculated through ingestion and dermal absorption pathways for adults and children were found to be lower than unity, indicating that the metals would not pose any adverse effect and non-carcinogenic health risk to the habitants. The results of carcinogenic risk assessment indicate that the Excess Lifetime Cancer Risk (ingestion and dermal exposure pathways) of metals exposure was in accordance to the acceptable lifetime risks for carcinogens in drinking water (10−6–10−4). Both non-carcinogenic and carcinogenic risks were mainly attributed to the ingestion pathways.
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Pakharukova, Mariya Yurievna, José Manuel Correia da Costa, and Viatcheslav Alekseevitch Mordvinov. "The liver fluke Opisthorchis felineus as a group III or group I carcinogen." 4open 2 (2019): 23. http://dx.doi.org/10.1051/fopen/2019016.
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Opisthorchiasis caused by the liver fluke Opisthorchis felineus is one of the most common helminthic infections in the Russian Federation. The largest area affected by opisthorchiasis felinea occupies almost the entire territory of Western Siberia and extends to northern Kazakhstan and a part of the Ural region. Natural endemic regions of opisthorchiasis also exist in the European part of Russia, and in the regions of Western and Eastern Europe. According to the official statistics of the Russian Federation, up to 40 000 patients with opisthorchiasis are registered annually in the country. Opisthorchiasis felinea affects the hepatobiliary system and causes serious liver disorders, including cancer of the biliary tract. Other parasitoses, opisthorchiasis viverrini and clonorchiasis, are widespread in the Southeast Asia and China. The causative agents of these diseases, liver flukes O. viverrini and Clonorchis sinensis, are officially recognized as Group 1 biological carcinogens and are classified as the main risk factors for cholangiocarcinoma. O. felineus is included in Group 3 of biological carcinogens and is not officially considered carcinogenic to humans. Studies on the carcinogenic potential of this liver fluke and the epidemiology of cholangiocarcinoma in the Russian Federation have started in earnest quite recently. Nevertheless, we have some evidence that infection with O. felineus leads to a precancerous state of the bile duct epithelium. This state, combined with additional risk factors, poses a real risk of cholangiocarcinoma. In our opinion, taking into consideration the accumulated facts, the classification of the carcinogenic potential of O. felineus requires revision. In this review, we focus on the relevant characteristics of the biology and epidemiology of this helminth as well as experimental data on opisthorchiasis felinea; this information might clarify the carcinogenicity of O. felineus to humans.
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Allen, D. G., G. Pearse, J. K. Haseman, and R. R. Maronpot. "Prediction of Rodent Carcinogenesis: An Evaluation of Prechronic Liver Lesions as Forecasters of Liver Tumors in NTP Carcinogenicity Studies." Toxicologic Pathology 32, no. 4 (June 2004): 393–401. http://dx.doi.org/10.1080/01926230490440934.
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The National Toxicology Program (NTP) developed the chronic 2-year bioassay as a mechanism for predicting the carcinogenic potential of chemicals in humans. The cost and duration of these studies has limited their use to small numbers of selected chemicals. Many different short-term methods aimed at increasing predictive accuracy and the number of chemicals evaluated have been developed in attempts to successfully correlate their results with evidence of carcinogenicity (or lack of carcinogenicity). Using NTP studies, the effectiveness of correlating prechronic liver lesions with liver cancer encompassing multiple studies using mice (83 compounds) and rats (87 compounds) was assessed. These lesions include hepatocellular necrosis, hepatocellular hypertrophy, hepatocellular cytomegaly, bile duct hyperplasia, and hepatocellular degeneration, along with increased liver weight. Our results indicate that pooling 3 of these prechronic data points (hepatocellular necrosis, hepatocellular hypertrophy, and hepatocellular cytomegaly) can be very predictive of carcinogenicity in the 2-year study ( p < 0 .05). The inclusion of increased liver weight as an endpoint in the pool of data points increases the number of rodent liver carcinogens that are successfully predicted ( p < 0 .05), but also results in the prediction of increased numbers of noncarcinogenic chemicals as carcinogens. The use of multiple prechronic study endpoints provides supplementary information that enhances the predictivity of identifying chemicals with carcinogenic potential.
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Maksimov, G. G., Yu G. Aznabaeva, E. V. Kirillova, O. N. Lipatov, and V. M. Akhmetov. "ECOLOGOEPIDEMIOLOGICAL CONNECTION OF LUNG CANCER MORBIDITY WITH ATMOSPHERIC AIR POLLUTION BY CARCINOGENS IN PETROCHEMICAL PROFILE REGIONS." Perm Medical Journal 35, no. 3 (December 15, 2018): 45–57. http://dx.doi.org/10.17816/pmj35345-57.
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Aim. To study the dynamics of lung cancer (LC) morbidity among the population of five cities of the Republic of Bashkortostan over the period from 2010 to 2016 and the structure of industrial emissions for grounding of adequate integral index, connected with LC morbidity and development of preventive measures to decrease malignant neoplasms. Materials and methods. The structure of gross emissions of industrial enterprises and ecologohygienic assessment of atmospheric air was conducted according to the materials of the Department of Rospotrebnadzor in Bashkortostan for 2010-2016. Lung cancer morbidity in the above mentioned territories was studied by the materials of Republican Clinical Oncological Dispensary. To estimate the influence of gross emissions on LC morbidity, modeling technique, adequate to panel analysis of spatially dynamic structural data, was applied. Results. The assessment of carcinogenic risk of atmospheric air emissions, taking into account not separate carcinogens, but their combined effect as substances with similarly directed impact, detected accurate correlation of dependence of high LC morbidity on the resultant carcinogens action. Conclusions. High LC morbidity in the cities of Bashkortostan is connected with high gross emission of carcinogens into the atmospheric air. Information on gross emissions of carcinogens and their structure can serve as an integral criterion of atmospheric pollution impact on lung cancer morbidity.
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Stiborová, Marie, Karel Naiman, Markéta Martínková, Václav Martínek, Martina Svobodová, Heinz Schmeiser, and Eva Frei. "Genotoxic mechanisms for the carcinogenicity of the environmental pollutants and carcinogens o-anisidine and 2-nitroanisole follow from adducts generated by their metabolite N-(2-methoxyphenyl)hydroxylamine with deoxyguanosine in DNA." Interdisciplinary Toxicology 2, no. 1 (March 1, 2009): 24–27. http://dx.doi.org/10.2478/v10102-009-0004-4.
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Genotoxic mechanisms for the carcinogenicity of the environmental pollutants and carcinogenso-anisidine and 2-nitroanisole follow from adducts generated by their metaboliteN-(2-methoxyphenyl)hydroxylamine with deoxyguanosine in DNAAn aromatic amine,o-anisidine (2-methoxyaniline) and its oxidative counterpart, 2-nitroanisole (2-methoxynitrobenzene), are the industrial and environmental pollutants causing tumors of the urinary bladder in rats and mice. Both carcinogens are activated to the same proximate carcinogenic metabolite,N-(2-methoxyphenyl)hydroxylamine, which spontaneously decomposes to nitrenium and/or carbenium ions responsible for formation of deoxyguanosine adducts in DNAin vitroandin vivo. In other words, generation ofN-(2-methoxyphenyl)hydroxylamine is responsible for the genotoxic mechanisms of the o-anisidine and 2-nitroanisole carcinogenicity. Analogous enzymes of human and rat livers are capable of activating these carcinogens. Namely, human and rat cytochorme P450 2E1 is the major enzyme oxidizingo-anisidine toN-(2-methoxyphenyl)hydroxylamine, while xanthine oxidase of both species reduces 2-nitroanisole to this metabolite. Likewise,O-demethylation of 2-nitroanisole, which is the detoxication pathway of its metabolism, is also catalyzed by the same human and rat enzyme, cytochorme P450 2E1. The results demonstrate that the rat is a suitable animal model mimicking the fate of both carcinogens in humans and suggest that both compounds are potential carcinogens also for humans.
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MITSUMORI, Kunitoshi. "POSSIBLE MECHANISM ON ENHANCED CARCINOGENESIS OF GENOTOXIC CARCINOGENS AND UNSOLVED MECHANISMS ON LESSER CARCINOGENIC SUSCEPTIBILITY TO SOME CARCINOGENS IN RASH2 MICE." Journal of Toxicological Sciences 28, no. 5 (2003): 371–83. http://dx.doi.org/10.2131/jts.28.371.
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Lijinsky, William, Barbara J. Thomas, and Robert M. Kovatch. "Local and Systemic Carcinogenic Effects of Alkylating Carcinogens in Rats Treated by Intravesicular Administration." Japanese Journal of Cancer Research 82, no. 9 (September 1991): 980–86. http://dx.doi.org/10.1111/j.1349-7006.1991.tb01931.x.
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Adrianovskii, V., G. Lipatov, E. Kuzmina, and N. Zlygosteva. "Applying of Technique for Assessing Occupational Cancerogenic Risks for Workers Used in Metallurgical Shops With Different Methods of Blister Copper Production." Journal of Global Oncology 4, Supplement 2 (October 1, 2018): 206s. http://dx.doi.org/10.1200/jgo.18.83600.
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Background: Exposure to carcinogens at workers used in the enterprises of copper metallurgy making urgent the task of assessing carcinogenic risks in the nonferrous metallurgy. In particular, melting and conversion of copper are characterized by the exposure of arsenic, cadmium, lead, nickel, benz(a)pyrene. Aim: Assessment of professional carcinogenic risks for workers used in shops with a shaft and reflective copper smelting ore, compared with one of the modern methods of producing blister copper. Carcinogenic risk was estimated from each of the substances and in total from their combination for 25 years of work experience. When inappropriate carcinogen risk calculated duration time of operation, at which the allowable upper limit of occupational risk. Methods: A hygienic assessment of the contribution of the working environment to the formation of a carcinogenic risk for workers engaged in reverberatory and blast smelting of copper-bearing ores in comparison with autogenous processes was carried out. To calculate the carcinogenic risks, we used 8 hours concentration in the working air as well as slope factors for inhalation exposure (SFi) of arsenic, cadmium, lead, nickel, and benz(a)pyrene. Results: It is shown that when copper is smelted, inorganic arsenic compounds are the main factor that forms a carcinogenic risk: reverberatory smelting - 67.8%; shaft smelting - 88.9%; melting furnaces in “molten bath” - 96.2%. The highest predicted values of carcinogenic risk for similar occupations of metallurgical shops are observed with reverberatory (2.9 × 10−2) and blast smelting (1.8 × 10−2), rather than with bath smelting (5.2 × 10−3). It is due to the difference in the used equipment. The highest values of carcinogenic risks identified in the batch loader, working conditions which are characterized by exposure to high concentrations of dust in the workplace area, and the least - for the metal spiller. Among the professions of the copper smelting shop, in which reflective smelting is used, the values of the length of service in contact with carcinogenic substances were in the range from 6.5 to 1.1 years. A little more was the duration of the maximum work experience in mine melting - from 1.38 to 1.56 years. In the smelting shop with smelting furnaces in a “liquid bath” the amount of acceptable work experience varied from 3.13 to 6.41 years. Conclusion: When all the existing methods for producing blister copper carcinogenic risk due to exposure to arsenic, cadmium, lead, chromium (VI), and benzo(a)pyrene is in an unacceptable range (>1.0 × 10−3). The main measure to reduce the carcinogenic risk of blister copper production should be the technical re-equipment of smelter shops with the introduction of autogenous processes (melting furnaces in “molten bath”).