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Synthetic Compounds vs. Phytochemicals for the Treatment of Human Cutaneous Malignant Melanoma
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Jacqueline Maphutha, Namrita Lall
Carcinogenesis refers to the initiation of a tumor due to cancer-causing agents referred to as carcinogens. Carcinogens can be characterized as chemical carcinogens, biological carcinogens and physical carcinogens. Chemical carcinogens such as polycyclic aromatic hydrocarbons (PAHs), released into the environment from the combustion of materials containing carbon, elicit mutations in the tumor suppressor gene TP53 (Soliman, 2018). The protein (p53) enables uncontrolled cellular proliferation, which is evident in breast cancer. Furthermore, human papillomaviruses (HPV) such as HPV16 and HPV18 (biological carcinogens) produce an oncoprotein E6, which elicits mutations in the tumor suppressor gene TP53, resulting in uncontrolled proliferation. Human papillomaviruses predominantly lead to the initiation and progression of cervical cancer (Burd, 2003; Pal and Kundu, 2020; Scheffner et al., 1990).
Environmental Inhaled Agents and Their Relation to Lung Cancer
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Animal studies are used to identify individual carcinogens and to explore the interaction among the effects of carcinogens in cancer induction. Animal models for exposure of the lungs to respiratory carcinogens through inhalation have been developed (Nettesheim and Griesemer, 1978), and are especially suitable for testing volatile chemicals, for example, benzo(a) pyrene inhalation by hamsters and bis(chloromethyl)ethyl inhalation by rats and hamsters (Harris, 1983). The extrapolations of animal data to human, are however, fraught with problems and uncertainties (Alderson, 1982; Samuels and Adamson, 1985; Upton, 1982), particularly extrapolations across species and across differences in dose and conditions of exposure. Arsenic, for instance, has not been shown to be carcinogenic in animal models (Frank, 1982) despite its well known effect in humans.
Our Radiation Environment
Published in T. D. Luckey, Radiation Hormesis, 2020
One benefit of nuclear power is that it limits pollution by carcinogens from coal-fired power plants. Coal-fired plants release more radioactive waste into the air than nuclear power plants of equivalent capacity. They are a major source of radon and airborne organic carcinogens. The choice of fuel in coal-fired plants is either soft coal, from mines in the eastern U.S. or hard coal from the Rocky Mountains. The former contains much sulfur, considered to be a major cause of acid rain; the latter contains more radionuclides.558 Both are sources of toxic elements, e.g., mercury, selenium, arsenic, lead, cadmium, gallium, and vanadium. Uranium released into the atmosphere from burning eastern coal in a plant with a very efficient filter system was 15 to 38 μg/g fly ash; the slag contained 16 to 95 μg/g. This was emphasized by the statement of Lord Marshall, chairman of the British Central Electricity Generating Board (CEGB): “I have to inform you that yesterday the CEGB released about 300 kg of uranium, together with all its radioactive decay products, into the environment. Furthermore, we released some 300 kg of uranium the day before that. We shall be releasing the same amount of uranium today, and we plan to do the same tomorrow. In fact, we do it every day of the year so long as we burn coal in our power stations. And we do not call that ‘radioactive waste’, we call it coal ash.”54
Global burden of tracheal, bronchus, and lung cancer attributable to occupational carcinogens in 204 countries and territories, from 1990 to 2019: results from the global burden of disease study 2019
Published in Annals of Medicine, 2023
Yan Zhang, Mi Mi, Ning Zhu, Zhijun Yuan, Yuwei Ding, Yingxin Zhao, Yier Lu, Shanshan Weng, Ying Yuan
Occupational carcinogen exposure is an important preventable cause of TBL cancer [5, 49]. The results of our and previous studies highlight the need for all countries to work to eliminate or control occupational carcinogen exposure, which is insufficient in many lower SDI countries and is sometimes comparable to the high-exposure levels experienced in high-income countries over the past few decades. Suitable approaches include further development of global and regional frameworks for the control of occupational carcinogens; adopting and enforcing relevant legislation; strengthening exposure and outcome data collection and reporting at the country level and emphasizing the importance of primary prevention [50]. At the same time, early TBL cancer detection must be implemented, with a special emphasis on strengthening treatment to reduce disease progression and severity [51].
The WHO claims estrogens are ‘carcinogenic’: is this true?
Published in Climacteric, 2023
According to definition, a ‘carcinogen’ can induce a new cancer cell. In terms of both mechanisms, estrogens themselves cannot be defined as ‘carcinogenic’ as they only induce cancer cells in combination with additional endogenous and/or exogenous factors. For this reason, societies such as the International Menopause Society (IMS) and the International Society of Gynecological Endocrinology (ISGE) have not accepted the WHO statement [6,7]. Furthermore, it takes many years before the first ‘clinical cancer’ cell develops; here we will focus on breast cancer. Another important aspect is that experimental as well as clinical data suggest ‘carcinoprotective’ estrogen metabolites; that is, a decrease in breast cancer risk during estrogen treatment – a sharp contrast to the claim made by the WHO.
Approaches for the setting of occupational exposure limits (OELs) for carcinogens
Published in Critical Reviews in Toxicology, 2023
According to the German Senate Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area (known as the MAK Commission), advances in our understanding of the MoAs and the potency of carcinogens have enabled an improved differentiation of carcinogenic substances. Therefore, carcinogens are classified in five categories (summarised in Table 5). In the methodology for the derivation of MAK-values (maximum workplace concentration), it is said that no scientifically justifiable MAK-value can be proposed in the absence of a NOAEL (DFG 2019). The benchmark approach is not mentioned. It should be noted that the MAK Commission approach is a hybrid in that categories 1–3 are largely based on strength of evidence, while categories 4–5 are based on MoA considerations.