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Polycyclic aromatic hydrocarbons (PAHs) adsorbed on cigarette sidestream smoke particulates (CSSPs) have been regarded as important contributors to lung carcinogenesis in never smokers. However, limited information is available on PAH levels in cigarette sidestream smoke. Here we determine the concentrations of 22 PAHs, including 16 US EPA priority PAHs, in CSSPs generated from a high market-share domestic brand in Taiwan. Five of the 22 PAHs are undetectable. The remaining 17 PAHs constitute about 0.022% of the total mass of CSSPs. Near one fifth of the PAH mass come from IARC group 1 and group 2 carcinogens. Carcinogenic potency is equivalent to 144 ng benzo[a]pyrene per cigarette converted according to potency equivalency factors (PEFs). The CSSP condensate could activate AhR activity and induce AhR target gene expression. High concentrations of CSSPs also exhibited AhR-independent cytotoxicity. However, mixing the 17 PAHs as the composition in the CSSP condensate could not reconstitute either capacity. Since AhR activation and cytotoxicity are important mechanisms underlying carcinogenic potency, the results suggest that other component compounds play a more active role in carcinogenesis. The approach of individual PAH profiling plus PEF conversion commonly used in risk assessment is likely to underestimate the risk caused by environmental cigarette smoke exposure. 相似文献
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It is widely accepted that tobacco smoke is responsible for the vast majority of lung cancers worldwide. There are many known and suspected carcinogens present in cigarette smoke, including α-emitting radioisotopes. Epidemiologic studies have shown that increased lung cancer risk is associated with exposure to ionizing radiation, and it is estimated that the majority of smoking-induced lung cancers may be at least partly attributable to the inhaled and deposited radiation dose from radioisotopes in the cigarette smoke itself. Recent research shows that silencing of the tumor suppressor gene p16INK4a (p16) by promoter methylation plays a role in smoking-related lung cancer. Inactivation of p16 has also been associated with lung cancer incidence in radiation-exposed workers, suggesting that radionuclides in cigarette smoke may be acting with other compounds to cause smoking-induced lung cancer. We evaluated the mechanism of ionizing radiation as an accepted cause of lung cancer in terms of its dose from tobacco smoke and silencing of p16. Because both radiation and cigarette smoking are associated with inactivation of p16, and p16 inactivation has been shown to play a major role in carcinogenesis, ionizing radiation from cigarette smoke likely plays a role in lung cancer risk. How large a role it plays, relative to chemical carcinogens and other modes of action, remains to be elucidated. 相似文献
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烟草行业的火灾特点及其监测方法的讨论 总被引:1,自引:0,他引:1
烟厂是火灾危险性较大的部门,加强其火灾的早期探测报警是防止火灾发生、减少火灾损失的重要方面。本文对烟厂中各主要生产环节的火灾特点作了分析,指出应针对各部分的特殊性采取适当的火灾探测方法并对现在常用的一些火灾探测技术在烟厂中的适用性作了讨论,认为现有的光束式火灾探测器较适用于内部空间较大的烟厂仓库和厂房。对安装了电视监控系统的企业,建议将其与计算机图象分析技术相结合,增加其防火监视功能。 相似文献
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To evaluate the effects of cigarette smoking and biomass (dried dung) smoke on the oxidant–antioxidant status, three groups each with 5 rabbits were used. Groups of rabbits were exposed to either cigarette smoke, dried dung smoke or dry air, 1?h daily for one month. Protein carbonyls, prostaglandin F2α and malondialdehyde levels were significantly increased and protein sulfhydryls levels were significantly decreased in the cigarette smoke group compared with the control group. Only protein sulfhydryls levels were significantly decreased in dung group compared with the control group. Short course exposure to both cigarette smoke and biomass smoke decreased plasma antioxidant levels but only cigarette smoke increased plasma oxidant levels, whereas biomass smoke did not produce any change. 相似文献
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