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生物标志物数据在临床和环境干预中的应用。

Utilization of biomarker data for clinical and environmental intervention.

作者信息

Christiani D C

机构信息

Occupational Medicine and Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA.

出版信息

Environ Health Perspect. 1996 Oct;104 Suppl 5(Suppl 5):921-5. doi: 10.1289/ehp.96104s5921.

DOI:10.1289/ehp.96104s5921
PMID:8933035
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1469688/
Abstract

Of the 189 air toxics listed in the Clean Air Act, a substantial number are important in potentially causing adverse health effects in several organ systems. Although the major health effects are manifested as respiratory diseases, especially airways disease, these agents may cause cancer and premature mortality, probably from cardiopulmonary disease. Validated biologic markers may be useful in identifying early effects to improve our understanding of exposure-response relationships and clarify susceptibility. However, the knowledge obtained from epidemiologic studies utilizing these new molecular tools will reduce morbidity and mortality from air toxics only when they can be applied effectively in the prevention and control of disease. Intervention strategies using these markers can be used to identify etiologic factors and assess the effectiveness of exposure reduction, and, in some instances, chemoprevention. This paper illustrates examples of these intervention strategies and reviews the current strengths and limitations of environmental molecular epidemiology in controlling disease caused by air toxics.

摘要

《清洁空气法》列出的189种空气有毒物质中,有相当一部分对多个器官系统潜在地造成不良健康影响具有重要意义。虽然主要健康影响表现为呼吸系统疾病,尤其是气道疾病,但这些物质可能导致癌症和过早死亡,可能是由于心肺疾病。经过验证的生物标志物可能有助于识别早期影响,以增进我们对暴露-反应关系的理解并阐明易感性。然而,只有当利用这些新分子工具进行的流行病学研究结果能够有效应用于疾病的预防和控制时,才能降低空气有毒物质导致的发病率和死亡率。使用这些标志物的干预策略可用于识别病因因素并评估减少暴露的效果,在某些情况下还可用于化学预防。本文举例说明了这些干预策略,并综述了环境分子流行病学在控制空气有毒物质所致疾病方面目前的优势和局限性。

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本文引用的文献

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K-ras mutations in human adenocarcinoma of the lung: association with smoking and occupational exposure to asbestos.人类肺腺癌中的K-ras突变:与吸烟及职业性石棉暴露的关联
Int J Cancer. 1993 Jan 21;53(2):250-6. doi: 10.1002/ijc.2910530213.
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Oxidants, antioxidants, and the degenerative diseases of aging.氧化剂、抗氧化剂与衰老性退行性疾病
Proc Natl Acad Sci U S A. 1993 Sep 1;90(17):7915-22. doi: 10.1073/pnas.90.17.7915.
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Polymorphisms of the CYP1A1 and glutathione S-transferase genes associated with susceptibility to lung cancer in relation to cigarette dose in a Japanese population.在日本人群中,CYP1A1和谷胱甘肽S-转移酶基因多态性与肺癌易感性的关系及与吸烟剂量的关联
Cancer Res. 1993 Jul 1;53(13):2994-9.
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Invited commentary--"molecular epidemiology": new pathway or new travelling companion?特邀评论——“分子流行病学”:新途径还是新伙伴?
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Mutations in the p53 gene in lung cancer are associated with cigarette smoking and asbestos exposure.肺癌中p53基因的突变与吸烟和接触石棉有关。
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Molecular epidemiology and carcinogen-DNA adduct detection: new approaches to studies of human cancer causation.分子流行病学与致癌物-DNA加合物检测:人类癌症病因研究的新方法。
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Chemical and biochemical dosimetry of exposure to genotoxic chemicals.遗传毒性化学物质暴露的化学和生化剂量测定法。
Environ Health Perspect. 1985 Oct;62:5-18. doi: 10.1289/ehp.85625.