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DNA Adducts and Lung Cancer Risk: A Prospective Study

¹ Cancer Risk Factor Branch and ² Molecular and Nutritional Epidemiology Unit, CSPO-Scientific Institute of Tuscany Region, Florence, Italy; ³ Department of Environmental and Occupational Health, Utrecht University; ⁴ Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, the Netherlands; ⁵ WHO, European Centre for Environment and Health, Bonn, Germany; ⁶ ISI Foundation; ⁷ University of Turin, Turin, Italy; ⁸ Istituto Mario Negri; ⁹ Genetics Research Institute; ¹⁰ Department of Epidemiology, National Cancer Institute, Milan, Italy; ¹¹ Department of Environmental and Occupational Medicine, Aarhus, Denmark; ¹² Department of Oncology, University of Cambridge; ¹³ Medical Research Council Dunn Human Nutrition Unit, Cambridge, United Kingdom; ¹⁴ IARC, Lyon, France; ¹⁵ Department of Clinical Epidemiology, Aalborg Hospital, Aarhus University Hospital, Aalborg, Denmark; ¹⁶ Institute of Cancer Epidemiology, Danish Cancer Society, Copenhagen, Denmark; ¹⁷ Institut National de la Sante et de la Recherche Medicale U521, Institut Gustave Roussy, Villejuif, France; ¹⁸ Division of Clinical Epidemiology, Deutsches Krebsforschungszentrum, Heidelberg, Germany; ¹⁹ German Institute of Human Nutrition, Potsdam-Rehbücke, Germany; ²⁰ Department of Hygiene and Epidemiology, Medical School, University of Athens, Athens, Greece; ²¹ Cancer Registry, Azienda Ospedaliera "Civile MP Arezzo," Ragusa, Italy; ²² Dipartimento di Medicina Clinica e Sperimentale, Università Federico II, Naples, Italy; ²³ Centre for Nutrition and Health, National Institute for Public Health and the Environment, Bilthoven, the Netherlands; ²⁴ Institute of Community Medicine, University of Tromso, Tromso, Norway; ²⁵ Department of Epidemiology, Catalan Institute of Oncology, Barcelona, Spain; ²⁶ Andalusian School of Public Health, Granada, Spain; ²⁷ Department of Public Health of Guipuzkoa, San Sebastian, Spain; ²⁸ Public Health Institute, Navarra, Spain; ²⁹ Epidemiology Department, Murcia Health Council, Murcia, Spain; ³⁰ Dirección General de Salud Pública, Consejería de Salud y Servicios Sanitarios Asturias, Oviedo, Spain; ³¹ Malmö Diet and Cancer Study, Lund University, Malmö, Sweden; ³² Department of Nutritional Research, University of Umeå, Umeå, Sweden; ³³ Cancer Research UK Epidemiology Unit, University of Oxford, Oxford, United Kingdom; and ³⁴ Imperial College London, London, United Kingdom

Requests for reprints: Marco Peluso, Cancer Risk Factor Branch, CSPO-Scientific Institute of Tuscany Region, Villa Delle Rose, Via Cosimo il Vecchio N. 2, Florence, Italy 50139. Phone: 39-55-32-697867; Fax: 39-55-32-6978; E-mail: m.peluso{at}cspo.it.

Objectives were to investigate prospectively the ability of DNA adducts to predict cancer and to study the determinants of adducts, especially air pollutants. DNA adducts were measured in a case-control study nested in the European Prospective Investigation into Cancer and Nutrition (EPIC) investigation. Cases included newly diagnosed lung cancer (n = 115), upper respiratory cancers (pharynx and larynx; n = 82), bladder cancer (n = 124), leukemia (n = 166), and chronic obstructive pulmonary disease or emphysema deaths (n = 77) accrued after a median follow-up of 7 years among the EPIC former smokers and never-smokers. Three controls per case were matched for questionnaire analyses and two controls per case for laboratory analyses. Matching criteria were gender, age, smoking status, country of recruitment, and follow-up time. Individual exposure to air pollution was assessed using concentration data from monitoring stations in routine air quality monitoring networks. Leukocyte DNA adducts were analyzed blindly using ³²P postlabeling technique. Adducts were associated with the subsequent risk of lung cancer, with an odds ratio (OR) of 1.86 [95% confidence interval (95% CI), 0.88-3.93] when comparing detectable versus nondetectable adducts. The association with lung cancer was stronger in never-smokers (OR, 4.04; 95% CI, 1.06-15.42) and among the younger age groups. After exclusion of the cancers occurring in the first 36 months of follow-up, the OR was 4.16 (95% CI, 1.24-13.88). A positive association was found between DNA adducts and ozone (O₃) concentration. Our prospective study suggests that leukocyte DNA adducts may predict lung cancer risk of never-smokers. Besides, the association of DNA adduct levels with O₃ indicates a possible role for photochemical smog in determining DNA damage.

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