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Träfflista för sökning "swepub ;lar1:(umu);pers:(Riboli Elio);pers:(Krogh Vittorio);spr:eng;pers:(Martínez Carmen);pers:(Autrup Herman);pers:(Krzyzanowski Michal)"

Sökning: swepub > Umeå universitet > Riboli Elio > Krogh Vittorio > Engelska > Martínez Carmen > Autrup Herman > Krzyzanowski Michal

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1.
  • Airoldi, Luisa, et al. (författare)
  • 4-Aminobiphenyl-hemoglobin adducts and risk of smoking-related disease in never smokers and former smokers in the European Prospective Investigation into Cancer and Nutrition prospective study.
  • 2005
  • Ingår i: Cancer Epidemiology Biomarkers & Prevention. - 1055-9965. ; 14:9, s. 2118-24
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim of this study was to evaluate whether biomarkers of environmental tobacco smoke exposure [i.e, 4-aminobiphenyl-hemoglobin (4-ABP-Hb) adducts] were predictive of the risk of tobacco-related cancers and diseases. We did a case control study nested within the European Prospective Investigation into Cancer and Nutrition, involving 190 controls and 149 cases (incident cancer of the lung, bladder, pharynx, larynx, oral cavity, leukemias, and chronic obstructive pulmonary disease or emphysema deaths). All individuals were never smokers or ex smokers for > 10 years. 4-ABP-Hb adducts were analyzed in peripheral blood collected before the onset of the disease (median, 7 years). Overall, 4-ABP-Hb adducts were higher, although not statistically significantly so, in cases (as a whole) than controls. In the control population, high fruit and vegetable consumption significantly lowered the frequency of detectable adducts (Fisher's exact test, P = 0.025). Restricting the analysis to women, 4-ABP-Hb adducts were higher in cases than controls (Mann-Whitney P = 0.036) and the odds ratio (OR) for the presence/absence of adducts was 2.42 [95% confidence interval (95% CI), 1.18-4.981. Moreover, the association of adducts with the individual cancer types was stronger in women than in the whole study population, although statistically significant only for leukemias (OR, 2.77; 95% CI, 1.06-7.20). The results provide some evidence that women may be more susceptible to environmental tobacco smoke, as suggested by their higher adduct levels. The most important finding of this prospective study is that, at least in women, 4-ABP-Hb adducts may help identify subjects at high risk of cancers related to environmental tobacco smoke exposure.
2.
  • Vineis, Paolo, et al. (författare)
  • Air pollution and risk of lung cancer in a prospective study in Europe.
  • 2006
  • Ingår i: Int J Cancer. - 0020-7136. ; 119:1, s. 169-74
  • Tidskriftsartikel (refereegranskat)abstract
    • To estimate the relationship between air pollution and lung cancer, a nested case-control study was set up within EPIC (European Prospective Investigation on Cancer and Nutrition). Cases had newly diagnosed lung cancer, accrued after a median follow-up of 7 years among the EPIC exsmokers (since at least 10 years) and never smokers. Three controls per case were matched. Matching criteria were gender, age (+/- 5 years), smoking status, country of recruitment and time elapsed between recruitment and diagnosis. We studied residence in proximity of heavy traffic roads as an indicator of exposure to air pollution. In addition, exposure to air pollutants (NO2, PM10, SO2) was assessed using concentration data from monitoring stations in routine air quality monitoring networks. Cotinine was measured in plasma. We found a nonsignificant association between lung cancer and residence nearby heavy traffic roads (odds ratio = 1.46, 95% confidence interval, CI, 0.89-2.40). Exposure data for single pollutants were available for 197 cases and 556 matched controls. For NO2 we found an odds ratio of 1.14 (95% CI, 0.78-1.67) for each increment of 10 mu g/m(3), and an odds ratio of 1.30 (1.02-1.66) for concentrations greater than 30 mu g/m(3). The association with NO2 did not change after adjustment by cotinine and additional potential confounders, including occupational exposures. No clear association was found with other pollutants. (c) 2006 Wiley-Liss, Inc.
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3.
  • Peluso, Marco, et al. (författare)
  • DNA adducts and lung cancer risk: A prospective study
  • 2005
  • Ingår i: Cancer Research. - American Association for Cancer Research. - 1538-7445. ; 65:17, s. 8042-8048
  • Tidskriftsartikel (refereegranskat)abstract
    • 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 (32)p 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), 0.88-3.931 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 (O-3) 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 O-3 indicates a possible role for photochemical smog in determining DNA damage.
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