4 0-1 risk alleles Smoking habit Nonsmokerc Former smoker Smoker <40 years Smoker ≥40 years Status Controlsc Benign lung disease Lung cancer 2 risk alleles Smoking habit Nonsmokerc Former smoker Smoker <40 years Smoker ≥40 years Status Controlsc Benign lung disease Lung cancer 3-4 risk alleles Smoking habit Nonsmokerc Former smoker Smoker ≥40 years Status Controlsc Benign lung disease Lung cancer Na 6 12 2 5 13 4 8 7 10 5 9 12 7 12 5 20 9 12 15 11 Table 2: Means of DNA adducts ± standard error (SE) case-control status considering the number of DNA repair risk alleles plus the parameter estimates of the multivariate regression model. Meansb ± S.E. Odds Ratio C.I. P-value 1.7 ± 1.5 0.4 ± 0.1 0.3 ± 0.2 1.3 ± 1.1 1.3 ± 0.7 0.4 ± 0.1 0.5 ± 0.2 0.4 ± 0.1 0.7 ± 0.4 0.8 ± 0.6 1.7 ± 0.6 0.5 ± 0.2 1.1 ± 0.6 1.3 ± 0.5 0.4 ± 0.2 1.7 ± 0.7 2.9 ± 1.3 1.5 ± 0.6 2.1 ± 0.9 2.3 ± 1.1 1 0.08 0.33 0.16 1 1.23 0.43 1 2.46 0.86 20.91 1 1.11 2.39 1 9.47 36.38 1 0.45 4.54 Journal of Nucleic Acids .302 .686 .480 .884 .458 .560 .933 .091 .928 .447 .130 .040 .460 .259 0.00–9.76 0.00–67.26 0.00–27.05 0.08–19.30 0.05–4.00 0.12–50.98 0.03–28.37 0.62–709.04 0.12–10.00 0.25–22.62 0.52–173.16 1.17–1132.84 0.06–3.69 0.33–62.93 aSome ﬁgures do not add up to the total because of missing values. bLevels per 108 normal nucleotides. cReference level. DNA adducts were associated with benign or malignant lung chronic diseases. The question of the utility of PBLs as a valid surrogate for a speciﬁc organ like lung, representing the events occurring in the target tissue, is still open [19]. Nev- ertheless, some studies have indicated that the use of PBLs such as a biological marker, may help in the identiﬁcation of subjects at elevated risk [6–8]. PBLs are considered suitable to monitor environmental and occupational carcinogen exposure and to estimate the burden of DNA adducts in respiratory tissue [5, 20–22]. In fact, increased amount of PBL DNA adducts have been found among subjects heavily exposed to air pollution [21]. The relationship with target tissue DNA adducts may vary between type of carcinogen and target tissue although signiﬁcant correlations have been seen between the levels of DNA damage in PBLs and bronchial mucosa [20]. Uppermost, we have considered the eﬀect of smoking on DNA adduct levels. Our ﬁndings show that the levels of DNA adducts of smokers were higher than those of former and nonsmokers. Our ﬁnding shows that PBL DNA adduct may reﬂect exposures to carcinogens, such as those contained in tobacco smoke better than other surrogate tissues, such as leukocyte DNA adducts. However, discrepant results have been also reported with PBLs [18]. This is probably due to methodical diﬀerences in the 32P- DNA postlabelling protocol applied from research laborato- ries. Next results show that the eﬀect of smoking on DNA damage was more marked in the subjects that reported to smoke for more than 40 years. Although detailed infor- mation on smoking history, for example, number of pack of cigarettes smoked per years was missing, our ﬁndings