Papers by Sofia Pavanello
Arthritis & …, 2009
Objective. Juvenile idiopathic arthritis (JIA) is a chronic rheumatic disease of childhood. Two w... more Objective. Juvenile idiopathic arthritis (JIA) is a chronic rheumatic disease of childhood. Two well-established genetic factors known to contribute to JIA susceptibility, HLA and PTPN22, account for less than half of the genetic susceptibility to disease; therefore, additional ...
Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 2002
We investigated the polymorphic enzymes cytochrome P450 1A2 (CYP1A2), N-acetyltransferase (NAT2),... more We investigated the polymorphic enzymes cytochrome P450 1A2 (CYP1A2), N-acetyltransferase (NAT2), glutathione S-transferase (GST) M1 (GSTM1), and T1 (GSTT1) in relation to cigarette smoking-associated urinary mutagenicity detected on YG1024 Salmonella typhimurium strain with S9 mix in 97 smokers. In each subject, cigarette smoke intake was checked by analysis of urinary nicotine plus its metabolites. NAT2 and CYP1A2 phenotypes were determined by the molar ratio of urinary caffeine metabolites detected by high-performance liquid chromatography, and GSTT1 and GSTM1 genotypes were determined by PCR. An increase in urinary mutagenicity was significantly related to levels of exposure to cigarette smoke and CYP1A2 N-hydroxylation activity (linear multiple regression analysis t = 4.51 and P < 0.001 and t = 3.09 and P = 0.003; F = 6.31, P < 0.001). Urinary mutagenicity was significantly higher in CYP1A2 extensive metabolizer smokers (n = 49) than in CYP1A2 poor metabolizer ones (n = 4...
Occupational and Environmental Medicine, 2009
To assess exposure to polycyclic aromatic hydrocarbons (PAHs) using 13 unmetabolised PAHs (U-PAHs... more To assess exposure to polycyclic aromatic hydrocarbons (PAHs) using 13 unmetabolised PAHs (U-PAHs) and 12 monohydroxy metabolites (OHPAHs) in urine, and to compare the utility of these biomarkers. 55 male Polish coke oven workers collected urine spot samples after a workshift. U-PAHs (naphthalene, acenaphtylene, acenaphthene, fluorene, phenanthrene, anthracene, fluoranthene, pyrene, benzo[a]anthracene, chrysene, benzo[k]fluoranthene, benzo[b]fluoranthene, benzo[a]pyrene) were determined by automatic solid phase micro-extraction followed by gas chromatography/mass spectrometry (GC/MS). OHPAHs (1- and 2-hydroxynaphthalene, 2- and 9-hydroxyfluorene, 4-, 9-, 3-, 1- and 2-hydroxyphenanthrene, 1-hydroxypyrene, 6-hydroxychrysene, 3-hydroxybenzo[a]pyrene) were determined, after liquid/liquid extraction and derivatisation, by GC/MS. U-PAHs from naphthalene to chrysene were found in 100% of samples, and heavier U-PAHs in 7-22% of samples. OHPAHs up to 1-hydroxypyrene were found in 100% of samples, while 6-hydroxychrysene and 3-hydroxybenzo[a]pyrene were always below the quantification limit. Median naphthalene, phenanthrene, pyrene, chrysene and benzo[a]anthracene levels were 0.806, 0.721, 0.020, 0.032 and 0.035 microg/l, while hydroxynaphthalenes, hydroxyphenanthrenes and 1-hydroxypyrene levels were 81.1, 18.9 and 15.4 microg/l. For each chemical, the ratio between U-PAH and the corresponding OHPAH ranged from 1:26 to 1:1000. Significant correlations between logged values of U-PAHs and OHPAHs, between U-PAHs, and between OHPAHs were found, with Pearson&#39;s r ranging from 0.27 to 0.97. Current analytical techniques allow specific and simultaneous measurement of several urinary determinants of PAHs in humans. The results of these measurements support the use of U-PAHs as biomarkers of exposure and suggest the spectrum of chemicals to be investigated, including carcinogenic chrysene and benzo[a]anthracene, should be widened.
Cancer research, Jan 15, 2014
A genome-wide association study (GWAS) of bladder cancer identified a genetic marker rs8102137 wi... more A genome-wide association study (GWAS) of bladder cancer identified a genetic marker rs8102137 within the 19q12 region as a novel susceptibility variant. This marker is located upstream of the CCNE1 gene, which encodes cyclin E, a cell-cycle protein. We performed genetic fine-mapping analysis of the CCNE1 region using data from two bladder cancer GWAS (5,942 cases and 10,857 controls). We found that the original GWAS marker rs8102137 represents a group of 47 linked SNPs (with r(2) ≥ 0.7) associated with increased bladder cancer risk. From this group, we selected a functional promoter variant rs7257330, which showed strong allele-specific binding of nuclear proteins in several cell lines. In both GWASs, rs7257330 was associated only with aggressive bladder cancer, with a combined per-allele OR = 1.18 [95% confidence interval (CI), 1.09-1.27, P = 4.67 × 10(-5)] versus OR = 1.01 (95% CI, 0.93-1.10, P = 0.79) for nonaggressive disease, with P = 0.0015 for case-only analysis. Cyclin E pr...
International Archives of Occupational and Environmental Health, 2014
Central Italy. Evaluation of surface contamination and dermal exposure to ANPD was assessed by de... more Central Italy. Evaluation of surface contamination and dermal exposure to ANPD was assessed by determining cyclophosphamide (CP) on selected surfaces (wipes) and on exposed nurses' clothes (pads). The concentration of unmetabolized CP-as a biomarker of internal dosewas measured in end-shift urine samples. Biomonitoring of genotoxic effects (i.e., biological effect monitoring) was conducted by analyzing micronuclei (MN) and chromosome aberrations (CA) in peripheral blood lymphocytes. Genetic polymorphisms for enzymes involved in metabolic detoxification (i.e., glutathione S-transferases) were analyzed as well.
Human molecular genetics, Jan 15, 2014
Genome-wide association studies (GWAS) have mapped risk alleles for at least 10 distinct cancers ... more Genome-wide association studies (GWAS) have mapped risk alleles for at least 10 distinct cancers to a small region of 63 000 bp on chromosome 5p15.33. This region harbors the TERT and CLPTM1L genes; the former encodes the catalytic subunit of telomerase reverse transcriptase and the latter may play a role in apoptosis. To investigate further the genetic architecture of common susceptibility alleles in this region, we conducted an agnostic subset-based meta-analysis (association analysis based on subsets) across six distinct cancers in 34 248 cases and 45 036 controls. Based on sequential conditional analysis, we identified as many as six independent risk loci marked by common single-nucleotide polymorphisms: five in the TERT gene (Region 1: rs7726159, P = 2.10 × 10(-39); Region 3: rs2853677, P = 3.30 × 10(-36) and PConditional = 2.36 × 10(-8); Region 4: rs2736098, P = 3.87 × 10(-12) and PConditional = 5.19 × 10(-6), Region 5: rs13172201, P = 0.041 and PConditional = 2.04 × 10(-6); a...
Toxicology Letters, 2010
Aim of the study was the assessment of exposure of coke-oven workers to polycyclic aromatic hydro... more Aim of the study was the assessment of exposure of coke-oven workers to polycyclic aromatic hydrocarbons (PAHs) by determination of urinary profiles of hydroxylated and unmetabolized PAHs. Fifty-five Polish coke-oven workers were investigated by measurement of 12 hydroxylated metabolites of PAHs (OHPAHs) (1-, 2-hydroxynaphthalene; 2-, 9-hydroxyfluorene; 1-, 2-, 3-, 4-, 9-hydroxyphenanthrene; 1-hydroxyypyrene, 6-hydroxychrysene and 3-hydroxybenzo[a]pyrene) and 13 unmetabolized PAHs (U-PAHs) (from naphthalene to benzo[a]pyrene), in spot urine samples collected at the end of the workshift. U-PAHs with four or less rings were detected in all samples. In particular, median levels for urinary naphthalene, phenanthrene, pyrene, chrysene and benz[a]anthracene were 0.806, 0.721, 0.020, 0.032 and 0.035 g/L. OHPAHs up to 1-hydroxypyrene were found in all samples, while high molecular-weight OHPAHs were always below quantification limit. Median level of 1-hydroxyypyrene was 15.4 g/L. In all subjects significant correlations between OHPAHs and U-PAHs were observed (0.27 < r < 0.70, p < 0.01). Our results suggest that both hydroxylated metabolites and unmetabolized PAHs in urine are useful biomarkers of exposure to PAHs. Moreover, the simultaneous determination of several biomarkers permits to obtain specific excretion profiles that might help in exposure characterization and in better defining the excretion patterns.
Polycyclic Aromatic Compounds, 2002
... Clonfero Section of Occupational Health, Department of Environmental Medicine and Public Heal... more ... Clonfero Section of Occupational Health, Department of Environmental Medicine and Public Health University of Padova, Padova, Italy Paola Simioli Silvia Lupi Pasquale Gregorio Section ... H. Bartsch, U. Nair, A. Risch, M. Rojas, H. Wikman, and K. Alexandrov, Cancer Epidemiol ...
PLoS ONE, 2014
DNA adducts are considered an integrate measure of carcinogen exposure and the initial step of ca... more DNA adducts are considered an integrate measure of carcinogen exposure and the initial step of carcinogenesis. Their levels in more accessible peripheral blood lymphocytes (PBLs) mirror that in the bladder tissue. In this study we explore whether the formation of PBL DNA adducts may be associated with bladder cancer (BC) risk, and how this relationship is modulated by genetic polymorphisms, environmental and occupational risk factors for BC. These complex interrelationships, including direct and indirect effects of each variable, were appraised using the structural equation modeling (SEM) analysis. Within the framework of a hospital-based case/control study, study population included 199 BC cases and 213 non-cancer controls, all Caucasian males. Data were collected on lifetime smoking, coffee drinking, dietary habits and lifetime occupation, with particular reference to exposure to aromatic amines (AAs) and polycyclic aromatic hydrocarbons (PAHs). No indirect paths were found, disproving hypothesis on association between PBL DNA adducts and BC risk. DNA adducts were instead positively associated with occupational cumulative exposure to AAs (p = 0.028), whereas XRCC1 Arg 399 (p,0.006) was related with a decreased adduct levels, but with no impact on BC risk. Previous findings on increased BC risk by packyears (p,0.001), coffee (p,0.001), cumulative AAs exposure (p = 0.041) and MnSOD (p = 0.009) and a decreased risk by MPO (p, 0.008) were also confirmed by SEM analysis. Our results for the first time make evident an association between occupational cumulative exposure to AAs with DNA adducts and BC risk, strengthening the central role of AAs in bladder carcinogenesis. However the lack of an association between PBL DNA adducts and BC risk advises that these snapshot measurements are not representative of relevant exposures. This would envisage new scenarios for biomarker discovery and new challenges such as repeated measurements at different critical life stages.
Mutation Research/Reviews in Mutation Research, 2000
International scientific publications on the influence of metabolic genotypes on biological indic... more International scientific publications on the influence of metabolic genotypes on biological indicators of genotoxic risk in environmental or occupational exposure are reviewed. Biomarkers of exposure (substance or its metabolites in biological fluids, urinary mutagenicity, protein and DNA adducts) and of effects (chromosome aberrations (CAs), sister chromatid exchanges (SCEs), micronuclei (Mn), COMET assay, HPRT mutants) have been evaluated according to different genotypes (or phenotypes) of several activating/detoxifying metabolic activities. In less than half the studies (43 out of 95), the influence of genotype on the examined biological indicator was found, of which four report poorly reliable results (i.e., with scarce biological plausibility, because of the inconsistency of modulated effect with the type of enzymatic activity expressed). As regards urinary metabolites, the excretion of mercapturic acids (MA) is greater in subjects with high GST activity, that of 1-pyrenol and other PAH metabolites turns out to be significantly influenced by genotypes CYP1A1 or GSTM1 null, and that of exposure indicators to aromatic amines (AA) (acetylated and non-acetylated metabolites) is modulated by NAT2. In benzene exposure, preliminary results suggest an increase in urinary t,t-muconic acid (t,t-MA) in subjects with some genotypes. On urinary mutagenicity of PAH-exposed subjects, the effects of genotype GSTM1 null, alone or combined with NAT2 slow are reported. When DNA adduct levels are clearly increased in PAH-exposed group (18 out of 22), 7 out of 18 studies report the influence of GSTM1 null on this biomarker, and of the five studies which also examined genotype CYP1A1, four report the influence of genotype CYP1A1, alone or in combination with GSTM1 null. A total of 25 out of 41 publications (61%) evaluating the influence of metabolic polymorphisms on biomarkers of effect (cytogenetic markers, COMET assay, HPRT mutants) do not record any increase in the indicator due to exposure to the genotoxic agents studied, confirming the scarce sensitivity of these indicators (mainly HPRT mutants, Mn, COMET assay) for assessing environmental or occupational exposure to genotoxic substances. Concluding, in determining urinary metabolites for monitoring exposure to genotoxic substances, there is sufficient evidence that genetically-based metabolic polymorphisms must be taken into account in the future. The unfavourable association for the activating/detoxifying metabolism of PAH is also confirmed as a risk factor due to the formation of PAH-DNA adducts. The clearly protective role played by GSTT1 on DEB (and/or related compound)-induced sister chromatid exchanges (SCEs) should be noted. The modulating effects of genotypes on protein adduct levels in environmental and occupational exposure have not yet been documented, and most studies on the influence of genotype on biological indicators of early genotoxic effects report negative results.
Mutation Research/Genetic Toxicology and Environmental Mutagenesis, 2006
We evaluated determinants of anti-benzo[a]pyrenediolepoxide-(B[a]PDE)-DNA adduct formation (adduc... more We evaluated determinants of anti-benzo[a]pyrenediolepoxide-(B[a]PDE)-DNA adduct formation (adduct induced by the ultimate carcinogenic metabolite of B[a]P) in lymphomonocytes of subjects environmentally exposed to low doses of polycyclic aromatic hydrocarbons (PAHs) (B[a]P). Our study population consisted of 585 Caucasian subjects, all municipal workers living in North-East Italy and recruited during their periodic check-ups after informed consent. PAH (B[a]P) exposure was assessed by questionnaire. Anti-B[a]PDE-DNA levels were measured by HPLC fluorescence analysis. We found that cigarette smoking (smokers (22%) versus non-smokers, p&amp;amp;amp;amp;amp;amp;lt;0.0001), dietary intake of PAH-rich meals (&amp;amp;amp;amp;amp;amp;gt; or =52 (38%) versus &amp;amp;amp;amp;amp;amp;lt;52 times/year, p&amp;amp;amp;amp;amp;amp;lt;0.0001), and outdoor exposure (&amp;amp;amp;amp;amp;amp;gt; or =4 (19%) versus &amp;amp;amp;amp;amp;amp;lt;4h/day; p=0.0115) significantly influenced adduct levels. Indoor exposure significantly increased the frequency of positive subjects (&amp;amp;amp;amp;amp;amp;gt; or =0.5 adducts/10(8) nucleotides; chi(2) for linear trend, p=0.051). In linear multiple regression analysis the major determinants of increased DNA adduct levels (ln values) were smoking (t=6.362, p&amp;amp;amp;amp;amp;amp;lt;0.0001) and diet (t=4.035, p&amp;amp;amp;amp;amp;amp;lt;0.0001). In this statistical analysis, indoor and outdoor exposure like other factors of PAH exposure had no influence. In non-smokers, the influence of diet (p&amp;amp;amp;amp;amp;amp;lt;0.0001) and high indoor exposure (p=0.016) on anti-B[a]PDE-DNA adduct formation became more evident, but not that of outdoor exposure, as was confirmed by linear multiple regression analysis (diet, t=3.997, p&amp;amp;amp;amp;amp;amp;lt;0.0001 and high indoor exposure, t=2.522, p=0.012). This study indicates that anti-B[a]PDE-DNA adducts can be detected in the general population and are modulated by PAH (B[a]P) exposure not only with smoking - information already known from studies with limited number of subjects - but also with dietary habits and high indoor exposure. In non-smokers, these two factors are the principal determinants of DNA adduct formation. The information provided here seems to be important, since DNA adduct formation in surrogate tissue is an index of genotoxic exposure also in target organs (e.g., lung) and their increase may also be predictive of higher risk for PAH-related cancers.
Mutation Research/Genetic Toxicology and Environmental Mutagenesis, 2004
The influence of the genetic deletion polymorphism of glutathione S-transferase 1 (GSTM1 * 0/ * 0... more The influence of the genetic deletion polymorphism of glutathione S-transferase 1 (GSTM1 * 0/ * 0) on levels of anti (±)-r-7,t-8-dihydroxy-t-9,10-oxy-7, 8,9,10-tetrahydrobenzo[a]pyrene (anti-BPDE-DNA) adduct in the peripheral blood lymphocyte plus monocyte fraction (LMF) of coke-oven workers was investigated. A total of 95 male Polish coke-oven workers (60% current smokers) from two different plants comprised the sample population.
Mutation Research/Genetic Toxicology and Environmental Mutagenesis, 2002
In this study, the correlation of indicators of external (i.e. mean daily intake of condensate, n... more In this study, the correlation of indicators of external (i.e. mean daily intake of condensate, nicotine, tobacco and tobacco proteins, and daily number of cigarettes smoked) and of internal tobacco-smoke exposure (i.e. urinary 1-pyrenol, nicotine and its metabolites and trans,trans-muconic acid) with urinary mutagenicity, detected on YG1024 Salmonella typhimurium strain with S9, were examined in 118 smokers.
Life Sciences, 2009
Aims: In this study, the effects of four single nucleotide polymorphisms (SNPs), − 3860G N A, −24... more Aims: In this study, the effects of four single nucleotide polymorphisms (SNPs), − 3860G N A, −2467delT, − 739T N G and − 163C N A, of CYP1A2 gene on lung cancer were evaluated in Tunisian population. Main methods: Four polymorphisms of CYP1A2 gene were analysed in 109 healthy smokers and in 101 lung cancer cases, including 63 with squamous cell carcinoma (SCC) and 41 with adenocarcinoma (AD). The genotyping for the SNPs − 3860 G NA, − 2467delT, − 739T N G and − 163C N A was performed by polymerase chain reaction (PCR)-restriction fragment length polymorphism analysis. Key findings: The results showed that smokers with CYP1A2 gene polymorphisms were associated with an increased risk for the development of lung AD. There was however no significant increased risk of developing lung SCC in smokers having CYP1A2 gene polymorphisms. An increased risk of developing AD was observed in smokers who are carriers of at least one copy of − 3680A or − 739G giving a significant odds ratio (OR) of 6.02 (CI = 2.91-12.9) and 3.01 (CI = 1.54-5.98), respectively. Significance: These genotyping data are consistent with the hypothesis that tobacco-specific-N-nitrosamines (TSN) such as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) are major contributors to the development of lung AD and that CYP1A2 gene product plays an important role in the metabolic activation of NNK. This study suggests that SNPs of CYP1A2 could be considered as promising biomarkers in the aetiology of lung AD in smokers.
International Journal of Hygiene and Environmental Health, 2014
Aim: A new solid phase microextraction-gas chromatography-mass spectrometry method (SPME-GC-MS) t... more Aim: A new solid phase microextraction-gas chromatography-mass spectrometry method (SPME-GC-MS) to detect urinary unmetabolized 3-, 6-ring polycyclic aromatic hydrocarbons (PAHs) was applied to coke oven workers and general population subjects with the aim to assess exposure to carcinogenic PAHs, to evaluate the role of occupational and environmental variables on PAHs levels, and to compare present results with those previously obtained with a less sensitive method. Methods: A total of 104 coke oven workers (CW) from Poland [recruited in 2000 (CW-2000; n = 55) and 2006 (CW-2006; n = 49)]
International Journal of Cancer, 2009
We investigated the effect of chronic exposure to polycyclic aromatic hydrocarbons (PAHs) on DNA ... more We investigated the effect of chronic exposure to polycyclic aromatic hydrocarbons (PAHs) on DNA methylation states (percentage of methylated cytosines (%mC)) in Polish male nonsmoking coke-oven workers and matched controls. Methylation states of gene-specific promoters (p53, p16, HIC1 and IL-6) and of Alu and LINE-1 repetitive elements, as surrogate measures of global methylation, were quantified by pyrosequencing in peripheral blood lymphocytes (PBLs). DNA methylation was evaluated in relation to PAH exposure, assessed by urinary 1-pyrenol and anti-benzo[a]pyrene diolepoxide (anti-B[a]PDE)-DNA adduct levels, a critical genetic damage from B[a]P. We also evaluated whether PAHinduced DNA methylation states were in turn associated with micronuclei in PBLs, an indicator of chromosomal instability. ' 2009 UICC
International Journal of Cancer, 2011
Alcohol abuse leads to earlier onset of aging-related diseases, including cancer at multiple site... more Alcohol abuse leads to earlier onset of aging-related diseases, including cancer at multiple sites. Shorter telomere length (TL) in peripheral blood leucocytes (PBLs), a marker of biological aging, has been associated with alcohol-related cancer risks. Whether alcohol abusers exhibit accelerated biological aging, as reflected in PBL-TL, has never been examined.
Food and Chemical Toxicology, 2002
In this work the phenotyping approach was used to study the influence of metabolic polymorphisms ... more In this work the phenotyping approach was used to study the influence of metabolic polymorphisms NAT2 and CYP1A2 on S9mediated urinary mutagenicity, detected with Salmonella strain YG1024, in 50 subjects after a meal of pan-fried hamburgers. All 50 post-meal samples, but not pre-meal ones, were clearly mutagenic (number of urine samples able to double number of spontaneous revertants was 50 to 0, respectively). CYP1A2 positively influences urinary mutagenicity: a rise in CYP1A2 activity increases levels of post-meal urinary mutagens (1.16AE 0.91 vs 1.72 AE 1.19 7-h minimum mutagenic doses (MMDs)/intake), especially in NAT2 slow acetylators (2.18 AE1.33 vs 0.90 AE 0.54 7-h MMDs/intake, Mann-Whitney U-test, P<0.05). NAT2 rapid acetylators exert lower post-meal urinary mutagenicity than slow ones (1.41AE 1.02 vs 1.77 AE 2.45 7-h MMDs/intake) and even more if the latter are extensive CYP1A2 metabolizers (1.41 AE1.02 vs 2.18 AE 1.33 7-h MMDs/intake), but the difference did not reach statistical significance. In conclusion, this study indicates that CYP1A2 and NAT2 activities influence the presence of urinary mutagens after a meal of panfried hamburger (rich in HHAs) and consequently their potential genotoxic risk. #
Environmental and Molecular Mutagenesis, 2007
Urinary mutagenicity was evaluated in relation to environmental mutagen exposure (i.e., diet, ind... more Urinary mutagenicity was evaluated in relation to environmental mutagen exposure (i.e., diet, indoor/outdoor activities, residential area etc.) on the day prior to sample collection, and also considering factors that contribute to the variability of Salmonella mutagenicity assay results. Overnight urine samples from 283 healthy non-smoking residents of northeast Italy (46% males, 20-62 years) were analyzed for mutagenicity on sensitive Salmonella typhimurium strain YG1024 with S9 mix employing the preincubation version of the plate incorporation assay (i.e., the Salmonella reverse mutation test). Urinary mutagenicity varied between 0.02 and 9.84 rev/ equiv. ml, and 7% of samples were positive (i.e., sample elicited a two-fold increase in revertants). There was an evident increase in mutagenicity in subjects with increased intake of mutagen-rich meals (n ¼ 80) (P < 0.01 and positive urine 13% vs. 5%, P ¼ 0.025). Indoor-exposed subjects (n ¼ 65) also showed a higher percentage of positive urine (14% vs. 5%, P ¼ 0.015). In particular, those subjects exposed to cooking fumes the previous evening (n ¼ 28) revealed higher urinary mutagenicity (P ¼ 0.035, positive urine 25% vs. 5%, P < 0.001) than non-indoor exposed. The sources of variability of the mutagenicity assay, mainly the histidine content of the urine concentrate (z ¼ 4.06, P < 0.0001), and to a lesser extent bacterial inoculum size (z ¼ 2.33, P ¼ 0.019), also significantly influenced urinary mutagenicity values. In a linear multiple regression analysis, their effects were still significant (i.e., histidine content P ¼ 0.026 and inoculum size P ¼ 0.021), but the effects of diet, indoor exposure, and other environmental exposures (i.e., traffic and heating system exhausts, residential area) were not. It is concluded that the previous day's exposure to mutagen-rich meals and cooking fumes may influence the presence of mutagenic activity in the overnight urine of non-smoking subjects. This mutagenic activity, which remains in contact with bladder mucosa for several hours, could be considered risk factors for colorectal adenoma and possibly other cancers (i.e., bladder) in nonsmokers. Accurate control of histidine content and bacterial inoculum size is strongly recommended when investigating the mutagenic activity of urine from non-smokers. Environ. Mol. Mutagen. 48:143-150, 2007. V V C 2007 Wiley-Liss, Inc.
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Papers by Sofia Pavanello