Objectives-To investigate the risk of cancer and non-neoplastic respiratory diseases among workers who manufacture carbon electrodes, as this industry entails exposure to mixtures of polycyclic aromatic hydrocarbons.Methods-A historical cohort study was carried out of 1006 male workers employ ed for at least 1 year between 1945 and 1971 in a carbon (graphite) electrode production plant in central Italy, who were followed up for mortality between 1955 and 1996. The ratio of observed to expected deaths (standardised mortality ratios, SMRs) was computed from both national and (for the period 1964-96) regional age and period specific mortalities. A multivariate Poisson regression analysis was performed to investigate the relative risk (RR) of death according to duration of employment and time since first employment in the factory.Results-A total of 424 workers had died, 538 were still alive, and 44 were lost to follow up, Mortalities from all causes, all cancers, and respiratory tract cancer were in Line with the regional figure. An excess was found over the expected deaths from skin cancer including melanoma (SMR 3.16, 95% confidence interval (95% CI) 0.65 to 9.23) and from non-neoplastic respiratory diseases (SMR 1.58, 95% CI 1.16 to 2.11). Poisson regression analysis including age as a covariate showed an increased risk of dying from gastric cancer with increasing duration of employment, and an increase in the RR of dying from lung cancer and from nonneoplastic respiratory diseases with increasing time since first employment, although the linear trend was not significant.Conclusion-This study supports previous findings that working in the carbon electrode manufacturing industry may not increase the risk of dying from respiratory cancer. However, a possible association with non-malignant respiratory diseases cannot be excluded.

We performed a case-control study to assess the role of hepatitis B virus (HBV), hepatitis C virus (HCV), GB virus C/hepatitis G virus (HGV), TT virus, alcohol intake, and tobacco smoking as risk factors for hepatocellular carcinoma (HCC) in the presence or absence of cirrhosis. We prospectively recruited 174 patients with a first diagnosis of HCC admitted to the main hospitals in Brescia, North Italy. On the basis of histological, clinical, and radiological criteria, the presence of cirrhosis was established in 142 cases, excluded in 21 cases, and remained undefined in 11 cases. Among the HCC cases without cirrhosis, a histological picture of normal liver was found in a single patient, chronic viral hepatitis was found in 11 patients, alcoholic hepatitis was found in 5 patients, nonspecific reactive hepatitis was found in 3 patients, and hemochromatosis was found in 1 patient. As controls, we also included 610 subjects unaffected by hepatic diseases and admitted to the same hospitals as cases. The odds ratios for having HCC according to positivity for HCV RNA, HBsAg and/or HBV DNA, and alcohol intake > 80 g/day (95% confidence interval) were as follows, in the presence and absence of cirrhosis, respectively: (a) 33.5 (17.7-63.4) and 19.7 (6-64.8) for HCV RNA; (b) 17.6 (9.0-34.4) and 20.3 (5.7-72.6) for HBsAg; and (c) 5.5 (3.1-9.7) and 4.6 (1.5-13.8) for alcohol intake. No association was found with HGV or TT virus infections or tobacco. This study has shown that most HCC cases arising in the area are due to HBV, HCV, or alcohol intake, in both the presence and absence of cirrhosis.

We performed a case-control study to evaluate the risk of hepatocellular carcinoma (HCC) for hepatitis C virus (HCV) infection. A total of 305 newly diagnosed HCC cases (80% males) and 610 subjects (81% males) unaffected by clinically evident hepatic disease admitted to the 2 main hospitals in Brescia, North Italy, were recruited as cases and controls, respectively. Among the 122 HCC cases positive for HCV RNA, genotype 1b was found in 83 patients (68%), genotype 2 in 36 (29.5%) and genotype 1a in 3 (2.5%). Among the controls, 15 were infected with genotype 1b and 15 with type 2. Analysis of HCV envelope 1 nucleotide sequence among 25 cases and 8 controls infected with genotype 2 showed subtype 2c in 96% of cases and in all controls, and subtype 2a in 1 HCC case. The odds ratio (OR) for HCV RNA positivity adjusted for hepatitis B virus (HBV) markers and alcohol intake was 26.3 [95% confidence interval (CI): 15.8-44], and it was higher for genotype 1b (OR = 34.2) than type 2 (OR = 14.4). The OR for HCV RNA was 35.6 (95% CI: 14.5-87.1) when the HBV markers were all negative and 132 (15.3-890) when HBsAg positivity was present; the OR was 26.1 (95% CI: 12.6-54.0) among subjects with alcohol intake of 0-40 g/day and increased to 62.6 (23.3-168) and 126 (42.8-373) with an alcohol intake of 41-80 and >80 g/day, respectively. In conclusion, synergism was found between HCV infection and HBV infection and alcohol intake in causing HCC.

Objective: To assess the role of hepatitis G virus (HGV) in cryptogenic chronic liver disease (CLD), we investigated the prevalence of HGV RNA among patients with cryptogenic CLD, patients with nonviral CLD (primary biliary cirrhosis [PBC] and Wilson’s disease [WD]) and subjects without clinically evident liver disease (controls). Methods: Ninety patients with cryptogenic CLD (43 with chronic hepatitis, 20 with cirrhosis, and 27 with hepatocellular carcinoma [HCC]), 143 patients with PBC, 22 patients with WD, and 134 controls were recruited. HGV RNA was detected by reverse transcription-polymerase chain reaction (RT-PCR) and antibodies against HGV E2 protein (anti-E2) by an immunoassay test. Results: HGV RNA was detected in 7.8% of patients with cryptogenic CLD (chronic hepatitis, 9.3%; cirrhosis, 5.0%; HCC, 7.4%), in 2.4% of patients with PBC or WD, and in 2.2% of controls. As a consequence, a positive association of HGV infection with cryptogenic CLD was found (odds ratio, 3.1; 95% confidence interval [CI], 1.0–9.7; p = 0.05). No difference was observed between HGV RNA-positive and -negative patients by age, sex, histology, or liver function tests. Anti-E2 prevalence did not differ between patients with cryptogenic CLD (26.5%), patients with PBC (28.1%), and controls (22.1%). Transfusion history was associated with HGV RNA but not with anti-E2 seropositivity. Conclusions: Although an association was found between cryptogenic CLD and HGV infection, the role of the virus seems far from important, the proportion of cryptogenic CLD attributable to it being only 5.2%.

Objectives: We carried out a case–control study to investigate the role of history of liver cancer in a first-degree relative as a risk factor for hepatocellular carcinoma (HCC).

We performed a case-control study to evaluate the association of a new human DNA virus named TT virus (TTV) with hepatocellular carcinoma (HCC). We recruited 174 subjects hospitalized for HCC (84% males; mean age: 64 years) and 118 patients hospitalized for non-liver diseases in Brescia, northern Italy, as controls (94% males; mean age: 66 years). TTV DNA was found in serum by polymerase chain reaction (PCR) in 26 cases (15%) and 11 controls (9.3%) (P >. 1). TTV group 2 infection was identified in 16 cases (61.5%) and 4 controls (36.4%) (P >.1) using a type-specific PCR method. Sequence analysis of 222 nt of TTV DNA demonstrated that the remaining 10 cases and 7 controls were all infected by group 1. The odds ratio (OR) for TTV-DNA positivity, adjusted for demographic variables, hepatitis B surface antigen (HBsAg), hepatitis C virus (HCV) RNA, and heavy alcohol intake was 1.8 (95% CI: 0.7-4.8; P >.1). The OR did not change when the analysis was restricted to 14 HCC cases and 56 controls who were negative for each known risk factor for HCC (OR = 1.7; 95% CI: 0.8-4.0). TTV-DNA positivity was not associated with transfusion history. The prevalence of TTV DNA was higher among HCC cases positive for HBsAg (10 of 38 [26.3%]) than among those positive for HCV RNA (8 of 62 [12.9%]) or negative for hepatitis B virus (HBV), HCV, and hepatitis G virus (HGV) infections (5 of 62 [8. 1%]) (P =.02). This study does not support the hypothesis of an association between TTV infection and HCC.

All the male students in a high school in Brescia, North Italy (about 195,000 inhabitants) in Grades 9 through 13 were given a self-administered anonymous questionnaire during school time. Among the 1,462 students who filled in a valid questionnaire, 29.1 % claimed to practice one or more sports regularly (at least 4 hours/week for 9 months/ year or more), 30.2% practice sports occasionally, and 40.7% no sports at all. The percentage of current smokers (at least one cigarette a month) increased from 9th grade (11.1%) to 10th (13.2%), 11th (15.2%), 12th (27.7%), and 13th (23.7%) grade. The percentage of smokers showed a steady linear increase from the lowest to the highest grade in students practicing no or occasional activity but no increase in those who regularly practice sports. Students' smoking was negatively associated with the regular practice of sports among 12th-13th grade students.

Background: Evidence on gender-related differences in susceptibility to alcohol-induced liver diseases is questionable with regard to both methodologic and clinical aspects. With the aim to assess the role of gender in the risk of liver cirrhosis, independently and in combination with known risk factors, data from three case-control studies performed in various Italian areas were analysed. Methods: The cases were 462 cirrhotic patients (300 men and 162 women) admitted for the first time to hospital for liver decompensation. Controls were 651 patients (355 men and 296 women) admitted to the same hospitals during the same period as the cases, for acute diseases unrelated to alcohol. Alcohol consumption was expressed as lifetime daily alcohol intake. Results: A significant and independent associations between alcohol intake, chronic hepatitis B and C virus infections, and the risk of liver cirrhosis was observed. The effect of alcohol intake was multiplicatively increased in women. The odds ratio (OR) increased from 1.0 (reference category: men, lifetime abstainers) to 31.4 (95% confidence interval (CI), 10.3-95.8) in men drinking more than 100 g/day of alcohol, and from 2.2 (95% CI, 1.0-7.1) in abstaining women to 44.8 (95% CI, 8.2-224.0) in women drinking more than 100 g/day of alcohol. An increased risk of liver cirrhosis associated with female gender independently of alcohol consumption and virus infection was also observed. Conclusions: A higher susceptibility to alcohol-induced liver diseases was confirmed for women, and an independent effect of female sex on the risk of cirrhosis was observed. Besides alcohol and viruses, some unknown gender-related factor might then be involved in the occurrence of the disease.

A new hepatitis-associated RNA virus of the Flaviviridae family has been identified and named GB virus C/ hepatitis G virus (HGV). We carried out a case-control study to evaluate the association of HGV infection with hepatocellular carcinoma (HCC). We recruited 170 patients hospitalized for HCC (143 male and 27 female, mean age 64 years) and 306 patients hospitalized for nonliver diseases (controls) in Brescia, Italy. HGV RNA was detected by reverse transcription-polymerase chain reaction (RT-PCR) and antibodies against HGV E2 protein (anti-E2) by an immunoassay test. HGV RNA was found in 8 cases (4.7%) and 4 controls (1.3%). The relative risk (RR) for HGV RNA positivity adjusted for demographic variables and hepatitis B surface antigen (HBsAg), hepatitis C virus (HCV) RNA, and alcohol was 7.3 (95% confidence interval, 1.7-30.6; P = .009). No HGV RNA-positive subject was also positive for anti-E2. Anti-E2 prevalence did not differ significantly between cases (20%) and controls (15.3%), and no RR increase was found by this marker. Among subjects with HGV exposure (HGV RNA plus anti-E2 positive), a greater proportion of cases (40%) than controls (14%) had transfusion history. The possible role of HGV in HCC etiology seems modest because the population-attributable risk is lower (4%) than those for HBsAg (22%), HCV RNA (36%), and heavy alcohol intake (52%). This study supports the hypothesis of an association between HGV infection and HCC, although at present there are insufficient data on the causality of the association.

Aims and background We evaluated some standardized criteria for classifying incident cases of liver cancer into either primary liver cancer (PLC) or unspecified liver cancer (ULC) on the basis of the diagnostic examinations performed and their results. Methods A pilot hospital-based study (98 cases) was carried out in Verona, northern Italy, with the main aim of assessing the feasibility of the method. The same procedures were subsequently applied in a population-based study (349 cases) in Brescia, northern Italy. Results Diagnosis was made on histologic data in 38.7% and 41.8% of the hospital based and population-based studies, respectively, with a wide variation among different hospitals. The percentage of cases classified as PLC was 78.6% in the hospital-based study and 78.8% in the population-based study. No differences in the proportion of cases attributed to PLC were found according to patients’ age and sex or hospital of admission. The repeatibility of the procedure was assessed by a cross-panel review of 198 cases, and concordance was found in 91.9% of them. Conclusions An operational method for case definition of PLC based on the results of the diagnostic examinations currently performed and some suggestions for cancer registration are proposed.

We defined some standardised criteria for classifying incident cases of liver cancer into either Primary Liver Cancer (PLC) or Unspecified Liver Cancer (ULC), on the basis of the diagnostic procedures performed. A pilot hospital-based study (98 cases) was carried out in Verona, northern Italy, in order to assess the feasibility of the method. The same protocol was subsequently applied in a population-based study (349 cases) in Bresica, northern Italy. The percentage of cases with histological verification was 38.7 and 41.8%, respectively, with a wide variation among different hospitals. The percentage of cases we attributed to the PLC category was 78.6% in the hospital-based study and 78.8% in the population-based study. No differences in the proportion of cases attributed to PLC were found according to patients' age, sex or hospital of admission. Repeatability of the method was assessed through a cross-panel review of 198 cases, with a 91.9% interobserver agreement. Implications of this method are discussed and some suggestions for cancer registration and future research are proposed.

The incidence rate for primary liver cancer (PLC) was investigated in the Health Unit of Brescia (about 325,000 inhabitants), North Italy, in the 5-year period 1986-90, in order to ascertain whether there was a high risk for developing the disease in the area as suggested by mortality data. A total of 349 incident cases were observed (male: female ratio = 3.4: 1), of which 182 (52.1%) were diagnosed through histology. The cumulative risk was about 5% and 1% in males and females, respectively. The crude incidence rates were 34.5/100,000 in males and 9.4/100,000 in females, and the age-standardized rates were the highest among all those observed in the 9 Italian areas covered by Cancer Registries. Although about half of the cases in males can be attributed to either chronic alcoholic disease or HBV infection or both, further research is needed to investigate the role of known risk factors for PLC in the Health Unit.