The role of cigarette smoking on the risk of Hodgkin's disease remains controversial. To provide further information on the issue, we analysed data of a case-control study from northern Italy. The cases were 158 patients with incident, histologically confirmed Hodgkin's disease, and the controls were 316 patients, frequency-matched to the cases by age, sex and study centre, and admitted to the same network of hospitals for acute, non-neoplastic, non-alcohol- or non-tobacco-related conditions. Compared with those who had never smoked, the multivariate odds ratio was 0.54 for former and 0.85 for current smokers. No trend in risk was found for either the number of cigarettes smoked or the duration of consumption. None of the estimates, or the corresponding trends in risk, was statistically significant. Our results are consistent with those of several studies indicating no direct association between cigarette smoking and risk of Hodgkin's disease.

In two case-control studies from Italy covering 3533 cases of colorectal cancer and 7062 hospital controls, the odds ratios were 1.04 after cholecystectomy for colorectal, 1.08 for colon and 1.03 for rectal cancers. The results did not differ significantly by gender, colon subsite or time since diagnosis.

As Beer et al.1 mention in their letter, our case-control studies started before the issue of acrylamide and cancer was first raised.2 Consequently, no information was collected on the browning degree of fried and baked potatoes, as well as on their cooking temperature and duration, that have been related to the concentration of acrylamide in foods.3 In any case, the reliability and validity of any such information would be undefined. Beer et al.1 also indicate that other foods or beverages, particularly coffee, contain smaller amounts of acrylamide but are widely consumed. Consequently, they may be responsible of an important proportion of acrylamide intake. In fact, according to Swiss data, coffee consumption contribute for about a third to a fifth of total acrylamide intake (Swiss Federal Office of Public Health assessment of acrylamide intake by duplicate diet study; www.bag.admin.ch). To provide further information on the issue, we include in Table I published data4, 5, 6, 7, 8, 9, 10 from the same network of case-control studies,2 as well as from other Italian and Swiss case-control studies of breast and colorectal cancers,6, 7, 8, 9 on the role of coffee consumption on the risk of selected cancers. The number of cases and controls included in the studies, odds ratios (ORs) and 95% confidence intervals for selected cancers according to consumption of coffee are given in Table I. As compared to the lowest level of coffee consumption, the ORs for the highest one were 0.6 for oral/pharyngeal and esophageal cancers, 0.8 for laryngeal cancer, 0.8 (in Italy) and 0.4 (in Switzerland) for colorectal cancer and around unity for breast and ovarian cancers. Coffee has been widely studied in relation to cancer risk, and our findings are in broad agreement with most studies on the issue.11 Although coffee is considered as a possible carcinogenic agent to the urinary bladder, an excess risk of other cancers considered has been excluded.11, 12 The inverse relation between coffee drinking and colorectal cancer has also been reported.11, 12 No noticeable differences were observed between Italian and Swiss median values of coffee consumption (about 2 cups/day), computed on the control groups. These values were similar to those reported in the Swiss assessment of acrylamide intake (mean, 2.4 servings/day; www.bag.admin.ch). Coffee is prepared in different ways in Italy and Switzerland, and its acrylamide contents may be different, too. Nevertheless, the ORs computed from the two countries were comparable. The present data confirm therefore that in the populations investigated, coffee drinking was not related to excess risk of selected cancers. Finally, a Swedish case-control study found no considerable impact of various measures of acrylamide intake on risk of large bowel, bladder and kidney cancers.13 Yours sincerely, Conducted with the financial support of the Italian Association for Cancer Research and the Italian and Swiss Leagues Against Cancer. The authors thank Mrs. M.P. Bonifacino for editorial assistance. Claudio Pelucchi, Carlo La Vecchia, Silvia Franceschi, Fabio Levi

Pizza has been favourably related to the risk of prostate cancer in North America. Scanty information, however, is available on sex hormone-related cancer sites. We therefore studied the role of pizza consumption on the risk of breast, ovarian and prostate cancers using data from three hospital-based case-control studies conducted in Italy between 1991 and 2002. These included 2569 women with breast cancer, 1031 with ovarian cancer, 1294 men with prostate cancer, and a total of 4864 controls. Compared with non-pizza eaters, the multivariate odds ratios for eaters were 0.97 (95% confidence interval (CI) 0.86-1.10) for breast, 1.06 (95% CI 0.89-1.26) for ovarian and 1.04 (95% CI 0.88-1.23) for prostate cancer. Corresponding estimates for regular eaters (i.e. > or =1 portion per week) were 0.92 (95% CI 0.78-1.08), 1.00 (95% CI 0.80-1.25) and 1.12 (95% CI 0.88-1.43), respectively. Our results do not show a relevant role of pizza on the risk of sex hormone-related cancers. The difference with selected studies from North America suggests that dietary and lifestyle correlates of pizza eating vary between different populations and social groups.

Alcohol drinking during meals was inversely related with risk of acute MI, whereas alcohol drinking outside meals only was unrelated to risk.

To investigate the relation between occupational and recreational physical activity (PA) in different periods of life and the risk of benign prostatic hyperplasia (BPH), we conducted a hospital-based, case-control study in Italy. The study included 1,369 histologically confirmed BPH and 1,451 controls, admitted to the same hospitals for acute, nonneoplastic diseases. Odds ratios (ORs) and 95% confidence intervals (CIs) of BPH, according to lifetime PA, were obtained by unconditional multiple logistic regression models, including terms for age, study center and education. Compared to the lowest level of occupational PA, the multivariate ORs for BPH for the heavy/strenuous level were 0.6 (95% CI, 0.4-0.8) at age 15-19, 0.6 (95% CI, 0.4-0.8) at age 30-39 and 0.7 (95% CI, 0.5-0.9) at age 50-59. Moreover, compared to <2 hr/week of recreational PA, the ORs for BPH for the highest level (>or=5 hr/week) were 0.5 (95% CI, 0.4-0.7) at age 15-19, 0.6 (95% CI, 0.5-0.8) at age 30-39, and 0.7 (95% CI, 0.5-0.8) at age 50-59. All inverse trends in risk were significant, and no heterogeneity was found by reason of BPH-diagnosis, age at diagnosis, and body mass index (BMI). The inverse association between PA and BPH risk may be due to favorable hormonal correlates of PA, but residual confounding by socioeconomic covariates cannot be excluded. A moderate PA at any ages may help reducing a sizeable number of BPH.

The role of family history on the risk of cervical cancer has been investigated in an article including data from 2 studies, from Costa Rica and the Eastern United States (US).1 In the case-control study from Costa Rica, women with a family history of cervical cancer had a 2.4 times (95% confidence Interval [CI] 1.2–4.7) higher risk of developing cervical cancer or severe cervical dysplasia than women without affected first-degree relatives.1 In the case-control study from the Eastern US, the odds ratio (OR) in women with a family history of cervical cancer in first-degree relatives was 2.6 (95% CI 1.1–6.4) for squamous cell carcinoma (SCC) of the cervix and 1.3 (95% CI 0.4–3.9) for cervical adenocarcinoma.1 In the latter study, women with a family history of noncervical gynaecological malignancies had an OR of cervical SCC of 1.2 (95% CI 0.4–3.6), whereas the OR of cervical adenocarcinoma was 1.8 (95% CI 0.7–4.9).1 There is scant additional information on family history of cancer and risk of cervical cancer. In the Swedish Family-Cancer Database, having an affected daughter or mother doubled the risk of developing cervical cancer.2 The risk of developing cervical SCC was 2.0 (95% CI 1.5–2.5) in women with a mother diagnosed with the same cancer and 1.5 (95% CI 0.4–3.3) in women whose mother had had an adenocarcinoma of the cervix.3 We analysed the issue using data from an Italian case-control study. A hospital-based case-control study of invasive cervical cancer was conducted from 1981–1993 in the greater Milan area on 786 women (median age 53, range 17–79 years) with histologically confirmed invasive cervical cancer.4, 5 The histology was adenocarcinoma for 96 cases, SCC for 471 cases and unknown for 219 cases. We grouped cases with unknown histology with SCC because the latter represented the vast majority of cervical cancers in Italy.6 Controls were 917 women (median age 54, range 16–79 years) admitted to the same network of hospitals as cases for a wide spectrum of nongynaecological, nonneoplastic acute conditions unrelated to known or potential risk factors for cervical cancer. Among controls, 31% had traumatic conditions, 30% nontraumatic orthopedic disorders, 12% acute surgical conditions and 27% miscellaneous other illnesses. All interviews were conducted in hospital using a structured questionnaire including information on personal characteristics and habits.4, 5 Information on family history included number of sisters and if the mother or a sister had had a cancer of the breast, ovary, cervix uteri, corpus uteri or an unspecified uterine cancer. We estimated the OR of cervical cancer according to history of cancer at selected sites in first-degree relatives using unconditional multiple logistic regression models.7 We present ORs adjusted for age, education and lifetime number of sexual partners. Further adjustment for area of residence, smoking, parity, number of pap smears (excluding the one(s) leading to the diagnosis), oral contraceptive use and number of sisters did not substantially modify the ORs. Table I shows the ORs of cervical cancer in relation to history of selected cancers in first-degree relatives. A family history of breast or ovarian cancer was not associated with cervical cancer risk. Several women reporting a history of cancer of the uterus in the family were not able to specify whether the cancer was at the corpus or at the cervix uteri. The OR of SCC was 2.2 (95% CI 0.9–5.8) in women reporting a family history of cervical cancer, 0.8 (95% CI 0.3–2.0) in women reporting a family history of endometrial cancer, 2.5 (95% CI 1.0–5.9) for a family history of an unspecified uterine cancer, and 1.6 (95% CI 1.0–2.7) for a family history of any type of uterine cancer. No cervical adenocarcinoma case reported a family history of cervical cancer, whereas the OR of adenocarcinoma of the cervix were 2.9 (95% CI 0.9–9.2), 5.1 (95% CI 1.2–22) and 2.7 (95% CI 1.1–6.6) for a family history of endometrial, unspecified uterine and any uterine cancer, respectively. For all cervical cancers combined, the ORs were similar to those for SCC. After adjustment for additional potential confounders, the OR for all histologies combined became 0.9 (95% CI 0.6–1.5) for a family history of breast cancer, 1.6 (95% CI 0.5–5.2) for ovarian cancer, 1.9 (95% CI 0.7–5.1) for cervical cancer, 1.1 (95% CI 0.4–2.5) for endometrial cancer, 2.5 (95% CI 1.0–6.2) for an unspecified uterine cancer and 1.7 (95% CI 1.0–2.9) for any uterine cancer (not shown). Some limitations must be considered when interpreting the present findings. This study is based on information provided by the subjects, without any confirmation from other sources, and inaccuracies in reporting cancer in first-degree relatives must be taken into account.8 Several women, particularly cases, were not able to distinguish between cancer of the cervix and cancer of the corpus uteri in the relatives, and we also lacked information on age and other correlates of cancer risk in first-degree relatives. Furthermore, the power of the study was limited, in particular when adenocarcinoma was analysed separately. Moreover, the use of hospital controls has long been debated,7 since they may differ from the general population. However, we carefully excluded any admission diagnosis for controls potentially related to cervical cancer, and the similar hospital setting of interview in cases and controls may have improved comparability of medical data.9 In this study, the risk of cervical cancer overall was about 2-fold higher in women with a family history of cervical cancer, or of an unspecified cancer of the uterus, but not in women with a first-degree relative affected with breast, ovarian or endometrial cancer, in agreement with previous studies.1, 3 Of interest is the suggestion in the present study, as well as in the study from the Eastern US,1 that the risk of adenocarcinoma of the cervix is enhanced more by a family history of endometrial/gynaecologic noncervical cancers than by a family history of cervical cancer. Although the major determinant of both adenocarcinoma and SCC of the cervix is HPV infection, and the 2 histologic types appear to share several risk factors,10, 11 some differences have also been observed.11, 12, 13 Cervical adenocarcinoma, but not SCC, appears to share some risk factors with endometrial cancer too, such as obesity, hypertension and diabetes.12 In this study, the OR of adenocarcinoma of the cervix was 1.9 (95% CI 1.0–3.5) for women with a body mass index > 30 kg/m2 compared to women with a body mass index < 25 kg/m2. Since most endometrial cancers are adenocarcinomas, our data would suggest an inherited susceptibility to develop a specific histologic type of cancer. Although the data from the Swedish Family-Cancer Database lend some support to the hypothesis that in general inherited susceptibility may be histology specific, results were less convincing for cervical cancer, which were, however, based on small numbers.14 Since obesity, hypertension and diabetes also tend to aggregate in families, the association between adenocarcinoma of the cevix and endometrial cancer may be due, at least in part, to shared environmental exposure or genetic predisposition to these risk factors. Our study and the case-control study from the Eastern US1 included approximately 100 adenocarcinomas each, and consequently the confidence intervals were wide. Because of the small samples and of the limits in our data discussed above, the possibility that the observed differences between histologic types are due to chance or bias cannot be ruled out. In conclusion, our data confirm that cervical cancer aggregates in families and suggest that some differences may exist in familial predisposition to SCC and adenocarcinoma of the cervix. The authors thank Mrs. I. Garimoldi for editorial assistance. Yours sincerely, Eva Negri, Carlo La Vecchia, Cristina Bosetti, Silvia Franceschi, Fabio Parazzini

This study was conducted to investigate the incidence of ovarian cancer in women who had undergone previous hysterectomy with or without unilateral oophorectomy. In 4 different regions of Italy, from January 1992 to September 1999, 1031 patients with primary invasive epithelial ovarian cancer were interviewed for information about personal health and clinical characteristics, including family history of cancer, use of oral contraceptives or hormone replacement therapy, and clinical history, especially hysterectomy with or without oophorectomy. Also interviewed were 2411 control patients who were recruited from women admitted to the same network of hospitals who were near the same ages as study patients (median, 57 years; range, 17–79 years). Control patients were being treated for indications other than cancer, hormonal, or gynecologic conditions and had no known risk factors for ovarian cancer. All interviews were conducted while patients were in the hospital. Surgical information was confirmed in the medical records. Among all 64 (6.2%) study patients and 248 (10.3%) controls who had previous pelvic surgery, including hysterectomy (n = 40, 3.9%) unilateral oophorectomy (n = 10, 1%), or hysterectomy with unilateral oophorectomy (n = 14, 1.4%), the risk of developing ovarian cancer was less than the risk for women with no previous pelvic surgery (odds ratio [OR], 0.6; 95% confidence interval [CI], 0.5–0.9). The risk decreased as the length of time since surgery increased. For women 1 to 7 years from surgery, the OR was 0.8 (95% CI, 0.5–1.4), and for those 15 or more years from surgery, the OR was 0.5 (95% CI, 1.3–0.8) (P = .005). Age at the time of surgery did not affect the results. The risk of developing ovarian cancer after pelvic surgery was greater among women under 60 years of age than among those 60 years old or more (OR, 0.9; 95% CI, 0.6–1.3 vs. OR, 0.4; 95% CI, 0.2–0.6). Neither family history of breast or ovarian cancer nor parity affected the outcome of the analysis.

Carbon or graphite electrode manufacturing may lead to exposure to polycyclic aromatic hydrocarbons, some of which are considered human carcinogens. To provide comprehensive evidence on cancer risk, we have considered five cohort studies from the USA, France, Sweden and Italy, including about 6,500 workers and 80,000 man-years at risk. In two studies providing data on incidence, 52 incident cases of all neoplasms were reported versus 56.28 expected, corresponding to a standardized incidence ratio (SIR) of 0.92. There were nine cases of lung cancer (SIR=0.91) and three of urinary cancers (SIR=0.81). Four studies gave data on mortality. Overall, 853 deaths were observed versus 1,065.2 expected, corresponding to a standardized mortality ratio (SMR) of 0.80 (95% confidence interval, CI, 0.75-0.86). There were 269 deaths from all neoplasms, versus 292.1 expected (SMR=0.92, 95% CI 0.81-1.04), 82 deaths from respiratory cancers versus 95.8 expected (SMR=0.86), and 15 deaths from bladder and urinary cancers versus 12.7 expected (SMR=1.18). None of these estimates were significant, and for none of the other cancer sites there was evidence of excess risk. Thus, epidemiological data allow excluding any appreciable risk of cancer--in particular of the respiratory and the urinary tract--in carbon electrode workers.

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