Pancreatic cancer mortality has appreciably increased for both sexes in Italy over the last few decades, although Italian rates are still relatively low or a European scale (7.0/100000 men, 4.1/100000 women, world standard). These rises are likely due, at least in part, to improved diagnosis and certification of the disease, and are related to increased exposure to tobacco smoking-the best recognised risk factor for the disease-in subsequent generations of Italian men and women. Besides cigarette smoking, pancreatitis is a recognised risk factor for pancreatic cancer, although it accounts only for a small proportion of cases, whereas a potential association with diabetes mellitus is restricted-or stronger-to the few years before diagnosis of the disease. A diet rich in fats and poor in fresh fruits and vegetables is apparently related to increased risk, but the dietary correlates of pancreatic cancer are still poorly understood. No consistent association has been reported between coffee and alcohol consumption and pancreatic cancer risk.

Infant mortality is an important indicator of the improvements in health observed in CEE countries over the last decade.

Although nutrition and diet have been related to renal cell carcinoma (RCC), the role of specific foods or nutrients on this cancer is still controversial. We evaluated the relation between a wide range of foods and the risk of RCC in an Italian case-control study including 767 patients (494 men and 273 women) younger than 79 years with incident, histologically confirmed RCC, and 1,534 controls (988 men and 546 women) admitted to the same hospitals as cases for a wide spectrum of acute, non-neoplastic conditions, not related to long term diet modifications. A validated and reproducible food frequency questionnaire, including 78 foods and beverages, plus a separate section on alcohol drinking, was used to assess patients' dietary habits 2 years before diagnosis or hospital admission. Multivariate odds ratios (OR) were obtained after allowance for energy intake and other major confounding factors. A significant direct trend in risk was found for bread (OR = 1.94 for the highest versus the lowest intake quintile), and a modest excess of risk was observed for pasta and rice (OR = 1.29), and milk and yoghurt (OR = 1.27). Poultry (OR = 0.74), processed meat (OR = 0.64) and vegetables (OR = 0.65) were inversely associated with RCC risk. No relation was found for coffee and tea, soups, eggs, red meat, fish, cheese, pulses, potatoes, fruits, desserts and sugars. The results of this study provide further indications on dietary correlates of RCC, and in particular indicate that a diet rich in refined cereals and poor in vegetables may have an unfavorable role on RCC.

We conducted a multicenter prospective study to assess the effects of occupational exposure to ethylenebisdithiocarbamate fungicides and/or other pesticides on self-reported asthma and asthmatic symptoms. This multicenter study was conducted among 248 workers exposed to pesticides and 231 non-exposed workers from five field studies. The five field studies were carried out in The Netherlands, Italy, Finland, and two studies in Bulgaria. Subjects constituting this cohort completed a self-administered questionnaire at baseline (before the start of exposure). Ethylenethiourea in urine was determined to assess exposure to ethylenebisdithiocarbamates. In multivariate analyses adjusted for all potential confounders (age, education, residence, smoking, gender, and field study), we found inverse associations, all not statistically significant, between occupational exposure to pesticides and asthma diagnosis (OR 0.41; 95% CI 0.15-1.11), complains of chest tightness (OR 0.60; 95% CI 0.36-1.02), wheeze (OR 0.56; 95% CI 0.32-0.98), asthma attack (OR 0.52; 95% CI 0.12-2.25), and asthma medication (OR 0.79; 95% CI 0.25-2.53). Furthermore, we reported null associations for multivariate analysis using ethylenethiourea as determinant for exposure. Although exposure to pesticides remains a potential health risk, our results do not suggest an association between exposure to ethylenebisdithiocarbamates and/or other pesticides used in our study on asthma and asthmatic symptoms.

Individuals diagnosed with skin cancer have elevated risk of non-Hodgkin lymphoma, and those with non-Hodgkin lymphoma have excess rates of various types of skin cancers. Sunshine and other sources of ultraviolet radiation are major risk factors for skin cancer, and hence a potential common link between skin cancer and non-Hodgkin lymphoma. We analyzed the relationship between occupational exposure to ultraviolet radiation and the risk for non-Hodgkin lymphoma using data from a case-control study conducted in Northern Italy between 1985 and 1997. Cases were 446 patients with histologically confirmed incident non-Hodgkin lymphoma, and controls were 1295 patients admitted to hospital for acute non-neoplastic, non-immunological conditions. The multivariate odds ratios were computed after allowance for age, sex, area of residence, education and smoking. The odds ratio for patients reporting ever ultraviolet exposure at work was 1.01 (95% confidence interval 0.72-1.43) and 1.03 (95% confidence interval 0.72-1.49) for exposure longer than 10 years. The odds ratio was 1.09 for manual workers and 0.79 for farmers exposed to ultraviolet radiation, compared with those with other occupations not exposed to ultraviolet radiation. Our study found no association between occupational exposure to ultraviolet radiation and the risk of non-Hodgkin lymphoma.

Using data from a case-control study conducted between 1985 and 1992 in northern Italy on 828 cases of colon cancer, 498 cases of rectal cancer and 2,024 controls in hospital for acute, non-neoplastic, non-digestive tract disorders, we estimated the percent population attributable risk (PAR) for colorectal cancer in relation to β-carotene, vitamin C (as markers of a diet rich in fruit and vegetables), red meat and seasoning fat intake, daily meal frequency and family history of the disease. On the basis of multivariate odds ratios, adjusted for total calorie intake, a low intake of β-carotene accounted for 39% of all the cases and a low intake of vitamin C for 14%. These two micronutrients together explained 43% of all colorectal cancer cases in this population. A high frequency of intake of red meat consumption explained 17% of all cases, and a high score of seasoning fats 4%. A higher daily meal frequency was responsable for 13% of the cases, and these 5 dietary factors together explained 63% of colorectal cancer cases in this population. Family history of colorectal cancer accounted for 4% of all cases. These estimates were similar for colon and rectal cancers separately, in males and females, and in younger and elderly subjects, except for seasoning fats and family history, whose PARs were apparently greater for colon cancer and at younger age. Thus, even though available dietary data were limited in several aspects, and the PAR estimates were based on somewhat arbitrary assumptions regarding the exposure distribution, about two-thirds of all colorectal cancers in this population could be explained in terms of a few risk factors or risk indicators considered. This would correspond to the avoidance of a large proportion of the over 18,000 deaths from colorectal cancer registered per year in the whole of Italy. © 1996 Wiley-Liss, Inc.

We thank Dr. Grant for his interest in our work.1 We cannot make inference on latitude of exposure, specifically, on latitudes south of about 40°. The subjects diagnosed with skin cancer are most likely, than those without skin cancer, to have been heavily exposed to sun in this Swiss population. Exposure may have occurred in the country with mountainous areas, where sun irradiation is stronger than at sea level,2, 3 or abroad. With reference to smoking, according to the Monograph 83 of the International Agency for Research on Cancer,4 there is evidence suggesting the lack of carcinogenicity of tobacco smoking for female breast cancer. There is clear evidence for the risk of neither prostate cancer nor skin cancer. There is some evidence from prospective cohort and case-control studies that the risk of colorectal cancer is increased among tobacco smokers. However, it is not possible to conclude that the association between tobacco smoking and colorectal cancer is causal (abstracted from reference4, pp. 1183–86). It is, therefore, unlikely that smoking has introduced any major bias, confounding, or modifying effect in the results of our study. The evidence from population-based cohort studies like ours1, 5-7 is open to criticism, but is in any case more valid than that of correlation (ecologic) ones often quoted by Dr. Grant in support of his views. Dr. Soerjomataram and Dr. de Vries suggest to provide additional information to address the issue of surveillance bias and stratified or sub-group analysis in our study.1 Although we caution toward inference based on subgroups, we are glad to provide the information requested, when available. With reference to potential surveillance bias, the number of male skin cancer cases in Vaud and Neuchatel, Switzerland were 15,246 when compared with 13,541 in the Dutch study, and that of population years at risk was 109,176. There is no reason to suppose that inclusion—rather than exclusion—of early prostate cancer introduces selection bias. In the mid 1990's, about 10% of men aged 65 or over may have undergone prostate-specific antigen (PSA) testing in Vaud and Neuchatel,8 and this proportion has risen over more recent years, in the absence, however, of any organised screening programme. The standardised incidence ratio (SIR) of prostate cancer was 1.18 (95% confidence interval (CI): 0.93–1.47) in the first, 1.24 (95% CI: 0.97–1.57) in the second, 1.16 (95% CI: 0.88–1.49) in the third year after diagnosis of skin cancer, and 1.13 (95% CI: 1.02–1.25) in subsequent years. Corresponding values were 1.34, 1.06, 0.89, 1.08 for colorectal, and 1.07, 1.20, 1.09, 1.06 for breast cancer. This weighs against the hypothesis of an early reduction in risk, which levels off with time, due to potentially reduced sunshine exposure after skin cancer diagnosis. With reference to strata of sex, the SIR of colorectal cancer were 1.06 (95% CI: 0.94–1.19) in men, and 1.14 (95% CI: 1.00–1.30) in women. The estimates were not significantly heterogeneous across sexes. We have information on stage and grade of prostate cancer only for recent years; thus numbers of subsequent cancers are inadequate now for any inference. Thus, none of the additional or subgroup analyses indicated by Dr. Soerjomataram and Dr. de Vries modify our conclusion that incidence of colorectal, breast, and prostate cancers is not reduced in patients diagnosed with skin cancer. We agree with Dr. Soerjomataram and Dr. de Vries that collaborative studies would help clarify the issue, and provide acceptable statistical power for subgroup analyses. Dr. Robert Tarone, from the International Epidemiology Institute, Rockville, MD, USA, kindly pointed to us that the expected rates in Table I were smaller than those in Table II.1 The correct Table I is, therefore, enclosed below. The first paragraph of the results section consequently reads as follows: “Table 1 gives the numbers of observed and expected cancers of the prostate, breast, and colorectum following basal and squamous cell skin cancers, skin melanomas, and all skin cancers combined. Overall, 680 prostate cancers were observed vs. 593.4 expected (SIR = 1.15; 95% CI: 1.06–1.24), 440 breast cancers were observed vs. 402.3 expected (SIR = 1.09; 95% CI: 0.99–1.20), and 535 colorectal cancers were observed vs. 488.0 expected (SIR = 1.10; 95% CI: 1.01–1.19). We, also, considered the risk of prostate, breast, and colorectal cancers in separate strata of age at diagnosis, location (head and neck vs. other), and time since skin cancer diagnosis, but found no indication of reduced risk in any of the strata considered, most SIRs for prostate, breast, and colorectal cancers being around or slightly above unity. The SIRs of colorectal cancer were 1.06 (95% CI: 0.94–1.19) for men, based on 292 observed vs. 275.4 expected, and 1.14 (95% CI: 1.00–1.30) for women, based on 243 vs. 212.6 expected.” These changes do not modify the inference and conclusions of our work. We apologize, nonetheless, the readers for the correction, and again thank Dr. Tarone for his careful reading and valuable help. Yours sincerely, Fabio Levi, Lalao Randimbison, Van-Cong Te, Manuela Maspoli Conconi, Carlo La Vecchia

The role of specific food groups and diet variety on the risk of oral and pharyngeal cancer has been considered using data from a case-control study conducted between 1992 and 1997 in the Swiss Canton of Vaud. Cases were 156 patients (126 males, 30 females) aged under 75 (median age 56) years with incident, histologically confirmed cancer of the oral cavity and pharynx, and controls were 284 subjects (246 males, 38 females, median age 57 years), admitted to the same university hospital for a wide spectrum of acute, non-neoplastic conditions unrelated to tobacco and alcohol consumption or to long-term modification of diet. After allowance for education, alcohol, tobacco and total energy intake, significant trends of increasing risk with more frequent intake emerged for eggs (OR = 2.3 for the highest tertile), red meat (OR = 2.1) and pork and processed meat (OR = 3.2). Inverse trends in risk were observed for milk (OR = 0.4 for the highest tertile), fish (OR = 0.5), raw vegetables (OR = 0.3), cooked vegetables (OR = 0.1), citrus fruit (OR = 0.4) and other fruits (OR = 0.2). The addition of a serving per day of fruit or vegetables was associated with an about 50% reduction in oral cancer risk. The most favourable diet for oral cancer risk is therefore given by infrequent consumption of red and processed meat and eggs and, most of all, frequent vegetable and fruit intake. Diet diversity was inversely related to oral and pharyngeal cancer: ORs were 0.35 for the highest tertile of total diversity, 0.24 for vegetable and 0.34 for fruit diversity. In terms of attributable risk, high meat intake accounted for 49% of oral and pharyngeal cancers in this population, low vegetable intake for 65% and low fruit intake for 54%. Int. J. Cancer 77:705–709, 1998. © 1998 Wiley-Liss, Inc.