Mortality from the most common cancers in Italy showed a favorable trend over recent years, the maintenance and potential improvement of which would require a strategy focusing on the control of tobacco and alcohol consumption, nutrition and diet. Early diagnosis for selected neoplasms can also have a relevant impact, together with advancements in treatments.

Only scant information is available on the association between family history of kidney cancer and risk of renal cell cancer (RCC), particularly as concerns the variation of the risk according to sex, age, and type of relative or the association of family history of other cancers with RCC. We thus investigated the issue using data from a large multicentric case-control study conducted in Italy between 1992 and 2004 on 767 patients (494 men and 273 women) under age 80 years, with incident, histologically confirmed RCC, and 1,534 controls under age 80 years, admitted to hospital for a wide spectrum of acute, nonneoplastic conditions and frequency matched 2:1 to cases by center, sex, and age. Conditional logistic regression models, conditioned on center, sex, and age and adjusted for year of interview, smoking, body mass index, and number of brothers and sisters were used to estimate odds ratios (OR). Eighteen RCC and 8 controls reported a family history of kidney cancer in one first-degree relative [OR, 5.2; 95% confidence interval (95% CI), 2.2-12.2]. No significant heterogeneity emerged according to sex or age of the proband or of the affected relative, or smoking habits, body mass index, and history of hypertension of the proband. Although not significant, the OR was higher when the affected relative was a sibling (OR, 7.0; 95% CI, 1.8-27.7) rather than a parent or child (OR, 4.3; 95% CI, 1.5-12.9), as suggested from previous studies. The OR of RCC was also significantly elevated for a family history of prostate cancer (OR, 1.9), leukemias (OR, 2.2), or any cancer (OR, 1.5).

In a previous report,1 we provided information on the relation between acrylamide intake and risk of cancers of the upper aero-digestive tract, colorectum, breast, ovary and prostate, using data from a series of Italian and Swiss case-control studies. No significant association emerged for any of the cancer sites considered, with odds ratios (OR) for the highest level of acrylamide intake ranging between 0.92 for prostate cancer and 1.23 for laryngeal cancer. New data are now available on renal cell cancer (RCC) from an Italian case-control study conducted using the same methods and food frequency questionnaire. To our knowledge, only 2 Swedish case-control studies have provided data on the issue,2, 3 and found no association between acrylamide intake (OR = 0.8; 95% confidence interval (CI), 0.4–1.7, and OR = 1.1; 95% CI, 0.7–1.8, for the highest versus lowest quartile) and risk of kidney and RCC, respectively. The general scheme of the study and methods have been described elsewhere.1, 4 Briefly, a case-control study of RCC was conducted between 1992 and 2004 in 4 Italian areas. Cases were 767 patients (494 men, 273 women) with incident, histologically confirmed RCC, recruited in a network of major teaching and general hospitals in the areas under surveillance. Controls were 1,534 subjects (988 men, 546 women), matched with cases by study centre, sex and age, admitted to the same hospitals for acute non-neoplastic conditions, unrelated to known or potential risk factors for RCC nor to long-term modifications of diet. Cases and controls were questioned during their hospital stay by trained interviewers. Information on diet was based on a food frequency questionnaire including 78 foods and recipes, that showed satisfactory validity and reproducibility.5, 6 Among the items in the food frequency questionnaire, those considered for the estimation of acrylamide intake were consumption of fried/baked potatoes, coffee, “cappuccino” (white coffee), bread, pizza, fried meat and fish, sweet biscuits, crackers, breadsticks and melba toast. The mean acrylamide content of each food was obtained from resources made available on the Internet by the World Health Organization (WHO, http://www.who.int/foodsafety/chem/en/) and the French Agency for Food Safety (AFSSA, http://www.afssa.fr).7, 8 For those foods that are prepared in a similar way in Italy and France (e.g., bread), we preferred - when available - data from the latter source. We estimated the ORs and the corresponding 95% CI using multiple conditional logistic regression models, conditioned on study centre, sex and quinquennia of age, and adjusted for year of interview, education (<7, 7–11, ≥12 years), smoking habit (never, ex, current smokers of <15, 15 to < 25, ≥25 cigarettes per day), alcohol consumption (never, ex, current drinkers of <21, ≥21 drinks per week), body mass index (<25, 25 to < 30, ≥30 kg/m2), occupational physical activity (mainly standing/sitting, intermediate, heavy/strenuous), family history of kidney cancer and energy intake (in quintiles). Table I shows the frequency distribution of cases and controls, ORs and 95% CI according to consumption of selected foods containing acrylamide and total acrylamide intake. Fried/baked potatoes was the food item that contributed most to total dietary acrylamide (29.6%), and its consumption was not related with RCC (OR = 1.06, 95% CI 0.78–1.43, for >1 portion/week as compared to no consumption). White bread contributed for 28.6% of total acrylamide intake, and the corresponding OR of RCC for high consumption was 1.70 (95% CI, 1.25–2.30). Sweet biscuits (15.0% of total dietary acrylamide, OR = 0.93 for high consumption), coffee (12.4%, OR = 1.03), crackers (6.5%, OR = 1.07) and other food items that contributed to a minor proportion of total acrylamide intake were not associated with RCC risk. Our estimate of average acrylamide intake (37 μg/kg, 0.475 μg/kg body weight/day) was consistent with published data from other populations.9 The ORs for increasing quartiles of total acrylamide intake were 1.21 (95% CI, 0.94–1.57), 1.14 (95% CI, 0.86–1.51) and 1.20 (95% CI, 0.88–1.63) as compared to the lowest quartile, with no trend in risk (p = 0.35). When we excluded the contribution of white bread consumption from the estimate of acrylamide intake, the OR for the highest vs. lowest quartile of acrylamide was 0.87 (95% CI, 0.65–1.14). Risk of RCC according to total acrylamide intake was consistent across strata of sex and age (data not shown). With reference to potential bias of this study, there is no reason to assume a different recall of foods containing acrylamide between cases and controls, because most of these foods are not known to be related with cancer risk. Further, the similar interview setting of cases and controls provides reassurance against information bias. The almost complete participation of cases and controls and the inclusion of acute conditions unrelated to diet in the comparison group weigh against any major role of selection bias. Moreover, the main dietary results of this study are in broad agreement with data from previous investigations.4 Another potential source of bias is misclassification of acrylamide intake. In a sensitivity analysis, we used median acrylamide content instead of mean values from the French database. Although estimated intakes were about 10% lower, none of the results was materially different. Therefore, this study confirms the absence of significant relations between dietary acrylamide and risk of RCC, in line with the findings of 2 Swedish case-control studies.2, 3 These also reported no association between food items containing elevated levels of acrylamide and risk of kidney and RCC. On the other hand, the modest increase in risk observed in our study for the 3 upper quartiles of acrylamide intake compared to the lowest one is likely attributable to the direct relation found between white bread consumption and RCC. This might be explained by the high glycemic index of this food and its consequent effect on insulin-like growth factors levels,10 as was discussed in an earlier report from this study.4 Yours sincerely, This work was conducted with the contribution of the Italian Association for Cancer Research, and the Italian League Against Cancer. The authors thank Ms. I. Garimoldi for editorial assistance. Claudio Pelucchi*, Carlotta Galeone, Luigino Dal Maso, Renato Talamini, Maurizio Montella, Valerio Ramazzotti, Eva Negri, Silvia Franceschi, Carlo La Vecchia.

The role of various micronutrients on the risk of renal cell cancer (RCC) was examined in a multicentric case-control study from Italy, in which information on dietary habits were collected using a validated food-frequency questionnaire. Cases were 767 patients (494 men and 273 women) with incident, histologically confirmed RCC; controls were 1,534 subjects (988 men and 546 women) admitted to the same hospitals as cases for a wide spectrum of acute, nonneoplastic conditions. After allowing for energy and other major covariates, a significant inverse association was found for vitamin E (odds ratio, OR, for the highest quintile of intake versus the lowest one 0.56, 95% confidence interval, CI 0.41-0.75), and vitamin C (OR = 0.72, 95% CI = 0.54-0.96), although the trend in risk for vitamin C was of borderline significance. No significant trend of decreasing risk was found for other micronutrients analyzed, although for most of them the risk estimates were below unity for intakes above the lowest. The ORs for the upper quintile of intake when compared with the lowest one were 0.80 (95% confidence interval, CI = 0.59-1.08) for retinol, 0.82 (95% CI = 0.61-1.10) for alpha-carotene, 0.90 (95% CI = 0.68-1.20) for beta-carotene, 0.94 (95% CI = 0.73-1.21) for beta-criptoxanthin, 0.85 (95% CI = 0.63-1.14) for lutein/zeaxanthin, 0.76 (95% CI = 0.57-1.01) for vitamin D, 0.75 (95% CI = 0.55-1.01) for thiamine, 0.88 (95% CI = 0.66-1.19) for riboflavin, 0.85 for vitamin B6 (95% CI = 0.64-1.13), 0.85 (95% CI = 0.64-1.12) for folate and 0.80 (95% CI = 0.60-1.07) for niacin. No meaningful associations emerged for lycopene (OR = 1.11). The present findings support a possible beneficial effect of vitamin E and C on RCC.

In some areas of China, indoor air pollution (IAP) originating principally from the combustion of solid fuels has a relevant role in lung cancer. Most previous studies focused on the female population and only a few on both the sexes. We analyzed the relationship between IAP from solid fuel use and selected chronic lung diseases and lung cancer risk in Harbin, Northeast China, an area with a very high base line risk of lung cancer for both the sexes. We used data from a case-control study conducted between 1987 and 1990, including 218 patients with incident, histologically confirmed lung cancer and 436 controls admitted to the same hospitals as cases. We calculated an index of IAP from solid fuel use exposure using data on heating type, cooking fuel used, and house measurements. Cases reported more frequently than controls an exposure to coal fuel for house heating and/or cooking, and the odds ratio (OR) for ever versus never exposed was 2.19 [95% confidence interval (CI): 1.08-4.46]. The ORs of lung cancer according to subsequent tertiles of IAP exposure index were 1.82 (95% CI: 1.14-2.89) and 1.99 (95% CI: 1.26-3.15) as compared with the lowest tertile. The ORs of lung cancer for participants with a history of chronic bronchitis and tuberculosis were 3.79 (95% CI: 2.38-6.02) and 3.82 (95% CI: 1.97-7.41), respectively. This study gives further support and quantification of the positive association between IAP, history of selected nonmalignant lung diseases, and lung cancer risk for both the sexes.

We considered the risk of second basal cell cancers (BCC) of the skin using a population-based series of 1,868 BCC collected between 1976 and 1985 in the Swiss Cantons of Vaud and Neuchâtel, and followed-up to the end of 2003. Overall, 507 second BCC were observed versus 59.98 expected, corresponding to a standardized incidence ratio (SIR) of 8.45 (95% CI: 7.73-9.22). The SIRs were similar in men and women in subsequent calendar periods, but tended to decline with advancing age at diagnosis of first BCC, from 13.98 below age 50 to 7.13 at age 70 or over. Consequently, the rate of first BCC increased to approximately 30-fold between 7/100,000 at age 30-39 and 200/100,000 at age 70-79, but the rate of second BCC increased only about 3-fold between 31/1,000 at age 30-39 and 110/1,000 at age 70-79. The cumulative risk of second BCC was 11% at 5 years, 21% at 10 years and 40% at 20 years. This study indicates that the relative (but not the absolute) risk of second BCC is greater at younger age and declines with advancing age, and is therefore compatible with an excess baseline risk in a population of susceptible individuals.

This study reviews the association between alcohol, tobacco, and the risk of cancers of the upper digestive and respiratory tract (i.e. oral cavity and pharynx, larynx, and esophagus) and liver. Alcohol drinking and tobacco smoking are the major risk factors for upper aerodigestive tract cancers, accounting for a large proportion (i.e. about three-quarters) of cases in developed countries. Consumption amount is the strongest alcohol-related determinant of risk, whereas the pattern of alcohol-related risk with duration is inconsistent. Both dose and duration of smoking have important effects on the risk of upper aerodigestive tract cancers. The combined exposure to alcohol and tobacco has a multiplicative effect on carcinogenesis of this tract. Alcohol and tobacco consumption are also causally related to liver cancer, although the associations are moderate and a lower fraction of neoplasms is attributable to these factors as compared with cancers of the upper aerodigestive tract. An interaction between alcohol drinking and tobacco smoking has been reported, but the issue is not adequately assessed.

a'Mario Negri' Institute for Pharmacological Research bInstitute of Medical Statistics and Biostatistics, University of Milan, Milan, Italy Correspondence to Professor Carlo La Vecchia, Istituto di Ricerche Farmacologiche 'Mario Negri', via Eritrea 62, 20157 Milan, Italy Tel: +39 02 3901 4527; e-mail: [email protected]