The relation between coffee, decaffeinated coffee, and tea intake and renal cell carcinoma (RCC) risk was analyzed in a case-control study conducted in Italy between 1992 and 2004. Cases were 767 subjects with incident histologically confirmed RCC and controls were 1,534 patients in hospital for acute non neoplastic conditions. Odds ratios (OR) and 95% confidence intervals (CI) for RCC were computed by multiple logistic regression models, conditioned on study center, sex, and age. Coffee intake (mostly espresso and mocha) was not associated with RCC risk, with an OR of 1.02 (95% CI 0.73-1.43) in drinkers of > or = 4 cups/day compared with drinkers of < 1 cup/day. The corresponding ORs were 1.34 (95% CI 0.87-2.07) in men and 0.67 (95% CI 0.38-1.18) in women, 1.91 (95% CI 0.85-4.31) in current smokers and 0.74 (95% CI 0.41-1.31) in never smokers, with no trend in risk with dose. No relation was observed with decaffeinated coffee (OR = 1.38, 95% CI 0.94-2.03 for drinkers compared with nondrinkers) and tea intake (OR = 0.78, 95% CI 0.59-1.05 for drinkers of > or = 1 cup/day compared with nondrinkers). No significant heterogeneity was found for coffee intake across strata of age, education, body mass index, and consumption of sugar. This study, based on a large dataset, provides further evidence that coffee, decaffeinated coffee, and tea consumption are not related to RCC risk.

The objective of this study was to provide information on recent trends in cancer mortality in Mexico. We analyzed data provided by the World Health Organization, using joinpoint analysis to detect changes in trends between 1981 and 2007. For most cancers, mortality was upward but started to decline in the late 1980's/early 1990's for both sexes. Overall cancer mortality was 75.53/100 000 men, world standard, and 69.2/100 000 women in 2005-2007. Mortality from uterine cancer declined by approximately 2.5% per year in the 1990s, and by approximately 5% per year in the last decade, but its rates remained exceedingly high (9.7/100 000 in 2005-2007). Other major declines over recent years were those of stomach cancer (approximately 2.5% per year, with rates of 6.6/100 000 in men and 4.9/100 000 in women in 2005-2007) and lung cancer (2-2.5% per year, 11.0/100 000 in men and 4.5/100 000 in women in 2005-2007). Mortality leveled off only since the early 1990s for breast and prostate, and since the late 1990s for colorectal cancer. Death rates from cancer in Mexico remained low on a worldwide scale and showed favorable trends over more recent calendar years. Mortality from (cervix) uterine cancer still represents a major public health priority in this country.

To evaluate the association between coffee, decaffeinated coffee, and tea consumption and pancreatic cancer risk in a pooled analysis of two Italian case-control studies, between 1983 and 2008, we conducted two case-control studies in Northern Italy, including a total of 688 pancreatic cancer cases and 2204 hospital controls with acute, non-neoplastic diseases. We computed multivariate odds ratios (ORs) and 95% confidence intervals (CIs) for coffee drinking (mostly espresso and mocha), adjusting for age, sex, center, year of interview, education, body mass index, tobacco smoking, alcohol drinking, and diabetes. Compared with coffee nondrinkers, the multivariate OR for coffee drinkers was 1.34 (95% CI: 1.01-1.77). However, there was no trend in risk with respect to dose and duration. The OR for an increment of one cup per day was 1.05 (95% CI: 0.98-1.11). There was no heterogeneity in strata of age, sex, and other covariates, including tobacco smoking. No association emerged for decaffeinated coffee (for drinkers the OR was 0.87, 95% CI: 0.60-1.26, compared with decaffeinated coffee nondrinkers) or tea (for tea drinkers the OR was 0.92, 95% CI: 0.75-1.14). The lack of relationship with dose and duration weighs against a causal association between coffee and pancreatic cancer, which is in agreement with most evidence on the issue.

mCAC is a better predictor of CVE and all-cause mortality than FEV1 and emphysema extent and may contribute to the identification of high-risk individuals in a lung cancer screening setting.

Extension of the smoking ban to selected outdoor areas is supported by the large majority of the Italian population. The overwhelming majority of support for smoke-free school grounds and outdoor areas surrounding hospitals indicates that legislative action is required.

We performed a pooled analysis of data on atopic disease and risk of non-Hodgkin lymphoma (NHL) from 13 case-control studies, including 13,535 NHL cases and 16,388 controls. Self-reported atopic diseases diagnosed 2 years or more before NHL diagnosis (cases) or interview (controls) were analyzed. Pooled odds ratios (OR) and 95% confidence intervals (95% CI) were computed in two-stage random-effects or joint fixed-effects models, and adjusted for age, sex, and study center. When modeled individually, lifetime history of asthma, hay fever, specific allergy (excluding hay fever, asthma, and eczema), and food allergy were associated with a significant reduction in NHL risk, and there was no association for eczema. When each atopic condition was included in the same model, reduced NHL risk was only associated with a history of allergy (OR, 0.80; 95% CI, 0.68-0.94) and reduced B-cell NHL risk was associated with history of hay fever (OR, 0.85; 95% CI, 0.77-0.95) and allergy (OR, 0.84; 95% CI, 0.76-0.93). Significant reductions in B-cell NHL risk were also observed in individuals who were likely to be truly or highly atopic-those with hay fever, allergy, or asthma and at least one other atopic condition over their lifetime. The inverse associations were consistent for the diffuse large B-cell and follicular subtypes. Eczema was positively associated with lymphomas of the skin; misdiagnosis of lymphoma as eczema is likely, but progression of eczema to cutaneous lymphoma cannot be excluded. This pooled study shows evidence of a modest but consistent reduction in the risk of B-cell NHL associated with atopy.

The smoking prevalence is the lowest estimate reported since 1957, and the gap between men and women has diminished. Compared to earlier birth cohorts, the lower current estimate among younger adults suggests that the rates will decrease in the future.

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We read with great interest the article by Welzel et al.1 The study reported a positive association between metabolic syndrome and hepatocellular carcinoma (HCC), but the results were restricted to people aged ≥65 years of age. Although the incidence of obesity and/or metabolic syndrome is showing no sign of decline, the epidemic of hepatitis B (HBV) and C (HCV) viruses is at its peak, thus increasing the incidence of HCC.2, 3 To provide further insights on the association of HCC and metabolic syndrome on the interaction with HBV/HCV infection, we report data from an Italian case–control study on HCC. The study was conducted between 1999 and 2002 in the province of Pordenone, Northeastern Italy, and in Naples, Southern Italy.4 Cases comprised 185 patients aged 43-84 years (50% below age 65 years) with incident HCC, who had not yet received any cancer treatment at study entry. The control group included 412 cancer-free patients from the same areas as the cases.4 Metabolic syndrome was associated with a four-fold higher risk of HCC. The association was confirmed among hepatitis B surface antigen (HBsAg)-negative and antibody to HCV (anti-HCV)-negative subjects (odds ratio [OR] = 4.00; 95% confidence interval [CI] = 1.30-12.27). According to the individual preexisting medical condition, only diabetes was significantly associated with HCC risk (OR = 3.75; 95% CI = 1.66-8.44; Table 1). This result was in agreement with a recent study.5 Our results are therefore in agreement with the study by Welzel et al.1; in particular, our study confirms that metabolic syndrome is also a risk factor for HCC in people younger than 65 years (50% of our study population). Our results on metabolic syndrome, together with heavy drinking (in the North) and high HCV prevalence (in the South), contribute to explain the high incidence of and mortality rates from HCC in Italy.3, 6 In order to reduce the burden of liver cancer, actions to control the recent epidemic of metabolic syndrome should be promoted. The authors gratefully acknowledge The Italian League Against Cancer (LILT), Project n. 11/2008. Maurizio Montella M.D.*, Jerry Polesel Sc.D. , Renato Talamini M.D. , Anna Crispo Sc.D.*, Aldo Giudice Sc.D.*, Francesco Izzo M.D. , Carlo La Vecchia Ph.D.§ ¶, * Unità di Epidemiologia, stituto Nazionale dei Tumori Fondazione “G. Pascale” Naples, Italy, Dipartimento di Epidemiologia e Biostatistica, Centro di Riferimento Oncologico—IRCCS, Aviano, Italy, Divisione di Chirurgia “D”, Istituto Nazionale dei Tumori Fondazione “G. Pascale,” Naples, Italy, § Istituto di Ricerche Farmacologiche “Mario Negri,” Milan, Italy, ¶ Istituto di Statistica Medica e Biometria “G. A. Maccacaro,” Università degli Studi di Milano, Milan, Italy.

Although cigarette smoking and alcohol consumption increase risk for head and neck cancers, there have been few attempts to model risks quantitatively and to formally evaluate cancer site-specific risks. The authors pooled data from 15 case-control studies and modeled the excess odds ratio (EOR) to assess risk by total exposure (pack-years and drink-years) and its modification by exposure rate (cigarettes/day and drinks/day). The smoking analysis included 1,761 laryngeal, 2,453 pharyngeal, and 1,990 oral cavity cancers, and the alcohol analysis included 2,551 laryngeal, 3,693 pharyngeal, and 3,116 oval cavity cancers, with over 8,000 controls. Above 15 cigarettes/day, the EOR/pack-year decreased with increasing cigarettes/day, suggesting that greater cigarettes/day for a shorter duration was less deleterious than fewer cigarettes/day for a longer duration. Estimates of EOR/pack-year were homogeneous across sites, while the effects of cigarettes/day varied, indicating that the greater laryngeal cancer risk derived from differential cigarettes/day effects and not pack-years. EOR/drink-year estimates increased through 10 drinks/day, suggesting that greater drinks/day for a shorter duration was more deleterious than fewer drinks/day for a longer duration. Above 10 drinks/day, data were limited. EOR/drink-year estimates varied by site, while drinks/day effects were homogeneous, indicating that the greater pharyngeal/oral cavity cancer risk with alcohol consumption derived from the differential effects of drink-years and not drinks/day.

This updated analysis, with almost 60% of the cohort having died, confirmed the excess mortality from pleural and peritoneal cancers and from several alcohol-related causes.