Background: In 1997, a Monograph from the International Agency for Research on Cancer (IARC) classified occupational exposure to crystalline silica as carcinogenic to humans. Large amounts of ...epidemiological data have been published subsequently.
Methods: We conducted a systematic review of epidemiological investigations on silica exposure and lung cancer risk published after the IARC Monograph, including 28 cohort, 15 case–control and two proportionate mortality ratio (PMR) studies. These were identified in the available literature.
Results: The pooled RR of lung cancer, calculated using random effects models, from all cohort studies considering occupational exposure to silica was 1.34. The RRs were 1.69 in cohort studies of silicotics only, 1.25 in studies where silicosis status was undefined and 1.19 among non silicotic subjects. The pooled RR was 1.41 for all case–control studies. The RRs were 3.27 in case–control studies of silicotics only, 1.41 in studies where silicosis status was undefined and 0.97 among non silicotic subjects. The RR was 1.24 for PMR studies.
Conclusions. In this re-analysis, the association with lung cancer was consistent for silicotics, but the data were limited for non silicotic subjects and not easily explained for undefined silicosis status workers. This leaves open the issue of dose–risk relation and pathogenic mechanisms and supports the conclusion that the carcinogenic role of silica per se in absence of silicosis is still unclear.
Objectives:To provide further information on mortality from cancer and other causes among chrysotile asbestos miners several years after exposure ceased, we updated the analyses from the Balangero ...mine worker cohort with follow-up to the end of 2003.Methods:The cohort included 1056 men, for a total of 34 432 man-years of observation. We obtained employment data from factory personnel records, and ascertained vital status and causes of death through population registers and death certificates from municipal registration offices. We computed expected numbers of deaths and standardised mortality ratios (SMRs) for relevant causes using the province of Turin and national death rates, for each 5-year calendar period and age group.Results:We found a significant excess mortality from pleural cancer only (4 deaths, SMR 4.67) and pleural and peritoneal cancers combined (5 deaths, SMR 3.16). All pleural and peritoneal cancer deaths occurred 30 or more years after first exposure. The SMRs were 1.27 for lung cancer (45 deaths), 1.82 for laryngeal cancer (8 deaths) and 1.12 for all cancers (142 deaths). Cumulative dust exposure and the various time factors considered did not show a clear pattern of risk associated with mortality from lung cancer. There were 57 deaths from cirrhosis (SMR 2.94) and 54 from accidents and violence (SMR 1.88). Overall, we observed a total of 590 deaths as compared to 412.9 expected (SMR 1.43).Conclusions: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.
To quantify the magnitude of the association between alcohol and oral and pharyngeal cancer (OPC) by sex, smoking habits, type of alcoholic beverage and other factors.
We combined findings from all ...case-control and cohort studies published until September 2010 and present in this article the results classified by these factors, using a meta-analytic approach. Summary relative risks (RRs) were obtained using random-effects models; heterogeneity was assessed using the χ(2) test.
The association between alcohol and OPC risk was similar in men and women, with similar dose-response relationships. No notable differences were found with respect to geographic area and other factors, both for drinking overall and heavy (≥4 drinks/day) drinking. Among never/non-current smokers, the pooled RRs were 1.32 (95% confidence interval, CI, 1.05-1.67) for drinking, and 2.54 (95% CI, 1.80-3.58) for heavy drinking. The corresponding RRs in smokers were 2.92 (95% CI, 2.31-3.70) and 6.32 (95% CI, 5.05-7.90). The pooled RRs for any drinking irrespective of smoking were 2.12 (95% CI, 1.37-3.29) for wine-, 2.43 (95% CI, 1.92-3.07) for beer- and 2.30 (95% CI, 1.78-2.98) for spirits-only drinking. The corresponding RRs for heavy drinking were 4.92 (95% CI, 2.80-8.65), 4.20 (95% CI, 1.43-12.38) and 5.20 (95% CI, 2.77-9.78).
The alcohol-related RRs are similar with respect to sex, geographic area and type of alcoholic beverage. The association between alcohol and OPC is stronger in smokers than in non-smokers.
Background/Objectives: The aim of this study is to investigate whether adherence to the Mediterranean diet changed during the period 1991–2006 in an Italian population. Subjects/Methods: We derived ...data from the comparison groups of a network of case–control studies on cancer and acute myocardial infarction conducted in the greater Milan area between 1991 and 2006. Subjects were 3247 adults (1969 women, 1278 men; median age 59 years) admitted to major teaching and general hospitals for a wide spectrum of acute conditions unrelated to long-term modifications of diet. Trained interviewers collected data on selected socioeconomic and demographic characteristics, lifestyle habits and other personal and familial factors. Information on diet was collected through an interviewer-administered, reproducible and validated food-frequency questionnaire. We computed a Mediterranean diet score (MDS) on the basis of nine a priori defined peculiar characteristics of the Mediterranean dietary pattern. Results: In multiple linear regression models, adjusted for age, education, place of birth and residence, and total energy intake, there was no significant association between the period of interview and MDS in both sexes. Subjects aged 55–64 years, those with high education, and those born in central and southern Italy showed the highest adherence to the Mediterranean diet in both sexes. Conclusions: In this population, adherence to the Mediterranean diet showed no significant change over the last 15 years.
Whether an association between alcohol drinking and non-Hodgkin lymphoma (NHL) risk exists is an open question. In order to provide quantification of the issue, we carried out a meta-analysis of ...published data.
We identified 21 case–control and 8 cohort studies, including a total of 18 759 NHL cases. We derived meta-analytic estimates using random-effects models, taking into account correlation between estimates.
The overall relative risk (RR) of NHL for drinkers versus non-drinkers was 0.85 95% confidence interval (CI) 0.79–0.91. Compared with non-drinkers, the pooled RRs were 0.88 for light (≤1 drink per day), 0.87 for moderate (1 to <4 drinks per day), and 0.84 for heavy (≥4 drinks per day) alcohol drinking. There was no association for light drinkers in cohort studies, whereas for moderate and heavy drinkers, the RRs were similar in case–control (0.85 for moderate, 0.92 for heavy) and cohort (0.89 for moderate, 0.79 for heavy) studies. The inverse relation with alcohol consumption (drinkers versus non-drinkers) was similar in men (RR = 0.83) and women (RR = 0.86), but apparently stronger in studies from Asia (RR = 0.69) than other world areas (RR = 0.88).
This meta-analysis provides quantitative evidence of a favourable role of alcohol drinking on NHL risk, though the lack of a biological explanation suggests caution in the interpretation of results.
We aimed at investigating the risk of bladder cancer at different levels of alcohol consumption by conducting a meta-analysis of epidemiological studies.
In October 2010, we carried out a systematic ...literature search in the Medline database, using PubMed. We identified 16 case–control and 3 cohort studies, including a total of 11219 cases of bladder cancer, satisfying the inclusion criteria for this meta-analysis. Moderate alcohol intake was defined as <3 drinks per day (i.e. <37.5g of ethanol per day) and heavy intake as ≥3 drinks/day. Pooled estimates of the relative risks (RR) and the corresponding 95% confidence intervals (CI) were calculated using random effects models.
Compared with non-drinkers, the pooled RRs of bladder cancer were 1.00 (95% CI 0.92–1.09) for moderate and 1.02 (95% CI 0.78–1.33) for heavy alcohol drinkers. When we excluded four studies that did not adjust for tobacco smoking, the corresponding estimates were 0.98 (95% CI 0.89–1.07) and 0.97 (95% CI 0.72–1.31).
This meta-analysis of epidemiological studies provides definite evidence on the absence of any material association between alcohol drinking and bladder cancer risk, even at high levels of consumption.
Alcohol is capable of traversing the blood–brain barrier and is thus a possible risk factor for brain cancer. Several epidemiological studies have been published on the issue, a number of those ...during recent years, with inconsistent findings.
We performed a systematic literature search in the Medline and EMBASE databases. We found a total of 19 studies providing risk estimates for total alcohol or specific alcoholic beverages. Pooled estimates of the relative risks (RR) and 95% confidence intervals (CI) were calculated using random-effects models.
The pooled RR of brain cancer for alcohol drinkers versus non-drinkers was 0.97 (95% CI 0.82–1.15; based on 12 studies). Moderate (<2 drinks/day) and heavy alcohol drinkers had RRs of 1.01 (95% CI 0.81–1.25) and 1.35 (95% CI 0.85–2.15), respectively. With reference to specific alcoholic beverages, the RRs were 1.01 (95% CI 0.70–1.48) for wine, 0.96 (95% CI 0.82–1.12) for beer, and 1.20 (95% CI 1.01–1.42) for spirit consumption. The RRs for drinkers versus non-drinkers were 0.93 (95% CI 0.81–1.07) for glioma and 0.71 (95% CI 0.45–1.12) for meningioma.
Alcohol drinking does not appear to be associated with adult brain cancer, though a potential effect of high doses deserves further study.
Abstract Objective In order to provide an updated quantification of the association between alcohol drinking and epithelial ovarian cancer risk, we conducted a meta-analysis of published ...observational studies. Methods Using PubMed, we performed a literature search of all case–control and cohort studies published as original articles in English up to September 2011. We included 27 observational studies, of which 23 were case–control studies, 3 cohort studies and one pooled analysis of prospective cohort studies, including a total of 16,554 epithelial ovarian cancer cases. We derived pooled meta-analytic estimates using random-effects models. Results The pooled relative risk (RR) for any alcohol drinking compared with non/occasional drinking was 1.00 95% confidence interval (CI), 0.95–1.05. The RRs were 0.97 (95% CI, 0.92–1.02), 1.03 (95% CI, 0.96–1.11) and 1.09 (95% CI, 0.80–1.50) for light (≤ 1 drink/day), moderate (> 1 to < 3 drinks) and heavy drinking (≥ 3 drinks/day), respectively. In particular, the pooled RR for invasive epithelial ovarian cancers was 1.00 (95% CI, 0.95–1.06), while for borderline cancers was 0.96 (95% CI, 0.74–1.26). Stratified analyses across cancer histotypes revealed a modest protective effect of alcohol on endometrioid epithelial ovarian tumors (RR = 0.82, 95% CI, 0.70–0.96), while no association was found for serous (RR = 1.00, 95% CI, 0.84–1.19), mucinous (RR = 0.91, 95% CI, 0.78–1.08) and clear cell (RR = 0.93, 95% CI, 0.76–1.14) cancers. There was no evidence of publication bias. Conclusions This comprehensive meta-analysis provided no evidence of a material association between alcohol drinking and epithelial ovarian cancer risk.
A cohort of 889 men and 1077 women employed for at least 1 month between 1946 and 1984 by a former Italian leading asbestos (mainly textile) company, characterised by extremely heavy exposures often ...for short durations, was followed up to 1996, for a total of 53,024 person-years of observation. Employment data were obtained from factory personnel records, while vital status and causes of death were ascertained through municipality registers and local health units. We observed 222 cancer deaths compared with 116.4 expected (standardized mortality ratio, SMR=191). The highest ratios were found for pleural (SMR=4105), peritoneal (SMR=1817) and lung (SMR=282) cancers. We observed direct relationships with duration of employment for lung and peritoneal cancer, and with time since first employment for lung cancer and mesothelioma. Pleural cancer risk was independent from duration (SMR=3428 for employment <1 year, 7659 for 1-4 years, 2979 for 5-9 years and 2130 for > or =10 years). Corresponding SMRs for lung cancer were 139, 251, 233 and 531. Nonsignificantly increased ratios were found for ovarian (SMR=261), laryngeal (SMR=238) and oro-pharyngeal (SMR=226) cancers. This study confirms and further quantifies the central role of latency in pleural mesothelioma and of cumulative exposure in lung cancer.
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