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Paolo Boffetta

Publications and source records attributed to Paolo Boffetta.

At least 145 records · Page 8Linked to original sources
PubMed2002

Pooled analysis and meta-analysis of glutathione S-transferase M1 and bladder cancer: a HuGE review.

Smoking is a known risk factor for bladder cancer. The product of the GSTM1 gene, glutathione S-transferase M1 (GSTM1), is involved in the detoxification of polycyclic aromatic hydrocarbons found in tobacco smoke; a homozygous deletion of this gene in approximately 50% of Caucasians and Asians results in a lack of GSTM1 enzyme activity. Most studies examining the relation between bladder cancer and GSTM1 have reported an increased risk associated with a lack of GSTM1 activity. The authors performed meta- and pooled analyses of published and unpublished, case-control, genotype-based studies that examined this association (17 studies, 2,149 cases, 3,646 controls) and excluded studies conducted in populations with a high prevalence of exposure to known bladder cancer risk factors other than tobacco smoke. Using random effects models in the meta-analysis, the authors obtained a summary odds ratio of 1.44 (95% confidence interval (CI): 1.23, 1.68) for GSTM1 null status with all studies included. Results from studies with at least 100 cases and 100 controls produced a summary odds ratio of 1.42 (95% CI: 1.26, 1.60). Pooled analyses using original data sets from 10 studies (1,496 cases and 1,444 controls) and adjusting for age, sex, and race produced similar results. There was no evidence of multiplicative interaction between the GSTM1 null genotype and ever smoking in relation to bladder cancer, although there was a suggestion of additive interaction (additive interaction = 0.45, 95% CI: -0.03, 0.93). These results indicate that, among populations studied to date, GSTM1 null status is associated with a modest increase in the risk of bladder cancer.

Benzo(a)pyrene↗
PubMed2002

O6-Alkylguanine-DNA-alkyltransferase activity in peripheral leukocytes, smoking and risk of lung cancer.

The level of activity of O6-alkylguanine-DNA-alkyltransferase (AGT), a DNA repair enzyme, in blood lymphocytes may be a marker of susceptibility to lung cancer. We measured the AGT activity level, expressed as pmoles of repaired bases/mg protein, in leukocytes of 153 lung cancer cases (of whom 80 were never smokers) and 106 controls (76 never smokers) enrolled in eight centres from seven countries. Subjects were interviewed with respect to active smoking and exposure to environmental tobacco smoke (ETS). Among never smokers, the odds ratios (ORs) of lung cancer were 1.3 (95% confidence interval 0.5-3.9), 1.5 (0.6-4.1) and 1.4 (0.5-3.8) in quartiles of decreasing AGT activity level, as compared to the upper quartile (P value of test for linear trend 0.6). Corresponding ORs among smokers were 3.4 (0.9-13), 2.0 (0.5-8.3) and 0.4 (0.1-1.6) (P value of test for linear trend 0.4). No interaction was suggested between AGT activity level and either cumulative smoking or exposure to ETS. Reduced AGT activity was not clearly associated with increased lung cancer risk in either smokers or non-smokers. However, the small size of our study argues for a prudent interpretation of our results.

Aged↗
PubMed2002

Mortality and cancer incidence in New Zealand pulp and paper mill workers.

AIMS: To evaluate mortality and cancer incidence in a cohort of workers employed in the New Zealand pulp and paper industry, and to identify the exposures responsible for any increased risk. METHODS: A total of 8456 workers employed for at least one year in three pulp and paper mills between 1978 and 1990 were followed up until 1992. The observed number of deaths and cancer cases was compared with expected numbers calculated using five-year age-specific rates for the New Zealand population. RESULTS: Vital status was determined for 81% of the cohort, and for 93% of the total person-years at risk. Mortality from all causes (standardised mortality ratios (SMR) = 0.80, 95% confidence intervals [CI] 0.71-0.89; 314 deaths), and from all malignant neoplasms (SMR = 0.95, 95% CI 0.78-1.15, 103 deaths), was lower than expected. Mortality from lung cancer (SMR = 1.33, 95% CI 0.94-1.83, 37 deaths) was marginally increased. CONCLUSIONS: No overall increase in mortality from cancer or other causes was observed in this cohort. A small increase in lung cancer risk is suggested, although this was not statistically significant. Numbers of cases were too small for detailed analyses of associations between disease and specific exposures.

Adult↗
PubMed2002

Dose-specific meta-analysis and sensitivity analysis of the relation between alcohol consumption and lung cancer risk.

Alcohol drinking increases the risk of several types of cancer, but studies of the relation between alcohol and lung cancer risk are complicated by smoking. The authors carried out meta-analyses for four study designs and conducted sensitivity analyses to assess the results. Pooled smoking-unadjusted relative risks (RRs) for brewery workers and alcoholics were 1.17 (95% confidence interval (CI): 0.99, 1.39) and 1.99 (95% CI: 1.66, 2.39), respectively, relative to population rates. For cohort and case-control studies, the authors conducted dose-specific meta-analyses for ethanol consumption of 1-499, 500-999, 1,000-1,999, and > or = 2,000 g/month, relative to nondrinking. Smoking-adjusted RRs for ascending dose groups in cohort studies were 0.98 (95% CI: 0.79, 1.21), 0.92 (95% CI: 0.81, 1.04), 1.04 (95% CI: 0.88, 1.22), and 1.53 (95% CI: 1.04, 2.25), respectively. Smoking-adjusted odds ratios for ascending groups in case-control studies were 0.63 (95% CI: 0.51, 0.78), 1.30 (95% CI: 0.98, 1.70), 1.13 (95% CI: 0.46, 2.75), and 1.86 (95% CI: 1.39, 2.49), respectively. Elevated odds ratios were seen for hospital-based case-control studies but not for population-based case-control studies. Sensitivity analyses indicated that smoking explained the elevated RRs in studies of alcoholics and that strong misclassification of smoking status could produce an elevated smoking-adjusted RR in cohort and case-control studies. Overall, evidence for a smoking-adjusted association between alcohol and lung cancer risk is limited to very high consumption groups in cohort and hospital-based case-control studies. At lower levels, any associations observed appear to be explained by confounding.

Alcohol Drinking↗
PubMed2002

Familial cancer aggregation and the risk of lung cancer.

CONTEXT: Around 90% of lung cancer worldwide is attributable to cigarette smoking, although less than 20% of cigarette smokers develop lung cancer. Other factors such as diet, chronic lung diseases, occupation and possibly environmental agents also contribute to this cancer. Genetic factors seem to play a role in lung cancer, but the precise characteristics influencing lung cancer susceptibility are not known, since genetic factors are easily obscured by the strong environmental determinants of lung cancer, particularly smoking. OBJECTIVE: To estimate the effect that cancer occurrence among first-degree relatives has on the risk of lung cancer. DESIGN: Hospital-based case-control study. SETTING: The metropolitan region of São Paulo, Brazil. PARTICIPANTS: 334 incident lung cancer cases and 578 controls matched by hospitals. MAIN MEASUREMENTS: By means of a structured questionnaire, cases and controls were interviewed about cancer occurrence in first-degree relatives, tobacco smoking, exposure to passive smoking, occupation, migration and socioeconomic status. Non-conditional logistic regression was used to calculate the risk of familial cancer aggregation, the effect of cancer in first-degree relatives and smoking in conjunction, and for controlling confounders. RESULTS: The adjusted odds ratio (OR) revealed a slight, but not statistically significant, excess risk of lung cancer for subjects with a history of lung cancer in relatives (OR 1.21; 95% confidence interval [CI] 0.50 - 2.92). The same was found among those with a history of other tobacco-related cancers in relatives (OR 1.36; 95% CI 0.87 - 2.14). A step gradient effect was observed regarding lung cancer risk, in accordance with increases in the number of pack-years of cigarette consumption. An interaction between familial cancer aggregation and tobacco smoking was detected. CONCLUSIONS: A mildly elevated risk of lung cancer among persons with a positive history of lung and other tobacco-related cancers was observed. The finding of an interaction between the variables of familial cancer aggregation and smoking suggests that familial cancer aggregation could be considered as a marker of susceptibility, increasing the risk of lung cancer among smokers. These results improve our knowledge of lung carcinogenesis and can guide future cancer genetic studies.

Adult↗
PubMed2002

Assessment of feasibility of workplace health promotion.

BACKGROUND: A simple empirically based method for assessment of the feasibility of workplace health promotion programs is described, focusing on cancer hazards (lifestyles, workplace hazards, deficient early detection). The basic components of feasibility are addressed: extent of hazards; needs of employees for hazard reduction and acceptability of WHP; and social context. METHODS: The procedure consists of six modules: guidelines on feasibility assessment; employee questionnaire; interview checklists for probing attitudes of management and partners (social context); data form; debriefing; and assessment of feasibility. Pretesting was completed in 16 workplace communities representing industry, construction, transport, telecommunications, health care, lodging and catering, teaching, and municipality jobs in five countries; a total of 1,085 subjects completed the employee questionnaire on health hazards, needs, and acceptability. RESULTS: The method demonstrated its utility in obtaining and summarizing the necessary data. Feasibility was assessed for the 16 test communities. CONCLUSION: The procedure can be customized; it has a high degree of face validity or understandability, and it is applicable in a wide variety of settings.

Attitude to Health↗
PubMed2002

Diet and adenocarcinoma of the lung: a case-control study in Uruguay.

With the objective of examining the relationship between diet and adenocarcinoma of the lung, a case-control study was carried out in Uruguay. Red meat, total meat and fatty foods were associated with a significant increase in risk (odds ratios (OR) for red meat intake 1.92, 95% CI 1.27-2.90). On the other hand, fruits, tubers and all plant foods displayed significant inverse associations with adenocarcinoma of the lung (OR for total plant foods 0.39, 95% CI 0.26-0.61). Among nutrients, total fat, other fats (saturated fat) and cholesterol were associated with an increased risk of adenocarcinoma of the lung (OR for high consumption of total fat 2.28, 95% CI 1.48-3.54). The risk associated with cholesterol intake was even higher after controlling for total fat, suggesting that both nutrients (fat and cholesterol) have independent effects. Carotenoids and vitamin E displayed significantly protective effects. This effect was markedly attenuated, when these micronutrients were adjusted for total plant intake. Furthermore, red meat, fat, and cholesterol showed attenuation in its effects after adjustment for total plant foods. It could be concluded that tobacco smoking is the strongest risk factor for adenocarcinoma of the lung. Low consumption of plant foods, and in a lesser degree, high consumption of red meat, total fat and cholesterol contribute to a high risk of adenocarcinoma of the lung.

Adenocarcinoma↗
PubMed2002

Food groups and risk of lung cancer in Uruguay.

The objective of the present study was to estimate the risk of lung cancer associated with several food groups. The study included 1,032 cases with lung cancer and 1,030 hospitalized controls, admitted to the Cancer Institute of Montevideo in the period 1988-2000. Total meat intake was directly associated with lung cancer (OR 1.6, 95% CI 1.2-2.2) whereas total vegetables and total fruits were inversely associated with lung cancer risk. When vegetable and fruit intakes were further adjusted for smoking status, years since quit, cigarettes/day and age at start, the protective effect was attenuated for plant foods (total vegetables and fruits). Also, the effect of vegetables and fruits was closest to the null among smokers of black tobacco and hand-rolled cigarettes. Thus, the present study is consistent in showing moderate associations with major food groups (meat, vegetables and fruits), and strongly suggests that the stringent control of tobacco smoking is mandatory in studies dealing with diet and lung cancer risk.

Adult↗
PubMed2002

Alcohol intake and risk of adenocarcinoma of the lung. A case-control study in Uruguay.

In order to examine in detail the relationship between alcohol drinking and risk of adenocarcinoma of the lung, a case-control study involving 160 cases of this cell type and 520 hospitalized controls was conducted in Uruguay in the time period January 1998-July 2000. Total alcohol intake was not associated with risk of adenocarcinoma of the lung (OR 1.2, 95% CI 0.6-2.1). Also beer drinking was not associated with risk of carcinoma (OR 0.6, 95% CI 0.3-1.6). On the other hand, wine drinking displayed a marginally significant reduction in risk (OR 0.4, 95% CI 0.2-1.1). On the contrary, hard liquor intake was associated with a 40% increase in risk of adenocarcinoma of the lung. These findings suggest that wine drinking has a protective effect in adenocarcinoma of the lung, whereas hard liquor increases moderately the risk of this cell type of lung cancer.

Adenocarcinoma↗
PubMed2002

Analysis of nonresponse bias in a population-based case-control study on lung cancer.

The objective of this study was to identify characteristics of nonrespondents and late respondents in a population-based case-control study on lung cancer conducted in the city of Turin (Italy). Information about demographic and socioeconomic variables of 634 cases and 859 controls who responded to an interview, as well as of 154 cases and 154 controls who did not respond were obtained from census and the public register of Turin. The socioeconomic level of nonrespondents was high in cases but low in controls. Late respondent controls (i.e., individuals who responded after contact through their general practitioner) had socioeconomic characteristics comparable with those of nonrespondents, while they were similar to respondents with respect to demographic variables. The interview of late respondents halved, from 14 to 7%, the magnitude of the bias introduced by nonresponse on the estimate of the association between educational level and lung cancer. Nonresponse, associated with socioeconomic status, is an important potential source of bias in population-based case-control studies, which should always be considered and discussed. The direction and magnitude of the bias can be quantified. General practitioners may contribute to decrease nonresponse bias. Caution should be used in inferring characteristics of nonrespondents on the basis of those of late respondents.

Aged↗
PubMed2002

Sinonasal cancer and occupational exposures: a pooled analysis of 12 case-control studies.

OBJECTIVE: In order to examine the associations between sinonasal cancer and occupational exposures other than wood dust and leather dust, the data from 12 case-control studies conducted in seven countries were pooled and reanalyzed. METHODS: The pooled data set included 195 adenocarcinoma cases (169 men and 26 women), 432 squamous cell carcinomas (330 men and 102 women), and 3136 controls (2349 men and 787 women). Occupational exposures to formaldehyde, silica dust, textile dust, coal dust, flour dust, asbestos, and man-made vitreous fibers were assessed with a job-exposure matrix. Odds ratios (ORs) were adjusted for age, study, wood dust, and leather dust, or other occupational exposures when relevant. 95% confidence intervals (CIs) were estimated by unconditional logistic regression. RESULTS: A significantly increased risk of adenocarcinoma was associated with exposure to formaldehyde. The ORs for the highest level of exposure were 3.0 (Cl = 1.5-5.7) among men and 6.2 (CI=2.0-19.7) among women. An elevated risk of squamous cell carcinoma was observed among men (OR=2.5, CI=0.6-10.1) and women (OR = 3.5, CI = 1.2-10.5) with a high probability of exposure to formaldehyde. Exposure to textile dust was associated with non-significantly elevated risk of adenocarcinoma, among women only: the OR for the high level of cumulative exposure was 2.5 (CI = 0.7-9.0). High level of asbestos exposure was associated with a significantly increased risk of squamous cell carcinoma among men (OR = 1.6, CI = 1.1-2.3). CONCLUSIONS: The results of this pooled analysis support the hypothesis that occupational exposure to formaldehyde increases the risk of sinonasal cancer, particularly of adenocarcinoma. They also indicate an elevated risk of adenocarcinoma among women exposed to textile dust, and suggest that exposure to asbestos may increase the risk of squamous cell carcinoma.

Adenocarcinoma↗
PubMed2002

Meta- and pooled analyses of the effects of glutathione S-transferase M1 polymorphisms and smoking on lung cancer risk.

Susceptibility to lung cancer may in part be attributable to inter-individual variability in metabolic activation or detoxification of tobacco carcinogens. The glutathione S-transferase M1 (GSTM1) genetic polymorphism has been extensively studied in this context; two recent meta-analyses of case-control studies suggested an association between GSTM1 deletion and lung cancer. At least 15 studies have been published after these overviews. We undertook a new meta-analysis to summarize the results of 43 published case-control studies including >18 000 individuals. A slight excess of risk of lung cancer for individuals with the GSTM1 null genotype was found (odds ratio (OR) = 1.17, 95% confidence interval (CI) 1.07-1.27). No evidence of publication bias was found (P = 0.4), however, it is not easy to estimate the extent of such bias and we cannot rule out some degree of publication bias in our results. A pooled analysis of the original data of about 9500 subjects involved in 21 case-control studies from the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens (GSEC) data set was performed to assess the role of GSTM1 genotype as a modifier of the effect of smoking on lung cancer risk with adequate power. Analyses revealed no evidence of increased risk of lung cancer among carriers of the GSTM1 null genotype (age-, gender- and center-adjusted OR = 1.08, 95% CI 0.98-1.18) and no evidence of interaction between GSTM1 genotype and either smoking status or cumulative tobacco consumption.

Case-Control Studies↗
PubMed2002

Lung cancer among rock and slag wool production workers.

BACKGROUND: Previous cohort studies have found an elevated risk of lung cancer among rock and slag wool (RSW) production workers. The aim of the present study was to investigate the risk of lung cancer associated with exposure to RSW while controlling for other occupational exposures and tobacco smoking. METHODS: Since 1971, a total of 196 lung cancer cases occurred among men who worked in seven plants in Denmark, Norway, Sweden, and Germany, with start of production between 1937 and 1950. We obtained information on occupational history and extra-occupational factors from either the subject or the next of kin for 133 cases and 513 matched controls. We assessed occupational exposure on the basis of interview data combined with information from expert panels set up in each factory. RESULTS: For cumulative exposure to RSW assessed with a 15-year lag, the smoking-adjusted odds ratios in the second, third, and fourth quartiles of exposure were 1.3 (95% confidence interval [CI] = 0.7-2.3), 1.0 (CI = 0.5-1.9), and 0.7 (CI = 0.3-1.3). Similar results were obtained when we included only those workers employed for more than 1 year, when we included other indicators of RSW exposure, and after control for co-exposures. CONCLUSIONS: This study provides no evidence of a carcinogenic effect on the lung of rock and slag wool under exposure circumstances in the production industry during the last four to five decades.

Adult↗
PubMed2002

Exposure to asbestos and lung and pleural cancer mortality among pulp and paper industry workers.

We studied the mortality from lung and pleural cancers in a cohort of 62,937 male workers employed for at least 1 year in the pulp and paper industry in 13 countries during 1945 to 1996. Mill departments were classified according to probability and level of exposure to asbestos on the basis of available dust measurements and mill-specific information on exposure circumstances. Thirty-six percent of workers were classified as ever exposed to asbestos. Standardized mortality ratios of lung cancer were 0.99 (95% confidence interval [CI], 0.90 to 1.08) among unexposed and 1.00 (95% CI, 0.90 to 1.11) among ever exposed workers. The number of pleural cancer deaths among unexposed workers was 10; that among exposed workers was 14, most of which occurred among maintenance workers. In internal analyses, a trend in mortality from either neoplasm was suggested for estimated cumulative exposure to asbestos, weighted for the individual probability of exposure within the department and for duration of exposure (relative risk for lung cancer for 0.78+ f/cc-years, as compared with < or = 0.01 f/cc-years: 1.44; 95% CI, 0.85 to 2.45; corresponding relative risk for pleural cancer: 2.43; 95% CI, 0.43 to 13.63). Despite a possible nondifferential misclassification of exposure and outcome, this study suggests that the carcinogenic effect of asbestos can be detected among workers employed in industries such as the pulp and paper industry, in which it is not considered to be a major hazard.

Air Pollutants, Occupational↗
PubMed2002

Cancer of the brain and nervous system and occupational exposures in Finnish women.

Occupational agents were evaluated for the risk of brain-nervous system cancer in a cohort of 413,877 Finnish women with blue-collar occupations in 1970. Observed and expected numbers of incident cases and the intensities of exposure to 25 agents were generated for 183 job titles from 1971 to 1995. Poisson regression models linked incidence and exposure data. Increased risks were found for medium/high intensities of iron (standardized incidence ratio [SIR], 2.15; 95% confidence interval [CI], 0.96 to 4.80), oil mist (1.95; 0.97 to 3.90), any chromium compounds (1.51; 0.85 to 2.67), electromagnetic fields (1.37; 0.98 to 2.10), aliphatic and alicyclic hydrocarbon compounds (1.34; 0.80 to 2.27), lead (1.27; 0.81 to 2.01), cadmium (1.26; 0.72 to 2.22), and aromatic hydrocarbon compounds (1.20; 0.71 to 2.03). Strengths of the study include fair number of cases, virtually complete case coverage, and a high-quality job exposure matrix. Ecological design and cross-sectional job assessment introduced exposure misclassification and tended to drive risk estimates toward unity.

Brain Neoplasms↗
PubMed2002

Mortality from lung cancer in workers exposed to sulfur dioxide in the pulp and paper industry.

Our objective in this study was to evaluate the mortality of workers exposed to sulfur dioxide in the pulp and paper industry. The cohort included 57,613 workers employed for at least 1 year in the pulp and paper industry in 12 countries. We assessed exposure to SO(2) at the level of mill and department, using industrial hygiene measurement data and information from company questionnaires; 40,704 workers were classified as exposed to SO(2). We conducted a standardized mortality ratio (SMR) analysis based on age-specific and calendar period-specific national mortality rates. We also conducted a Poisson regression analysis to determine the dose-response relations between SO(2) exposure and cancer mortality risks and to explore the effect of potential confounding factors. The SMR analysis showed a moderate deficit of all causes of death [SMR = 0.89; 95% confidence interval (CI), 0.87-0.96] among exposed workers. Lung cancer mortality was marginally increased among exposed workers (SMR = 1.08; 95% CI, 0.98-1.18). After adjustment for occupational coexposures, the lung cancer risk was increased compared with unexposed workers (rate ratio = 1.49; 95% CI, 1.14-1.96). There was a suggestion of a positive relationship between weighted cumulative SO(2) exposure and lung cancer mortality (p-value of test for linear trend = 0.009 among all exposed workers; p = 0.3 among workers with high exposure). Neither duration of exposure nor time since first exposure was associated with lung cancer mortality. Mortality from non-Hodgkin lymphoma and from leukemia was increased among workers with high SO(2) exposure; a dose-response relationship with cumulative SO(2) exposure was suggested for non-Hodgkin lymphoma. For the other causes of death, there was no evidence of increased mortality associated with exposure to SO(2). Although residual confounding may have occurred, our results suggest that occupational exposure to SO(2) in the pulp and paper industry may be associated with an increased risk of lung cancer.

Air Pollutants↗