9 research outputs found

    Association Between Acute non-Lymphocytic Leukemia and Sources of Exposure to Tobacco Smoke. The SETIL Study, Italy, 1998–2003.

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    <p>Abbreviations: 95%CI, 95% confidence interval; cigs, cigarettes; ETS, environmental tobacco smoke; OR, odds ratio; Ref, reference category.</p>a<p>Logistic regression models conditioned on matching variables (date of birth, sex, residence area of the child).</p>b<p>Logistic regression model adjusted by age class and maternal educational level.</p>c<p>Logistic regression model adjusted by age class and maternal educational level.</p>d<p>Logistic regression model adjusted by duration of breastfeeding and paternal educational level.</p>e<p>Logistic regression model adjusted by age class, maternal and paternal educational level.</p>f<p>Logistic regression model adjusted sex, age class, residence area, birth order, birth weight, duration of breastfeeding, maternal and paternal age at child birth, maternal and paternal educational level, birth year of the mother, and parental occupational exposure to benzene (inverse probability weighting).</p><p>Association Between Acute non-Lymphocytic Leukemia and Sources of Exposure to Tobacco Smoke. The SETIL Study, Italy, 1998–2003.</p

    Characteristics of Acute Non-Lymphocytic Leukemia Cases and Controls in the SETIL Case-Control Study, Italy, 1998-2003.

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    <p>Abbreviations: AnLL, acute non-lymphocytic leukemia; NA, not appropriate.</p>a<p>Comparison between cases and all controls sampled in the SETIL study (AnLL controls + ALL controls).</p>b<p><i>P</i> values from χ2 test.</p>c<p><i>P</i> values from Fisher exact test.</p>d<p>Matching variables.</p><p>Characteristics of Acute Non-Lymphocytic Leukemia Cases and Controls in the SETIL Case-Control Study, Italy, 1998-2003.</p

    Factors Affecting Asbestosis Mortality Among Asbestos-Cement Workers in Italy

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    Objectives This study was performed with the aim of investigating the temporal patterns and determinants associated with mortality from asbestosis among 21 cohorts of Asbestos-Cement (AC) workers who were heavily exposed to asbestos fibres. Methods Mortality for asbestosis was analysed for a cohort of 13 076 Italian AC workers (18.1% women). Individual cumulative asbestos exposure index was calculated by factory and period of work weighting by the different composition of asbestos used (crocidolite, amosite, and chrysotile). Two different approaches to analysis, based on Standardized Mortality Ratios (SMRs) and Age-Period-Cohort (APC) models were applied. Results Among the considered AC facilities, asbestos exposure was extremely high until the end of the 1970s and, due to the long latency, a peak of asbestosis mortality was observed after the 1990s. Mortality for asbestosis reached extremely high SMR values [SMR: males 508, 95% confidence interval (CI): 446–563; females 1027, 95% CI: 771–1336]. SMR increased steeply with the increasing values of cumulative asbestos exposure and with Time Since the First Exposure. APC analysis reported a clear age effect with a mortality peak at 75–80 years; the mortality for asbestosis increased in the last three quintiles of the cumulative exposure; calendar period did not have a significant temporal component while the cohort effect disappeared if we included in the model the cumulative exposure to asbestos. Conclusions Among heaviest exposed workers, mortality risk for asbestosis began to increase before 50 years of age. Mortality for asbestosis was mainly determined by cumulative exposure to asbestos

    [Time trend in mesothelioma and lung cancer risk in asbestos workers in Italy]

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    This study aims at investigating, in asbestos exposed workers, the time trend of their risk of mesothelioma and of other neoplasm after very long latency and after the cessation of asbestos exposure. We pooled a large number of Italian cohorts of asbestos workers and updated mortality follow-up. The pool of data for statistical analyses includes 51,988 workers, of which 6,058 women: 54.2% was alive at follow-up, 42.6% was dead, and 2.8%was lost. Cause of death is known for 94.3%: 2,548 deaths from lung cancer, 748 frompleural cancer, 173 fromperitoneal cancer, and 434 from asbestosis. An exposure index is being developed to compare the different cohorts. Data analysis is in progress. This study will have the size for analysing not only time trends in mesothelioma, but also the occurrence of rarer diseases and cancer specific mortality in women

    Risk of childhood leukaemia and non-Hodgkin's lymphoma after parental occupational exposure to solvents and other agents: the SETIL Study

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    Aim In the context of the Italian Multicentric Epidemiological Study on Risk Factors for Childhood Leukaemia and Non-Hodgkin's Lymphoma (SETIL), the risk of childhood cancer was investigated in relation to parental occupational exposures. Methods All cases of childhood leukaemia and non-Hodgkin's lymphoma (NHL) in children aged 0-10 years were identified. Controls were chosen at random from the local population in each region. Parents were interviewed using a structured questionnaire. The collected data were blindly reviewed by expert industrial hygienists in order to estimate exposure to a list of agents. Statistical analyses were performed for each agent using unconditional multivariable logistic regression models, taking into account timing of exposure. Results 683 cases of acute childhood leukaemia, 97 cases of NHL and 1044 controls were identified. Increased risk of childhood leukaemia was found for maternal exposure to aliphatic (OR 4.3) or aromatic hydrocarbons (OR 3.8) in the preconception period, and for paternal exposure to diesel exhaust (OR 1.4), lead exposure (OR 1.4) and mineral oils (OR 1.7). Risk of NHL appeared to be related to paternal exposure to oxygenated solvents (OR 2.5) and petrol exhaust (OR 2.2). Conclusions We found increased risk for childhood leukaemia associated with maternal occupational exposure to aromatic and aliphatic hydrocarbons, particularly in the preconception period; increased risks were also observed for paternal exposure to diesel exhaust fumes, mineral oils and lead. The risk of NHL appeared to be related to paternal exposure to oxygenated solvent and petrol exhausts
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