Cumulative asbestos exposure and mortality from asbestos related diseases in a pooled analysis of 21 asbestos cement cohorts in Italy

Background: Despite the available information on cancer risk, asbestos is used in large areas in the world, mostly in the production of asbestos cement. Moreover, questions are raised regarding the shape of the dose response relation, the relation with time since exposure and the association with neoplasms in various organs. We conducted a study on the relationship between cumulative asbestos exposure and mortality from asbestos related diseases in a large Italian pool of 21 cohorts of asbestos-cement workers with protracted exposure to both chrysotile and amphibole asbestos. Methods: The cohort included 13,076 workers, 81.9% men and 18.1% women, working in 21 Italian asbestos-cement factories, with over 40 years of observation. Exposure was estimated by plant and period, and weighted for the type of asbestos used. Data were analysed with consideration of cause of death, cumulative exposure and time since first exposure (TSFE), and by gender. SMRs were computed using reference rates by region, gender and calendar time. Poisson regression models including cubic splines were used to analyse the effect of cumulative exposure to asbestos and TSFE on mortality for asbestos-related diseases. 95% Confidence Intervals (CI) were computed according to the Poisson distribution. Results: Mortality was significantly increased for ‘All Causes’ and ‘All Malignant Neoplasm (MN)’, in both genders. Considering asbestos related diseases (ARDs), statistically significant excesses were observed for MN of peritoneum (SMR: men 14.19; women 15.14), pleura (SMR: 22.35 and 48.10), lung (SMR: 1.67 and 1.67), ovary (in the highest exposure class SMR 2.45), and asbestosis (SMR: 507 and 1023). Mortality for ARDs, in particular pleural and peritoneal malignancies, lung cancer, ovarian cancer and asbestosis increased monotonically with cumulative exposure. Pleural MN mortality increased progressively in the first 40 years of TSFE, then reached a plateau, while peritoneal MN showed a continuous increase. The trend of lung cancer SMRs also showed a flattening after 40 years of TSFE. Attributable proportions for pleural, peritoneal, and lung MN were respectively 96, 93 and 40%. Conclusions: Mortality for ARDs was associated with cumulative exposure to asbestos. Risk of death from pleural MN did not increase indefinitely with TSFE but eventually reached a plateau, consistently with reports from other recent studie

Italian pool of asbestos workers cohorts: asbestos related mortality by industrial sector and cumulative exposure

Objective. Italy has been a large user of asbestos and asbestos containing materials until the 1992 ban. We present a pooled cohort study on long-term mortality in exposed workers. Methods. Pool of 43 Italian asbestos cohorts (asbestos cement, rolling stock, shipbuilding, glasswork, harbors, insulation and other industries). SMRs were computed by industrial sector for the 1970-2010 period, for the major causes, using reference rates by age, sex, region and calendar period. Results. The study included 51 801 subjects (5741 women): 55.9% alive, 42.6% died (cause known for 95%) and 1.5% lost to follow-up. Asbestos exposure was estimated at the plant and period levels. Asbestos related mortality was significantly increased. All industrial sectors showed increased mortality from pleural malignancies, and most als

TOBACCO SMOKE AND RISK OF CHILDHOOD LEUKAEMIA: FINDINGS FROM THE SETIL CASE-CONTROL STUDY

Introduction. Tobacco smoke could cause childhood leukaemia through at least two different pathways: 1) prenatal parental smoking; 2) childhood exposure to environmental tobacco smoke (ETS). Objectives. To explore these two possible risk factors for acute lymphoblastic leukaemia (ALL) and acute myeloid leukaemia (AML), we analyzed data collected in a large case control study (SETIL) primarily designed to evaluate the role of electromagnetic fields in childhood haematopoietic malignancies. Methods.We focused on incident cases (with informed consent) of ALL (n=602) and AML (n=83) in 14 Italian Regions during 1998- 2001, individually matched (2:1) by age, sex and Region with controls randomly drawn from the general population (matching was broken in the present analysis). We conducted separate logistic regressions for ALL and AML, conditioned to Region and adjusted for child age and sex. Results. Analysis of AML data showed a 3-way interaction (p=0.003) between paternal preconception smoking, maternal smoking during pregnancy, and maternal age. Remarkably, heavy smokers (>10 cigarettes/day) appeared to be at raised risk of having a child affected by childhood AML when maternal age was <30 years (OR 5.4; 95%CI 1.6-18.2; reference category, never-smoker parents); we were unable to find any sign of smoking-related risk above this cut-off (based on median maternal age). No clear association emerged for ETS. Analysis of ALL data showed raised risk for children regularly exposed (>=1 cigarette/day) to ETS (OR 1.5; 95%CI 1.1-2.0; reference, never exposed); intriguingly, risk appeared more pronounced (OR 2.5; 95%CI 1.4-4.4) in “late-onset” cases (age >=6 years). No association was detected with prenatal exposure. Conclusion.We hypothesize that young maternal age could modulate risks of childhood AML determined by parental smoking (plausibly due to age-related metabolic differences). This study also supports the concept that childhood exposure to ETS could be a risk factor for ALL

TOBACCO SMOKE AND RISK OF CHILDHOOD LEUKAEMIA: FINDINGS FROM THE SETIL CASE-CONTROL STUDY

Introduction. Tobacco smoke could cause childhood leukaemia through at least two different pathways: 1) prenatal parental smoking; 2) childhood exposure to environmental tobacco smoke (ETS). Objectives. To explore these two possible risk factors for acute lymphoblastic leukaemia (ALL) and acute myeloid leukaemia (AML), we analyzed data collected in a large case control study (SETIL) primarily designed to evaluate the role of electromagnetic fields in childhood haematopoietic malignancies. Methods.We focused on incident cases (with informed consent) of ALL (n=602) and AML (n=83) in 14 Italian Regions during 1998- 2001, individually matched (2:1) by age, sex and Region with controls randomly drawn from the general population (matching was broken in the present analysis). We conducted separate logistic regressions for ALL and AML, conditioned to Region and adjusted for child age and sex. Results. Analysis of AML data showed a 3-way interaction (p=0.003) between paternal preconception smoking, maternal smoking during pregnancy, and maternal age. Remarkably, heavy smokers (>10 cigarettes/day) appeared to be at raised risk of having a child affected by childhood AML when maternal age was <30 years (OR 5.4; 95%CI 1.6-18.2; reference category, never-smoker parents); we were unable to find any sign of smoking-related risk above this cut-off (based on median maternal age). No clear association emerged for ETS. Analysis of ALL data showed raised risk for children regularly exposed (>=1 cigarette/day) to ETS (OR 1.5; 95%CI 1.1-2.0; reference, never exposed); intriguingly, risk appeared more pronounced (OR 2.5; 95%CI 1.4-4.4) in “late-onset” cases (age >=6 years). No association was detected with prenatal exposure. Conclusion.We hypothesize that young maternal age could modulate risks of childhood AML determined by parental smoking (plausibly due to age-related metabolic differences). This study also supports the concept that childhood exposure to ETS could be a risk factor for ALL

TOBACCO SMOKE AND RISK OF CHILDHOOD LEUKAEMIA: FINDINGS FROM THE SETIL CASE-CONTROL STUDY

Introduction. Tobacco smoke could cause childhood leukaemia through at least two different pathways: 1) prenatal parental smoking; 2) childhood exposure to environmental tobacco smoke (ETS). Objectives. To explore these two possible risk factors for acute lymphoblastic leukaemia (ALL) and acute myeloid leukaemia (AML), we analyzed data collected in a large case control study (SETIL) primarily designed to evaluate the role of electromagnetic fields in childhood haematopoietic malignancies. Methods.We focused on incident cases (with informed consent) of ALL (n=602) and AML (n=83) in 14 Italian Regions during 1998- 2001, individually matched (2:1) by age, sex and Region with controls randomly drawn from the general population (matching was broken in the present analysis). We conducted separate logistic regressions for ALL and AML, conditioned to Region and adjusted for child age and sex. Results. Analysis of AML data showed a 3-way interaction (p=0.003) between paternal preconception smoking, maternal smoking during pregnancy, and maternal age. Remarkably, heavy smokers (>10 cigarettes/day) appeared to be at raised risk of having a child affected by childhood AML when maternal age was =1 cigarette/day) to ETS (OR 1.5; 95%CI 1.1-2.0; reference, never exposed); intriguingly, risk appeared more pronounced (OR 2.5; 95%CI 1.4-4.4) in “late-onset” cases (age >=6 years). No association was detected with prenatal exposure. Conclusion.We hypothesize that young maternal age could modulate risks of childhood AML determined by parental smoking (plausibly due to age-related metabolic differences). This study also supports the concept that childhood exposure to ETS could be a risk factor for ALL

Tobacco smoke and risk of childhood acute lymphoblastic leukemia: findings from the SETIL case-control study.

Tobacco smoke could cause childhood acute lymphoblastic leukemia (ALL) through at least three pathways: (1) prenatal parental smoking; (2) fetal exposure through maternal smoking during pregnancy; and (3) childhood exposure to secondhand smoke (SHS). We tested these hypotheses in a large population-based case-control study (SETIL) primarily designed to evaluate the role of electromagnetic fields in childhood hematopoietic malignancies.From 1998 to 2003, we enrolled 602 incident cases of ALL from 14 Italian Regions, and 918 controls were individually matched by birthdate, sex, and area of residence. Cases (n = 557) and controls (n = 855) with complete information were analyzed; odds ratios (OR) and 95 \% confidence intervals (95 \% CI) were estimated with logistic regression models conditioned on matching variables and adjusted by birth order, birthweight, duration of breastfeeding, parental age at delivery, education, and occupational exposure to benzene.No evidence associating paternal smoking in the conception period or maternal smoking during the pregnancy with ALL was found. An association of ALL with maternal exposure to SHS during pregnancy (adjusted OR for mothers exposed more than 4 h/day = 2.18, 95 \% CI 1.39-3.42) was observed, but recall bias cannot be excluded. Exposure of the children to SHS was associated with ALL only in unadjusted analysis (unadjusted OR for highly exposed children = 1.64; 95 \% CI 1.10-2.45).This study does not support the hypothesis that parental active smoking is associated with ALL. We found very weak evidence of increased risk of ALL for children exposed to SHS. Maternal exposure to SHS was associated with ALL, but recall bias is likely to inflate our estimates