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The objective of this study was to determine the contribution of a familial history of cancer (FHC) to the development of leukemia in children below 2 years of age. This is a national hospital-based case-control study of children 0-24 months of age recruited from 15 Brazilian hospitals from several regions providing oncological care and local general hospitals. Participants' FHC antecedents were obtained through face-to-face interviews with the mothers of cases and controls using a standardized questionnaire. Unconditional logistic regression was used to determine crude and adjusted (adj.) odds ratios (OR), and the respective 95% confidence intervals (CI), of acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) after adjustment for selected variables. FHC antecedents were obtained from 178 ALL, 51 AML, and 428 controls. FHC in second-degree relatives (grandparents, uncles, cousins) showed an adj. OR=1.66 (95% CI 1.12-2.45) for ALL. Antecedents of two or more relatives with cancer showed a statistically significant two-fold higher risk of either ALL or AML. Paternal, and joint paternal and maternal antecedents of cancer also showed statistically significant higher adj. OR, respectively: 1.80 and 1.89 for ALL, and 2.34 and 3.23 for AML. Hematological malignancies among second-degree relatives showed an adj. OR=3.48 (95% CI 1.72-7.09) for ALL. According to the anatomic site, antecedents of leukemia/lymphoma among case relatives, compared with the control ones, showed an OR=2.98 (95% CI 1.52-5.82) for ALL, whereas stomach cancer antecedents showed an OR=3.55 (95% CI 1.02-12.39) for AML. The observed results support the hypothesis that FHC antecedents are associated with leukemogenesis in children below 2 years of age.

Background: An association between pesticide exposure and cancer has been suggested. Infant leukemia is a rare neoplasm and its association with maternal pesticide exposure has been poorly explored. Objectives: We investigated the association between pesticide exposure during pregnancy and leukemia in children < 2 years of age. Methods: A hospital-based case–control study was carried out in 13 Brazilian states during 1999–2007. Mothers of 252 cases and those of 423 controls were interviewed. Information on pesticide exposures 3 months before pregnancy, throughout pregnancy, and during breastfeeding was obtained. Unconditional logistic regression was used to estimate adjusted odds ratios (aORs) for associations between pesticide exposures and leukemia. Results: Associations with ever use of pesticides during pregnancy were observed for acute lymphoid leukemia (ALL) (aOR = 2.10; 95% CI: 1.14, 3.86) and acute myeloid leukemia (AML) (aOR = 5.01; 95% CI: 1.97, 12.7) in children 0–11 months of age, and with ALL (aOR = 1.88; 95% CI: 1.05, 5.23) at 12–23 months of age. According to reported maternal exposure to permethrin, higher risk estimates were verified for children 0–11 months of age (aOR = 2.47; 95% CI: 1.17, 5.25 for ALL; and aOR = 7.28; 95% CI: 2.60, 20.38 for AML). Maternal pesticide exposure related to agricultural activities showed an aOR of 5.25 (95% CI: 1.83, 15.08) for ALL, and an aOR of 7.56 (95% CI: 1.83, 31.23) for AML. Conclusions: These results support the hypothesis that pesticide exposure during pregnancy may be involved in the etiology of acute leukemia in children < 2 years of age.

O presente estudo objetiva explorar as relações inaparentes que diversos fatores relativos às exposições ambientais e características individuais existentes em nosso meio possam ter no processo de desenvolvimento da leucemia na infância. A partir de um banco de dados clínicos e epidemiológicos obtido com estudo caso-controle de base hospitalar sobre fatores de risco para leucemias na infância, foi realizada análise multivariada exploratória por meio do emprego de análise de componentes principais e análise fatorial. Esta investigação é parte de um estudo multicêntrico nacional, que incluiu 292 casos de leucemias em crianças com idade entre 0 e 12 anos e 541 controles da mesma faixa etária, hospitalizados por causas não neoplásicas em hospitais gerais próximos aos centros de origem dos casos. As informações de exposições ambientais selecionadas foram obtidas por meio de entrevistas realizadas com mães de casos e controles, por meio de questionário padronizado. O modelo com maior poder explicativo da variância observada nos dados analisados foi da ordem de 52%, apresentando três fatores considerados mais adequados na predição da leucemogênese na infância, cada um incluindo variáveis com cargas fatoriais maiores que 0,6: fator "condições relacionadas a exposições químicas na gestação", o qual explicou 20% da variância final e incluiu as variáveis exposição a pesticidas, exposição a solventes e exposição a tintas na gravidez; fator "hábitos de vida durante a gestação", tendo explicado 17% da variância e incluindo exposição a tinturas de cabelo e cosméticos para alisamento; e fator "consumo de serviços de saúde durante a gestação", explicando 15% da variância e incluindo as variáveis tipo de parto (cesariana ou parto normal) e uso de radiografia na gestação. Na análise de regressão logística, foi encontrada associação estatisticamente significativa entre o desenvolvimento de leucemias na infância e antecedentes de exposição química materna durante a gestação (OR=1,36; 95% IC=1,16-1,59) e consumo de serviços de saúde durante a gestação (OR=1,27; 95%IC =1,08-1,49). Os resultados encontrados são sugestivos quanto à contribuição conjunta das exposições ambientais, e não apenas individualizadas, no desenvolvimento das leucemias na infância, sendo apoiados pelas evidências na literatura de que o processo de carcinogênese, em geral, e o da leucemogênese, em particular, resultem de efeitos de múltiplas mutações relacionadas a exposições ambientais conjuntas. El presente estudio tiene como objetivo explorar las relaciones no aparentes que diversos factores relacionados con exposiciones ambientales, y características individuales existentes en nuestro medio, pueden llegar a tener en el proceso de desarrollo de la leucemia en la infancia. A partir de un banco de datos clínicos y epidemiológicos, obtenido con un estudio de control de casos de base hospitalaria sobre factores de riesgo para leucemias en la infancia, se realizó un análisis multivariado exploratorio, mediante el empleo de un análisis de componentes principales y análisis factorial. Esta investigación es parte de un estudio multicéntrico nacional que incluyó 292 casos de leucemias en niños con edades comprendidas entre 0 y 12 años y 541 controles de la misma franja etaria, hospitalizados por causas no neoplásicas en hospitales generales, cercanos a los centros de origen de los casos. La información sobre las exposiciones ambientales seleccionadas se obtuvo mediante entrevistas realizadas con madres de casos y controles a través de un cuestionario padronizado. El modelo con mayor poder explicativo de la variancia observada en los datos analizados fue del orden de un 52%, presentando tres factores considerados como más adecuados en la predicción de la leucemogénesis en la infancia, cada uno incluyendo variables con cargas factoriales mayores que 0,6: factor "condiciones relacionadas con las exposiciones químicas en la gestación", el cual explicó un 20% de la variancia final e incluyó las variables exposición a pesticidas, exposición a solventes y exposición a tintas en el embarazo; factor "hábitos de vida durante la gestación", habiendo explicado un 17% de la variancia e incluyendo exposición a tintes de pelo y cosméticos para el alisamiento; el factor "consumo de servicios de salud durante la gestación", explicando un 15% de la variancia e incluyendo las variables tipo de parto (cesárea o parto normal) y uso de radiografías en la gestación. En el análisis de regresión logística, fue encontrada una asociación estadísticamente significativa entre el desarrollo de leucemias en la infancia y antecedentes de exposición química materna durante la gestación (OR=1,36; 95% IC=1,16-1,59) y consumo de servicios de salud durante la gestación (OR=1,27; 95%IC =1,08-1,49). Los resultados encontrados son sugestivos en lo que se refiere a la contribución conjunta de las exposiciones ambientales, y no sólo individualizadas, en el desarrollo de las leucemias en la infancia. Siendo apoyados por evidencias en la literatura especializada de que el proceso de carcinogénesis, en general, y/o de la leucemogénesis en particular, resultan de efectos de múltiples mutaciones relacionadas a exposiciones ambientales conjuntas. This study aims to explore the unapparent relations that several factors related to environmental exposure and individual characteristics existing in our environment may have with the process of developing childhood leukemia. From a database obtained from a clinical and epidemiological hospital-based, case-control study on risk factors for childhood leukemia, an exploratory multivariate analysis was performed using principal component analysis and factor analysis. This research is part of a national multicenter study that included 292 cases of leukemia in children aged 0 to 12 years and 541 controls of the same age, hospitalized for non-neoplastic causes in general hospitals near the centers the cases originated in. Information on selected environmental exposure was obtained in interviews with the mothers of both cases and controls by means of a standardized questionnaire. The model with the greatest explanatory power for the variance observed in the data analyzed was of approximately 52%. Three factors were considered most appropriate for predicting leukemogenesis in childhood, each including variables with factor loadings greater than 0.6: factor "conditions related to chemical exposures during pregnancy", which explained 20% of the final variance and included the variables pesticide exposure, exposure to solvents and paint exposure in pregnancy; factor "lifestyle habits during pregnancy" explained 17% of the variance and included exposure to hair dyes and cosmetics for hair straightening; and factor "use of health services during pregnancy", which explained 15% of the variance and included the variables type of delivery (vaginal or caesarean) and use of radiography in pregnancy. Logistic regression analysis revealed a statistically significant association between the development of leukemia in childhood and maternal history of chemical exposure during pregnancy (OR=1.36, 95% CI=1.16-1.59) and use of health services during pregnancy (OR=1.27, 95% CI=1.08-1.49). The results indicate the joint contribution of not just individual but environmental exposure in the development of leukemia in childhood, and are supported by evidence in the literature that the process of carcinogenesis in general and of leukemogenesis in particular, result from effects of multiple mutations related to joint environmental exposure.

Objectives: To analyze trends in childhood leukemia mortality in the state of Rio de Janeiro, Brazil, between 1980 and 2006. Method: Gender-stratified leukemia mortality data for children aged < 15 years from 1980 to 2006 were retrieved from the Brazilian Mortality Information System for the state of Rio de Janeiro. Data were stratified by place of death (city of Rio de Janeiro proper, the state capital; Rio de Janeiro Metropolitan Region, excluding the capital; and rest of the state). Leukemia deaths were defined according to death certificate ICD-9 and ICD-10 coding (for deaths occurring in 1980-1995 and 1996-2006 respectively). Leukemia mortality rates were calculated by age and calendar year and age-adjusted to a standard world population. Polynomial linear regression with a 5% significance level was used to evaluate mortality trends in the study regions. Results: The three studied regions revealed similar trends, with a continuous downward pattern; the most substantial decline was detected in the municipality of Rio de Janeiro (city proper). In all studied areas, leukemia mortality was highest among males. Conclusions: A downward trend in childhood leukemia mortality was detected throughout the state of Rio de Janeiro. The most pronounced reduction occurred in the state capital.

Objectives. To investigate the association between the maternal alcohol consumption during pregnancy and early age leukemia (EAL) in offspring.Methods. Datasets were analyzed from a case-control study carried out in Brazil during 1999–2007. Data were obtained by maternal interviews using a standardized questionnaire. The present study included 675 children (193 acute lymphoid leukemia (ALL), 59 acute myeloid leukemia (AML), and 423 controls). Unconditional logistic regression was performed, and adjusted odds ratios (adj. OR) on the association between alcohol consumption and EAL were ascertained.Results. Alcohol consumption was reported by 43% of ALL and 39% of AML case mothers and 35.5% of controls’. Beer consumption before and during pregnancy was associated with ALL in crude analysis (OR = 1.54, 95% CI, 1.08–2.19), although in adjusted analysis no statistical significance was found. For weekly intake of ≤1 glass (adj. OR = 1.30, 95% CI, 0.71–2.36) and ≥1 glass/week (adj. OR = 1.47, 95% CI, 0.88–2.46) a potential dose-response was observed (Ptrend < 0.03).Conclusion. This study failed to support the hypothesis of an increased risk of EAL associated with maternal alcohol intake during pregnancy, neither with the interaction with tobacco nor with alcohol consumption.

Childhood leukemia etiology and mainly the interactions of genetic and environmental risk factors remains largely unexplored. This national hospital-based case-control study was carried out in Brazil among children aged 0-23 months who were recruited at cancer and general hospitals in 13 states. Maternal medicine intake during pregnancy including analgesic intake was assessed by face-to-face interviews with the mothers of 231 leukemia patients and 411 controls. Unconditional logistic regression was used to ascertain crude and adjusted odds ratios (ORs) and their 95% confidence intervals (CIs) for the association between maternal analgesic use during pregnancy and early age leukemia. Acetaminophen use during the first trimester of pregnancy showed an OR=0.39 (95% CI 0.17-0.93) for acute lymphocytic leukemia and an OR=0.37 (95% CI 0.16-0.88) for use in the second trimester. For acute myeloid leukemia an OR=0.11 (95% CI 0.02-0.97) was found following acetaminophen use in the second trimester. For acute lymphocytic leukemia the exclusive use of dipyrone during preconception showed an OR=1.63 (95% CI 1.06-2.53) and dipyrone intake during lactation showed an OR=2.00 (95% CI 1.18-3.39). These results suggest that acetaminophen use during pregnancy may protect against development of early age leukemia in the offspring whereas dipyrone use may act as a risk factor for such an outcome. © 2015 Wolters Kluwer Health Inc. All rights reserved.

Background: Cigarette smoking has been associated with acute myeloid leukemia but hypothesis on the association between maternal smoking during pregnancy and childhood leukemia is unclear. Objectives: To investigate the association between maternal exposure to tobacco smoking during pregnancy and early age (< 2 yr.) leukemia (EAL). Methods: A hospital-based multicenter case-control study aiming to explore EAL risk factors was carried out in Brazil during 1999-2007. Data were collected by direct interview with the biological mothers using a standardized questionnaire. The present study included 675 children, being 193 acute lymphoblastic leukemia (ALL), 59 acute myeloid leukemia (AML), and 423 controls, being the latter age frequency matched and paired by area of residence with the cases. Unconditional logistic regression was performed, and odds ratios (OR) on the association between tobacco smoking (3 months before pregnancy, during pregnancy, and 3 months after delivery) and EAL were ascertained after adjustment for selected variables (maternal age at birth and education, birth weight, infant skin color, and oral contraceptives use during pregnancy).Results: Smoking was reported by 17.5% of case mothers and 20.6% of controls´. Among women who reported to have smoked 20 or more cigarettes during the index pregnancy, an adjusted OR = 5.28 (95% C.I. 1.40-19.95) for ALL was observed. Heavy smoking during breastfeeding yielded an adjusted risk estimate for ALL, OR = 7.78 (95% C.I. 1.33-45.5). No dose-response effect was observed according to smoking exposure during pregnancy and EAL. An association between secondhand smoking during pregnancy or breastfeeding was not observed. Conclusion: An association between maternal smoking and AAL in the offspring was restricted to women who have reported an intense exposure to tobacco smoke during pregnancy and breastfeeding.

Background and Aims: Childhood leukemia is a rare hematological neoplasm and several factors related to environmental exposures and individual characteristics existing in our environment may have o...

Background and Aims: Infant leukemia (IL) is a rare hematological neoplasm associated with MLL gene rearrangements. Maternal exposures during pregnancy to pesticides, hormones, dipyrone, and topois...

The aim of this study was to explore the unapparent relationships that several factors related to environmental exposures and individual characteristics existing in our environment seem to be involved with childhood leukaemia. From a database of clinical and epidemiological data obtained from hospital-based multicenter case-control study on risk factors for childhood leukaemia, exploratory multivariate analysis was performed the principal component and factor analysis. Further, an unconditional logistic regression was carried out aiming to ascertain the magnitude of association between the selected factors, and their composing variables, with childhood leukaemia. The model displaying the highest power explained 52% of the total variance, including three factors, each one of the showing factors loadings higher than 0.6: “conditions related to chemical exposure during pregnancy”, which explained 20% of the variance; “lifestyle exposures”, such as smoking and hair dyes and hair cosmetics use during pregnancy, explaining 17% of the total variance; and “consumption of health services during pregnancy”, such as x-rays and delivery type (cesarean or vaginal delivery), explaining 15% of the total variance. Logistic modelling revealed statistically significant association between childhood leukaemia and chemical exposure during pregnancy (OR=1.36; 95% CI 1.16 to 1.59), and also with consumption of health services during pregnancy (OR=1.27; 95% CI 1.08 to 1.49). The observed results are suggestive of the contribution of environmental exposures to childhood leukaemia development, not just individually, which has been supported by the literature according to carcinogenesis in general, and to leukaemogenesis in particular, as resulting from several mutations triggered by joint environmental exposures.