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Objective: To assess prenatal air toxics exposure and risk for childhood germ cell tumors (GCTs) by histological subtype (yolk sac tumor and teratoma)., Methods: In this case-control study, GCT cases less than 6 years (n = 243) identified from California Cancer Registry records were matched by birth year to cancer-free population controls (n = 147,100), 1984 to 2013. Routinely monitored air toxic exposures were linked to subjects' birth address. Logistic regression estimated GCT risks per interquartile range increase in exposure., Results: Prenatal exposure to various highly-correlated, traffic-related air toxics during the second trimester increased GCT risk, particularly 1,3-butadiene (odds ratio [OR] = 1.51; 95% confidence interval [CI] = 1.01, 2.26) and meta/para-xylene (OR = 1.56; 95% CI = 1.10, 2.21). Analyses by subtype indicated elevated ORs for yolk sac tumors but not teratomas., Conclusion: Our estimated ORs are consistent with positive associations between some prenatal traffic-related air toxics and GCT risk, notably yolk sac tumors.

Studies of environmental exposures and childhood cancers that rely on records often only use maternal address at birth or address at cancer diagnosis to assess exposures in early childhood, possibly leading to exposure misclassification and questionable validity due to residential mobility during early childhood. Our objective was to assess patterns and identify factors that may predict residential mobility in early childhood, and examine the impact of mobility on early childhood exposure assessment for agriculturally applied pesticides and childhood cancers in California. We obtained the addresses at diagnosis of all childhood cancer cases born in 1998-2011 and diagnosed at 0-5 years of age (n = 6478) from the California Cancer Registry (CCR), and their birth addresses from linked birth certificates. Controls were randomly selected from California birth records and frequency matched (20:1) to all cases by year of birth. We obtained residential histories from a public-record database LexisNexis for both case (n = 3877 with age at diagnosis 1-5 years) and control (n = 99,262) families. Logistic regression analyses were conducted to assess the socio-demographic factors in relation to residential mobility in early childhood. We employed a Geographic Information System (GIS)-based system to estimate children's first year of life exposures to agriculturally applied pesticides based on birth vs diagnosis address or residential histories based upon Lexis-Nexis Public Records and assessed agreement between exposure measures using Spearman correlations and kappa statistics. Over 20% of case and control children moved in their first year of life, and 55% of children with cancer moved between birth and diagnosis. Older age at diagnosis, younger maternal age, lower maternal education, not having a Hispanic ethnic background, use of public health insurance, and non-metropolitan residence at birth were predictors of higher residential mobility. There was moderate to strong correlation (Spearman correlation = 0.76-0.83) and good agreement (kappa = 0.75-0.81) between the first year of life exposure estimates for agricultural pesticides applied within 2 km of a residence relying on an address at birth or at diagnosis or LexisNexis addresses; this did not differ by outcome status, but agreement decreased with decreasing buffer size, and increasing distance moved or age at diagnosis. These findings suggest that residential addresses collected at one point in time may represent residential history in early childhood to a reasonable extent; nevertheless, they exposure misclassification in the first year of life remains an issue. Also, the highest proportion of women not captured by LexisNexis were Hispanic women born in Mexico and those living in the lowest SES neighborhoods, i.e. possibly those with the higher environmental exposures, as well as younger women and those with less than high school education. Though LexisNexis only captures a sub-population, its data may be useful for augmenting address information and assessing the extent of exposure misclassification when estimating environmental exposures in large record linkage studies. Future research should investigate how to correct for exposure misclassification introduced by residential mobility that is not being captured by records., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Objectives Recent meta-analyses suggest a physical activity health paradox: high levels of occupational physical activity (OPA) increase cardiovascular disease (CVD) risk, while leisure-time physical activity (LTPA) decreases risk. However, studies of women and cerebrovascular disease are limited. This report examines physical activity effects on stroke and transient ischemic attack (TIA) among working women in the United States. Methods OPA history, health status, and lifestyle were assessed by baseline interviews of 31 270 employed Sister Study participants aged 35-74 years. OPA was assessed at six intensity levels (lowest: "mostly sitting"); the highest three were combined as "high intensity work." Independent OPA and LTPA effects on 6-year cerebrovascular disease incidence were estimated in adjusted Cox proportional hazard models. Results Stroke (N=441) and TIA (N=274) risk increased with more standing and higher intensity work at current and longest held job. Compared with mostly sitting, high intensity work at the current job increased TIA risk by 57% [hazard ratio (HR) 1.57, 95% confidence interval (CI) 1.04-2.38]. High intensity OPA at the longest held job increased risk for stroke by 44% (HR 1.44; 95% CI 1.08-1.93). Among women with CVD, sitting and standing equally, especially at the current job, increased risks up to two-fold (TIA HR 1.98, 95% CI 1.10-3.55) compared with mostly sitting at work. LTPA showed inverse associations. Conclusions Higher intensity levels of OPA increased stroke and TIA risks, while LTPA decreased risks; results corroborate the physical activity health paradox for women and cerebrovascular disease. More standing at work increased cerebrovascular disease risks, especially for women with CVD.

Background: Melanoma, the deadliest form of skin cancer, is the second most common cancer diagnosed before age 30. Little is known about potentially modifiable or intervenable risk factors specific to developing melanoma at a young age. The objective was to determine if high birth weight or higher early-life ultraviolet (UV) radiation exposure would be associated with increased risk of melanoma in young patients., Methods: Population-based, case-control study of 1,396 cases of melanoma diagnosed before age 30 in 1988-2013 and 27,920 controls, obtained by linking cancer registry data to birth records in California., Results: High birth weight (>4,000 g) was associated with 19% higher risk of melanoma (OR = 1.19; 95% CI = 1.02, 1.39), while low birth weight (<2,500 g) was associated with 41% lower risk (OR = 0.59; 95% CI = 0.43, 0.82), compared with normal birth weight (2,500-4,000 g); dose-response per 1,000 g increase was also evident (OR = 1.24; 95% CI = 1.13, 1.36). All quartiles of birthplace UV greater than the lowest quartile were associated with increased melanoma risk. The strongest relation between birthplace UV and melanoma was for 15-19 years of age at diagnosis., Conclusions: High birth weight and high early-life UV exposure may be important independent risk factors for melanoma diagnosis before age 30. The implication is that adopting skin-protective behaviors as early as infancy could be important for primary prevention of melanoma in younger people. However, research that accounts for early-life behavioral patterns of skin protection during infancy is needed to advance our understanding of how birth weight and early-life UV may influence the development of early-onset melanoma.

Advanced parental age has been associated with adverse health effects in the offspring including childhood (0-14 years) acute lymphoblastic leukemia (ALL), as reported in our meta-analysis of published studies. We aimed to further explore the association using primary data from 16 studies participating in the Childhood Leukemia International Consortium. Data were contributed by 11 case-control (CC) studies (7919 cases and 12,942 controls recruited via interviews) and five nested case-control (NCC) studies (8801 cases and 29,690 controls identified through record linkage of population-based health registries) with variable enrollment periods (1968-2015). Five-year paternal and maternal age increments were introduced in two meta-analyses by study design using adjusted odds ratios (OR) derived from each study. Increased paternal age was associated with greater ALL risk in the offspring (OR CC 1.05, 95% CI 1.00-1.11; OR NCC 1.04, 95% CI 1.01-1.07). A similar positive association with advanced maternal age was observed only in the NCC results (OR CC 0.99, 95% CI 0.91-1.07, heterogeneity I 2  = 58%, p = 0.002; OR NCC 1.05, 95% CI 1.01-1.08). The positive association between parental age and risk of ALL was most marked among children aged 1-5 years and remained unchanged following mutual adjustment for the collinear effect of the paternal and maternal age variables; analyses of the relatively small numbers of discordant paternal-maternal age pairs were not fully enlightening. Our results strengthen the evidence that advanced parental age is associated with increased childhood ALL risk; collinearity of maternal with paternal age complicates causal interpretation. Employing datasets with cytogenetic information may further elucidate involvement of each parental component and clarify underlying mechanisms.

Background: Prenatal exposure to air pollution and smoking increases the risk of pregnancy complications and adverse birth outcomes, but pathophysiologic mechanisms are still debated. Few studies to date have examined the influence of air pollution on uterine vascular resistance and no studies have examined the independent impact of these exposures. We aimed to assess the impact of prenatal exposure to traffic-related air pollution and smoking on uterine vascular resistance., Methods: Our study included 566 pregnant women recruited between 1993 and 1996 in Los Angeles who completed visits at three gestational ages. Information on smoking was collected and uterine vascular resistance was measured at each visit by Doppler ultrasound. We calculated three resistance indices: the resistance index (RI), the pulsatility index (PI), and the systolic/diastolic (S/D) ratio. We estimated exposure to NO 2 at the home address of the mother using a land use regression (LUR) model and to NO x using CALINE4 air dispersion modeling. We used generalized linear mixed models to estimate the effects of air pollution and smoking on uterine vascular resistance indices., Results: LUR-derived NO 2 and CALINE4-derived NO x exposure increased the risk of high uterine artery resistance in late pregnancy. Smoking during pregnancy also increased the risk of higher uterine resistance and contributed to bilateral notching in mid-pregnancy., Conclusion: Our results suggest that uterine vascular resistance is a mechanism underlying the association between smoking and air pollution, and adverse birth outcomes., Competing Interests: The authors declare they have no actual or potential competing financial interests.

Objectives: We examined associations between parental occupational chemical exposures up to 10 years before conception and the risk of sporadic retinoblastoma among offspring., Methods: In our multicentre study on non-familial retinoblastoma, parents of 187 unilateral and 95 bilateral cases and 155 friend controls were interviewed by telephone. Exposure information was collected retroactively through a detailed occupational questionnaire that asked fathers to report every job held in the 10 years before conception, and mothers 1 month before and during the index pregnancy. An industrial hygienist reviewed all occupational data and assigned an overall exposure score to each job indicating the presence of nine hazardous agents., Results: We estimated elevated ORs for unilateral and bilateral retinoblastoma among offspring of fathers who were exposed to polycyclic aromatic hydrocarbons or paints in the 10 years before conception. However, only for exposure to paints did confidence limits exclude the null for bilateral disease (OR: 8.76, 95% CI: 1.32 to 58.09). Maternal prenatal exposure to at least one of the nine agents was related to increased risk of unilateral disease in their children (OR: 5.25, 95% CI: 1.14 to 24.16). Fathers exposed to at least one of the nine agents and who were ≥30 years of age were at increased risk of having a child diagnosed with bilateral retinoblastoma (OR: 6.59, 95% CI: 1.34 to 32.42)., Conclusions: Our results suggest a role for several hazardous occupational exposures in the development of childhood retinoblastoma., Competing Interests: Competing interests: None declared., (© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Purpose: We aimed to examine the influence of pre-pregnancy diabetes, pre-pregnancy body mass index (BMI), gestational diabetes, and gestational weight gain on childhood cancer risk in offspring., Methods: We identified cancer cases (n = 11,149) younger than age 6 years at diagnosis from the California Cancer Registry registered between 1988 and 2013. Controls (n = 270,147) were randomly sampled from California birth records, and frequency matched by year of birth to all childhood cancers during the study period. Exposure and covariate information were extracted from birth records. Unconditional logistic regression models were generated to assess the importance of pre-pregnancy diabetes, pre-pregnancy BMI, gestational diabetes, and gestational weight gain on childhood cancer risk., Results: We observed increased risks of acute lymphoblastic leukemia and Wilms' tumor in children of mothers with pre-pregnancy diabetes [odds ratio (OR) 95 % confidence interval (CI) 1.37 (1.11, 1.69); OR (95 % CI) 1.45 (0.97, 2.18), respectively]. When born to mothers who were overweight prior to pregnancy (BMI 25-<30), children were at increased risk of leukemia [OR (95 % CI) 1.27 (1.01, 1.59)]. Insufficient gestational weight gain increased the risk of acute myeloid leukemia [OR (95 % CI) 1.50 (0.92, 2.42)] while excessive gestational weight gain increased the risk of astrocytomas [OR (95 % CI) 1.56 (0.97, 2.50)]. No associations were found between gestational diabetes and childhood cancer risk in offspring., Conclusions: We estimated elevated risks of several childhood cancers in the offspring of mothers who had diabetes and were overweight prior to pregnancy, as well as mothers who gained insufficient or excessive weight. Since few studies have focused on these factors in relation to childhood cancer, replication of our findings in future studies is warranted.

Smoking during pregnancy is a plausible risk factor for childhood cancer, yet previous studies have yielded conflicting results, and few prospective studies have been published. Data on maternal smoking were obtained from California birth certificates. We linked California birth certificates (births 2007-2011) with California Cancer Registry records for childhood cancer cases (diagnosed January 2007-September 2013) that were ages 5 or younger at diagnosis (N cases = 2,021). Controls (N = 40,356) were frequency-matched by birth year and randomly selected from birth certificate records. We used unconditional logistic regression to obtain odds ratios (OR) and 95% confidence intervals (CI) to assess the association between smoking during pregnancy and childhood cancer. We observed positive associations for gliomas (OR = 1.8, 95% CI: 1.0-3.4) and retinoblastoma (OR = 3.0, 95% CI: 1.4-6.6), particularly bilateral retinoblastoma (OR = 9.4, 95% CI 3.6-24.7) with maternal smoking in pregnancy. Maternal smoking during pregnancy may be a risk factor for retinoblastoma and certain types of childhood brain tumors., (© 2016 UICC.)

Background: Little is known about the influence of environmental factors on the etiology of childhood brain tumors., Objectives: We examined risks for brain tumors in children after prenatal and infant exposure to monitored ambient air toxics., Methods: We ascertained all cases of medulloblastoma, central nervous system primitive neuroectodermal tumor (PNET), and astrocytoma before 6 years of age diagnosed in 1990-2007 from the California Cancer Registry and selected controls randomly from birth rolls matched by birth year. Exposures to air toxics during pregnancy/infancy for 43 PNET, 34 medulloblastoma, and 106 astrocytoma cases and 30,569 controls living within 5 mi of a monitor were determined. With factor analysis we assessed the correlational structures of 26 probable carcinogenic toxics, and estimated odds ratios by brain tumor type in logistic regression models., Results: PNETs (≤ 38 cases) were positively associated with interquartile range (IQR) increases in prenatal exposure to acetaldehyde [odds ratio (OR) = 2.30; 95% CI: 1.44, 3.67], 1,3-butadiene (OR = 2.23; 95% CI: 1.28, 3.88), benzene, and toluene; and with IQR increases in exposure during the first year of life to ortho-dichlorobenzene (OR = 3.27; 95% CI: 1.17, 9.14), 1,3-butadiene (OR = 3.15; 95% CI: 1.57, 6.32), and benzene. All exposures except ortho-dichlorobenzene loaded on the same factor. Medulloblastoma (≤ 30 cases) was associated with prenatal exposure to polycyclic aromatic hydrocarbons (PAHs combined: OR = 1.44; 95% CI: 1.15, 1.80). Exposures to lead and some PAHs during the first year of life were positively associated with astrocytoma, but the confidence intervals included the null value (e.g., for lead, OR = 1.40; 95% CI: 0.97, 2.03)., Conclusions: Our data suggest that in utero and infancy exposures to air toxics generated by industrial and road traffic sources may increase the risk of PNET and medulloblastoma, with limited support for increased risks for astrocytoma in children up to age 6., Citation: von Ehrenstein OS, Heck JE, Park AS, Cockburn M, Escobedo L, Ritz B. 2016. In Utero and early-life exposure to ambient air toxics and childhood brain tumors: a population-based case-control study in California, USA. Environ Health Perspect 124:1093-1099; http://dx.doi.org/10.1289/ehp.1408582.

Importance: The Hispanic epidemiologic paradox is the phenomenon that non-US-born Hispanic mothers who immigrate to the United States have better pregnancy outcomes than their US-born counterparts. It is unknown whether this advantage extends to childhood cancer risk., Objective: To determine whether the risk for childhood cancers among Hispanic children varies by maternal birthplace., Design, Setting, and Participants: In this population-based case-control study conducted in June 2015, cohort members were identified through California birth records of children born in California from January 1, 1983, to December 31, 2011. Information on cancer diagnoses was obtained from California Cancer Registry records from 1988 to 2012. Cases (n = 13 666) were identified from among children younger than 6 years in the California Cancer Registry and matched to California birth certificates. Control children (n = 15 513 718) included all other children born in California during the same period. Maternal birthplace and ethnic ancestry were identified from the birth certificate., Main Exposures: Maternal race/ethnicity and birthplace., Main Outcomes and Measures: We used Cox proportional hazards modeling to estimate hazard ratios (HRs) of childhood cancer., Results: Included in the study were 4 246 295 children of non-Hispanic white mothers (51.3% male), 2 548 822 children of US-born Hispanic mothers (51.0% male), and 4 397 703 children of non-US-born Hispanic mothers (51.0% male). Compared with children of non-Hispanic white mothers, the children of non-US-born Hispanic mothers had a reduced risk for glioma (HR, 0.50; 95% CI, 0.44-0.58), astrocytoma (HR, 0.43; 95% CI, 0.36-0.51), neuroblastoma (HR, 0.47; 95% CI, 0.40-0.54), and Wilms tumor (HR, 0.70; 95% CI, 0.59-0.82). For these cancer types, the risk estimates for children of US-born Hispanic mothers fell between those of the children of US-born white and non-US-born Hispanic mothers. Children of Mexican-born mothers had a higher risk of yolk sac tumors (HR, 1.46; 95% CI, 0.99-2.17), while children of US-born Hispanic mothers with ancestry from countries other than Mexico had a higher risk for unilateral retinoblastoma (HR, 2.03; 95% CI, 1.33-3.11)., Conclusions and Relevance: For several cancers, we observed differential risk by maternal place of birth. Examining the differences in health behaviors and environment between Hispanic groups may shed light on childhood cancer etiology.

We examined ambient exposure to specific air toxics in the perinatal period in relation to retinoblastoma development. Cases were ascertained from California Cancer Registry records of children diagnosed between 1990 and 2007 and matched to California birth certificates. Controls were randomly selected from state birth records for the same time period. We chose 27 air toxics for the present study that had been listed as possible, probable, or established human carcinogens by the International Agency for Research on Cancer. Children (103 cases and 30,601 controls) included in the study lived within 5 miles of an air pollution monitor. Using logistic regression analyses, we modeled the risk of retinoblastoma due to air toxic exposure, separately for exposures in pregnancy and the first year of life. With a per interquartile range increase in air toxic exposure, retinoblastoma risk was found to be increased with pregnancy exposure to benzene (OR=1.67, 95% CI: 1.06, 2.64) and other toxics which primarily arise from gasoline and diesel combustion: toluene, 1,3-butadiene, ethyl benzene, ortho-xylene, and meta/para-xylene; these six toxics were highly correlated. Retinoblastoma risk was also increased with pregnancy exposure to chloroform (OR=1.35, 95% CI: 1.07, 1.70), chromium (OR=1.29, 95% CI: 1.04, 1.60), para-dichlorobenzene (OR=1.24, 95% CI: 1.04, 1.49), nickel (OR=1.48, 95% CI: 1.08, 2.01), and in the first year of life, acetaldehyde (OR=1.62, 95% CI: 1.06, 2.48). Sources of these agents are discussed.

Purpose: Previous studies have suggested a role for parental diet in childhood cancer prevention, but there are few studies of retinoblastoma. The aim of this study was to examine the relation between maternal diet and unilateral retinoblastoma., Methods: A case-control study of 163 unilateral RB cases and 136 controls ascertained information on maternal diet during pregnancy using a standardized food frequency questionnaire. Logistic regression was used to assess the relation between retinoblastoma and food groups and dietary patterns., Results: We observed a negative association between retinoblastoma and intake of fruit [odds ratio (OR) 0.38, 95 % confidence interval (CI) 0.14-1.02]. Positive associations were seen with intake of cured meats (OR 5.07, 95 % CI 1.63-15.70) and fried foods (OR 4.89, 95 % CI 1.72-13.89). A food pattern of high fruits and vegetables and low fried food and sweets was negatively associated with disease (OR 0.75, 95 % CI 0.61-0.92)., Conclusion: Our study provides preliminary evidence that mothers who consume diets higher in fruit and lower in fried foods and cured meats during pregnancy may reduce the risk of unilateral retinoblastoma in their offspring.

Leukemia is the most frequent malignant disease affecting children. To date, the etiology of childhood leukemia remains largely unknown. Few risk factors (genetic susceptibility, infections, ionizing radiation, etc.) have been clearly identified, but they appear to explain only a small proportion of cases. Considerably more uncertain is the role of other environmental risk factors, such as indoor and outdoor air pollution. We sought to summarize and quantify the association between traffic-related air pollution and risk of childhood leukemia, and further examined results according to method of exposure assessment, study quality, leukemia subtype, time period, and continent where studies took place. After a literature search yielded 6 ecologic and 20 case-control studies, we scored the studies based on the Newcastle-Ottawa Scale. The studies assessed residential exposure to pollutants from motorized traffic by computing traffic density in the neighboring roads or vicinity to petrol stations, or by using measured or modeled nitrogen dioxide and benzene outdoor air levels. Because heterogeneity across studies was observed, random-effects summary odds ratios (OR) and 95% confidence intervals (CI) were reported. Whenever possible we additionally conducted stratified analyses comparing acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). Limiting the analysis to high-quality studies (Newcastle-Ottawa Scale ≥ 7), those using traffic density as the exposure assessment metric showed an increase in childhood leukemia risk in the highest exposure category (OR = 1.07, 95% CI 0.93-1.24). However, we observed evidence of publication bias. Results for NO2 exposure and benzene showed an OR of 1.21 (95% CI 0.97-1.52) and 1.64 (95% CI 0.91-2.95) respectively. When stratifying by leukemia type, the results based upon NO2 were 1.21 (95% CI 1.04-1.41) for ALL and 1.06 (95% CI 0.51-2.21) for AML; based upon benzene were 1.09 (95% CI 0.67-1.77) for ALL and 2.28 (95% CI 1.09-4.75) for AML. Estimates were generally higher for exposures in the postnatal period compared to the prenatal period, and for European studies compared to North American studies. Overall, our results support a link between ambient exposure to traffic pollution and childhood leukemia risk, particularly due to benzene.

There are few established causes of leukemia, the most common type of cancer in children. Studies in adults suggest a role for specific environmental agents, but little is known about any effect from exposures in pregnancy to toxics in ambient air. In our case-control study, we ascertained 69 cases of acute lymphoblastic leukemia (ALL) and 46 cases of acute myeloid leukemia (AML) from California Cancer Registry records of children

Background: Epidemiologic studies indicate that infections in early childhood may protect against pediatric acute lymphoblastic leukemia (ALL)., Methods: We identified 3,402 ALL cases among children 0 to 5 years of age using the California Cancer Registry. From California birth records we randomly selected controls in a 20:1 ratio and frequency matched them to cases by birth year. We investigated markers of exposure to infections, including month of birth, timing of birth in relation to influenza and respiratory syncytial virus (RSV) seasons, and birth order based on data from California birth certificates and national infection surveillance systems., Results: We observed an increased risk of ALL for spring and summer births, and for those first exposed to an influenza or RSV season at nine to twelve months of age compared with those exposed during the first three months of life, and this association was stronger among first born children [odds ratios (OR), 1.44 and 95% confidence intervals (CI), 1.13-1.82, for influenza exposure at nine to twelve months of age]. Decreased risk was observed with increasing birth order among non-Hispanic whites but not Hispanics (OR, 0.76 and 95% CI, 0.59-096, for fourth or higher birth order among whites)., Conclusion: Our results support the hypothesis that infections in early childhood decrease risk of ALL., Impact: Our findings implicate early life exposure to infections as protective factors for ALL in young children., (©2014 American Association for Cancer Research.)

Objective: Our understanding of the influence of maternal race/ethnicity and nativity and childhood autistic disorder (AD) in African Americans/blacks, Asians, and Hispanics in the United States is limited. Phenotypic differences in the presentation of childhood AD in minority groups may indicate etiologic heterogeneity or different thresholds for diagnosis. We investigated whether the risk of developing AD and AD phenotypes differed according to maternal race/ethnicity and nativity., Methods: Children born in Los Angeles County with a primary AD diagnosis at ages 3 to 5 years during 1998-2009 were identified and linked to 1995-2006 California birth certificates (7540 children with AD from a cohort of 1,626,354 births). We identified a subgroup of children with AD and a secondary diagnosis of mental retardation and investigated heterogeneity in language and behavior., Results: We found increased risks of being diagnosed with AD overall and specifically with comorbid mental retardation in children of foreign-born mothers who were black, Central/South American, Filipino, and Vietnamese, as well as among US-born Hispanic and African American/black mothers, compared with US-born whites. Children of US African American/black and foreign-born black, foreign-born Central/South American, and US-born Hispanic mothers were at higher risk of exhibiting an AD phenotype with both severe emotional outbursts and impaired expressive language than children of US-born whites., Conclusions: Maternal race/ethnicity and nativity are associated with offspring's AD diagnosis and severity. Future studies need to examine factors related to nativity and migration that may play a role in the etiology as well as identification and diagnosis of AD in children., (Copyright © 2014 by the American Academy of Pediatrics.)

Background: The literature on traffic-related air pollution and childhood cancers is inconclusive, and little is known on rarer cancer types., Objectives: We sought to examine associations between childhood cancers and traffic-related pollution exposure., Methods: The present study included children < 6 years of age identified in the California Cancer Registry (born 1998-2007) who could be linked to a California birth certificate (n = 3,590). Controls were selected at random from California birthrolls (n = 80,224). CAlifornia LINE Source Dispersion Modeling, version 4 (CALINE4) was used to generate estimates of local traffic exposures for each trimester of pregnancy and in the first year of life at the address indicated on the birth certificate. We checked our findings by additionally examining associations with particulate matter (≤ 2.5 μm in aerodynamic diameter; PM2.5) pollution measured by community-based air pollution monitors, and with a simple measure of traffic density., Results: With unconditional logistic regression, a per interquartile range increase in exposure to traffic-related pollution during the first trimester (0.0538 ppm carbon monoxide, estimated using CALINE4) was associated with acute lymphoblastic leukemia [ALL; first trimester odds ratio (OR) = 1.05; 95% CI: 1.01, 1.10]; germ cell tumors (OR = 1.16; 95% CI: 1.04, 1.29), particularly teratomas (OR = 1.26; 95% CI: 1.12, 1.41); and retinoblastoma (OR = 1.11; 95% CI: 1.01, 1.21), particularly bilateral retinoblastoma (OR = 1.16; 95% CI: 1.02, 1.33). Retinoblastoma was also associated with average PM2.5 concentrations during pregnancy, and ALL and teratomas were associated with traffic density near the child's residence at birth., Conclusions: We estimated weak associations between early exposure to traffic pollution and several childhood cancers. Because this is the first study to report on traffic pollution in relation to retinoblastoma or germ cell tumors, and both cancers are rare, these findings require replication in other studies.

Exposure to air pollution during pregnancy has been linked to the risk of childhood cancer, but the evidence remains inconclusive. In the present study, we used land use regression modeling to estimate prenatal exposures to traffic exhaust and evaluate the associations with cancer risk in very young children. Participants in the Air Pollution and Childhood Cancers Study who were 5 years of age or younger and diagnosed with cancer between 1988 and 2008 were had their records linked to California birth certificates, and controls were selected from birth certificates. Land use regression-based estimates of exposures to nitric oxide, nitrogen dioxide, and nitrogen oxides were assigned based on birthplace residence and temporally adjusted using routine monitoring station data to evaluate air pollution exposures during specific pregnancy periods. Logistic regression models were adjusted for maternal age, race/ethnicity, educational level, parity, insurance type, and Census-based socioeconomic status, as well as child's sex and birth year. The odds of acute lymphoblastic leukemia increased by 9%, 23%, and 8% for each 25-ppb increase in average nitric oxide, nitrogen dioxide, and nitrogen oxide levels, respectively, over the entire pregnancy. Second- and third-trimester exposures increased the odds of bilateral retinoblastoma. No associations were found for annual average exposures without temporal components or for any other cancer type. These results lend support to a link between prenatal exposure to traffic exhaust and the risk of acute lymphoblastic leukemia and bilateral retinoblastoma.

Background: Hepatoblastoma is a malignant embryonal tumor typically diagnosed in children younger than five years of age. Little is known on hepatoblastoma etiology., Methods: We matched California Cancer Registry records of hepatoblastomas diagnosed in children younger than age 6 from 1988 to 2007 to birth records using a probabilistic record linkage program, yielding 261 cases. Controls (n=218,277), frequency matched by birth year to all cancer cases in California for the same time period, were randomly selected from California birth records. We examined demographic and socioeconomic information, birth characteristics, pregnancy history, complications in pregnancy, labor and delivery, and abnormal conditions and clinical procedures relating to the newborn, with study data taken from birth certificates., Results: We observed increased risks for hepatoblastoma among children with low [1500-2499 g, Odds Ratio (OR)=2.02, 95% confidence interval (CI) 1.29-3.15] and very low birthweight (<1500 g, OR=15.4, 95% CI 10.7-22.3), preterm birth <33 weeks (OR=7.27, 95% CI 5.00, 10.6), small size for gestational age (OR=1.75, 95% CI 1.25-2.45), and with multiple birth pregnancies (OR=2.52, 95% CI 1.54-4.14). We observed a number of pregnancy and labor complications to be related to hepatoblastoma, including preeclampsia, premature labor, fetal distress, and congenital anomalies., Conclusion: These findings confirm previously reported associations with low birthweight and preeclampsia. The relation with multiple birth pregnancies has been previously reported and may indicate a relation to infertility treatments., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Background: Studies have shown that higher solar UV radiation exposure (UVR) may be related to lower risk of some cancers in adults. Recently, an ecologic study reported lower risks of some cancers among children living in higher UVR cities and countries. In a large population-based case-control study in California, we tested the hypothesis that childhood cancers may be influenced by UVR., Methods: Cancers in children ages 0 to 5 years were identified from California Cancer Registry records for 1988 to 2007 and linked to birth certificate data. Controls were sampled from the birth certificates at a ratio of 20:1. Based on birth address, we assigned UVR exposure in units of Watt-hours/m(2) using a geostatistical exposure model developed with data from the National Solar Radiation Database., Results: For cases with UVR exposure of 5,111 Watt-hours/m(2) or above, we estimated a reduction in odds of developing acute lymphoblastic leukemia (OR: 0.89, 95% CI: 0.81-0.99), hepatoblastoma (OR: 0.69, 95% CI: 0.48-1.00), and non-Hodgkin's lymphoma (OR: 0.71, 95% CI: 0.50-1.02) adjusting for mother's age, mother's race, and child's year of birth. We also observed a small increase in odds for intracranial/intraspinal embryonal tumors (OR: 1.29, 95% CI: 1.01-1.65)., Conclusions: Our findings suggest that UVR during pregnancy may decrease the odds of some childhood cancers. Future studies should explore additional factors that may be correlated with UVR exposure and possibly include biomarkers of immune function and vitamin D., Impact: This study shows protective associations of UVR with some childhood cancers.

Background: Rhabdoid tumors are a rare and aggressive cancer subtype which is usually diagnosed in early childhood. Little is known about their etiology. The purpose of this study was to describe the epidemiology of rhabdoid tumors and examine their relation to perinatal characteristics., Methods: We identified 44 atypical teratoid/rhabdoid tumors (AT/RT) of the central nervous system (CNS) and 61 rhabdoid sarcomas (renal and extra-renal non-CNS tumors) from California Cancer Registry records of diagnoses 1988-2007 among children <6 years of age. We randomly selected 208,178 controls from California birthrolls. Multivariable logistic regression was used to examine associations between rhabdoid tumors and perinatal characteristics., Results: After adjustment for demographic characteristics, low birthweight (<2,500 g) strongly increased risk for developing both rhabdoid sarcomas (OR = 2.43, 95% CI 1.09, 5.41) and AT/RT (OR = 2.99, 95% CI 1.31, 6.84). Both preterm delivery (<37 weeks gestation, OR = 2.63, 95% CI 1.34, 5.17) and late term delivery (>42 weeks, OR = 3.66, 95% CI 1.54, 8.71) also increased risk of rhabdoid sarcomas. Rhabdoid sarcoma cases (OR = 3.08, 95% CI 1.11, 8.55) and AT/RT cases (OR = 3.16, 95% CI 1.23, 8.13) also were more likely to be multiple births., Conclusion: The excess of twin pregnancies may suggest an association with infertility treatments. This is the first population-based epidemiologic study to examine these rare tumors., (Copyright © 2012 Wiley Periodicals, Inc.)

Purpose: The etiology of retinoblastoma remains poorly understood. In the present study, we examined associations between perinatal factors and retinoblastoma risk in California children., Methods: We identified 609 retinoblastoma cases (420 unilateral, 187 bilateral, and 2 with laterality unknown) from California Cancer Registry records of diagnoses 1988-2007 among children < 6 years of age. We randomly selected 209,051 controls from California birth rolls. The source of most study data was birth certificates. Multivariable logistic regression was used to examine associations between retinoblastoma and perinatal characteristics., Results: Bilateral retinoblastoma was associated with greater paternal age [for fathers over 35, crude odds ratio (OR) = 1.73, 95 % confidence interval (CI) 1.20, 2.47] and with twin births (OR = 1.93, 95 % CI 0.99, 3.79). Among unilateral cases, we observed an increased risk among children of US-born Hispanic mothers (OR = 1.34, 95 % CI 1.01, 1.77) while a decreased risk was observed for infants born to mothers with less than 9 years of education (OR = 0.70, 95 % CI 0.49, 1.00), a group that consisted primarily of mothers born in Mexico. We observed that maternal infection in pregnancy with any STD (OR = 3.59, 95 % CI 1.58, 8.15) was associated with bilateral retinoblastoma., Conclusions: This study supports the findings of previous investigations reporting associations between parental age, HPV infection, and retinoblastoma.

Background: Betel quid is chewed by 600 million people worldwide and it has been linked to obesity and cardiovascular disease. The purpose of our study was to examine the prevalence and predictors of betel quid chewing in a rural area of Bangladesh, and determine its effects on body mass index (BMI) and blood pressure., Methods: In this population-based prospective study, we analysed data on 19 934 Bangladeshi adults. Linear and multivariate logistic regression was used to determine the socio-demographic predictors of betel quid chewing and the effect of betel quid on change in BMI and on systolic and diastolic blood pressure, pulse pressure, arterial pressure, overweight or obesity, and hypertension., Results: At baseline, betel quid was chewed by 33.2% of the cohort (35.5% of men, 31.6% of women). In a subsample in which we collected methods of use, 17.5% chewed it without tobacco and 82.5% chewed it with tobacco. In multivariate analysis, betel quid chewing was associated with female sex, older age, tobacco smoking and lower socio-economic status, as measured by fewer years of formal education and not owning land. Betel quid was chewed more times per day among women and older persons. At follow-up, persons who chewed betel quid without tobacco had higher systolic blood pressure, diastolic blood pressure and arterial pressure in comparison with never users. After controlling for other explanatory variables, chewing betel quid without tobacco was associated with general hypertension [odds ratio (OR) 1.48, 95% confidence interval (CI) 1.04-2.10] and systolic hypertension (OR 1.55, 95% CI 1.01-2.37). We did not observe associations of betel quid chewing with BMI or overweight., Conclusions: Betel quid chewing is likely contributing to high blood pressure in Bangladesh, particularly among women.

Background: The countries of Central and Eastern Europe have among the highest worldwide rates of renal cell cancer (RCC). Few studies have examined whether genetic variation in xenobiotic metabolic pathway genes may modify risk for this cancer., Methods: The Central and Eastern Europe Renal Cell Cancer study was a hospital-based case-control study conducted between 1998 and 2003 across seven centers in Central and Eastern Europe. Detailed data were collected from 874 cases and 2053 controls on demographics, work history, and occupational exposure to chemical agents. Genes [cytochrome P-450 family, N-acetyltransferases,, Nad(p)h: quinone oxidoreductase I (NQO1), microsomal epoxide hydrolase (mEH), catechol-O-methyltransferase (COMT), uridine diphosphate-glucuronosyltransferase (UGT)] were selected for the present analysis based on their putative role in xenobiotic metabolism. Haplotypes were calculated using fastPhase. Odds ratios and 95% confidence intervals were estimated by unconditional logistic regression adjusted for country of residence, age, sex, smoking, alcohol intake, obesity, and hypertension., Results: We observed an increased risk of RCC with one SNP. After adjustment for multiple comparisons it did not remain significant. Neither NAT1 nor NAT2 slow acetylation was associated with disease., Conclusion: We observed no association between this pathway and renal cell cancer.

We investigated the association between diet and head and neck cancer (HNC) risk using data from the International Head and Neck Cancer Epidemiology (INHANCE) consortium. The INHANCE pooled data included 22 case-control studies with 14,520 cases and 22,737 controls. Center-specific quartiles among the controls were used for food groups, and frequencies per week were used for single food items. A dietary pattern score combining high fruit and vegetable intake and low red meat intake was created. Odds ratios (OR) and 95% confidence intervals (CI) for the dietary items on the risk of HNC were estimated with a two-stage random-effects logistic regression model. An inverse association was observed for higher-frequency intake of fruit (4th vs. 1st quartile OR = 0.52, 95% CI = 0.43-0.62, p (trend) < 0.01) and vegetables (OR = 0.66, 95% CI = 0.49-0.90, p (trend) = 0.01). Intake of red meat (OR = 1.40, 95% CI = 1.13-1.74, p (trend) = 0.13) and processed meat (OR = 1.37, 95% CI = 1.14-1.65, p (trend) < 0.01) was positively associated with HNC risk. Higher dietary pattern scores, reflecting high fruit/vegetable and low red meat intake, were associated with reduced HNC risk (per score increment OR = 0.90, 95% CI = 0.84-0.97).

Background: Sexual contact may be the means by which head and neck cancer patients are exposed to human papillomavirus (HPV)., Methods: We undertook a pooled analysis of four population-based and four hospital-based case-control studies from the International Head and Neck Cancer Epidemiology (INHANCE) consortium, with participants from Argentina, Australia, Brazil, Canada, Cuba, India, Italy, Spain, Poland, Puerto Rico, Russia and the USA. The study included 5642 head and neck cancer cases and 6069 controls. We calculated odds ratios (ORs) of associations between cancer and specific sexual behaviours, including practice of oral sex, number of lifetime sexual partners and oral sex partners, age at sexual debut, a history of same-sex contact and a history of oral-anal contact. Findings were stratified by sex and disease subsite., Results: Cancer of the oropharynx was associated with having a history of six or more lifetime sexual partners [OR = 1.25, 95% confidence interval (CI) 1.01, 1.54] and four or more lifetime oral sex partners (OR = 2.25, 95% CI 1.42, 3.58). Cancer of the tonsil was associated with four or more lifetime oral sex partners (OR = 3.36, 95 % CI 1.32, 8.53), and, among men, with ever having oral sex (OR = 1.59, 95% CI 1.09, 2.33) and with an earlier age at sexual debut (OR = 2.36, 95% CI 1.37, 5.05). Cancer of the base of the tongue was associated with ever having oral sex among women (OR = 4.32, 95% CI 1.06, 17.6), having two sexual partners in comparison with only one (OR = 2.02, 95% CI 1.19, 3.46) and, among men, with a history of same-sex sexual contact (OR = 8.89, 95% CI 2.14, 36.8)., Conclusions: Sexual behaviours are associated with cancer risk at the head and neck cancer subsites that have previously been associated with HPV infection.

Background: Little is known about the carcinogenic potential of arsenic in areas with low to moderate concentrations of arsenic (< 100 microg/L) in drinking water., Objectives: We examined associations between arsenic and lung cancer., Methods: A population-based case-control study of primary incident lung cancer was conducted in 10 counties in two U.S. states, New Hampshire and Vermont. The study included 223 lung cancer cases and 238 controls, each of whom provided toenail clippings for arsenic exposure measurement by inductively coupled-plasma mass spectrometry. We estimated odds ratios (ORs) of the association between arsenic exposure and lung cancer using unconditional logistic regression with adjustment for potential confounders (age, sex, race/ethnicity, smoking pack-years, education, body mass index, fish servings per week, and toenail selenium level)., Results: Arsenic exposure was associated with small-cell and squamous-cell carcinoma of the lung [OR = 2.75; 95% confidence interval (CI), 1.00-7.57] for toenail arsenic concentration > or = 0.114 microg/g, versus < 0.05 microg/g. A history of lung disease (bronchitis, chronic obstructive pulmonary disease, or fibrosis) was positively associated with lung cancer (OR = 2.86; 95% CI, 1.39-5.91). We also observed an elevated risk of lung cancer among participants with a history of lung disease and toenail arsenic > or = 0.05 microg/g (OR = 4.78; 95% CI, 1.87-12.2) than among individuals with low toenail arsenic and no history of lung disease., Conclusion: Although this study supports the possibility of an increased risk of specific lung cancer histologic types at lower levels of arsenic exposure, we recommend large-scale population-based studies.