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Objective To evaluate the relationship between birth weight (along with a variety of pre and perinatal characteristics) and the risk of paediatric Hodgkin lymphoma (HL) diagnosed at age <20 years. Method We linked California statewide birth records from 1978–2009 and cancer diagnosis data from 1988–2011 to conduct a population-based case–control study with 1216 cases and 4485 controls (matched on birth month and year, sex, and race/ethnicity). Conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (95% CI) of paediatric HL overall and by age of diagnosis, controlling for other perinatal factors. Results Compared to children with a normal birth weight (2500–3999 g), those who had a high birth weight (≥4000 g) had an increased risk of paediatric HL overall (OR = 1.23, 95% CI: 1.02–1.48) after adjusting for birth order, maternal age at the time of delivery, and paternal age at the time of delivery. The magnitude of association appeared larger for subgroups of children whose age of diagnosis was 0–10 years (OR = 1.56, 95% CI: 1.04–2.24) or 15–19 years (OR = 1.43, 95% CI: 1.11–1.83), while no association was observed in 11–14 year olds. Compared with firstborn children, those who were third or higher in birth order had a reduced risk of paediatric HL overall (OR = 0.80, 95% CI: 0.67–0.95), and this association also varied by age of diagnosis. Conclusions In this study with the largest number of paediatric HL cases, high birth weight was associated with an increased disease risk for most but not all ages of diagnosis. The different findings by age of diagnosis regarding both birth weight and birth order underscore the importance to stratify paediatric HL by age at diagnosis in future etiological investigations. [ABSTRACT FROM AUTHOR]

Background: Incidence rates of thyroid cancer in children and young adults (age 0–19 years) have nearly doubled over a recent 15-year period in the United States. Children with thyroid cancer may require long-term therapy and surveillance and are at greater risk for second primary malignancies. High-dose exposure to ionizing radiation is the only known nongenetic risk factor; the vast majority of cases have an unknown etiology. Methods: We conducted a population-based nested case-control study to evaluate the relationship between a range of birth characteristics and the risk of pediatric thyroid cancer. Using linked birth records and cancer registry data from California, we included 1012 cases who were diagnosed with first primary thyroid cancer at the age of 0–19 years from 1988 to 2015 and 50,600 birth-year matched controls (1:50 case to control ratio). We estimated adjusted odds ratios (OR) and 95% confidence intervals (CI) by using multivariable logistic regression models applied to the full population and stratified by thyroid cancer subtypes (papillary and follicular), race/ethnicity (white and Hispanic), and age at diagnosis (0–14 and 15–19 years). Results: Hispanic ethnicity (OR: 1.20 [CI 1.01–1.42]), higher birth weight (OR: 1.11 [CI 1.04–1.18] per 500g), and higher maternal education (13–15 years OR: 1.35 [CI 1.09–1.68], 16+ years OR: 1.35 [CI 1.07–1.71]) were associated with an increased risk of pediatric thyroid cancer, while male sex (OR: 0.21 [CI 0.18–0.25]) and higher birth order (third or higher OR: 0.81 [CI 0.68–0.98]) were associated with a decreased risk. Some heterogeneity was observed across subtype, most notably an elevated OR with higher birth order for follicular thyroid cancer, in contrast to the reduced risk for this category among papillary thyroid cancer cases (p-value for interaction = 0.01). Hispanic ethnicity was a risk factor for papillary, but not follicular thyroid cancer (p-value for interaction = 0.07). Conclusions: In this population-based study of birth characteristics and pediatric thyroid cancer, we identified several important risk factors for pediatric thyroid cancer, including female sex, Hispanic ethnicity, higher birth weight, higher maternal educational attainment, and lower birth order. Our data provide new areas for replication and investigation of biological mechanisms for this poorly understood malignancy. [ABSTRACT FROM AUTHOR]