Background Though the association between parental age at child’s birth and the risk of childhood cancer has been previously investigated, the evidence to date is inconclusive and scarce for rarer cancer types. Methods Cancer cases (N=5,856) were selected from all children born from 1968–2014 and diagnosed from 1968–2015 in Denmark at less than 16 years of age listed in the nationwide Danish Cancer Registry. Cases were individually matched to controls (1:100) on sex and year of birth with a total of 585,594 controls randomly sampled from all live births in Denmark from the Danish Central Population Registry. Parental age at child’s birth was extracted from the Central Population Registry. Conditional logistic regression models were used to estimate odds ratios for the association between parental age at child’s birth and childhood cancer risk. Parental age was modeled as both categorical (referent group, parents aged 25–29) and continuous per 5-year increase in age. Results Offspring of older mothers were at an increased risk of acute lymphoblastic leukemia (ALL) [OR=1.10, 95% CI: (1.02, 1.19) per 5-year increase in age]. Older maternal age (40+) increased the risk of non-Hodgkin lymphoma (NHL) [OR=1.96, 95%CI: (1.12, 3.43)]. The risk of Wilms’ tumor also appeared elevated with older paternal age [OR=1.11, 95% CI: (0.97, 1.28) per 5-year increment in age]. Conclusion Older parental age was a risk factor for various childhood cancers in Danish children. Further investigation of the biological and social factors that may be contributing to these associations is warranted.

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 1988–2013. 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 was 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 (ALL) and Wilms’ tumor in children of mothers with pre-pregnancy diabetes [odds ratio (OR) =1.37, 95% confidence interval (CI): (1.11, 1.69), OR=1.45, 95% CI: (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=1.27, 95% CI: (1.01, 1.59)]. Insufficient gestational weight gain increased the risk of acute myeloid leukemia (AML) [OR=1.50 (95% CI: 0.92, 2.42)] while excessive gestational weight gain increased the risk of astrocytomas [OR=1.56, 95% CI: (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.

The parallel epidemics of childhood asthma and obesity over the past few decades have spurred research into obesity as a risk factor for asthma. However, little is known regarding the role of asthma in obesity incidence. We examined whether early-onset asthma and related phenotypes are associated with the risk of developing obesity in childhood.This study includes 21 130 children born from 1990 to 2008 in Denmark, France, Germany, Greece, Italy, The Netherlands, Spain, Sweden and the UK. We followed non-obese children at 3-4 years of age for incident obesity up to 8 years of age. Physician-diagnosed asthma, wheezing and allergic rhinitis were assessed up to 3-4 years of age.Children with physician-diagnosed asthma had a higher risk for incident obesity than those without asthma (adjusted hazard ratio (aHR) 1.66, 95% CI 1.18-2.33). Children with active asthma (wheeze in the last 12 months and physician-diagnosed asthma) exhibited a higher risk for obesity (aHR 1.98, 95% CI 1.31-3.00) than those without wheeze and asthma. Persistent wheezing was associated with increased risk for incident obesity compared to never wheezers (aHR 1.51, 95% CI 1.08-2.09).Early-onset asthma and wheezing may contribute to an increased risk of developing obesity in later childhood.

Purpose of Review Diabetes mellitus is a top contributor to the global burden of mortality and disability in adults. There has also been a slow, but steady rise in prediabetes and type 2 diabetes in youth. The current review summarizes recent findings regarding the impact of increased exposure to air pollutants on the type 2 diabetes epidemic. Recent Findings Human and animal studies provide strong evidence that exposure to ambient and traffic-related air pollutants such as particulate matter (PM), nitrogen dioxide (NO2), and nitrogen oxides (NOx) play an important role in metabolic dysfunction and type 2 diabetes etiology. This work is supported by recent findings that have observed similar effect sizes for increased exposure to air pollutants on clinical measures of risk for type 2 diabetes in children and adults. Further, studies indicate that these effects may be more pronounced among individuals with existing risk factors, including obesity and prediabetes. Summary Current epidemiological evidence suggests that increased air pollution exposure contributes to alterations in insulin signaling, glucose metabolism, and beta (β)-cell function. Future work is needed to identify the specific detrimental pollutants that alter glucose metabolism. Additionally, advanced tools and new areas of investigation present unique opportunities to study the underlying mechanisms, including intermediate pathways, that link increased air pollution exposure with type 2 diabetes onset.

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.