IMPORTANCE Birth defects affect approximately 1 in 33 children. Some birth defects are known to be strongly associated with childhood cancer (eg, trisomy 21 and acute leukemia). However, comprehensive evaluations of childhood cancer risk in those with birth defects have been limited in previous studies by insufficient sample sizes. OBJECTIVES To identify specific birth defect-childhood cancer (BD-CC) associations and characterize cancer risk in children by increasing number of nonchromosomal birth defects. DESIGN, SETTING, AND PARTICIPANTS This multistate, population-based registry linkage study pooled statewide data on births, birth defects, and cancer from Texas,
Background Data-linkage studies have reported an association between congenital anomalies and childhood cancer. However, few studies have focused on the differences in the effect of congenital anomalies on cancer as a function of attained age. We aimed to examine associations between anomalies and childhood cancer as a function of attained age among children born in Oklahoma. Methods Data were obtained from the Oklahoma State Department of Health from 1997-2009 (n=591,235). We linked Vital Statistics records for singleton deliveries to the Oklahoma Birth Defects Registry and the Oklahoma Central Cancer Registry using name and birth date. In order to assess the relation between anomalies and childhood cancer, we used Cox regression analysis allowing for a non-proportional hazards for anomalies as a function of age. Results There were 23,368 (4.0%) children with anomalies and 531 (0.1%) children with cancer. When considering 3-year age intervals, we detected an increased hazard of any childhood cancer in children with anomalies compared to those without anomalies before one year of age (HR: 14.1, 95% CI: 8.3, 23.7) and at three years of age (HR: 2.3, 95% CI: 1.6, 3.2). The increased hazard declined with increasing time since birth, with the effect diminished by six years of age. Conclusions Our results were consistent with previous studies indicating an increased rate of childhood cancer among children with anomalies at younger ages. Furthermore, our study added a methodological refinement of assessing the effect of anomalies as a function of attained age.
Objectives Previous studies have identified racial/ethnic disparities in infertility care, but patterns among American Indian/Alaska Natives (AI/AN) have not been reported. Our objective was to evaluate infertility services use in the US by race/ethnicity using data from the National Survey of Family Growth (NSFG). Methods We analyzed female respondent data from the pooled NSFG cycles 2002, 2006-2010 and 2011-2013. Respondents reported use of infertility services and types of services. We calculated weighted crude and adjusted prevalence proportion ratios (PPR) and 95% confidence intervals (95% CI) using modified Poisson regression with robust error variances accounting for the complex survey design to compare infertility services use across race/ethnicities. Results Overall, 8.7% of women reported using medical services to get pregnant. The prevalence of using any medical service to help get pregnant was lower for American Indian/Alaska Native (AI/AN) (PPR: 0.60, 95% CI 0.43-0.83) and black (PPR: 0.53, 95% CI 0.44-0.63) compared to white women and in Hispanic compared to non-Hispanic women (PPR: 0.57, 95% CI 0.48-0.67). The prevalence of accessing treatment, testing, and advice also differed by race and ethnicity. Conclusions for Practice We observed disparities in accessing services to get pregnant among AI/AN and black women and reduced use of advice among Asian/Pacific Islanders compared to whites. We also observed reduced service utilization for Hispanic compared to non-Hispanic women. Differential utilization of specific services suggests barriers to infertility care may contribute to reproductive health disparities among underserved populations.
Background The prevalence of infertility in American Indian/Alaska Native (AI/AN) populations is unknown. The objective of our study was to estimate the prevalence of infertility and impaired fecundity in the AI/AN population and other racial and ethnic groups. Methods We analyzed female respondent data from the pooled National Survey of Family Growth (NSFG) cycles 2002, 2006‐2010, and 2011‐2013. We used modified Poisson regression with robust error variance accounting for survey weighting to estimate prevalence proportion ratios (PPR) and 95% confidence intervals (CI) for NSFG definitions of infertility and impaired fecundity by race and Hispanic ethnicity. Results The prevalence of infertility and impaired fecundity in the pooled NSFG was 6.4% (95% CI 5.7, 7.0) and 11.0% (95% CI 11.0, 12.2), respectively. Compared to whites, blacks had a 1.45 times greater adjusted prevalence of infertility (95% CI 1.15, 1.83) and AI/ANs had a 1.37 times greater prevalence of infertility (95% CI 0.91, 2.06) compared to whites. We observed a 1.30 times greater prevalence of impaired fecundity among AI/AN (95% CI 1.04, 1.62) compared to whites. We observed no differences in impaired fecundity for black or Asian/Pacific Islander women compared to whites or for Hispanic compared to non‐Hispanic women. Conclusions Inequalities in the burden of reproductive impairments among blacks and AI/AN women warrant further evaluation to identify opportunities for prevention and disparity reduction.
Background Although childhood cancer is a leading cause of childhood mortality in the US, evidence regarding the etiology is lacking. The goal of this study was to evaluate the association between benzene, a known carcinogen, and childhood acute leukemia. Methods We conducted a case-control study including cases diagnosed with acute leukemia between 1997 and 2012 (n=307) from the Oklahoma Central Cancer Registry and controls matched on week of birth from birth certificates (n=1,013). We used conditional logistic regression to evaluate the association between benzene, measured with the 2005 National-Scale Air Toxics Assessment (NATA) at census tract of the birth residence, and childhood acute leukemia. Results We observed no differences in benzene exposure overall between cases and controls. However, when stratified by year of birth, cases born from 2005-2010 had a three–fold increased unadjusted odds of elevated exposure compared to controls born in this same time period (4th Quartile OR: 3.53, 95% CI: 1.35, 9.27). Furthermore, the estimates for children with acute myeloid leukemia (AML) were stronger than those with acute lymphoid leukemia, though not statistically significant. Conclusions While we did not observe an association between benzene and childhood leukemia overall, our results suggest that acute leukemia is associated with increased benzene exposure among more recent births, and children with AML may have increased benzene exposure at birth. Using the NATA estimates allowed us to assess a specific pollutant at the census tract level, providing an advantage over monitor or point source data. Our study, however, cannot rule out the possibility that benzene may be a marker of other traffic-related exposures and temporal misclassification may explain the lack of an association among earlier births.
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