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OBJECTIVES To compare risks of distant-stage colorectal cancer (CRC) diagnosis between whites and American Indian/Alaska Natives (AI/ANs) and to explore effect modification by area-based socioeconomic status (SES). DESIGN Retrospective cohort study using data from the Oklahoma Central Cancer Registry. SETTING Oklahoma. PARTICIPANTS White and AI/AN cases of CRC diagnosed in Oklahoma between 2001 and 2008 (N = 8 438). A subanalysis was performed on the cohort of those aged 50 years and older (N = 7 728). MAIN OUTCOME MEASURE Risk of distant-stage CRC diagnosis stratified by SES score. RESULTS Race and SES were independently associated with distant-stage diagnosis. In SES-stratified analyses, AI/ANs in the 2 lowest SES groups experienced increased risks in the overall cohort and among those aged 50 years and older. In multivariable models, risks remained significant among those aged 50 years and older in the lowest SES groups (Adjusted risk ratio SES score of 2: 1.31, 95% confidence interval: 1.06-1.63 and adjusted risk ratio SES score of 1: 1.21, 95% confidence interval: 1.01-1.44). CONCLUSION Socioeconomic status is an effect modifier in the association between race/ethnicity and stage at CRC diagnosis. Disparities in stage at CRC diagnosis exist between AI/ANs and whites with lower estimated SES. Efforts are needed to increase CRC screening among lower SES AI/ANs.

Previous studies suggest arsenic exposure may increase the risk of gestational diabetes mellitus (GDM). However, prior assessments of total arsenic concentrations have not distinguished between toxic and nontoxic species. Our study aimed to investigate the relationships between inorganic arsenic exposure, arsenic methylation capacity, and GDM. Sixty-four cases of GDM and 237 controls were analyzed for urinary concentrations of inorganic arsenic species and their metabolites (arsenite (As3), arsenate (As5), monomethylarsonic acid (MMA), and dimethylarsinic acid (DMA)), and organic forms of arsenic. Inorganic arsenic exposure was defined as the sum of inorganic and methylated arsenic species (iSumAs). Methylation capacity indices were calculated as the percentage of inorganic arsenic species [iAs% = (As3 + As5)/iSumAs, MMA% = MMA/iSumAs, and DMA% = DMA/iSumAs]. Multivariable logistic regression was performed to evaluate the association between inorganic arsenic exposure, methylation capacity indices, and GDM. We did not observe evidence of a positive association between iSumAs and GDM. However, women with GDM had an increased odds of inefficient methylation capacity when comparing the highest and lowest tertiles of iAs% (adjusted odds ratio (aOR) = 1.48, 95% CI 0.58–3.77) and MMA% (aOR = 1.95 (95% CI 0.81–4.70) and a reduced odds of efficient methylation capacity as indicated by DMA% (aOR = 0.62 (95% CI 0.25–1.52), though the confidence intervals included the null value. While the observed associations with arsenic methylation indices were imprecise and warrant cautious interpretation, the direction and magnitude of the relative measures reflected a pattern of lower detoxification of inorganic arsenic exposures among women with GDM.

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.

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: No research exists on American Indian pregnancy rates following infertility treatment. Most racial/ethnic fertility research has focused on pregnancy following in vitro fertilization, with only rare studies looking at intrauterine insemination (IUI). The objective of our study was to compare fecundability following IUI by race/ethnicity, with a special focus on American Indians. METHODS: This was a retrospective analysis of subjects undergoing IUI July 2007—May 2012 at a university-based infertility clinic. The primary outcome was positive pregnancy test, with a secondary outcome of ongoing pregnancy/delivery (OP/D). We calculated risk ratios (RR) and 95% confidence intervals (CI) using cluster-weighted generalized estimating equations method to estimate modified Poisson regression models with robust standard errors to account for multiple IUI cycles in the same patient. RESULTS: A total of 663 females (median age 32) undergoing 2007 IUI cycles were included in the analysis. Pregnancy rates overall were 15% per IUI cycle. OP/D rates overall were 10% per IUI cycle. The American Indian patients had significantly lower pregnancy (RR 0.34, 95%CI 0.16–0.72) and OP/D rates (RR 0.33, 95%CI 0.12–0.87) compared to non-Hispanic whites when patient and cycle characteristics were controlled. Pregnancy and OP/D rates for blacks, Asians and Hispanics did not differ from non-Hispanic whites. CONCLUSIONS: Our finding of lower IUI treatment success among American Indian patients is novel, as no published studies of assisted reproductive technology or other fertility treatments have examined this subgroup separately. Further investigation of patient and clinical factors that may mediate racial/ethnic disparities in fertility treatment outcomes is warranted.

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 = 1013). 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 to 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.

Little is known about the etiology of hepatoblastoma. We aimed to confirm the results of a previous study evaluating the association between parental occupational exposures and hepatoblastoma. In our case-control study, we identified cases (n=383) from the Children's Oncology Group and controls from birth certificates (n=387), which were frequency matched to cases on year and region of birth, sex, and birth weight. Occupational exposure in the year before and during the index pregnancy was collected through maternal interview and analyzed using unconditional logistic regression. The odds of both paternal and maternal "Likely" exposure to paints was elevated among cases compared with controls (paternal odds ratio (OR): 1.71, 95% confidence interval (CI): 1.04, 2.81; maternal OR: 3.29, 95% CI: 0.32, 33.78) after adjustment for matching factors and the confounding factors of maternal race (maternal only) and household income. In addition, paternal exposure to other chemicals was also elevated when adjusting for matching factors only (OR: 1.53, 95% CI: 1.02, 2.30). The results of our study provide further evidence of an association between parental occupation and hepatoblastoma. These results warrant further investigation of the etiologically relevant timing of occupational exposure to fumes and chemicals related to hepatoblastoma.

Background Female breast, prostate, lung, and colorectal cancers are the leading incident cancers among American Indian and Alaska Native (AI/AN) and non-Hispanic White (NHW) persons in the United States. To understand racial differences, we assessed incidence rates, analyzed trends, and examined geographic variation in incidence by Indian Health Service regions. Methods To assess differences in incidence, we used age-adjusted incidence rates to calculate rate ratios (RRs) and 95% confidence intervals (CIs). Using joinpoint regression, we analyzed incidence trends over time for the four leading cancers from 1999 to 2015. Results For all four cancers, overall and age-specific incidence rates were lower among AI/ANs than NHWs. By Indian Health Service regions, incidence rates for lung cancer were higher among AI/ANs than NHWs in Alaska (RR: 1.46; 95% CI: 1.37, 1.56) and Northern (RR: 1.29; 95% CI: 1.25, 1.33) and Southern (RR: 1.06; 95% CI: 1.03, 1.09) Plains. Similarly, colorectal cancer incidence rates were higher in AI/ANs than NHWs in Alaska (RR: 2.29; 95% CI: 2.14, 2.45) and Northern (RR: 1.04; 95% CI: 1.00, 1.09) and Southern (RR: 1.11; 95% CI: 1.07, 1.15) Plains. Also, AI/AN women in Alaska had a higher incidence rate for breast cancer than NHW women (RR: 1.05; 95% CI: 1.05, 1.20). From 1999 to 2015, incidence rates for all four cancers decreased in NHWs, but only rates for prostate (average annual percent change: -4.70) and colorectal (average annual percent change: -1.80) cancers decreased considerably in AI/ANs. Conclusion Findings from this study highlight the racial and regional differences in cancer incidence.

Background Cervical cancer, a preventable cancer, has disproportionately affected African American women. To better understand the burden of cervical cancer, we assessed incidence and mortality rates and analyzed trends among non-Hispanic (NH) African American and White women in the US from 1999 to 2015. Methods From age-adjusted cervical cancer incidence and mortality rates, rate ratios (RR) and 95% confidence intervals (CI) were calculated for comparison between the two races. Trends were analyzed using joinpoint regression and expressed as annual percent change (APC) and average annual percent change (AAPC). Results Cervical cancer incidence rates were significantly higher (RR: 1.46; 95% CI: 1.44, 1.47) among NH African Americans (10.8 per 100,000 females) than NH Whites (7.4 per 100,000 females). Similarly, mortality rates were significantly higher (RR: 2.05; 95% CI: 2.01, 2.09) in NH African Americans (4.4 per 100,000 females) compared to NH Whites (2.1 per 100,000 females). From 1999 to 2015, overall incidence and mortality trends decreased significantly for both races. Mortality rates steadily increased with age for both races, and incidence rates only increased with age in NH African American women. Conclusion NH African American women had significantly higher cervical cancer incidence and mortality rates than NH Whites. Even as incidence and mortality trends declined significantly, older NH African Americans had three times the rate of cervical cancer than NH Whites. Prevention and treatment programs need to be enhanced for African Americans as failure to do so may widen cancer disparities.

It is estimated that 300,000 children 0-14 years of age are diagnosed with cancer worldwide each year. While the absolute risk of cancer in children is low, it is the leading cause of death due to disease in children in high-income countries. In spite of this, the etiologies of pediatric cancer are largely unknown. Environmental exposures have long been thought to play an etiologic role. However, to date, there are few well-established environmental risk factors for pediatric malignancies, likely due to technical barriers in collecting biological samples prospectively in pediatric populations for direct measurements. In this review, we propose the use of novel or underutilized biospecimens (dried blood spots and teeth) and molecular approaches for exposure assessment (epigenetics, metabolomics, and somatic mutational profiles). Future epidemiologic studies of pediatric cancer should incorporate novel exposure assessment methodologies, data on molecular features of tumors, and a more complete assessment of gene-environment interactions.

Background While many studies have evaluated the association between acute childhood leukemia and environmental factors, knowledge is limited. Ambient air pollution has been classified as a Group 1 carcinogen, but studies have not established whether traffic-related air pollution is associated with leukemia. The goal of our study was to determine if children with acute leukemia had higher odds of exposure to traffic-related air pollution at birth compared to controls. Methods We conducted a case-control study using the Oklahoma Central Cancer Registry to identify cases of acute leukemia in children diagnosed before 20 years of age between 1997 and 2012 (n=307). Controls were selected from birth certificates and matched to cases on week of birth (n=1013). Using a novel satellite-based land-use regression model of nitrogen dioxide (NO 2 ) and estimating road density based on the 2010 US Census, we evaluated the association between traffic-related air pollution and childhood leukemia using conditional logistic regression. Results The odds of exposure to the fourth quartile of NO 2 (11.19–19.89 ppb) were similar in cases compared to controls after adjustment for maternal education (OR: 1.08, 95% CI: 0.75, 1.55). These estimates were stronger among children with acute myeloid leukemia (AML) than acute lymphoid leukemia, with a positive association observed among urban children with AML (4th quartile odds ratio: 5.25, 95% confidence interval: 1.09, 25.26). While we observed no significant association with road density, male cases had an elevated odds of exposure to roads at 500 m from the birth residence compared to controls (OR: 1.39, 95% CI: 0.93, 2.10), which was slightly attenuated at 750 m. Conclusions Although we observed no association overall between NO 2 or road density, this was the first study to observe an elevated odds of exposure to NO 2 among children with AML compared to controls suggesting further exploration of traffic-related air pollution and AML is warranted.

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 to 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. To assess the relation between anomalies and childhood cancer, we used Cox regression analysis allowing for a nonproportional 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 with those without anomalies before 1 year of age (hazard ratio, 14.1; 95% confidence interval, 8.3–23.7) and at 3 years of age (hazard ratio, 2.3; 95% confidence interval, 1.6–3.2). The increased hazard declined with increasing time since birth, with the effect diminished by 6 years of age. Conclusion 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. Birth Defects Research (Part A), 2016. © 2016 Wiley Periodicals, Inc.

Background The twin prevention strategies of HPV vaccination and cervical cancer screening reduce new cases and averts deaths, yet women still develop or die from cervical cancer. To assess and better understand the burden of cervical cancer in Oklahoma, we analyzed incidence and mortality trends in Oklahoma from 1999 to 2013. Methods We obtained age-adjusted cervical cancer incidence and mortality rates and calculated standardized rate ratios (RR) for women in Oklahoma compared to the US. To evaluate temporal changes in annual age-adjusted incidence and mortality, we calculated the annual percent change (APC) using the Joinpoint Regression Program. Results We observed higher age-adjusted incidence (RR: 1.2; 95% CI: 1.1, 1.3) and mortality (RR: 1.2; 95% CI: 1.1, 1.2) rates among women in Oklahoma compared to the US. The overall incidence and mortality rates in Oklahoma were 9.7 and 2.9 per 100,000 women, respectively. In Oklahoma, the highest age-adjusted incidence rates were in American Indian/Alaska Native (AI/AN) (14.8 per 100,000 females) and Asian or Pacific Islander (API) (11.7 per 100,000 females) women and the highest mortality rates were in AI/AN (4.5 per 100,000 females) and African American (AA) (3.9 per 100,000 females) women. Incidence rates decreased for AA women (APC: −4.0; 95% CI: −7.7, −0.2), but were stable for all other races and ethnicities in Oklahoma (APC: −0.8; 95% CI: −2.2, 0.7). A stable trend for mortality was observed in Oklahoma (APC: 0.1; 95% CI: −2.2, 2.5) each year. Conclusion Women in Oklahoma had a higher cervical cancer incidence and mortality rate than the US. A disproportionately higher incidence of cervical cancer among AI/AN and API women and deaths among AI/AN and AA women were observed signaling continuing racial disparities.

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, Arkansas, Michigan, and North Carolina on 10 181 074 children born from January 1, 1992, to December 31, 2013. Children were followed up to 18 years of age for a diagnosis of cancer. Data were retrieved between September 26, 2016, and September 21, 2017, and data analysis was performed from September 2, 2017, to March 21, 2019. Exposures Birth defects diagnoses (chromosomal anomalies and nonchromosomal birth defects) recorded by statewide, population-based birth defects registries. Main Outcomes and Measures Cancer diagnosis before age 18 years, as recorded in state cancer registries. Cox regression models were used to generate hazard ratios (HRs) and 95% CIs to evaluate BD-CC associations and the association between number of nonchromosomal defects and cancer risk. Results Compared with children without any birth defects, children with chromosomal anomalies were 11.6 (95% CI, 10.4-12.9) times more likely to be diagnosed with cancer, whereas children with nonchromosomal birth defects were 2.5 (95% CI, 2.4-2.6) times more likely to be diagnosed with cancer before 18 years of age. An increasing number of nonchromosomal birth defects was associated with a corresponding increase in the risk of cancer. Children with 4 or more major birth defects were 5.9 (95% CI, 5.3-6.4) times more likely to be diagnosed with cancer compared with those without a birth defect. In the analysis of 72 specific BD-CC patterns, 40 HRs were statistically significant (adjustedP Conclusions and Relevance Several significant and novel associations were observed between specific birth defects and cancers. Among children with nonchromosomal birth defects, the number of major birth defects diagnosed was significantly and directly associated with cancer risk. These findings could inform clinical treatment for children with birth defects and may elucidate mechanisms that lead to these complex outcomes.

Despite well-established clinical guidelines for breast cancer treatment, Standard of Care (SOC) is not universal in the U.S. The purpose of this study was to describe the extent to which patients receive guideline-based, stage-specific treatments for localized female breast cancer in Oklahoma. Data were obtained from the Oklahoma Central Cancer Registry for the period 2003–2006. We included localized, invasive female breast cancers and analyzed both treatment and demographic factors. We used the National Comprehensive Cancer Network (NCCN) treatment guidelines to determine SOC. Among women who received breast conserving surgery (BCS), we used logistic regression to evaluate factors related to SOC. In Oklahoma, 92 percent of the 4,177 localized breast cancer patients were treated with recognized SOC. In women aged ≥65 years with BCS, those ≥75 years had a lower adjusted odds of meeting SOC than did those without insurance, with comorbid conditions, or whose comorbid status was unknown. Among women aged

Introduction Studies have assessed rates of childhood obesity in diverse populations, but few have been able to compare the weight status of American Indian and white children living in the same community and attending the same schools. The objective of this study was to measure and compare the weight status of American Indian and white elementary school students (kindergarten through 5th grade) from 2005 through 2009 in an Oklahoma school district. Methods We assessed height, weight, age, and sex to calculate body mass index, body mass percentile, and categorical weight status of students, based on the Centers for Disease Control and Prevention 2000 Growth Charts. We used binomial regression to generate risk ratios (RRs) to compare student weight status by race, sex, and age. Results An average of 753 students was measured in each year; mean age was 8.3 years. From 2005 through 2009, 45.4% of American Indian students and 65.1% of white students were healthy weight or underweight. Greater proportions of American Indian children were very obese (weighted average RR, 2.0); obese (weighted average RR, 1.6), or overweight (weighted average RR, 1.8) compared with white children. The overall prevalence of excess weight changed little during the study period. Conclusion American Indian children had a greater risk of being overweight, obese, or very obese than white children from the same rural environment.