Congenital anomalies associated with oil and gas development and resource extraction: a population-based retrospective cohort study in Texas.

BACKGROUND: Oil and gas extraction-related activities produce air and water pollution that contains known and suspected teratogens. To date, health impacts of in utero exposure to these activities is largely unknown. OBJECTIVE: We investigated associations between in utero exposure to oil and gas extraction activity in Texas, one of the highest producers of oil and gas, and congenital anomalies. METHODS: We created a population-based birth cohort between 1999 and 2009 with full maternal address at delivery and linked to the statewide congenital anomaly surveillance system (n = 2,234,138 births, 86,315 cases). We examined extraction-related exposures using tertiles of inverse distance-squared weighting within 5 km for drilling site count, gas production, oil production, and produced water. In adjusted logistic regression models, we calculated odds of any congenital anomaly and 10 specific organ sites using two comparison groups: 1) 5 km of future drilling sites that are not yet operating (a priori main models), and 2) 5-10 km of an active well. RESULTS: Using the temporal comparison group, we find increased odds of any congenital anomaly in the highest tertile exposure group for site count (OR: 1.25; 95% CI: 1.21, 1.30), oil production (OR: 1.08; 95% CI: 1.04, 1.12), gas production (1.20; 95% CI: 1.17, 1.23), and produced water (OR: 1.17; 95% CI: 1.14, 1.20). However, associations did not follow a consistent exposure-response pattern across tertiles. Associations are highly attenuated, but still increased, with the spatial comparison group in the highest tertile exposure group. Cardiac and circulatory defects are strongly and consistently associated with all exposure metrics. SIGNIFICANCE: Increased odds of congenital anomalies, particularly cardiac and circulatory defects, were associated with exposures related to oil and gas extraction in this large population-based study. Future research is needed to confirm findings, examine specific exposure pathways, and identify potential avenues to reduce exposures among local populations. IMPACT: About 5% of the U.S. population (~17.6 million people) resides within 1.6 km of an active oil or gas extraction site, yet the influence of this industry on population health is not fully understood. In this analysis, we examined associations between oil and gas extraction-related exposures and congenital anomalies by organ site using birth certificate and congenital anomaly surveillance data in Texas (1999-2009). Increased odds of congenital anomalies, particularly cardiac and circulatory defects, were associated with exposures related to oil and gas extraction in this large population-based study. Future research is needed to confirm these findings.

Associations between residential proximity to oil and gas extraction and hypertensive conditions during pregnancy: a difference-in-differences analysis in Texas, 1996-2009.

BACKGROUND: Oil and gas extraction produces air pollutants that are associated with increased risks of hypertension. To date, no study has examined residential proximity to oil and gas extraction and hypertensive conditions during pregnancy. This study quantifies associations between residential proximity to oil and gas development on gestational hypertension and eclampsia. METHODS: We utilized a population-based retrospective birth cohort in Texas (1996-2009), where mothers reside <10 km from an active or future drilling site (n = 2 845 144.) Using full-address data, we linked each maternal residence at delivery to assign exposure and evaluate this exposure with respect to gestational hypertension and eclampsia. In a difference-in-differences framework, we model the interaction between maternal health before (unexposed) or after (exposed) the start of drilling activity (exposed) and residential proximity near (0-1, >1-2 or >2-3 km) or far (≥3-10 km) from an active or future drilling site. RESULTS: Among pregnant women residing 0-1 km from an active oil or gas extraction site, we estimate 5% increased odds of gestational hypertension [95% confidence interval (CI): 1.00, 1.10] and 26% increased odds of eclampsia (95% CI: 1.05, 1.51) in adjusted models. This association dissipates in the 1- to 3-km buffer zones. In restricted models, we find elevated odds ratios among maternal ages ≤35 years at delivery, maternal non-Hispanic White race, ≥30 lbs gained during pregnancy, nulliparous mothers and maternal educational attainment beyond high school. CONCLUSIONS: Living within 1 km of an oil or gas extraction site during pregnancy is associated with increased odds of hypertensive conditions during pregnancy.

Associations between Residential Proximity to Oil and Gas Drilling and Term Birth Weight and Small-for-Gestational-Age Infants in Texas: A Difference-in-Differences Analysis.

BACKGROUND: Oil and natural gas extraction may produce environmental pollution at levels that affect reproductive health of nearby populations. Available studies have primarily focused on unconventional gas drilling and have not accounted for local population changes that can coincide with drilling activity. OBJECTIVE: Our study sought to examine associations between residential proximity to oil and gas drilling and adverse term birth outcomes using a difference-in-differences study design. METHODS: We created a retrospective population-based term birth cohort in Texas between 1996 and 2009 composed of mother-infant dyads (n=2,598,025) living <10km from an oil or gas site. We implemented a difference-in-differences approach to estimate associations between drilling activities and infant health: term birth weight and term small for gestational age (SGA). Using linear and logistic regression, we modeled interactions between births before (unexposed) or during (exposed) drilling activity and residential proximity near (0-1, 1-2, or 2-3km) or far (3-10km) from an active or future drilling site, adjusting for individual- and neighborhood-level characteristics. RESULTS: The adjusted mean difference in term birth weight for mothers living 0-1 vs. 3-10km from a current or future drilling site was -7.3g [95% confidence interval (CI): -11.6, -3.0] for births during active vs. future drilling. The corresponding adjusted odds ratio for SGA was 1.02 (95% CI: 0.98, 1.06). Negative associations with term birth weight were observed for the 1-2 and 2-3km near groups, and no consistent differences were identified by type of drilling activity. Larger, though imprecise, adverse associations were found for infants born to Hispanic women, women with the lowest educational attainment, and women living in cities. CONCLUSIONS: Residing near oil and gas drilling sites during pregnancy was associated with a small reduction in term birth weight but not SGA, with some evidence of environmental injustices. Additional work is needed to investigate specific drilling-related exposures that might explain these associations. https://doi.org/10.1289/EHP7678.

Sex differences in associations between birth characteristics and childhood cancers: a five-state registry-linkage study.

BACKGROUND: There is a well-recognized male excess in childhood cancer incidence; however, it is unclear whether there is etiologic heterogeneity by sex when defined by epidemiologic risk factors. METHODS: Using a 5-state registry-linkage study (cases n = 16,411; controls n = 69,816), we estimated sex-stratified odds ratios (OR) and 95% confidence intervals (95% CI) between birth and demographic characteristics for 16 pediatric cancers. Evidence of statistical interaction (p-interaction < 0.01) by sex was evaluated for each characteristic in each cancer. RESULTS: Males comprised > 50% of cases for all cancers, except Wilms tumor (49.6%). Sex interacted with a number of risk factors (all p-interaction < 0.01) including gestational age for ALL (female, 40 vs. 37-39 weeks OR: 0.84, 95% CI 0.73-0.97) and ependymoma (female, 40 vs. 37-39 OR: 1.78, 95% CI 1.14-2.79; female, ≥ 41 OR: 2.01. 95% CI 1.29-3.14), birth order for AML (female, ≥ 3rd vs. 1st OR: 1.39, 95% CI 1.01-1.92), maternal education for Hodgkin lymphoma (male, any college vs. < high school[HS] OR: 1.47, 95% CI 1.03-2.09) and Wilms tumor (female, any college vs. HS OR: 0.74, 95% CI 0.59-0.93), maternal race/ethnicity for neuroblastoma (male, black vs. white OR: 2.21, 95% CI 1.21-4.03; male, Hispanic vs. white OR: 1.86, 95% CI 1.26-2.75; female, Asian/Pacific Islander vs. white OR: 0.28, 95% CI 0.12-0.69), and paternal age (years) for hepatoblastoma in males (< 24 vs. 25-29 OR: 2.17, 95% CI 1.13-4.19; ≥ 35 vs. 25-29 OR: 2.44, 95% CI 1.28-4.64). CONCLUSIONS: These findings suggest etiologic heterogeneity by sex for childhood cancers for gestational age, maternal education, and race/ethnicity and paternal age.

Assessing the effectiveness of vehicle emission regulations on improving perinatal health: a population-based accountability study.

BACKGROUND: Since the 1990s, extensive regulations to reduce traffic-related air pollution (TRAP) have been implemented, yet the effectiveness of these regulations has not been assessed with respect to improving infant health. In this study, we evaluate how infant health risks associated with maternal residences near highways during pregnancy have changed over time. METHODS: We created a population-based retrospective birth cohort with geocoded residential addresses in Texan metropolitan areas from 1996 through 2009 (n = 2 259 411). We compared term birthweight (37-42 weeks of gestation) among maternal residences <300 m from a highway (high TRAP exposure) (n = 394 346) and 500-3500 m from a highway (comparison group) (n = 1 865 065). We implemented linear regressions to evaluate interactions between high TRAP exposure and birth year, adjusting for demographics, socioeconomic status and neighbourhood context. In addition, we used propensity score matching to further reduce residual confounding. RESULTS: From 1996 to 2009, outdoor NO2 decreased by 51.3%, based on regulatory monitoring data in Texas. Among pregnant women who resided in the high TRAP zone during pregnancy, interaction terms between residential location and birth year show that birthweight increased by 1.1 g [95% confidence interval CI): 0.7, 1.5) in unadjusted models and 0.3 g (95% CI: 0.0, 0.6) in matched models. Time-stratified models also show decreasing impacts of living in high TRAP areas on birthweight when comparing infants born in 1996-97 with 2008-09. Sensitivity analyses with alternative exposure and control groups show consistent results. CONCLUSIONS: Infant health risks associated with maternal residence near highways have reduced over time, paralleling regulatory measures to improve exhaust pipe emissions.

Association Between Birth Defects and Cancer Risk Among Children and Adolescents in a Population-Based Assessment of 10 Million Live Births.

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 (adjusted P < .05) after accounting for multiple comparisons. Cancers most frequently associated with nonchromosomal defects were hepatoblastoma and neuroblastoma. 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.

Parental Age and Risk of Infant Leukaemia: A Pooled Analysis.

BACKGROUND: Infant leukaemia (IL) is extremely rare with fewer than 150 cases occurring each year in the United States. Little is known about its causes. However, recent evidence supports a role of de novo mutations in IL aetiology. Parental age has been associated with several adverse outcomes in offspring, including childhood cancers. Given the role of older parental age in de novo mutations in offspring, we carried out an analysis of parental age and IL. METHODS: We evaluated the relationship between parental age and IL in a case-control study using registry data from New York, Minnesota, California, Texas, and Washington. Records from 402 cases [219 acute lymphoblastic leukaemia (ALL), 131 acute myeloid leukaemia (AML), and 52 other] and 45 392 controls born during 1981-2004 were analysed. Odds ratios (OR) and 95% confidence intervals (CI) were calculated by logistic regression. Estimates were adjusted for infant sex, birth year category, maternal race, state, and mutually adjusted for paternal or maternal age, respectively. RESULTS: Infants with mothers' age ≥40 years had an increased risk of developing AML (OR 4.80, 95% CI 1.80, 12.76). In contrast, paternal age <20 was associated with increased risk of ALL (OR 3.69, 95% CI 1.62, 8.41). CONCLUSION: This study demonstrates increased risk of infant ALL in relation to young paternal age. Given record linkage, there is little concern with recall or selection bias, although data are lacking on MLL gene status and other potentially important variables. Parent of origin effects, de novo mutations, and/or carcinogenic exposures may be involved in IL aetiology.

Associations between multiple green space measures and birth weight across two US cities.

INTRODUCTION: Several measures of green space exposure have been used in epidemiological research, but their relevance to health, and representation of exposure pathways, remains unclear. Here we examine the relationships between multiple urban green space metrics and associations with term birth weight across two diverse US cities. METHODS: We used Vital Statistics data to create a birth cohort from 2005 to 2009 in the cities of Portland, Oregon (n = 90,265) and Austin, Texas (n = 88,807). These cities have similar green space levels but very different population and contextual characteristics. Green space metrics derived from mother's full residential address using multiple buffer distances (50-1000m) included: Landsat Normalized Difference Vegetation Index (NDVI), % tree cover, % green space, % street tree buffering, and access to parks (using US EPA EnviroAtlas Data). Correlation between green space metrics were assessed and mixed models were used to determine associations with term birth weight, controlling for a comprehensive set of individual and neighborhood factors. City-specific models were run to determine how contextual and population differences affected green space associations with birth weight. RESULTS: We observed moderate to high degrees of correlation between different green space metrics (except park access), with similar patterns between cities. Unadjusted associations demonstrated consistent protective effects of NDVI, % green space, % tree cover, and % street tree buffering for most buffer sizes on birth weight; however, in fully adjusted models most metrics were no longer statistically significant and no clear patterns remained. For example, in Austin the difference in birth weight for the highest versus lowest quartile of % green space within 50m was 38.3g (95% CI: 30.4, 46.1) in unadjusted and -1.5g (98% CI: -8.8, 6.3) in adjusted models compared to 55.7g (95%CI: 47.9, -63.6) and 12.9g (95% CI: 4.4, 21.4) in Portland. Maternal race, ethnicity and education had the largest impact on reducing green space and birth weight associations. However, consistent positive associations were observed for the high density areas of both cities using several green space metrics at small buffer distances. CONCLUSIONS: This study highlights the importance of understanding the individual and contextual factors that may confound and/or modify green space and birth weight associations.

Childhood cancer risk in those with chromosomal and non-chromosomal congenital anomalies in Washington State: 1984-2013.

BACKGROUND: The presence of a congenital anomaly is associated with increased childhood cancer risk, likely due to large effects of Down syndrome and chromosomal anomalies for leukemia. Less is known about associations with presence of non-chromosomal anomalies. METHODS: Records of children diagnosed with cancer at <20 years of age during 1984-2013 in Washington State cancer registries were linked to their birth certificates (N = 4,105). A comparison group of children born in the same years was identified. Congenital anomalies were assessed from birth records and diagnosis codes in linked hospital discharge data. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) for cancer, and for specific cancer types in relation to the presence of any anomaly and specific anomalies. RESULTS: Having any congenital anomaly was associated with an increased risk of childhood cancer (OR: 1.46, 95% CI 1.28-1.65). Non-chromosomal anomalies were also associated with increased childhood cancer risk overall (OR: 1.35; 95% CI: 1.18-1.54), and with increased risk of several cancer types, including neuroblastoma, renal, hepatoblastoma, soft-tissue sarcoma, and germ cell tumors. Increasing number of non-chromosomal anomalies was associated with a stronger risk of childhood cancer (OR for 3+ anomalies: 3.11, 95% CI: 1.54-6.11). Although central nervous system (CNS) anomalies were associated with CNS tumors (OR: 6.05, 95% CI 2.75-13.27), there was no strong evidence of other non-chromosomal anomalies being specifically associated with cancer occurring in the same organ system or anatomic location. CONCLUSIONS: Non-chromosomal anomalies increased risk of several cancer types. Additionally, we found that increasing number of non-chromosomal anomalies was associated with a stronger risk of cancer. Pooling similar data from many regions would increase power to identify specific associations in order to inform molecular studies examining possible common developmental pathways in the etiologies of birth defects and cancer.

Evaluation of maternal health and labor and delivery conditions as risk factors for childhood leukemias in children with Down syndrome.

Children with Down syndrome (DS) have a remarkably high risk of developing leukemia during childhood; the mechanisms driving that risk are not well understood, and no clear prevention strategies exist. We conducted a nested case-control study in a Texas DS birth cohort to investigate possible links between maternal health, labor/delivery conditions, and leukemia risk. For most of the factors studied there was no evidence of an increased risk of total leukemias, or the subtypes acute lymphoid or acute myeloid leukemia. Ultrasound use showed an almost 2-fold increased odds of leukemia, but this result is likely an example of confounding by indication. There was a pattern of increased risk seen for presence of co-occurring heart anomalies, including tetralogy of Fallot, ventricular septal defects, atrial septal defects, and patent ductus arteriosus. Further investigation of the links between co-occurring heart defects in children with DS and development of leukemia may provide new understanding of cancer mechanisms, and ultimately lead to prevention opportunities for this high-risk population.

In vivo contaminant partitioning to silicone implants: Implications for use in biomonitoring and body burden.

Silicone polymers are used for a wide array of applications from passive samplers in environmental studies, to implants used in human augmentation and reconstruction. If silicone sequesters toxicants throughout implantation, it may represent a history of exposure and potentially reduce the body burden of toxicants influencing the risk of adverse health outcomes such as breast cancer. Objectives of this research included identifying a wide variety of toxicants in human silicone implants, and measuring the in vivo absorption of contaminants into silicone and surrounding tissue in an animal model. In the first study, eight human breast implants were analyzed for over 1400 organic contaminants including consumer products, chemicals in commerce, and pesticides. A total of 14 compounds including pesticides such as trans-nonachlor (1.2-5.9ng/g) and p,p'-DDE (1.2-34ng/g) were identified in human implants, 13 of which have not been previously reported in silicone prostheses. In the second project, female ICR mice were implanted with silicone and dosed with p,p'-DDE and PCB118 by intraperitoneal injection. After nine days, silicone and adipose samples were collected, and all implants in dosed mice had p,p'-DDE and PCB118 present. Distribution ratios from silicone and surrounding tissue in mice compare well with similar studies, and were used to predict adipose concentrations in human tissue. Similarities between predicted and measured chemical concentrations in mice and humans suggest that silicone may be a reliable surrogate measure of persistent toxicants. More research is needed to identify the potential of silicone implants to refine the predictive quality of chemicals found in silicone implants.

Infant birthweight and risk of childhood cancer: international population-based case control studies of 40 000 cases.

BACKGROUND: High birthweight is an established risk factor for childhood leukaemia. Its association with other childhood cancers is less clear, with studies hampered by low case numbers. METHODS: We used two large independent datasets to explore risk associations between birthweight and all subtypes of childhood cancer. Data for 16 554 cases and 53 716 controls were obtained by linkage of birth to cancer registration records across five US states, and 23 772 cases and 33 206 controls were obtained from the UK National Registry of Childhood Tumours. US, but not UK, data were adjusted for gestational age, birth order, plurality, and maternal age and race/ethnicity. RESULTS: Risk associations were found between birthweight and several childhood cancers, with strikingly similar results between datasets. Total cancer risk increased linearly with each 0.5 kg increase in birthweight in both the US [odds ratio 1.06 (95% confidence interval 1.04, 1.08)] and UK [1.06 (1.05, 1.08)] datasets. Risk was strongest for leukaemia [USA: 1.10 (1.06, 1.13), UK: 1.07 (1.04, 1.10)], tumours of the central nervous system [USA: 1.05 (1.01, 1.08), UK: 1.07 (1.04, 1.10)], renal tumours [USA: 1.17 (1.10, 1.24), UK: 1.12 (1.06, 1.19)] and soft tissue sarcomas [USA: 1.12 (1.05, 1.20), UK: 1.07 (1.00, 1.13)]. In contrast, increasing birthweight decreased the risk of hepatic tumours [USA: 0.77 (0.69, 0.85), UK: 0.79 (0.71, 0.89) per 0.5 kg increase]. Associations were also observed between high birthweight and risk of neuroblastoma, lymphomas, germ cell tumours and malignant melanomas. For some cancer subtypes, risk associations with birthweight were non-linear. We observed no association between birthweight and risk of retinoblastoma or bone tumours. CONCLUSIONS: Approximately half of all childhood cancers exhibit associations with birthweight. The apparent independence from other factors indicates the importance of intrauterine growth regulation in the aetiology of these diseases.

Are children with birth defects at higher risk of childhood cancers?

Birth defects may influence the risk of childhood cancer development through a variety of mechanisms. The rarity of both birth defects and childhood cancers makes it challenging to study these associations, particularly for the very rare instances of each. To address this limitation, the authors conducted a record linkage-based cohort study among Texas children born between 1996 and 2005. Birth defects in the cohort were identified through the Texas Birth Defects Registry, and children who developed cancer were identified by using record linkage with Texas Cancer Registry data. Over 3 million birth records were included; 115,686 subjects had birth defects, and there were 2,351 cancer cases. Overall, children with a birth defect had a 3-fold increased risk of developing cancer (incidence rate ratio (IRR) = 3.05, 95% confidence interval (CI): 2.65, 3.50), with germ cell tumors (IRR = 5.19, 95% CI: 2.67, 9.41), retinoblastomas (IRR = 2.34, 95% CI: 1.21, 4.16), soft-tissue sarcomas (IRR = 2.12, 95% CI: 1.09, 3.79), and leukemias (IRR = 1.39, 95% CI: 1.09, 1.75) having statistically significant elevated point estimates. All birth defect groups except for musculoskeletal had increased cancer incidence. Untangling the strong relation between birth defects and childhood cancers could lead to a better understanding of the genetic and environmental factors that affect both conditions.

Birth order and risk of childhood cancer: a pooled analysis from five US States.

The causes of childhood cancers are largely unknown. Birth order has been used as a proxy for prenatal and postnatal exposures, such as frequency of infections and in utero hormone exposures. We investigated the association between birth order and childhood cancers in a pooled case-control dataset. The subjects were drawn from population-based registries of cancers and births in California, Minnesota, New York, Texas and Washington. We included 17,672 cases <15 years of age who were diagnosed from 1980 to 2004 and 57,966 randomly selected controls born 1970-2004, excluding children with Down syndrome. We calculated odds ratios and 95% confidence intervals using logistic regression, adjusted for sex, birth year, maternal race, maternal age, multiple birth, gestational age and birth weight. Overall, we found an inverse relationship between childhood cancer risk and birth order. For children in the fourth or higher birth order category compared to first-born children, the adjusted OR was 0.87 (95% CI: 0.81, 0.93) for all cancers combined. When we examined risks by cancer type, a decreasing risk with increasing birth order was seen in the central nervous system tumors, neuroblastoma, bilateral retinoblastoma, Wilms tumor and rhabdomyosarcoma. We observed increased risks with increasing birth order for acute myeloid leukemia but a slight decrease in risk for acute lymphoid leukemia. These risk estimates were based on a very large sample size, which allowed us to examine rare cancer types with greater statistical power than in most previous studies, however the biologic mechanisms remain to be elucidated.

Childhood cancer in relation to parental race and ethnicity: a 5-state pooled analysis.

BACKGROUND: Children of different racial/ethnic backgrounds have varying risks of cancer. However, to the authors' knowledge, few studies to date have examined cancer occurrence in children of mixed ancestry. METHODS: This population-based case-control study examined cancer among children aged <15 years using linked cancer and birth registry data from 5 US states from 1978 through 2004. Data were available for 13,249 cancer cases and 36,996 controls selected from birth records. Parental race/ethnicity was determined from birth records. Logistic regression analysis was used to examine the association of cancer with different racial/ethnic groups. RESULTS: Compared with whites, blacks had a 28% decreased risk of cancer (odds ratio [OR], 0.72; 95% confidence interval [95% CI], 0.65-0.80), whereas both Asians and Hispanics had an approximate 15% decrease. Children of mixed white/black ancestry also were found to be at decreased risk (OR, 0.71; 95% CI, 0.56-0.90), but estimates for mixed white/Asian and white/Hispanic children did not differ from those of whites. Compared with whites: 1) black and mixed white/black children had decreased ORs for acute lymphoblastic leukemia (OR, 0.39 [95% CI, 0.31-0.49] and OR, 0.58 [95% CI, 0.37-0.91], respectively); 2) Asian and mixed white/Asian children had decreased ORs for brain tumors (OR, 0.51 [95% CI, 0.39-0.68] and OR, 0.79 [95% CI, 0.54-1.16], respectively); and 3) Hispanic and mixed white/Hispanic children had decreased ORs for neuroblastoma (OR, 0.51 [95% CI, 0.42-0.61] and OR, 0.67 [95% CI, 0.50-0.90], respectively). CONCLUSIONS: Children of mixed ancestry tend to have disease risks that are more similar to those of racial/ethnic minority children than the white majority group. This tendency may help formulate etiologic studies designed to study possible genetic and environmental differences more directly.

Occurrence of conotruncal heart birth defects in Texas: a comparison of urban/rural classifications.

PURPOSE: (1) Determine if there is an association between 3 conotruncal heart birth defects and urban/rural residence of mother. (2) Compare results using different methods of measuring urban/rural status. METHODS: Data were taken from the Texas Birth Defects Registry, 1999-2003. Poisson regression was used to compare crude and adjusted birth prevalence. FINDINGS: Based on residences of births in Texas, the values for urban influence code (UIC), rural urban continuum code (RUCC), and rural urban commuting area (RUCA) were highly correlated with each other and, less highly, to percentage of land in crops. For tetralogy of Fallot, the most rural category consistently showed the highest prevalence ratio for all measures. The adjusted prevalence ratio for highest percentage cropland was 1.73 [95% CI, 1.14-2.51] using natural breaks and 1.42 [95% CI, 1.07-1.86] using quartiles. The trend with cropland percentage was significant (P < .03), whether crude or adjusted. The crude trend was also significant using RUCC. Neither truncus arteriosus nor transposition of the great arteries exhibited consistent associations with urban or rural residence. CONCLUSIONS: The urban/rural measures were generally correlated with each other; as a broad measure, RUCA has advantages for many health studies. Tetralogy of Fallot was most prevalent in rural areas; that pattern was strongest using percentage of land in crops.

Risks of childhood cancer among Texas watersheds, based on mothers' living locations at the time of birth.

Cancer is the most common fatal disease among US children. The fetus has reduced resistance to toxic injury and is especially prone to mutagenic injury because of the high rate of cell division. A fetus can be exposed to environmental toxins through maternal consumption of contaminated water. The objective of this study was to estimate the incidence risk for childhood cancers within each watershed in Texas. The approach modeled risk for 19 cancer histotypes incorporating correlations among the cancer types and spatial correlation. Several watersheds in a very large area known as the Central Great Plains of North Texas were associated with increased risk for astrocytoma. Two watersheds near Houston, Buffalo-San Jacinto and West Galveston Bay, had increased risk for renal cancer and acute lymphoid leukemia, respectively. A watershed in South Texas, the South Laguna Madre, had increased risk for atypical leukemias. The possibility that waterborne toxins cause these childhood cancers should be investigated further.