Neighborhood and Social Environmental Influences on Child Chronic Disease Prevalence

We investigate how distinct residential environments uniquely influence chronic child disease. Aggregating over 200,000 pediatric geocoded medical records to the census tract of residence and linking them to neighborhood-level measures, we use multiple data analysis techniques to assess how heterogeneous exposures of social and environmental neighborhood conditions influence an index of child chronic disease (CCD) prevalence for the neighborhood. We find there is a graded relationship between degree of overall neighborhood disadvantage and children’s chronic disease such that the highest neighborhood CCD scores reside in communities with the highest concentrated disadvantage. Finally, results show that higher levels of neighborhood concentrated disadvantage and air pollution exposure associate with higher risks of having at least one chronic condition for children after also considering their individual- and family-level characteristics. Overall, our analysis serves as a comprehensive start for future researchers interested in assessing which neighborhood factors matter most for child chronic health conditions

Child Obesity and the Interaction of Family and Neighborhood Socioeconomic Context

The literature on neighborhoods and child obesity links contextual conditions to risk, assuming that if place matters, it matters in a similar way for everyone in those places. We explore the extent to which distinctive neighborhood types give rise to social patterning that produces variation in the odds of child obesity. We leverage geocoded electronic medical records for a diverse sample of over 135,000 children aged 2 to 12 and latent profile modeling to characterize places into distinctive neighborhood contexts. Multilevel models with cross-level interactions between neighborhood type and family socioeconomic standing (SES) reveal that children with different SES, but living in the same neighborhoods, have different odds of obesity. Specifically, we find lower-SES children benefit, but to a lesser degree, from neighborhood advantages and higher-SES children are negatively influenced, to a larger degree, by neighborhood disadvantages. The resulting narrowing of the gap in obesity by neighborhood disadvantage helps clarify how place matters for children’s odds of obesity and suggests that efforts to improve access to community advantages as well as efforts to address community disadvantages are important to curbing obesity and improving the health of all children

Comprehensive Neighborhood Portraits and Child Asthma Disparities Introduction

Objectives Previous research has established links between child, family, and neighborhood disadvantages and child asthma. We add to this literature by first characterizing neighborhoods in Houston, TX by demographic, economic, and air quality characteristics to establish differences in pediatric asthma diagnoses across neighborhoods. Second, we identify the relative risk of social, economic, and environmental risk factors for child asthma diagnoses. Methods We geocoded and linked electronic pediatric medical records to neighborhood-level social and economic indicators. Using latent profile modeling techniques, we identified Advantaged, Middle-class, and Disadvantaged neighborhoods. We then used a modified version of the Blinder-Oaxaca regression decomposition method to examine differences in asthma diagnoses across children in these different neighborhoods. Results Both compositional (the characteristics of the children and the ambient air quality in the neighborhood) and associational (the relationship between child and air quality characteristics and asthma) differences within the distinctive neighborhood contexts influence asthma outcomes. For example, unequal exposure to PM2.5 and O3 among children in Disadvantaged and Middle-class neighborhoods contribute to asthma diagnosis disparities within these contexts. For children in Disadvantaged and Advantaged neighborhoods, associational differences between racial/ethnic and socioeconomic characteristics and asthma diagnoses explain a significant proportion of the gap. Conclusions for Practice Our results provide evidence that differential exposure to pollution and protective factors associated with non-Hispanic White children and children from affluent families contribute to asthma disparities between neighborhoods. Future researchers should consider social and racial inequalities as more proximate drivers, not merely as associated, with asthma disparities in children

Genetic architecture of laterality defects revealed by whole exome sequencing

Aberrant left-right patterning in the developing human embryo can lead to a broad spectrum of congenital malformations. The causes of most laterality defects are not known, with variants in established genes accounting for <20% of cases. We sought to characterize the genetic spectrum of these conditions by performing whole-exome sequencing of 323 unrelated laterality cases. We investigated the role of rare, predicted-damaging variation in 1726 putative laterality candidate genes derived from model organisms, pathway analyses, and human phenotypes. We also evaluated the contribution of homo/hemizygous exon deletions and gene-based burden of rare variation. A total of 28 candidate variants (26 rare predicted-damaging variants and 2 hemizygous deletions) were identified, including variants in genes known to cause heterotaxy and primary ciliary dyskinesia (ACVR2B, NODAL, ZIC3, DNAI1, DNAH5, HYDIN, MMP21), and genes without a human phenotype association, but with prior evidence for a role in embryonic laterality or cardiac development. Sanger validation of the latter variants in probands and their parents revealed no de novo variants, but apparent transmitted heterozygous (ROCK2, ISL1, SMAD2), and hemizygous (RAI2, RIPPLY1) variant patterns. Collectively, these variants account for 7.1% of our study subjects. We also observe evidence for an excess burden of rare, predicted loss-of-function variation in PXDNL and BMS1- two genes relevant to the broader laterality phenotype. These findings highlight potential new genes in the development of laterality defects, and suggest extensive locus heterogeneity and complex genetic models in this class of birth defects

Disparities in insurance coverage among hospitalized adult congenital heart disease patients before and after the Affordable Care Act

BackgroundData are lacking regarding the insurance status of adults with congenital heart disease (ACHD). We investigated whether the Affordable Care Act (ACA) impacted insurance status among hospitalized ACHD, identified associated sociodemographic factors, and compared coverage to adults with other chronic childhood conditions.MethodsSerial cross‐sectional analysis of National Inpatient Sample hospitalizations from 2007 to 2016 was performed for patients 18–64 years old. ACHD were identified using ICD‐9/10‐CM codes and compared to patients with sickle cell disease (SCD), cystic fibrosis (CF), and the general population. Age was dichotomized as 18–25 years (transition aged) or 26–64 years. Groups were compared by era (pre‐ACA [January 2007–June 2010]; early‐ACA [July 2010–December 2013], which eliminated pre‐existing condition exclusions; and full‐ACA [January 2014–December 2016]) using interrupted time series and multivariable Poisson regression analyses.ResultsOverall, uninsured hospitalizations decreased from pre‐ACA (12.0%) to full‐ACA (8.5%). After full ACA implementation, ACHD had lower uninsured rates than the general hospitalized population (6.0 vs. 8.6%, p < .01), but higher rates than those with other chronic childhood diseases (SCD [4.5%]; CF [1.6%]). Across ACA eras, transition aged ACHD had higher uninsured rates than older patients (8.9 vs. 7.6%, p < .01), and Hispanic patients remained less insured than other groups.ConclusionsHospitalized ACHD were better insured than the general population but less insured than those with SCD or CF. Full ACA implementation was associated with improved insurance coverage for all groups, but disparities persisted for transition aged and Hispanic patients. Ongoing evaluation of the effects of insurance and health policy on ACHD remains critical to diminish health disparities.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/167545/1/bdr21878_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/167545/2/bdr21878.pd

Neighborhoods Matter; but for Whom? Heterogeneity of Neighborhood Disadvantage on Child Obesity by Sex

Although evidence suggests that neighborhood context, particularly socioeconomic context, influences child obesity, little is known about how these neighborhood factors may be heterogeneous rather than monolithic. Using a novel dataset comprised of the electronic medical records for over 250,000 children aged 2–17 nested within 992 neighborhoods in the greater Houston area, we assessed whether neighborhoods influenced the obesity of children differently based on sex. Results indicated that neighborhood disadvantage, assessed using a comprehensive, multidimensional, latent profile analysis-generated measure, had a strong, positive association with the odds of obesity for both boys and girls. Interactions revealed that the relationship between disadvantage and obesity was stronger for girls, relative to boys. Our findings demonstrated the complex dynamics underlying the influence of residential neighborhood context on obesity for specific subgroups of children

US Mortality Attributable to Congenital Heart Disease Across the Lifespan From 1999 Through 2017 Exposes Persistent Racial/Ethnic Disparities

Background: Congenital heart disease (CHD) accounts for ≈40% of deaths in US children with birth defects. Previous US data from 1999 to 2006 demonstrated an overall decrease in CHD mortality. Our study aimed to assess current trends in US mortality related to CHD from infancy to adulthood over the past 19 years and determine differences by sex and race/ethnicity. Methods: We conducted an analysis of death certificates from 1999 to 2017 to calculate annual CHD mortality by age at death, race/ethnicity, and sex. Population estimates used as denominators in mortality rate calculations for infants were based on National Center for Health Statistics live birth data. Mortality rates in individuals ≥1 year of age used US Census Bureau bridged-race population estimates as denominators. We used joinpoint regression to characterize temporal trends in all-cause mortality, mortality resulting directly attributable to and related to CHD by age, race/ethnicity, and sex. Results: There were 47.7 million deaths with 1 in 814 deaths attributable to CHD (n=58 599). Although all-cause mortality decreased 16.4% across all ages, mortality resulting from CHD declined 39.4% overall. The mean annual decrease in CHD mortality was 2.6%, with the largest decrease for those \u3e65 years of age. The age-adjusted mortality rate decreased from 1.37 to 0.83 per 100 000. Males had higher mortality attributable to CHD than females throughout the study, although both sexes declined at a similar rate (≈40% overall), with a 3% to 4% annual decrease between 1999 and 2009, followed by a slower annual decrease of 1.4% through 2017. Mortality resulting from CHD significantly declined among all races/ethnicities studied, although disparities in mortality persisted for non-Hispanic Blacks versus non-Hispanic Whites (mean annual decrease 2.3% versus 2.6%, respectively; age-adjusted mortality rate 1.67 to 1.05 versus 1.35 to 0.80 per 100 000, respectively). Conclusions: Although overall US mortality attributable to CHD has decreased over the past 19 years, disparities in mortality persist for males in comparison with females and for non-Hispanic Blacks in comparison with non-Hispanic Whites. Determining factors that contribute to these disparities such as access to quality care, timely diagnosis, and maintenance of insurance will be important moving into the next decade

US Mortality Attributable to Congenital Heart Disease Across the Lifespan From 1999 Through 2017 Exposes Persistent Racial/Ethnic Disparities

Background: Congenital heart disease (CHD) accounts for ≈40% of deaths in US children with birth defects. Previous US data from 1999 to 2006 demonstrated an overall decrease in CHD mortality. Our study aimed to assess current trends in US mortality related to CHD from infancy to adulthood over the past 19 years and determine differences by sex and race/ethnicity. Methods: We conducted an analysis of death certificates from 1999 to 2017 to calculate annual CHD mortality by age at death, race/ethnicity, and sex. Population estimates used as denominators in mortality rate calculations for infants were based on National Center for Health Statistics live birth data. Mortality rates in individuals ≥1 year of age used US Census Bureau bridged-race population estimates as denominators. We used joinpoint regression to characterize temporal trends in all-cause mortality, mortality resulting directly attributable to and related to CHD by age, race/ethnicity, and sex. Results: There were 47.7 million deaths with 1 in 814 deaths attributable to CHD (n=58 599). Although all-cause mortality decreased 16.4% across all ages, mortality resulting from CHD declined 39.4% overall. The mean annual decrease in CHD mortality was 2.6%, with the largest decrease for those \u3e65 years of age. The age-adjusted mortality rate decreased from 1.37 to 0.83 per 100 000. Males had higher mortality attributable to CHD than females throughout the study, although both sexes declined at a similar rate (≈40% overall), with a 3% to 4% annual decrease between 1999 and 2009, followed by a slower annual decrease of 1.4% through 2017. Mortality resulting from CHD significantly declined among all races/ethnicities studied, although disparities in mortality persisted for non-Hispanic Blacks versus non-Hispanic Whites (mean annual decrease 2.3% versus 2.6%, respectively; age-adjusted mortality rate 1.67 to 1.05 versus 1.35 to 0.80 per 100 000, respectively). Conclusions: Although overall US mortality attributable to CHD has decreased over the past 19 years, disparities in mortality persist for males in comparison with females and for non-Hispanic Blacks in comparison with non-Hispanic Whites. Determining factors that contribute to these disparities such as access to quality care, timely diagnosis, and maintenance of insurance will be important moving into the next decade

Birth Defect Survival for Hispanic Subgroups

Background: Previous studies demonstrate that infant and childhood mortality differ among children with birth defects by maternal race/ethnicity, but limited mortality information is published for Hispanic ethnic subgroups. Methods: We performed a retrospective cohort study using data for children with birth defects born to Hispanic mothers during 1999–2007 from 12 population-based state birth defects surveillance programs. Deaths were ascertained through multiple sources. Survival probabilities were estimated by the Kaplan-Meier method. Cox proportional hazards regression was used to examine the effect of clinical and demographic factors on mortality risk. Results: Among 28,497 Hispanic infants and children with major birth defects, 1-year survival was highest for infants born to Cuban mothers at 94.6% (95% confidence intervals [CI] 92.7–96.0) and the lowest for Mexicans at 90.2% (95% CI 89.7–90.6; p \u3c .0001). For children aged up to 8 years, survival remained highest for Cuban Americans at 94.1% (95% CI 91.8–95.7) and lowest for Mexican Americans at 89.2% (95% CI 88.7–89.7; p = .0002). In the multivariable analysis using non-Hispanic White as the reference group, only infants and children born to Mexican mothers were noted to have a higher risk of mortality for cardiovascular defects. Conclusions: This analysis provides a better understanding of survival and mortality for Hispanic infants and children with selected birth defects. The differences found in survival, particularly the highest survival rates for Cuban American children and lowest for Mexican American children with birth defects, underscores the importance of assessing Hispanic ethnic subgroups, as differences among subgroups appear to exist