Characteristics of Mothers and Infants Living in Homeless Shelters and Public Housing in New York City.

Introduction Homelessness can result in poor health. The number of families with children living in NYC homeless shelters increased 55% from 2008 to 2014. Half of children living in shelter in 2014 were younger than 6 years old. We compared demographics and health outcomes of mothers and infants residing in NYC homeless shelters to those residing in public housing in this cross-sectional study. Methods Addresses of NYC Department of Homeless Services shelters and NYC Housing Authority (NYCHA) developments were matched to NYC Department of Health birth certificate data for the years 2008-2013. Sociodemographic and health characteristics of newborns residing in shelters were compared to newborns in NYCHA housing using Chi square tests. Results Mothers residing in shelters were younger, more likely to be black and less likely to be Hispanic, more likely to have been born outside NYC and reside in the Bronx. Babies born to mothers living in shelter were more likely to have low birth weight (< 2500 g), be born preterm (< 37 gestational weeks), require assisted ventilation immediately following delivery, have a NICU admission, and use Medicaid. They were less likely to breastfeed within 5 days of delivery and be discharged to their residence. Discussion Homeless mothers and infants had poorer health outcomes compared with those living in public housing. Understanding the health disparities of homeless infants can provide guidance for developing future policies and research initiatives, which may be used to inform the development of new policies to improve health outcomes of homeless infants and their mothers.

Trends in Cardiovascular Disease Mortality Among Persons With HIV in New York City, 2001-2012.

BACKGROUND: Cardiovascular disease (CVD) has become more prominent among human immunodeficiency virus (HIV)-infected individuals. The extent to which CVD mortality rates are changing is unclear. METHODS: We analyzed surveillance data for all persons aged ≥13 years with HIV infection between 2001 and 2012 reported to the New York City HIV Surveillance Registry. We examined age-specific and age-standardized mortality rates due to major CVDs. We compared mortality time trends among persons with HIV with the general population, and examined differences among HIV-infected persons by RNA level. RESULTS: There were 29 588 deaths reported among 145 845 HIV-infected persons. Ten percent of deaths were attributed to CVD as the underlying cause, including chronic ischemic heart disease (42% of CVD deaths), hypertensive diseases (27%), and cerebrovascular diseases (10%). While proportionate mortality due to CVD among persons with HIV increased (6% in 2001 to 15% in 2012, P < .001), the CVD mortality rate decreased from 5.1 to 2.7 per 1000 person-years. After controlling for sex, race/ethnicity, borough of residence, and year, those with HIV had significantly higher CVD mortality than the general population in all age groups through age 65. The CVD mortality rate was highest among viremic persons (adjusted rate ratio [RR], 3.53 [95% confidence interval {CI}, 3.21-3.87]) but still elevated among virally suppressed (<400 copies/mL) persons (adjusted RR, 1.53 [95% CI, 1.41-1.66]) compared with the general population. CONCLUSIONS: Our findings support continued emphasis by HIV care providers on both viremic control and preventive measures including smoking cessation, blood pressure control, and lipid management.

Effect of cause-of-death training on agreement between hospital discharge diagnoses and cause of death reported, inpatient hospital deaths, New York City, 2008-2010.

INTRODUCTION: Accurate cause-of-death reporting is required for mortality data to validly inform public health programming and evaluation. Research demonstrates overreporting of heart disease on New York City death certificates. We describe changes in reported causes of death following a New York City health department training conducted in 2009 to improve accuracy of cause-of-death reporting at 8 hospitals. The objective of our study was to assess the degree to which death certificates citing heart disease as cause of death agreed with hospital discharge data and the degree to which training improved accuracy of reporting. METHODS: We analyzed 74,373 death certificates for 2008 through 2010 that were linked with hospital discharge records for New York City inpatient deaths and calculated the proportion of discordant deaths, that is, death certificates reporting an underlying cause of heart disease with no corresponding discharge record diagnosis. We also summarized top principal diagnoses among discordant reports and calculated the proportion of inpatient deaths reporting sepsis, a condition underreported in New York City, to assess whether documentation practices changed in response to clarifications made during the intervention. RESULTS: Citywide discordance between death certificates and discharge data decreased from 14.9% in 2008 to 9.6% in 2010 (P < .001), driven by a decrease in discordance at intervention hospitals (20.2% in 2008 to 8.9% in 2010; P < .001). At intervention hospitals, reporting of sepsis increased from 3.7% of inpatient deaths in 2008 to 20.6% in 2010 (P < .001). CONCLUSION: Overreporting of heart disease as cause of death declined at intervention hospitals, driving a citywide decline, and sepsis reporting practices changed in accordance with health department training. Researchers should consider the effect of overreporting and data-quality changes when analyzing New York City heart disease mortality trends. Other vital records jurisdictions should employ similar interventions to improve cause-of-death reporting and use linked discharge data to monitor data quality.

Mortality of New York children with sickle cell disease identified through newborn screening.

PURPOSE: Long-term follow-up of newborn screening for conditions such as sickle cell disease can be conducted using linkages to population-based data. We sought to estimate childhood sickle cell disease mortality and risk factors among a statewide birth cohort with sickle cell disease identified through newborn screening. METHODS: Children with sickle cell disease identified by newborn screening and born to New York residents in 2000-2008 were matched to birth and death certificates. Mortality rates were calculated (using numbers of deaths and observed person-years at risk) and compared with mortality rates for all New York children by maternal race/ethnicity. Stratified analyses were conducted to examine associations between selected factors and mortality. RESULTS: Among 1,911 infants with sickle cell disease matched to birth certificates, 21 deaths were identified. All-cause mortality following diagnosis was 3.8 per 1,000 person-years in the first 2 years of life and 1.0 per 1,000 person-years at ages 2-9 years. The mortality rate was significantly lower among children of foreign-born mothers and was significantly higher among preterm infants with low birth weight. The mortality rates were not significantly higher for infants after 28 days with sickle cell disease than for all New York births, but they were 2.7-8.4 times higher for children 1 through 9 years old with homozygous sickle cell disease than for those of all non-Hispanic black or Hispanic children born to New York residents. CONCLUSION: Estimated mortality risk in children with homozygous sickle cell disease remains elevated even after adjustment for maternal race/ethnicity. These results provide evidence regarding the current burden of child mortality among children with sickle cell disease despite newborn screening.Genet Med 17 6, 452-459.

Programmatic impact of 5 years of mortality surveillance of New York City homeless populations.

A homeless mortality surveillance system identifies emerging trends in the health of the homeless population and provides this information to key stakeholders in a timely and ongoing manner to effect evidence-based, programmatic change. We describe the first 5 years of the New York City homeless mortality surveillance system and, for the first time in peer-reviewed literature, illustrate the impact of key elements of sustained surveillance (i.e., timely dissemination of aggregate mortality data and real-time sharing of information on individual homeless decedents) on the programs of New York City's Department of Homeless Services. These key elements had a positive impact on the department's programs that target sleep-related infant deaths and hypothermia, drug overdose, and alcohol-related deaths among homeless persons.

Impact of a hospital-level intervention to reduce heart disease overreporting on leading causes of death.

INTRODUCTION: The quality of cause-of-death reporting on death certificates affects the usefulness of vital statistics for public health action. Heart disease deaths are overreported in the United States. We evaluated the impact of an intervention to reduce heart disease overreporting on other leading causes of death. METHODS: A multicomponent intervention comprising training and communication with hospital staff was implemented during July through December 2009 at 8 New York City hospitals reporting excessive heart disease deaths. We compared crude, age-adjusted, and race/ethnicity-adjusted proportions of leading, underlying causes of death reported during death certification by intervention and nonintervention hospitals during preintervention (January-June 2009) and postintervention (January-June 2010) periods. We also examined trends in leading causes of death for 2000 through 2010. RESULTS: At intervention hospitals, heart disease deaths declined by 54% postintervention; other leading causes of death (ie, malignant neoplasms, influenza and pneumonia, cerebrovascular disease, and chronic lower respiratory diseases) increased by 48% to 232%. Leading causes of death at nonintervention hospitals changed by 6% or less. In the preintervention period, differences in leading causes of death between intervention and nonintervention hospitals persisted after controlling for race/ethnicity and age; in the postintervention period, age accounted for most differences observed between intervention and nonintervention hospitals. Postintervention, malignant neoplasms became the leading cause of premature death (ie, deaths among patients aged 35-74 y) at intervention hospitals. CONCLUSION: A hospital-level intervention to reduce heart disease overreporting led to substantial changes to other leading causes of death, changing the leading cause of premature death. Heart disease overreporting is likely obscuring the true levels of cause-specific mortality.

A case study of the impact of inaccurate cause-of-death reporting on health disparity tracking: New York City premature cardiovascular mortality.

OBJECTIVES: Heart disease death overreporting is problematic in New York City (NYC) and other US jurisdictions. We examined whether overreporting affects the premature (< 65 years) heart disease death rate disparity between non-Hispanic Blacks and non-Hispanic Whites in NYC. METHODS: We identified overreporting hospitals and used counts of premature heart disease deaths at reference hospitals to estimate corrected counts. We then corrected citywide, age-adjusted premature heart disease death rates among Blacks and Whites and a White-Black premature heart disease death disparity. RESULTS: At overreporting hospitals, 51% of the decedents were White compared with 25% at reference hospitals. Correcting the heart disease death counts at overreporting hospitals decreased the age-adjusted premature heart disease death rate 10.1% (from 41.5 to 37.3 per 100,000) among Whites compared with 4.2% (from 66.2 to 63.4 per 100,000) among Blacks. Correction increased the White-Black disparity 6.1% (from 24.6 to 26.1 per 100,000). CONCLUSIONS: In 2008, NYC's White-Black premature heart disease death disparity was underestimated because of overreporting by hospitals serving larger proportions of Whites. Efforts to reduce overreporting may increase the observed disparity, potentially obscuring any programmatic or policy-driven advances.

Sickle cell disease incidence among newborns in New York State by maternal race/ethnicity and nativity.

PURPOSE: Sickle cell disease is estimated to occur in 1:300-400 African-American births, with higher rates among immigrants from Africa and the Caribbean, and is less common among Hispanic births. This study determined sickle cell disease incidence among New York State newborns stratified by maternal race/ethnicity and nativity. METHODS: Newborns with confirmed sickle cell disease born to New York State residents were identified by the New York State newborn screening program for the years 2000-2008 and matched to birth records to obtain birth and maternal information. Annual incidence rates were computed and bivariate analyses were conducted to examine associations with maternal race/ethnicity and nativity. RESULTS: From 2000 to 2008, 1,911 New York State newborns were diagnosed with sickle cell disease and matched to the birth certificate files. One in every 1,146 live births was diagnosed with sickle cell disease. Newborns of non-Hispanic black mothers accounted for 86% of sickle cell disease cases whereas newborns of Hispanic mothers accounted for 12% of cases. The estimated incidence was 1:230 live births for non-Hispanic black mothers, 1:2,320 births for Hispanic mothers, and 1:41,647 births for non-Hispanic white mothers. Newborns of foreign-born non-Hispanic black mothers had a twofold higher incidence of sickle cell disease than those born to US-born non-Hispanic black mothers (P < 0.001). CONCLUSION: This study provides the first US estimates of sickle cell disease incidence by maternal nativity. Women born outside the United States account for the majority of children with sickle cell disease born in New York State. Such findings identify at-risk populations and inform outreach activities that promote ongoing, high-quality medical management to affected children.

An intervention to improve cause-of-death reporting in New York City hospitals, 2009-2010.

INTRODUCTION: Poor-quality cause-of-death reporting reduces reliability of mortality statistics used to direct public health efforts. Overreporting of heart disease has been documented in New York City (NYC) and nationwide. Our objective was to evaluate the immediate and longer-term effects of a cause-of-death (COD) educational program that NYC's health department conducted at 8 hospitals on heart disease reporting and on average conditions per certificate, which are indicators of the quality of COD reporting. METHODS: From June 2009 through January 2010, we intervened at 8 hospitals that overreported heart disease deaths in 2008. We shared hospital-specific data on COD reporting, held conference calls with key hospital staff, and conducted in-service training. For deaths reported from January 2009 through June 2011, we compared the proportion of heart disease deaths and average number of conditions per death certificate before and after the intervention at both intervention and nonintervention hospitals. RESULTS: At intervention hospitals, the proportion of death certificates that reported heart disease as the cause of death decreased from 68.8% preintervention to 32.4% postintervention (P < .001). Individual hospital proportions ranged from 58.9% to 79.5% preintervention and 25.9% to 45.0% postintervention. At intervention hospitals the average number of conditions per death certificate increased from 2.4 conditions preintervention to 3.4 conditions postintervention (P < .001) and remained at 3.4 conditions a year later. At nonintervention hospitals, these measures remained relatively consistent across the intervention and postintervention period. CONCLUSION: This NYC health department's hospital-level intervention led to durable changes in COD reporting.

Excess mortality among injection drug users with AIDS, New York City (1999-2004).

We calculated proportions and trends in contributing causes of death among persons with AIDS (PWA) and a history of injection drug use (IDU) in New York City and compared the proportions with those among PWA with a transmission risk of high-risk heterosexual sex (HRH) and men who have sex with men (MSM). We included all 10,575 injection drug user, HRH, and MSM residents aged 13+ years with AIDS reported by September 30, 2006 , who died from 1999 through 2004. Accidental drug overdose was the most frequent contributing cause of death among IDUs (20.5%). Overdose prevention initiatives may greatly and immediately reduce deaths among PWA.

Etiology of nonspecific cause of death coding in New York City motor vehicle crash-related fatalities.

OBJECTIVES: Nearly 20 percent of New York City's (NYC) accidental deaths are related to motor vehicles crashes (MVCs). Detailed International Classification of Disease (ICD-10; World Health Organization [WHO] 2007) cause-of-death coding of MVC-related fatalities improves surveillance and resulting identification of prevention strategies. We investigated ICD-10 codes in these fatalities and the potential to make them more specific. METHODS: We defined "nonspecific" MVC ICD-10 codes as all globally unspecific codes (V870-V878, V892) and any codes with nonspecific components regarding vehicle involved, decedent position in vehicle, or MVC setting. We calculated nonspecific-code frequency for 1999-2008 MVC deaths. We reviewed a random 10 percent sample of 2007-2008 MVC deaths (N=61) and medical examiner (ME) records of all nonspecific death certificates (N=52), including police accident reports ("full PAR") and summaries prepared by onsite police officers ("brief PAR") to determine whether MEs had sufficient information available but did not include that information at death certification. RESULTS: Among 1999-2008 NYC MVC deaths, 82.9 percent had nonspecific ICD-10 cause-of-death codes. Similarly, of the 61 recent randomly sampled MVC deaths, 52 (85.2%) had nonspecific codes. Of 52 nonspecific death certificates from the random sample, 38 (73.1%) death certificates had adequate information available on full or brief PAR to be more specific at the time of death certification. Consistent with MEs' reports of high reliance on the brief PAR, most nonspecific death certificates (76.9%) lacked adequate information in the brief PAR to be more specific. CONCLUSION: Specific ICD-10 codes for MVC deaths depends on the level of detail provided by the ME in the "How Injury Occurred" and "If Transportation Injury Specify" death certificates sections. We have worked to ensure that key information is available to MEs in the brief PAR and educated MEs on the importance of this information to reduce the frequency of nonspecific codes and enhance injury prevention research.

Overreporting of deaths from coronary heart disease in New York City hospitals, 2003.

INTRODUCTION: New York City has one of the highest reported death rates from coronary heart disease in the United States. We sought to measure the accuracy of this rate by examining death certificates. METHODS: We conducted a cross-sectional validation study by using a random sample of death certificates that recorded in-hospital deaths in New York City from January through June 2003, stratified by neighborhoods with low, medium, and high coronary heart disease death rates. We abstracted data from hospital records, and an independent, blinded medical team reviewed these data to validate cause of death. We computed a comparability ratio (coronary heart disease deaths recorded on death certificates divided by validated coronary heart disease deaths) to quantify agreement between death certificate determination and clinical judgment. RESULTS: Of 491 sampled death certificates for in-hospital deaths, medical charts were abstracted and reviewed by the expert panel for 444 (90%). The comparability ratio for coronary heart disease deaths among decedents aged 35 to 74 years was 1.51, indicating that death certificates overestimated coronary heart disease deaths in this age group by 51%. The comparability ratio increased with age to 1.94 for decedents aged 75 to 84 years and to 2.37 for decedents aged 85 years or older. CONCLUSION: Coronary heart disease appears to be substantially overreported as a cause of death in New York City among in-hospital deaths.

Methods for assessing familial aggregation: family history measures and confounding in the standard cohort, reconstructed cohort and case-control designs.

OBJECTIVES: To test whether case-control-based familial aggregation studies produce estimates of risk to relatives that are inherently biased or confounded by age and family size, and to compare case-control-derived estimates with those from the reconstructed cohort method. In addition, we test if the definition of family history affects the accuracy of results obtained from either design. We use simulated data, which allows us to know the true data origin. METHODS: We simulated populations of three generation families. Both a dominant genetic disease and a non-genetic disease were present in the population. We compared the effect estimates from different measures of family history with those derived from the actual genetic cause of disease. RESULTS: Effect estimates from family history measures that used multiple family members were more accurate than those derived from measures based on a single relative. Neither family size nor age of family members defining family history were confounders in the case-control design. CONCLUSION: The case-control and reconstructed cohort designs are equally valid in assessing familial aggregation of disease.

Partnership for preparedness: a model of academic public health.

The New York City Department of Health and Mental Hygiene and the Columbia University Mailman School of Public Health's National Center for Disaster Preparedness undertook a collaborative project to establish a model academic health department. The goals were to increase student participation at the health department, increase faculty participation in health department activities, and facilitate health department faculty appointments at the school. As a result, 17 students were placed in full-time summer research projects designed by health department staff specifically for the project, 154 health department staff attended a series of six lectures presented by faculty, and five health department professionals applied for academic appointments at the school. The benefits of the efforts toward establishing an academic health department extend to all areas of public health practice, including those of preparedness.

Construction of the model for the Genetic Analysis Workshop 14 simulated data: genotype-phenotype relationships, gene interaction, linkage, association, disequilibrium, and ascertainment effects for a complex phenotype.

The Genetic Analysis Workshop 14 simulated dataset was designed 1) To test the ability to find genes related to a complex disease (such as alcoholism). Such a disease may be given a variety of definitions by different investigators, have associated endophenotypes that are common in the general population, and is likely to be not one disease but a heterogeneous collection of clinically similar, but genetically distinct, entities. 2) To observe the effect on genetic analysis and gene discovery of a complex set of gene x gene interactions. 3) To allow comparison of microsatellite vs. large-scale single-nucleotide polymorphism (SNP) data. 4) To allow testing of association to identify the disease gene and the effect of moderate marker x marker linkage disequilibrium. 5) To observe the effect of different ascertainment/disease definition schemes on the analysis. Data was distributed in two forms. Data distributed to participants contained about 1,000 SNPs and 400 microsatellite markers. Internet-obtainable data consisted of a finer 10,000 SNP map, which also contained data on controls. While disease characteristics and parameters were constant, four "studies" used varying ascertainment schemes based on differing beliefs about disease characteristics. One of the studies contained multiplex two- and three-generation pedigrees with at least four affected members. The simulated disease was a psychiatric condition with many associated behaviors (endophenotypes), almost all of which were genetic in origin. The underlying disease model contained four major genes and two modifier genes. The four major genes interacted with each other to produce three different phenotypes, which were themselves heterogeneous. The population parameters were calibrated so that the major genes could be discovered by linkage analysis in most datasets. The association evidence was more difficult to calibrate but was designed to find statistically significant association in 50% of datasets. We also simulated some marker x marker linkage disequilibrium around some of the genes and also in areas without disease genes. We tried two different methods to simulate the linkage disequilibrium.