Medical Misadventures as Errors and Mistakes and Motor Vehicular Accidents in the Disproportionate Burden of Childhood Mortality among Blacks/African Americans in the United States: CDC Dataset, 1968-2015.

PURPOSE: Racial disparities in infant mortality in the United States persist after adjustment for known confounders of race and mortality association, as well as heterogeneity assessment. Epidemiologic and clinical data continue to show the survival disadvantages of Black/AA children: when Black/AAs are compared to whites, they are three times as likely to die from all-cause mortality. The persistent inability to remove the variance in race-mortality association is partly due to unobserved, unmeasured, and residual confounding, as well as implicit biases in public health and clinical medicine in health equity transformation. This current epidemiologic-perspective explanatory model study aimed to examine the possible explanation of racial differences in U.S. infant mortality using medical misadventures as errors and mistakes, and infants' involvement in motor vehicular traffic accidents. MATERIALS AND METHOD: Using CDC WONDER ecologic data from 1968 to 2015, we assessed the infant mortality-rate ratio and percent change associated with medical misadventures as well as motor vehicular accidents or trauma. The rate ratio and percent change were estimated using stratification analysis and trend homogeneity, respectively. RESULTS: There was a Black-white racial difference in medical misadventures during the study period. Relative to the years 1968-1978 (rate ratio [RR], 1.43), there was a steady increase in the mortality-rate ratio in 1979-1998 (52%, RR = 1.52), and mortality was more than two times as likely in 1999-2015 (RR = 2.37). However, with respect to motor vehicular accident/trauma mortality, the mortality ratio, although lower among Blacks in 1968-1978 (RR, 0.92), increased in 1979-1998 by 27% (RR = 1.27) but decreased in 1999-2015 (RR, 1.17), though there was still an excess of 17% mortality among Black/AAs. The percent change for medical misadventures indicated an increasing trend from 9.3% in 1998 to 52% in 2015. However, motor vehicular-related mortality indicated a positive trend in 1998 (38.5%) but a negative trend in 2015 (-8.4%). CONCLUSIONS: There were substantial race differentials or variances in infant mortality associated with medical misadventures compared to traffic accidents, and Black/AA children relative to whites experienced a survival disadvantage. These comparative findings are suggestive of medical misadventures and motor vehicular trauma as potential explanations for some of the persistent Black-white disparities in overall infant mortality in the U.S. From these findings, we recommend a national effort to address these issues, thus narrowing the observed disparities in the U.S. infant mortality burden among Black/AAs.

Risk Differences in Disease-Specific Infant Mortality Between Black and White US Children, 1968-2015: an Epidemiologic Investigation.

PURPOSE: Black/African American (AA) infants have been persistently observed with survival disadvantage compared to White infants in the USA, implying excess mortality. While reliable epidemiologic data continue to illustrate these disparities, data are yet to provide a substantial explanation to the observed rates and risk differences over the past six decades. We aimed in this study to examine the infant mortality risk differences by temporal trends and to provide an ecologic and non-concurrent explanation for the persisted variability. METHODS: A retrospective design with aggregate data from the Center for Disease Control and Prevention (CDC) was used to access the risk difference in cause-specific mortality, while stratification analysis was utilized for the risk ratio estimation. We also estimated the percent change for mortality trends. RESULTS: The cumulative infant mortality (IM) incidence was two times as likely for Black/AA relative to White, risk ratio (RR), 2.05. There were temporal trends in IM between 1968 and 2015 with excess IM among Black/AA children. Specifically, between 1968 and 2015, the percent change (% change) for digestive system disorders (58.43%); genito-urinary tract system disorders (58.20%); muscle, skeleton, and connective tissue disorders (66.60%); congenital anomalies (23.79%); and certain perinatal causes (38.65%) indicated upward trends in infant mortality Black/AA and White risk ratio. Except for neoplasm, and the initial study period (1968-1978) for congenital anomalies, Black/AA infants indicated survival disadvantage, implying excess mortality ratio relative to their White counterparts. CONCLUSION: Disease-specific infant mortality is higher among black/AA except for neoplasm, and increasing percent changes are observed in digestive; genito-urinary; and muscle, skeleton, and connective tissue disorders. These findings are suggestive of the pressing needs to examine the cause of these disparities namely social determinants of health and social inequity for specific risk-adapted intervention in achieving health equity in US infant mortality.

An Acute Respiratory Infection of a Physiologically Anemic Infant is a More Likely Cause of SIDS than Neurological Prematurity.

INTRODUCTION: The cause of the sudden infant death syndrome (SIDS) is perhaps the oldest of unsolved mysteries of medicine, possibly dating back to Exodus in Biblical times when Egyptian children died in their sleep as if from a plague. It occurs when infants die unexpectedly with no sufficient cause of death found in a forensic autopsy, including death scene investigation and review of medical history. That SIDS is an X-linked recessive death from infectious respiratory disease of a physiologically anemic infant and not a simple anomalous cardiac or neurological condition is an extraordinary claim that requires extraordinary evidence. If it were by a simple cause, it would have already been solved, with over 11,000 papers on SIDS listed now in PubMed. Our aim is to use mathematical models of SIDS to explain: (1) its 50% excess male death rate; (2) its 4-parameter lognormal distribution of ages at death; (3) its winter maxima and summer minima; and (4) its increasing rate with live-birth order. METHODS: From extensive SIDS vital statistics data and published epidemiologic studies, we developed probability models to explain the mathematical behavior of SIDS meeting the four constraints mentioned above. We, then, compare these SIDS properties to infant death from acute respiratory infection (ARI), and infant death from encephalopathy, unspecified (EU). RESULTS: Comparisons show that SIDS are congruent with ARI and are not consistent with EU and that these probability models not only fit the SIDS data but they also predict and fit the male fraction of all infant and child mortality from birth through the first 5 years of their life. CONCLUSION: SIDS are not rejected as an X-linked disease involving ARI and are not explained by a triple risk model that has been commonly accepted by the SIDS medical community, as implicating a neurological causation process in a subset of SIDS.

Is excess male infant mortality from sudden infant death syndrome and other respiratory diseases X-linked?

AIM: Male excess infant mortality is well known but unexplained. In 2004, we reported sudden infant death syndrome (SIDS) and other infant respiratory deaths showed a ~50% male excess in the United States between 1979 and 2002. This study analyses expanded US data from 1968 to 2010 to see whether infant respiratory deaths still show similar ~50% male excess and may be X-linked. METHODS: The analysis compared infant mortality data from the US Centers for Disease Control and Prevention, 1968-2010, with 11 World Health Organization International Classification of Diseases (ICD) rubric groups for respiratory deaths by accidents, congenital anomalies, respiratory diseases and causes unknown. RESULTS: The 11 ICD groupings presented male excesses of ~50% and combining the 453,953 US cases produced a male fraction of 0.6034, a 52.1% male excess. A further 72,380 non-US respiratory cases showed a similar 0.6055 male fraction, a 53.5% male excess. CONCLUSION: The constant ~50% male excess for quite different causes of respiratory death suggests they all have a common terminal event and that is acute anoxic encephalopathy. We hypothesise that this constant male excess phenomenon must be caused by a single X-linked gene, with a recessive condition, leading to a predisposition to succumb to acute anoxic encephalopathy.

Estimating perchlorate exposure from food and tap water based on US biomonitoring and occurrence data.

Human biomonitoring data show that exposure to perchlorate is widespread in the United States. The predominant source of intake is food, whereas drinking water is a less frequent and far smaller contributor. We used spot urine samples for over 2700 subjects and estimated 24 h intake using new creatinine adjustment equations. Merging data from surveys of national health (NHANES) with drinking water monitoring (UCMR), we categorized survey participants according to their potential exposure through drinking water or food. By subtracting daily food doses of perchlorate from the oral reference dose (RfD), we derive an allowances for perchlorate in tap water for several populations. The calculated mean food perchlorate dose in the United States was 0.081 µg/kg/day compared to 0.101 µg/kg/day for those who also had a potential drinking water component. The calculated 95th percentile doses, typically falling between 0.2 and 0.4 µg/kg/day, were well below the RfD (0.7 µg/kg/day) in all populations analyzed. Children aged 6-11 years had the highest mean perchlorate doses in food (0.147 µg/kg/day), with an additional water contribution of only 0.003 µg/kg/day representing just 2% of exposure. Pregnant women had a mean food dose of 0.093 vs 0.071 µg/kg/day for all women of reproductive age. At the 95th percentile intake for both the total population and women of child-bearing age (15-44), the perchlorate contribution from food was 86% and from drinking water 14% (respectively, 30% and 5% of the RfD). At the mean for the same groups, the food to water contribution ratio is approximately 80:20. We calculate that an average 66 kg pregnant woman consuming a 90th percentile food dose (0.198 µg/kg/day) could also drink the 90th percentile of community water for pregnant women (0.033 l/kg/day) containing 15 µg/l perchlorate without exceeding the 0.7 µg/kg/day reference dose.

A Unifying Theory for SIDS.

The Sudden Infant Death Syndrome (SIDS) has four distinctive characteristics that must be explained by any theory proposed for it. (1) A characteristic male fraction of approximately 0.61 for all postneonatal SIDS in the US; (2) a distinctive lognormal-type age distribution arising from zero at birth, mode at about 2 months, median at about 3 months, and an exponential decrease with age going towards zero beyond one year; (3) a marked decrease in SIDS rate from the discovery that changing the recommended infant sleep position from prone to supine reduced the rate of SIDS, but it did not change the form of the age or gender distributions cited above; (4) a seasonal variation, maximal in winter and minimal in summer, that implies subsets of SIDS displaying evidence of seasonal low-grade respiratory infection and nonseasonal neurological prematurity. A quadruple-risk model is presented that fits these conditions but requires confirmatory testing by finding a dominant X-linked allele protective against cerebral anoxia that is missing in SIDS.

Creatinine corrections for estimating children's and adult's pesticide intake doses in equilibrium with urinary pesticide and creatinine concentrations.

A urine contaminant concentration per se has uncertain meaning for human health because of dilution by hydration. However, the estimation of the health-related daily intake dose of pollutant (mg/kg/day) that equilibrates with a spot urinary concentration of a pesticide residue or metabolite, or other analyte, can be made using creatinine-corrected toxicant levels (mg analyte/mg creatinine) multiplied by an estimate of the subjects' expected creatinine excretion rates (mg creatinine/kg/day). The objective was to develop a set of equations predicting a person's expected daily creatinine excretion (mg/kg) as a function of age, gender, race and morphometry, from birth to old age. We review the creatinine excretion literature where infants, children and adults provided 24 h total urine samples for creatinine analysis. Equations are developed for infants (or=18 years) that match at 3 and 18 years. A series of equations that estimate daily creatinine excretion (mg/day) are developed that are piecewise continuous from birth through infancy through adolescence and through adulthood for males and females, and Black and White races. Complicating factors such as diet, health status and obesity are discussed. We propose that these equations, with caveat, can now be used with measured urine concentrations to consistently estimate the corresponding equilibrium intake doses of toxicants at ages from birth to 92 years for the healthy non-obese. We recommend that this system of equations be considered for future development and reporting of applied doses in mg/kg/day of pollutants and toxicants that are measured in urine samples, as in the National Health and Nutrition Examination Survey.