Search

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.

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.

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.

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., (©2013 Foundation Acta Paediatrica. Published by John Wiley & Sons Ltd.)

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.

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.

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.

There is currently no accepted explanation in the medical literature for the lower female total mortality rate in infancy, childhood and adulthood. We review the pediatric mortality data provided by Centers for Disease Control and Prevention (CDC) and the World Health Organization (WHO) and show that for causes of respiratory infant death that are apparently independent of gender (e.g., suffocation from inhalation of food or other object), there is a consistently one-third lower rate of mortality in the female than in the male. This one-third lower mortality for causes of death with a respiratory terminal event is hypothesized to be due to an X-linked dominant allele that occurs with frequency 1/3. It appears as if a second X chromosome provides the one-third extra probability of protection afforded for an XX female compared with an XY male. It is suggested that the allele's function is unmasked during transient periods of cerebral anoxia, requiring a mechanism for anaerobic oxidation to prevent the death of respiratory control neurons in the brain stem. Examples of the female one-third extra chance of resistance to hypoxia are given for causes of death in infancy, such as infant respiratory distress syndrome (IRDS) and sudden infant death syndrome (SIDS), and for causes of suffocation in childhood and asphyxiation in adulthood. DNA testing of the X chromosome of probands from causes of respiratory death, such as SIDS and IRDS, where there is a one-third lower female than male death rate, is a future direction that can verify the existence of the proposed allele.

The Third National Health and Nutrition Examination Survey gathered health and job data from a sample of the US population. Researchers collected urine samples from a subset of subjects and analyzed it for 12 pesticide residues or metabolites (ie, analytes). They investigated the relationship between the industries and jobs reported and the analytes detected in the urine samples. The authors found an association between several jobs and the concentration for one or more pesticide analytes above the 90th percentile. They applied a job exposure matrix to categorize subjects on their potential for job exposures to pesticides. For the detected analytes, the subjects with the highest potential for occupational exposures to insecticides were more likely to have an analyte concentration above the 90th percentile and to have an average analyte concentration score 30% higher than that of subjects reporting jobs with the lowest exposure potential. These findings indicate that occupational exposure may not be a major source of pesticide exposure among the general population.

The Third National Health and Nutrition Examination Survey (NHANES-III) of the Centers for Disease Control and Prevention (CDC) recorded data on the urinary concentrations of 12 chemicals (analytes), which were either pesticides or their metabolites, that represent exposure to certain pesticides, in urine samples collected from 1988 to 1994 from a cohort of 978 volunteer subjects, aged 20-59 years. We have used each subject's urinary creatinine concentration and their individual daily creatinine excretion rate (g/day) computed from their age, gender, height and weight, to estimate their daily excretion rate in microg analyte/kg/day. We discuss the mechanisms of excretion of the analytes and certain assumptions needed to compute the equivalent daily dietary intake (microg/kg/day) of the most likely parent pesticide compounds for each excreted analyte. We used literature data on the average amount of parent compound ingested per unit amount of the analyte excreted in the urine, and compared these estimated daily intakes to the US EPA's reference dose (RfD) values for each of those parent pesticides. A Johnson S(B) distribution (four-parameter lognormal) was fit to these data to estimate the national distribution of exclusive exposures to these 12 parent compounds. Only three such pesticides had a few predicted values above their RfD (lindane 1.6%; 2,4-dichlorophenol 1.3%; chlorpyrifos 0.02%). Given the possibility of a subject's dietary intake of a pesticide's metabolites incorporated into treated food, our results show that few, if any, individuals in the general US population aged 20-59 years and not employed in pesticide application were likely to have exceeded the USEPA RfD for these parent compounds during the years studied.

Objective: To test whether the sudden infant death syndrome (SIDS) rate displays the universal winter maximum and summer minimum in Hawaii where there is no appreciable seasonal variation of temperature., Design: The null hypothesis is tested that there is no seasonal variation of necropsied SIDS in Hawaii. The numbers of live births and SIDS cases by month for the years 1979 to 2002 were collected and the monthly SIDS distribution is predicted based on the age at death distribution., Setting: The state of Hawaii, located in the midst of the Pacific Ocean, has a semi-tropical climate with temperatures fluctuating diurnally as 25 +/- 5 degrees C throughout the year. Therefore homes are unheated and infants are not excessively swaddled. The Hawaii State Department of Health maintains vital statistics of all infant births and deaths., Main Results: The results reject the null hypothesis of no seasonal variation of SIDS (p = 0.026). An explanation for the seasonal effect of the winter maximum and summer minimum for Hawaiian SIDS is that it arises from the cycle of the school session and summer vacation periods that represent variable intensity of a possible viral infection vector. SIDS rates in both Hawaii and the United States increase with parity, also indicating a possible role of school age siblings as carriers., Conclusions: The winter peak of the SIDS in Hawaii is support for the hypothesis that a low grade viral infection, insufficient by itself to be a visible cause of death at necropsy, may be implicated as contributing to SIDS in vulnerable infants.

Aim: To test whether infant mortality from clearly respiratory causes has a consistent male excess that is different from the male excess in most cardiac conditions., Methods: Analysis of male excess in infant mortality data from the United States and from north European countries. Data are analyzed for the period 1979-2002 in autopsied and unautopsied cohorts., Results: Several modes of respiratory death in infancy are characterized by an approximate 50% male excess. This common excess is demonstrated in vital statistics for infant respiratory distress syndrome, sudden infant death syndrome, inhalation of food and other objects causing obstruction of respiratory tract or suffocation, congenital pneumonia, viral pneumonia, bronchiolitis and bronchitis, and accidental drowning. Results are presented for these and other respiratory causes of mortality in all United States infant deaths from 1979-1998 and for sudden infant death syndrome from the United Kingdom and Scandinavia. In sudden infant death syndrome, the common male excess appears to exist only for the autopsied post-neonatal cases. Comparisons are made to the male excess mortality from congenital cardiac anomalies showing a similarly large male excess for those conditions resulting in severe hypoxic and ischemic hypoxia., Conclusion: Because these respiratory disease conditions are quite different, it is proposed that their common approximately 50% male excess implies a common terminal hypoxic condition and mechanism of death reached via the different pathways. We hypothesize that an unknown X-linkage may be responsible for this consistent male excess in infant mortality.

Sudden Infant Death Syndrome is characterized globally by a 50% excess in males per 1000 live births of each gender. We previously hypothesized that this male excess may arise from a single X-linked gene locus with a dominant allele (p = 1/3) that is protective against potentially terminal cerebral anoxia by catalyzing anaerobic oxidation and a recessive allele (q = 2/3) that is unprotective. We now hypothesize this same terminal mechanism for all other causes of infant respiratory death (50% male excess) and that infant cardiac death is equally probable for males and females (0% male excess). With these hypotheses, we model the male excess of all infant mortality (under 5 years) as 25% per 1000 live births of each gender. We show for the USA (1979-2000) that this model of a 25% male excess accurately predicts the male excess mortality under 1 year (24.15%), from 1 to 4 years (25.42%), and under 5 years (24.51%).

Using a cohort study of all deaths in infants under 12 months in Dundee born between 1882-91 we set out to compare the aetiology of sudden unexpected infant deaths in Dundee at the end of the 19th Century with the aetiology of present day Sudden Infant Death Syndrome (SIDS). During 1882-1891, 361 infants died suddenly and unexpectedly and without obvious cause while in bed with their parents. The sex ratio of deaths was even (0.51 male) whereas the typical male fraction of SIDS today is 0.61. The mean age at death was almost two and one-half weeks younger in the Dundee cohort than for SIDS in modern Scotland. The infants in the Dundee cohort were discovered more frequently early in the morning than is typical. Their social class distribution was different in that no overlying cases were found in the higher classes whereas SIDS affects all classes. The overlying rate for illegitimate infants was lower than that reported for SIDS today. The epidemiological characteristics of the Dundee cohort and of those dying from present day SIDS differ considerably. The Dundee cohort apparently died from overlying rather than from SIDS as it is classified today. Present day advice that co-sleeping is safe should be given more cautiously until the safety of co-sleeping is resolved. It might be prudent to inform parents that co-sleeping is a risk factor for SIDS and that it should therefore be avoided.

Kitchen-area 22-h gravimetric PM2.5 and passive diffusion stain-tube carbon monoxide (CO) concentrations were measured in homes with open fire and improved wood cookstoves in two studies. In the first study (Guat-2), which also studied homes with gas cookstoves, three samples were collected per stove condition from each of three test houses. In the second study (Guat-3), one sample was collected per house from 15 open fire and 25 improved-stove houses. CO personal samples were also taken for mother and child in both studies. Spearman correlation coefficients (R) between kitchen-area CO and PM2.5 levels in homes using open fires or impoved wood cookstoves were high ranging from 0.92 (Guat-2) to 0.94 (Guat-3), as were those between the personal samples for mother and child ranging from 0.85 (Guat-3) to 0.96 (Guat-2). In general, the correlations were lower for less-polluted conditions. The study found that CO is a good proxy for PM2.5 in homes using open fires or planchas (improved wood cookstove with chimney) but not under gas stove use conditions. It also determined that mother personal CO is a good proxy for child's (under 2 years of age) personal CO and that area CO measurements are not strongly representative of personal CO measurements. These results generally support the use of Draeger CO passive diffusion tubes as a proxy for PM2.5 in such cases where a single type of emission source is the predominant source for CO and PM2.5.

Modern epidemiology has shown that fluctuations of mortality data are statistically significantly correlated with fluctuations of ambient particulate matter (PM) concentration data. This relation cannot be confounded by exposure to PM of indoor origin because the concentrations of ambient PM are not correlated with concentrations of PM of indoor origin. It has been suggested, given the above understanding, that modern PM exposure measurements and analysis should create separate estimates of exposure to all PM of ambient origin and exposure to all PM of nonambient origin (primarily of indoor origin), and not exposure to total PM. This paper reviews the developments of the form of the general microenvironmental mass balance equation that can be utilized for estimating human exposure to PM of ambient origin and for estimating the portion of total PM exposure that is attributable to nonambient origin PM. The equation is perfectly general and can be applied to conditions of time-varying factors that influence exposure, such as rapidly changing air-exchange rates in a home as doors and windows are opened and closed, and turning on and off air cleaners in a home. It is suggested that this procedure be applied in exposure assessment studies and validated using independent techniques of estimating exposure to PM of ambient origin available in the literature.

This paper discusses the legal and scientific reasons for separating personal exposure to PM into ambient and nonambient components. It then demonstrates by several examples how well-established models and data typically obtained in exposure field studies can be used to estimate both individual and community average exposure to ambient-generated PM (ambient PM outdoors plus ambient PM that has infiltrated indoors), indoor-generated PM, and personal activity PM. Ambient concentrations are not highly correlated with personal exposure to nonambient PM or total PM but are highly correlated with personal exposure to ambient-generated PM. Therefore, ambient concentrations may be used in epidemiology as an appropriate surrogate for personal exposure to ambient-generated PM. Suggestions are offered as to how exposure to ambient-generated PM may be obtained and used in epidemiology and risk assessment.

The frequency of self-reported high pesticide exposure events (HPEE) has been recorded in the NCI/EPA/NIEHS Agricultural Health Study (AHS). Fourteen percent (14%) of the enrolled applicators responding reported "an incident or experience while using any pesticide which caused an unusually high exposure." These data show, as expected, that the probability of a report of an HPEE increases with the cumulative number of days of pesticide application reported by the applicator. We have developed a three-parameter model that predicts the risk odds ratio (OR) of an HPEE as a function of the number of days that pesticides are applied. These events are costly in terms of resulting health-care visits, lost time from work, and potential risk for cancer and other chronic diseases. We propose that failure to carefully follow all the pesticide manufacturer's label requirements, inexperience, and random events (i.e., breaking hose) are the three factors responsible for the events observed. Special precautions for new or infrequent users of pesticides are indicated.

Data on recent and historic pesticide use, pesticide application methods, and farm characteristics were collected from 35,879 restricted-use pesticide applicators in the first 2 years of the Agricultural Health Study, a prospective study of a large cohort of private and commercial licensed pesticide applicators that is being conducted in Iowa and North Carolina. (In Iowa, applicators are actually "certified," while in North Carolina they are "licensed"; for ease of reference the term license will be used for both states in this paper.) Commercial applicators (studied in Iowa only) apply pesticides more days per year than private applicators in either state. When the types of pesticides being used by different groups are compared using the Spearman coefficient of determination (r2), we find that Iowa private and Iowa commercial applicators tend to use the same type of pesticides (r2=0.88). White and nonwhite private applicators tended to use the same type of pesticides (North Carolina r2=0.89), as did male and female private applicators (Iowa r2=0.85 and North Carolina r2=0.84). There was less similarity (r2=0. 50) between the types of pesticides being used by Iowa and North Carolina private applicators. A greater portion of Iowa private applicators use personal protective equipment than do North Carolina private applicators, and pesticide application methods varied by state. This heterogeneity in potential exposures to pesticides between states should be useful for subsequent epidemiologic analyses using internal comparison groups., (Copyright 1999 Academic Press.)

Characteristics of persons who report high pesticide exposure events (HPEE) were studied in a large cohort of licensed pesticide applicators from Iowa and North Carolina who enrolled in the Agricultural Health Study between December 1993 and December 1995. Fourteen percent reported having "an incident or experience while using any pesticide which caused an unusually high personal exposure. " After taking into account total number of applications made and education, females (OR=0.76), applicators from NC (OR=0.65), and privately licensed applicators (OR=0.65) were less likely to have reported an HPEE. Work practices more common among both private and commercial applicators with an HPEE included delay in changing clothing or washing after pesticide application, mixing pesticide application clothing with the family wash, washing up inside the house after application, applying pesticides within 50 yards of their well, and storing pesticides in the home. Job characteristics more common among those with an HPEE included self-repair of application equipment and first pesticide use more than 10 years in the past. These job characteristics explained much of the difference in reported HPEE between males and females, but not between IA and NC subjects or between commercial or private applicators., (Copyright 1999 Academic Press.)