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.

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.

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.

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.

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.

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.)

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.)

We combine two major approaches currently used in human air pollution exposure assessment, the direct approach and the indirect approach. The direct approach measures exposures directly using personal monitoring. Despite its simplicity, this approach is costly and is also vulnerable to sample selection bias because it usually imposes a substantial burden on the respondents, making it difficult to recruit a representative sample of respondents. The indirect approach predicts exposures using the activity pattern model to combine activity pattern data with microenvironmental concentrations data. This approach is lower in cost and imposes less respondent burden, thus is less vulnerable to sample selection bias. However, it is vulnerable to systematic measurement error in the predicted exposures because the microenvironmental concentration data might need to be "grafted" from other data sources. The combined approach combines the two approaches to remedy the problems in each. A dual sample provides both the direct measurements of exposures based on personal monitoring and the indirect estimates based on the activity pattern model. An indirect-only sample provides additional indirect estimates. The dual sample is used to calibrate the indirect estimates to correct the systematic measurement error. If both the dual sample and the indirect-only sample are representative, the indirect estimates from the indirect-only sample is used to improve the precision for the overall estimates. If the dual sample is vulnerable to sample selection bias, the indirect-only sample is used to correct the sample selection bias. We discuss the allocation of the resources between the two subsamples and provide algorithms which can be used to determine the optimal sample allocation. The theory is illustrated with applications to the empirical data obtained from the Washington, DC, Carbon Monoxide (CO) Study.

The microenvironmental components of the CO concentration in two cities are compared by subtracting the ambient background concentration from personal exposures measured in Denver, Colorado, and Washington, DC. Two surrogate measures for the ambient background concentration are tested. Both improve the similarity of the means in the two cities, but the Denver standard deviations are higher than those in Washington, DC. Microenvironments containing the internal combustion engine have both higher means and standard deviations in Denver compared with Washington, DC. The Washington, DC, mean concentration for automobiles, for example, was 59% of the Denver mean (2.0 ppm versus 4.9 ppm). Washington, DC, had approximately 57% of the Denver emissions, and the difference in mean CO concentrations is roughly consistent with the lower emissions in Washington, DC, due to lower elevation. A surprising finding is that mean CO exposure levels caused by cooking with gas stoves in Washington, DC, were only 58% of the levels in Denver (1.9 ppm and 3.3 ppm, respectively). This result suggests that elevation may exert an influence on gas stove emissions that is similar to its influence on internal combustion engines. Using an averaging time model, analysis of the autocorrelation of sleeping and office microenvironments suggests that considerable serial dependency exists. The microenvironmental data and findings in this paper have important implications for constructing human exposure-activity pattern models. For future human exposure field studies, the findings emphasize the importance of measuring background values in a location that is extremely close to each microenvironment studied.