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David T Mage

Publications and source records attributed to David T Mage.

11 recordsLinked to original sources
PubMed2004

The X-linkage hypotheses for SIDS and the 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%).

Cause of Death↗
PubMed2004

Estimating pesticide dose from urinary pesticide concentration data by creatinine correction in the Third National Health and Nutrition Examination Survey (NHANES-III).

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.

Adult↗
PubMed2004

Seasonal variation of sudden infant death syndrome in Hawaii.

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.

Age Distribution↗
PubMedDate not supplied

Female resistance to hypoxia: does it explain the sex difference in mortality rates?

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.

Centers for Disease Control and Prevention, U.S.↗