Richard L. Naeye

Male infants have an excessive risk of neonatal death by comparison with females. It has never been clear whether this male disadvantage is due to specific disease processes or is a general biologic feature of being male. In an analysis of 2,735 consecutive newborn autopsies, the ratio of males to females was 1.28:, which differs significantly from the 1.05:1 ratio for all U.S. livebirths. There was a near equal male to female ratio for most disorders in stillborn infants while disorders arising after birth demonstrated a strong male disadvantage. The still-born ratios presumably reflect a predominant maternal influence while birth and removal from the maternal environment uncovers an inherent biologic disadvantage of being male, a disadvantage not selectively related to specific disease processes. This nonspecificity is confirmed by the finding of several disorders in which sex ratios for stillborns are quite different than the ratios recorded for liveborn infants. The sex ratio for liveborn Caucasians was significantly greater than for nonwhites, and the nonpoor had a significantly greater ratio than the poor. About half of these differences appear related to a greater incidence of prenatal bacterial infections in the poor and nonwhites.

Data were analyzed from a large prospective study to try to determine whether or not women's smoking during pregnancy affects their children's mental development. Many confounding variables were controlled by multiple regression analysis and by intrapair comparisons of siblings whose mothers had smoked during one but not in the other of the two pregnancies. Hyperactivity, short attention span, and lower scores on spelling and reading tests were more frequent for children whose mothers had smoked throughout pregnancy. The cognitive abnormalities were mild, with achievement test scores only 2 to 4% lower in children whose mothers had smoked during pregnancy. The behavioral abnormalities in children of smokers were associated with elevated neonatal hemoglobin levels and low birth weights, suggesting that fetal hypoxemia possibly may contribute to the genesis of behavioral abnormalities.

Fourteen of 28 sudden-infant-death syndrome (SIDS) victims had an abnormal proliferation of astroglial fibers in their brain stems and an enlarged mass of chromaffin cells in their adrenal medullas. Both of these abnormalities were associated with greater than normal muscle in the small pulmonary arteries, abnormal brown fat retention, and retained extramedullary erythropoiesis. These latter three findings are probably evidences of chronic alveolar hypoventilation and hypoxemia. The brain stem and adrenal abnormalities are probably also secondary to chronic hypoxemia.

Infants with known chronic hypoxemia before death retained a large proportion of the brown fat cells that are normally replaced by white fat cells after birth. Many of these hypoxemic infants also had an abnormal retention of extramedullary hematopoiesis. These same abnormalities were found in many victims of the sudden infant death syndrome.