The fifty percent male excess of infant respiratory mortality
Article first published online: 2 JAN 2007
Volume 93, Issue 9, pages 1210–1215, September 2004
How to Cite
Mage, D. and Donner, E. (2004), The fifty percent male excess of infant respiratory mortality. Acta Paediatrica, 93: 1210–1215. doi: 10.1111/j.1651-2227.2004.tb02751.x
- Issue published online: 2 JAN 2007
- Article first published online: 2 JAN 2007
- Received Sept. 11, 2003; revision received Jan. 7, 2004; accepted Mar. 9, 2004
- Congenital anomalies;
- male excess;
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 ∼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.