In utero exposure to smoking and peripheral chemoreceptor function

The common physiopathology of sudden unexplained infant and perinatal death is attributed to impaired developmental processes in the peripheral chemoreceptors, i.e., in the carotid and aortic bodies and the aorticopulmonary paraganglia. At the functional level, a sudden death implies a defective resetting, slow or incomplete, of the sensitivity to hypoxia and hypercapnia and/or a defective processing of signals in the cardiorespiratory centers of the brainstem. A normal infant’s nervous system receives prompt information on a progressive hypercapnia and hypoxia event, and triggers respiration or arousal. In infants with peripheral or central chemoreception defects, these protective reflexes are not initiated at normal levels of hypoxia and hypercapnia, and prolonged apnea can develop until blood gas alterations reach the higher level required to initiate new respiration or arousal. These prolonged apnea may lead to fatal apnea and sudden death. Smoke exposure in utero acts as a triggering phenomenon in fetuses and infants with developmental abnormalities located the in brainstem centers regulating vital functions or in the cardiac conduction system. Prevention of stillbirth and SIDS is the object of the bill S. 3142 introduced in 2008 in the Senate of the United States, which will enhance public health activities related to understanding and preventing stillbirth and sudden unexpected infant deaths. The aim of the bill is to significantly reduce the toll in human life, the promotion of anatomoclinical, genetic and epidemiological research, and awareness and information campaigns, and the implementation of programs and projects for the psychological support of victims’ families.