Human pregnancy differs from that of many other species in showing no abrupt changes in maternal levels of estrogen and progesterone at the start of labor. The fetus appears to play a relatively minor role in initiating parturition since mean pregnancy length is not markedly affected by major disorders of the fetal hypothalamus, pituitary or adrenals. Human pregnancy cannot be induced by estrogen treatment and corticosteroids are ineffective except in women beyond term. Prostaglandins are released into the maternal circulation and amniotic fluid during labor but there is no unequivocal evidence of their involvement in initiation of labor. However, there is circumstantial evidence favoring a local mechanism involving the fetal membranes and deciduum that controls prostaglandin release. These tissues contain glycerophospholipids enriched with arachidonic acid in the sn 2 position, phospholipase A2 activity and prostaglandin synthetase. The local mechanism is readily activated by local trauma. It is proposed that the onset of labor is mainly the outcome of a genetically determined maturational event in the amnion and/or chorion. The fetus itself and the mother may modulate, but rarely control, the time of birth.