Does heat damage fetuses?

Abstract

Temperature affects phenotypic variation during critical developmental stages in all forms of life that have been studied thus far. In animal studies of heat teratogenicity, adverse effects have ranged from disruption of the normal cell cycle leading to decreased numbers of cells, to the induction of developmental abnormalities by means of embryonic cell death. The heat shock response is a universal cellular stress reaction in which the transcriptional and translational mechanisms of the cell are pre-empted by preferential induction of heat shock protein synthesis. Occurrence of such a phenomenon during prenatal life could lead to the absence of essential gene products at critical stages of development. The crucial question of whether temperature induced cellular and genetic effects ever occur during human fetal development has been considered only in relation to maternal hyperthermia, which is generally viewed as not being of significance in human teratology. We propose that teratogenicity may result from fetal hyperthermia unrelated to maternal hyperthermia, caused either by impaired fetomaternal heat dissipation due to reduced placental blood flow (extrinsic fetal hyperthermia) or by increased fetal heat production during hypermetabolic states (intrinsic fetal hyperthermia). The need for further studies in this regard is emphasized.