Clinical investigations of human fetuses have revealed that placentas may occasionally exhibit harbour chromosomal aberrations that are absent from the fetus 1 . The basis of this genetic segregation of the placenta, termed confined placental mosaicism, remains unknown. Here, we investigated the phylogeny of human placentas reconstructed from somatic mutations, using whole genome sequencing of 86 placental bulk samples biopsies and of 106 microdissections.We found that every placental bulk sample biopsy represented a clonal expansion that is genetically distinct. Biopsies exhibited a genomic landscape akin to childhood cancer, in terms of mutation burden and mutational imprints. Furthermore, unlike any other human normal tissue studied to date, placental genomes commonly harboured copy number changes.Reconstructing phylogenetic relationships between tissues from the same pregnancy, revealed that developmental bottlenecks genetically isolate confined placental tissues, by separating trophectodermal from inner cell mass-derived lineages. Of particular note were cases in which inner cell mass-derived and placental lineages fully segregated within a few cell divisions of the zygote. Such early embryonic bottlenecks may enable the normalisation normalization of zygotic aneuploidy. We observed direct evidence for this in a case of mosaic trisomic rescue.Our findings reveal extensive cancer-like mutagenesis in placental tissues and portray confined mosaicism as a the normal feature outcome of placental development.