Effects of the insecticide chlordecone (Kepone) on female reproduction in birds and mammals were reviewed. In different avian species, chlordecone inhibited or reduced reproduction and decreased egg hatchability and survival of the newborn. In Japanese quail, chronic chlordecone ingestion decreased total egg production and clutch size and increased egg breakage. Eggs produced by treated quail were significantly weaker and thinner. Chlordecone also decreased follicular development, induced ovarian regression, and inhibited ovulation and egg laying. Histological studies showed that when chlordecone was fed to sexually immature quail, the oviducts exhibited accelerated growth, cytodifferentiation, cellular hypertrophy, secretory activity, and maturation. Ultrastructure of the oviduct surface showed increased growth of microvilli and profuse ciliation. Chlordecone also stimulated granular endoplasmic reticulum and Golgi development and induced full secretory activity in the cytoplasm of estrogen‐sensitive quail oviduct cells. In addition to mimicking estrogen in the quail oviduct, chlordecone produced abnormal apical protrusions of oviduct cells, disoriented and twisted cilia, disorganized Golgi apparatus, induced myelin figure formation, and swollen or abnormal mitochondria in oviduct cells that produce egg white protein and eggshell. Chlordecone also detrimentally effected mammalian reproduction. Mice ingesting chlordecone produced decreased litters, and the adult females exhibited constant estrus, decreased corpora lutea, and hormonal imbalance resulting in decreased luteinizing hormone levels. In pregnant mice and rats, chlordecone produced fetal toxicity, abnormalities, and malformations. In neonatal or weanling rats, chlordecone induced rapid uterine growth, precocious vaginal opening, decreased corpora lutea, and persistent vaginal estrus. In adult rats, chlordecone inhibited female reproduction, which was only partially restored after chlordecone ingestion ceased. In neonatal female mice, chlordecone induced development of the entire reproductive tract. Both oviduct and uterus showed accelerated growth, cellular hypertrophy, and hyperplasia, whereas vaginal epithelium became keratinized. Ultra‐structure of chlordecone‐treated neonatal mouse oviduct and uterus surfaces revealed increased cell size and cell surfaces, rapid growth of microvilli and cilia, and discharge of numerous secretory granules. However, numerous oviduct and uterine cells exhibited severe apical protrusions in the form of swelling, and in the oviduct cilia appeared disorganized and twisted. In immature avian and mammalian reproductive tracts, chlordecone appears to produce similar alterations and abnormalities. Such stimulatory changes are not surprising, since recent reports indicate that chlordecone estrogenicity is apparently due to its competition for and binding to estrogen receptors in mammalian uterus and avian oviduct cells.