Figure 1: Summary diagram of the putative mechanisms underlying the development of reproductive disorders in human male fetuses. Different classes of endocrine-disrupting chemicals (EDCs) inhibit the production of androgens and insulin-like factor 3 (Insl3) by fetal Leydig cells (FLCs) in the sensitive androgen-dependent period of male reproductive organ development. Under-masculinization disturbs the proper formation and growth of the penis, increasing the risk of developing hypospadias and micropenis. A lack of Insl3 alters the normal testis descent, leading to cryptorchidism. EDCs can impair Sertoli cell (SC) differentiation from their progenitors and alter the proliferation of gonocytes that may lead to poor semen quality in postnatal life. EDCs may also directly impair the development of the reproductive organs by antiandrogenic or estrogen-mediated mechanisms and affect the methylation and/or acetylation status of the fetal testicular cells, which may create an abnormal genetic background and an increased risk of testicular cancer in postnatal life.