In his 1991 article Screening for Congenital Hypothyroidism, Delbert A. Fisher in the US reported on the implementation and impact of mass neonatal screening programs for congenital hypothyroidism (CH) from the early 1970s through 1991. CH is a condition that causes stunted mental and physical development in newborns unless treatment begins within the first three months of the newborn's life. In the early 1970s, regions in Canada and the US had implemented screening programs to diagnose and treat CH as quickly as possible after the infant's birth. By 1991 many other countries had adopted the early screening program, and Fisher estimated that 10 to 12 million newborns per year were tested in the early 1990s. The screening programs, along with physician education and improved screening techniques, such as radioimmunoassay, helped significantly reduce the incidence of abnormal newborn development resulting from untreated congenital hypothyroidism.

Our Bodies, Ourselves, a succession to a pamphlet of resources pulled from co-ops of women in and around Boston, Massachusetts was published in New York in 1973 by Simon and Schuster. Retitled from the original Women and Their Bodies, Our Bodies, Ourselves was an effort by a group of educated, middle class women to reinforce women's ownership of their bodies. There have been eight editions of Our Bodies, Ourselves, as well as sequels such as Our Bodies, Ourselves: Pregnancy and Birth and Our Bodies, Ourselves: Menopause. Our Bodies, Ourselves has sold more than four million copies and been printed in twenty foreign-language editions.

Teratogens are substances that may produce physical or functional defects in the human embryo or fetus after the pregnant woman is exposed to the substance. Alcohol and cocaine are examples of such substances. Exposure to the teratogen affects the fetus or embryo in a variety of ways, such as the duration of exposure, the amount of teratogenic substance, and the stage of development the embryo or fetus is in during the exposure. Teratogens may affect the embryo or fetus in a number of ways, causing physical malformations, problems in the behavioral or emotional development of the child, and decreased intellectual quotient IQ in the child. Additionally, teratogens may also affect pregnancies and cause complications such as preterm labors, spontaneous abortions, or miscarriages. Teratogens are classified into four types: physical agents, metabolic conditions, infection, and finally, drugs and chemicals.

The concept Fetal Alcohol Syndrome (FAS) refers to a set of birth defects that occur in children born to mothers who abused alcohol during pregnancy. The alcohol-induced defects include pre- and post-natal growth deficiencies, minor facial abnormalities, and damage to the developing central nervous system (CNS). FAS is the most serious condition physicians group under the heading of Fetal Alcohol Spectrum Disorders, which also includes Alcohol-Related Birth Defects, like alcohol-induced congenital cardiac defects that are unrelated to a diagnosis of FAS, and Alcohol-Related Neurodevelopmental Disorders, which occur in the absence of any facial birth defects or growth delays. The severity of birth defects associated with FAS can vary depending on the intensity, duration, and frequency of exposure to alcohol during gestation. In addition to these dose-related concerns, maternal factors such as the mother's genetics or how quickly she metabolizes alcohol, and the timing of exposure during prenatal development also impact alcohol-induced abnormalities. As birth defects and anomalies can arise when pregnant women consume alcohol, alcohol is a teratogen, an environmental agent that negatively impacts the course of normal embryonic or fetal development.

Early 1990s research conducted by Peter Koopman, John Gubbay, Nigel Vivian, Peter Goodfellow, and Robin Lovell-Badge, showed that chromosomally female (XX) mice embryos can develop as male with the addition of a genetic fragment from the Y chromosome of male mice. The genetic fragment contained a segment of the mouse Sry gene, which is analogous to the human SRY gene. The researchers sought to identify Sry gene as the gene that produced the testis determining factor protein (Tdf protein in mice or TDF protein in humans), which initiates the formation of testis. Koopman's team published their results in 1991 in Male Development of Chromosomally Female Mice Transgenic for Sry gene. Their results showed that Sry gene partly determines the sex of an embryo and is the only gene on the Y chromosome necessary for initiation of male development in mice.

Carl Richard Moore was a professor and researcher at the University of Chicago in Chicago, Illinois who studied sex hormones in animals from 1916 until his death in 1955. Moore focused on the role of hormones on sex differentiation in offspring, the optimal conditions for sperm production, and the effects of vasectomy or testicular implants on male sex hormone production. Moore's experiments to create hermaphrodites in the laboratory contributed to the theory of a feedback loop between the pituitary and fetal gonadal hormones to control sex differentiation. Moore showed that the scrotal sac controls the temperature for the testes, which is necessary for sperm production. He also helped distinguish the hormones testosterone, and androsterone from testicular extracts.

Congenital rubella syndrome (CRS) can occur in children whose mothers contracted the rubella virus, sometimes called German measles, during pregnancy. Depending on the gestational period when the mother contracts rubella, an infant born with CRS may be unaffected by the virus or it may have severe developmental defects. The most severe effects of the virus on fetal development occur when the mother contracts rubella between conception and the first trimester. Defects from maternal rubella in the first trimester are included in the term congenital rubella syndrome, but physicians and researchers specifically refer to those defects as rubella embryopathy. Developmental defects are less severe if the mother contracts rubella in the second trimester, and they are generally negligible if the infection occurs in the third trimester. Prenatal rubella infection can cause birth defects which include deafness, compromised vision, abnormal heart development, and damage to the central nervous system which can lead to compromised cognition and learning disabilities.