Michael R. Harrison worked as a pediatric surgeon in the US throughout the late-twentieth century and performed many fetal surgeries, including one of the first successful surgeries on a fetus in utero, or while it is still in its gestational carrier’s body, also called open fetal surgery. A fetus is an organism developing inside of the uterus that is anywhere from eight weeks old to birth. Harrison hypothesized that open fetal surgery could correct developmental defects that may become fatal to the fetus at birth. After years of research, Harrison and his colleagues at the University of California, San Francisco, in San Francisco, California, performed surgery on the fetus of a woman in her seventh month of pregnancy to correct the fetus’s developmental defects. The surgery was successful, as the fetus developed into a healthy child. Harrison’s work led to advancements in fetal treatment techniques, such as a method to conduct open fetal surgery that will not harm the fetus or pregnant woman, as well as the establishment of one of the first fetal treatment centers in the US.

In 1996, Michael R. Harrison published “Fetal Surgery” in the American Journal of Obstetrics and Gynecology. In the article, Harrison describes the importance of fetal surgery and the techniques used to correct defects in fetuses. As a fetus develops in the uterus, it can develop abnormalities that may become debilitating or fatal. Harrison discusses cases that show how physicians can use fetal surgery to repair such abnormalities, including obstructions in the heart or urinary tract, or organs or muscles whose malformations impair function. Harrison states where knowledge is lacking within the field or where surgery would be inappropriate, such as in the modification of a cleft lip, which can be fixed after birth and as such does not merit the risks of surgery. In the article, Harrison provides a summary of what information existed about fetal surgeries in 1996, which helped physicians explore fetal surgery and make further advancements.

Sprayed extensively by the US military in Vietnam, Agent Orange contained a dioxin contaminant later found to be toxic to humans. Despite reports by Vietnamese citizens and Vietnam War veterans of increased rates of stillbirths and birth defects in their children, studies in the 1980s showed conflicting evidence for an association between the two. In 1996, the US National Academy of Sciences reported that there was evidence that suggested dioxin and Agent Orange exposure caused spina bifida, a birth defect in which the spinal cord develops improperly. The US Department of Veterans Affairs' subsequent provision of disability compensation for spina bifida-affected children marked the US government's first official acknowledgement of a link between Agent Orange and birth defects. By 2016, spina bifida and related neural tube defects were the only birth defects associated with Agent Orange.

Spina bifida is a birth defect that affects the spines of developing fetuses and infants, and research in the 20th century indicated that chemicals in the herbicide Agent Orange likely lead to the birth defect. People with spina bifida can have nerve damage, paralysis, and mental disabilities. During the Vietnam War in the 1960s, the US military employed Agent Orange and other herbicides to destroy enemy crops and forest cover until 1970. Though studies of the link between Agent Orange exposure and birth defects were at first inconclusive, in 1995 the US National Academy of Sciences concluded that one birth defect, spina bifida, was associated with paternal Agent Orange exposure. Spina bifida was, by the twenty-first century, the only birth defect that the US Veterans Administration connected to Agent Orange exposure.