By October 1945, DDT was available for public sale in the United States, used both as an agricultural pesticide and as a household insecticide.  Although its use was promoted by government and the agricultural industry, US scientists such as FDA pharmacologist Herbert O. Calvery expressed concern over possible hazards associated with DDT as early as 1944.    As its production and use increased, public response was mixed. At the same time that DDT was hailed as part of the "world of tomorrow," concerns were expressed about its potential to kill harmless and beneficial insects (particularly pollinators ), birds, fish, and eventually humans. The issue of toxicity was complicated, partly because DDT's effects varied from species to species, and partly because consecutive exposures could accumulate, causing damage comparable to large doses. A number of states attempted to regulate DDT.   In the 1950s the federal government began tightening regulations governing its use.  These events received little attention. Women like Dorothy Colson and Mamie Ella Plyler of Claxton, Georgia gathered evidence about DDT's effects and wrote to the Georgia Department of Public Health, the National Health Council in New York City, and other organizations. 
Genetic females (46,XX karyotype) have two X chromosomes, thus have two AR genes. A mutation in one (but not both) results in a minimally affected, fertile, female carrier. Some carriers have been noted to have slightly reduced body hair, delayed puberty, and/or tall stature, presumably due to skewed X-inactivation.   A female carrier will pass the affected AR gene to her children 50% of the time. If the affected child is a genetic female, she, too, will be a carrier. An affected 46,XY child will have AIS.