The presence of drugs or chemicals in an organism's environment can also influence gene expression in the organism. Cyclops fish are a dramatic example of the way in which an environmental chemical can affect development. In 1907, researcher C. R. Stockard created cyclopean fish embryos by placing fertilized Fundulus heteroclitus eggs in 100 mL of seawater mixed with approximately 6 g of magnesium chloride. Normally, F. heteroclitus embryos feature two eyes; however, in this experiment, half of the eggs placed in the magnesium chloride mixture gave rise to one-eyed embryos (Stockard, 1907).

A second example of how chemical environments affect gene expression is the case of supplemental oxygen administration causing blindness in premature infants (Silverman, 2004). In the 1940s, supplemental oxygen administration became a popular practice when doctors noticed that increasing oxygen levels converted the breathing pattern of premature infants to a "normal" rhythm. Unfortunately, there is a causal relationship between oxygen administration and retinopathy of prematurity (ROP), although this relationship was unknown at the time; thus, by 1953, ROP had blinded approximately 10,000 infants worldwide. Finally, in 1954, a randomized clinical trial identified supplemental oxygen as the factor causing blindness. Complicating the issue is the fact that too little oxygen results in a higher rate of brain damage and mortality in premature infants. Unfortunately, even today, the optimal amount of oxygenation necessary to treat premature infants while completely avoiding these complications is still not clear.

Yet another example of the way in which chemicals can alter gene expression involves thalidomide, a sedative, antiemetic, and nonbarbiturate drug that was first manufactured and marketed during the mid-1950s. While thalidomide has no discernable effect on gene expression and development in healthy adults, it has a profoundly detrimental effect on developing fetuses. When the drug was first created, however, its impact on fetuses was not known. Moreover, because of its apparent lack of toxicity in adult human volunteers, thalidomide was marketed as the safest available sedative of its time and rapidly became popular in Europe, Australia, Asia, and South America for countering the effects of morning sickness. (In the United States, the drug failed to receive Food and Drug Administration approval because its side effects included tingling hands and feet after long-term administration, which led to concerns that the drug might be associated with neuropathy.) Not until 1961 did Australian researcher William McBride and German researcher Widukind Lenz independently report that thalidomide was a teratogen, meaning that its use was associated with birth defects. Another study associated thalidomide use with neuropathies. Sadly, the drug was withdrawn too late to prevent severe developmental deformities in approximately 8,000 to 12,000 infants, many of whom were born with stunted limb development. Interestingly, despite the fact that thalidomide is dangerous during embryonic development, the drug continues to be used in certain instances yet today. For example, it has therapeutic potential in treating leprosy, and in recent years, it has also been used to treat cancers and enhance the effectiveness of cancer vaccines (Bartlett et al., 2004; Fraser, 1988).