Chemical exposures can cause adverse effects on the endocrine system. Some chemicals, for example oral contraceptives, are designed to modulate or disrupt the human reproductive endocrine system, proving the plausibility that chemicals can have such effects. Other chemicals, such as diethylstilbestrol (DES) have caused unintended adverse effects on offspring exposed during particularly sensitive periods of in utero development, proving that humans are susceptible. While those human effects were at pharmacological levels, recent studies have raised concerns that human endocrine changes could have been caused by environmental exposures. Increases in breast cancer, testicular cancer, hypospadia, cryptorchidism, and drops in sperm count have all been reported. It has been hypothesized that those effects were caused by industrial chemical exposures. Further evidence that environmental chemicals might be endocrine disruptors come from various wildlife studies. Birds in contaminated areas of the Great Lakes, fish in the UK, and alligators in Florida have shown decreased fertility or increased reproductive abnormalities, supporting the position that environmental chemical exposures can affect wildlife. Plant and fungal toxins are also known to alter reproductive function, for example clover contains sufficient coumestrol to adversely affect reproductive function in sheep showing that natural chemicals can also affect endocrine function. Recent research indicates that some of these agents act synergistically in vitro; they may do the same in vivo. In conclusion, research has demonstrated that chemicals can affect reproductive health via an endocrine mechanism. This, therefore, constitutes a real risk to human health that must be addressed.