stances. 2,4-D enters the brain, but only to a limited extent, and its uptake by the brain appears to be an energy-dependent process. Cacodylic acid is one of the major metabolic products of ingested arsenic in mammals. Studies using skin taken from mice report that the absorption of cacodylic acid is influenced by the substance in which it is dissolved and the length of time that cacodylic acid remains in contact with the skin.
TCDD, unlike the herbicides, stays in the body for a long time. In humans about half is eliminated every 8.5 years. It is removed from the body as it is metabolized to less toxic forms that are more easily eliminated in the urine than TCDD itself. The length of time that TCDD remains in the body increases with increasing body fat.
New evidence based on animal models suggests that rats and humans tend to handle TCDD in body tissues in similar ways. However, rats tend to excrete TCDD more quickly. Rats are most likely to absorb TCDD through food and air and this fact may carry over to humans. However, the types of TCDD and other dioxins that accumulate in the body may differ markedly between humans and rodents.
Little is known about the way in which the herbicides produce toxic effects in animals. Recent studies have focused on the mechanisms of cellular toxicity of 2,4,5-T. For example, some studies using animal tissues suggest that 2,4,5-T may alter nerve and muscle function by interacting with chemicals that participate in nervous system function. 2,4,5-T may induce mutations at different stages of cell development. Finally, it may alter the cellular process involved in the elimination of harmful carcinogens.
To date, the consensus is that TCDD is not directly toxic to the body's genetic material. However, it may affect enzymes and hormone levels, which in turn may produce adverse effects.
Recent studies confirm earlier findings that most of the toxic effects of TCDD are caused by its binding to a protein called the aryl hydrocarbon receptor (AhR). The binding of TCDD to this protein triggers various events that result in toxic sequelae. However, some tests suggest that other events, in addition to the binding of TCDD to the AhR, are involved. Studies of the AhR and its partner protein Arnt (aryl hydrocarbon nuclear translocator protein) indicate that similar proteins exist in different species and interact with a number of other proteins to produce an effect. Researchers have recently bred mice that lack the AhR protein. It is anticipated that these mice will allow more informative studies of the way TCDD reacts with the AhR to produce a toxic effect.
Disease outcomes associated with herbicide exposures continue to be debated. Some cellular-level effects have been identified, although it is not clear