The intended purpose of dispersants is to dissolve or suspend the medium to heavy fractions of oil in the sea water. Reports have surfaced of very large (~100s of square mile) plumes of suspended small droplets of oil in subsurface layers of the Gulf. There are two benefits to this suspension of the oil: 1) protection of important and vulnerable wetlands from fouling with surface oil, and 2) increased biodegradation. The rate of biodegradation will be greatly increased by the increase of surface area of the small oil drops in suspension over the surface area of a sheet of surface oil. The US government dispersant monitoring program includes tracking the dissolved oxygen level presumably to avoid creation of 'dead zones' from the increased oxygen demand created by the rapid biodegredation.
BP is spraying and injecting the dispersant Corexit 9527A as the second named dispersant used in their Deepwater Horizon disaster. It seems likely that this dispersant is a replacement for the 9500, as such it is or will become the primary dispersant used on the oil in the Gulf of Mexico. The amount of dispersant used is approaching 1 Million gallons so it represents a few percent of the total amount of chemicals dumped in the Gulf. Crude oil is itself a stew of toxic materials and must contain the primary toxicity of the Gulf Oil spill. However, the dispersants applied by BP represent an additional toxic load placed by BP on the Gulf.
Toxicity -- I intended in this blog to look at the toxicity of EGBE - ethylene glycol butyl ether or 2-Butoxyethanol. Over 50 million pounds of EGBE is made annually in the US and it is used in " a wide variety of industrial and consumer products like cleaning products, paints, brake fluids and inks."  The Dow Product Safety Assessment on EGBE also says "Consumers will likely have contact with EGBE." . EGBE is 30-60% of Corexit 9527.
The Dow MSDS  notes that the OSHA PEL for EGBE is 25 ppm (skin). Jargon translation MSDS = Material Safety Data Sheet; OSHA = Occupational Safety and Health (US gov't); PEL = Permissible Exposure Level. The EPA toxicity study  says EGBE is more readily absobed through respiration (breathing) but is also absorbed through the skin (10-20% of total) when the exposure airborne. Environmental EGBE is expected to end up in groundwater if released into the air because of its high solubility in water.
The short answer on EGBE toxicity is that there is no short answer to the toxicity of this chemical. The EPA summary  does show that humans are less susceptible to EGBE than lab rats and mice. There is also a general trend of some higher toxicity in females over males. The toxicity appears to be very different in rodents and humans. In rodents the mechanism is hemolysis (red blood cell breakage) creating damage through secondary effects: clots causing tissue damage (high dose), spleen growth (increased red blood cell production) and liver damage (iron poisoning). In humans the toxicity mechanism appears to be a more of a direct chemical poisoning involving acidosis (blood pH too low). This noticeable species difference is attributed to 1) different breakdown paths where BAA (butoxy acetic acid) is formed by the rodents (BAA causes hemolysis) whereas humans combine much of the potential BAA with nucleic acids into different products. Additionally, human red blood cells are much less susceptible to BAA's hemolytic effects (50-150 times less). So, who can say what it does to fish, birds or amphibians?
Europe has likely banned the spraying of this chemical on the ocean due to the Precautionary Principle - in Europe chemicals must be proven safe (or at least be understood) before environmental or internal uses. It seems that BP and other users of EGBE have chosen not to try to fight this presumptive ban or have tried and failed. I am fairly sure that the lack of a short answer on toxicity of EGBE and the variance of toxicity of related glycol ethers is why the EPA has asked that BP stop (or maybe reduce ... please?) spraying this into the Gulf.
other notes: In the EPA studies some of the human cases are accidental poisonings and suicide attempts others were inhalation and absorption studies. In some cases, toxicity arose hours after the exposure.
note to Kerry:
Quote EPA: Osterhoudt (2002, 100186) reported on a 16-month-old girl who ingested an unknown amount of cleaning solution containing EGBE (10–30%), monoethanolamine (5–10%), alkoxylated linear alcohols (1–5%), ethylenediaminetetraacetic acid (1–5%), and potassium hydroxide (1–5%). Metabolic acidosis was manifest, and a single dose (15 mg/kg) of the ALDH [aldehyde dehydrogenase] inhibitor fomepizole was administered. Within 2 hours, the metabolic acidosis was completely resolved, and there was no evidence of alkaline mucosal injury, hepatic or renal dysfunction, or hemolysis.
 Product Safety Assessment (PSA): Ethylene Glycol Butyl Ether; http://www.dow.com/productsafety/finder/egbe.htm -- note almost all of the outlinks from this document are broken - the egep.com domain (Ethylene Glycol Enthusiasts and Promoters?) is for sale as of 5/28/10.
 Dow MSDS for Glycol Ethers: Ecological and Toxicological Data of Dow Glycol Ethers; http://www.dow.com/PublishedLiterature/dh_0058/0901b8038005889d.pdf?filepath=oxysolvents/pdfs/noreg/110-00761.pdf&fromPage=GetDoc
 TOXICOLOGICAL REVIEW OF ETHYLENE GLYCOL MONOBUTYL ETHER (EGBE); CAS No. 111-76-2; http://www.epa.gov/iris/toxreviews/0500tr.pdf