as monoesters and do not undergo phase II biotransformation processes such as hydroxylation and oxidation unlike the well-known banned molecule DEHP. Human safety Acute exposure to DMP via inhalation in humans and animals have shown to result in irritation to the eyes, nose and throat. Although some research has shown the association between the susceptibility of the reproductive system and phthalates esters, most phthalates demonstrate low acute toxicity. The chronic (long term) effects, reproductive effects, and carcinogenicity of DMP on humans and animals have yet to be fully established as compared to some other phthalate esters. This is due to insufficient animal evidence and inadequate lifetime-exposure carcinogenicity studies available. However, DMP does appear to have less potential towards inducing health hazards than other phthalates, such as DEHP and BBP. Animal toxicity Studies have shown that DMP is readily absorbed in the gastrointestinal tract of rats. After an orally administered dose of 0.1mL of DMP, about 77% of monomethyl phthalate and 8% of DMP have been detected in urine collected for 24 hours from male rats. Acute oral toxicity results in an LD50 of 8,2, 5,2, 2,9, 10,1 and 8,6 mg/kg for rats, rabbits, guinea pigs, chicks, and mice respectively. Another study on Sprague-Dawley albino rats resulted in a lower LD50 of 4,39 mg/kg in females and 5,12 mg/kg in males. Treatment was applied and for dead subjects, necropsy revealed toxic effects in the lungs, stomach and intestines of rats. Based on this animal data, DMP does not fit the definition of ''acute toxic'' under FHSA via oral exposure. Hematoxicity At high doses (1000 mg/kg), DMP may cause red blood cells (RBCs) to lose their oxygen-carrying function. In both in vitro and in vivo rat studies, DMP-incubated red blood cells released iron. Iron is the site of oxygen binding for hemoglobin, without it, hemoglobin is unable to bind to oxygen and transport it to the rest of the body. Release of iron from RBCs was not found in RBCs not incubated with DMP, nor at low and medium doses of DMP. One mechanism of iron release is the oxidative stress-induced on RBCs by DMP. A separate study found that the oxidative stress induced by DMP also decreased the immune functions of erythrocytes. The oxidative stress damages the structure and function of erythrocytes, in particular RBC-complement 3b (C3b) receptors. Hepatotoxicity Animal studies on oral exposure of DMP in rats have established hepatotoxic