2-,3-, and 4-Methylhippuric acid

Optimal Result: 0 - 0.6 nmol/mg Creatinine.

2-Methylhippuric Acid (2MHA), 3-Methylhippuric Acid (3MHA), 4-Methylhippuric Acid (4MHA)
These are metabolites of xylenes, solvents found in paints, lacquers, cleaning agents, pesticides, and gasoline. Exposure to xylenes generates methylhippuric acid isomers.

Avoid/reduce exposure to these substances.

Xylenes (dimethylbenzenes) are found not only in common products such as paints, lacquers, pesticides, cleaning fluids, fuel and exhaust fumes, but also in perfumes and insect repellents. Xylenes are oxidized in the liver and bound to glycine before eliminated in urine. High exposures to xylene create an increase in oxidative stress, causing symptoms such as nausea, vomiting, dizziness, central nervous system depression, and death. Occupational exposure is often found in pathology laboratories where xylene is used for tissue processing.

What does it mean if your 2-,3-, and 4-Methylhippuric acid result is too high?

Methylhippuric acid (2,-3,4-MHA) is the result of exposure to the solvent xylene that is widespread in the environment. Xylene is found in paints, lacquers, cleaning agents, pesticides, and gasoline. It is also used in the pathology laboratory for tissue processing.

High exposure to xylene may cause nausea, vomiting, dizziness, incoordination, central nervous system depression, and even death. An exposure to 100 ppm xylene in the air resulted in a urine value of 3140 µg/g creatinine for methylhippuric acid.

Rats given xylene experienced a significant decrease in locomotor activity, deficits in learning ability and memory loss. These xylene -induced behavioral changes were associated with a decrease in beta-endorphins.

Possible treatment options:

Treatment begins with removing all potential sources of exposure. Elimination of xylene can be accelerated by sauna treatment, the Hubbard detoxification protocol employing niacin supplementation, supplementation with glycine to encourage metabolism of xylene to methylhippuric acid in the liver, or by glutathione (reduced) supplementation (oral, intravenous, transdermal, or precursors such as N-acetyl cysteine [NAC]).

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