Author:
Seidel Shawn,Barranco Wade T.,Shi Quan
Abstract
Abstract
Propylene‐series glycol ethers are produced by the reaction of propylene oxide (PO) with primary alcohols. Chain prolongation occurs by further reaction of the glycol ether with excess propylene oxide during the production process. Therefore, a mixture of mono‐, di‐, tri‐, and higher propylene glycol ethers are formed, which are separated from each other by distillation. Due to the flexibility of using different alcohol groups and the number of propylene glycol ether linkages, P‐series glycol ethers can provide unique solvency characteristics by conveying both polar and nonpolar characteristics, and reduction of surface tension. Due to their physical–chemical characteristics, P‐series glycol ethers are used in many applications ranging from electronics to protective coatings and cleaners. The P‐series glycol ethers, and glycol ethers in general, have a robust toxicology data set covering a wide range of endpoints following oral, dermal, and inhalation routes of exposure. Due to the nature of the PO molecule, two structural isomers can be formed for each PO unit in the glycol ether molecule, i.e., two isomers for mono‐, four for di‐, eight for tri‐, and so on. The key difference is the resulting environment for the hydroxy group between the isomers. For the monos, the α‐isomer contains a secondary hydroxyl group (hence, sometimes also called the secondary isomer) whilst the β‐isomer has a primary hydroxyl group. This difference in hydroxyl group environment between the two isomers results in different metabolism routes being available, with higher toxicity from the β‐isomer due to its ability to oxidize to the acid form. It should be emphasized, however, that this predicted higher toxicity has only been seen with the β‐isomer of methoxypropanol. During production, the α‐isomer is thermodynamically favored and, when needed, the β‐isomer is controlled to reduce its presence. The P‐series glycol ether products as commercially produced are of low toxicity with the primary effects from long‐term exposure being adaptive changes to the liver and rat‐specific (α‐2μ‐globulin) kidney effects.