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Propylene glycol ethers (PGE) and ethylene glycol ethers (EGE) are the most common derivatives of the glycol ethers family. Among the PGE family, propylene glycol monomethyl ether (PGME, CAS # 107-98-2) and propylene glycol monobutyl ether (PGBE, CAS # 5131-66-8) are widely used. Regulations for PGME limit the \u03b2-isomer to &lt;\u20095% due to its metabolism to alkoxy propionic acid, which has been associated reproductive and neurotoxic effects similar to those observed with ethylene glycol ethers. Other PGEs do not have such restrictions despite similar isomeric composition. Propylene glycol ethers are used in many commercial products, including cleaning products, and enter the body rapidly via lungs, skin, and ingestion. We hypothesized that PGBE is metabolized to 2-butoxypropionic acid (2-BPA), as suggested by in vitro hepatocyte experiments, and that 2-BPA would be quantifiable in urine from healthy participants (\n                    <jats:italic>N<\/jats:italic>\n                    \u2009=\u200917) following a 2-h exposure to a vapor mixture containing 15 ppm PGBE and 35 ppm PGME. Metabolites were quantified with liquid chromatography with quadrupole mass spectrometry (LC-MS\/MS). Our in vitro hepatocyte experiments showed that PGBE was metabolized to 2-BPA. Urinary metabolite concentrations from the participants were greater for PGBE compared to PGME, and their peak elimination occurred at 1 h post exposure. Our findings show that \u03b2-isomers in commercial propylene glycol ethers can readily metabolize to the corresponding alkoxy propionic acid. However, current toxicological hazard assessments are insufficient to evaluate possible health implications.\n                  <\/jats:p>","DOI":"10.1007\/s00204-026-04338-7","type":"journal-article","created":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T19:28:47Z","timestamp":1773170927000},"page":"2367-2379","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Urinary metabolite elimination from inhaled propylene glycol butyl ether (PGBE) and propylene glycol methyl ether (PGME) in healthy participants"],"prefix":"10.1007","volume":"100","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4490-6109","authenticated-orcid":false,"given":"Nancy B.","family":"Hopf","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susanne","family":"Kaspar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4453-9457","authenticated-orcid":false,"given":"Jamal","family":"Bouitbir","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-1399-4191","authenticated-orcid":false,"given":"Jennifer","family":"Pache","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-9296-2671","authenticated-orcid":false,"given":"Sylvain","family":"Le Gludic","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregory","family":"Plateel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicole","family":"Charriere","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6326-0614","authenticated-orcid":false,"given":"Myriam","family":"Borgatta","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,3,10]]},"reference":[{"issue":"2","key":"4338_CR1","doi-asserted-by":"publisher","first-page":"151","DOI":"10.1007\/s10565-020-09537-1","volume":"37","author":"J Allard","year":"2021","unstructured":"Allard J, Bucher S, Massart J, Ferron PJ, Le Guillou D, Loyant R, Daniel Y, Launay Y, Buron N, Begriche K, Borgne-Sanchez A, Fromenty B (2021) Drug-induced hepatic steatosis in absence of severe mitochondrial dysfunction in HepaRG cells: proof of multiple mechanism-based toxicity. 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