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A combination of mass spectrometry, DFT calculations and 31 P{ 1 H} NMR spectroscopy has been used to define the mode of action of the commercial cobalt extractant, bis(2,4,4-trimethylpentyl)phosphinic acid (CYANEX®272, L 1 H) in Co recovery. The nature of the Co II complexes formed in the water-immiscible phase is determined largely by the propensity of phosphinates to form strong interligand H-bonds in the outer coordination sphere and also to form stable μ 2 -Co-O-P-O-Co bridges. At low Co loading levels, the predominant species is the 4:1 complex, [Co(L 1 ·L 1 H) 2 ], in which coordinated neutral phosphinic acid ligands form strong H-bonds to adjacent anionic phosphinates. At higher Co loading, oligomers such as [a]

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Sulfhemoglobin is formed by the irreversible bonding of sulfur atoms to the heme molecule. Oxygen is then unable to bind the heme molecule, rendering the hemoglobin molecule unable to carry oxygen. The most common etiology of sulfhemoglobinemia is the use/misuse of sulfur-containing medications such as AZO. Unlike methemoglobin, sulfhemoglobin, due to its irreversible binding, has no antidote, and the treatment is ultimately supportive. We present a case of a 53-year-old female who presented to the emergency room endorsing dysuria and was noted to have abnormally low oxygen saturation (SpO2) despite having high arterial oxygen pressure (PaO2) on blood gas. History was significant for dysuria developed while traveling and the use of over-the-counter AZO four times daily for the past 10 days. She was diagnosed with a presumed dyshemoglobinemia and, upon return of send-out labs, was confirmed to have sulfhemoglobinemia attributed to phenazopyridine. This case highlights the importance of the recognition of potential dyshemoglobinemias and consideration of sulfhemoglobinemia as a potential causative etiology, especially in patients taking sulfur-containing medications.