Oxidation of organic contaminants by sulfate radical (SO₄ ^•-) is becoming more popular for the treatment of hazardous waste sites by in situ chemical oxidation (ISCO) and industrial wastewater by advanced oxidation processes (AOPs). It is well documented that SO₄ ^•- can produce similar oxygen-containing transformation products as hydroxyl radical-based treatment processes, but SO₄ ^•- also has the potential to produce organosulfates by radical addition. Experiments conducted with a suite of 23 aromatic and 5 aliphatic compounds, including several contaminants typically detected at hazardous waste sites, demonstrated the formation of at least one stable sulfate-containing product for 25 of the compounds. These compounds likely exhibit higher mobility in the subsurface due to a lower affinity for surfaces (e.g., aquifer solids, activated carbon) than most other transformation products. Although the health risks associated with organosulfates are still uncertain, some aromatic organosulfates produced in this study (i.e. phenyl sulfate and p-cresyl sulfate) are known to be harmful uremic toxins. Further study of organosulfate formation, fate, and toxicity is needed before SO₄ ^•--based treatment processes are more widely employed.

Chemical disinfectants employed in water and wastewater treatment can produce a variety of transformation products, including carbonyl compounds (e.g., saturated and unsaturated aldehydes and ketones). Experiments conducted under conditions relevant to chlorination at drinking water treatment plants and residual chlorine application in distribution systems indicate that α,β-unsaturated carbonyl compounds readily react with free chlorine and free bromine over a wide pH range but react slowly with combined chlorine (i.e., NH₂Cl). For nearly all of the 11 α,β-unsaturated carbonyl compounds studied, the apparent second-order rate constants for the reaction with free chlorine increased in a linear manner with hypochlorite (OCl^-) concentrations, yielding species-specific second-order rate constants for the reaction with OCl^- ranging from 0.21 to 12 M^-1 s^-1. Predictions based on the second-order rate constants indicate that a substantial fraction (i.e., >60%) of several of the more prominent α,β-unsaturated carbonyls (e.g., acrolein, crotonaldehyde) will be transformed to an appreciable extent in distribution systems by free chlorine. Products from the reaction of chlorine with acrolein, crotonaldehyde, and methyl vinyl ketone were tentatively identified using nuclear magnetic resonance (NMR) and gas chromatography coupled to high-resolution time-of-flight mass spectrometry (GC-HRT-MS). These products lacked unsaturated carbons and, in some cases, contained multiple halogens.

Per- and polyfluoroalkyl substances (PFASs) from aqueous film forming foams (AFFFs) can hinder bioremediation of co-contaminants such as trichloroethene (TCE) and benzene, toluene, ethylbenzene, and xylene (BTEX). Anaerobic dechlorination can require bioaugmentation of Dehalococcoides, and for BTEX, oxygen is often sparged to stimulate in situ aerobic biodegradation. We tested PFAS inhibition to TCE and BTEX bioremediation by exposing an anaerobic TCE-dechlorinating coculture, an aerobic BTEX-degrading enrichment culture, and an anaerobic toluene-degrading enrichment culture to n-dimethyl perfluorohexane sulfonamido amine (AmPr-FHxSA), perfluorohexane sulfonamide (FHxSA), perfluorohexanesulfonic acid (PFHxS), or nonfluorinated surfactant sodium dodecyl sulfate (SDS). The anaerobic TCE-dechlorinating coculture was resistant to individual PFAS exposures but was inhibited by >1000× diluted AFFF. FHxSA and AmPr-FHxSA inhibited the aerobic BTEX-degrading enrichment. The anaerobic toluene-degrading enrichment was not inhibited by AFFF or individual PFASs. Increases in amino acids in the anaerobic TCE-dechlorinating coculture compared to the control indicated stress response, whereas the BTEX culture exhibited lower concentrations of all amino acids upon exposure to most surfactants (both fluorinated and nonfluorinated) compared to the control. These data suggest the main mechanisms of microbial toxicity are related to interactions with cell membrane synthesis as well as protein stress signaling.