Wavelength-dependent time–dose reciprocity and stress mechanism for UV-LED disinfection of Escherichia coli

Ultraviolet (UV) disinfection efficiency by low-pressure (LP) mercury lamp depends on the UV fluence (dose): the product of incident irradiance (fluence rate) and exposure time, with correction factors. Time–dose reciprocity may not always apply, as higher UV–LP inactivation of E. coli was obtained at a higher irradiance over shorter exposure time, for the same UV fluence. Disinfection by UV LEDs is limited by low radiant flux compared to mercury LP lamps. Our goal was to determine the UV-LED time–dose reciprocity of E. coli for four different central LED wavelengths (265, 275, 285 and 295 nm) under different fluence rates. Inactivation kinetics determined at UV-LED265 was not affected by the fluence rate or exposure time for a given UV fluence. In contrast, UV-LED275, UV-LED285, and UV-LED295 led to higher inactivation at low fluence rate coupled to high exposure time, for the same UV fluence. The intracellular damage mechanisms for each LED central wavelength were determined by using the bioreporters RecA as an indicator of bacterial DNA damage and SoxS as an indicator of oxidative stress. For 265 nm, higher DNA damage was observed, whereas for 285 and 295 nm, higher oxidative stress (possibly due to reactive oxygen species [ROS] damage) was observed. ROS inactivation of E. coli was predicted to be more effective when keeping the ROS concentration low but allowing longer exposure, for a given UV fluence. [Display omitted] •Time–dose reciprocity law was examined for E. coli with 265, 275, 285, 295 nm LEDs•E. coli inactivation at 265 nm depended on the UV-LED fluence and not fluence rate•E. coli inactivation at 285 and 295 nm did not follow the Bunsen–Roscoe law•UV-LED intracellular damage was examined using bioreporters RecA and SoxS•At 265 nm, DNA damage was higher; at 295 nm, ROS damage was higher