Investigation of membrane fouling and mechanism induced by extracellular organic matter during long-term exposure to pharmaceuticals and personal care products.

This study investigated ultrafiltration membrane fouling by extracellular organic matter (EOM) and the mechanism operating during long-term exposure to pharmaceuticals and personal care products. The results indicated that carbamazepine and diclofenac in algal-laden water altered the filtration flux and membrane fouling by EOM. Exposure to low-concentration carbamazepine (0.25 μg/L) improved the filtration flux and the total (R) and reversible fouling resistance (R), whereas the filtration flux and R and R were reduced when EOM was used during long-term exposure to high carbamazepine concentrations (>1 μg/L). Both R and R were increased when algae were exposed to 0.25 μg/L diclofenac, whereas the filtration flux and R and R were alleviated when algae were exposed to >1 μg/L diclofenac. Moreover, carbamazepine and diclofenac (0.25 μg/L - 1000 μg/L) in water enhanced the irreversible fouling resistance (R) when ultrafiltration was used to treat algal-laden waters. The mechanism indicated that membrane fouling induced by standard blocking was transformed to complete blocking when EOM was exposed to high levels of carbamazepine (>0.25 μg/L) in the initial filtration process, whereas cake layer formation played an important role during the later filtration process; with low carbamazepine levels (0.25 μg/L), standard blocking of EOM was dominant during the entire filtration process. The membrane fouling mechanism also changed when algal-laden waters were exposed to diclofenac, the membrane fouling was transformed from complete blocking to standard blocking when DFC was present in the initial filtration process, whereas cake layer formation exerted an important role during the late filtration process. This research provides important information on the long-term risks caused by pharmaceutical and personal care products and potential threats to membrane treatment.