Toxic cyanobacteria have been shown to accumulate in drinking water treatment plants that are susceptible to algal blooms. However, the risk for plants that do not experience algal blooms, but that receive a low influx of cells, is not well known. This study determined the extent of cell accumulation and presence of cyanotoxins across the treatment trains of four plants in the Great Lakes region. Samples were collected for microscopic enumeration and enzyme-linked immunosorbent assay (ELISA) measurements for microcystins, anatoxin-a, saxitoxin, cylindrospermopsin, and β-methylamino-L-alanine (BMAA). Low cell influxes (under 1000 cells/mL) resulted in significant cell accumulations (over 1 × 105 cells/mL) in clarifier sludge and filter backwash samples. Microcystins peaked at 7.2 µg/L in one clarifier sludge sample, exceeding the raw water concentration by a factor of 12. Anatoxin-a was detected in the finished drinking water of one plant at 0.6 µg/L. BMAA may have been detected in three finished water samples, though inconsistencies among the BMAA ELISAs call these results into question. In summary, the results show that plants receiving a low influx of cells can be at risk of toxic cyanobacterial accumulation, and therefore, the absence of a bloom at the source does not indicate the absence of risk.

Increases in the global use of plastics have caused concerns regarding potential adverse effects on human health. Plastic products contain hundreds of potentially toxic chemical additives, yet the exact chemicals which drive toxicity currently remain unknown. In this study, we employed nontargeted analysis and in vitro bioassays to identify the toxicity drivers in plastics. A total of 56 chemical additives were tentatively identified in five commonly used plastic polymer pellets (i.e., PP, LDPE, HDPE, PET, and PVC) by employing suspect screening and nontargeted analysis. Phthalates and organophosphates were found to be dominant in PVC pellets. Triphenyl phosphate and 2-ethylhexyl diphenyl phosphate accounted for a high amount (53.6%) of the inhibition effect of PVC pellet extract on human carboxylesterase 1 (hCES1) activity. Inspired by the high abundances of chemical additives in PVC pellets, six different end-user PVC-based products including three widely used PVC water pipes were further examined. Among them, extracts of PVC pipe exerted the strongest PPARγ activity and cell viability suppression. Organotins were identified as the primary drivers to these in vitro toxicities induced by the PVC pipe extracts. This study clearly delineates specific chemical additives responsible for hCES1 inhibition, PPARγ activity, and cell viability suppression associated with plastic.

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