Elucidating the surface macroplastic load, types and distribution in mangrove areas around Cebu Island, Philippines and its policy implications.

The Philippines is identified as one of the major marine plastic litter polluters in the world with a discharge of approximately 0.75 million tons of marine plastic debris per year. However, the extent of the plastic problem is yet to be defined systematically because of limited research. Thus, this study aims to quantify plastic litter occurrence in mangrove areas as they function as sinks for plastic litter due to their inherent nature of trapping plastics. To define the extent of marine plastic pollution on an island scale, mangrove areas in 14 municipalities around Cebu Island were sampled, with 3 to 9 transects in each site depending on the length of coastline covered by mangroves. Sampling and characterization of both plastics and the mangrove ecosystem was performed in three locations along the transect - landward, middle, and seaward. A total of 4501 plastic items were sampled throughout the study sites with an average of 1.29 ± 0.67 items/m2 (18.07 ± 8.79 g/m2). The average distribution of plastic loads were 2.68 ± 1.9 items/m2 (38.52 ± 25.35 g/m2), 0.27 ± 0.10 items/m2 (6.65 ± 4.67 g/m2), and 0.94 ± 0.61 items/m2 (9.04 ± 4.28 g/m2) for the landward, middle, and seaward locations, respectively. The most frequent plastic types found were i) packaging, ii) plastic bags and iii) plastic fragments. The plastic loads and types suggest that most plastic wastes trapped in mangroves come from the nearby communities. Fishing-related plastics originated from the sea and were transported across the mangrove breadth. The findings confirm that mangroves are major traps of plastic litter that might adversely affect the marine ecosystem. The study underscores the urgent need for waste mitigation measures, including education, community engagement, infrastructure, technological solutions and supporting policies.

The environmental release and ecosystem risks of illicit drugs during Glastonbury Festival.

Reported high drug use at music festivals coupled with factors such as public urination can lead to the direct release of illicit drugs into the environment. Glastonbury Festival 2019 had 203,000 attendees, its site is intercepted by the Whitelake River providing a direct route for illicit drug pollution into the local environment. We tested for popular illicit drugs such as cocaine and MDMA in the river upstream and downstream of the festival site as well as in the neighbouring Redlake River. Both rivers were sampled the weeks before, during and after the festival. Cocaine, benzoylecgonine and MDMA were found at all sample sites; concentrations, and mass loads (mass carried by the river per unit of time) were significantly higher in the Whitelake site, downstream of the festival. MDMA mass loads were 104 times greater downstream in comparison to upstream sites (1.1-61.0 mg/h vs 114.7 mg/h; p < .01). Cocaine and benzoylecgonine mass loads were also 40 times higher downstream of the festival (1.3-4.2 mg/h vs 50.4 mg/h; p < .01) (22.7-81.4 mg/h vs 854.6 mg/h; p < .01). MDMA reached its highest level during the weekend after the festival with a concentration of 322 ng/L. This concentration is deemed harmful to aquatic life using Risk Quotient assessment (RQ) and provides evidence of continuous release after the festival due to leaching of MDMA from the site. Cocaine and benzoylecgonine concentrations were not at levels deemed harmful to aquatic life according to RQ assessment yet were three times higher than MDMA concentrations. Redlake River experienced no significant changes (p > .05) in any illicit drug levels, further confirming that drug release was likely dependent on the festival site. The release of environmentally damaging levels of illicit drugs into Whitelake River during the period of Glastonbury Festival suggests an underreported potential source of environmental contamination from greenfield festival sites.

The drinking water contaminant dibromoacetonitrile delays G1-S transition and suppresses Chk1 activation at broken replication forks.

Chlorination of drinking water protects humans from water-born pathogens, but it also produces low concentrations of dibromoacetonitrile (DBAN), a common disinfectant by-product found in many water supply systems. DBAN is not mutagenic but causes DNA breaks and elevates sister chromatid exchange in mammalian cells. The WHO issued guidelines for DBAN after it was linked with cancer of the liver and stomach in rodents. How this haloacetonitrile promotes malignant cell transformation is unknown. Using fission yeast as a model, we report here that DBAN delays G1-S transition. DBAN does not hinder ongoing DNA replication, but specifically blocks the serine 345 phosphorylation of the DNA damage checkpoint kinase Chk1 by Rad3 (ATR) at broken replication forks. DBAN is particularly damaging for cells with defects in the lagging-strand DNA polymerase delta. This sensitivity can be explained by the dependency of pol delta mutants on Chk1 activation for survival. We conclude that DBAN targets a process or protein that acts at the start of S phase and is required for Chk1 phosphorylation. Taken together, DBAN may precipitate cancer by perturbing S phase and by blocking the Chk1-dependent response to replication fork damage.