Investigation and analysis of microplastics in sewage sludge and biosolids: A case study from one wastewater treatment works in the UK.

There is an increasing concern about the impacts of microplastic pollution in the terrestrial environment. Identifying sources, pathways and sinks of terrestrial microplastics is crucial to determining environmental exposure and applying efficient intervention measures. In the UK alone, 3.5 million tonnes (wet weight) of biosolids from the wastewater industry are recycled each year to agricultural land, raising the possibility that recycling of biosolids could be a significant source of microplastic pollution to the terrestrial environment. To address this issue, the present study determined the presence of microplastics from across the whole sludge treatment stream from one exemplar wastewater treatment works in the UK. Both sewage sludge (a liquid by-product produced from the wastewater treatment processes) and biosolids (sewage sludge that has undergone a treatment process) were examined as a source of microplastics to the terrestrial environment. Microplastics were detected in all samples taken from across the treatment process with concentrations ranging from 37.7-286.5 number of microplastics/g of sludge (dry weight). The microplastic load in the final biosolid products produced at the site ranged from 37.7-97.2 number of microplastics/g of sludge (dry weight). The wastewater treatment works in this study produces 900 tonnes of anaerobically digested sludge cake and 690 tonnes of lime stabilised cake per month. Based on the results from this study, the application of these biosolids to agricultural land as fertilisers can potentially release 1.61 × 1010 and 1.02 × 1010 microplastics in anaerobically digested and lime stabilised sludge respectively, every month (equivalent to the same volume as >20,000 plastic bank cards). The results illustrate the extent to which microplastics may enter the terrestrial environment through this route.

Germline hypomorphic CARD11 mutations in severe atopic disease.

Few monogenic causes for severe manifestations of common allergic diseases have been identified. Through next-generation sequencing on a cohort of patients with severe atopic dermatitis with and without comorbid infections, we found eight individuals, from four families, with novel heterozygous mutations in CARD11, which encodes a scaffolding protein involved in lymphocyte receptor signaling. Disease improved over time in most patients. Transfection of mutant CARD11 expression constructs into T cell lines demonstrated both loss-of-function and dominant-interfering activity upon antigen receptor-induced activation of nuclear factor-κB and mammalian target of rapamycin complex 1 (mTORC1). Patient T cells had similar defects, as well as low production of the cytokine interferon-γ (IFN-γ). The mTORC1 and IFN-γ production defects were partially rescued by supplementation with glutamine, which requires CARD11 for import into T cells. Our findings indicate that a single hypomorphic mutation in CARD11 can cause potentially correctable cellular defects that lead to atopic dermatitis.