A model to rapidly assess informal electronic waste systems.

Electronic waste (e-waste) policies have traditionally been based on extended producer responsibility (EPR) principles. In practice, EPR-based e-waste policies primarily involve the creation of regulated collection and recycling channels, with success tied to achieving high collection quotas. However, the majority of EPR programs, particularly those in the Global South, have achieved little success due to competition with the informal sector. Despite this, strikingly little is known of the scope and dynamics of informal e-waste flows and actors during the formulation of e-waste management policies. This study develops and pilots a replicable three-stage model for solid waste researchers, practitioners and policymakers to rapidly assess these informal e-waste systems. This model is demonstrated in Cuenca, Ecuador, and determined the destination of 50-80% of Cuenca's e-waste over a period of three days. The methods used and findings that emerge from this study offer a strategy to rapidly quantify and understand the dynamics of informal e-waste systems to inform EPR-based policies in ways that place informal recyclers at the core of e-waste management. This not only provides creative opportunities for formal systems to achieve e-waste collection quotas through partnerships with the informal sector, but offers a pathway to preserve the livelihoods of marginalized populations reliant on e-waste recycling and decrease environmental harm.

Toward Active Community Environmental Policing: Potentials and Limits of a Catalytic Model.

This paper offers a field tested community environmental policing model to address the pressing environmental management challenges of reducing e-waste burning in informal e-waste hubs, and enforcement against informal polluting industries more broadly. This is based on our intervention to reduce e-waste burning in a substantial informal e-waste hub in the West Bank, Palestine, a 45 km2 region in which an estimated 5-10 metric tonnes of cables are burnt daily, causing serious environmental and public health consequences. In analogous e-waste hubs in the global South, environmental management solutions have focused on economically attractive alternatives to replace cable burning or policies that integrate informal recyclers with formal e-waste management systems-achieving little success. Our paper describes a two-pronged intervention in Palestine's e-waste hub, which reduced e-waste burning by 80% through a combination of economically competitive cable grinding services and an "active" community environmental policing initiative that lowered barriers to and successfully advocated for governmental policing of e-waste burning. Our discussion of this intervention addresses the community environmental policing literature, which has documented few successes stories of real improvements to the enforcement of environmental violations. We argue that existing strategies have relied on "passive" approaches comprised of monitoring and reporting environmental violations to advocate for change. Our strategy offers a template to improve outcomes through a more "active" approach, moving from monitoring environmental violations through understanding the rationale and dynamics of violators, identifying environmental policing barriers, and implementing a feasible and persuasive strategy to overcome them.

A strong spatial association between e-waste burn sites and childhood lymphoma in the West Bank, Palestine.

A paper in the International Journal of Cancer analyzed Palestinian cancer registry data in the West Bank from 1998 to 2007, showing a cluster of elevated cancer incidence in rural villages in south-west Hebron, with a 4.10 risk ratio for childhood lymphoma (p = 0.0023). The paper called for investigation of the environmental or genetic etiologies of this cluster in an otherwise unremarkable rural area.1 Our research in these same villages shows them to be the center of an extensive informal electronic and electrical waste (e-waste) dismantling industry in Palestine, operating for almost two decades. This entails extensive open-burning of e-waste components to extract valuable metals or dispose of nonvaluable waste, releasing high concentrations of hazardous contaminants, which may be an important factor in the elevated cancer incidence. We offer a first step in assessing this link. We applied a novel multitemporal object-based method to map the prevalence and intensity of e-waste burn sites in the entire Hebron Governorate (1,060 km2 ) between 1999 and 2007. A weighted standard deviation ellipse of cumulative burn activity covers a smaller area (247 km2 ) very closely matching the childhood lymphoma cluster: it contains 85% of the core cluster area (RR of 4.1), and falls almost entirely (95%) within the broader area of elevated risk (RR of 2.8). Extensive international evidence linking informal e-waste processing to elevated cancer incidence and this strong spatial association of e-waste burning activity with a distinct unexplained cancer cluster in the Palestinian context signals the urgent need for investigation and intervention.

Bacurd1/Kctd13 and Bacurd2/Tnfaip1 are interacting partners to Rnd proteins which influence the long-term positioning and dendritic maturation of cerebral cortical neurons.

BACKGROUND: The development of neural circuits within the embryonic cerebral cortex relies on the timely production of neurons, their positioning within the embryonic cerebral cortex as well as their terminal differentiation and dendritic spine connectivity. The RhoA GTPases Rnd2 and Rnd3 are important for neurogenesis and cell migration within the embryonic cortex (Nat Commun 4:1635, 2013), and we recently identified the BTB/POZ domain-containing Adaptor for Cul3-mediated RhoA Degradation family member Bacurd2 (also known as Tnfaip1) as an interacting partner to Rnd2 for the migration of embryonic mouse cortical neurons (Neural Dev 10:9, 2015). FINDINGS: We have extended this work and report that Bacurd1/Kctd13 and Bacurd2/Tnfaip1 are interacting partners to Rnd2 and Rnd3 in vitro. Given that these genes are expressed during cortical development, we performed a series of in utero electroporation studies in mice and found that disruptions to Bacurd1/Kctd13 or Bacurd2/Tnfaip1 expression impair the long-term positioning of E14.5-born cortical neurons within the postnatal (P17) mouse cerebral cortex. We also find that forced expression of Bacurd1/Kctd13 and Bacurd2/Tnfaip1 alters the branching and dendritic spine properties of layer II/III projection neurons. CONCLUSIONS: We identify Bacurd1/Kctd13 and Bacurd2/Tnfaip1 as interacting partners to Rnd proteins which influence the development of cortical neurons. Their neurodevelopmental functions are likely to be relevant to human brain development and disease.

Bacurd2 is a novel interacting partner to Rnd2 which controls radial migration within the developing mammalian cerebral cortex.

BACKGROUND: During fetal brain development in mammals, newborn neurons undergo cell migration to reach their appropriate positions and form functional circuits. We previously reported that the atypical RhoA GTPase Rnd2 promotes the radial migration of mouse cerebral cortical neurons (Nature 455(7209):114-8, 2008; Neuron 69(6):1069-84, 2011), but its downstream signalling pathway is not well understood. RESULTS: We have identified BTB-domain containing adaptor for Cul3-mediated RhoA degradation 2 (Bacurd2) as a novel interacting partner to Rnd2, which promotes radial migration within the developing cerebral cortex. We find that Bacurd2 binds Rnd2 at its C-terminus, and this interaction is critical to its cell migration function. We show that forced expression or knockdown of Bacurd2 impairs neuronal migration within the embryonic cortex and alters the morphology of immature neurons. Our in vivo cellular analysis reveals that Bacurd2 influences the multipolar-to-bipolar transition of radially migrating neurons in a cell autonomous fashion. When we addressed the potential signalling relationship between Bacurd2 and Rnd2 using a Bacurd2-Rnd2 chimeric construct, our results suggest that Bacurd2 and Rnd2 could interact to promote radial migration within the embryonic cortex. CONCLUSIONS: Our studies demonstrate that Bacurd2 is a novel player in neuronal development and influences radial migration within the embryonic cerebral cortex.