Applying the Pennsylvania Environmental Rights Amendment Meaningfully to Climate Disruption

The Pennsylvania Constitution contains a unique Environmental Rights Amendment (ERA), which recognizes an individual right to “clean air, pure water, and to the preservation of the natural, scenic, historic and esthetic values of the environment.” The ERA also includes a public trust element that makes “Pennsylvania’s public natural resources . . . the common property of all the people, including generations yet to come.” It makes the Commonwealth the “trustee of these resources,” requiring it to “conserve and maintain them for the benefit of all the people.” Recent decisions by the Pennsylvania Supreme Court (the Court) in Robinson Township v. Commonwealth and Pennsylvania Environmental Defense Foundation v. Commonwealth provide significant support for Pennsylvania regulations to address the threat of climate disruption posed by greenhouse gas (GHG) emissions to achieve net zero carbon emissions by the middle of this century. In light of the threats that climate disruption poses to Pennsylvania’s public natural resources, the text of the ERA, and the principles articulated in those recent cases, we argue that a stable climate (a climate that has not been disrupted by anthropogenic emissions of GHGs) should be considered protected by the rights recognized by the ERA, and the public trust duties it creates. We argue that these rights and duties require Pennsylvania to employ regulatory measures to reduce GHG emissions to the level warranted by the social cost of carbon and to achieve carbon neutrality (net zero emissions) by mid-century. Further, we argue that there are judicially recognizable standards to compel the Commonwealth to exercise its existing authority to limit GHG emissions. In light of existing legislative authority, the obligations imposed by the United Nations Framework Convention on Climate Change, the Paris Agreement, and the federal Clean Air Act, we make the case that this regulatory program should take the form of an economy-wide cap-and-trade program providing for the auction of allowances with a reserve price based on the social cost of carbon and additional measures to prevent leakage and a cap reaching carbon neutrality by mid-century

Exploring Metapopulation-Scale Suppression Alternatives for a Global Invader in a River Network Experiencing Climate Change

Invasive species can dramatically alter ecosystems, but eradication is difficult, and suppression is expensive once they are established. Uncertainties in the potential for expansion and impacts by an invader can lead to delayed and inadequate suppression, allowing for establishment. Metapopulation viability models can aid in planning strategies to improve responses to invaders and lessen invasive species’ impacts, which may be particularly important under climate change. We used a spatially-explicit metapopulation viability model to explore suppression strategies for ecologically-damaging invasive brown trout (Salmo trutta), established in the Colorado River and a tributary within Grand Canyon National Park. Our goals were to: 1) estimate the effectiveness of strategies targeting different life stages and subpopulations within a metapopulation, 2) quantify the effectiveness of a rapid response to a new invasion relative to delaying action until establishment; and 3) estimate whether future hydrology and temperature regimes related to climate change and reservoir management affect metapopulation viability and alter the optimal management response. We included scenarios targeting different life-stages with spatially-varying intensities of electrofishing, redd destruction, incentivized angler harvest, piscicides, and a weir. Quasi-extinction (QE) was obtainable only with metapopulation-wide suppression targeting multiple life-stages; subpopulations were most sensitive to age-0 and large adult mortality. The duration of suppression needed to reach QE for a large established subpopulation was triple compared to a rapid response to a new invasion. Isolated subpopulations were vulnerable to suppression; however, connected tributary subpopulations enhanced metapopulation persistence by serving as climate refuges. Water shortages driving changes in reservoir storage and subsequent warming would cause brown trout declines, but metapopulation QE was only achieved by re-focusing and increasing suppression. Our modeling approach improved our understanding of invasive brown trout metapopulation dynamics, which could lead to more focused and effective invasive species suppression strategies, and ultimately, maintenance of populations of endemic fishes

Pharmocologic inhibitors of the mitogen activated protein kinase cascade have the potential to interact with ionizing radiation exposure to induce cell death in carcinoma cells by multiple mechanisms

Recent studies have shown that inhibition of stress-induced signaling via the mitogen activated protein kinase (MAPK) pathway can potentiate the toxic effects of chemotherapeutic drugs and ionizing radiation. Because of these observations, we have further investigated the impact upon growth and survival of mammary (MDA-MB-231, MCF7, T47D), prostate (DU145, LNCaP, PC3) and squamous (A431) carcinoma cells following irradiation and combined long-term exposure to MEK1/2 inhibitors. Exposure of carcinoma cells to ionizing radiation resulted in MAPK pathway activation initially (0-4h) and modestly enhanced MAPK activity at later times (24h-96h). Inhibition of radiation-induced MAPK activation using MEK1/2 inhibitors potentiated radiation-induced apoptosis in two waves, at 21-30h and 96-144h after exposure. The potentiation of apoptosis was not observed in MCF7, LNCaP, or PC3 cells. At 24h, the potentiation of apoptosis was independent of radiation dose whereas at 108h, apoptosis correlated with increasing dose. Removal of the MEK1/2 inhibitor either 6h or 12h after exposure abolished the potentiation of apoptosis at 24h. At this time, the potentiation of apoptosis correlated with cleavage of pro-caspases -8, -9 and -3, and with release of cytochrome c into the cytosol. Inhibition of caspase function using a pan-caspase inhibitor ZVAD blocked the enhanced apoptotic response at 24h. Selective inhibition of caspase 9 with LEHD or caspase 8 with IETD partially blunted the apoptotic response in MDA-MB-231, DU145 and A431 cells, whereas inhibition of both caspases reduced the response by >90%. Removal of the MEK1/2 inhibitor either 24h or 48h after exposure abolished the potentiation of apoptosis at 108h. Incubation of cells with ZVAD for 108h also abolished the potentiation of apoptosis. In general agreement with the finding that prolonged inhibition of MEK1/2 was required to enhance radiation-induced apoptosis at 108h, omission of MEK1/2 inhibitor from the culture media during assessment of clonogenic survival resulted in either little or no significant alteration in radiosensitivity. Collectively, our data show that combined exposure to radiation and MEK1/2 inhibitors can reduce survival in some, but not all, tumor cell types. Prolonged blunting of MAPK pathway function following radiation exposure is required for MEK1/2 inhibitors to have any effect on carcinoma cell radiosensitivity.Fil: Qiao, Liang. Virginia Commonwealth University; Estados UnidosFil: Yacoub, Adly. Virginia Commonwealth University; Estados UnidosFil: McKinstry, Robert. Virginia Commonwealth University; Estados UnidosFil: Park, Jong Sung. Virginia Commonwealth University; Estados UnidosFil: Caron, Ruben Walter. Virginia Commonwealth University; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Fisher, Paul B.. Columbia University. College of Physicians and Surgeons; Estados UnidosFil: Hagan, Michael P.. Virginia Commonwealth University; Estados UnidosFil: Grant, Steven. Virginia Commonwealth University; Estados UnidosFil: Dent, Paul. Virginia Commonwealth University; Estados Unido

Four problems with global carbon markets: a critical review

This article offers a critique of global carbon markets and trading, with a special focus on the Clean Development Mechanism of the Kyoto Protocol. It explores problems with the use of tradable permits to address climate change revolving around four areas: homogeneity, justice, gaming, and information. Homogeneity problems arise from the non-linear nature of climate change and sensitivity of emissions, which complicate attempts to calculate carbon offsets. Justice problems involve issues of dependency and the concentration of wealth among the rich, meaning carbon trading often counteracts attempts to reduce poverty. Gaming problems include pressures to promote high-volume, least-cost projects and the consequences of emissions leakage. Information problems encompass transaction costs related to carbon trading and market participation and the comparatively weak institutional capacity of project evaluators