Warming caused by cumulative carbon emissions towards the trillionth tonne

Global efforts to mitigate climate change are guided by projections of future temperatures1. But the eventual equilibrium global mean temperature associated with a given stabilization level of atmospheric greenhouse gas concentrations remains uncertain1, 2, 3, complicating the setting of stabilization targets to avoid potentially dangerous levels of global warming4, 5, 6, 7, 8. Similar problems apply to the carbon cycle: observations currently provide only a weak constraint on the response to future emissions9, 10, 11. Here we use ensemble simulations of simple climate-carbon-cycle models constrained by observations and projections from more comprehensive models to simulate the temperature response to a broad range of carbon dioxide emission pathways. We find that the peak warming caused by a given cumulative carbon dioxide emission is better constrained than the warming response to a stabilization scenario. Furthermore, the relationship between cumulative emissions and peak warming is remarkably insensitive to the emission pathway (timing of emissions or peak emission rate). Hence policy targets based on limiting cumulative emissions of carbon dioxide are likely to be more robust to scientific uncertainty than emission-rate or concentration targets. Total anthropogenic emissions of one trillion tonnes of carbon (3.67 trillion tonnes of CO2), about half of which has already been emitted since industrialization began, results in a most likely peak carbon-dioxide-induced warming of 2 °C above pre-industrial temperatures, with a 5–95% confidence interval of 1.3–3.9 °C.

Carbon management, local governance and community engagement

This article examines the role of communities in carbon management as it relates to both climate change and energy policy at the local level and as a seedbed for grassroots activity. The article considers some of the implications of recent policy developments, particularly the ways in which the ‘lines of responsibility’ are now being drawn at the local level. Drawing upon in-depth interviews with local authorities in the UK and the USA, the article examines the political distinctions that are evident between the two situations and the ramifications of these for practical community engagement in carbon management at the local level. Community engagement is likely to be central to the delivery of CO2 reductions, but evidence so far points to a series of challenges that will require a greater emphasis on partnership working between community groups and formal decision-making bodies.

Mobilising community action towards a low-carbon future: Opportunities and challenges for local government in the UK

Over the last decade the important role that local authorities can play in catalyzing communityaction on climate change has been repeatedly emphasised by the UK Government. The paper examines this policy context and explores the options available to local authorities in terms of reaching and engaging their communities. The type of progressive response shown by some UKlocal authorities is illustrated with empirical evidence gathered through a study conducted in the London Borough of Islington focusing on their recently established ‘Green Living Centre’. The results confirm interest in this major council-led community initiative, with positive attitudes expressed by the majority of those questioned in terms of the advice and information available. However, it is also clear that many participants had preexisting pro-environmental attitudes and behavioural routines. Results from a broader sample of Islington residents indicate a substantial challenge in reaching the wider community, where enthusiasm for sustainability change and interest in this type of scheme were more mixed. The prospect for local government in addressing this challenge – and their ability to trigger and capitalize upon concepts of social change at the community level towardsalowercarbon future – is discussed in the final part of the paper.

Effect of mountain breeze in ventilating the city under calm and neutral atmospheric environment: Interaction of airflow structures and ventilation efficiency

Many modern cities locate in the mountainous areas, like Hong Kong, Phoenix City and Los Angles. It is confirmed in the literature that the mountain wind system developed by differential heating or cooling can be very beneficial in ventilating the city nearby and alleviating the UHI effect. However, the direct interaction of mountain wind with the natural-convection circulation due to heated urban surfaces has not been studied, to our best knowledge. This kind of unique interaction of two kinds of airflow structures under calm and neutral atmospheric environment is investigated in this paper by CFD approach. A physical model comprising a simple mountain and three long building blocks (forming two street canyons) is firstly developed. Different airflow structures are identified within the conditions of different mountain-building height ratios (R=Hm/Hb) by varying building height but fixing mountain height. It is found that the higher ventilation rate in the street canyons is expected in the cases of smaller mountain-building ratios, indicating the stronger natural convection due to increasing heated building surfaces. However, there is the highest air change rate (ACH) in the lowest-building-height case and most of the air is advective into the street canyon through the top open area, highlighting the important role played by the mountain wind. In terms of the ventilation efficiency, it is shown that the smallest R case enjoys the best air change efficiency followed by the highest R case, while the worst ventilative street canyons occur at the middle R case. In the end, a gap across the streets is introduced in the modeling. The existence of the gap can greatly channel the mountain wind and distribute the air into streets nearby. Thus the ACH can be doubled and air quality can be significantly improved.

The ethics of carbon offsetting

Carbon offsetting can be loosely characterized as a mechanism by which an organization or individual contributes to a scheme that is projected either to remove carbon dioxide from the atmosphere or to deliver carbon dioxide emission reductions on the part of other organizations or individuals. An activity that has been offset therefore purports to make no long-term net contribution to atmospheric greenhouse gas concentrations. The ethical basis for using carbon offsetting as an approach to tackling climate change is very much contested. We seek to expose some of the underlying reasons for these ethical disagreements. We show that they relate both to empirical disagreements about what the likely benefits of offsetting are and, more fundamentally, to principled disagreements about the right way to discharge duties to deliver carbon reductions.

Assessment of potential climate change impacts on peatland dissolved organic carbon release and drinking water treatment from laboratory experiments

Catchments draining peat soils provide the majority of drinking water in the UK. Over the past decades, concentrations of dissolved organic carbon (DOC) have increased in surface waters. Residual DOC can cause harmful carcinogenic disinfection by-products to form during water treatment processes. Increased frequency and severity of droughts combined with and increased temperatures expected as the climate changes, have potentials to change water quality. We used a novel approach to investigate links between climate change, DOC release and subsequent effects on drinking water treatment. We designed a climate manipulation experiment to simulate projected climate changes and monitored releases from peat soil and litter, then simulated coagulation used in water treatment. We showed that the ‘drought’ simulation was the dominant factor altering DOC release and affected the ability to remove DOC. Our results imply that future short-term drought events could have a greater impact than increased temperature on DOC treatability.

Surface chemistry of glycine on Pt{111} in different aqueous environments

Adsorption of glycine on Ptf111g under UHV conditions and in different aqueous environments was studied by XPS (UHV and ambient pressure) and NEXAFS. Under UHV conditions, glycine adsorbs in its neutral molecular state up to about 0.15 ML. Further deposition leads to the formation of an additional zwitterionic species, which is in direct contact with the substrate surface, followed by the growth of multilayers, which also consist of zwitterions. The neutral surface species is most stable and decomposes at 360 K through a multi-step process which includes the formation of methylamine and carbon monoxide. When glycine and water are co-adsorbed in UHV at low temperatures (< 170 K) inter-layer diffusion is inhibited and the surface composition depends on the adsorption sequence. Water adsorbed on top of a glycine layer does not lead to significant changes in its chemical state. When glycine is adsorbed on top of a pre-adsorbed chemisorbed water layer or thick ice layer, however, it is found in its zwitterionic state, even at low coverage. No difference is seen in the chemical state of glycine when the layers are exposed to ambient water vapor pressure up to 0.2 Torr at temperatures above 300 K. Also the decomposition temperature stays the same, 360 K, irrespective of the water vapor pressure. Only the reaction path of the decomposition products is affected by ambient water vapor.

Carbon monoxide mediates the anti-apoptotic effects of heme oxygenase-1 in medulloblastoma DAOY cells via K+ channel inhibition

Tumor cell survival and proliferation is attributable in part to suppression of apoptotic pathways, yet the mechanisms by which cancer cells resist apoptosis are not fully understood. Many cancer cells constitutively express heme oxygenase-1 (HO-1), which catabolizes heme to generate biliverdin, Fe(2+), and carbon monoxide (CO). These breakdown products may play a role in the ability of cancer cells to suppress apoptotic signals. K(+) channels also play a crucial role in apoptosis, permitting K(+) efflux which is required to initiate caspase activation. Here, we demonstrate that HO-1 is constitutively expressed in human medulloblastoma tissue, and can be induced in the medulloblastoma cell line DAOY either chemically or by hypoxia. Induction of HO-1 markedly increases the resistance of DAOY cells to oxidant-induced apoptosis. This effect was mimicked by exogenous application of the heme degradation product CO. Furthermore we demonstrate the presence of the pro-apoptotic K(+) channel, Kv2.1, in both human medulloblastoma tissue and DAOY cells. CO inhibited the voltage-gated K(+) currents in DAOY cells, and largely reversed the oxidant-induced increase in K(+) channel activity. p38 MAPK inhibition prevented the oxidant-induced increase of K(+) channel activity in DAOY cells, and enhanced their resistance to apoptosis. Our findings suggest that CO-mediated inhibition of K(+) channels represents an important mechanism by which HO-1 can increase the resistance to apoptosis of medulloblastoma cells, and support the idea that HO-1 inhibition may enhance the effectiveness of current chemo- and radiotherapies.

Peroxynitrite mediates disruption of Ca2+ homeostasis by carbon monoxide via Ca2+ ATPase degradation

CO stimulates formation of NO and reactive oxygen species which, via peroxynitrite formation, inhibit Ca(2+) extrusion via PMCA, leading to disruption of Ca(2+) signaling. We propose this contributes to the neurological damage associated with CO toxicity.

Carbon monoxide induces cardiac arrhythmia via induction of the late Na+ current

Our data indicate that the proarrhythmic effects of CO arise from activation of NO synthase, leading to NO-mediated nitrosylation of Na(V)1.5 and to induction of the late Na(+) current. We also show that the antianginal drug ranolazine can abolish CO-induced early after-depolarizations, highlighting a novel approach to the treatment of CO-induced arrhythmias.

Carbon monoxide protects against oxidant-induced apoptosis via inhibition of Kv2.1

Oxidative stress induces neuronal apoptosis and is implicated in cerebral ischemia, head trauma, and age-related neurodegenerative diseases. An early step in this process is the loss of intracellular K(+) via K(+) channels, and evidence indicates that K(v)2.1 is of particular importance in this regard, being rapidly inserted into the plasma membrane in response to apoptotic stimuli. An additional feature of neuronal oxidative stress is the up-regulation of the inducible enzyme heme oxygenase-1 (HO-1), which catabolizes heme to generate biliverdin, Fe(2+), and carbon monoxide (CO). CO provides neuronal protection against stresses such as stroke and excitotoxicity, although the underlying mechanisms are not yet elucidated. Here, we demonstrate that CO reversibly inhibits K(v)2.1. Channel inhibition by CO involves reactive oxygen species and protein kinase G activity. Overexpression of K(v)2.1 in HEK293 cells increases their vulnerability to oxidant-induced apoptosis, and this is reversed by CO. In hippocampal neurons, CO selectively inhibits K(v)2.1, reverses the dramatic oxidant-induced increase in K(+) current density, and provides marked protection against oxidant-induced apoptosis. Our results provide a novel mechanism to account for the neuroprotective effects of CO against oxidative apoptosis, which has potential for therapeutic exploitation to provide neuronal protection in situations of oxidative stress.

Ion channels as effectors in carbon monoxide signaling

A wealth of recent studies has highlighted the diverse and important influences of carbon monoxide (CO) on cellular signaling pathways. Such studies have implicated CO, and the enzymes from which it is derived (heme oxygenases) as potential therapeutic targets, particularly (although not exclusively) in inflammation, immunity and cardiovascular disease.1 In a recent study,2 we demonstrated that CO inhibited cardiac L-type Ca(2+) channels. This effect arose due to the ability of CO to bind to mitochondria (presumably at complex IV of the electron transport chain) and so cause electron leak, which resulted in increased production of reactive oxygen species. These modulated the channel's activity through interactions with three cysteine residues in the cytosolic C-terminus of the channel's major, pore-forming subunit. Our study provided a potential mechanism for the cardioprotective effects of CO and also highlighted ion channels as a major potential target group for this gasotransmitter.

Carbon monoxide inhibits L-type Ca2+ channels via redox modulation of key cysteine residues by mitochondrial reactive oxygen species

Conditions of stress, such as myocardial infarction, stimulate up-regulation of heme oxygenase (HO-1) to provide cardioprotection. Here, we show that CO, a product of heme catabolism by HO-1, directly inhibits native rat cardiomyocyte L-type Ca2+ currents and the recombinant alpha1C subunit of the human cardiac L-type Ca2+ channel. CO (applied via a recognized CO donor molecule or as the dissolved gas) caused reversible, voltage-independent channel inhibition, which was dependent on the presence of a spliced insert in the cytoplasmic C-terminal region of the channel. Sequential molecular dissection and point mutagenesis identified three key cysteine residues within the proximal 31 amino acids of the splice insert required for CO sensitivity. CO-mediated inhibition was independent of nitric oxide and protein kinase G but was prevented by antioxidants and the reducing agent, dithiothreitol. Inhibition of NADPH oxidase and xanthine oxidase did not affect the inhibitory actions of CO. Instead, inhibitors of complex III (but not complex I) of the mitochondrial electron transport chain and a mitochondrially targeted antioxidant (Mito Q) fully prevented the effects of CO. Our data indicate that the cardioprotective effects of HO-1 activity may be attributable to an inhibitory action of CO on cardiac L-type Ca2+ channels. Inhibition arises from the ability of CO to promote generation of reactive oxygen species from complex III of mitochondria. This in turn leads to redox modulation of any or all of three critical cysteine residues in the channel's cytoplasmic C-terminal tail, resulting in channel inhibition.