Growth in stratospheric chlorine from short-lived chemicals not controlled by the Montreal Protocol.

We have developed a chemical mechanism describing the tropospheric degradation of chlorine containing very short-lived substances (VSLS). The scheme was included in a global atmospheric model and used to quantify the stratospheric injection of chlorine from anthropogenic VSLS ( ClyVSLS) between 2005 and 2013. By constraining the model with surface measurements of chloroform (CHCl3), dichloromethane (CH2Cl2), tetrachloroethene (C2Cl4), trichloroethene (C2HCl3), and 1,2-dichloroethane (CH2ClCH2Cl), we infer a 2013 ClyVSLS mixing ratio of 123 parts per trillion (ppt). Stratospheric injection of source gases dominates this supply, accounting for ∼83% of the total. The remainder comes from VSLS-derived organic products, phosgene (COCl2, 7%) and formyl chloride (CHClO, 2%), and also hydrogen chloride (HCl, 8%). Stratospheric ClyVSLS increased by ∼52% between 2005 and 2013, with a mean growth rate of 3.7 ppt Cl/yr. This increase is due to recent and ongoing growth in anthropogenic CH2Cl2-the most abundant chlorinated VSLS not controlled by the Montreal Protocol.

Molecular hydrogen (H2) emissions from gasoline and diesel vehicles.

This study assesses individual-vehicle molecular hydrogen (H2) emissions in exhaust gas from current gasoline and diesel vehicles measured on a chassis dynamometer. Absolute H2 emissions were found to be highest for motorcycles and scooters (141+/-38.6 mg km(-1)), approximately 5 times higher than for gasoline-powered automobiles (26.5+/-12.1 mg km(-1)). All diesel-powered vehicles emitted marginal amounts of H2 ( approximately 0.1 mg km(-1)). For automobiles, the highest emission factors were observed for sub-cycles subject to a cold-start (mean of 53.1+/-17.0 mg km(-1)). High speeds also caused elevated H2 emission factors for sub-cycles reaching at least 150 km h(-1) (mean of 40.4+/-7.1 mg km(-1)). We show that H2/CO ratios (mol mol(-1)) from gasoline-powered vehicles are variable (sub-cycle means of 0.44-5.69) and are typically higher (mean for automobiles 1.02, for 2-wheelers 0.59) than previous atmospheric ratios characteristic of traffic-influenced measurements. The lowest mean individual sub-cycle ratios, which correspond to high absolute emissions of both H2 and CO, were observed during cold starts (for automobiles 0.48, for 2-wheelers 0.44) and at high vehicle speeds (for automobiles 0.73, for 2-wheelers 0.45). This finding illustrates the importance of these conditions to observed H2/CO ratios in ambient air. Overall, 2-wheelers displayed lower H2/CO ratios (0.48-0.69) than those from gasoline-powered automobiles (0.75-3.18). This observation, along with the lower H2/CO ratios observed through studies without catalytic converters, suggests that less developed (e.g. 2-wheelers) and older vehicle technologies are largely responsible for the atmospheric H2/CO ratios reported in past literature.

Observations of long-lived anthropogenic halocarbons at the high-Alpine site of Jungfraujoch (Switzerland) for assessment of trends and European sources.

Anthropogenic halocarbons, such as chlorofluorocarbons (CFCs), hydrochlorofluorocarbons (HCFCs), hydrofluorocarbons (HFCs), bromocarbons (halons) and long-lived chlorinated solvents have been measured continuously at the high-Alpine site of Jungfraujoch (Switzerland) since January 2000. Chloro- and bromo-containing halocarbons are responsible for the stratospheric ozone depletion and will be globally banned from usage within the next years. With the exception of the stable CFC-12 (CF2 Cl2), all major CFCs and chlorinated solvents show a negative trend in recent years in their background concentrations at Jungfraujoch. HCFCs, as their first-generation substitute, are still increasing with a few percent per year. However, the frequency and the strength of HCFCs pollution events, which are caused by regional European emissions, are already declining. This can be seen as a sign of the impending ban of these gases within the next years in Europe. On the other hand, HFCs as the second-generation substitutes, are increasing with relative rates of at least 10% per year (e.g. almost 5 ppt per year for HFC-134a). An allocation of European sources was attempted by combining measured concentrations with trajectories of air masses reaching the Jungfraujoch during pollution events. Potential source regions could be detected in Italy, France, Spain and Germany.

Localization of source regions of selected hydrofluorocarbons combining data collected at two European mountain stations.

Ground-based in situ measurements of hydrofluorocarbons HFC-125, HFC-134a, and HFC-152a, which are regulated under the Kyoto Protocol, are carried out at four European sites within the SOGE (System of Observation of Halogenated Greenhouse Gases in Europe) program. Concentrations measured at the high mountain stations of Jungfraujoch (Switzerland) and Mte Cimone (Italy) together with back-trajectory statistical analysis are used in order to identify potential source regions on a European scale. Combining concentration data recorded at the two sites allows to reduce one of the problem which is inherent to the back-trajectory approach, i.e. the localisation of "ghost" sources in the wake of real sources. In this way, a more reliable picture of the location of European potential source regions is given.

An evaluation of the current radiative forcing benefit of the Montreal Protocol at the high-Alpine site Jungfraujoch.

A combination of reconstructed histories, long-term time series and recent quasi-continuous observations of non-CO2 greenhouse gases at the high-Alpine site Jungfraujoch is used to assess their current global radiative forcing budget and the influence of regulations due to the Montreal Protocol on Substances that Deplete the Ozone Layer in terms of climate change. Extrapolated atmospheric greenhouse gases trends from 1989 assuming a business-as-usual scenario, i.e. no Montreal Protocol restriction, are presented and compared to the observations. The largest differences between hypothetical business-as-usual mixing ratios and current atmospheric observations over the last 16 years were found for chlorinated species, in particular methyl chloroform (CH3CCl3) at 167 to 203 ppt and chlorofluorocarbon-12 (CFC-12) at 121 to 254 ppt. These prevented increases were used to estimate the effects of their restrictions on the radiative forcing budget. The net direct effect due to the Montreal Protocol regulations reduces global warming and offsets about 14 to 30% of the positive greenhouse effect related to the major greenhouse gases CO2, CH4, N2O and also SF6, and about 12 to 22% of the hypothetical current radiative forcing increase without Montreal Protocol restrictions. Thus, the Montreal Protocol succeeded not only in reducing the atmospheric chlorine content in the atmosphere but also dampened global warming. Nevertheless, the Montreal Protocol controlled species still add to global warming.

Response of a gamma delta+ T cell receptor invariant subset during bacterial infection.

Murine gamma delta T cells can be divided into subsets based on the TCR gamma-chains they express. Most of these subsets have variable TCR junctions, but two, both associated with epithelia, express invariant TCRs. The absence of receptor variability in these cells implies uniformity of their ligands. This was previously taken as evidence to suggest that gamma delta T cells recognize host-derived, stress-induced ligands. We now demonstrate, for the first time, the response of a gamma delta TCR invariant subset during bacterial infection, a potential cause of stress. After infection with Listeria monocytogenes, absolute numbers of all T cells in the liver, including alpha beta and gamma delta T cell subsets, increased markedly. However, responses of a gamma delta T cell subset varied. We noted a decrease in the relative frequency of V delta 6.3+ cells, which are, for the most part, included in the V gamma 1+ subset. In contrast, cells bearing the invariant V gamma 6/V delta 1 TCR increased substantially in proportion to other gamma delta T cells, as determined by PCR analysis of liver T cell RNA and by comparing liver gamma delta T cell hybridomas made from normal mice to those from mice infected with Listeria. V gamma 6/V delta 1+ cells have been previously reported as a TCR invariant intraepithelial subset in the female reproductive tract and tongue. We show here that V gamma 6/V delta 1+ cells reactive in Listeria-infected liver are polyclonally derived, but still bear TCR chains with invariant junctional sequences, identical with those of the female reproductive tract. Although the Ag that stimulates these cells is unknown, our results indicate that only diverse, but also invariant, gamma delta T cell subsets can become involved in the host response to a bacterial infection.

Allelic differences in TCR gamma-chains alter gamma delta T cell antigen reactivity.

Mouse gamma delta T cell hybridomas from various strains that express a TCR-V gamma 1/V delta 6 respond weakly to an autologous Ag and more strongly to a short segment of the mycobacterial heat shock protein-60 (HSP-60). However, V gamma 1/V delta 6 hybridomas derived from AKR mice show greatly reduced or absent responses to these stimuli. To determine whether the lack of response in these AKR hybridomas is caused by polymorphisms found in the expressed AKR gamma and TCR-delta genes or, instead, stems from other genes in AKR, we crossed an AKR mouse with a responder mouse, C57BL/10 (B10), and prepared hybridomas from F1 progeny. Expression of an AKR V gamma 1-J gamma 4-C gamma 4 gene correlated with nonresponsiveness, whereas expression of a B10 V gamma 1-J gamma 4-C gamma 4 gene in most hybridomas ensured responses to both self Ag and the HSP-60 peptide. An allelic difference in the expressed V gamma 6 gene was irrelevant to these responses. Moreover, transfection of a functional B10 V gamma 1-J gamma 4-C gamma 4 gene into an F1 hybridoma variant that had lost the AKR version of this gene restored responses. The allelic gamma gene products differ at nine amino acids in the V region, and three amino acids in the C region. In addition, the AKR C gamma 4 region contains a 16-amino acid insertion. We propose that amino acid differences among those encoded by the AKR V gamma 1-J gamma 4-C gamma 4 gene are responsible for the lack of response, and reduce the ability of the TCR-gamma delta to bind the relevant Ag.

Liver gamma delta T cells. TCR junctions reveal differences in heat shock protein-60-reactive cells in liver and spleen.

The liver of mice contains elevated percentages of gamma delta T cells when compared with peripheral lymphoid organs. We have now analyzed these cells clonally, by generating a random collection of liver gamma delta T cell hybridomas and sequencing the productively rearranged TCR-gamma and -delta genes in each hybridoma clone. Examining C57BL/10 mice of various ages, we have found that over half of their normal gamma delta T cells are one of two types, V delta 4+ or V delta 6.3+. gamma delta T cell hybridomas generated from mouse liver contain clones that are "spontaneously" reactive, and respond to purified protein derivative from mycobacteria and to a 17-amino acid peptide from mycobacterial heat shock protein-60 (HSP-60). Like similar cells found in newborn thymus or adult spleen, all of the cells showing this HSP-60 reactivity pattern were found to express V gamma 1-J gamma 4-C gamma 4, most in conjunction with V delta 6-J delta 1-C delta, particularly with V delta 6.3. However, the gamma and delta junctional sequences of the V gamma 1/V delta 6+ cells isolated from adult liver differed from those found in adult spleen; being less diverse, their receptors instead resemble those of similar cells from newborn thymus. These data suggest that HSP-60-reactive gamma delta cells in adult murine liver and spleen are independent of each other and may be resident in their respective sites.