Methanogenic community changes, and emissions of methane and other gases, during storage of acidified and untreated pig slurry.

AIMS: Acidification with concentrated H(2)SO(4) is a novel strategy to reduce NH(3) emissions from livestock slurry. It was recently found that also CH(4) emissions from acidified slurry are reduced. This study investigated the microbiological basis and temporal stability of these effects. METHODS AND RESULTS: Pig slurry from two farms, acidified by different techniques or untreated, was stored for 83 days in a pilot-scale facility. Methanogens were characterized before and after storage by T-RFLP and qPCR targeting mcrA. Emissions of NH(3) and CH(4) during storage were quantified. Acidified slurry pH was nearly constant at values of 5·5 and 6·5. Ammonia losses were reduced by 84 and 49%, respectively, while CH(4) emission with both acidification techniques was reduced by >90%. T-RFLP fingerprints showed little effect of acidification or storage time. A major T-RF of 105 bp could represent methanogens related to Thermoplasmata (Tp). No treatment effects on gene copy numbers were seen with universal methanogen primers, whereas effects were found with Tp-specific primers. CONCLUSION: Methane emissions were reduced >90% during storage. Thermoplasmata-related methanogens could be involved in CH(4) emissions from pig slurry. SIGNIFICANCE AND IMPACT OF THE STUDY: The effect of acidification on CH(4) emissions during storage of pig slurry was quantified for the first time. Acidification with sulphuric acid holds promise as a novel greenhouse gas mitigation strategy for confined livestock production.

The United States Department of Energy's Regional Carbon Sequestration Partnerships Program Validation Phase.

This paper reviews the Validation Phase (Phase II) of the Department of Energy's Regional Carbon Sequestration Partnerships initiative. In 2003, the U.S. Department of Energy created a nationwide network of seven Regional Carbon Sequestration Partnerships (RCSP) to help determine and implement the technology, infrastructure, and regulations most appropriate to promote carbon sequestration in different regions of the nation. The objectives of the Characterization Phase (Phase I) were to characterize the geologic and terrestrial opportunities for carbon sequestration; to identify CO(2) point sources within the territories of the individual partnerships; to assess the transportation infrastructure needed for future deployment; to evaluate CO(2) capture technologies for existing and future power plants; and to identify the most promising sequestration opportunities that would need to be validated through a series of field projects. The Characterization Phase was highly successful, with the following achievements: established a national network of companies and professionals working to support sequestration deployment; created regional and national carbon sequestration atlases for the United States and portions of Canada; evaluated available and developing technologies for the capture of CO(2) from point sources; developed an improved understanding of the permitting requirements that future sequestration activities will need to address as well as defined the gap in permitting requirements for large scale deployment of these technologies; created a raised awareness of, and support for, carbon sequestration as a greenhouse gas (GHG) mitigation option, both within industry and among the general public; identified the most promising carbon sequestration opportunities for future field tests; and established protocols for project implementation, accounting, and management. Economic evaluation was started and is continuing and will be a factor in project selection. During the Validation Phase, the seven regional partnerships will put the knowledge learned during the Characterization Phase into practice through field tests that will validate carbon sequestration technologies that are best suited to their respective regions of the country. These tests will verify technologies developed through DOE's core R&D effort and enable implementation of CO(2) sequestration on a large scale, should that become necessary. Pilot projects will have a site-specific focus to test technology; assess formation storage capacity and injectivity; validate and refine existing CO(2) formation models used to determine the transport and fate of CO(2) in the formation; demonstrate the integrity of geologic seals to contain CO(2); validate monitoring, mitigation, and verification (MMV) technologies; define project costs and compare costs of alternatives; assess potential operational and long-term storage risks; address regulatory requirements; and engage and evaluate public acceptance of sequestration technologies. Field validation tests involving both sequestration in geologic formations and terrestrial sequestration are being developed. The results from the Validation Phase will help to confirm the estimates made during the Characterization Phase and will be used to update the regional atlases and NatCarb. Answers to many questions about the effectiveness and safety of carbon sequestration technologies will be instrumental in planning for a Deployment Phase, in which large volume tests will be planned to further sequestration as an option that can mitigate GHG emissions in the United States.

Decreased toxicity to terrestrial plants associated with a mixture of methyl tert-butyl ether and its metabolite tert-butyl alcohol.

The influence of the main fuel oxygenate methyl tert-butyl ether (MTBE) and its key metabolite, tert-butyl alcohol (TBA), on the growth of a plant seedling was studied separately and in combination. The test plants were mung bean (Phaseolus radiatus), cucumber (Cucumis sativus), wheat (Triticum aestivum), sorghum (Sorghum bicolor), kale (Brassica alboglabra), Chinese cabbage (Brassica campestris), and sweet corn (Zea mays). The growth of all the plants was adversely affected by TBA and MTBE. The 5-d median effective concentration (EC50) for the plants exposed to MTBE and TBA were in the range of 680 to 1,000 mg MTBE/kg soil (dry wt) and 1,200 to 3,500 mg TBA/kg soil (dry wt), respectively. The relative order of the sensitivity rankings is almost the same for MTBE and TBA. Methyl tert-butyl ether is more toxic than TBA to most of the test species. Based on the EC50 values, MTBE is approximately 1.5 to 3 times more potent than TBA. The sum of the toxic unit (TU) at 50% inhibition of the mixture (EC50mix) was calculated from the dose (TU-based)-response relationships using the trimmed Spearman-Karber method. The combined effect of MTBE + TBA on the plant growth was less than additive because the EC50mix values were greater than I TU. This phenomenon may be due to the competition of MTBE and TBA in terms of their intake by plants. The combined effects of MTBE and TBA should be taken into account to assess their risk in gasoline-contaminated sites.

Ethylenediurea (EDU) affects the growth of ozone-sensitive and tolerant ash (Fraxinus excelsior) trees under ambient O3 conditions.

Adult ash trees (Fraxinus excelsior L.), known to be sensitive or tolerant to ozone, determined by presence or absence of foliar symptoms in previous years, were treated with ethylenediurea (EDU) at 450 ppm by gravitational trunk infusion over the 2005 growing season (32.5 ppm h AOT40). Tree and shoot growth were recorded in May and September. Leaf area, ectomycorrhizal infection, and leaf and fine root biomass were determined in September. EDU enhanced shoot length and diameter, and the number and area of leaves, in both O3-sensitive and tolerant trees. However, no EDU effects were recorded at the fine root and tree level. Therefore, a potential for EDU protection against O3-caused growth losses of forest trees should be evaluated during longer-term experiments.

Alveolar macrophage cytokine production in response to air particles in vitro: role of endotoxin.

The interaction of air particles and alveolar macrophages (AMs) may result in the release of proinflammatory cytokines. Normal mouse AMs were treated with concentrated air particle (CAPs) suspensions in vitro. After 5 h, cytokine release [macrophage inflammatory protein-2 (MIP-2) and tumor necrosis factor-alpha (TNF-alpha)] and phagocytosis of ambient air particles were measured. CAPs samples collected from urban air (Boston) on different days were used. The CAPs samples and their soluble and solid components caused significant MIP-2 and TNF-alpha production. Variability in the potency of samples collected on different days was observed. Trace endotoxin was measured in CAPs samples (EU/mg: 2.3 +/- 0.7, mean +/- SE, n = 10). A majority of biologic activity (cytokine induction) and endotoxin content was associated with the solid components. Neutralization of endotoxin by polymyxin B abrogated >80% of TNF-alpha induction by CAPs samples, but inhibited MIP-2 production by only approximately 40%. The trace endotoxin present in CAPs caused much more MIP-2 production than predicted by concentration alone (28 +/- 8-fold increase, n = 9), indicating synergistic interaction with other AM-activating components of the particles. Data suggest that low levels of endotoxin may interact with air particles to activate lung macrophages.

Suppression of rat and mouse lymphocyte function by urban air particulates (Ottawa dust) is reversed by N-acetylcysteine.

Epidemiology studies have demonstrated increased pulmonary morbidity such as allergy and infection with episodes of high particulate air pollution (size range 0.1-10 microm diameter, PM10), but the mechanism(s) for this association is not yet well defined. The present study was undertaken to evaluate the effects of EHC-93 urban particles (Ottawa dust) on immune functions of peripheral blood mononuclear cells (PBMCs) and splenocytes from male Fischer 344 rats and C57Bl/6 mice. Immune function endpoints evaluated included cell viability, lymphocyte blastogenesis stimulated by T-cell mitogen (concanavalin A, Con A) or B-cell mitogens [lipopolysaccharide (LPS) or LPS/dextran sulfate], intracellular Ca2+ concentration, interleukin 2 (IL-2) production, and expression of receptors for transferrin (TfR) and IL-2 (IL-2R). In addition, the effect of N-acetylcysteine (NAC), an antioxidant, on the toxicity of EHC-93 particles was evaluated. Total EHC-93 particles, water leachate of EHC-93, and washed EHC-93 suppressed proliferation of PBMCs and splenocytes to T- and B-cell mitogens. Treatment of splenocytes with EHC-93 particles did not alter intracellular Ca2+ concentration or mitogen-induced expression of TfR and IL-2R expression, but increased IL-2 production assayed by enzyme-linked immunosorbent assay (ELISA). In spite of an increase in IL-2 production, exogenous IL-2 when added to cultures was able to reverse the suppression of Con A-induced lymphocyte proliferation by EHC-93 particles. Furthermore, the suppressive effect of EHC-93 particles on mitogen-induced lymphocyte proliferation was completely abolished by addition of the antioxidant NAC to cultures, suggesting a possible role of oxidative factors for the toxicity of EHC-93 particles.

Air pollution and its effect on the upper respiratory tract and on allergic rhinosinusitis.

The nose is the first organ system encountered by inhaled air and its associated pollutants. Pollutants are deposited during inspiration through the nose. They accumulate on mucus and are absorbed in the nasal mucosa, resulting in a number of deleterious effects on the body. Irritation of the nose and sinus from these pollutants, resulting from direct contact with the nasal mucosa, leads to inflammation, edema, swelling, and blocked sinuses. The result is acute and chronic sinusitis. Absorption of these chemicals into the body produces systemic effects. Their effect on the immune system, although subtle, leads to dramatic changes in the allergic diathesis. The T suppressor cell is the most sensitive cell of the immune system and the first to be affected by exposure to chemical pollutants. Diminution of the suppressor activity and the relative increase in helper activity in turn lead to increased immunoglobulin production and the manifestation of allergy symptoms. The underlying biochemical reaction is caused by the effects of pollutants on the T suppressor cell. Patients with existing allergies become brittle and difficult to treat with the exacerbation of the allergic diathesis. Removal of these chemical pollutants from the body as quickly as possible is essential for effective treatment of this problem. Dietary antioxidants help reduce the oxidizing effect of the pollutants and act as conjugators to remove the pollutants from the body.

Intratracheally administered liposomal alpha-tocopherol protects the lung against long-term toxic effects of paraquat.

Paraquat is a broad-spectrum herbicide known to produce lung injury via oxidative stress-mediated mechanisms. Different pharmacological strategies have been explored to reduce the formation of these reactive oxygen species and/or prevent their toxic effects in the treatment of paraquat poisoning. The present study was carried out to investigate whether the antioxidant alpha-tocopherol, incorporated into liposomes and delivered directly to the lungs of rats, could protect the organ against the long-term toxic effects of paraquat. Plain liposomes (composed of dipalmitoylphosphatidylcholine, DPPC) or alpha-tocopherol liposomes (8 mg alpha-tocopherol/kg body weight) were administered intratracheally to animals 24 h prior to an intraperitoneal injection of paraquat dichloride (20 mg/kg) and rats were killed 0, 1, 4, 6, 8, 10, 12, 16, 19 or 24 days after paraquat treatment. Results of this study showed that lungs of animals treated with paraquat were extensively damaged, as evidenced by significant increases in lung weight and decreases in lung angiotensin converting enzyme (ACE) and alkaline phosphatase enzyme (AKP) activities. Moreover, paraquat treatment: resulted in a significant reduction in the number of neutrophils in the blood of rats with a concurrent increase in the pulmonary myeloperoxidase activity, suggestive of neutrophil infiltration in the lungs of treated animals. Pretreatment of rats with liposomes alone did not significantly alter the paraquat-induced changes of all parameters examined. On the other hand, pretreatment of rats with alpha-tocopherol liposomes, 24 h prior to paraquat challenge, attenuated paraquat-induced changes in ACE, AKP and myeloperoxidase activities but failed to prevent increases in lung weight. Thus, pretreatment of rats with liposome-associated alpha-tocopherol appears to protect the lung against some of the toxic effects of paraquat.

[Optimization on slow-release inhibition of biomethane and the kinetics model of diffusion].

The diffusion mechanism of acetylene,which can inhibit the activity of methanogens, was studied. Paraffin wax and rosin were used as matrix of slow-release and calcium carbide was used as inhibition material. Based on the T. Higuchi equation and the characteristics of slow-release inhibitors, a mechanism model was derived. Moreover, the effective diffusion coefficients (De) can be acquired by this model. During the diffusion process, the reaction heat of calcium carbide and water could make acetylene gas expansion and caused the slow-release inhibitors expansion if the hardness of the slow-release inhibitors is inadequate. The hardness and compactness were enhanced and the effective diffusion coefficients reached 2.2849 x 10(-8) cm2/min (R2 = 0.9901) when the mass faction of rosin was 20% and the mass ratio of matrix to calcium carbide was 1/1. Hence,the mitigation the methane generation with municipal solid waste (MSW) can be achieved by the technology of slow-release inhibition.

Air pollution effect of O3 on crop yield in rural India.

Measurement of surface ozone (O(3)) mixing ratio was made from January 2006 to December 2007 in Ahmednagar (19.1°N, 74.8°E, 657 m above sea level), India. The monthly average of daytime maximum of O(3) mixing ratio ranged from 14 to 57 parts per billion by volume (ppbv) with an annual average of about 20 ppbv. The estimated winter wheat and summer crop yield reduction by 10% and 15%, respectively from present O(3) pollution level associated with AOT40 (accumulation exposure of O(3) concentration over a threshold of 40 ppbv) index values 7370-9150 ppbv h in rural areas.

Cellular basis of the role of diesel exhaust particles in inducing Th2-dominant response.

There is growing evidence that diesel exhaust particles (DEP) can induce allergic diseases with increased IgE production and preferential activation of Th2 cells. To clarify the cellular basis of the role of DEP in the induction of Th2-dominant responses, we examined the effects of DEP on the cytokine production by T cells stimulated with anti-CD3/CD28 Ab and on that by monocyte-derived dendritic cells (MoDCs) stimulated with CD40L and/or IFN-gamma. We examined IFN-gamma, IL-4, IL-5, IL-8, and IL-10 produced by T cells and TNF-alpha, IL-1beta, IL-10, and IL-12 produced by MoDCs using real-time PCR analysis or by ELISA. To highlight the effects of DEP, we compared the effects of DEP with those of dexamethasone (DEX) and cyclosporin A (CyA). DEP significantly suppressed IFN-gamma mRNA expression and protein production, while it did not affect IL-4 or IL-5 mRNA expression or protein production. The suppressive effect on IFN-gamma mRNA expression was more potent than that of DEX and comparable at 30 mug/ml with 10(-7) M CyA. The suppressive effect on IFN-gamma production was also more potent than that of either DEX or CyA. DEP suppressed IL-12p40 and IL-12p35 mRNA expression and IL-12p40 and IL-12p70 production by MoDCs, while it augmented IL-1beta mRNA expression. Finally, by using a thiol antioxidant, N-acetyl cysteine, we found that the suppression of IFN-gamma production by DEP-treated T cells was mediated by oxidative stress. These data revealed a unique characteristic of DEP, namely that they induce a Th2 cytokine milieu in both T cells and dendritic cells.