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Aug 16, 2014 - Carbon Capture and Sequestration: An Exploratory Inhalation ... 6N mice were exposed for 7 days by inhalation of 25 ppm neat amine or...
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Carbon Capture and Sequestration: An Exploratory Inhalation Toxicity Assessment of Amine-Trapping Solvents and Their Degradation Products Jacob D. McDonald,*,† Dean Kracko,† Melanie Doyle-Eisele,† C. Edwin Garner,† Chris Wegerski,† Al Senft,† Eladio Knipping,‡ Stephanie Shaw,‡ and Annette Rohr‡ †

Chemistry and Inhalation Exposure Program (CIEP), Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive Southeast, Albuquerque, New Mexico 87108, United States ‡ Electric Power Research Institute (EPRI), 3420 Hillview Avenue, Palo Alto, California 94304, United States S Supporting Information *

ABSTRACT: Carbon dioxide (CO2) absorption with aqueous amine solvents is a method of carbon capture and sequestration (CCS) from flue gases. One concern is the possible release of amine solvents and degradation products into the atmosphere, warranting evaluation of potential pulmonary effects from inhalation. The CCS amines monoethanolamine (MEA), methyldiethanolamine (MDEA), and piperazine (PIP) underwent oxidative and CO2-mediated degradation for 75 days. C57bl/ 6N mice were exposed for 7 days by inhalation of 25 ppm neat amine or equivalant concentration in the degraded mixture. The aqueous solutions were nebulized to create the inhalation atmospheres. Pulmonary response was measured by changes in inflammatory cells in bronchoalveolar lavage fluid and cytokine expression in lung tissue. Ames mutagenicity and CHOK1 micronucleus assays were applied to assess genotoxicity. Chemical analysis of the test atmosphere and liquid revealed complex mixtures, including acids, aldehydes, and other compounds. Exposure to oxidatively degraded MEA increased (p < 0.05) total cells, neutrophils, and lymphocytes compared to control mice and caused inflammatory cytokine expression (statistical increase at p < 0.05). MEA and CO2-degraded MEA were the only atmospheres to show statistical (p < 0.05) increase in oxidative stress. CO2 degradation resulted in a different composition, less degradation, and lower observed toxicity (less magnitude and number of effects) with no genotoxicity. Overall, oxidative degradation of the amines studied resulted in enhanced toxicity (increased magnitude and number of effects) compared to the neat chemicals.

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INTRODUCTION

Given the potential of large-scale CCS applications, for both high volumetric flows and geographically widespread usage, potential environmental consequences of implementing this technology need to be evaluated. Amine scrubbing has been employed in a number of industrial applications, but the environmental releases of the amines and potential degradation products are not generally well-characterized. In CCS applications, amine solvent may be lost by chemical degradation along with evaporation and aerosol formation at the outlets of absorber and desorber columns.27,39 For the frequently used alkanolamine, monoethanolamine (MEA), the emission loss to air, relative to all sources of solvent consumption pathways, has been estimated to be ∼3% for a natural gas power station under normal operation.39 For a 420 MW gas power plant at Karsto, Norway, it is estimated that amine loss to the environment may approach 40−160 tons/

Amine scrubbing technology has been used since 1930 in the oil and chemical industries for removal of hydrogen sulfide and carbon dioxide (CO2) from flue gas streams.3,15,19 It is the most well-developed of technologies for CO2 capture and sequestration (CCS);10 however, it has not yet been applied at full scale to coal-fired power plant flue gases. The technology is currently being evaluated at a number of pilot- and demonstration-scale projects worldwide. In the amine-scrubbing process, flue gas is passed through the solvent, which reacts with CO2 via carbamate or bicarbonate formation, as shown in Figure 1.13,32 The reaction of primary and secondary amines with CO2 is rapid, and the stoichiometry is 0.5 mol of CO2 for each mole of amine.14 Tertiary amines react more slowly than primary or secondary amines, but the stoichiometry is 1:1.14,31 The system is regenerated by desorption of CO2 with heating, whereby released CO2 may be compressed for either further use or storage, and the remaining amine solvent is recycled and reused. © XXXX American Chemical Society

Received: March 1, 2013 Revised: July 23, 2014 Accepted: August 16, 2014

A

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Figure 1. CO2 sequestration reactions of primary, secondary, and tertiary amines.

annum.2 This loss could result in environmental exposures through air or other media. Amines used in CCS processes have been shown to degrade via thermal and oxidative mechanisms as well as via carbamate polymerization. The MEA example is shown in Figure 2.1,11

comparison to oxidative and thermal degradation pathways, the atmospheric reactions are more complex and would give a larger range of products.3,20 The main products of atmospheric degradation are amides, but a number of aldehydes, nitrosamines, and nitramines may potentially be formed.3,20 Because of the potential for release to the environment, the toxicity of several of the amines has been proposed for use along with many of their potential solvent and atmospheric degradation products. Amines, such as MEA, methyldiethanolamine (MDEA), and piperazine (PIP), can be respiratory irritants at high inhalation doses, and PIP has also been shown to be a sensitizer. MEA and PIP studied at high oral doses resulted in reproductive, neurotoxicity, and target organ toxicity but little or no mutagenic and carcinogenic properties.18,19 Overall, these effects only occur at high doses in laboratory animals. As a result, the allowable exposure limits for the amines are typically high (i.e., 1−10 ppm over 8 h).21 There remains some concern, however, about the potential for the complex mixtures produced from the amine degradations to result in enhanced toxicity, as both irritants because of the formation of aldehydes and, potentially, carcinogens if nitrosamines are confirmed to be present in sufficient quantities. This study was conducted to evaluate the pulmonary inflammatory potential of several amines used for CCS and their degradant mixtures. MEA, MDEA, and PIP were used as model amines. Their inhalation toxicity and genotoxicity in aerosolized aqueous amine or degraded mixtures were evaluated. The experimental matrix included MEA, MDEA, and PIP compared to both oxidatively and CO2-mediated degraded solvent amines (nine total groups plus their corresponding controls). The amine and amine degradation mixture exposures were conducted at the same total hydrocarbon concentration to facilitate direct comparison of the “potency” of the response. This relative comparison across a number of pulmonary inflammatory metrics can provide focus for future research. The composition of the mixtures was also evaluated with particular attention given to the extent of degradation and assessment of several potential compounds of concern. This study should be interpreted as a demonstration of the successful development of degradation and exposure methodologies for inhalation toxicological evaluation of amines and their degradation mixtures as well as a preliminary assessment of toxicity. Future research, such as dose−response assessment, when coupled with information on emissions and exposure, will aid in risk assessment associated with the use of amine solvents for CCS.

Figure 2. Examples of pathways of chemical degradation of MEA.1

The rate and mechanism of degradation are dependent upon the chemical properties of the amine along with the temperature and oxygen content of the emission stream.22 The most well-studied capture agent, MEA, has been shown to degrade by as much as 25% via oxidative pathways and 6% via carbamate polymerization in power station CO2-trapping processes.39 Oxidation of MEA produces a variety of lowmolecular-weight carbamates, aldehydes, carboxylic acids, ethers, amides, imidazoles, and other compounds.1 Chemical transformations can also take place in the atmosphere once amines or their degradation products are released. Recent reports from the Norwegian Institute for Air Research and the University of Oslo have provided some initial descriptions of reactions and reaction mechanisms in air.3,20 In B

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MATERIALS AND METHODS Amines. MEA, PIP, and MDEA were purchased from Aldrich (St. Louis, MO) and were of ≥99% purity. MEA is a primary amine; PIP is a secondary amine; and MDEA is a tertiary amine. Amine Degradation. Amine degradation was carried out in a 1 L stainless-steel vessel maintained at 150 °C and approximately 15 psi (Figure 3). Laboratory-scale reactor

the system below 15 psi or at least once per week. Degradation was carried out for 75 days. This length of time was selected on the basis of the time to achieve significant oxidative breakdown of MEA, the first amine evaluated in series. This experimental configuration was subsequently applied to all amines for the follow-up experiments. Amine degradation was evaluated as defined below for amine content (specific to each amine) to confirm the extent of degradation (expressed as percentage of amine remaining = amount amine remaining/initial amine × 100) and to characterize degradation products. Chemical Analysis of Amines and Amine Degradation Products. Chemical analysis of the amine degradant mixtures was conducted to evaluate the extent of degradation, assess the composition of the mixture, and evaluate the presence of specific compounds of concern. The choice of analytical systems was made based on previous work characterizing degradation products for MEA, MDEA, and PIP.1,4,7,8,23,33 This directed analysis focused on amines, carbonyls, and nitrosamines to define the quantity of amine, degree of oxidation, and potential for nitrosamine formation because they are putative carcinogens.9,12,26,34 MEA was analyzed by high-pressure liquid chromatography (HPLC) analysis after collection on SKC tubes pretreated with 1-naphthyl-isothiocyanate (NITC) to derivitize the amine. MDEA and PIP samples were collected through a SKC Anasorb 708 cartridge (Eighty Four, PA) and analyzed by an Agilent 6950 series gas chromatograph connected to an Agilent (Foster City, CA) 5973N (inert) mass spectrometric detector (GC−MSD). The samples were analyzed by single ion monitoring (SIM). Additional details on the analytical methods are provided in the Supporting Information. Degradant Analysis. The extent of oxidative degradation was estimated by detection of oxidative carbonyl-containing products in each reaction mixture. Volatile carbonyl compounds were analyzed by HPLC−mass spectrometry (MS) after collection on 2,4-dinitrophenylhydrazine cartridges. NNitrodimethylamine (nitramine), acetamide, and formamide were analyzed by GC−MSD [1 ng/mL limit of detection (LOD)]. For liquid chromatography−mass spectrometry (LC−MS) analysis to determine possible nitrosamine components of the amine degradation mixtures, two techniques were applied. First, targeted analysis of predicted nitrosamines from reaction mechanisms and the literature was conducted. Second, a nitrosamine screening method [dual neutral loss (DNL)] was developed that conducts non-discriminately for unique molecular ions associated with nitrosamines. This method is described in the Supporting Information. Those identified nitrosamines were further elucidated when possible or characterized as unidentified nitrosamines. In addition to the targeted analysis defined above, mass spectral analysis was used to determine components of the amine degradation mixtures in scanning mode. Spectral interpretation was conducted by comparison versus spectral libraries and structural elucidation based on interpretation of fragmentation patterns. Animal Strain and Husbandry. Male C57bl/6N mice (n = 8/group), 6−8 weeks old on arrival, were purchased from Harlan LabBloks (Madison, WI) and quarantined for 2 weeks before use. Mice were housed in whole-body exposure chambers for the duration of the exposure period with water provided ad libitum and food (Harlan, Madison, WI) provided during non-exposure hours. Light/dark cycles were 12:12 h,

Figure 3. Schematic of the amine degradation system. The headspace of the sealed, heated reaction vessel is charged with gases to simulate oxidative degradation (shown) or CO2 degradation (NO2, air, and CO2).

designs, such as this, are often used to investigate amine solvent degradation. These vessels model industrial conditions by providing excess reactants and high temperatures under pressurized conditions. During laboratory degradation studies, gases, such as O2, CO2, and NO2, are usually bubbled into the alkanolamine solution or used to pressurize the reactor headspace.4,7,8,23,33 For the current studies, the system was configured to determine degradation with and without CO2. This was performed to distinguish oxidative and CO2-mediated reaction products that would differ in composition. In general, the approach was modeled after the work by Lepaumier et al.23 with a combination of reactants that focused on CO2/oxygen and the inclusion of NO2 that would also be present (and may be important for degradant formation). The vessel was placed on a heating mantle, wrapped in electronically controlled heat tape, and coupled to gas cylinders for the introduction of gaseous reactants (Figure 1). For the oxidative degradation conductions, NO2 (0.06 L min−1, Scott Specialty Gases, Plumsteadville, PA) at 200 ppm was combined with purified air (0.5 L min−1, Matheson, Albuquerque, NM) and delivered through the aqueous amine mixture at 0.5 L min−1 for 10 min. The exhaust port on the vessel was then sealed, and the chamber was pressurized to 15 psi with NO2 and purified air prior to closing the inlet. For CO2-mediated degradation, the vessel was pressurized with 5% CO2 (0.5 L min−1) in addition to the gas mixture defined above. The vessel was heated to 150 °C. Once the reactants were added and the system was pressurized, it was left in a static condition until the addition of additional reactants the following day. Reactants were added from gas cylinders when the pressure decreased in C

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Salmonella Mutagenicity Test Kit (Molecular Toxicology, Inc., Boone, NC). Details of the methodology for each of the assays below are provided in the Supporting Information. Statistics. Statistical analysis of biological response by oneway analysis of variance (ANOVA) and Student’s t test for exposure-related effects was conducted with GraphPad Prism software, version 5.01 (GraphPad Software, San Diego, CA). The criterion for statistical significance was set at p = 0.05 with n = 8 animals per group.

and exposures were conducted during the light phase. Each experiment included a set of control animals exposed to filtered air (FA). All procedures were approved by the Institutional Animal Care and Use Committee of the Lovelace Respiratory Research Institute. Inhalation Exposures. Exposures to amines, amine degradation products, or filtered air were conducted in a whole body chamber inhalation exposure system for 6 h/day for 7 consecutive days. The test article (diluted in purified water) was delivered by a Hospitak nebulizer connected to a continuous feed reservoir at 20−30 psi. Forced air dilution through the delivery line was set at 13−15 L min−1, and exhaust was set at approximately 25 L min−1. Exposures to amines were conducted at 25 ppm total concentration. The exposure concentration of amine degradation products was based on levels of total degradation from reaction vessel experiments (i.e., an initial target of amine at 25 ppm minus the percentage degraded). For example, MEA showed 30% degradation; therefore, the exposure target was 17.5 ppm MEA, with the remainder being the degradation products. In Vivo Pulmonary Inflammation Assessment. At 18− 24 hours after final exposure, the animals were euthanized by an overdose of pentobarbital-based solution and then subjected to total lung lavage and bronchoalveolar lavage (BAL) analysis. Briefly, the lungs of the mice from each exposure group were lavaged 2 times with approximately 0.5 mL of phosphatebuffered saline. The cell content of BAL was then evaluated using a hemocytometer (Bright-Line model 4200, Reichert Scientific Instruments, Buffalo, NY). Differential cell types were evaluated on a Diff-Quick-stained cytocentrifuge preparation. A panel of tissue cytokines that are expressed in response to tissue injury or inflammation were measured in collected BAL as an index of inflammation. The concentrations of selected cytokines [granulocyte macrophage colony-stimulating factor (GM-CSF)], interleukin-4 (IL-4), IL-1β, IL-6, IL-10, IL-12, interferon-γ (IFN-γ), growth-regulated oncogene-α/keratinocyte-derived cytokine (GRO-KC), chemokine (C−C motif) ligand 5 [also known as regulated and normal T cell expressed and secreted (RANTES)], tumor necrosis factor-α (TNF-α), vascular endothelial growth factor (VEGF), and monocyte chemoattractant protein-1 (MCP-1) were determined using a Luminex BioPlex 100 multiplex instrument (BioSource, human 30-plex) and performed as recommended by the supplier.35 To assess oxidative stress in the lung, lipid peroxidation markers in the lung tissue were assessed using a thiobarbituric acid reactive substances (TBARS) assay, as previously described.24 Briefly, right middle-lung lobe tissue was homogenized and sonicated for 15 s. These homogenates were diluted 1:10 weight/volume in normal saline. A TBARS assay kit was used to measure TBARS levels in whole tissue homogenates. Duplicate samples were read on a spectrophotometer at 530 nm (PerkinElmer Lambda 35, Boston, MA), and results were expressed as malondialdehyde (MDA) equivalents using a MDA standard curve (OXItek, ZeptoMetrix Corp, Buffalo, NY). In Vitro Genotoxicity. Genotoxicity was evaluated by either directly applying the mixture to the cell media or exposing the cells in the exposure chamber for up to 6 h. A flow-cytometrybased micronucleus assay of CHO-K1 cells was used to determine the percentage micronuclei after exposure to degraded MEA. Mutagenic activity was evaluated by the Salmonella/ microsome assay, using the Salmonella typhimurium tester strains TA98, and TA100, with (+S9) and without (−S9) metabolization per instructions provided in the Moltox

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RESULTS AND DISCUSSION Characterization of Amine Degradation Products. MEA, PIP, and MDEA were used as model primary, secondary, and tertiary amines, respectively, to evaluate their degradation in CO2-rich and oxidative conditions. The amines showed a wide range in degradation under the conditions of these experiments (Figure 4). Degradation was higher under

Figure 4. Percent degradation of each amine tested after approximately 75 day in a controlled 150 °C and 15 psi atmosphere. Amine degradation was evaluated by HPLC for MEA and GC−MS for MDEA and PIP.

oxidative conditions compared to CO2-mediated degradation. Under oxidative conditions, PIP showed the least amount of degradation (12%) and MDEA showed the greatest amount of degradation (60%) over the approximately 75 day period. When subjected to CO2-mediated degradation, MEA was most susceptible to degradation. Amine degradation products identified in the exposure atmospheres for degraded MEA, MDEA, and PIP are shown in the Supporting Information. The degraded samples were complex mixtures of organic compounds, mostly dimers and heterocyclic compounds. No degradation products were observed in the neat, non-degraded amine atmospheres (data not shown). Carbonyls were detected in the parts per billion (ppb) concentration range (see the Supporting Information). Because of their carcinogenicity, particular attention was focused on evaluating the potential presence of nitrosamines.29,36 The formation of N-nitrosodiethanolamine (NDELA) was observed via LC−MS analysis using multiple reaction monitoring (MRM) of laboratory-degraded MEA in the CO2 atmosphere (Figure 5). Importantly, DEA, which is a precursor to NDELA, was also detected by LC−MS (data not shown) in CO2/MEA and oxidative MDEA samples. The MEA sample used in the degradation experiment was investigated for any DEA impurity that might have led to the presence of NDELA. No DEA was detected in the MEA sample, indicating D

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The expression of a panel of inflammatory cytokines in the lung of C57bl/6N mice exposed to MEA, MDEA, PIP, and their degradants was assessed (Table 2). The oxidatively degraded MDEA atmosphere resulted in the strongest cytokine response of amines tested, with statistically significant increases in GRO-KC, MCP-1, IL-6, and GM-CSF expression compared to controls. The CO2-degraded PIP atmosphere showed a statistically significant increase in GRO-KC expression. Both the oxidative and CO2-degraded atmospheres resulted in significant decreases in MCP-1 compared to controls. Other tissue cytokines evaluated did not show statistically significant responses (data not shown). Genotoxicity of Samples Containing Nitrosamines. The nitrosamines detected in degraded amine compounds used for CO2 sequestration are a potential concern for genotoxicity that would not be captured in an acute rodent inhalation study. The Ames test and micronucleus assay were performed to assess mutagenic effects of the parent compounds as well as CO2- and O2-degraded amine mixtures. None of the parent amines (MEA, MDEA, or PIP) nor the CO2- and O2-degraded amine mixtures when added directly into media at multiple dilutions or by aerosol exposure met criteria (described in the Supporting Information) to be “positive” for mutagenicity (data provided in the Supporting Information). Similar results were found in the micronucleus assay using CHO-K1 cells (data provided in the Supporting Information). The parent amines as well as the CO2- and O2-degraded amine mixtures were directly cytotoxic to the CHO-K1 cells in a dose-dependent manner; however, there was not a significant increase in micronucleus formation. Aerosol exposure of the CHO-K1 cells to parent amines as well as the CO2- and O2-degraded amine mixtures had no impact on micronucleus formation. A limitation to this study is that CHO-K1 cells do not possess metabolic machinery to act on nitrosamines that may be formed during degradation; therefore, we are unable to fully assess the mutagenic potential of these compounds in the CHO-K1 experimental system. Together, data suggest that the nitrosamines detected in the mixtures do not reach concentrations sufficient to cause genotoxicity with limitations of the experimental system. Amine-based CO2-scrubbing technologies have been used for decades in the oil and gas industry. However, because these applications have been somewhat limited in scale, there has not been a perceived need to comprehensively evaluate potential health and environmental risks. With the prospect of full-scale application to coal-fired power plants across the United States and abroad, this issue has increased in importance. In the current study, we successfully demonstrated the development of degradation and exposure methodologies for inhalation toxicological evaluation of amines and their degradation mixtures as well as a preliminary assessment of toxicity. We identified known amine degradation products in degraded mixtures and observed toxicological effects associated primarily with these mixtures. Although these studies were limited in

Figure 5. Nitrosamines detected by LC−MS MRM and DNL methods.

that NDELA is a true degradation product. Because it is a precursor, MDEA in the oxidative atmosphere suggested the presence of NDELA and 2-(1-methyl-2-oxohydrazino)ethanol (MOHE) nitrosamines. Detection was confirmed using authentic standards but was not quantitatively analyzed because the method was not validated for quantitation. Degradation products of MEA, MDEA, and PIP from both CO2 and O2 degradation atmospheres were screened by LC−MS using the DNL method. The MEA CO2 and O2 degradation samples both indicated the presence of two additional undetermined nitrosamine compounds, each with a m/z of 117.4, indicating a molecular weight of 116.4 because all nitrosamines tested gave [M + H]+ parent ions. The other CO2- and O2-degraded samples from MDEA and PIP did not show evidence for nitrosamines other than those determined by MRM with authentic standards. Inhalation Toxicity of Amines and Amine Degradation Products. Oxidatively degraded MEA was the only atmosphere causing an increase in inflammatory cells measured in BAL fluid (0.44 × 106 cells/mL of MEA degraded versus 0.25 × 106 cells/mL of control; p = 0.02). This increase was driven by increases in neutrophils (0.07 × 106 cells/mL of MEA degraded versus 0.005 × 106 cells/mL of control; p = 0.007) and lymphocytes (0.008 × 106 cells/mL of MEA degraded versus 0.0004 × 106 cells/mL of control; p = 0.04). Oxidative stress response in the lung was estimated by changes in measured TBARS (Table 1). MEA alone caused a statistically significant (p < 0.05) decrease in TBARS in mouse lung relative to controls, while CO2-degraded MEA caused a significant increase in TBARS compared to controls. MDEA after CO2 degradation showed the highest increase in TBARS, but the increase was not statistically significant because of large variance in the control response. No other atmospheres resulted in significant TBARS changes.

Table 1. TBARS in Lungs of C57bl/6N Mice Exposed to MEA, PIP, MDEA, or Their Respective Degradant Mixturesa MEA

MDEA

PIP

neat

O2 degraded

CO2 degraded

neat

O2 degraded

CO2 degraded

neat

O2 degraded

CO2 degraded

0.6 (0.3)b

1.1 (0.3)

1.5 (0.3)b

1.2 (0.3)

0.8 (0.2)

3.2 (3.2)

1.1 (0.3)

1 (0.2)

1.5 (0.5)

a

Data are presented as the mean/standard error fold increase over the control, indicated at 1.0. Values are fold change from the control, with mean (SD). bRepresents p < 0.05 compared to the control. E

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Table 2. Cytokine Expression in Lungs of C57bl/6N Mice Exposed to MEA, PIP, MDEA, or Their Respective Degradant Mixturesa MEA neat KC MCP1 GMCSF IL-12 IL-4 IL-1β IL-6 IL-10 IFN-Y RAINTES TNF-α VEGF

1.2 0.9 1.0 1.0 1.0 0.9 0.8 1.1 0.9 0.9 0.7 0.9

(1.2) (0.3) (0.3) (0.4) (0.1) (0.3) (0.4)b (0.3) (0.3) (0.1) (0.2) (0.2)

O2 degraded 1.0 0.6 4.9 1.3 1.0 1.2 0.0 1.0 0.9 0.0 0.9 0.9

(0.8) (0.3)b (1.4) (0.2) (0.2) (0.2)b (0.0) (0.3) (0.3) (0.0) (0.9) (0.1)b

MDEA CO2 degraded 0.7 0.4 0.0 10.4 0.9 0.9 1.1 0.5 0.6 0.9 0.0 1.0

(0.1) (0.3)b (0.0) (4.5) (0.3) (0.1) (0.3) (0.4) (0.2b) (0.2)b (0.0) (0.1)

neat 0.6 0.6 1.1 0.9 5.3 1.1 0.0 0.8 1.0 1.0 1.0 1.0

O2 degraded

(0.4)b (0.3) (0.3) (0.4) (4.7) (0.3) (0.0) (0.5) (0.5) (0.3) (0.4) (0.2)

11.1 3.8 1.5 1.2 0.0 0.8 1.5 1.0 1.2 0.8 1.0 0.5

(10.0)b (3.5)b (0.5)b (0.4) (0.0) (0.2)b (0.4)b (0.5) (0.4) (0.2)b (0.2) (0.2)b

PIP CO2 degraded 1.3 0.9 0.8 1.1 1.0 1.0 1.1 1.1 1.3 1.0 3.6 0.8

(0.4)b (0.2) (0.7) (0.2) (0.0) (0.1) (0.2) (0.2) (0.6)b (0.1) (7.6) (0.2)b

neat 1.8 1.6 1.1 0.8 0.0 0.8 0.8 0.8 0.7 1.0 0.9 0.8

(2.0) (1.5) (0.2) (0.3) (0.0) (0.1) (0.7) (1.1) (0.6) (0.1) (0.1) (0.1)

O2 degraded 0.7 0.9 1.5 1.2 0.0 1.0 0.9 0.8 1.1 1.1 1.0 1.4

(0.5) (0.7) (1.1) (0.8) (0.0) (0.5) (0.8) (2.5) (1.4) (0.3) (0.4) (1.5)

CO2 degraded 1.4 1.1 1.2 0.8 1.0 0.9 1.7 1.3 0.9 1.0 7.2 0.9

(0.4)b (0.3) (0.7) (0.3) (0.0) (0.2) (0.3) (1.0) (0.2) (0.1) (11.5) (0.2)b

a

Data are presented as the mean/standard error fold increase over the control, indicated at 1.0. The sample size to evaluate GM-CSF expression for MEA and degraded MEA and MCP-1 expression for MEA was too low for analysis and is presented as 1.0. Values are fold change from the control, with mean (SD). bRepresents p < 0.05 compared to the control.

important driver of the potential risk of amines used in CCS. In these studies, in vitro genotoxicity assays were applied to the CO2 MEA-degraded mixtures because that mixture showed the highest abundance of nitrosamines. No mutagenicity or chromosomal damage was observed. The degraded mixtures were both applied as an aerosol to the cells, and in a separate set of experiments, the liquid mixture was directly applied after dilution in media to achieve a high dose. The high doses used were not sufficient to cause genotoxicity, suggesting that the potential genotoxic compounds are formed at too low of a concentration to cause an effect. Alternatively, other compounds in the complex mixture may suppress any potential genotoxic response. We found that exposure to high concentrations of amines or amine degradation product mixtures resulted in inflammatory responses in mice that were especially pronounced for degraded amine mixtures. This enhanced toxicity may be linked to the increase in oxidative products, such as carbonyls, known to cause pulmonary inflammation. The concentrations used in these studies (25 ppm) are high relative to likely environmental exposures, which would likely be in the ppb concentration range.16 However, these concentrations were selected to achieve a response to directly compare the relative hazard of the amines and their degradant mixtures. Initial studies with MEA at 10 ppm resulted in no inflammatory response (data not shown). As a result of this initial experiment, subsequent studies were conducted at higher concentrations. We found that the oxidatively degraded MEA atmosphere was the only atmosphere to result in significant increases in inflammatory cells and oxidative response (TBARS) in the lung. Cytokine expression was modulated in multiple atmospheres, suggesting that an inflammatory signal was observed, but at the time point at which biological response was assessed, there was no significant inflammation or oxidative stress, as measured by cell counts and TBARS. The cytokine expression signal was most prevalent in the degraded mixtures and, in particular, oxidatively degraded MDEA. CO2-degraded mixtures showed less response compared to the oxidatively degraded mixtures, perhaps because the latter was more degraded. This, of course, assumes that the degradants were more inflammatory, which is somewhat expected given the nature of some of the degradation products.

scope, we found that pulmonary toxicity was relatively low considering the high doses investigated. We used a simulated degradation scenario that included air or CO2 and NO2. There was a range of degradations, depending upon the amine, and the degradation process led to a complex mixture of nitrogenous organic compounds, mostly dimers and heterocyclic compounds. Oxidative degradation caused a greater loss of the parent amine compared to degradation with CO2. In both cases, degradation resulted in increases in carbonyls and other oxidants, such as acids (albeit at low concentrations). Qualitative analysis of the mixtures revealed a complex mixture of nitrogen-based organic compounds. Tentative identification of selected degradant peaks (see the Supporting Information) by GC−MS included nitrogen-containing dimers and heterocyclic amine/amine derivatives, amine carboxylic acids, and amides, suggesting a component of degradation via carbamate condensation. A number of similar compounds have been identified or postulated in previous studies.1,22,37 Although there were some differences in reaction conditions, many of the reaction products showed similarity in type (acids, amine heterocyclics, and carbonyls), as previously reported.22 The conditions studied here included oxidation that would occur through interaction of flue gases with oxygen, NO2, and CO2 but did not include other gases, such as sulfur dioxide (SO2). Among the tentatively identified compounds of concern from amine degradation are nitrosamines, which may form in the presence of nitrogen oxides.17,30 These compounds have recently been reported in the trapping solutions of pilot-plant CCS systems using MEA, N-methyldiethanolamine, and PIP.4 In this study, degraded MDEA in the CO2 atmosphere along with MEA and PIP in both CO2 and O2 degradation atmospheres did not demonstrate nitrosamine formation by MRM. However, 1-nitrosopiperazine and 1,4-dinitrosopiperazine have been previously shown to form by simulated industrial post-combustion CO2 capture processes using PIP as a capture solvent.6,15 Nitrosamines are of particular interest because of their designation as probable carcinogens by the National Toxicology Program, International Agency for Research on Cancer, and the U.S. Environmental Protection Agency.5,11,25,28,38,39 Because of this designation, these compounds could be an F

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This study was aimed at investigating the pulmonary inflammatory potential of inhaled amines and degradation products, such as those that could be released in treated flue gas. Other discharge streams, including liquid or solid materials, should also be included in a comprehensive evaluation of the potential environmental or health impacts of amine solvent usage for CCS. The scope of the biological responses studied here was limited to acute inflammatory responses in the lung. The potential to cause long-term effects or effects outside of the lung was not evaluated. Cancer risk would be a minimal concern for amines themselves based on published literature;21 however, because of potential formation of nitrosamines, the cancer risk associated with degraded amines needs to be better evaluated. At the current time, risk assessment is uncertain because of a lack of knowledge of emission composition and concentration and subsequent potential for exposure. The results of this study suggest that inhalation exposure to amines at high concentrations poses minimal risk for pulmonary inflammation under acute exposure conditions. The oxidative degradation products of the amines used caused inflammatory responses in the lung, albeit at unrealistically high concentrations compared to likely environmental exposure scenarios. Nitrosamines, a class of compound of concern for this technology, were detected in MEA and MDEA degradation mixtures at low concentrations; however, these samples were not mutagenic in an Ames assay. The emissions of these products and, therefore, the resulting exposures are currently unknown. The current research was intended to demonstrate the successful development of degradation and inhalation exposure methodologies to allow for laboratory investigation of the toxicity of amine solvents and their degradation products. The toxicological assessment constitutes a preliminary evaluation of the potential health impacts associated with exposure to these materials. A dose−response assessment to include lower exposure levels will be necessary to more fully elucidate the potential hazard, which was beyond the scope of this study.

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ASSOCIATED CONTENT

S Supporting Information *

Details on the analytical methodology for the degraded amine characterization, additional supporting analytical data, and detailed methodology and results from the in vitro Ames and micronucleus assays. This material is available free of charge via the Internet at http://pubs.acs.org.

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AUTHOR INFORMATION

Corresponding Author

*Telephone: 505-348-9455. Fax: 505-348-4980. E-mail: [email protected]. Notes

The authors declare no competing financial interest.

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ACKNOWLEDGMENTS Research was funded by the Electric Power Research Institute. REFERENCES

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