Isocyanic acid (HNCO) and its fate in the atmosphere: a review

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Abstract

Isocyanic acid (HNCO) has recently been identified in ambient air at potentially concerning concentrations for human health. Since its first atmospheric detection, significant progress has been made in understanding its sources and sinks. The chemistry of HNCO is governed by its partitioning between the gas and liquid phases, its weak acidity, its high solubility at pH above 5, and its electrophilic chemical behaviour. The online measurement of HNCO in ambient air is possible due to recent advances in mass spectrometry techniques, including chemical ionization mass spectrometry for the detection of weak acids. To date, HNCO has been measured in North America, Europe and South Asia as well as outdoors and indoors, with mixing ratios up to 10s of ppbv. The sources of HNCO include: (1) fossil fuel combustion such as coal, gasoline and diesel, (2) biomass burning such as wildfires and crop residue burning, (3) secondary photochemical production from amines and amides, (4) cigarette smoke, and (5) combustion of materials in the built environment. Then, three losses processes can occur: (1) gas phase photochemistry, (2) heterogenous uptake and hydrolysis, and (3) dry deposition. HNCO lifetimes with respect to photolysis and OH radical oxidation are on the order of months to decades. Consequently, the removal of HNCO from the atmosphere is thought to occur predominantly by dry deposition and by heterogeneous uptake followed by hydrolysis to NH ₃ and CO ₂. A back of the envelope calculation reveals that HNCO is an insignificant global source of NH ₃, contributing only around 1%, but could be important for local environments. Furthermore, HNCO can react due to its electrophilic behaviour with various nucleophilic functionalities, including those present in the human body through a reaction called protein carbamoylation. This protein modification can lead to toxicity, and thus exposure to high concentrations of HNCO can lead to cardiovascular and respiratory diseases, as well as cataracts. In this critical review, we outline our current understanding of the atmospheric fate of HNCO and its potential impacts on outdoor and indoor air quality. We also call attention to the need for toxicology studies linking HNCO exposure to health effects.

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Measurements of volatile organic compounds in the earth's atmosphere using proton-transfer-reaction mass spectrometry.

Joost de Gouw, Carsten Warneke (2006)

Proton-transfer-reaction mass spectrometry (PTR-MS) allows real-time measurements of volatile organic compounds (VOCs) in air with a high sensitivity and a fast time response. The use of PTR-MS in atmospheric research has expanded rapidly in recent years, and much has been learned about the instrument response and specificity of the technique in the analysis of air from different regions of the atmosphere. This paper aims to review the progress that has been made. The theory of operation is described and allows the response of the instrument to be described for different operating conditions. More accurate determinations of the instrument response involve calibrations using standard mixtures, and some results are shown. Much has been learned about the specificity of PTR-MS from inter-comparison studies as well the coupling of PTR-MS with a gas chromatographic interface. The literature on this issue is reviewed and summarized for many VOCs of atmospheric interest. Some highlights of airborne measurements by PTR-MS are presented, including the results obtained in fresh and aged forest-fire and urban plumes. Finally, the recent work that is focused on improving the technique is discussed. (c) 2006 Wiley Periodicals, Inc.

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Protein carbamylation links inflammation, smoking, uremia and atherogenesis.

Outi Kummu, Zeneng Wang, Stanley Hazen … (2007)

Post-translational modification and functional impairment of proteins through carbamylation is thought to promote vascular dysfunction during end-stage renal disease. Cyanate, a reactive species in equilibrium with urea, carbamylates protein lysine residues to form epsilon-carbamyllysine (homocitrulline), altering protein structure and function. We now report the discovery of an alternative and quantitatively dominant mechanism for cyanate formation and protein carbamylation at sites of inflammation and atherosclerotic plaque: myeloperoxidase-catalyzed oxidation of thiocyanate, an anion abundant in blood whose levels are elevated in smokers. We also show that myeloperoxidase-catalyzed lipoprotein carbamylation facilitates multiple pro-atherosclerotic activities, including conversion of low-density lipoprotein into a ligand for macrophage scavenger receptor A1 recognition, cholesterol accumulation and foam-cell formation. In two separate clinical studies (combined n = 1,000 subjects), plasma levels of protein-bound homocitrulline independently predicted increased risk of coronary artery disease, future myocardial infarction, stroke and death. We propose that protein carbamylation is a mechanism linking inflammation, smoking, uremia and coronary artery disease pathogenesis.