Isoprene In Air Research Articles

UV-Vis spectrophotometric determination of isoprene in atmosphere based on Diels–Alder reaction

ABSTRACT Isoprene is the most abundant biogenic volatile organic compound in the atmosphere. Till now, chromatography is the main detection method for isoprene, dependent on sophisticated instruments and complex operations. An UV-Vis spectrophotometric method based on the Diels–Alder (D-A) reaction was developed to detect isoprene in the atmosphere. The fast D-A reaction between the probe 4-phenyl−1,2,4-triazolin−3,5-dione (PTAD) and isoprene may cause absorbance decrease, which enable it to detect isoprene in solution at 118 nmol·L−1 level. Further, isoprene in air at the level of ppbv was detected using this method. Compared with chromatography this method has the advantages of low cost, fast and less dependence on instrument.

The Stable Carbon Isotope Ratio of Biogenic Emissions of Isoprene and the Potential Use of Stable Isotope Ratio Measurements to Study Photochemical Processing of Isoprene in the Atmosphere

A technique was developed that allows the determination of the stable carbon isotope ratio of isoprene in air. The method was used for a limited number of ambient measurements as well as laboratory studies of isoprene emitted from Velvet Bean (Mucana pruriens L. var. utilis), including the light and temperature dependence. The mean stable carbon isotope ratio (δ 13C) of isoprene emitted from Velvet Bean (Mucana pruriens L. var. utilis) for all our measurements is –27.7‰ ± 2.0‰ (standard deviation for 23 data points). Our results indicate a small dependence of the stable carbon isotope ratios on leaf temperature and photosynthetic photon flux density (PPFD). The light dependence is 0.0026 ± 0.0012‰/(μ mol of photons m−2 s−1) for the studied range from 400 to 1700 μ mol of photons m−2 s−1. The temperature dependence is 0.16 ± 0.09‰/K. On average, the emitted isoprene is 2.6 ± 0.9‰ lighter than the leaf carbon. An uncertainty analysis of the possibility to use stable carbon isotope ratio measurements of isoprene for estimates of its mean photochemical age suggests that meaningful results can be obtained. This is supported by the results of a small number of measurements of the stable carbon isotope composition of ambient isoprene at different locations. The results range from approximately –29‰ to –16‰. They are consistent with vegetation emissions of isoprene that is slightly depleted in 13C relative to the plant material and enrichment of 13C in the atmosphere due to isotope fractionation associated with the reaction with OH-radicals. The stable carbon isotope ratio of ambient isoprene at locations directly influenced by isoprene emissions is very close to the values we found in our emission studies, whereas at sites located remote from isoprene emitting vegetation we find substantial enrichment of 13C. This suggests that stable carbon isotope ratio measurements will be a valuable, quantitative method to determine the extent of photochemical processing of isoprene in ambient air.

Toxicokinetics of inhaled and endogenous isoprene in mice, rats, and humans

Isoprene (IP) is ubiquitous in the environment and is used for the production of polymers. It is metabolized in vivo to reactive epoxides, which might cause the tumors observed in IP exposed rodents. Detailed knowledge of the body and tissue burden of inhaled IP and its intermediate epoxides can be gained using a physiological toxicokinetic (PT) model. For this purpose, a PT-model was developed for IP in mouse, rat, and human. Experimentally determined partition coefficients were taken from the literature. Metabolic parameters were obtained from gas-uptake experiments. The measured data could be described by introducing hepatic and extrahepatic metabolism into the model. At exposure concentrations up to 50 ppm, the rate of metabolism at steady-state is 14 times faster in mice and about 8 times faster in rats than in humans (2.5 μmol/h/kg at 50 ppm IP in air). IP does accumulate only barely due to its fast metabolism and its low thermodynamic partition coefficient whole body:air. IP is produced endogenously. This production is negligible in rodents compared to that in humans (0.34 μmol/h/kg). About 90% of IP produced endogenously in humans is metabolized and 10% is exhaled unchanged. The blood concentration of IP in non-exposed humans is predicted to be 9.5 nmol/l. The area under the blood concentration–time curve (AUC) following exposure over 8 h to 10 ppm IP is about 4 times higher than the AUC resulting from the unavoidable endogenous IP over 24 h. A comparison of such AUCs can be used for establishing workplace exposure limits. For estimation of the absolute risk, knowledge of the body burden of the epoxide intermediates of IP is required. Unfortunately, such data are not yet available.

Ion chemistry for the detection of isoprene and other volatile organic compounds in ambient air

A chemical ionization mass spectrometer (CIMS) and a flowing afterglow apparatus were used to study reactions of benzene cations (C6H6+ and (C6H6)2+) with a series of volatile organic compounds (VOCs). Both cations react at the collision rate with compounds of lower ionization potential than benzene, such as isoprene (C5H8), other conjugated dienes, and aromatics. These ions are generally unreactive with substances of higher ionization potential such as alkanes, simple alcohols, simple carbonyls, etc. The results demonstrate that C6H6+ and (C6H6)2+ are excellent reagent ions for the sensitive detection of isoprene in air with a CIMS. However, 2‐methyl‐3‐buten‐2‐ol (MBO) and C5H8 conjugated dienes were identified as potential interferences to this technique. This indicates that the selectivity of the CIMS isoprene measurement must be tested by intercomparison with well‐established methods, e.g. gas chromatography techniques.

Product distributions from the OH radical-induced oxidation of but-1-ene, methyl-substituted but-1-enes and isoprene in NOx-free air

Product distributions resulting from the OH-induced oxidation of but-1-ene, 2-methylbut-1-ene, 3-methylbut-1-ene and isoprene in air were measured in the absence of nitrogen oxides and compared with predictions based on currently accepted oxidation mechanisms. In the case of butenes, the observed distributions of carbonyl compounds, hydroxyketones, hydroxyalkanals and diols were evaluated to obtain probabilities for the initial attack of OH radical on the outer position of the double bond (γ = 0.90 ± 0.03 for 2-Me-but-1-ene and γ = 0.76 ± 0.05 for both but-1-ene and 3-Me-but-1-ene), for the probability of formation of stable products in the self-reaction of secondary β-hydroxyperoxyl radicals (kssb/kss = 0.29 ± 0.07 for but-1-ene and kssb/kss = 0.19 ± 0.06 for 3-Me-but-1-ene), and for the ratio of the reaction with oxygen s. decomposition of β-hydroxyalkoxyl radicals, k3[O2]/(k4 + k3[O2]) = 0.25 ± 0.04 for but-1-ene and = 0.38 ± 0.04 for 3-Me-but-1-ene. The last two values disagree with other published data, which suggest a smaller effect of oxygen. The oxidation of isoprene produced methacrolein and methyl vinyl ketone with a ratio 0.93 ± 0.10, the ratio of methyl vinyl ketone and 3-methylfuran was 7.3 ± 1.0. Other products were 1-hydroxy-3-methylbut-3-en-2-one (identified by mass spectrometry) and 3-methyl-3-oxo-butane (tentatively identified). The overall product distribution was complex and could not be fully elucidated. Computer simulations based on several mechanisms applied the relative probabilities for OH addition found for the but-1-enes. Comparison with the experimental data suggests probabilities for OH addition to the methylated double bond of 0.504 ± 0.027 (outer position) and 0.056 ± 0.003 (inner position), and to the non-methylated double bond of 0.335 ± 0.023 (outer position) and 0.105 ± 0.008 (inner position).

Cigarette smoke chemistry: conversion of nitric oxide to nitrogen dioxide and reactions of nitrogen oxides with other smoke components as studied by Fourier transform infrared spectroscopy

Nitric oxide is both a critical biological toxin and an important messenger molecule, signalling events as diverse as nerve transmission and smooth muscle relaxation. Fresh cigarette smoke contains from 300 to 500 ppm nitric oxide. While there have been reports of the rate of oxidation of nitric oxide to nitrogen dioxide in cigarette smoke, none have utilized a real-time method and provided detailed kinetic data and modelling. In this paper we present a Fourier transform infrared spectroscopy (FT-IR) method for the simultaneous determination of nitric oxide and nitrogen dioxide in gas phase cigarette smoke and in a number of gaseous mixtures that model smoke. The method uses multivariate least-squares regression analysis, which allows simultaneous quantitation of several components even in the presence of overlapping peaks, and fast data acquisition for kinetic analysis. Model systems containing mixtures of nitric oxide and isoprene, methanol, and/or acrolein and acetaldehyde in air were studied. The concentrations of nitric oxide, isoprene, etc., in the model systems were chosen to duplicate those in authentic cigarette smoke. In our best model (a mixture of nitric oxide, methanol, and isoprene in air) the disappearance of nitric oxide and the appearance of nitrogen dioxide follow time courses that closely duplicate those for cigarette smoke. Furthermore, the production of nitrogen dioxide follows a time course that agrees with our previously published rate of the development of organic free radicals in cigarette smoke. The present work, therefore, substantiates the steady-state mechanism we previously proposed for the production of free radicals in gas phase cigarette smoke.

Mechanisms of cigarette smoke toxicity: the inactivation of human α-1-proteinase inhibitor by nitric oxide/isoprene mixtures in air

A mixture of nitric oxide (NO) and isoprene in air has been studied as a model for gas-phase cigarette smoke. We have shown that this model system duplicates many of the properties of cigarette smoke including the inactivation of human alpha-1-proteinase inhibitor (a1PI). In this study, buffered solutions of a1PI were exposed to puffs of air containing 300 ppm NO and 400 ppm isoprene. Bubbling of the NO/air/isoprene gas stream directly through buffered protein solutions causes a1PI to undergo a fast loss of inhibitory capacity. This fast inactivation is not observed when a1PI is exposed to aqueous extracts of the NO/air/isoprene mixture. Both direct exposure and exposure to aqueous extracts, however, cause a1PI to undergo a slow loss of activity that continues for several days as the protein is incubated in the buffer solutions. Gas-phase cigarette smoke has already been shown to cause this same two-phase inactivation of a1PI. The inactivation of a1PI by the model system is dependent on the presence of oxygen in the gas stream, suggesting that the oxidation of nitric oxide to nitrogen dioxide in air is involved in the formation of the inactivating species. The nature of these species remains to be determined; however, small alkoxyl or peroxyl radicals (such as are spin-trappable from gas-phase smoke as well as from the NO/air/isoprene system) do not appear to inactivate a1PI. One possibility is that the inactivating species are metastable compounds formed by radical processes in the gas phase of both cigarette smoke and our model system. Our data suggest that one possible class of species is peroxynitrates.