Gas and particle-phase size distribution concentrations of PAHs and their derivative compounds quinones in traffic environments
JUANA MARI DELGADO-SABORIT (1), Christopher Stark (1), Roy M. Harrison (1)
(1) Division of Environmental Health and Risk Management; School of Geography, Earth and Environmental Sciences; University of Birmingham; Birmingham; B15 2TT; United Kingdom
Abstract Number: 58
Preference: Platform Presentation
Last modified: October 9, 2009
Working Group: sq1
Polycyclic aromatic hydrocarbons (PAH) are amongst the best-known chemical carcinogens occurring widely in the environment. The main sources of PAH emission to the atmosphere are combustion processes such as traffic and heating, as well as some industrial combustion processes. PAHs are a group of many compounds characterised by fused aromatic rings whose individual carcinogenicity varies significantly. According to their molecular weight and hence vapour pressure, some PAH compounds exist predominantly in the atmosphere in the vapour phase and others mainly associated with particles. The more carcinogenic species tend to be particle-associated . Quinones are an oxidation product of PAHs in the atmosphere, which have the ability to produce reactive oxygen species , resulting in oxidative stress, which is a casual factor in the pathology of many diseases (e.g. cardiovascular diseases) .
The aim of this study is to quantify the levels of PAHs and their derivative compounds quinones in a traffic environment in order to quantify the levels of carcinogenic and toxic compounds emitted by traffic sources.
Gas and particulate PAH and quinones have been measured using a sampling train consisting of XAD-4 coated denuders, MOUDI sampler and backup PUF filters (500 cm3). The MOUDI sampled the size ranges of 3.2-10.0 micro-m (stage-1), 1.8-3.2 micro-m (stage-2), 1.0-1.8 micro-m (stage-3), 0.2-1.0 micro-m (stage-4) and less than 0.2 micro-m (stage-5) in quartz fibre filters.
The levels of benzo(a)pyrene in the gas ranged between 0.02-0.04 ng/m3 whilst the levels in size-fractionated particle phase ranged between 0.05-0.016 ng/m3, 0.011-0.015 ng/m3, 0.013-0.030 ng/m3, 0.003-0.019± ng/m3 and 0.041-0.064 ng/m3 for stages 1-5 respectively. As regards the levels of quinones, most of the quinones (i.e. 2-methylanthraquinone, acenaphthenequinone, 2,3-dimethylanthraquinone, benzo[a]anthracene-7,12-dione and 5,12-naphthacenequinone) were more abundant in the particulate phase (e.g. benzo[a]anthracene-7,12-dione particle-phase ranged between 0.01-0.70 ng/m3 in stage-1 vs. gas-phase 0.01-0.06 ng/m3), except for methyl-1,4-benzoquinone and 2,6-ditertbutyl-1,4-benzoquinone which were evenly distributed in the gas and particulate phase (e.g. methyl-1,4-benzoquinone particle-phase ranged between 0.5-1.7 ng/m3 in stage-1 vs. gas-phase 0.02-3.9 ng/m3). Methyl-1,4-benzoquinone was the most abundant quinone in both phases, followed by 2,6-ditertbutyl-1,4-benzoquinone (i.e. particle-phase ranged between 0.2-1.7 ng/m3 in stage-1 and gas-phase 0.1-3.4 ng/m3). The rest of the quinones were one order of magnitude lower (e.g. 2,3-dimethylanthraquinone particle-phase ranged between 0.09-0.30 ng/m3 in stage 1 and gas-phase 0.001-0.01 ng/m3). Quinones were present in all size ranges; however 2,6-ditertbutyl-1,4-benzoquinone was more frequent in the size range below 1.8 micro-m.
The occurrence of quinones and carcinogenic PAH in association with fine particles and vapour confers upon them a capacity to penetrate to the deeper regions of the respiratory tract.
1. EPAQS, A recommendation for a United Kingdom air quality standard for polycyclic aromatic hydrocarbons. , T.a.R.E.P.o.A.Q.S. Department of the Environment, Editor. 1999, The Stationery Office.
2. Kumagai, Y. and N. Shimojo, Induction of Oxidative Stress and Dysfunction of Nitric Oxide-Dependent Vascular Tone Caused by Quinones Contained in Diesel Exhaust Particles. Journal of Health Science, 2001. 47(5): p. 439-445.
3. Heitzer, T., et al., Endothelial dysfunction, oxidative stress, and risk of cardiovascular events in patients with coronary artery disease. Circulation, 2001. 104(22): p. 2673-2678.