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Pregled bibliografske jedinice broj: 191658

How dangerous is ground level ozone


Butković, Vjera; Cvitaš, Tomislav; Kezele, Nenad; Klasinc, Leo; Kovač, Elvira; Šorgo, Glenda
How dangerous is ground level ozone // Regional Biophysics Meeting 2005
Zreče, Slovenija, 2005. (poster, nije recenziran, neobjavljeni rad, znanstveni)


Naslov
How dangerous is ground level ozone

Autori
Butković, Vjera ; Cvitaš, Tomislav ; Kezele, Nenad ; Klasinc, Leo ; Kovač, Elvira ; Šorgo, Glenda

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, neobjavljeni rad, znanstveni

Skup
Regional Biophysics Meeting 2005

Mjesto i datum
Zreče, Slovenija, 16.-20.03.2005

Vrsta sudjelovanja
Poster

Vrsta recenzije
Nije recenziran

Ključne riječi
Tropospheric ozone

Sažetak
Life, when it just emerged on Earth, began to influence the composition of the atmosphere and finally, determined that in which we live today. To be sure, certain catastrophic events of cosmic, geophysical or even chaotic nature have had sudden influences on both the life itself as well as the atmosphere. Science anticipates, however, that the strong feedback between life forms and atmospheric composition provides an effective buffering effect, and warrants both recovery from catastrophe as well as long term stability. One hundred years after the discovery of ozone, atmospheric chemists became aware due to human activities (mainly production of nitrogen oxides) have caused the concentrations of ozone in ground level air to increase, and that this trend continues. This increase engenders much concern because, in the entire history of Earth, life has never experienced such elevated ozone concentrations for such long periods. Recent communications1, 2 concerned with the high mortality related to air pollution in the UK and the Netherlands during the 2003 heat wave have linked it to particulate matter and ozone concentrations. These findings raise the specter that high oxidant levels may well have an important impact on life. The situation is somewhat analogous to that of 2000 million years ago, when the atmospheric oxygen started to accumulate (Fig.1) and certain anaerobic life forms began to use oxygen for "breathing" and energy production. Oxygen was toxic for anaerobic life forms, much as ozone is now for existing aerobes. Actually, oxygen itself or, more particularly, some of its metabolic products (e.g., peroxides, oxyradicals and super oxide radical) may be detrimental for living organisms. These organisms, however, have evolved defense and repair mechanisms and they use antioxidants to handle the treat. Could it be that present life forms will develop also similar but more efficient defense and repair mechanisms for ozone, much as already exist for oxidants, uv and even some level of ionizing radiation (e.g. Deinococcus radiodurans and the recent study of the DNA sequence of Dehalococcoides ethenogenes, which appears in the January 7 , 2005 issue of Science, found evidence that the soil bacterium may have developed the metabolic capability to consume chlorinated solvents fairly recently, possibly by acquiring genes in an adaptation related to the increasing prevalence of the pollutants). Because, momentarily at least, we are unable to reduce or even stop the rise of surface ozone concentrations, it is pertinent to ask if we should be concerned for the existent life forms, ourselves included, or if we should be prepared for the evolution of new life forms, an emergent class of "superoxidative" organisms. It is possible that our extensive use of oxidants spurs this process on. Recent papers on possible ozone "production" and functions within the human body engender such suspicions.3-7 However, we consider the endogeneous ozone production as highly improbable. Besides thermodynamic objections especially the argument that ozone is an agent detrimental to the organism speaks against its "on purpose" synthesis as antimicrobial agent. Thus, if reaction products with ozone signature are found to be produced from plaque it should still be considered that the source of the ozone is outside i.e. from the atmosphere. Numerous studies have established the ability of ozone to react with species present in the lung ; they include the amino acids, peptides and pro-teins.2, 3 However, the primary target of ozone is thought to be the unsatu-rated fatty acids (UFA) in the fluid layer of the lung lining and in the epi-thelial cell membranes of the lung.4-6 Because of its reactivity, ozone does not penetrate far into the cells that line the airways. The cascade hypothesis states that lipid ozonation products (LOP) relay the effects of ozone into deeper tissue strata at the lung-air interface than ozone itself can reach. LOP, rather than products from ozonation of proteins or nucleic acids, are thought to be signal transduction species because ozonation of UFA leads to small, diffusible, stable or metastable species, and because lipid oxidation products are known to act as signal transduction agents in other systems. Thus, the likely candidates for signal transduction species are LOP produced in the Criegee ozonation process, which gives a predictable spectrum of products.8-11 Recent results by Friedman, Pryor and coworkers strongly support this hypothesis.12-17 Therefore, if the human body has developed some defense against such "ozone toxicity" it should target the ozonide because the LOPs are the detrimental products and the ozonide formation is the fastest (diffusion controlled) reaction step. Thus, if one has to explain atmospheric "ozone" survival into the arteries and final appearance as plaque? We see the answer in formation of (relatively) stable lipid ozonides which the body tries to convert into products less detrimental than the Criegee ozonolysis products. This conversion may result in products which cary the signature of a reaction with ozone. The formation of stable lipid ozonide we have shown in experiments performed during 1999 while applying for a Fogarty international research collaboration award on the role of nitrogen oxides in ozone toxicity. In these experiments the lipid POPC dissolved in CH2Cl2 and spread as a thin film (after evaporation) inside the reaction column was allowed to react for 10 min with a stream of 100 ppb ozone in air ; the reacted film was again dissolved in CH2Cl2, after evaporation mixed into a cryogenic matrix of 3-nitrobenzyl alcohol and its mass spectrum recorded by MALDI-FTMS. The single laser shot spectrum shows along with protonated POPC and some ozonation products PC/ALD and PC/AC a considerable amount of ozonide indicating its remarkable stability which enabled it survive the procedures before recording the spectrum. Therefore, we suggest that an organism breathing the air with ozone produces in the lung besides the "signal transduction species" a steady flow of ozonides into the organism. Some repair mechanisms there must take care of their disposal. A possibility not to be overlooked is that plaque is result of such (un)successful cleanup.

Izvorni jezik
Engleski

Znanstvena područja
Kemija



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