Development of damage function for stratospheric ozone layer depletion

The purpose of our study was to develop damage functions due to ozone layer depletion, that related the emission of ozone depleting substances (ODS) to the damage of category endpoints. The ozone layer depletion causes many types of damage such as skin cancer, cataract, adverse effect to crop and plant growth. We assessed the increase of skin cancer incidence risk. The damage function have been developed with connecting the main processes on ozone depletion, emission of ODS, increase of tropospheric ODS, increase of stratospheric ODS, change of total ozone, change of B region ultra-violet (UV-B) at the surface, and the increase of skin cancer incidence. As the result, we could introduce damage functions of melanoma and non-melanoma skin cancer incidence for 13 species of ODSs and damage factors based on the disability-adjusted life years (DALYs). We also compared the DALYs value with the damage factors of Eco-indicator 99 (egalitarian and hierarchic value), and it was found that our result was several ten times as small except methyl bromide. Furthermore, a case study for refrigerator was performed and it showed that shifting to less ozone depleting substances reduced the risk of skin cancer incidence to one-fourteenth in DALYs.     

Toxic effects of ozone on murine L929 fibroblasts. Enzyme inactivation and glutathione depletion.

Exposure of L929 murine fibroblasts to ozone resulted in K+ leakage and inhibition of several enzymes. Most sensitive to ozone exposure were glyceraldehyde-3-phosphate dehydrogenase and pyruvate kinase. The activities of another cytosolic enzyme, lactate dehydrogenase, the mitochondrial enzymes glutamate dehydrogenase, succinate dehydrogenase, cytochrome c oxidase and the activity of the lysosomal enzymes acid phosphatase and beta-glucuronidase were, initially, not or only slightly affected. The localization of the lysosomal enzymes did not change during ozone exposure. After prolonged exposure complete deterioration of the cells was observed and all enzyme activities declined. The activity of the enzymes was also monitored during ozone exposure of a sonicated cell suspension and it was shown that all these enzymes are in fact susceptible to ozone. These observations clearly demonstrate that, besides the structure and amino acid composition of an enzyme, the localization in the cell plays an important role in its susceptibility to ozone. The intracellular levels of reduced and oxidized glutathione were affected as well. The ATP content, however, proved to be insensitive to ozone exposure.     

Mechanisms of the acute effects of inhaled ozone in humans

Ambient air ozone (O₃) is generated photochemically from oxides of nitrogen and volatile hydrocarbons. Inhaled O₃ causes remarkably reversible acute lung function changes and inflammation. Approximately 80% of inhaled O₃ is deposited on the airways. O₃ reacts rapidly with CC double bonds in hydrophobic airway and alveolar surfactant-associated phospholipids and cholesterol. Resultant primary ozonides further react to generate bioactive hydrophilic products that also initiate lipid peroxidation leading to eicosanoids and isoprostanes of varying electrophilicity. Airway surface liquid ascorbate and urate also scavenge O₃. Thus, inhaled O₃ may not interact directly with epithelial cells.Acute O₃–induced lung function changes are dominated by involuntary inhibition of inspiration (rather than bronchoconstriction), mediated by stimulation of intraepithelial nociceptive vagal C-fibers via activation of transient receptor potential (TRP) A1 cation channels by electrophile (e.g., 4-oxo-nonenal) adduction of TRPA1 thiolates enhanced by PGE₂-stimulated sensitization.Acute O₃-induced neutrophilic airways inflammation develops more slowly than the lung function changes. Surface macrophages and epithelial cells are involved in the activation of epithelial NFkB and generation of proinflammatory mediators such as IL-6, IL-8, TNFa, IL-1b, ICAM-1, E-selectin and PGE₂. O₃-induced partial depolymerization of hyaluronic acid and the release of peroxiredoxin-1 activate macrophage TLR4 while oxidative epithelial cell release of EGFR ligands such as TGFa or EGFR transactivation by activated Src may also be involved. The ability of lipid ozonation to generate potent electrophiles also provides pathways for Nrf2 activation and inhibition of canonical NFkB activation. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.     

The effects on human health from stratospheric ozone depletion and its interactions with climate change.

Ozone depletion leads to an increase in the ultraviolet-B (UV-B) component (280-315 nm) of solar ultraviolet radiation (UVR) reaching the surface of the Earth with important consequences for human health. Solar UVR has many harmful and some beneficial effects on individuals and, in this review, information mainly published since the previous report in 2003 (F. R. de Gruijl, J. Longstreth, M. Norval, A. P. Cullen, H. Slaper, M. L. Kripke, Y. Takizawa and J. C. van der Leun, Photochem. Photobiol. Sci., 2003, 2, pp. 16-28) is discussed. The eye is exposed directly to sunlight and this can result in acute or long-term damage. Studying how UV-B interacts with the surface and internal structures of the eye has led to a further understanding of the location and pathogenesis of a number of ocular diseases, including pterygium and cataract. The skin is also exposed directly to solar UVR, and the development of skin cancer is the main adverse health outcome of excessive UVR exposure. Skin cancer is the most common form of malignancy amongst fair-skinned people, and its incidence has increased markedly in recent decades. Projections consistently indicate a further doubling in the next ten years. It is recognised that genetic factors in addition to those controlling pigment variation can modulate the response of an individual to UVR. Several of the genetic factors affecting susceptibility to the development of squamous cell carcinoma, basal cell carcinoma and melanoma have been identified. Exposure to solar UVR down-regulates immune responses, in the skin and systemically, by a combination of mechanisms including the generation of particularly potent subsets of T regulatory cells. Such immunosuppression is known to be a crucial factor in the generation of skin cancers. Apart from a detrimental effect on infections caused by some members of the herpesvirus and papillomavirus families, the impact of UV-induced immunosuppression on other microbial diseases and vaccination efficacy is not clear. One important beneficial effect of solar UV-B is its contribution to the cutaneous synthesis of vitamin D, recognised to be a crucial hormone for bone health and for other aspects of general health. There is accumulating evidence that UVR exposure, either directly or via stimulation of vitamin D production, has protective effects on the development of some autoimmune diseases, including multiple sclerosis and type 1 diabetes. Adequate vitamin D may also be protective for the development of several internal cancers and infections. Difficulties associated with balancing the positive effects of vitamin D with the negative effects of too much exposure to solar UV-B are considered. Various strategies that can be adopted by the individual to protect against excessive exposure of the eye or the skin to sunlight are suggested. Finally, possible interactions between ozone depletion and climate warming are outlined briefly, as well as how these might influence human behaviour with regard to sun exposure.     

Effects of stratospheric ozone depletion and climate change on materials damage.

Nanoscale inorganic fillers with average particle sizes smaller by an order of magnitude or more compared to those of conventional fillers are becoming commercially available. The efficacy of these fillers used in polymer formulations and particularly their effect as photostabilizers are beginning to be investigated. These may enhance or retard photodegradation depending on the surface coating of the particles or their chemical nature. Some recent data indicate their use as effective photostabilizers in some common polymers. However, the potential deleterious interaction of the nanoscale fillers with other additives in the formulation has also been pointed out. Depending on the efficiency of stabilization and the economics of their use nanofillers may provide a useful route to UV-stabilization of plastics and rubber used outdoors. Insufficient data are available at this time to assess their potential impact on material and coatings stabilization. Organic fillers such as lignocellulose continue to be investigated for outdoor applications. Their cost advantage makes them attractive despite the somewhat reduced engineering properties of their composites. Recent reports, however, suggest the photostability of these composites to depend on the source of fiber as well as the processing techniques employed in fabricating products from them. Identification of the key determinants in terms of species, isolation and processing of polymer-wood composites is critical to developing them for long-term outdoor use. Efforts are continuing on the synthesis of new light stabilizers, particularly those based on a hindered amine light stabilizers (HALS), and on identifying synergistic combinations of known stabilizers for common thermoplastics. Variants of HALS-type stabilizers that reduce the loss of stabilizer via leaching or migration were recently reported. Studies on the permanence of the stabilizers themselves when exposed to solar UV wavelengths have also been reported in recent work. Identification of relevant mechanisms is important not only to understand the interactions of climate changes and higher UV solar environments with materials damage, but also to guide future design of light-stabilizers.     

Environmental effects of ozone depletion and its interactions with climate change: progress report, 2004.

The complexity of the linkages between ozone depletion, UV-B radiation and climate change has become more apparent.