Questions and answers about the effects of the depletion of the ozone layer on humans and the environment.

The ozone molecule contains three atoms of oxygen and is mainly formed by the action of the ultraviolet rays of the sun on the diatomic oxygen molecules in the upper part of the Earth's atmosphere (called the stratosphere). Atmospheric pollution near the Earth's surface can form localized areas of ozone. The stratospheric ozone layer protects life on Earth by absorbing most of the harmful ultraviolet radiation from the sun. In the mid 1970s it was discovered that some manmade products destroy ozone molecules in the stratosphere. This destruction can result in damage to ecosystems and to materials such as plastics. It may cause an increase in human diseases such as skin cancers and cataracts. The discovery of the role of the synthetic ozone-depleting chemicals such as chlorofluorocarbons (CFCs) stimulated increased research and monitoring in this field. Computer models predicted a disaster if no action was taken to protect the ozone layer. Based on this research and monitoring, the nations of the world took action in 1985 with the Vienna Convention for the Protection of the Ozone Layer followed by the Montreal Protocol on Substances that Deplete the Ozone Layer in 1987. The Convention and Protocol were amended and adjusted several times as new knowledge was obtained. The Meetings of the Parties to the Montreal Protocol appointed three Assessment Panels to review the progress in scientific knowledge on their behalf. These panels are the Scientific Assessment Panel, the Technological and Economic Assessment Panel and the Environmental Effects Assessment Panel. Each panel covers a designated area and there is a natural level of overlap. The main reports of the Panels are published every four years as required by the Meeting of the Parties. All the reports have an executive summary that is distributed more widely than the main report itself. It became customary to add a set of questions and answers--mainly for non-expert readers--to the executive summaries. This document contains the questions and answers prepared by experts who comprise the Environmental Assessment Panel. It is based mainly on the 2006 report of the Panel but also contains information from previous assessments. Readers who need detailed information on any question should consult the full reports for a more complete scientific discussion. This set of questions refers mainly to the environmental effects of ozone depletion and climate change. The report of the Scientific Assessment Panel contains questions and answers related to the other scientific issues addressed by that Panel. All these reports can be found on the UNEP website (http://ozone.unep.org).     

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.     

Review of the genotoxicity of ozone.

Ozone is a powerful oxidant, reactive to biomolecules. In aqueous solution it decomposes to give hydrogen peroxide, superoxide and hydroxy radicals which can take part in secondary reactions. Ozone is a disinfectant that inactivates both viruses and bacteria. Although other reactions are primarily responsible for the inactivation, cellular DNA is also damaged. Ozone is genotoxic to microorganisms, plants and cell cultures in vitro. The results from in vivo cytogenetic studies with laboratory animals after inhalation exposure are contradictory. Chromosome aberrations in lymphocytes, but not SCEs, have been demonstrated in Chinese hamsters but not in mice. Chromatid deletions were induced in pulmonary macrophages in rats. No cytogenetic effects have been reported for bone marrow cells or spermatocytes. The few experimental and epidemiological studies with human subjects do not allow a conclusion on the cytogenetic effects of ozone in lymphocytes in humans. No life-long cancer studies have been performed with ozone. However, after 4 and 6 months of inhalation exposure, lung adenomas were induced in strain A/J mice, but not in Swiss-Webster mice.     

Exercise responses following ozone exposure.

We have tested the response of 28 subjects to a three-stage ergometer test, with loads adjusted to 45, 60, and 75% of maximum aerobic power following ozone exposure. The subjects were exposed to one of 0.37, 0.50, or 0.75 ppm O3 for 2 h either at rest (R) or while exercising intermittently (IE) (15 min rest alternated with 15 min exercise at approximately 50 W. sufficient to increase VE by a factor of 2.5). Also, all subjects completed a mock exposure VE, respiratory frequency (fR), mixed expired PO2 and PCO2, and electrocardiogram were monitored continuously during the exercise test. Neither submaximal exercise oxygen consumption nor minute ventilation was significantly altered following any level of ozone exposure. The major response noted was an increase in respiratory frequency during exercise following ozone exposure. The increase in fR was closely correlated with the total dose of ozone (r = 0.98) and was accompanied by a decrease in tidal volume (r = 0.91) so that minute volume was unchanged. It is concluded that through its irritant properties, ozone modifies the normal ventilatory response to exercise, and that this effect is dose dependent.     

An evaluation of the sporicidal activity of ozone.

This study was undertaken to determine the feasibility of sterilizing surfaces with ozone-saturated water by the methods of the Association of Official Analytical Chemists (AOAC). Initially, it was determined that there was no apparent difference in ozone resistance between spores of Bacillus subtilis and Clostridium sporogenes when they are suspended in water. Both species were inactivated by a 10-min exposure at ambient temperature. Resistance was increased when the spores were dried on AOAC carriers. Viable organisms were recovered after an exposure of 40 min at ambient temperature. An increase in the reactor water temperature to 60 degrees C did not improve the effectiveness of the ozone in sterilizing AOAC carriers. Dried spores of C. sporogenes were more resistant than B. subtilis spores because of a greater accumulation of organic matter on the carriers. No significant sporicidal activity was demonstrated after 40 min for spores of either species when they were inoculated on silk suture loops. The data suggest that organic loading and poor ozone penetrability are key factors in effecting the ability of ozone to sterilize surfaces rapidly.     

Inactivation of human and simian rotaviruses by ozone.

The inactivation of simian rotavirus SA-11 and human rotavirus type 2 (Wa) by ozone was compared at 4 degrees C by using single-particle virus stocks. Although the human strain was clearly more sensitive, both virus types were rapidly inactivated by ozone concentrations of 0.25 mg/liter or greater at all pH levels tested. Comparison of the virucidal activity of ozone with that of chlorine in identical experiments indicated little significant difference in rotavirus-inactivating efficiencies when the disinfectants were used at concentrations of 0.25 mg/liter or greater.     

Mechanism of enteroviral inactivation by ozone.

The mechanism of enteroviral inactivation by ozone was investigated with poliovirus 1 (Mahoney) as the model virus. Ozone was observed to alter two of the four polypeptide chains present in the viral protein coat of poliovirus 1. However, the alteration of the protein coat did not significantly impair virus adsorption or alter the integrity of the virus particle. Damage to the viral RNA after exposure to ozone was demonstrated by velocity sedimentation analysis. It was concluded that the damage to the viral nucleic acid is the major cause of poliovirus 1 inactivation by ozone.     

Ontogeny of the mouse motor cortex. The polymorph layer or layer VI. A Golgi and electronmicroscopical study

Summary The development of neurons and their synapses of the mouse motor cortex has been studied from the first postnatal day up to an age of three weeks both electronmicroscopically and with the Golgi method. Special attention has been paid to the maturation of the different cell types in the sixth cortical layer and their dendritic organization within this layer.The polymorph layer is subdivided into two zones: an internal (VIb) and an external one (VIa). In these zones six different cell types can be identified both electronmicroscopically and with the Golgi method: large, small and inverted pyramidal cells in VIa; horizontal cells, star cells and small pyramidal cells in VIb.Spines of apical dendrites of large pyramidal cells in sublayer VIa can be detected as early as the 6th postnatal day. About the ninth day the basal dendrites as well show emerging spines. Somatic spines are found only on the large pyramidal cells and disappear slowly towards the end of the 3rd postnatal week.The small pyramidal cells show developing spines on their apical dendrite in the first half of the second postnatal week. The final density and distribution of spines is reached by the stem dendrites towards the end of the second week, by the basal dendrites during the third week. The maturation process of the improperly orientated neurons occurs in time in between the large and the small pyramidal cells.The axo-somatic synapses appear in general at a later date than the axo-dendritic ones. In the horizontal cells axo-somatic synapses are visible already at the seventh postnatal day.At the end of the first week especially in layer VIb many immature neurons with an ovoid or round nucleus are present having little if any endoplasmic reticulum organised as ergastoplasm.Towards the end of the second week however most neurons in the polymorph layer have a well developed endoplasmic reticulum.Electronmicroscopical pictures reveal in outgrowing dendrites many enlargements filled with vesicles, these correspond to the varicosities seen in Golgi pictures. At nine days postnatally the first myelinated fibres appear.Aided by grant (R-209-67) from the United Cerebral Palsy Research and Educational Foundation, New York.     

近地层高臭氧浓度对水稻生长发育影响研究进展

臭氧（O₃）被认为是最主要的空气污染物之一.目前地球对流层大气中平均O₃浓度已经从工业革命前的38 nl·L^-1（25～45 nl·L^-1,夏季每天8 h平均）上升到2000年的50 nl·L^-1,悲观估计到2100年近地层O₃浓度将上升到80 nl·L^-1.水稻是世界上最重要的粮食作物,准确评估近地层O₃浓度升高对水稻生长发育的影响具有重要意义.本文从叶片伤害特征、光合作用、水分关系、生育期、物质生产与分配、叶片膜保护系统、籽粒产量及产量构成因素等方面,系统收集和整理了气室条件下（包括封闭气室、开放式气室）高O₃浓度对水稻生长发育影响的研究进展,并对该领域有待深入研究的方向进行了展望.     

Oxidative damage to plasma constituents by ozone.

The reaction of ozone (O3) with human blood plasma was studied to help understand possible events that could occur in the respiratory tract. Uric acid (quantitatively the most important scavenger) and ascorbic acid were oxidized quickly, protein-SH groups were lost more slowly, and there was no loss of bilirubin or alpha-tocopherol. There was little formation of lipid hydroperoxides and no detectable formation of 4-hydroxynoneal, hexanal or nonanal, or changes in lipoprotein electrophoretic mobility. Uric acid in human upper airway secretions may play a significant role in removing inhaled O3. Oxidative damage to lipids must not be assumed to be the key mechanism of respiratory tract O3 toxicity.