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.
Atmosphere↗
Biomedical subjects
Jan C van der Leun
Publications and source records attributed to Jan C van der Leun.
Ultraviolet tanning equipment: six questions.
Recreational tanning, particularly as promoted by commercial salons with 'sunbeds' or booths, has generated increasing attention from the regulatory and the biomedical communities. Several agencies have weighed in with opinions on recommended modifications in guidelines, training procedures, regulatory controls, and consumer awareness. Currently there is little uniformity in the guidance provided by trade groups, in recommendations supplied by health agencies and medical associations, or in regulatory approaches taken or proposed by the many countries involved. In an effort to provide a clearer focus for its concerns in this area, the EU Directorate General Health and Consumer Affairs formulated six questions on ultraviolet (UV) tanning, all of a technical or biomedical nature. The questions were stimulated in part by the fact that the European Commission no longer regards the European standard EN 60335-2-27:1997 ('Particular requirements for appliances for skin exposure to ultraviolet and infrared radiation') as giving presumption of conformity to the Low Voltage Directive 73/23/EEC. (The latter Directive governs marketing of electrical devices in EC countries.) Initially, the questions were posed to an EU Scientific Committee. Subsequently, industry representatives and the European Commission jointly requested that the scientific community provide answers to the questions. We received the questions with a request for our technical responses and opinions. Our response was in the form of the following essay, submitted earlier this year to the European Commission. We offer it here in the hope of stimulating constructive discussion and comment.
Beauty Culture↗
The ozone layer.
BACKGROUND/PURPOSE: The intention of this paper is to stimulate the interest for the ozone layer, especially among young colleagues in photobiology; the "layer" is not only important, but also fascinating. CONCLUSION: In spite of remarkably effective action, the recovery of the ozone layer will be a long-term process. It will need the attention, also of scientists, for decades to come.
Atmosphere↗
Immunochemical study of DNA modifications in the nuclei of UV-damaged lymphocytes.
Studies of UV-induced skin cancers show that malignisation of skin cells, as well as alterations in anti-tumor immune control, are triggered by UV-induced lesions in cellular DNA. Such lesions can probably appear in the human mononuclear leukocytes (lymphocytes) during exposure of skin to sunlight. With the aim of studying the processing of UV-induced DNA lesions in these cells, we used flow cytometry and labelling of their partially denatured nuclei with the monoclonal antibody (H3) that binds cyclobutane pyrimidine dimers in single-stranded DNA. After the first few hours of cultivation of the irradiated cells, we found an increase in H3-specific fluorescence from cellular nuclei, while there was a decrease in the number of H3-positive sites in isolated DNA from these cells. We examined cells cultured under different conditions and concluded that the effect of enhancement of H3 labelling of nuclei did not result from changes in temperature and culture medium. Furthermore, we have found that this effect, as well as the decrease in H3 labelling in isolated DNA, are both prevented by pretreatment of the cells with Novobiocin, which we used as an inhibitor for the topoisomerase II-induced relaxation of supercoiled DNA prior to repair-specific incision. The inhibition by Novobiocin of the above-mentioned changes in H3 labelling in cellular nuclei and isolated DNA of the irradiated cells clearly indicate the association of both effects with an excision repair-related DNA modification. While the partial loss of H3-binding sites from isolated DNA is obviously a result of excision of some fraction of pyrimidine dimers, the enhancement of the H3 labelling of nuclei might be due to the formation of open structures at dipyrimidine-containing DNA fragments in preparation for incision. We suggest that formation of open structures predominates quantitatively over dual incision and excision of these fragments, and leads to enhanced exposure of the pyrimidine dimers in nuclei to H3 binding. Thus, unstimulated human lymphocytes appear to be capable of performing pre-incision steps for removal of these DNA lesions.
Cell Nucleus↗
Standardized protocols for photocarcinogenesis safety testing.
Solar ultraviolet radiation (UVR) is recognized as a major cause of non-melanoma skin cancer in man. Skin cancer occurs most frequently in the most heavily exposed areas and correlates with degree of outdoor exposure. The incidence of skin cancer is also increased by contact with photosensitizing drugs and chemicals such as psoralens, coal tars and petroleum stocks. Other substances which do not act as photosensitizers, such as immunosuppressants taken by organ transplant recipients, also increase the risk of skin cancer. The U.S. Food and Drug Administration requests, on a case-by-case basis, that risk of enhanced photocarcinogenesis is assessed for many classes of drugs. Health Canada's Therapeutic Products Programme has issued a Notice of Intent to regulate pharmaceutical products which may enhance carcinogenicity of the skin induced by ultraviolet radiation. Other national regulatory agencies review such data when they exist, but their own requirements emphasize batteries of short-term in vitro and in vivo tests. While they may support drug development strategies, short-term tests have yet to be validated as predictors of the ability of drugs or chemicals to enhance photocarcinogenesis. Published protocols now describe study designs and procedures capable of determining whether test agents enhance the rate of formation of UVR-induced skin tumors.
Animals↗
Health effects from stratospheric ozone depletion and interactions with climate change.
The potential health effects of elevated levels of ambient UV-B radiation are diverse, and it is difficult to quantify the risks, especially as they are likely to be considerably modified by human behaviour. Nevertheless epidemiological and experimental studies have confirmed that UV radiation is a definite risk factor for certain types of cataract, with peak efficacy in the UV-B waveband. The causal link between squamous cell carcinoma and cumulative solar UV exposure has been well established. New findings regarding the genetic basis of skin cancer, including studies on genetically modified mice, have confirmed the epidemiological evidence that UV radiation contributes to the formation of basal cell carcinomas and cutaneous melanomas, For the latter, animal models have demonstrated that UV exposure at a very young age is more detrimental than exposure in adulthood. Although suppression of certain immune responses has been recognised following UV exposure, the impact of this suppression on the control of infectious and autoimmune diseases is largely unknown. However, studies on several microbial infections have indicated significant consequences in terms of symptoms or reactivation of disease. The possibility that the immune response to vaccination could be depressed by UV-B exposure is of considerable concern. Newly emerging possibilities regarding interactions between ozone depletion and global climate change further complicate the risk assessments for human health but might result in an increased incidence of cataracts and skin cancer, plus alterations in the patterns of certain categories of infectious and other diseases.
Cataract↗
UV doses of young adults.
Since 1986, people have been informed that they get about 80% of their lifetime ultraviolet (UV) dose by the age of 18. This belief originated from the mathematical conclusion that diligent use of sunscreens (sun protection factor 15 or higher) during the first 18 years of life would reduce the lifetime incidence of nonmelanoma skin cancers by 78%. These data were misconstrued to mean that individuals also got about 80% of their lifetime dose of UV by the age of 18 (linear relationship). However, these calculations were based on the incidence of nonmelanoma skin cancers being related to the square of the UV dose. Careful analysis of UV exposure data shows that Americans actually get less than 25% of their lifetime UV dose by the age of 18. This finding also appears to be true worldwide because Australia, UK and The Netherlands report a similar UV exposure pattern. UV-initiated damage early in life can be promoted by subsequent exposures to progress into tumors later in life. For example, the nonmelanoma skin cancer, squamous cell carcinoma, is dependent on the cumulative UV dose. Thus, a better educational approach for reducing skin cancers would be to instruct fair-skinned individuals to protect themselves throughout their lives from being exposed to too much UV radiation.
Adolescent↗
Physical variables in experimental photocarcinogenesis and quantitative relationships between stages of tumor development.
Solar ultraviolet (UV) radiation is a prominent environmental carcinogen, but it does not penetrate any deeper than the skin. The UV-related skin cancers are by far the most common form of cancer among white Caucasians in the USA and Australia, and this poses a serious public health problem. Chronic UV exposure of hairless mice is a well established model for squamous cell carcinomas in man. It is important to identify the essential physical variables, and explore fully how photocarcinogenesis evolves in dependence of these variables. The 3 main physical variables in photocarcinogenesis are (i) the wavelength of the radiation, (ii) the exposure and (iii) time. A good quantitative description of tumor induction and precursing stages can be given in terms of these variables. An analysis of this description shows us that the early induction of clusters of epidermal cells that over-express mutant p53 ('p53 patches') are closely and, most likely, causally linked to the eventual tumors. These p53 patches may thus serve as early indicators of tumor risk. The induction of an immune-tolerance toward the UV-induced tumors precedes the actual occurrence of the tumors at high daily doses, but extrapolation indicates that this order of events may be reversed at low daily doses. This disparity between the dose-time relationships for the tumor tolerance and the tumors needs to be investigated further. It could imply a shift to non-immunogenic tumors at low daily doses.
Animals↗
Climate change and skin cancer.
Depletion of the ozone layer and climate change by the increasing greenhouse effect are distinctly different processes. It is becoming quite clear, however, that the two global environmental problems are interlinked in several ways [D. L. Albritton, P. J Aucamp, G. Mégie, R. T. Watson, Scientific Assessment of Ozone Depletion, 1998, World Meteorological Organization, Global Ozone Research and Monitoring Project, Report No. 44 (WMO, Geneva, 1998)]. In the present analysis we deal with the possibility of such an interlinkage within one effect on human health, namely, skin cancer. The increase in the incidence of skin cancer is one of the most extensively studied effects of increasing ultraviolet radiation by ozone depletion (F. R. de Gruijl, Skin cancer and solar radiation, Eur. J Cancer, 1999, 35, 2003-2009). We wondered if this impact could also be influenced by increasing environmental temperatures. Here we show that it is likely that such an influence will occur. For the same reason, it is likely that the baseline incidence of skin cancer will be augmented by rising temperatures, which may become significant in magnitude.
Animals↗