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Ultraviolet (UV) radiation drives the net production of tropospheric ozone (O 3 ) and a large fraction of particulate matter (PM) including sulfate, nitrate, and secondary organic aerosols. Ground-level O 3 and PM are detrimental to human health, leading to several million premature deaths per year globally, and have adverse effects on plants and the yields of crops. The Montreal Protocol has prevented large increases in UV radiation that would have had major impacts on air quality. Future scenarios in which stratospheric O 3 returns to 1980 values or even exceeds them (the so-called super-recovery) will tend to ameliorate urban ground-level O 3 slightly but worsen it in rural areas. Furthermore, recovery of stratospheric O 3 is expected to increase the amount of O 3 transported into the troposphere by meteorological processes that are sensitive to climate change. UV radiation also generates hydroxyl radicals (OH) that control the amounts of many environmentally important chemicals in the atmosphere including some greenhouse gases, e.g., methane (CH 4 ), and some short-lived ozone-depleting substances (ODSs). Recent modeling studies have shown that the increases in UV radiation associated with the depletion of stratospheric ozone over 1980-2020 have contributed a small increase (~ 3%) to the globally averaged concentrations of OH. Replacements for ODSs include chemicals that react with OH radicals, hence preventing the transport of these chemicals to the stratosphere. Some of these chemicals, e.g., hydrofluorocarbons that are currently being phased out, and hydrofluoroolefins now used increasingly, decompose into products whose fate in the environment warrants further investigation. One such product, trifluoroacetic acid (TFA), has no obvious pathway of degradation and might accumulate in some water bodies, but is unlikely to cause adverse effects out to 2100., (© 2023. The Author(s).)

The composition of the air we breathe is determined by emissions, weather, and photochemical transformations induced by solar UV radiation. Photochemical reactions of many emitted chemical compounds can generate important (secondary) pollutants including ground-level ozone (O 3 ) and some particulate matter, known to be detrimental to human health and ecosystems. Poor air quality is the major environmental cause of premature deaths globally, and even a small decrease in air quality can translate into a large increase in the number of deaths. In many regions of the globe, changes in emissions of pollutants have caused significant changes in air quality. Short-term variability in the weather as well as long-term climatic trends can affect ground-level pollution through several mechanisms. These include large-scale changes in the transport of O 3 from the stratosphere to the troposphere, winds, clouds, and patterns of precipitation. Long-term trends in UV radiation, particularly related to the depletion and recovery of stratospheric ozone, are also expected to result in changes in air quality as well as the self-cleaning capacity of the global atmosphere. The increased use of substitutes for ozone-depleting substances, in response to the Montreal Protocol, does not currently pose a significant risk to the environment. This includes both the direct emissions of substitutes during use and their atmospheric degradation products (e.g. trifluoroacetic acid, TFA).

UV radiation is an essential driver for the formation of photochemical smog, which includes ground-level ozone and particulate matter (PM). Recent analyses support earlier work showing that poor outdoor air quality is a major environmental hazard as well as quantifying health effects on regional and global scales more accurately. Greater exposure to these pollutants has been linked to increased risks of cardiovascular and respiratory diseases in humans and is associated globally with several million premature deaths per year. Ozone also has adverse effects on yields of crops, leading to loss of billions of US dollars each year. These detrimental effects also may alter biological diversity and affect the function of natural ecosystems. Future air quality will depend mostly on changes in emission of pollutants and their precursors, but changes in UV radiation and climate will contribute as well. Significant reductions in emissions, mainly from the energy and transportation sectors, have already led to improved air quality in many locations. Air quality will continue to improve in those cities/states that can afford controls, and worsen where the regulatory infrastructure is not available. Future changes in UV radiation and climate will alter the rates of formation of ground-level ozone and photochemically-generated particulate matter and must be considered in predictions of air quality. The decrease in UV radiation associated with recovery of stratospheric ozone will, according to recent global atmospheric model simulations, lead to increases in ground-level ozone at most locations. If correct, this will add significantly to future ground-level ozone trends. However, the spatial resolution of these global models is insufficient to inform policy at this time, especially for urban areas. UV radiation affects the atmospheric concentration of hydroxyl radicals, ˙OH, which are responsible for the self-cleaning of the atmosphere. Recent measurements confirm that, on a local scale, ˙OH radicals respond rapidly to changes in UV radiation. However, on large (global) scales, models differ in their predictions by nearly a factor of two, with consequent uncertainties for estimating the atmospheric lifetime and concentrations of key greenhouse gases and air pollutants. Projections of future climate need to consider these uncertainties. No new negative environmental effects of substitutes for ozone depleting substances or their breakdown-products have been identified. However, some substitutes for the ozone depleting substances will continue to contribute to global climate change if concentrations rise above current levels.

The authors modeled the possible consequences for US cataract incidence of increases in ultraviolet B radiation due to ozone depletion. Data on the dose-response relation between ocular exposure to ultraviolet B radiation and cortical cataract were derived from a population-based study (the Salisbury Eye Evaluation Project, Salisbury, Maryland) in which extensive data on cataract and ultraviolet radiation were collected in persons aged 65-84 years. Exposure estimates for the US population were derived using estimated ultraviolet radiation fluxes as a function of wavelength. US Census data were used to obtain the age, ethnicity, and sex distribution of the population. Predicted probabilities of cataract were derived from the age-, sex-, and ethnicity-specific ocular ultraviolet exposure data and were modeled under conditions of 5-20% ozone depletion. The analysis indicated that by 2050, the prevalence of cortical cataract will increase above expected levels by 1.3-6.9%. The authors estimate that with 5-20% ozone depletion, there will be 167,000-830,000 additional cases of cortical cataract by 2050. Because of the high prevalence of cataract in older persons, at a 2003 cost of 3,370 dollars per cataract operation, this increase could represent an excess cost of 563 million dollars to 2.8 billion dollars.

A possible contribution of the immune system to the pathogenesis of virus-induced diabetes mellitus was investigated using the D-variant of encephalomyocarditis (EMC-D) virus. Studies on the F1 and backcross progeny of susceptible and resistant strains of mice gave no suggestion of a linkage between susceptibility and the major histocompatibility locus. Immuno-suppression by antilymphocyte serum did not prevent the induction of EMC-D-induced diabetes. Athymic nude mice infected with EMC-D virus showed a nearly identical diabetogenic response as compared with heterozygous littermates. Passive transfer of lymphocytes from mice made diabetic with EMC-D virus into normal mice failed to produce diabetes. From these and other studies, we conclude that the development of EMC-D-induced diabetes is due to the direct destruction of beta-cells by the virus and that the contribution of the immune response to the pathogenesis of this disease is, at the most, minor.