Urban Air Pollution Levels Research Articles

Transport and Urban Air Pollution in India

The rapid growth in motor vehicle activity in India and other rapidly industrializing low-income countries is contributing to high levels of urban air pollution, among other adverse socio-economic, environmental, health and welfare impacts. This paper first discusses the local, regional and global impacts associated with air pollutant emissions resulting from motor vehicle activity, and the technological, behavioural and institutional factors that have contributed to these emissions, in India. The paper then discusses some implementation issues related to various policy measures that have been undertaken, and the challenges of the policy context. Finally, the paper presents insights and lessons based on the recent Indian experience, for better understanding and more effectively addressing the transport air pollution problem in India and similar countries, in a way that is sensitive to their needs, capabilities and constraints.

Tandem repeat DNA: applications in mutation analysis

Non-coding tandem repeat DNA sequences have high rates of mutation that facilitate the measurement of induced mutation in small sample sizes. It has been suggested that these loci may be useful biomarkers for heritable genetic mutation induced by exposure to genotoxic agents. Significant induction of mutation is quantifiable in the germline of mice exposed to mutagens. The primary focus of this work has been on exposure to radiation. The data suggest that meiosis or DNA replication/repair may be required for induction of mutation in the germline at tandem repeats. Mutations arise via indirect mechanisms rather than by direct damage to the repeat locus itself, therefore reflecting genomic instability rather than targeted DNA damage. These markers have also been used to measure induced germline mutations in animals exposed to ambient levels of urban air pollution. The mutagenicity is associated with particulate matter in the air but the exact chemical nature of the mutagens is unknown. Lack of knowledge of the relationship between ESTR instability and gene mutation, and lack of understanding of the mechanisms resulting in instability prevent inference on the health-related implications of induced tandem repeat mutation. We have developed single-molecule PCR approaches to study ESTR instability in vitro. This method circumvents the requirement of sub-cloning and allows for many more individual ESTR alleles to be examined. These types of laboratory-based experiments will be crucial in clarifying the types of chemicals that can generate tandem repeat instability and thereby provide insight into the mechanisms of action and the putative mutagens found in complex environmental matrices.

HEALTH IMPACT ASSESSMENT OF LONG TERM EXPOSURE TO FINE PARTICLES IN FRENCH CITIES

ISEE-567 Abstract: In the framework of the preparation of the National Environment Health Action Plan, a health impact assessment study was conducted in a large number of French metropolitan areas, following the rationale proposed by Künzli et al [2000]. Based on the latest international epidemiological evidence [Pope et al 2002] the number of air pollution attributable cases (lung cancer and cardiopulmonary mortality) was derived, with fine particles as single indicator of urban air pollution. Retrospective urban background PM10 concentration data were retrieved from the Ambient Air Quality National Database covering 76 Urban Units and 15 259 590 adults 30 years old and over. PM10 data were converted into PM2.5 estimates applying a 60 % PM2.5/PM10 ratio. Attributable number of deaths and potentially avoidable cases were computed for year 2002, assuming a 15 year retrospective exposure. The “no risk” baseline exposure level was ranging from 4.5μg/m3 to 9μg/m3, while the average 2002 urban background PM2.5 concentration was 12μg/m3. A set of scenarios was used to forecast ambient air concentrations over the next 20 years. The main results for lung cancer mortality, based on the lowest baseline exposure level (4.5μg/m3), are the following: In 2002, the estimated attributable number of deaths due to the previous 16 years of exposure is 670 [89-1 257]CI95%, which corresponds to an attributable fraction of 6 %. When the target for PM2.5 in year 2020 is set at 4.5μg/m3 (in the “volunteer” scenario), the estimated number of lung cancer attributable cases is 575 [76-1 084] in 2010 and 335 [43-644] in 2020. Under the assumption of a linear reduction of the annual impacts between 2002, 2010 and 2020, the potentially avoidable total number of attributable deaths until 2020 (by comparison with a situation “leave it as it is in 2002”) is 2 698. Results are also available for cardio-pulmonary mortality (figures are about 5 fold greater). A sensitivity analysis was carried out for different exposure reference levels, ambient air quality objectives and RR estimates exposed in the paper by Pope et al. Sources of uncertainty are discussed along with the impact assessment process. Results are put into perspective with a parallel output proposing some action scenarios to reduce urban air pollution levels, and associated exposures.

Urban air pollution induces micronuclei in peripheral erythrocytes of mice in vivo

In this study, we explored the role of chronic exposure to urban air pollution in causing DNA damage (micronuclei frequency in peripheral erythrocytes) in rodents in vivo. Mice (n=20) were exposed to the urban atmosphere of São Paulo for 120 days (February to June 1999) and compared to animals (n=20) maintained in the countryside (Atibaia) for the same period. Daily levels of inhalable particles (PM10), CO, NO2, and SO2, were available for São Paulo. Occasional measurements of CO and O3 were made in Atibaia, showing negligible levels of pollution in the area. The frequency of micronuclei (repeated-measures ANOVA) increased with aging, the highest values obtained for the 90th day of experiment (P<0.001). The exposure to urban air pollution elicited a significant (P=0.016) increase of micronuclei frequency, with no significant interaction with time of study. Associations (Spearman's correlation) between pollution levels of the week that precede blood sampling and micronuclei counts were observed in São Paulo. The associations between micronuclei counts and air pollution were particularly strong for pollutants associated with automotive emissions, such as CO (P=0.037), NO2 (P<0.001), and PM10 (P<0.001). Our results support the concept that urban levels of air pollution may cause somatic mutations.

Air pollution and its health impacts: the changing panorama.

Urban air pollution levels are associated with increased mortality and cardiorespiratory morbidity. These health effects occur even at exposure levels below those stipulated in current air-quality guidelines, and it is unclear whether a safe threshold exists. Air pollution in Australia and New Zealand comes primarily from motor vehicle emissions, electricity generation from fossil fuels, heavy industry, and home heating using wood and coal. In individual patients a direct link between symptoms and air pollution exposure may be difficult to establish and may not change their clinical management. However, avoiding exposure during periods of peak pollution may be beneficial. Although there is some evidence that urban air pollution in Australia and New Zealand has been decreasing (through reduced car use, improved emission-control technology and use of more energy-efficient devices in the household and in industry), pollution levels are still unsatisfactory. Further reductions may prevent hundreds of cardiorespiratory hospital admissions and deaths each year.

Preferences over Prosperity and Pollution: Environmental Valuation based on Happiness Surveys

This paper uses cross–national data from happiness surveys, jointly with data on per capita income and pollution, to examine how self–reported well–being varies with prosperity and environmental conditions. This approach allows us to show that citizens care about prosperity and the environment, and to calculate the trade–off people are willing to make between them. The paper finds that the effect of urban air pollution on subjective well–being shows up as a considerable monetary valuation of improved air quality. For instance, a representative German citizen would need to be given more than 1900 $ per year in order to accept the typical urban air pollution level prevailing in Japan. The subjective marginal valuation of air pollution is compared with marginal abatement costs from the literature.

Privatization and Equity in Brazil and Russia

This paper uses cross–national data from happiness surveys, jointly with data on per capita income and pollution, to examine how self–reported well–being varies with prosperity and environmental conditions. This approach allows us to show that citizens care about prosperity and the environment, and to calculate the trade–off people are willing to make between them. The paper finds that the effect of urban air pollution on subjective well–being shows up as a considerable monetary valuation of improved air quality. For instance, a representative German citizen would need to be given more than 1900$ per year in order to accept the typical urban air pollution level prevailing in Japan. The subjective marginal valuation of air pollution is compared with marginal abatement costs from the literature.

Personal exposures to PM(2.5) and polycyclic aromatic hydrocarbons and their relationship to environmental tobacco smoke at two locations in Greece.

In the context of a large-scale molecular epidemiology study of biomarkers of genotoxicity of air pollution, 24-h mean personal exposures to airborne PM(2.5) (particulate matter <2.5 microm) and associated polycyclic aromatic hydrocarbon (PAHs) were measured in 194 non-smoking technical institute students living in the city of Athens, Greece (an area with moderately high levels of air pollution) and the nearby small town of Halkida anticipated to have lower pollution levels. Extensive information relevant to the assessment of long-term and recent exposure to PAH was obtained from questionnaires as well as a time-location-activity diary (TLAD) which was kept by all subjects during a 4-day observation period. During the last 24 h of this period, subjects underwent personal exposure monitoring for PM(2.5) and PAH, while a sample of blood was donated at the end of this period. All subjects were monitored in this way twice; once during a winter season (October-February) and once during the following summer season (June-September). Nine subjects with plasma cotinine levels above 20 ng/ml were considered as unreported smokers and excluded from the study. Winter PM(2.5) exposures were lower in Athens (geometric mean 39.7 microg/m(3)) than Halkida (geometric mean 56.2 microg/m(3)) (P<0.001), while there was no significant location difference during the summer (Athens: geometric mean 32.3 microg/m(3), Halkida: geometric mean 32.9 microg/m(3); P=0.79). On the other hand, PAH exposures (sum of the eight carcinogenic PAHs) were significantly higher in Athens than in Halkida during the winter (Athens: geometric mean 8.26 ng/m(3), Halkida: geometric mean 5.80 ng/m(3); P<0.001) as well as during the summer (Athens: geometric mean 4.44 ng/m(3), Halkida: geometric mean 1.48 ng/m(3); P<0.001). There was a significant difference in the profile of the PAH exposures at the two locations, the proportion of lighter PAH (benzo[a]anthracene, chrysene [CHRYS], benzo[k]fluoranthene, and benzo[b]fluoranthene) being higher, and that of heavier PAH (benzo[ghi]perylene [BPer] and indeno[1,2,3,cd]pyrene) lower, in Halkida than in Athens, regardless of season. This difference appeared to be related to individual exposure to environmental tobacco smoke (ETS), as indicated by (a) the correlation at the individual level between the CHRYS/BPer ratio and declared time of recent exposure to ETS as well as plasma cotinine levels, especially during the winter; (b) the parallel variation of the mean levels of all three markers (declared ETS exposure, cotinine levels, CHRYS/BPer ratio) among three subgroups of subjects (Athens subjects who had lowest levels of all three markers; Halkida subjects other than those living in the institute campus area; and Halkida subjects living in the institute campus area who had the highest levels of all three markers). This demonstrates that ETS can have a distinctive effect on the PAH exposure profile of subjects exposed to relatively low levels of urban air pollution.

Urban levels of air pollution modifies the progression of urethane-induced lung tumours in mice

This paper investigates the effects of air pollution in urethane-induced lung tumours in mice by means of histological, morphometrical, and DNA ploidy. The experimental exposure was done in locations with different air pollution profiles: a polluted area (downtown São Paulo) and a "clean" environment. Swiss mice were employed and urethane (3 g/kg) was used as a carcinogenic substance. All the animals, whether exposed or not to air pollution, were sacrificed after 6 months, and the lung lesions were analysed. The results showed a significant effect of air pollution on tumour progression, observed by changes in the phenotype of the tumour cells as demonstrated by morphometry and DNA ploidy. We observed more atypical adenomas in the air pollution-exposed group (p = 0.02). Coherently, morphometric differences were also detected between the two groups. Neoplasms of exposed mice exhibited an increase in the nuclear fraction (p = 0.002) and in the nucleus/cytoplasm ratio (p = 0.011), as a decrease in the stromal fraction (p < 0.001). There was a higher risk of aneuploidy in the 6-months-of-air-pollution-exposure group (relative risk: 1.58; 95% of confidence interval: 1.007 to 2.403). These results indicate that urban air pollution accelerates the process of progression towards malignancy.

Correlation between respiratory alterations and respiratory diseases due to urban pollution

Background: Air pollution is strongly correlated with allergic and infectious diseases. Chronicity of the stimulation and immaturity of the defense system make children prone to respiratory diseases. The aim of this study was to assess the adverse effects of urban levels of air pollution, correlating children’s respiratory diseases and ultrastructural studies in rats, compared to controls in a clean area. Methods: An epidemiological survey was conducted with 2000 school children (age range 7–14 years old), divided into two groups of 1000 children each: the Red group from São Paulo city (17 000 000 inhabitants) and the Green group from a rural area around the city of Tupã with no air pollution at all. A questionnaire was given to the children’s parents in order to estimate history of respiratory diseases and predisposing factors. A total of 69 rats were housed for 6 months in the center of São Paulo, and ultrastructural studies of the epithelium of the airways were done and compared to 56 control animals in the rural area. Results: The Red group of children had a statistically significant ( P<0.005) high prevalence of respiratory diseases such as rhinitis, sinusitis, and upper respiratory infections (URI). Rats exposed to air pollution developed ultrastructural ciliary alterations. Conclusion: The results obtained in the present investigation suggest that chronic exposure to urban levels of air pollution may cause respiratory diseases in children and ultrastructural ciliary alterations in the epithelium of the airways in rats, when compared to controls in a pollution-free rural area.

Molecular epidemiological approaches to the study of the genotoxic effects of urban air pollution

Direct epidemiological observations suggest that exposure to high levels of urban air pollution may result in increased risk of lung cancer, sufficient to account for a few (∼1–3) percent of total lung cancer incidence. Extrapolation from occupational exposure and risk data suggests that among potential carcinogens present in polluted urban air, polycyclic aromatic hydrocarbons (PAHs) may make a major contribution to air pollution-associated lung cancer risks. The use of biomarkers of genotoxocity in large-scale population studies may help to reduce the uncertainty involved in the assessment of such risks, especially those associated with relatively low pollution levels such as nowadays found in many Western cities. Increases in biomarkers of exposure to urban air PAHs as well as biomarkers of early effects have been detected in situations of relatively high levels of air pollution (e.g., ambient PAH concentrations of the order of a few tens of micrograms per cubic meter). Evidence has also been found about the modulation genetic damage accumulation in different individuals by polymorphisms in genes involved in the activation or detoxification of PAHs, especially of polymorphisms GSTM1 and CYP1A1 genes. However, the inconsistencies in the currently reported effects of genetic polymorphisms suggest that additional factors may also be important in the modulation of individual susceptibility to the accumulation of PAH-derived genetic damage. Biomarkers studies in populations exposed to relatively low ambient PAH concentrations (below 20 μg/m 3) have not demonstrated clear dose-related effects (e.g., on DNA adduct levels), possibly because of the existence of multiple sources and routes of human exposure to PAHs in addition to inhalation of urban air (including, for example, home heating, environmental tobacco smoke and diet), and the consequent difficulty of adequately and specifically assessing atmospheric air-related exposure. This makes it imperative that molecular epidemiology studies be designed in such a way as to allow adequate assessment of exposure to urban air PAHs at the individual level and over short-, medium- and long-term time periods which correspond to the expression times of different biomarkers.

Proposed Air Quality Objectives for Fine Particulate Air Pollution

Canada is now considering recommendations of the Federal-Provincial Working Group on Air Quality Objectives and Guidelines to adopt objectives for fine particulates that will be among the most stringent anywhere in the world and that may be technically unobtainable in the short term. No Canadian city would be in compliance at this time if these objectives were adopted. The fine particulate issue is also driving a fundamental change in the way that Canada harmonizes regulations on air pollution. In the United States, standards are set by the federal government for implementation by the states; the federal government has primacy. These standards are mandatory as a minimum level of control, although states may impose more stringent standards. By contrast, in the Canadian system the federal government does not have primacy and environmental protection at the local level is mandated to provincial governments. Canada has chosen to set guidelines negotiated between the federal government and representatives of provincial governments, in the expectation that these guidelines will influence the individual provinces to adopt similar standards. The role of guidelines, as opposed to standards, is to drive voluntary change and to influence public opinion. In the past, these guidelines were set to be more stringent than U.S. National Ambient Air Quality Standards and reflected the reality that urban air pollution levels in most large Canadian cities were generally lower than their U.S. counterparts. In 1997, a new process was initiated to bring the development of recommended air quality criteria into a more scientific formulation. National Ambient Air Quality Objectives will now be developed in a more transparent, accountable and science-based process. They will also be recommended rather than mandated but as objectives will carry the expectation that all jurisdictions in Canada will eventually harmonize their own standards to these norms. The first two objectives under this new process are fine particulates and ozone. For the purpose of this discussion, we shall confine our remarks to fine particulates. A large body of evidence was compiled into a report 1 that constituted the briefing document for a Stakeholder Consultation Workshop convened by the Atmospheric Environment Service of Environment Canada in December 1997. Included in this dossier was the report of the Federal Provincial Working Group recommending new air quality objectives for fine particulates. 2 The implication of these recommendations was staggering. Based on their reading of the available evidence, and driven primarily by estimates of lives saved through reductions in mortality associated with fine particulate levels in urban areas, the Federal Provincial Working Group recommended an objective for PM 10 of a 24hour average concentration of 40 µg/m 3 and for PM 2.5 of 20 µg/m 3 . This compares with the U.S. Environmental Protection Agency’s (EPA’s) previously proposed (now remanded) National Ambient Air Quality Standard of U.S. 24-hour averages of 150 and 65 µg/m 3 , respectively. Canada would have no equivalent to the previously proposed U.S. annual averages of 50 and 15 µg/m 3 , respectively, relying on the 24

Respiratory Changes due to Long-term Exposure to Urban Levels of Air Pollution: A Histopathologic Study in Humans

To evaluate the potential associations between long-term exposure to air pollution and histopathologic evidence of damage to the lungs in humans. Lung tissue samples were collected during necropsies of individuals who died due to violent causes, selected on the basis of their exposure background. The exposed group was composed of individuals who lived in Guarulhos, an area with high mean levels of inhalable particles. The control group was composed of individuals who lived in two cities with economies based on agricultural activities: Ribeirão Preto and Ourinhos. Information about cigarette smoking and occupational exposure was obtained from family members. Morphometric evaluation of the main bronchus was conducted to determine the volume ratio of submucosal glands. Histopathologic alterations of the bronchioli were evaluated by scoring the presence of inflammatory reaction, wall thickening, and secretory hyperplasia. The number of spots of carbon deposition was counted along the regions of lymphatic drainage (visceral pleura and axial connective tissue around bronchi and blood vessels). Statistical analysis was done by means of regression models controlled for age, smoking, and occupational exposure. Lungs collected from the high pollution area presented evidence of more histopathologic damage in comparison to those from the clean environments. These effects were observed even after controlling for individual differences in age, sex, and cigarette smoking levels. These results suggest that long-term exposure to air pollution may contribute to the pathogenesis of airway disease, and that urban levels of air pollution have adverse effects on the respiratory tract.

Cytological changes of the respiratory tract in young adults related to high levels of air pollution exposure.

Several histopathological and cytological studies have shown that lesions of the respiratory tract epithelium become increasingly severe with duration of exposure to high levels of urban air pollution as well as with ageing of studied population groups. In this study we investigated and compared findings of cytological abnormalities in sputa of young adults (21-25 years of age) exposed to high levels of air pollution since birth with those who were exposed in the last 2-3 years only. All subjects were non-smokers and were clinically healthy at the time of sampling. No significant differences in the incidence or severity of any of the cytological findings were found. The fact that even 10 times longer exposure to air pollution resulted in no major respiratory tract epithelial changes is, in our opinion, a result of the extremely efficient defence mechanisms and enormous regenerative potential of the respiratory tract of younger people.

Assessing the impact of the New Athens airport to urban air quality with contemporary air pollution models

The new airport of Athens will be constructed in the Spata area to the east of the Athens basin. In an attempt to study how the airport operation influences air quality in Athens, the wind flow and pollutant transport in the Athens basin and the Spata area are studied by applying a set of contemporary models, all constituents of the EUMAC Zooming Model (EZM): (1) the nonhydrostatic prognostic mesoscale model MEMO for simulating air flow and the dispersion of inert pollutants, and (2) two photochemical dispersion models, the three-dimensional model MARS and the three-layer model MUSE for describing the dispersion of reactive pollutants. Simulations were performed for meteorological conditions favouring the occurrence of air pollution episodes. Emphasis is put on the influence of the airport emissions on air quality assuming that the airport is operating either at its old location (Hellenikon) or at Spata. Comparison of simulation results for one selected scenario achieved with all three models reveals similar diurnal variations of nitrogen oxides in the Athens basin and the Spata area. The model results show that under conditions favoring air mass penetration from Athens to the Spata area the resulting pollutant transport causes an increase in air pollution levels without, however, leading to the exceedance of air quality standards. In the opposite case, the pollutant transport cannot have a noticeable adverse influence on the Athens air quality because of both the relatively high urban air pollution levels and the fact that the penetration depth is small.

Damage to the nasopharyngeal mucosa induced by current levels of urban air pollution: a field study in lambs

This study concerns the effects of urban air pollution on the nasopharyngeal epithelium, with the aim of evaluating the possible harmful activity of levels of atmospheric pollution which are not currently considered to be dangerous. Over a 3 month period, 10 lambs kept in a zone characterized by numerous vehicles were sacrificed at regular intervals, and their nasopharyngeal mucosa was examined by scanning electron microscopy and image analysis. Two lambs kept in a rural area were used as controls. The local levels of some airborne contaminants (NO(x), NO2, NO, SO2, CO and particulate matter with aerodynamic diameter < or =10 microm (PM10)) were monitored throughout the experiment. The urban air had an irritating effect, inducing hypersecretion of mucus and morphological damage to the ciliated epithelium. These alterations increased with the duration of exposure to urban air and with increasing pollution levels, although the levels remained below current legal levels. We conclude that the harmful effects of airborne contaminants are probably underestimated. Moreover, physicochemical evaluation of pollution parameters should be complemented by morphological study of upper respiratory epithelium in exposed animals, since this mucosa is a sensitive target for irritating agents.

Nasal lavage biomarkers in air pollution epidemiology.

Epidemiological studies have shown associations between air pollution and respiratory health effects (reviewed in Bascom et al., 1996). Adverse health effects at current levels of exposures have been found for ozone, acid aerosols and particulate matter smaller than 10 μm (PM10). Effects of ozone include pulmonary function decrements, increased non-specific bronchial responsiveness and inflammatory responses (Graham and Koren, 1990; Jorens et al., 1992; Koren et al., 1989). Data based on health effects associated with acute exposure to urban particulate air pollution is rapidly growing by consistent data from epidemiological studies (Bascom et al., 1996). These data indicate that increases in daily mortality, hospitalisation, asthma exacerbation, respiratory symptoms and lung function decline are associated with ambient low levels of urban particulate air pollution measured as PM10 and lower. Possibly, air pollution induced inflammatory reactions and related inflammatory mediators are involved in altered lung function and may have implications for respiratory allergy. It is possible that ozone induces mild to moderate immune disorders by shifting vulnerable balances in the immune system, such as T help-1 and T help-2 subset ratios, resulting in altered resistance to respiratory tract infections or altering the expression of respiratory allergy. Epidemiological studies focused on inflammatory responses include the use of biomarkers.

Using measurements of air pollution in streets for evaluation of urban air quality — meterological analysis and model calculations

Measurements of urban air pollution are usually confined to a few locations within a city area. Monitoring stations are often situated in streets with significant traffic levels or in places where severe pollution problems are expected. Such measurements are naturally influenced by very local conditions and care must be taken in interpreting the results. This is especially important when the measurements are used for estimating urban air pollution levels or comparing air quality in different cities. Another frequent application of street measurements is for public information or warning the population of elevated pollution levels. Estimating the dangers of long-term exposure to air pollution means careful consideration must be given to how representative these measurements actually are. In this paper the influence of local conditions on air pollution concentrations is discussed, regarding especially the dependency of pollution levels on street configuration and meteorolgical parameters. The examples used are based on measurements from locations in Copenhagen and on model calculations using the Danish Operational Street Pollution Model (OSPM). It is shown that large concentration gradients can occur in street canyons with leeward concentrations far higher than windward concentrations. Thus, street measurements are site-dependent and not representative for urban areas. Model calculations with OSPM agree well with measurements.

Urban Levels of Air Pollution Increase Lung Responsiveness in Rats

This study was designed to investigate if animals exposed to urban levels of air pollution develop pulmonary hyperresponsiveness and to test if this change was reversed after moving the animals to a nonpolluted environment. One hundred twenty male Wistar rats were kept in (a) São Paulo (polluted environment) for 3 months (SP3); (b) Atibaia (clean region), for 3 months (A3); (c) São Paulo for 3 months and then Atibaia for a further 3 months (SPA6); (d) Atibaia for 6 months (A6). After the exposure period, the rats were submitted to dose-response curves to inhaled methacholine. Older animals (SPA6 and A6) had lower responses to methacholine in terms of respiratory system resistance when compared to the animals studied after 3 months of experiment (SP3 and A3). However, the response in terms of respiratory system elastance of the SP3 group was significantly (P = 0.0004) greater than those of the other three groups. Our results suggest that the environmental conditions of the large urban centers can induce pulmonary hyperresponsiveness in rats that can be reversed when the animals are removed to a nonpolluted area.

Health effects of air pollution in southern Europe: are there interacting factors?

Recent results suggest that adverse health effects of air pollution exist at levels of pollutants around or even below air quality standards set by national and international institutions. Furthermore, there are indications that air pollution effects on health may be partly determined by specific mixtures of air pollutants and may be altered by other environmental, behavioral, and social patterns. Southern European countries share some common characteristics in terms of climate, geography, and life activity patterns. Results from studies undertaken in France, Greece, Italy, Portugal, and Spain investigating short- and long-term air pollution health effects are presented and their consistency demonstrated. These results provide adequate evidence that health effects--particularly short-term--of the currently measured urban air pollution levels exist. However, information available so far does not allow an assessment of regional differences in the health effects of air pollution as far as the Mediterranean region of Europe is concerned. It is suggested that the interaction between the traditional pollution (mainly characterized by high levels of black smoke and SO2) and photochemical pollution must be investigated in this area, as well as the possible interaction between air pollution and high temperature and other meteorologic factors. In addition, measurements of individual exposure to different pollutants, affected by the pollutant's levels in specific micro-environments and the individual's time-activity pattern, must be undertaken for a better understanding of the air pollution-health link. Finally, the importance of the reported air pollution health effects in terms of public health must be addressed more closely.