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What can we learn today from the Central European smog episode of 1985 (and earlier episodes)?

In January 1985 an extended smog episode occurred in Central Europe. The Rhine-Ruhr area (Western Germany) was affected for 5 days with maximum concentrations of 0.8 mg/m3 SO2 and 0.6 mg/m3 TSP (24h averages). Health effects were investigated during the smog period and a control period before and after the smog. Daily mortality increased by 8%, hospital admissions (for respiratory and cardiovascular causes, RC) by 15%, outpatients (RC) by 12% and ambulance transports (RC) by 28%. Patients with chronic bronchitis from the Ruhr area cities showed more exacerbations during the episode, and in school children from the Netherlands lung function was reduced. In Augsburg (Southern Germany) the smog episode was less severe (maximum concentrations 0.2 mg/m3 SO2 and 0.1 mg/m3 TSP, 24 h averages). Here--by chance--the prospective MONICA study was ongoing. During the episode a significant increase of plasma viscosity, C-reactive protein and heart rate was observed in the participants. The highest ambient concentrations (maximum 24h average of 3.6 mg/m3 SO2) were measured in Erfurt (Eastern Germany). Surprisingly, no measurable increase of mortality occurred. This was explained by premature deaths during the period before the smog, were the concentrations had already been clearly above 1 mg/m3 SO2. An earlier episode took place in December 1962 in the Rhine-Ruhr area for 5 days with maximum concentrations of 5.0 mg/m3 SO2 and 2.4 mg/m3 TSP (24 h average). Daily mortality on average increased by 19%. In 1962 and 1985 the effects were stronger in cities with pollution mainly from traffic than in areas with pollution from industrial sources. In total, between 1962 and 1987 two major and several smaller smog episodes occurred in Central Europe. Patients with cardiovascular diseases were more severely affected than patients with respiratory diseases. Health effects were more strongly correlated with TSP than with SO2.

Air Pollutants↗

[A study on the role of vascular endothelial growth factor in emphysema of rat caused by smog exposure].

OBJECTIVE: To explore the role of vascular endothelial growth factor (VEGF) in emphysema of rat caused by smog exposure. METHODS: Thirty-six 12-week male rats were randomly divided into 2 groups: a smog exposure group (S group), and a normal control group (N group). S group rats were randomly subdivided into 3 groups: S(1) group, S(2) group, S(3) group, which were exposed to smog for 2 weeks, 4 weeks, 8 weeks, respectively; N group rats were randomly subdivided into 3 groups: N(1) group, N(2) group, N(3) group, which were raised in normal oxygen condition for 0 week, 4 weeks, 8 weeks, respectively. The expressions of VEGF mRNA and VEGF protein and kinase-insert domain containing receptor (KDR) protein were determined by reverse transcription-polymerase chain reaction (RT-PCR) and modified SABC immunohistochemistry assay separately. The pathological change in smog exposure rat lung was determined by HE staining. MLI and MAN were determined as an index of emphysema. Variance analysis, nonparametric analysis and correlate analysis were conducted in SPSS 10.0. RESULTS: (1) There were airway inflammation in S group rat lungs, and an early-emphysema-like change in S(3) group rat lungs: MAN in S(3) group was significantly decreased compared with N(3) group, MLI in S(3) group was significantly increased compared with N(3) group (P < 0.05). (2) VEGF189 mRNA in lung and VEGF protein in alveolar and bronchial epithelium of rats in S(1) group were significantly lower than those in N(1) group (P < 0.01); VEGF189 mRNA, VEGF165 mRNA and VEGF121 mRNA of lung tissue and VEGF protein in alveolar and bronchial epithelium of rats in S(2) group were significantly lower than those in N(2) group (P < 0.01), too; VEGF protein in alveolar and bronchial epithelium and KDR expression in pulmonary vascular endothelium of rats in S(3) group was lower than that in N(3) group (P < 0.01, P < 0.01, P < 0.05), but VEGF mRNA have no difference (P > 0.05). (3) VEGF protein expression in alveolar epithelium and bronchial epithelium had a positive correlation with MAN (r = 0.43, r = 0.37, P < 0.05) and an inverse correlation with MLI (r = -0.42, r = -0.37, P < 0.05). CONCLUSIONS: Smog exposure decrease the expression of VEGF and KDR in rat lung. VEGF might involve in the pathology of emphysema caused by smog exposure.

Animals↗

Does smog increase the general practitioner's workload?

Dublin city experienced a week-long episode of intense smog in November 1988. A retrospective analysis was carried out in ten general practices of the numbers of patients seen during November. Each practice was situated in an area affected by high smog levels. The numbers of patients seen in surgery and on house-calls showed no differences during the weeks preceding the smog outbreak, during the period of high smog levels or during the week after this period. No qualitative data on the reasons for patients' visits were collected and no comments can be made on the nature of patients' illnesses during this period. There was no evidence for an increased workload in general practice caused by this episode of intense smog but a prospective study is necessary to confirm this finding and to examine the nature of patients' problems during such an episode.

Humans↗

[Biological effects of smog. VIII. Impulse cytophotometric cell cycle analysis of synchronized Syrian hamster kidney cell cultures (line 14-b)].

Syrian hamster kidney cultures of line 14-1b were synchronized by excess of thymidine. Thereafter in the phase of DNA synthesis cell cultures were exposed to extract and fractions of city smog, derived from a polluted area at the river Rhine and Ruhr. Using impulscytophotometry and estimation of mitotic frequency cell cycle analyses were conducted on synchronized exposed and control cultures. The total extract obtained by methanol treatment of city smog was further fractionated by organic solvents leading to fractions of cyclohexane, polyaromates and propanol. Cell cycle progression of synchronized cultures was inhibited in a dose dependent manner by increasing concentration of city smog extract and its fractions. This inhibition led to a prolongation of DNA synthetic phase and to an accumulation of cells in G2(+ M)-phase. The total cell cycle showed a prolongation of 3-5 h. The strongest effect was induced by the total extract. We have to emphasize that already amounts of city smog which were found in air volumes of 2-5 m3 exerted strong effects. With a declining sequence of toxicity followed the fractions of cyclohexane, propanol and of polyaromates. Our results show, that samples of city smog from polluted areas contain substances which induce heavy alterations in cell cycle progression of mammalian cells in vitro. These highly effective toxic substances are dangerous for human health, especially after a long-time exposition.

1-Propanol↗

Trends in photochemical smog in the Cape Peninsula and the implications for health.

There has been growing public concern over reports of increasing air pollution in the Cape Peninsula. Attention has been focused on the 'brown haze' and on photochemical smog. Because of deficiencies in the monitoring equipment, information on trends in photochemical smog levels over the past decade is limited. Trends in oxides of nitrogen, one of the main precursors of photochemical smog, and therefore an indicator of the potential for its formation, were examined for the period 1984-1993. Meaningful data for determining trends were available from only a single site. Increases in mean monthly levels, peak hourly levels and the number of times guidelines were exceeded were demonstrated. Given the dynamics of formation of photochemical smog and the particular role of motor vehicles, it is argued that the trends measured at this site are probably an underestimate of the trends in other parts of the Cape Town metropolitan area. Some of the precursors of photochemical smog, notably nitrogen dioxide, and some of its components, notably ozone, have been shown to be detrimental to respiratory health at levels close to, or below, current recommended guidelines. A continuing increase in these pollutants will therefore result in more respiratory illness, particularly among susceptible groups. This calls for an upgrading of monitoring of air pollution in Cape Town and for appropriate steps to prevent its further increase.

Air Pollutants↗

Health effects during a smog episode in West Germany in 1985.

In January 1985 a smog period occurred for 5 days in parts of West Germany, including the Rhur District. Mortality (24,000 death certificates), morbidity in hospitals (13,000 hospital admissions, 5400 outpatients, 1500 ambulance transports) and consultations in doctors' offices (1,250,000 contacts) were studied for a 6-week period including the smog episode and a time interval before and thereafter. The study region was the State of North Rhine-Westfalia (16 million inhabitants), but the analysis is restricted to the comparison of the polluted area and a control area (6 million inhabitants each). During the smog period, mortality and morbidity in hospitals increased in the polluted area, but there was no substantial increase in the control area. The increases were for the total number of deaths 8 vs. 2% (polluted area vs. control area), for hospital admissions 15 vs. 3%, for outpatients 12 vs. 5% and for deliveries by ambulance to hospitals 28% in the polluted area (not investigated in the control area). The effects were more pronounced for cardiovascular diseases than for respiratory diseases. The consultations in doctors' offices show a slight decrease (-2 vs. -4%). Regression analysis shows a moderate influence of temperature, but a strong influence of ambient air pollution. The maxima of the ambient concentrations are more important on the same day, whereas the influence of the daily averages is more pronounced after a delay of 2 days. The results are discussed considering other possible confounders such as indoor pollution and psychogenic influences of the alarm situation. In total, the study suggests moderate health effects due to increased air pollution during the smog episode.

Acid Rain↗

Transformation of rat and hamster embryo cells by extracts of city smog.

Extracts of particulate matter from condensates of city air were tested for their ability to transform rat or hamster cell cultures. Uninfected rat embryo cultures were not transformed, but cultures chronically infected with Rauscher leukemia virus were transformed by benzpyrene or by extracts of city smog. The smog extracts were 600 times more active than pure benzpyrene as transforming agents. Hamster embryo cultures infected with hamster leukemia virus were equally as sensitive as leukemia-infected rat cultures to the transforming effects of smog; uninfected hamster cultures were also transformed, although tenfold higher doses of smog extract were required.

Air Pollution↗

Source reconciliation of atmospheric gas-phase and particle-phase pollutants during a severe photochemical smog episode.

A comprehensive organic compound-based receptor model is developed that can simultaneously apportion the source contributions to atmospheric gas-phase organic compounds, semivolatile organic compounds, fine particle organic compounds, and fine particle mass. The model is applied to ambient data collected at four sites in the south coast region of California during a severe summertime photochemical smog episode, where the model determines the direct primary contributions to atmospheric pollutants from 11 distinct air pollution source types. The 11 sources included in the model are gasoline-powered motor vehicle exhaust, diesel engine exhaust, whole gasoline vapors, gasoline headspace vapors, organic solvent vapors, whole diesel fuel, paved road dust, tire wear debris, meat cooking exhaust, natural gas leakage, and vegetative detritus. Gasoline engine exhaust plus whole gasoline vapors are the predominant sources of volatile organic gases, while gasoline and diesel engine exhaust plus diesel fuel vapors dominate the emissions of semivolatile organic compounds from these sources during the episode studied at all four air monitoring sites. The atmospheric fine particle organic compound mass was composed of noticeable contributions from gasoline-powered motor vehicle exhaust, diesel engine exhaust, meat cooking, and paved road dust with smaller but quantifiable contributions from vegetative detritus and tire wear debris. In addition, secondary organic aerosol, which is formed from the low-vapor pressure products of gas-phase chemical reactions, is found to be a major source of fine particle organic compound mass under the severe photochemical smog conditions studied here. The concentrations of secondary organic aerosol calculated in the present study are compared with previous fine particle source apportionment results for less intense photochemical smog conditions. It is shown that estimated secondary organic aerosol concentrations correlate fairly well with the concentrations of 1,2-benzenedicarboxylic acid in the atmospheric fine particle mass, indicating that aromatic diacids may be useful in the quantification of certain sources of secondary organic aerosol in the atmosphere.

Atmosphere↗

Carcinogenic and cocarcinogenic effects of inhaled synthetic smog and ferric oxide particles.

The carcinogenic and cocarcinogenic activity of synthetic smog, ferric oxide (Fe2O3) dust, and a mixture of the two air contaminants was determined in a long-term inhalation study with Syrian hamsters. Inhaled Fe2O3 particles definitely enhanced diethylnitrosamine tumorigenicity in the peripheral lung. Synthetic smog did not. When tested at a concentration of 40 ppm methane equivalents or 40 mg/m3, respectively, neither air pollutant by itself appeared carcinogenic. Fe2O3 caused pulmonary fibrosis and synthetic smog caused alveolar bronchiolization in many of the exposed animals.

Air Pollutants↗

The impact of aerosols on solar ultraviolet radiation and photochemical smog.

Photochemical smog, or ground-level ozone, has been the most recalcitrant of air pollution problems, but reductions in emissions of sulfur and hydrocarbons may yield unanticipated benefits in air quality. While sulfate and some organic aerosol particles scatter solar radiation back into space and can cool Earth's surface, they also change the actinic flux of ultraviolet (UV) radiation. Observations and numerical models show that UV-scattering particles in the boundary layer accelerate photochemical reactions and smog production, but UV-absorbing aerosols such as mineral dust and soot inhibit smog production. Results could have major implications for the control of air pollution.

Aerosols↗

A retrospective assessment of mortality from the London smog episode of 1952: the role of influenza and pollution.

The London smog of 1952 is one of history's most important air pollution episodes in terms of its impact on science, public perception of air pollution, and government regulation. The association between health and air pollution during the episode was evident as a strong rise in air pollution levels was immediately followed by sharp increases in mortality and morbidity. However, mortality in the months after the smog was also elevated above normal levels. An initial government report proposed the hypothesis that influenza was responsible for high mortality during these months. Estimates of the number of influenza deaths were generated using multiple methods, indicating that only a fraction of the deaths in the months after the smog could be attributable to influenza. Sensitivity analysis reveals that only an extremely severe influenza epidemic could account for the majority of the excess deaths for this time period. Such an epidemic would be on the order of twice the case-fatality rate and quadruple the incidence observed in a general medical practice during the winter of 1953. These results underscore the need for diligence regarding extremely high air pollution that still exists in many parts of the world.

Adolescent↗

Potential oxidative stress in the bodies of electric arc welding operators: effect of photochemical smog.

OBJECTIVE: To investigate whether photochemical smog emitted during the process of electric arc welding might cause oxidative stress and potential oxidative damage in the bodies of welding operators. METHODS: Seventy electric arc welding operators (WOs) and 70 healthy volunteers (HVs) were enrolled in a randomized controlled study design, in which the levels of vitamin C (VC) and vitamin E (VE) in plasma as well as the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX), and the level of lipoperoxide (LPO) in erythrocytes were determined by spectrophotometry. RESULTS: Compared with the average values of the above experimental parameters in the HVs group, the average values of VC and VE in plasma as well as those of SOD, CAT and GPX in erythrocytes in the WOs group were significantly decreased (P < 0.005-0.0001), while the average value of LPO in erythrocytes in the WOs group was significantly increased (P < 0.0001). The findings from the partial correlation analysis on the controlling of age suggested that with a prolonged duration of exposure to photochemical smog the values of VC, VE, SOD, and GPX, except for CAT, in the WOs were decreased gradually (P < 0.05-0.005), the value of LPO in the WOs was increased gradually (P < 0.001), and that with the ozone dose increased in the air in each worksite VC, VE, SOD, CAT and GPX decreased (P < 0.005-0.001), but LPO increased (P < 0.001). The findings from the reliability analysis for the VC, VE, SOD, CAT, GPX, and LPO values which were used to reflect oxidative stress and potential oxidative damage in the WOs showed that the reliability coefficients' alpha (6 items) was 0.8021, P < 0.0001, and that the standardized item alpha was 0.9577, P < 0.0001. CONCLUSION: Findings in the present study suggest that there exists an oxidative stress induced by long-term exposure to photochemical smog in the bodies of WOs, thereby causing potential oxidative and lipoperoxidative damages in their bodies.

Adult↗

[Supplementary comments on the health effects of the 1985 smog period].

This paper discusses the objections made by Hompesch (1989) in this journal against our analysis of the smog episode 1985. We consider these claims and show that the complete data from the analysis of the smog episode are widely consistent internally and with external findings. Overall as before we conclude that during the smog episode small influences of air pollution on respiratory and cardiovascular diseases and mortality have been shown.

Cardiovascular Diseases↗

[Lung function and carboxyhemoglobin during the smog episode of January 1987].

During a phase of elevated ambient air pollution in January 1987 the alert level of the smog alarm recommendation in Northrhine Westfalia (FRG) was reached. The average concentrations during examinations were 0.255 mg/m3 SO2 and 3.2 mg/m3 CO at the closest station. In 111 healthy persons in Cologne and Düsseldorf, resistance measured by oscillatory method was elevated during this period compared to control examinations. In 59 patients with moderate airway-obstruction from different parts of West Germany lung function showed further deterioration during the smog phase: Airway resistance measured by body-plethysmography was higher than during a control period, FVC, FEV1, PEF and MEF75 were decreased. Finally levels of carboxyhemoglobin in blood also were increased in 46 healthy nonsmokers. The investigation shows, that even in moderate smog episodes (compared to earlier years) small, but consistent changes of lung function parameter can be measured.

Adolescent↗

[An investigation on the mortality during a smog situation in western Ruhrgebiet on the 17. January 1979 (author's transl)].

A smog-warning of the first degree was announced on the 19th January 1979 for the first time after the institution of the so called Smog-decree in Northrhine-Westphalia. This warning was calceled after a few hours, already. The mortality in the relevant areas did not increase during this period. The adequacy of the 1st stage of the smog-warning was thus confirmed. This stage signifies a prewarning, which indicates a situation with no expected harmful effects of air-pollution on the population.

Emergencies↗

The sequestration of ethane on Titan in smog particles.

Saturn's largest satellite, Titan, has a dense atmosphere of nitrogen with a few per cent of methane. At visible wavelengths its surface is hidden by dense orange-brown smog, which is produced in the stratosphere by photochemical reactions following the dissociation of methane by solar ultraviolet light. The most abundant of the products of these reactions is ethane, and enough of it should have been generated over the life of the Solar System to form a satellite-wide ocean one kilometre deep. Radar observations have found specular reflections in 75 per cent of the surface spots observed, but optical searches for a sun-glint off an ocean have been negative. Here I explain the mysterious absence or rarity of liquid ethane: it condenses onto the smog particles, instead of into liquid drops, at the cold temperatures in Titan's atmosphere. This dusty combination of smog and ethane, forming deposits several kilometres thick on the surface, including the observed dunes and dark areas, could be named 'smust'. This satellite-wide deposit replaces the ocean long thought to be an important feature of Titan.

Journal Article↗

Mortality during winter smog episodes 1982, 1985, 1987 and 1993 in the Czech Republic.

OBJECTIVES: Severe air pollution episodes were recorded during the 1980s and early 1990s in the Czech Republic as a result of widespread combustion of brown coal. A population-based retrospective study investigated the relationship between air pollution and daily mortality in six highly polluted areas of the Czech Republic during smog episodes in 1982, 1985, 1987, and 1993. METHODS: Total daily mortality, mortality by gender and age, cardiovascular mortality, respiratory mortality, data on weekly incidence of acute respiratory diseases and daily mean concentrations of sulphur dioxide and suspended particulate matter were used in the model. The effects of smog on daily mortality were estimated by multiple linear regression analysis. RESULTS: Significant increases in mortality were observed for the 1982 and 1987 episodes (6% and 9%). In 1982, mortality was significantly associated with mean concentration of sulphur dioxide (SO2) of the current and the preceding days and with the 4-day moving average. In the 1985 episode a significant increase in respiratory mortality in men and in both genders together, lagging by 2 and 3 days, was detected. During the 1987 episode significant associations of total daily mortality, mortality in persons over 65 years of age and mortality from cardiovascular or respiratory diseases with 4-day moving average of both pollutants were found. For the 1993 episode a significant association between mortality in women under 65, lagging by 3 days, and mean concentration of suspended particulate matter (SPM) was observed. CONCLUSIONS: Most of the results are consistent with other studies aimed at episodic air pollution during the 1950s and 1960s in Western Europe and the USA, in which outdoor air pollution was shown to be a significant predictor of mortality. However, non-significant or opposite associations between air pollution and mortality indicate that other factors may also play an important role. A stronger effect on men under 65 years of age, suggested by a previous Czech study was not confirmed.

Czech Republic↗

Acute respiratory effects of summer smog in primary school children.

In 535 primary school children we studied the effects of exposure to summer smog on respiratory health. Baseline measurements were performed during low air pollution levels (max. 24-h concentrations of SO2, O3 and NO2 were 55, 49 and 58 micrograms/m3, respectively) consisting of lung function measurements using spirometry and the forced oscillation technique (FOT) and the prevalence of respiratory symptoms, determined by a written questionnaire. During a summer smog episode, 212 randomly chosen children were re-examined, characterised by 8-h ozone levels > 120 micrograms/m3 (max. 163 micrograms/m3) and 1-h ozone levels > 160 micrograms/m3 (max. 215 micrograms/m3). Overall, small decrements were observed in the forced expiratory volume in 1 s (FEV1), (P < 0.05) and the forced expiratory volume between 25 and 75% of the vital capacity (FEF25-75%) (P < 0.01). On the contrary, there was a statistically significant decrease in resistance parameters. No increases were observed in the prevalence of acute respiratory symptoms. In conclusion, in this study we found small inconsistent changes in lung function and no increase of respiratory symptoms after short-time exposure to moderately high ozone levels.

Acute Disease↗