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PubMed1996

Low-level air pollution and hospital admissions for cardiac and cerebrovascular diseases in Helsinki.

OBJECTIVES: This study investigated whether low concentrations of ambient air pollutants are associated with hospital admissions for ischemic cardiac and cerebrovascular diseases. METHODS: Associations between daily concentrations of sulfur dioxide, nitric oxide, nitrogen dioxide, ozone, and particulates and daily hospital admissions due to ischemic cardiac and cerebrovascular diseases were studied in Helsinki, Finland, 1987 through 1989. The regression analyses controlled for weather, day of the week, season, long-term trends, and influenza epidemics. RESULTS: Admissions via emergency rooms due to ischemic cardiac diseases (n = 7005) were significantly associated with the prevailing levels of nitric oxide and ozone, and those due to cerebrovascular diseases (n = 3737) were associated with nitrogen dioxide; these levels were only moderate. Long-term transient myocardial ischemic attacks were related to particulates, and short-term ischemic attacks were related to nitrogen dioxide. CONCLUSIONS: Symptoms of ischemic cardiac and cerebrovascular diseases may be provoked by pollutants in concentrations lower than those given as guidelines in many countries and lower than previously shown.

Air Pollutants↗

PubMedDate not supplied

The Po River Delta (north Italy) indoor epidemiological study: effects of pollutant exposure on acute respiratory symptoms and respiratory function in adults.

The authors studied the effects of relatively low doses of nitrogen dioxide and respirable suspended particulate matter (i.e., < 2.5 mu) on acute respiratory symptoms and on peak expiratory flow in 383 adults (15-72 yr of age) who lived in the Po River Delta area, located near Venice. During 2 wk-1 wk in winter and 1 wk in summer--the authors monitored each participant's house to measure nitrogen dioxide (in parts per billion) and respirable suspended particulate (microgram/m3) concentration. Information on sex, age, height, weight, daily activity patterns, active and passive smoking, chronic respiratory diseases, daily peak expiratory flow, and presence of acute respiratory symptoms during the weeks monitoring occurred were also collected. Peak expiratory flow variation was studied as mean amplitude percentage (i.e., amplitude/mean) and percentage of diurnal variation (maximum/minimum). The exposure indices to nitrogen dioxide (nitrogen dioxide--index of exposure) and to respirable suspended particulate matter (respirable suspended particulate matter-index of exposure) were computed as the product of pollutant concentration and time of exposure. The authors considered indices as "low" or "high" on the basis of the median value. The median nitrogen dioxide was 20 ppb in winter and 14 ppb in summer; the highest nitrogen dioxide levels occurred in the kitchen in the winter (33 ppb) and summer (20 ppb). The median respirable suspended particulate matter was 68 micrograms/m3 in winter and 45 micrograms/m3 in summer. Only in winter were there significant associations between bronchitic/asthmatic symptoms and "high" nitrogen dioxide and respirable suspended particulate matter indices. In subjects who did not smoke, a significant influence of the "high" respirable suspended particulate matter-index of exposure was also observed in summer. With respect to peak expiratory flow and its variability, respirable suspended particulate matter-index of exposure was associated with an increase of both amplitude/mean and maximum/mean; however, with respect to the nitrogen dioxide--index of exposure, the association was significant only in subjects with chronic respiratory diseases (i.e., asthma and bronchitis). These relationships were significant only in winter. In conclusion, the results of the current study indicate that there is an association between relatively low doses of pollutants and acute respiratory symptoms and peak expiratory flow in adults.

Acute Disease↗

PubMed1998

[Asthma and household chemical pollutants (with the exception of tobacco)].

The relationship between allergens in a domestic environment and asthma has been extensively studied and it is only recently that studies have suggested the possibility of the role of chemical pollutants in the internal environment in the genesis of asthma. The pollutants studied are oxides of nitrogen (nitrogen dioxide NO2), volatile organic components (COV), formaldehyde, ozone (O3) and sulphur dioxide (SO2). The level of nitrogen dioxide in the interior of houses may be greater than those met outside. Normal values are 400 mcg per metre3 per hour and 150 mcg per metre3 in twenty four hours. In asthmatics challenge test to nitrogen dioxide and epidemiological studies suggest that internal nitrogen dioxide is capable of provoking asthmatic crises either by a direct pollutant effect or by potentialising the allergenic crises either by a direct pollutant effect or by potentialising the allergenic response of the bronchi. COV and formaldehyde are liberated by urea formaldehyde foams and by chipboard furniture. The levels of COV and formaldehyde inside a house may be up to 10 times higher than those outside. COV and formaldehyde perhaps would have an effect on the bronchi in asthmatics at significant levels which are rarely found in the domestic environment. Ozone is an external pollutant. However, from 5-80% of the external concentrations may be found inside some locations. Thus, in certain conditions which are relatively rare, the interior concentrations of dwelling places may attain levels which are capable of inducing, in healthy subjects who are sensitive to ozone, a drop in the FEV1. As regards asthmatics, only experimental work has been able to show any bronchospastic effect of ozone, either by a direct effect on the bronchi or by the potentiation of a bronchial response to allergens. It would be convenient to perform some epidemiological studies to determine if there is a relationship between exposure to ozone internally and to bronchial changes. The concentrations of SO2 inside houses increases when coal is burnt. The levels provoking a bronchial reaction are much greater than those found inside houses. The data and the literature which is mostly recent seems to stress the role of NO2 ozone and SO2 as a factor which might favour asthmatic crises induced by allergens in atopic subjects. However, other studies will be necessary to confirm the initial data.

Adult↗

PubMed1997

Genetic modeling of susceptibility to nitrogen dioxide-induced lung injury in mice.

We investigated the mode of inheritance of susceptibility to nitrogen dioxide (NO2)-induced lung injury in inbred mice. Susceptible C57BL/6J (B6) and resistant C3H/HeJ (C3) mice, as well as F1, F2, and backcross (BX) populations derived from them, were exposed to 15 parts per million NO2 for 3 h. Six hours after exposure, animals were lavaged, and differential cell counts and cell viability (cytotoxicity) were measured. Statistically significant (P < 0.05) differences in numbers of lavageable macrophages, epithelial cells, and dead cells were found between inbred strains. Distributions of cellular responses in F1 progeny overlapped both progenitors, and mean responses were intermediate. In C3:BX progeny, ranges of responses to NO2 closely resembled C3 mice, and means were not significantly different between populations. Ranges of cellular responses to NO2 in B6:BX and intercross progeny overlapped both progenitors; mean responses of both populations were intermediate to progenitors. Segregation analyses tested goodness of fit of phenotyping data with various inheritance models, and the highest likelihood for each cell response to NO2 was for the hypothesis two-unlinked loci general. We conclude that there are likely two major unlinked genes that account for differential susceptibility to acute NO2 exposure. The chromosomal location of the genes is not known.

Animals↗

PubMed1994

Nitrogen dioxide-induced phosphatidylserine biosynthesis and subcellular translocation in cultured pulmonary artery endothelial cells.

Exposure to nitrogen dioxide (NO2) increases phosphatidylserine (PS) content in the plasma membranes of pulmonary artery endothelial cells (PAEC). We examined whether the increased PS content is associated with increased uptake of L-serine and/or biosynthesis of PS. Exposure to 5 ppm NO2 increased uptake and incorporation of exogenous L-[14C]serine into whole cells, total cellular lipids, phospholipids, and phospholipid subclasses compared to control. Incorporation of L-[14C]serine into the total lipid extracts from isolated plasma membranes, mitochondria, and microsomes from NO2-exposed cells was increased by 45, 32, and 31%, respectively (p < 0.05 for all membranes). Increased incorporation of L-[14C]serine into the total phospholipids of plasma membranes, mitochondria, and microsomes of NO2-exposed cells was increased by 31, 48, and 33%, respectively (p < 0.05 for all membranes). Incorporation of L-[14C]serine into the PS of plasma membranes and microsomes from NO2-exposed cells was increased by 63 and 89%, respectively (p < 0.05 for both membranes). The incorporation of radioactivity from L-[14C]serine into the phosphatidylethanolamine and phosphatidylcholine contents of plasma membranes, mitochondria, and microsomes from NO2-exposed cells was also observed. Exposure of PAEC to NO2 resulted in a significant (p < 0.01) increase in the activity of PS synthase, the serine base-exchange enzyme located in the microsomes of these cells. When L-[14C]serine-prelabeled microsomes were incubated with unlabeled mitochondria from control and NO2-exposed cells, transfer of PS-derived radioactivity from microsomes to mitochondrial phospholipids was observed. These results demonstrate that exposure to NO2 increases uptake and incorporation of exogenous serine as well as intracellular biosynthesis of PS, resulting in increases in the PS content of PAEC and their plasma membranes.

Analysis of Variance↗

PubMed1996

Nitrogen dioxide-induced expression of a 78 kDa protein in pulmonary artery endothelial cells.

Exposure to nitrogen dioxide (NO2) activates signal transduction in cultured pulmonary artery endothelial cells (PAEC). We examined whether NO2-induced activation of signal transduction results in increased expression of proteins in PAEC. Exposure to 5 ppm NO2 for 4, 12, and 24 h had no significant effect on total protein synthesis. However, two-dimensional gel electrophoresis of [35S]-methionine-labeled PAEC exposed to NO2 for 24 h, but not 4 and 12 h, demonstrated increased synthesis of several proteins including a two- to five-fold increase of some proteins with molecular masses of 47, 64, 78, and 105 kDa compared to controls. N-terminal amino acid sequencing and immunodetection analysis identified the 78 kDa protein as 78 kDa glucose-regulated protein (GRP-78). Induction of GRP-78 by NO2 exposure was regulated at the transcriptional level, and the induction required de novo protein synthesis. Exposure to NO2 for 24 h also significantly (p < .05) decreased glycosylation of proteins in PAEC. Exposure of cell monolayers to tunicamycin, an inhibitor of protein glycosylation, mimicked the effect of NO2 exposure on expression of GRP-78. Increased expression of GRP-78 was also detected when cell monolayers were exposed to the calcium ionophore A 23187, to 2-deoxyglucose, or to glucose-free medium, which are also known to cause perturbations in protein glycosylation. These results demonstrate that exposure to NO2 increases expression of a number of proteins including GRP-78 in PAEC. Increased expression of GRP-78 in NO2-exposed cells appears to be associated with inhibition of glycosylation or through coordinated alterations in metabolic events that lead to inhibition of protein glycosylation.

Amino Acid Sequence↗

PubMed2003

Effect of short-term exposure to gaseous pollution on asthma hospitalisation in children: a bi-directional case-crossover analysis.

STUDY OBJECTIVE: Assess associations between short-term exposure to gaseous pollutants and asthma hospitalisation among boys and girls 6 to12 years of age. DESIGN: A bi-directional case-crossover analysis was used. Conditional logistic regression models were fitted to the data for boys and girls separately. Exposures averaged over periods ranging from one to seven days were used to assess the effects of gaseous pollutants on asthma hospitalisation. Estimated relative risks for asthma hospitalisation were calculated for an incremental exposure corresponding to the interquartile range in pollutant levels, adjusted for daily weather conditions and concomitant exposure to particulate matter. SETTING: Toronto, Ontario, Canada. PARTICIPANTS: A total of 7319 asthma hospitalisations for children 6 to 12 years of age (4629 for boys and 2690 for girls) in Toronto between 1981 and 1993. MAIN RESULTS: A significant acute effect of carbon monoxide on asthma hospitalisation was found in boys, and sulphur dioxide showed significant effects of prolonged exposure in girls. Nitrogen dioxide was positively associated with asthma admissions in both sexes. The lag time for certain gaseous pollutant effects seemed to be shorter in boys (around two to three days for carbon monoxide and nitrogen dioxide), as compared with girls (about six to seven days for sulphur dioxide and nitrogen dioxide). The effects of gaseous pollutants on asthma hospitalisation remained after adjustment of particulate matter. The data showed no association between ozone and asthma hospitalisation in children. CONCLUSIONS: The study showed positive relations between gaseous pollutants (carbon monoxide, sulphur dioxide, and nitrogen dioxide) at comparatively low levels and asthma hospitalisation in children, using bi-directional case-crossover analyses. Though, the effects of certain specific gaseous pollutants were found to vary in boys and girls.

Air Pollutants↗

PubMed1996

Air pollution and daily mortality in London: 1987-92.

OBJECTIVE: To investigate whether outdoor air pollution levels in London influence daily mortality. DESIGN: Poisson regression analysis of daily counts of deaths, with adjustment for effects of secular trend, seasonal and other cyclical factors, day of the week, holidays, influenza epidemic, temperature, humidity, and autocorrelation, from April 1987 to March 1992. Pollution variables were particles (black smoke), sulphur dioxide, ozone, and nitrogen dioxide, lagged 0-3 days. SETTING: Greater London. OUTCOME MEASURES: Relative risk of death from all causes (excluding accidents), respiratory disease, and cardiovascular disease. RESULTS: Ozone levels (same day) were associated with a significant increase in all cause, cardiovascular, and respiratory mortality; the effects were greater in the warm seasons (April to September) and were independent of the effects of other pollutants. In the warm season an increase of the eight hour ozone concentration from the 10th to the 90th centile of the seasonal change (7-36 ppb) was associated with an increase of 3.5% (95% confidence interval 1.7 to 5.3), 3.6% (1.04 to 6.1), and 5.4% (0.4 to 10.7) in all cause, cardiovascular, and respiratory mortality respectively. Black smoke concentrations on the previous day were significantly associated with all cause mortality, and this effect was also greater in the warm season and was independent of the effects of other pollutants. For black smoke an increase from the 10th to 90th centile in the warm season (7-19 microg/m3) was associated with an increase of 2.5% (0.9 to 4.1) in all cause mortality. Significant but smaller and less consistent effects were also observed for nitrogen dioxide and sulphur dioxide. CONCLUSION: Daily variations in air pollution within the range currently occurring in London may have an adverse effect on daily mortality.

Air Pollutants↗

PubMed1989

Potentiation of the expression of nitrogen dioxide-induced lung injury by postexposure exercise.

Previous investigations have indicated that postexposure exercise (E) can can potentiate nitrogen dioxide (NO2)-induced lung injury. In this report, we (1) further characterize the potentiation of expression of NO2-induced lung injury in the rat by E; (2) characterize the postexposure period during which such potentiation by E can occur, i.e., "window of susceptibility"; (3) assess whether two E bouts performed during the "window of susceptibility" have even greater potentiating effects; and (4) determine if early postexposure E can extend the window of susceptibility. Groups of Fischer-344 rats were exposed to 100 ppm NO2 for 15 min, exercised at times ranging from 30 min to 24 hr thereafter, and sacrificed during a 24-hr postexposure period. Other exposed rats were exercised 30 min to 24 hr thereafter and sacrificed for lung studies 30 min following the E runs. Still other exposed animals were exercised immediately and at 8 or 24 hr postexposure and sacrificed 30 min after the last E run. NO2-exposed but rested rats, and sham-air-exposed and rested or exercised rats served as controls. E immediately or at 8 hr post-NO2 exposure caused marked increases in lung wet weight (LWW) and right cranial lobe dry weights (RCLDW) and more pronounced histopathologic disturbances beyond those following NO2 exposure and rest only. Potentiation of injury was not observed in rats exercised 24 hr after exposure. The pattern of subsidence of the LWW and RCLDW increases after immediate or 8 hr E differed with the increases in the former being more persistent. Two E bouts (30 min and 8 hr postexposure) caused lung changes consistent with an additive effect. E performed immediately after NO2 exposure extended the window of susceptibility to E beyond 24 hr.

Animals↗

PubMed1978

Nitrogen dioxide-induced pulmonary disease: five new cases and a review of the leterature.

Twenty-three patients exposed to nitrogen dioxide in agriculture or industry were referred to the University of Wisconsin Medical Center. Eighteen experienced a transient upper respiratory tract syndrome; five developed pulmonary edema or bronchiolitis obliterans. This latter group responded to steroid therapy but all demonstrated evidence of persistent pulmonary dysfunction on follow-up studies. Combining our findings with those in the literature we concluded: (1) exposure to NO2 is more common than generally appreciated; (2) case fatality is high--29% for silo-filler's disease; (3) steroids are effective therapy and should be continued for at least eight weeks; (4) although the majority recover without significant sequelae, some individuals may develop persistent functional abnormalities; (5) there is no evidence that long-term exposure to low concentrations of NO2 leads to chronic airway obstruction; and, (6) NO2-induced pulmonary disease could be elminated with appropriate preventive measures.

Adult↗

PubMed2005

Roadside concentration of gaseous and particulate matter pollutants and risk assessment in Dar-es-Salaam, Tanzania.

This study used manual air sampling method to assess the contribution of road traffic to air pollution level in Dar-es-Salaam City, Tanzania. Samples were collected from 11 different sites. Parameters measured were: sulphur dioxide using pararosaniline method, nitrogen dioxide using saltzman method, particulate matter and particulate lead using filtration method and atomic absorption spectrometric method, respectively. Results showed that hourly average sulphur dioxide concentration range from 127 to 1385 microg/m3. The measured values of sulphur dioxide were above the recommended WHO guidelines with an hourly objective value of 350 microg/m3 at 87% of the sampling sites. The hourly average nitrogen dioxide concentration ranged from 18 to 53 microg/m3. The maximum hourly nitrogen dioxide concentration at 53 microg/m3 was below the WHO guideline value of 200 microg/m3. The hourly average suspended particulate matter (SPM) ranged from 98 to 1161 microg/m3, exceeding the recommended value of 230 microg/m3 by WHO at 87% of the sampling sites. The hourly average lead concentration was found to range from 0.60 to 25.6 microg/m3, exceeding again the WHO guideline value of 1.5 microg/m3 at 83% of the sampling sites. Results predicted by Gaussian model when compared with the measured values were found to have a correlation coefficient of 0.8, signifying a good correlation. The risk assessment was undertaken considering the people who spend a significant portion of their time near the roads, such as the Uhuru primary school pupils and the adult population who reside by the roadside. The unit risk realised was 18.2 x 10(-6) for adult population and 2.2 x 10(-6) for pupils, both scenarios showing risk higher than the United Sates of America Environmental Protection Agency (USEPA) acceptable limit of 1 x 10(-6). Considering the magnitude of the problem at hand, this study recommends an introduction of mandatory emission tests of SPM, lead and sulphur dioxide (SO2). The study further recommends the introduction of continuous and/or regular air quality monitoring and the use non-leaded petrol in Tanzania.

Air Pollutants↗

PubMed1977

A new personal dosimeter for the monitoring of industrial pollutants.

A new passive sampling device (GASBADGE dosimeter) has been developed for personal/ambient monitoring of industrial air pollutants. Compact and convenient to use (no pump, wet chemicals, or length of stain estimation required, etc.), it may be either worn or used for area monitoring. The operating principle is based upon Fick's first law of diffusion. Analysis of the collection element after exposure yields the time-weighted (TWA) exposure concentration. Promising results have been obtained to date in controlled exposures with sulfur dioxide and nitrogen dioxide. Preliminary data also indicate the applicability of the GASBADGE dosimeter to the monitoring of a wide variety of organic vapors.

Air Pollutants↗

PubMed1996

Association between air pollution and acute childhood wheezy episodes: prospective observational study.

OBJECTIVE: To examine the association between the air pollutants ozone, sulphur dioxide, and nitrogen dioxide and the incidence of acute childhood wheezy episodes. DESIGN: Prospective observational study over one year. SETTING: District general hospital. SUBJECTS: 1025 children attending the accident and emergency department with acute wheezy episodes; 4285 children with other conditions as the control group. MAIN OUTCOME MEASURES: Daily incidence of acute wheezy episodes. RESULTS: After seasonal adjustment, day to day variations in daily average concentrations of ozone and sulphur dioxide were found to have significant associations with the incidence of acute wheezy episodes. The strongest association was with ozone, for which a non-linear U shaped relation was seen. In terms of the incidence rate ratio (1 at a mean 24 hour ozone concentration of 40 microg/m3 (SD=19.1)), children were more likely to attend when the concentration was two standard deviations below the mean (incidence rate ratio=3.01; 95% confidence interval 2.17 to 4.18) or two standard deviations above the mean (1.34; 1.09 to 1.66). Sulphur dioxide had a weaker log-linear relation with incidence (1.12; 1.05 to 1.19 for each standard deviation (14.1) increase in sulphur dioxide concentration). Further adjustment for temperature and wind speed did not significantly alter these associations. CONCLUSIONS: Independent of season, temperature, and wind speed, fluctuations in concentrations of atmospheric ozone and sulphur dioxide are strongly associated with patterns of attendance at accident and emergency departments for acute childhood wheezy episodes. A critical ozone concentration seems to exist in the atmosphere above or below which children are more likely to develop symptoms.

Acute Disease↗

PubMed1996

Air pollution and daily mortality in three Swiss urban areas.

Particulate air pollution, in association with other common urban air pollutants, has been associated with various measured health endpoints, including the incidence and duration of respiratory symptoms, lung function, absence from work or school due to respiratory illness, hospitalization for respiratory disease, and cardiopulmonary disease mortality. In this study, the association between daily mortality and air pollution was assessed in Zurich, Basle, and Geneva (Switzerland) for the time period 1984 through 1989. Various regression modeling techniques were used to estimate the effect of air pollution on mortality, to control for time trends, seasonal factors, and weather variables, and to assess the sensitivity of the results. A positive, statistically significant association between daily mortality counts and measures of ambient air pollution in all three cities was observed. Mortality was associated with total suspended particulate pollution, sulfur dioxide, and nitrogen dioxide. The strongest association was with a 3-day moving average (including the concurrent day and the preceding 2 days) of these pollutants. The estimated mortality-air pollution effects were not highly sensitive to regression modeling techniques used to control for seasonality, long-term trends, and weather variables.

Aged↗

PubMedDate not supplied

Importance of the indoor environment in air pollution exposure.

A portable personal air pollution sampler was used to measure the exposure of twenty children to respirable particulates, sulfur dioxide, and nitrogen dioxide over a 24-hour period. Particulate exposures were significantly higher among children who lived with one or more smokers, and exceeded the primary air quality standard in nineteen of the twenty subjects. To a large extent, an individual's respirable particulate load appears to be determined by exposure to indoor rather than outdoor pollutants.

Adolescent↗

PubMed2004

Air pollution and sudden infant death syndrome.

BACKGROUND: Sudden infant death syndrome (SIDS) affects approximately 1 in 1000 live births and is the most common cause of infant death after the perinatal period. OBJECTIVE: To determine the influence of air pollution on the incidence of SIDS. METHODS: Time-series analyses were performed to compare the daily mortality rates for SIDS and the daily air pollution concentrations in each of 12 Canadian cities during the period of 1984-1999. Serial autocorrelation was controlled for by city, and then the city-specific estimates were pooled. Increased daily rates of SIDS were associated with increases, on the previous day, in the levels of sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide but not ozone or fine particles measured every sixth day. Effects persisted despite adjustments for season alone or the combination of daily mean temperature, relative humidity, and changes in barometric pressure for NO2 and SO2 but not carbon monoxide. RESULTS: Increases in both SO2 and NO2, equivalent to their interquartile ranges, were associated with a 17.72% increase in SIDS incidence. CONCLUSION: Ambient SO2 and NO2 may be important risk factors for SIDS.

Air Pollutants↗

PubMed2001

The potential impacts of climate variability and change on air pollution-related health effects in the United States.

Climate change may affect exposures to air pollutants by affecting weather, anthropogenic emissions, and biogenic emissions and by changing the distribution and types of airborne allergens. Local temperature, precipitation, clouds, atmospheric water vapor, wind speed, and wind direction influence atmospheric chemical processes, and interactions occur between local and global-scale environments. If the climate becomes warmer and more variable, air quality is likely to be affected. However, the specific types of change (i.e., local, regional, or global), the direction of change in a particular location (i.e., positive or negative), and the magnitude of change in air quality that may be attributable to climate change are a matter of speculation, based on extrapolating present understanding to future scenarios. There is already extensive evidence on the health effects of air pollution. Ground-level ozone can exacerbate chronic respiratory diseases and cause short-term reductions in lung function. Exposure to particulate matter can aggravate chronic respiratory and cardiovascular diseases, alter host defenses, damage lung tissue, lead to premature death, and possibly contribute to cancer. Health effects of exposures to carbon monoxide, sulfur dioxide, and nitrogen dioxide can include reduced work capacity, aggravation of existing cardiovascular diseases, effects on pulmonary function, respiratory illnesses, lung irritation, and alterations in the lung's defense systems. Adaptations to climate change should include ensuring responsiveness of air quality protection programs to changing pollution levels. Research needs include basic atmospheric science work on the association between weather and air pollutants; improving air pollution models and their linkage with climate change scenarios; and closing gaps in the understanding of exposure patterns and health effects.

Aerosols↗

PubMed1980

[Evaluation of the MPEL for SO2 and NO2 and the development of new MPELs for atmospheric pollutants based on modern epidemiological, ecological and toxicological studies].

Proceeding from modern experimental and natural observations on the effect of sulphur dioxide and nitrogen dioxide on live organism and environment, the now, operative in Bulgaria maximum allowable concentrations of these contaminants are reassessed. The maximal single and mean diurnal SO2 MAC are proposed to be reduced to 0.15 mg/m3 and 0.03 mg/m3, while those of NO2 remain the same. Based on data available in modern literature and equations proposed by the authors for express determination of MAC for some atmosphere contaminants, MAC for some nonstandardized contaminants in Bulgaria are suggested: ozone (maximal single - 0.06 mg/m3 and mean diurnal - 0.03 mg/m3 asbestos (mean dirnal - 0.25 fibers/cm3), zinc (mean diurnal - 0.05 mg/m3, copper (mean diurnal - 0.01 mg/m3. The use of mathematical equations for determination of MAC of differrent hydrocarbons is suggested.

Air Pollutants↗