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PubMed1995

Air pollution and allergic disease. Report of a Working Party of the British Society for Allergy and Clinical Immunology.

Asthma and other types of allergic disease such as allergic rhinitis are increasing in prevalence throughout the western world. This report has reviewed the available world literature to examine the evidence that this increase is related to air pollution and to identify areas of uncertainty which need further research. We have restricted our review to aspects which are of direct relevance to allergic disease. In particular we have not addressed links between air pollution and increased cardio-respiratory mortality. There is good evidence that a number of air pollutants including sulphur dioxide, nitrogen dioxide, ozone and particulates, if present at sufficiently high concentrations, can exacerbate existing allergic disease, particularly asthma. Such concentrations are not infrequently found in the U.K. during episodes of poor air quality. The evidence that air pollutants cause problems at concentrations below internationally accepted guidelines (which are not, however, comprehensive) is not conclusive, although there is no room for complacency. In view of the frequency with which guidelines are breached and the risk to health this poses, the working group regard reducing air pollution in the U.K. as an important priority. The evidence that air pollutants, either from 'old style' fossil fuel burning, or from automobiles has contributed to the increase in the prevalence of asthma and allergy, other than through unmasking occult disease, is inconclusive although definitive studies are lacking. Similarly evidence to support the hypothesis that air pollutants act as adjuvants to increase the risk of becoming atopic is weak. The working party recommends detailed and comprehensive monitoring of air pollution concentrations across the U.K., development of techniques to measure individual exposure, research into the interaction between air pollutants and allergens and a major research effort into the effects of particulates. We would also welcome large, long-term, cohort studies to answer as definitively as possible whether exposure to increased air pollution increases the risk of becoming allergic.

Air Pollution↗

PubMed1997

Use of unvented residential heating appliances--United States, 1988-1994.

Many heating appliances rely on combustion of carbon-based fuels and therefore are potential sources of health-threatening indoor air pollution. Most combustion heating appliances are vented to the outside of buildings to facilitate removal of the products of combustion, which include carbon monoxide (CO), carbon dioxide, nitrogen dioxide, and water vapor. However, some combustion heating devices may be unvented (e.g., kerosene- and propane-fueled space heaters, some gas-fueled log sets, and cooking devices used improperly for heating), and the use of such unvented devices in closed settings may be associated with risks for exposure to toxic gases and other emissions. This report presents an analysis of data from the Third National Health and Nutrition Examination Survey (NHANES III) to estimate the number and regional distribution of adults using unvented residential heating appliances and stoves or ovens misused as heating devices in the United States during 1988-1994. The findings indicate that the percentage of adults using these devices was higher in the South, among low-income groups, among blacks, and among rural residents, and underscore the need for public education about the health risks associated with exposure to elevated levels of combustion by-products. NHANES III collected data from approximately 20,000 adults about household characteristics, including the prevalence of various types of residential heating appliances, the use of unvented combustion space heaters, and use of stoves or ovens specifically for heating during the previous year. NHANES weights were used to obtain national estimates based on these responses. Because responses by race/ethnicity other than for whites and blacks were too small for reliable estimates, responses from all others were combined.

Air Pollution, Indoor↗

PubMed1994

Nitrogen dioxide-induced eosinophilia and mucosal injury in the nose of the guinea pig.

Nitrogen dioxide exposure-induced mucosal pathology of the guinea pig nose was studied. Guinea pigs were exposed to 3 ppm or 9 ppm of nitrogen dioxide for 6 h a day, 6 times weekly for 2 weeks, and sacrificed 24 h after the final exposure. Exposure to 3 ppm of nitrogen dioxide resulted in decreased ciliary activity and slight eosinophil accumulation on the epithelium and submucosal layer. More serious pathologies were observed in the nose of guinea pigs exposed to 9 ppm of nitrogen dioxide, including a more prominent eosinophil influx to the epithelium and epithelial injury due to activation of eosinophils. Epithelial damage induced by nitrogen dioxide could lead to hyperresponsiveness and may result in a prolonged allergic inflammation. Our study suggests that environmental nitrogen dioxide may contribute to hyperresponsiveness and thus be involved in the increased morbidity of allergic rhinitis.

Animals↗

PubMed1993

Nitrogen dioxide-induced eosinophilia and mucosal injury in the trachea of the guinea pig.

Nitrogen dioxide exposure-induced mucosal pathology of the guinea pig trachea was studied. Exposure to 3 or 9 ppm of nitrogen dioxide for 6 h a day, 6 times weekly for 2 weeks resulted in decreased ciliary activity as well as a dramatic eosinophil accumulation to the epithelium and submucosal layer. Especially exposure to 9 ppm of nitrogen dioxide induced epithelial injury through the activation of eosinophils accumulated in the tracheal mucosa. The epithelial damage induced by nitrogen dioxide could lead to hyperresponsiveness and prolonged allergic inflammation. Our study suggests that environmental nitrogen dioxide could contribute to the hyperresponsiveness and could most probably be involved in the development and chronicity of airway allergic disorders.

Animals↗

PubMed1982

[Occurrence of carbon monoxide, carbon dioxide and nitrogen oxides during the use of gas stoves].

The concentrations of carbon monoxide, carbon dioxide, nitrogen monoxide and nitrogen dioxide arising from gas burning have been measured under experimental and field conditions. In the test room propane, butane and town-gas have been burned, whereas in the apartments investigated only town-gas has been used. The most important influence on the concentration of the four substances arises from the changes in the burning conditions of the flame. Laboratory experiments have been carried out in the test room with open flames and with an aluminum block or a kettle on the flame. The following results have been obtained: (a) for CO the lowest concentration is obtained with open flames irrespective of the type of gas burned. Higher concentrations have been found with aluminum blocks, whereas the highest concentrations were associated with the use of kettles and pots, (b) the experimental conditions have only a small influence on the CO2 concentration, (c) NO concentrations are influenced by the gas type and by the experimental conditions. They are low with kettles but high with open flames, (d) NO2 concentrations are less influenced by the experimental conditions than are NO concentrations. The results of more than 1000 paired determinations of NO2 in kitchen and other rooms are presented. The concentrations which have been measured using diffusion tubes according to Palmes which were exposed for 48 h, were highest in kitchens of dwellings fully equipped with gas devices (heating, cooking, warming water). The mean value of the concentrations was about 50 micrograms/m3, whereas the mean for dwellings without any gas device has been found to be lower than 20 micrograms/m3.

Air Pollutants↗

PubMedDate not supplied

Nitrogen dioxide-induced reactive oxygen intermediates production by human alveolar macrophages and peripheral blood mononuclear cells.

Alveolar macrophages located on the alveolar surface have contact with air pollutants. We evaluated the dose-dependent effect of nitrogen dioxide exposure on the oxidative metabolism of alveolar macrophages and peripheral blood mononuclear cells by measuring the spontaneous and stimulated reactive oxygen intermediates production. Alveolar macrophages or peripheral blood mononuclear cells were placed on a polycarbonate membrane, which was in direct contact with the surface of a nutrient reservoir. The cells were exposed to nitrogen dioxide during different periods of time, varying between 30 and 120 min at concentrations ranging from 0.1 to 0.5 ppm. Exposure of alveolar macrophages to nitrogen dioxide for 30 min yielded a dose-dependent stimulation of reactive oxygen intermediates generation of 1.7- to 2.9-fold of control. An 120-min exposure to nitrogen dioxide at concentrations between 0.1 and 0.5 ppm resulted in a similar reactive oxygen intermediates production of about 1.9- to 2.2-fold of control at all concentrations tested. The nitrogen dioxide exposure to peripheral blood mononuclear cells yielded identical results. These experiments demonstrate that alveolar macrophages and peripheral blood mononuclear cells become activated by nitrogen dioxide and that concentrations up to 0.5 ppm nitrogen dioxide induce an increase in reactive oxygen intermediates production after 30 to 120 min exposure of the cells.

Aged↗

PubMedDate not supplied

Enhancement of nitrogen dioxide-induced lipid peroxidation and DNA strand breaking by cysteine and glutathione.

Nitrogen dioxide less than 100 ppm in air induced lipid peroxidation of liposome composed of 1-palmitoyl-2-arachidonylphosphatidylcholine as assessed by thiobarbituric acid reactivity. The nitrogen dioxide-induced lipid peroxidation was enhanced by cysteine, glutathione and bovine serum albumin. While the activity of nitrogen dioxide in air to induce single strand breaks of supercoiled plasmid DNA was low, the breaking was remarkably enhanced by cysteine, glutathione and bovine serum albumin. ESR spin trapping using 5,5-dimethyl-1-pyrroline N-oxide showed that certain strong oxidant(s) were generated by interaction of nitrogen dioxide and cysteine. The spin trapping using 3,5-dibromo-4-nitrosobenzene-sulfonate suggested that sulfur-containing radicals were generated by interaction of nitrogen dioxide and cysteine or glutathione. Hence, certain sulfur-containing radicals generated by the interaction which could effectively induce lipid peroxidation and DNA strand breaks.

1,2-Dipalmitoylphosphatidylcholine↗

PubMedDate not supplied

Short-term effects of air pollution on mortality in nine French cities: a quantitative summary.

Between 1990 and 1995, 9 French cities provided data on daily air pollution, total mortality, cardiovascular mortality, and respiratory mortality. Personnel in individual cities performed Poisson regressions, controlling for trends in seasons, calendar effects, influenza epidemics, temperature, and humidity, to assess the short-term effects of air pollution. The authors describe results obtained from the quantitative pooling of these local analyses. When no heterogeneity could be detected, a fixed-effect model was used; otherwise, a random-effect model was used. Significant and positive associations were found between total daily deaths in these cities and the 4 air pollution indicators studied: (1) Black Smoke, (2) sulfur dioxide, (3) nitrogen dioxide, and (4) ozone. A 50-microg/m3 increase in Black Smoke (24 hr), sulfur dioxide (24 hr), nitrogen dioxide (24 hr), or ozone (8 hr) was associated with increases in total mortality of 2.9% (95% confidence interval [CI]) = 1.3, 4.4), 3.6% (95% CI = 2.1, 5.2), 3.8% (95% CI = 2.0, 5.5), and 2.7% (95% CI = 1.3, 4.1), respectively. Similar results were obtained for cardiovascular mortality. Except for sulfur dioxide, positive--but not significant--associations were found with respiratory mortality. The internal consistency among the cities studied, as well as consistency with previously published results, favors a causal interpretation of these associations.

Adolescent↗

PubMed2003

Review of air pollution and health impacts in Malaysia.

In the early days of abundant resources and minimal development pressures, little attention was paid to growing environmental concerns in Malaysia. The haze episodes in Southeast Asia in 1983, 1984, 1991, 1994, and 1997 imposed threats to the environmental management of Malaysia and increased awareness of the environment. As a consequence, the government established Malaysian Air Quality Guidelines, the Air Pollution Index, and the Haze Action Plan to improve air quality. Air quality monitoring is part of the initial strategy in the pollution prevention program in Malaysia. Review of air pollution in Malaysia is based on the reports of the air quality monitoring in several large cities in Malaysia, which cover air pollutants such as Carbon monoxide (CO), Sulphur Dioxide (SO2), Nitrogen Dioxide (NO2), Ozone (O3), and Suspended Particulate Matter (SPM). The results of the monitoring indicate that Suspended Particulate Matter (SPM) and Nitrogen Dioxide (NO2) are the predominant pollutants. Other pollutants such as CO, O(x), SO2, and Pb are also observed in several big cities in Malaysia. The air pollution comes mainly from land transportation, industrial emissions, and open burning sources. Among them, land transportation contributes the most to air pollution. This paper reviews the results of the ambient air quality monitoring and studies related to air pollution and health impacts.

Air Pollutants↗

PubMed1995

Hospital admission rates for asthma and respiratory disease in the West Midlands: their relationship to air pollution levels.

BACKGROUND: A study was undertaken to determine the relationship between hospital admissions for asthma and all respiratory conditions in electoral wards in the West Midlands and ambient levels of smoke, sulphur dioxide, and nitrogen dioxide, and to establish whether the relationship is independent of social deprivation and ethnicity, and is different for young children and older individuals. METHODS: Data on hospital admissions for acute respiratory conditions were obtained by electoral ward from the West Midlands Regional Health Authority Information Department Körner inpatient data including asthma (ICD 493) and all acute respiratory disease (466, 480-486, 490-496) for the period April 1988 to March 1990. The population for each electoral ward, percentage of ward population that was from non-white ethnic groups, and Townsend deprivation score were all calculated from 1991 census information. Data on smoke and sulphur dioxide (SO2) levels were obtained for 24 wards in Birmingham, Coventry, Wolverhampton, Dudley, Stafford, and Burton-on-Trent, and on nitrogen dioxide (NO2) levels from 39 wards in the same local authority areas. All were background urban sites and most participated in the Warren Spring national quality control programme for SO2 and smoke monitoring. Indirect age-sex standardised hospitalisation rates (SHR) for all respiratory conditions and asthma were calculated using the 1991 rates for the West Midlands RHA as the standard. Multivariate regression models were used to assess the relationship between individual pollutants and the SHR. The Townsend score and percentage of the population from non-white ethnic groups were included in all models to adjust for ethnicity and socioeconomic deprivation. RESULTS: The SHR for asthma varied almost fourfold across the region, and all respiratory SHR showed more than three fold variation. Bivariate regression revealed both Townsend score and percentage of non-white individuals to be associated with SHR for asthma and all respiratory conditions at all ages, but not for children under 5 years. NO2 was associated with hospital admission rates for all ages including children under 5. SO2 and smoke were not associated with hospital admissions. Multivariate analysis including Townsend score and percentage of non-white subjects in the model revealed that NO2 was associated with hospital admission rates for all respiratory conditions only for children under 5. The Townsend score was associated with SHR for all respiratory conditions, and both the Townsend score and percentage of non-white subjects were associated with SHR for asthma in children under 5 in two of three models. The association between SHR for asthma and percentage of non-white subjects was negative. CONCLUSIONS: Socioeconomic deprivation, as measured by the Townsend score, is a significant predictor of hospital admission rates for respiratory disease in older individuals, and both the percentage of non-white subjects and the Townsend score are significant predictors of hospital admission rates for asthma in children. After correction for socioeconomic deprivation and ethnicity, background urban NO2 levels in the ward of residence are significantly associated with standardised hospital admission rates for all respiratory disease in children under 5. This may represent a causal effect of NO2 on the respiratory health of children, or the effect of confounding factors not corrected by use of the Townsend score.

Acute Disease↗

PubMedDate not supplied

Associations between outdoor air pollution and hospital admissions in Brisbane, Australia.

The authors investigated the effects of ambient air pollution on hospital admissions in Brisbane, Australia. The authors used the Air Pollution on Health: European Approach protocol to examine the effects of particles, ozone, sulfur dioxide, and nitrogen dioxide on daily hospital admissions for asthma and respiratory, cardiovascular, and digestive disorders (control diagnosis) that occurred during the period 1987-1994. Ozone was consistently associated with admissions for asthma and respiratory disease-with little evidence of a threshold. In two-pollutant models, the ozone effect was relatively unaffected by the control for high levels of other pollutants. Particulate pollution (measured by nephelometry) was associated positively with admissions for respiratory disease and admissions for asthma in summer, whereas a negative association was observed for cardiovascular admissions. Although sulfur dioxide was associated significantly with admissions for respiratory and cardiovascular disese, a significant association was also found for the control diagnosis of digestive disorders. No significant associations were found for nitrogen dioxide over the study period, although significantly positive seasonal interactions were found for asthma and respiratory disease in autumn, winter, and spring. It was concluded that current levels of ambient air pollution in Brisbane make a significant contribution to the variation in daily hospital admissions for asthma and respiratory disease.

Adolescent↗

PubMed2006

Valuing the adult health effects of air pollution in Chinese cities.

China's ongoing economic growth is accompanied by a large amount of air pollution that exacts significant health and economic costs on its people. Following up on some earlier work focusing upon general mortality and child-specific health effects, this article uses a larger data set, covering more than 90 Chinese cities, along with a set of China-based epidemiological functions, to estimate some of the adult health benefits of reducing urban air pollution. Projecting future air pollution based upon current conditions, it calculates the averted mortality and morbidity effects that would result from the cleanup of particulates, sulfur dioxide, and nitrogen dioxide. The inclusion of nitrogen dioxide in our analysis is particularly important because it is a growing problem and has not been included in most of the more widely known studies that examine Chinese air pollution. Finally, the economic valuation of these pollution-related health effects is developed, using a number of recent, China-based valuation studies.

Adult↗

PubMed2003

Basic processes in phytoremediation and some applications to air pollution control.

In this short review, basic processes for phytoremediation and plant enzymes that are potentially useful in phytoremediation are briefly summarized. The remaining part describes the applications of the basic processes to decontaminate pollutants in the environments that have been done in our laboratory. Our work includes (1) analysis of the capability of various naturally occurring plants to decontaminate atmospheric nitrogen dioxide and selection of nitrogen-dioxide-philic plants that grow with nitrogen dioxide as the sole nitrogen source, (2) production of transgenic plants to improve plants' capability to decontaminate atmospheric nitrogen dioxide, and (3) analysis of the denitrification process in plants to innovate a gas--gas-converting plants that convert nitrogen dioxide to nitrogen gas.

Air Pollution↗

PubMed2000

Subject-domain approach to the study of air pollution effects on schoolchildren's illness absence.

In this paper, the authors propose a new statistical modeling technique, the subject-domain approach, which is theoretically proven to be equivalent to the time-domain approach in detecting an association between exposure and response with time trends. The authors use an empirical data set from a school absence monitoring study conducted during the 1994-1995 school year in Taiwan to demonstrate this subject-domain approach's application to environmental epidemiologic studies. Because the subject-domain models can control the influential personal confounding factors in the models, they show greater statistical power than the traditional time-domain approaches in determining the relation between air pollution and illness absences. The authors' models found that the schoolchildren's risks of illness absence were significantly related to acute exposures to nitrogen dioxide and nitrogen oxides with a 1-day lag (p < 0.01) at levels below the World Health Organization's guidelines. By contrast, the authors could not detect significant associations between air pollution and schoolchildren's absenteeism using time-domain approaches. Such findings imply that the models built on subject domain may be a general solution to the problem of the ecologic fallacy, which is commonly encountered in environmental and social epidemiologic studies.

Absenteeism↗

PubMed1989

An outbreak of nitrogen dioxide-induced respiratory illness among ice hockey players.

During February 1987 an outbreak of nitrogen dioxide-induced respiratory illness occurred among players and spectators of two high school hockey games played at an indoor ice arena in Minnesota. The source of the nitrogen dioxide was the malfunctioning engine of the ice resurfacer. Case patients experienced acute onset of cough, hemoptysis, and/or dyspnea during, or within 48 hours of attending, a hockey game. One hundred sixteen cases were identified among hockey players, cheerleaders, and band members who attended the two games. Members of two hockey teams had spirometry performed at 10 days and 2 months after exposure; no significant compromise in lung function was documented. Nitrogen dioxide exposure in indoor ice arenas may be more common than currently is recognized; only three states require routine monitoring of air quality in ice arenas, and the respiratory symptoms caused by exposure to nitrogen dioxide are nonspecific and easily misdiagnosed.

Disease Outbreaks↗

PubMed1986

Nitrogen dioxide-induced changes in cell membrane fluidity and function.

Nitrogen dioxide (NO2), an environmental oxidant pollutant, is toxic to lung cells. One of the postulated mechanisms of NO2-induced pulmonary injury involves peroxidation of membrane lipids. Therefore, we evaluated the effect of 5 ppm NO2 exposure on membrane lipid fluidity, uptake of 5-hydroxytryptamine (5-HT), lactate dehydrogenase (LDH) release, and formation of lipid peroxides in porcine pulmonary artery and aortic endothelial cells in culture. After 3- to 24-h exposure, cells were labeled with 1,6-diphenyl-1,3,5-hexatriene (DPH), an aromatic hydrocarbon that partitions into the hydrophobic interior of the lipid bilayer of cell membranes. Membrane fluidity was monitored by measuring changes in rotational relaxation time (rho) for DPH by fluorescence spectroscopy. Reductions in membrane fluidity increase the value of rho. The 5-HT uptake was calculated from the disappearance of 1 X 10(-6) M 14C-5-HT from the medium, and LDH release and lipid peroxide formation were measured by spectrophotometric methods. The NO2 caused a significant increase in rhoDPH in both types of endothelial cells after 3 h and progressed with further exposure to NO2. Exposure to NO2 for 24 h, but not 3 or 12 h, significantly (p less than 0.05) reduced 5-HT uptake, increased (p less than 0.01) LDH release, and increased (p less than 0.05) lipid peroxide formation in both pulmonary artery and aortic endothelial cells. These results suggest that oxidant injury caused by NO changes the physical state of membrane lipids, impairs membrane function, and contributes to the biochemical and metabolic abnormalities in the cells.

Animals↗

PubMedDate not supplied

Associations between outdoor air pollution and daily mortality in Brisbane, Australia.

The results of several studies have indicated significant associations between daily mortality and air pollution, with little evidence of a threshold. In the current study, the authors examined daily mortality during the period 1987-1993 for the Brisbane region, which is the fastest-growing urban region in Australia (annual average concentration of particulate matter less than 10 microm in diameter = 27 microg/m3, maximum hourly sulfur dioxide level = 60 ppb, and maximum daily ozone hourly level = 118 ppb). The authors conducted a general estimating equation analysis, and they used autoregressive Poisson models for daily mortality to examine associations with air pollution variables. The authors used research methods developed in the Air Pollution on Health, European Approach (APHEA), project to control confounding effects of weather and temporal trends. The air pollutants examined included particulate pollution (measured by nephelometry [bsp data]), sulfur dioxide, ozone, and nitrogen dioxide. The results indicated that the associations between total daily mortality and particulate levels found in studies in the United States and other countries may be applicable in Brisbane, Australia. Ozone levels were also associated significantly with total daily mortality. There was little evidence of interaction between the ozone effects (mainly in summer) and particulates or with sulfur dioxide and nitrogen dioxide. The associations between pollutants (ozone, bsp) and daily mortality were significant only for individuals who were older than 65 y of age; positive associations were also found with cardiovascular disease categories, and the regression coefficients--when significant--were higher than those for total mortality. The results indicated a possible threshold for ozone levels, but a similar result for particulate levels was not apparent.

Age Factors↗

PubMed1998

Daily variations in air pollution and respiratory health in a multicentre study: the PEACE project. Pollution Effects on Asthmatic Children in Europe.

The Pollution Effects on Asthmatic Children in Europe (PEACE) study is a multicentre study of the acute effects of particles with a 50% cut-off aerodynamic diameter of 10 microm (PM10), black smoke (BS), sulphur dioxide (SO2) and nitrogen dioxide (NO2) on the respiratory health of children with chronic respiratory symptoms. The study was conducted in the winter of 1993/1994 by 14 research centres in Europe. A total of 2,010 children, divided over 28 panels in urban and suburban locations, was followed for at least 2 months. Exposure to air pollution was monitored on a daily basis. Health status was monitored by daily peak expiratory flow (PEF) measurements and a symptom diary. The association between respiratory health and air pollution levels was calculated with time series analysis. Combined effect estimates of air pollution on PEF or the daily prevalence of respiratory symptoms and bronchodilator use were calculated from the panel-specific effect estimates. Fixed effect models were used and, in cases of heterogeneity, random effect models. No clear associations between PM10, BS, SO2 or NO2 and morning PEF, evening PEF, prevalence of respiratory symptoms or bronchodilator use could be detected. Only previous day PM10 was negatively associated with evening PEF, but only in locations where BS was high compared to PM10 concentrations. There were no consistent differences in effect estimates between subgroups based on urban versus suburban, geographical location or mean levels of PM10, BS, SO2 and NO2. The lack of association could not be attributed to a lack of statistical power, low levels of exposure or incorrect trend specifications. In conclusion, the PEACE project did not show effects of particles with a 50% cut-off aerodynamic diameter of 10 microm, black smoke, sulphur dioxide or nitrogen dioxide on morning or evening peak expiratory flow or the daily prevalence of respiratory symptoms and bronchodilator use.

Air Pollution↗