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PubMed2005

Protein nitration by polluted air.

The effects of air pollution on allergic diseases are not yetwell-understood. Here, we show that proteins, in particular birch pollen proteins including the allergen Bet v 1, are efficiently nitrated by polluted air. This posttranslational modification of proteins is likely to trigger immune reactions and provides a molecular rationale for the promotion of allergies bytraffic-related air pollution. Enzyme immunoassays have been used to determine equivalent degrees of nitration (EDN) for protein samples exposed to urban outdoor air and synthetic gas mixtures. The observed rates of nitration were governed by the abundance of nitrogen oxides and ozone, and concentration levels typical for summer smog conditions led to substantial nitration within a few hours to days (EDN up to 20%). Moreover, nitrated proteins were detected in urban road dust, window dust, and fine air particulate matter (EDN up to 0.1%).

Air Pollutants↗
PubMed1993

Clinical ecology and its role in diagnosis of chronic diseases caused by environmental pollution. Indoor air pollution as a major factor.

The author discusses the four basic principles of clinical ecology, which include total load, such as exposure to chemicals, effects of physical factors (cold, heat, positive ions, radiation), exposure to bacteria, viruses and fungi, effects of consumed foods and psychological stress. Adaptation is discussed in detail as it pertains to chronic degenerative disease and chemical sensitivity. Lack of understanding of adaptive phenomena leads contemporary physicians to prescribe drugs instead of finding and eliminating the cause of disease to alleviate suffering. Body response to environmental stimuli during adaptive processes is biphasic in nature and is characterized by stimulatory and withdrawal reactions. Symptoms developed during these phases are described in detail. Effects of foods and chemicals on patients' health should be examined and considered before excluding in favour of idiopathic, mental or psychosomatic disturbances. In order to understand the variety of symptoms and signs developed during the process of degenerative disease one has to accept and apply the concept of biological individuality. Each patient should be assessed and dealt with carefully since each represents a unique clinical picture. The author further on discusses indoor air pollution, its causes and effects on health. Particular emphasis is placed on the indoor use of pesticides in the Canadian setting. Four groups of population have been defined as the result of exposure to chemicals and are discussed in brief. The author concludes with a comparison of traditional and environmental medicine in respect to history taking, the stage at which disease is diagnosed, the patient's viewpoint, specialization and therapies.

Adaptation, Physiological↗
PubMed1999

A synergistic decline in humoral and cellular immunity of diabetic mice on exposure to polluted air.

It is clinically known that diabetic patients are more prone to infectious diseases, due to low immune status. Since, some of the common air pollutants are reported to suppress immune system, how exposure to artificially polluted air influences the immune responses in experimental diabetic mice was studied. A diabetic state was induced by alloxan and mice were exposed to artificially polluted air for 30 days. During the period of exposure, the humoral (antibody titer) and cellular (foot and swelling) immune responses to antigenic challenges with sheep RBC were investigated. The exposure to polluted air produced a significant decline in the immune responses in non-diabetic mice whereas a synergistic decline was observed in diabetic group. Since, daily oral treatment with vitamin E (150 mg/kg) significantly prevented the pollution induced immunosuppression, the involvement of free radicals is suggested.

Air Pollution↗
PubMed2005

Use of multi-objective air pollution monitoring sites and online air pollution monitoring system for total health risk assessment in Hyderabad, India.

A consensus has been emerging among public health experts in developing countries that air pollution, even at current ambient levels, aggravates respiratory and cardiovascular diseases and leads to premature mortality. Recent studies have also presented well-founded theories concerning the biological mechanisms involved and the groups of people that are probably more susceptible to health effects caused or exacerbated by inhalation of ambient particulate matter (PM.). On the basis of prognostic studies carried out in Center for Environment, JNT University, Hyderabad "it has been estimated that in Hyderabad some 1,700 to 3,000 people per year die prematurely as a result of inhaling PM". These figures reflect only the effects of acute exposure to air pollution. If the long-term effects of chronic exposure are taken into account, 10,000-15,000 people a year could die prematurely in Hyderabad. This estimate of the chronic effects is based on other studies, which are not completely comparable with the Hyderabad situation. While the study designs and analyses in these other studies may indeed be different or irrelevant to Hyderabad, the fact they were carried out in other countries is irrelevant. Taking into account these considerations, a model for total health risk assessment for the city of Hyderabad, and its state of Andhra Pradesh in India has been developed using a multi-objective air pollution monitoring network and online and real time air pollution monitoring stations. For the model studies a number of potential monitoring sites were screened for general and site-specific criteria in a geographic information system (GIS) environment that may, on a local basis, affect the representativeness of the data collected. Local features that may affect either the chemical or meteorological parameters are evaluated to assure a minimum of interference. Finally, for monitoring air pollution, an online and real-time monitoring system was designed using advanced electrochemical sensor systems (sulphur dioxide, oxides of nitrogen, carbon monoxide, hydrocarbons, ozone, mercaptans and hydrogen sulphide) and a particulate matter analyzer (total suspended particulate matter TSPM), PM2.5 and PM10). The sensor and data acquisition systems are programmed to monitor pollution levels at 1/2 hour durations during peak hours and at 1-hour intervals at other times. Presently, extensive statistical and numerical simulations are being carried out at our center to correlate the individuals living in the monitored areas with respiratory infections with air pollution.

Air Pollutants↗
PubMed1976

Epidemiological evidence on the carcinogenic risk of air pollution.

In summary, higher lung cancer morbidity and mortality in urban than in rural areas and the presence of carcinogens in polluted air suggest that smoking habits and specific occupational exposures cannot account for all the urban air pollution may play a role in this disease. Surveys of lung cancer have shown that differences in excess. Positive correlations between lung cancer death rates and indices of pollution in different places, the experience of migrants and a possibile decline in lung cancer mortality with decline in pollution provide support for the view that air pollution is a factor in this disease. But the effect of pollution cannot be large. It is likely to be a small fraction (possibly a tenth) of the effect of cigarette smoking.

Adolescent↗
PubMed1997

Lung function and long term exposure to air pollutants in Switzerland. Study on Air Pollution and Lung Diseases in Adults (SAPALDIA) Team.

The effect of long-term exposure to air pollutants was studied in a cross-sectional population-based sample of adults (aged 18 to 60 yr; n = 9,651) residing in eight different areas in Switzerland. Standardized medical examination included questionnaire data, lung function tests, skin-prick testing, and end-expiratory CO concentration. The impact of annual means of air pollutants on FVC and FEV1 was tested (controlling for age and age squared, sex, height, weight, educational level, nationality, and workplace exposure). Analyses were done separately for healthy never-smokers, ex-smokers (controlling for pack-yr), for current smokers (controlling for cigarettes per day and pack-yr smoked), and for the whole population. Significant and consistent effects on FVC and FEV1 were found for NO2, SO2, and particulate matter < 10 microm (PM10) in all subgroups and in the total population, with PM10 showing the most consistent effect of a 3.4% change in FVC per 10 microg/m3. Results for ozone were less consistent. Atopy did not influence this relationship. The limited number of study areas and high intercorrelation between the pollutants make it difficult to assess the effect of one single pollutant. Our conclusion is that air pollution from fossil fuel combustion, which is the main source of air pollution with SO2, NO2, and PM10 in Switzerland, is associated with decrements in lung function parameters in this study.

Adolescent↗
PubMed1992

[Activity of bronchoalveolar cell population as an indicator of air pollution].

The aim of this study was the evaluation of cytological, immunocytological and cytochemical tests efficiency in describing the pulmonary alveoli cells activity in people chronically exposed to the polluted air. The detailed analysis of bronchoalveolar lavage (BAL) obtained by rinsing of pulmonary alveoli in 36 cases of prolonged exposure to silica and asbestos dust, divided into non-smokers and smokers, was performed. The control were the patients free of any pathological pulmonary symptoms, in this number the inhabitants of Cracow. The BAL cells contribution and activity was evaluated by following methods: routine cytology (the number and percentage of cells), computer cytomorphometry (for assessment macrophage area), nitro-blue-tetrazolium (NBT) reduction test (macrophage activity) and indirect immunofluorescence with use of monoclonal antibodies (macrophage subsets) and FACS-star-PLUS flow cytometer (lymphocyte subsets). In the individuals chronically exposed to the different forms of air pollution we found the changes in number and proportions of bronchoalveolar space cells, the alterations in cell activity (especially pulmonary macrophages) and decrease in CD4/CD8 lymphocyte ratio, that could indicate the apparent disturbances in the local cell resistance. According to our observation there is a synergistic action of tobacco smoking and air pollution. Finally, we may conclude, that BAL, was a non-invasive, repeatable method, useful for monitoring pulmonary changes due to dust exposure.

Adult↗
PubMed2003

Epidemiologic evidence of a relationship between airway hyperresponsiveness and exposure to polluted air.

BACKGROUND: There has been an increase in allergic diseases as a result of increased air pollution emanating from traffic and various industries. OBJECTIVE: This study evaluated the association between air pollution and airway hyperresponsiveness in a cross-sectional study of a cohort of 670 children, aged 10-13 years. METHODS: We measured spirometry and conducted allergic skin tests and methacholine challenge tests in 670 schoolchildren. The methacholine concentration causing a 20% fall in FEV1 (PC20) was used as the threshold of airway hyperresponsiveness (AHR). Thresholds of 16 mg/dl or less were assumed to indicate AHR. RESULTS: All of the schoolchildren had normal pulmonary function. Of the children, 257 (38.3%) had AHR. There was a significant increase in AHR in schoolchildren living near a chemical factory [45.0% (138/306), 6.50 +/- 0.48] compared to those in rural [31.9% (52/163), 9.84 +/- 0.83] and coastal [33.3% (67/201), 7.17 +/- 0.68] areas. Atopy was significantly more prevalent near the chemical factory vs the coastal and rural areas [35.6% (109/306) vs 27.3% (55/201) and 23.3% (38/163), respectively, P < 0.007]. Schoolchildren with atopy had lower PC20 than those without atopy (5.98 +/- 0.60 vs 8.15 +/- 0.45, P < 0.001). Positive allergy skin tests and living in a polluted area were risk factors in multivariate analyses adjusted for sex, parents' smoking habits, age, body mass index, nose symptoms and lung symptoms (odds ratio for location = 2.4875, confidence interval 1.6542-3.7406, P < 0.000; odds ratio for allergy skin test = 1.5782, confidence interval 1.1130-2.2379, P < 0.0104). CONCLUSION: Our findings demonstrate that more children living in polluted areas have airway hyperresponsiveness than do those living in less polluted areas.

Adolescent↗
PubMed1976

Immunoglobulins under the influence of nonspecific factors. III. Immunoglobulins, pertussis antibodies and lysozyme in three child populations exposed to different air pollution.

The levels of IgG, IgA, IgM, lysozyme, agglutinins against B. pertussis and B. parapertussis were followed in the blood serum of 306 children 9--10 years old in 3 areas of Central Bohemian region. In children dwelling in areas with more polluted air significantly higher levels of serum lysozyme and of parapertussis antibodies were found by the t-test. The distribution of these values shows significant differences between more polluted areas in comparison with lower-pollution area also in Kolmogorov-Smirnov test. The average levels of Ig approached statistically critical values but did not reach them, but significant differences in the distribution of values of IgG and IgA were shown by the F-test and chi2-test between lightly and heavily polluted areas. The values of immunological reactions in polluted areas were always higher than in the non-polluted group. This provides evidence for a hypothesis about a stimulatory effect of polluted air on immunological mechanisms in child population. The higher values of IgM observed recently by other authors in women were shown in girls of 9--10 years.

Agglutinins↗
PubMed1999

Transmission electron microscopy findings in the respiratory epithelium of guinea pigs exposed to the polluted air of southwest Mexico City.

We evaluated the nature and the extent of the damage to the respiratory epithelium of guinea pigs after a 4-month exposure to the mixture of air pollutants in southwest Mexico City. Guinea pigs were placed outdoors on the roof of our facility, 8 hours daily, from February to May 1995. At the same time, control guinea pigs were kept indoors breathing filtered air. Air pollutants, temperature, and humidity data were obtained from the nearest station of the Environmental Monitoring Net. The airways and lung parenchyma were analyzed after 120 days using transmission electron microscopy (TEM). During the 4-month exposure period, ozone (O3) exceeded the norm during 511 hours, and suspended particles less than 10 microm in diameter (PM10) during 52 hours. Both pollutants reached peak levels of more than twice the norm. TEM revealed no important abnormalities in the control group. In the exposed group, there was loss of cilia, detachment of epithelial cells, and eosinophil and macrophage migration toward alveolar spaces through type I pneumocytes with destruction of their basal membranes. In six guinea pigs in the exposed group, we noted bacteria along the airways, with associated inflammatory response. We explain the colonization of the respiratory epithelium by bacteria as the result of the impairment on the defense mechanism caused by the exposure to environmental O3 and PM10.

Air Pollutants↗
PubMed2006

Long-term effects of exposure to particulate air pollution.

Considerable work has been done to elucidate the effects of polluted air, most of which has studied acute effects of particles. Studies suggest that the effects of longer term exposures are more than just the daily sum of the acute effects. Because most of the studies of acute effects have examined changes in health status occurring within days of the exposure, this article takes a broad definition of long-term exposure to include averaging times of months to years. It concludes that health effects increase as length of exposure increases, but much of that increase occurs within the first year.

Air Pollutants↗
PubMed2003

Risk factors among elderly for short term deaths related to high levels of air pollution.

BACKGROUND: Air pollution has been linked to increased rates of mortality, but little is known about individual characteristics related to the increase in risk. AIMS: To examine short term effects of air pollution on daily mortality in elderly people in Bordeaux and compare characteristics of subjects > or =65 years old who died with levels of particulate air pollution. METHODS: Daily mortality data from Bordeaux were used to determine the core model of mortality for the period 1988-97. The air pollution indicator was regressed on the core model of mortality, allowing control of the main effect modifiers and confounding factors of air pollution on the same day. The residual series of this regression model was classified from the lowest to the highest to determine "low level days" and "high level days". A sample of 1469 elderly people in a French cohort study were studied. RESULTS: From 1988 to 1997, 543 subjects died; 55 deaths were during days with low air pollution and 51 during days with high air pollution. Only gender differed significantly according to both types of days, with a proportion of women significantly higher in high air pollution days than men. After adjustment for smoking habits, the odds ratio was 5.2 for women. CONCLUSION: The risk of mortality between women and men was determined on days with "high air pollution levels" above the 50-90th centiles compared to below the 10th centile. No clear pattern was observed between days with low levels of air pollution and the different centiles of exposure.

Aged↗
PubMed2004

Using air pollution based community clusters to explore air pollution health effects in children.

To study respiratory health effects of long-term exposure to ambient air pollutant mixture, we observed 7058 school children 5-16 years of age living in the four Chinese cities of Lanzhou, Chongqing, Wuhan, and Guangzhou. These children were enrolled from elementary schools located in eight districts, one urban district and one suburban district in each of the above cities. Ambient levels of PM(2.5), PM(10-2.5), total suspended particles (TSP), SO(2), and NO(x) were measured in these districts from 1993 to 1996. Based on a cluster analysis of arithmetic mean concentrations of PM(2.5), PM(10-2.5), (TSP-PM(10)), SO(2), and NO(x), we classified these children into four ordinal categories of exposure to ambient air pollutant mixtures. We tested for exposure-response relationships using logistic regression models, controlling for relevant covariates. We observed monotonic, positive relationships of exposure to the pollutant mixture with prevalence rates of cough with phlegm and wheeze. Other outcomes were not associated with the exposure in a monotonic exposure-response pattern. Even so, odds ratios for cough, phlegm, bronchitis, and asthma in the higher exposure district clusters were all higher than in the lowest exposure district cluster. We found evidence that exposure to the pollutant mixtures had adverse effects on children living in the four Chinese cities.

Adolescent↗
PubMed2005

Particulate air pollution and nonfatal cardiac events. Part II. Association of air pollution with confirmed arrhythmias recorded by implanted defibrillators.

Implanted cardioverter defibrillators (ICDs) monitor patients for episodes of cardiac arrhythmias and can initiate a therapeutic intervention to restore normal heart rhythm. These devices also record dates, times, and electrograms of these episodes. We examined the effects of air pollution on the incidence of arrhythmias in 195 cardiac patients with ICD devices in the Boston metropolitan area between July 1995 and July 2002. Gaseous air pollutant and meteorologic data were measured on essentially all days, fine particle mass on 80% of the days, and black carbon (BC) on 61% of the days. Date and time of detected arrhythmias, intracardiac electrograms, and therapeutic interventions were downloaded during the patients' regular follow-up visits every 3 months on average. A cardiac electrophysiologist reviewed electrograms recorded before, during, and after the arrhythmias and categorized them into ventricular and supraventricular events. Risk of arrhythmias associated with air pollution was estimated using logistic regression with adjustments for season, temperature, relative humidity, day of the week, and patient. We found increased relative risks of ventricular arrhythmias (VAs) associated with an increase in 2-day mean concentrations for all air pollutants considered, although these associations were not statistically significant. The relative risks of supraventricular arrhythmias (SVAs) increased in association with 2-day mean concentrations for all air pollutants, and this association was significant only for sulfur dioxide (SO2) at 4 ppb (odds ratio [OR] = 1.33; 95% confidence interval [CI] = 1.04, 1.70). The positive associations of VAs and SVAs with particulate matter less than 2.5microm in aerodynamic diameter (PM2.5; also referred to as fine particles), carbon monoxide (CO), nitrogen dioxide (NO2), BC, and SO2 suggest a link with motor vehicle pollutants. We explored patient characteristics that may have identified subjects susceptible to the effects of air pollution. The association of air pollution with SVAs was blunted by regularly prescribed beta-blockers. We found stronger associations of air pollution with VAs for episodes within 3 days of a previous arrhythmia, suggesting that VAs were triggered by air pollution episodes in combination with other factors that raised the patient's underlying risk. Although ICDs are specifically designed to monitor and treat only VAs, these results suggest that air pollution may trigger both VAs and SVAs.

Adult↗