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PubMed2005

Particulate air pollution and nonfatal cardiac events. Part I. Air pollution, personal activities, and onset of myocardial infarction in a case-crossover study.

We conducted a prospective case-crossover study to assess the association of particulate air pollution with onset of nonfatal myocardial infarction (MI). Patients who had survived MIs between February 1999 and July 2001 were identified based on the Coronary Event Registry in Augsburg, Southern Germany. The study included 851 MI subjects with known date and time of MI who had survived the first 24 hours and had completed the Registry's standard interview. Of these subjects, 691 provided case and control information for subject-specific MI triggers collected by a diary assessing the 4 days before symptom onset. The exposures of interest were the total number concentration (TNC) of particles as an indicator for ultrafine particles and the mass of particles with an aerodynamic diameter no larger than 2.5 microm (PM2.5). We conducted conditional logistic regression analyses using different control-selection strategies in a case-crossover approach, and Poisson regression analyses of the time-series data.

Activities of Daily Living↗
PubMed2006

[Evaluating health risk for workers due to polluted air in auxiliary workshops of heat power stations].

The authors evaluated health risk for workers of auxiliary workshops in heat power stations by workplace air,caused by workplace air pollution with solid particles, nitrogen dioxide, sulfur dioxide, phenol, carbon oxide, benzpyrene. This evaluation was a part of longstanding research designing measures to optimize work conditions. Kuznetsk heat power station served as an example to calculate mean air concentrations of chemicals, yearly individual risk of chronic intoxication, to determine contribution of each individual chemical into the overall risk, to assess individual risk due to benzpyrene inhalation.

Air Pollutants, Occupational↗
PubMed1985

The status of indoor air pollution.

Indoor air pollution, specifically restricted in its meaning to chemicals in home indoor air environment, presents a new and probably an important challenge to the researchers of the air pollution field. The general overview of this topic suggests that the voluminous data generated in the past ten or so years have only defined the rudiments of the problem, and significant areas of research still exist. Among the important areas where information is lacking, the exposures to contaminants generated by the use of consumer products and through hobbies and crafts represent perhaps the most urgent need for substantial research.

Air Pollution↗
PubMed2000

Construction and economics of a pilot/full-scale biological trickling filter reactor for the removal of volatile organic compounds from polluted air.

The design and the construction of an actual 8.7-m3 pilot/full-scale biotrickling filter for waste air treatment is described and compared with a previous conceptual scale-up of a laboratory reactor. The reactor construction costs are detailed and show that about one-half of the total reactor costs ($97,000 out of $178,000) was for personnel and engineering time, whereas approximately 20% was for monitoring and control equipment. A detailed treatment cost analysis demonstrated that, for an empty bed contact time of 90 sec, the overall treatment costs (including capital charges) were as low as $8.7/1000 m3air in the case where a nonchlorinated volatile organic compound (VOC) was treated, and $14/1000 m3air for chlorinated compounds such as CH2Cl2. Comparison of these costs with conventional air pollution control techniques demonstrates excellent perspectives for more field applications of biotrickling filters. As the specific costs of building and operating biotrickling filter reactors decrease with increasing size of the reactor, the cost benefit of biotrickling filtration is expected to increase for full technical-scale bioreactors.

Air Pollution↗
PubMed1994

Air pollution and childhood respiratory health: exposure to sulfate and ozone in 10 Canadian rural communities.

This study was designed to examine differences in the respiratory health status of preadolescent school children, aged 7-11 years, who resided in 10 rural Canadian communities areas of moderate and low exposure to regional sulfate and ozone pollution. Five of the communities were located in central Saskatchewan, a low-exposure region, and five were located in southwestern Ontario, an area with moderately elevated exposures resulting from long-range atmospheric transport of polluted air masses. In this cross-sectional study, the child's respiratory symptoms and illness history were evaluated using a parent-completed questionnaire, administered in September 1985. Respiratory function was assessed once for each child in the schools between October 1985 and March 1986, by the measurement of pulmonary function for forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1.0), peak expiratory flow rate (PEFR), mean forced expiratory flow rate during the middle half of the FVC curve (FEF25-75), and maximal expiratory flow at 50% of the expired vital capacity (V50max). The 1986 annual mean of the 1-hr daily maxima of ozone was higher in Ontario (46.3 ppb) than in Saskatchewan (34.1 ppb), with 90th percentile concentrations of 80 ppb in Ontario and 47 ppb in Saskatchewan. Summertime 1-hr daily maxima means were 69.0 ppb in Ontario and 36.1 ppb in Saskatchewan. Annual mean and 90th percentile concentrations of inhalable sulfates were three times higher in Ontario than in Saskatchewan; there were no significant differences in levels of inhalable particles (PM10) or particulate nitrates. Levels of sulfur dioxide (SO2) and nitrogen dioxide (NO2) were low in both regions. After controlling for the effects of age, sex, parental smoking, parental education, and gas cooking, no significant regional differences were observed in rates of chronic cough or phlegm, persistent wheeze, current asthma, bronchitis in the past year, or any chest illness that kept the child at home for 3 or more consecutive days during the previous year. Children living in southwestern Ontario had statistically significant (P < 0.01) mean decrements of 1.7% in FVC and 1.3% in FEV1.0 compared with Saskatchewan children, after adjusting for age, sex, weight, standing height, parental smoking, and gas cooking. There were no statistically significant regional differences in the pulmonary flow parameters (P > 0.05).

Air Pollutants↗
PubMed2000

Nitration and hydroxylation of aromatic amino acid and guanine by the air pollutant peroxyacetyl nitrate.

Peroxyacetyl nitrate (PAN) is a common gaseous photochemical compound in polluted air and cigarette smog. The toxicity of PAN has been found to depend on three pathways: (1) its oxidizing property that mimics peroxide or peroxynitrite; (2) its nitrating and hydroxylating properties similar to peroxynitrite; and (3) its acetylating property like acetic anhydride. The present investigations were intended to focus on the reactions of PAN with aromatic amino acids and guanine. When PAN interacted with tyrosine and guanine the major products were 3-nitrotyrosine, 3, 5-dinitrotyrosine, 8-hydroxyguanine and 8-nitroguanine. These compounds have been used as indicators for the presence of peroxynitrite in previous studies. When PAN interacted with phenylalanine, the products were 3-nitrotyrosine, 4-nitrophenylalanine, p-tyrosine, o-tyrosine and m-tyrosine. 5-Hydroxytryptophan is produced from the reaction of PAN with tryptophan. Furthermore, the formation of nitrated tyrosines was also found in the PAN-treated HL-60 cells. A high yield of dityrosine was formed when PAN and peroxynitrite were reacted with tyrosine, probably through free radical oxidation. We also found that peroxynitrite and PAN are similar in their oxidizing activity. From these findings, we suggest that peroxynitrite may be considered as the reactive intermediate of PAN.

Air Pollutants↗
PubMed1999

Exploring the clastogenic effects of air pollutants in São Paulo (Brazil) using the Tradescantia micronuclei assay.

This study was designed to determine the clastogenicity of particulate matter (aerodynamic diameter smaller than 10 microm) in the urban polluted air in the city of São Paulo. The Tradescantia-micronucleus (Trad-MCN) assay was used throughout this study to evaluate the clastogenicity of the extracts of the particulate matter. Tradescantia pallida (Rose) Hunt. cv. purpurea, an indigenous cultivar, was used in the Trad-MCN assay. The efficacy of this plant material for the Trad-MCN assay was validated with dose-response studies using formaldehyde and beta radiation. Dose-response curves were established with these known mutagens. The extracts of the PM10 particles at concentrations between 5 and 50 ppm induced a dose-related increase in MCN frequencies. The results indicate that T. pallida is equally sensitive to mutagens as the standard Tradescantia clone 4430 or 03 and the particulate matter in the urban air are clastogenic to the chromosomes of this plant. Inhalation of these particles by urban dwellers may affect their health by inducing similar genetic damage.

Air Pollutants↗
PubMed2000

[Air pollution and sperm quality].

BACKGROUND: It has been described that an exposition of males to chemical substances may significantly impoverish quality and quantity of produced spermatozoa. The aim of our study was to test whether the polluted air in the Teplice district has negative effects on the quality of sperm of males living in this district. METHODS AND RESULTS: 325 males 18-year-old living in the Teplice district and in the control district of Prachatice were tested. Samples were taken in 1992 and 1994, always at the end of winter and in autumn. According to WHO laboratory manual for investigation of the human sperm, basic parameters were determined: volume of the semen, pH, motility, number and morphology of spermatozoa. In selected groups of males the frequency of aneuploidia of spermatozoa was also examined. Examination of aneuploidia was done using three color fluorescence in situ hybridisation with satellite DNA proves specific for X, Z and 8 chromosomes. Logistic regression was used for the data analysis and Odd's Ratio was estimated (OR's). OR's was found for the morphology of spermatozoa (4.1 and 10.1 for medium and high exposition respectively), for the head morphology (6.1 and 4.1) and in the percentage of motile spermatozoa (9.8 and 3.5). More intensively exposed males had higher frequency of disomy in chromosomes X (p = 0.012), XY (p = 0.01), and Y (p < 0.001). CONCLUSIONS: Bio-indicators of toxic and genetic impairment have shown lower quality of sperm in males in Teplice district.

Adolescent↗
PubMed1970

The new airborne disease. Community air pollution.

Community air pollution is the new airborne disease of our generation's communities. It is caused by the increasing use of fuel, associated with both affluence and careless waste. Photochemical air pollution of the California type involves newly defined atmospheric reactions, is due mostly to motor vehicle exhaust, is oxidizing, and produces ozone, plant damage, impairment of visibility and eye and respiratory symptoms. Aggravation of asthma, impairment of lung function among persons with chronic respiratory disease and a possible causal role, along with cigarette smoking in emphysema and chronic bronchitis, are some of the effects of photochemical pollution. More subtle effects of pollution include impairment of oxygen transport by the blood due to carbon monoxide and interference with porphyrin metabolism due to lead. Carbon monoxide exposures may affect survival of patients who are in hospitals because of myocardial infarction. While many uncertainties in pollution-health reactions need to be resolved, a large number of people in California have health impairment due to airborne disease of this new type.

Air Pollution↗
PubMed2005

Exposure and measurement contributions to estimates of acute air pollution effects.

Air pollution health effect studies are intended to estimate the effect of a pollutant on a health outcome. The definition of this effect depends upon the study design, disease model parameterization, and the type of analysis. Further limitations are imposed by the nature of exposure and our ability to measure it. We define a plausible exposure model for air pollutants that are relatively nonreactive and discuss how exposure varies. We discuss plausible disease models and show how their parameterizations are affected by different exposure partitions and by different study designs. We then discuss a measurement model conditional on ambient concentrations and incorporate this into the disease model. We use simulation studies to show the impact of a range of exposure model assumptions on estimation of the health effect in the ecologic time series design. This design only uses information from the time-varying ambient source exposure. When ambient and nonambient sources are independent, exposure variation due to nonambient source exposures behaves like Berkson measurement error and does not bias the effect estimates. Variation in the population attenuation of ambient concentrations over time does bias the estimates with the bias being either positive or negative depending upon the association of this parameter with ambient pollution. It is not realistic to substitute measured average personal exposures into time series studies because so much of the variation in personal exposures comes from nonambient sources that do not contribute information in the time series design. We conclude that general statements about the implications of measurement error need to be conditioned on the health effect study design and the health effect parameter to be estimated.

Air Pollutants↗
PubMedDate not supplied

Short-term effects of air pollution on hospital admissions of respiratory diseases in Europe: a quantitative summary of APHEA study results. Air Pollution and Health: a European Approach.

The Air Pollution and Health: a European Approach (APHEA) project is a coordinated study of the short-term effects of air pollution on mortality and hospital admissions. Five West European cities (i.e., London, Amsterdam, Rotterdam, Paris, Milano) contributed several years of hospital admissions data for all respiratory causes. In the current study, the authors describe the results obtained from the quantitative pooling (meta-analysis) of local analyses. The diagnostic group was defined by ICD 460-519. The age groups studied were 15-64 y (i.e., adults) and 65+ y (elderly). The air pollutants studied were sulfur dioxide; particles (i.e., Black Smoke or total suspended particles); ozone; and nitrogen dioxide. The pollutants were obtained from existing fixed-site monitors in a standardized manner. We used Poisson models and standardized confounder models to examine the associations between daily hospital admissions and air pollution. We conducted quantitative pooling by calculating the weighted means of local regression coefficients. We used a fixed-effects model when no heterogeneity could be detected; otherwise, we used a random-effects model. When possible, the authors investigated the factors correlated with heterogeneity. The most consistent and strong finding was a significant increase of daily admissions for respiratory diseases (adults and elderly) with elevated levels of ozone. This finding was stronger in the elderly, had a rather immediate effect (same or next day), and was homogeneous over cities. The elderly were affected more during the warm season. The Sulfur dioxide daily mean was available in all cities, and it was not associated consistently with an adverse effect. Effects were present in areas in which more than one station was used in the assessment of daily exposure. Some significant associations were observed, although no conclusion that related to an overall particle effect could be drawn. The effect of Black Smoke was significantly stronger with high nitrogen dioxide levels on the same day, but nitrogen dioxide itself was not associated with admissions. The ozone results were in good agreement with the results of similar U.S. studies. The coherence of the results of this study and other results gained under different conditions strengthens the argument for causality.

Adolescent↗
PubMed1998

Copper-dependent inflammation and nuclear factor-kappaB activation by particulate air pollution.

Particulate air pollution causes increased cardiopulmonary morbidity and mortality, but the chemical determinants responsible for its biologic effects are not understood. We studied the effect of total suspended particulates collected in Provo, Utah, an area where an increase in respiratory symptoms in relation to levels of particulate pollution has been well documented. Provo particulates caused cytokine-induced neutrophil chemoattractant-dependent inflammation of rat lungs. Provo particulates stimulated interleukin-6 (IL-6) and IL-8 production, increased IL-8 messenger RNA (mRNA) and enhanced expression of intercellular adhesion molecule-1 (ICAM-1) in cultured BEAS-2B cells, and stimulated IL-8 secretion in primary cultures of human bronchial epithelium. Cytokine secretion was preceded by activation of the transcription factor nuclear factor-kappaB (NF-kappaB) and was reduced by treatment of cultures with superoxide dismutase, deferoxamine, or N-acetylcysteine. These biologic effects were replicated by culturing BEAS cells with quantities of Cu2+ found in Provo extract. IL-8 secretion by BEAS cells could be modified by addition of normal constituents of airway lining fluid to the culture medium. Mucin significantly reduced IL-8 secretion, and ceruloplasmin significantly increased IL-8 secretion and activation of NF-kappaB. These findings suggest that copper ions may cause some of the biologic effects of inhaled particulate air pollution in the Provo region of the United States, and may provide an explanation for the sensitivity of asthmatic individuals to Provo particulates that has been observed in epidemiologic studies.

Air Pollution↗
PubMed1992

Risk assessment of urban air pollution.

Urban air pollution, originating in western countries mainly from automotive engine exhausts, contains thousands of components, many of which are genotoxic, i.e. are putative cancer initiators. Other pollution components, such as NO2 and certain particles, may have cocarcinogenic/promotive effects, at least at higher exposure levels. Cancer risk assessment of this complex mixture has to combine data from the exposure history, from epidemiological studies as well as from animal carcinogenicity tests, and from in vitro studies of fractions and individual components. Data for metabolism and pharmaco-kinetics have also to be considered. A multiplicative linear model is assumed to be valid for cancer initiation at low levels. Attempts are being made to determine the target dose from ultimate carcinogens (reactive metabolites) via macromolecule adduct levels, and to base the risk assessment on the radiation-dose equivalent to the chemical dose. So far this has been possible only for simple alkenes, which are metabolized to epoxides, and indirectly, via benzo(a)pyrene (BaP), for particle-bound polycyclic aromatic hydrocarbons (PAH). The lifetime risk of cancer (all sites) from ethene is estimated accordingly to 1.4 x 10(-4) per microgram m-3, and from PAH to 12 x 10(-4) per ng m-3 BaP. For other components indicated to give risk contribution (NOx, volatile PAH, benzene, aldehydes, butadiene) essential data are lacking and only very rough estimates can be given at this time.

Air Pollutants↗
PubMed1997

Respiratory health and long-term exposure to air pollutants in Swiss schoolchildren. SCARPOL Team. Swiss Study on Childhood Allergy and Respiratory Symptoms with Respect to Air Pollution, Climate and Pollen.

The impact of long-term exposure to air pollution on respiratory and allergic symptoms and illnesses was assessed in a cross-sectional study of schoolchildren (ages 6 to 15 yr, n = 4,470) living in 10 different communities in Switzerland. Air pollution measurements (particulate matter less than 10 microns in diameter [PM10], nitrogen dioxide [NO2], sulfur dioxide [SO2], and ozone) and meteorologic data were collected in each community. Reported symptom rates of chronic cough, nocturnal dry cough, and bronchitis, adjusted for individual risk factors, were positively associated with PM10, NO2, and SO2. The strongest relationship was observed for PM10 (adjusted odds ratios for chronic cough, nocturnal dry cough, and bronchitis between the most and the least polluted community for PM10 were 3.07 [95% CI: 1.62 to 5.81], 2.88 [95% CI: 1.69 to 4.89], and 2.17 [95% CI: 1.21 to 4.89], respectively). The high correlation between the average concentrations of the pollutants makes the assessment of the relative importance of each pollutant difficult. No association between long-term exposure to air pollution and classic asthmatic and allergic symptoms and illnesses was found. There was some indication that frequency of fog is a risk factor of chronic cough and bronchitis, independent of air pollution. In conclusion, this study provides further evidence that rates of respiratory illnesses and symptoms among children augment with increasing levels of air pollution even in countries like Switzerland with moderate average air pollution concentrations.

Adolescent↗