Abstract  Air quality indices currently in use have been criticized because they do not capture additive effects of multiple pollutants, or reflect the apparent no-threshold concentration-response relationship between air pollution and health. We propose a new air quality health index (AQHI), constructed as the sum of excess mortality risk associated with individual pollutants from a time-series analysis of air pollution and mortality in Canadian cities, adjusted to a 0-10 scale, and calculated hourly on the basis of trailing 3-hr average pollutant concentrations. Extensive sensitivity analyses were conducted using alternative combinations of pollutants from single and multipollutant models. All formulations considered produced frequency distributions of the daily maximum AQHI that were right-skewed, with modal values of 3 or 4, and less than 10% of values at 7 or above on the 10-point scale. In the absence of a gold standard and given the uncertainty in how to best reflect the mix of pollutants, we recommend a formulation based on associations of nitrogen dioxide, ozone, and particulate matter of median aerodynamic diameter less than 2.5 μm with mortality from single-pollutant models. Further sensitivity analyses revealed good agreement of this formulation with others based on alternative sources of coefficients drawn from published studies of mortality and morbidity. These analyses provide evidence that the AQHI represents a valid approach to formulating an index with the objective of allowing people to judge the relative probability of experiencing adverse health effects from day to day. Together with health messages and a graphic display, the AQHI scale appears promising as an air quality risk communication tool. [ABSTRACT FROM AUTHOR] Copyright of Journal of the Air & Waste Management Association (1995) is the property of Air & Waste Management Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts)

Abstract  Background: A growing body of research suggests that prenatal exposure to air pollution may be harmful to fetal development. We assessed the association between exposure to air pollution during pregnancy and anthropometric measures at birth in four areas within the Spanish Children's Health and Environment (INMA) mother and child cohort study. Methods: Exposure to ambient nitrogen dioxide (NO2) and benzene was estimated for the residence of each woman (n = 2,337) for each trimester and for the entire pregnancy. Outcomes included birth weight, length, and head circumference. The association between residential outdoor air pollution exposure and birth outcomes was assessed with linear regression models controlled for potential confounders. We also performed sensitivity analyses for the subset of women who spent more time at home during pregnancy. Finally, we performed a combined analysis with meta-analysis techniques. Results: In the combined analysis, an increase of 10 µg/m3 in NO2 exposure during pregnancy was associated with a decrease in birth length of -0.9 mm [95% confidence interval (CI), -1.8 to -0.1 mm]. For the subset of women who spent ≥ 15 hr/day at home, the association was stronger (-0.16 mm; 95% CI, -0.27 to -0.04). For this same subset of women, a reduction of 22 g in birth weight was associated with each 10-µg/m3 increase in NO2 exposure in the second trimester (95% CI, -45.3 to 1.9). We observed no significant relationship between benzene levels and birth outcomes. Conclusions: NO2 exposure was associated with reductions in both length and weight at birth. This association was clearer for the subset of women who spent more time at home.

Abstract  Halogen atoms and oxides are highly reactive and can profoundly affect atmospheric composition. Chlorine atoms can decrease the lifetimes of gaseous elemental mercury(1) and hydrocarbons such as the greenhouse gas methane(2). Chlorine atoms also influence cycles that catalytically destroy or produce tropospheric ozone(3), a greenhouse gas potentially toxic to plant and animal life. Conversion of inorganic chloride into gaseous chlorine atom precursors within the troposphere is generally considered a coastal or marine air phenomenon(4). Here we report mid-continental observations of the chlorine atom precursor nitryl chloride at a distance of 1,400km from the nearest coastline. We observe persistent and significant nitryl chloride production relative to the consumption of its nitrogen oxide precursors. Comparison of these findings to model predictions based on aerosol and precipitation composition data from long-term monitoring networks suggests nitryl chloride production in the contiguous USA alone is at a level similar to previous global estimates for coastal and marine regions(5). We also suggest that a significant fraction of tropospheric chlorine atoms(6) may arise directly from anthropogenic pollutants.

Abstract  Multipollutant models are frequently used to differentiate roles of multiple pollutants in epidemiologic studies of ambient air pollution. In the presence of differing levels of measurement error across pollutants under consideration, however, they can be biased and as misleading as single-pollutant models. Their appropriate interpretation depends on the relationships among the pollutant measurements and the outcomes in question. In situations where two or more pollutant variables may be acting as surrogates for the etiologic agent(s), multipollutant models can help identify the best surrogate, but the risk estimates may be influenced by inclusion of a second variable that is not itself an independent risk factor for the outcome in question. In this paper, these issues will be illustrated in the context of an ongoing study of emergency visits in Atlanta. Emergency department visits from 41 of 42 hospitals serving the twenty-county Atlanta metropolitan area for the period 1993-2004 (n=10,206,389 visits) were studied in relation to ambient pollutant levels, including speciated particle measurements from an intensive monitoring campaign at a downtown station starting in 1998. Relative to our earlier publications, reporting results through 2000, the period for which the speciated data are now available is now tripled (six years in length). Poisson generalized linear models were used to examine outcome counts in relation to three-day moving average concentrations of pollutants of a priori interest (ozone, nitrogen dioxide, carbon monoxide, sulfur dioxide, oxygenated hydrocarbons, PM10, coarse PM, PM2.5, and the following components of PM2.5: elemental carbon, organic carbon, sulfate, water-soluble transition metals.) In the present analysis, we report results for two outcome groups: a respiratory outcomes group and a cardiovascular outcomes group. For cardiovascular visits, associations were observed with CO, 3 NO2, and PM2.5 elemental carbon and organic carbon. In multipollutant models, CO was the strongest predictor. For respiratory visits, associations were observed with ozone, PM10, CO and NO2 in single-pollutant models. In multipollutant models, PM10 and ozone persisted as predictors, with ozone the stronger predictor. Caveats and considerations in interpreting the multipollutant model results are discussed.

Abstract  This article describes the governing equations, computational algorithms, and other components entering into the Community Multiscale Air Quality (CMAQ) modeling system. This system has been designed to approach air quality as a whole by including state-of-the-science capabilities for modeling multiple air quality issues, including tropospheric ozone, fine particles, acid deposition, and visibility degradation. CMAQ was also designed to have multiscale capabilities so that separate models were not needed for urban and regional scale air quality modeling. By making CMAQ a modeling system that addresses multiple pollutants and different spatial scales, it has a "one-atmosphere" perspective that combines the efforts of the scientific community. To implement multiscale capabilities in CMAQ, several issues (such as scalable atmospheric dynamics and generalized coordinates), which depend on the desired model resolution, are addressed. A set of governing equations for compressible nonhydrostatic atmospheres is available to better resolve atmospheric dynamics at smaller scales. Because CMAQ is designed to handle scale-dependent meteorological formulations and a large amount of flexibility, its governing equations are expressed in a generalized coordinate system. This approach ensures consistency between CMAQ and the meteorological modeling system. The generalized coordinate system determines the necessary grid and coordinate transformations, and it can accommodate various vertical coordinates and map projections. The CMAQ modeling system simulates various chemical and physical processes that are thought to be important for understanding atmospheric trace gas transformations and distributions. The modeling system contains three types of modeling components (Models-3): a meteorological modeling system for the description of atmospheric states and motions, emission models for man-made and natural emissions that are injected into the atmosphere, and a chemistry-transport modeling system for simulation of the chemical transformation and fate. The chemical transport model includes the following process modules: horizontal advection, vertical advection, mass conservation adjustments for advection processes, horizontal diffusion, vertical diffusion, gas-phase chemical reactions and solvers, photolytic rate computation, aqueous-phase reactions and cloud mixing, aerosol dynamics, size distributions and chemistry, plume chemistry effects, and gas and aerosol deposition velocity estimation. This paper describes the Models-3 CMAQ system, its governing equations, important science algorithms, and a few application examples.

Abstract  Aims: To investigate the chronic effects of air pollution caused mainly by automobiles in healthy adult females. Methods: Respiratory symptoms were investigated in 5682 adult females who had lived in the Tokyo metropolitan area for three years or more in 1987; 733 of them were subjected to pulmonary function tests over eight years from 1987 to 1994. The subjects were divided into three groups by the level of air pollution they were exposed to during the study period. The concentrations of nitrogen dioxide and suspended particulate matter were the highest in group 1, and the lowest in group 3. Results: The prevalence rates of respiratory symptoms in group 1 were higher than those in groups 2 and 3, except for wheezing. Multiple logistic regression analysis showed significant differences in persistent phlegm and breathlessness. The subjects selected for the analysis of pulmonary function were 94, 210, and 102 females in groups 1, 2, and 3, respectively. The annual mean change of FEV1 in group 1 was the largest (-0.020 l/y), followed by that in group 2 (-0.015 l/y), and that in group 3 (-0.009 l/y). Testing for trends showed a significant larger decrease of FEV1 with the increase in the level of air pollution. Conclusions: The subjects living in areas with high levels of air pollution showed higher prevalence rates of respiratory symptoms and a larger decrease of FEV1 compared with those living in areas with low levels of air pollution. Since the traffic density is larger in areas with high air pollution, the differences among the groups may reflect the effect of air pollution attributable to particulate matter found in automobile exhaust.

Abstract  Gaseous nitrogen dioxide (NO2) was found to induce umuC gene expression in Salmonella typhimurium carrying the umuC-lacZ fusion plasmid. The induction level of the umu operon responsible for inducible mutagenesis was measured by the level of beta-galactosidase in the cell, encoded by the fusion gene. NO2 gas was bubbled into bacterial suspensions at 10, 30 and 90 microliters/l for 30 min at a flow rate of 100 ml/min. Expression of the umuC gene varied with the concentration, flow rate and bubbling time of the NO2 gas. Although NO2 gas induces SOS functions, mutagenesis due to it was not detectable in Salmonella typhimurium TA100 and TA102. Nitric oxide gas (NO) did not induce any umuC gene expression.

Abstract  Nitrogen dioxide induced SOS functions in Salmonella typhimurium and Escherichia coli K-12 and was mutagenic in Escherichia coli WP2. When a rabbit was administered aminopyrine intravenously and administered nitrogen dioxide by inhalation, N-nitrosodimethylamine was detected in its blood. Analysis was conducted with 15N-nitrosodimethylamine as an internal standard by a combination of capillary gas chromatography and mass spectrometry. Accompanying administration of cystamine increased the blood concentration of N-nitrosodimethylamine in the rabbit, suggesting inhibition of its metabolism. Concurrent sulfur trioxide inhalation increased N-nitrosodimethylamine formation in the rabbit.

Abstract  Nitric oxide (NO.) is a physiological messenger formed by several cell types. Reaction with O2 forms oxides that nitrosate amines at pH values near 7. We now report experiments in which NO. was added to intact human cells and to aerobic solutions of DNA, RNA, guanine, or adenine. TK6 human lymphoblastoid cells were mutated 15- to 18-fold above background levels at both the HPRT and TK gene loci. Xanthine and hypoxanthine, from deamination of guanine and adenine, respectively, were formed in all cases. NO. induced dose-responsive DNA strand breakage. Yields of xanthine ranged from nearly equal to about 80-fold higher than those of hypoxanthine. Yields of xanthine and hypoxanthine from nucleic acids were higher than those from free guanine and adenine. This was most pronounced for xanthine; 0.3 nmol/mg was formed from free guanine vs. 550 nmol/mg from calf thymus RNA. Nitric oxide added to TK6 cells produced a 40- to 50-fold increase in hypoxanthine and xanthine in cellular DNA. We believe that these results, plus the expected deaminations of cytosine to uracil and 5-methylcytosine to thymine, account for the mutagenicity of nitric oxide toward bacteria and mammalian cells.

Abstract  Male CD-1 mice were exposed to an nominal concentration of 20 p.p.m. of 15N-nitrogen dioxide (15NO2) for 6 h/day for 4 days and for 2 h on the day 5, and to 1 g morpholine/kg body wt by gavage daily for five consecutive days. N-Nitrosomorpholine (NMOR) was found in whole mice, stomachs, skins with hair, and remains. The sum of individual tissue concentrations measured separately was 3421 ng/tissue, where the average skin weighed 4.3 g, the average stomach weighed 1.0 g and the average remains weighed 22.2 g. The average whole mouse weighed 27.7 g and contained a total of 3903 ng of NMOR. The concentration of NMOR was highest in the skin, next highest in the stomach, and lowest in the remains. However, the total quantity of NMOR per tissue, while highest in the skin (83%), was next highest in the remains (14.8%) and lowest in the stomach (2.2%). GC-MS analysis served to distinguish between the NMOR of 15NO2 origin and that of other origin. All of the NMOR in the whole mouse homogenates was identified as 15NMOR. In the stomach 73% was identified as 14NMOR, representing 1.6% of the total NMOR in the mouse, and 27% as 15NMOR, representing 0.6% of the total NMOR in the mouse. N-Nitrosamine formation in vivo is discussed as a possibly ongoing mammalian process.

Abstract  Nitrogen dioxide (NO2) is a ubiquitous, pollutant gas that produces a broad range of pathological and physiological effects on the lung. Absorption of inhaled NO2 is coupled to near-interfacial reactions between the solute gas and constituents of the airway and alveolar epithelial lining fluid. Although alveolar surfactant imparts limited resistance to respiratory gas exchange compared with that contributed by either the pulmonary membrane or uptake in red blood cells, resistance to NO2 flux could have a significant effect on NO2 absorption kinetics. To investigate the effect of interfacial surfactant on NO2 absorption, we designed an apparatus permitting exposure of variably compressed monolayers. Our results suggest that compressed monolayers enriched in 1,2-dipalmitoyl-sn-3-glycero-phosphocholine present significant resistance to NO2 absorption even at surface tensions greater than those achieved in vivo. However, monolayers composed of pure unsaturated phospholipids failed to alter NO2 absorption significantly when compressed, in spite of similar reductions in surface tension. The results demonstrate that phospholipid monolayers appreciably limit NO2 absorption and further that monolayer-induced resistance to NO2 flux is related to physicochemical properties of the film itself rather than alterations within the aqueous and gas phases. On the basis of these findings, we propose that pulmonary surfactant may influence the intrapulmonary gas phase distribution of inhaled NO2.

Abstract  To determine if nitrogen dioxide (NO2), a gaseous free radical, modifies the protective antioxidant pool present in respiratory tract lining fluids, a random, double-blind study utilizing flexible fiberoptic bronchoscopy with bronchial and bronchoalveolar lavage was performed. Healthy, nonsmoking, asymptomatic subjects were exposed to filtered air and 2 ppm NO2 for 4 h on separate occasions. To examine the kinetics of the NO2-induced antioxidant reactions, 44 subjects were randomly assigned to one of three groups. Bronchoscopy was performed 1.5 h (group 1), 6 h (group 2) or 24 h (group 3) after each exposure. Reduced glutathione (GSH), uric acid, and ascorbic acid concentrations were determined in both bronchial and bronchoalveolar lavage fluid fractions. In addition, bronchoalveolar lavage fluid was screened for malondialdehyde as a marker of lipid peroxidation. Exposure to NO2 resulted in a rapid (1.5 h) loss of uric acid from the bronchial region, however by 6 h after exposure it had increased significantly above control uric acid concentration in this region. At 24 h after exposure, uric acid concentration had returned to the control level. A similar response of uric acid to NO2 was seen in the bronchoalveolar region. Ascorbic acid was also decreased in bronchial and bronchoalveolar lavage fluids 1.5 h after exposure to NO2, but returned to control values by 6 h. In marked contrast, significant increases in GSH concentration were seen at 1.5 and 6 h in bronchial lavage fluid after exposure to NO2, which subsequently returned to control levels by 24 h. No change in bronchoalveolar lavage fluid GSH concentration or malondialdehyde content was seen after NO2 exposure. These data support the view that antioxidants present in lung fluids react with, and hence modulate the impact of, NO2 on the lung.

Abstract  Several nasal nitric oxide (NO) measurement techniques have been described, but there is not a widespread measurement technique for measurement of nasal NO. In this study we evaluated the repeatability of one technique of nasal NO measurements using the nasal application of the NIOX system. METHODS: Three nasal NO measurements (NIOX Nitric Oxide Monitoring System, Aerocrine, Sweden) were made on a single occasion in 22 healthy subjects and 27 patients with asthma, aged 5-69 years. Nasal NO was sampled during breath hold from one nostril at a flow rate of 5 ml/s. RESULTS: The repeatability of nasal NO assessed by the coefficient of variation (CV) was 12.5% (95% Confidence interval (CI) 11.0-14.7%) for the total population. Healthy adults had a significantly better repeatability than healthy children (P<0.008). The mean NO level for the total population was 837 ppb. The mean NO levels in children were lower than in the adults (751 and 897 ppb, respectively). The mean breath hold length needed to obtain a steady NO plateau for all subject categories combined was 20.4+/-6.01 s. The average number of attempts needed to obtain three approved NO measurements was 5.4 (range 3-13) for the total population. There were no significant differences between the different subject categories. When using two measurements per session instead of three, the overall CV was 10.5% (95% CI 8.8-13.1%). Most subjects found the measurements easy to perform and all of them would accept to do the examination as a routine. CONCLUSIONS: Nasal NO measurements in NIOX may provide a useful reliable clinical tool to assess and monitor upper airways in different diseases, for example PCD and rhinitis, and are acceptable by both healthy and asthmatic adults and children, as a part of their routine visit to a physician.

Abstract  The Global Ozone Monitoring Experiment (GOME) is a new instrument aboard the European Space Agency's (ESA) Second European Remote Sensing Satellite (ERS-2), which was launched in April 1995. The main scientific objective of the GOME mission is to determine the global distribution of ozone and several other trace gases, which play an important role in the ozone chemistry of the earth's stratosphere and troposphere. GOME:measures the sunlight scattered from the earth's atmosphere and/or reflected by the surface in nadir viewing mode in the spectral region 240-790 nm at a moderate spectral resolution of between 0.2 and 0.4 nm. Using the maximum 960-km across-track swath width, the spatial resolution of a GOME ground pixel is 40 X 320 km(2) for the majority of the orbit and global coverage is achieved in three days after 43 orbits. Operational data products of GOME as generated by DLR-DFD, the German Data Processing and Archiving Facility (D-PAF) for GOME, comprise absolute radiometrically calibrated earthshine radiance and solar irradiance spectra (level 1 products) and global distributions of total column amounts of ozone and NO2, (level 2 products), which are derived using the DOAS aroach (Differential Optical Absorption Spectroscopy). (Under certain conditions and some restrictions, the operational data products are publically available from the European Space Agency via the ERS Helpdesk.) In addition to the operational data products, GOME has delivered important information about other minor trace gases such as OClO, volcanic SO2, H2CO from biomass burning, and tropospheric BrO. Using an iterative optimal estimation retrieval scheme, ozone vertical profiles can be derived from the inversion of the UV/VIS spectra. This paper reports on the GOME instrument, its operation mode, and the retrieval techniques, the latter with particular emphasis on DOAS (total column retrieval) and advanced optimal estimation (ozone profile retrieval). Observation of ozone depletion in the recent polar spring seasons in both hemispheres are presented. OClO observed by GOME under twilight conditions provides valuable information on the chlorine activation inside the polar vortex, which is believed to be responsible for the rapid catalytic destruction of ozone. Episodes of enhanced BrO in the Arctic, most likely contained in the marine boundary layer, were observed in early and late spring. Excess tropospheric nitrogen dioxide and ozone have been observed during the recent Indonesian fire in fall 1997. Formaldehyde could also clearly be identified by GOME and is known to be a by-product resulting from biomass burning.

Abstract  The heterogeneous reaction of NO2 with water on the surface of laboratory systems has been known for decades to generate HONO, a major source of OH that drives the formation of ozone and other air pollutants in urban areas and possibly in snowpacks. Previous studies have shown that the reaction is first order in NO2 and in water vapor, and the formation of a complex between NO2 and water at the airûwater interface has been hypothesized as being the key step in the mechanism. We report data from long path FTIR studies in borosilicate glass reaction chambers of the loss of gaseous NO2 and the formation of the products HONO, NO and N2O. Further FTIR studies were carried out to measure species generated on the surface during the reaction, including HNO3, N2O4 and NO2+. We propose a new reaction mechanism in which we hypothesize that the symmetric form of the NO2 dimer, N2O4, is taken up on the surface and isomerizes to the asymmetric form, ONONO2. The latter autoionizes to NO+NO3-, and it is this intermediate that reacts with water to generate HONO and surface-adsorbed HNO3. Nitric oxide is then generated by secondary reactions of HONO on the highly acidic surface. This new mechanism is discussed in the context of our experimental data and those of previous studies, as well as the chemistry of such intermediates as NO+ and NO2+ that is known to occur in solution. Implications for the formation of HONO both outdoors and indoors in real and simulated polluted atmospheres, as well as on airborne particles and in snowpacks, are discussed. A key aspect of this chemistry is that in the atmospheric boundary layer where human exposure occurs and many measurements of HONO and related atmospheric constituents such as ozone are made, a major substrate for this heterogeneous chemistry is the surface of buildings, roads, soils, vegetation and other materials. This area of reactions in thin films on surfaces (SURFACE=Surfaces, Urban and Remote: Films As a Chemical Environment) has received relatively little attention compared to reactions in the gas and liquid phases, but in fact may be quite important in the chemistry of the boundary layer in urban areas.

Abstract  The effect of exposure to irritant air pollutants on the development of allergic airway disease is poorly understood. This study examines the effects of the lower respiratory tract irritant, NO2, on the outcome of ovalbumin (OVA)-induced allergic airway disease. Male and female C57Bl/6 mice were sensitized by weekly intraperitoneal (ip) OVA injections for 3 wk followed by daily 1-h OVA aerosol inhalation challenge for 3 or 10 d. Initially, mice were exposed daily for 3 d to air or 0.7 or 5 ppm NO2 for 2 h following each OVA aerosol challenge. OVA exposure resulted in pronounced lower airway inflammation, as evidenced by a significant increase in bronchoalveolar lavage (BAL) total cellularity and eosinophil levels. BAL eosinophil levels were significantly lower in OVA-NO2 compared to OVA-air animals. The reduction was similar at both NO2 exposure concentrations. In a subsequent study, sensitized animals were exposed for 3 or 10 d to aerosolized OVA followed by air or 0.7 ppm NO2. BAL eosinophils were again reduced at 3 d by OVA-NO2 exposure compared to OVA-air mice. At 10 d the eosinophilia was virtually abolished. This reduction in OVA-induced cellular inflammation by NO2 was confirmed by histopathological analysis. Contrary to expectations, exposure to NO2 during the aerosol challenge to OVA dramatically diminished the outcome of allergic disease in lungs as measured by airway cellular inflammation.

Abstract  Morphometric procedures were used to determine the number of cells, cell volume, cell diameter, and surface areas of the airways in human and rat lungs. Nuclear sizes of epithelial cells from human bronchi were significantly larger than other lung cell nuclei. The average volume of human ciliated cell nuclei was 310 ± 30 Ám(3) and 167 ± 12 Ám(3) in bronchi and bronchioles, respectively. The smaller nuclei of human bronchioles were comparable to those of alveolar cells. In the pseudostratified epithelium of human bronchi, basal cells had a large surface area in contact with the basement membrane (51.3 ± 4.6 Ám(2) per cell) when compared with ciliated (1.1 ± 0.1 Ám(2)), goblet (7.6 ± 1.2 Ám(2)), or other secretory cells (12.0 ± 2.1 Ám(2)). In the first four airway generations distal to the trachea, basal cells account for 30% of the cells in human airway epithelium and 2% of the cells in rat airway epithelium. Total airway surface area from trachea to bronchioles was 2,471 ± 320 and 27.2 ± 1.7 cm(2) in human and rat lungs, respectively. These direct measurements of airway surface area are less than half of the estimates based on current lung models. The total number of airway epithelial cells were 10.5 x 10(9) for human and 0.05 X 10(9) for rat lungs. For both species, there were 18 times more alveolar cells than bronchial epithelial cells.

Abstract  This criteria document focuses on a review and assessment of the effects on human health and welfare of the nitrogen oxides, nitric oxide (NO) and nitrogen dioxide (NO2), and the related compounds, nitrites, nitrates, nitrogenous acids, and nitrosamines. Although the emphasis is on presentation of health and welfare effects data, other scientific data are presented in order to provide a better understanding of these pollutants in the environment. To this end, separate chapters are included which discuss the nitrogen cycle, sources and emissions, atmospheric chemical processes which transform emissions of nitrogen oxides into related airborne compounds, transport and removal processes, measurement methods, and atmospheric concentrations of nitrogenous pollutants.

Abstract  BACKGROUND: Recent studies have suggested that exposure to air pollutants may enhance the airway responsiveness of susceptible individuals to inhaled allergen. METHODS: To investigate the effect of exposure to nitrogen dioxide (NO2) on nasal airways resistance (NAR) and inflammatory mediators in nasal lavage fluid, eight subjects with a history of seasonal allergic rhinitis, who were tested out of season, were exposed in a randomized single-blind, crossover study to either air or 400 ppb NO2 for 6 hours. The changes in NAR and eosinophil cationic protein (ECP), mast cell tryptase (MCT), neutrophil myeloperoxidase (MPO), and interleukin-8 (IL-8) in nasal lavage fluid before and after exposure were evaluated. Another group of eight subjects with a history of seasonal allergic rhinitis were also randomized to exposure to air or 400 ppb NO2 for 6 hours and then challenged with allergen, before evaluation for changes in NAR and changes in ECP, MCT, MPO, and IL-8 in nasal lavage fluid. RESULTS: Exposure to air or NO2 did not alter either NAR or the levels of ECP, MCT, MPO, or IL-8 in nasal lavage fluid. Allergen challenge after exposure to both air and NO2 significantly (p < 0.05) increased levels of MCT, but not MPO and IL-8 in the nasal lavage fluid. In addition, allergen challenge after exposure to NO2 but not air, significantly increased levels of only ECP in nasal lavage fluid (p < 0.05). CONCLUSIONS: These results suggest that acute exposure to NO2 at concentrations found at the curbside in heavy traffic during episodes of pollution, may "prime" eosinophils for subsequent activation by allergen in individuals with a history of seasonal allergic rhinitis.

Abstract  The expanded Second Edition of Dr. Rothman's acclaimed Modern Epidemiology reflects the remarkable conceptual development of this evolving science and the engagement of epidemiologists with an increasing range of current public health concerns. This landmark work is the most comprehensive and cohesive text on the principles and methods of contemporary epidemiologic research.Coauthored by two leading epidemiologists, with 15 additional contributors, the Second Edition presents a much broader range of concepts and methods than Dr. Rothman's single-authored original edition. Coverage of basic measures and study types is more thorough and includes a new chapter on field methods. New chapters on advanced topics in data analysis, such as hierarchical regression, are also included. A new section covers specific areas of research such as infectious disease epidemiology, ecologic studies, disease surveillance, analysis of vital statistics, screening, clinical epidemiology, environmental and occupational epidemiology, reproductive and perinatal epidemiology, genetic epidemiology, and nutritional epidemiology.

Abstract  A mechanized wheel was constructed for use in evaluating the interaction of exercise and gaseous pollutants such as O3 and NO2. Immediately after the pollutant exposure, both exercised and nonexercised female mice (CD-1) were combined with controls, challenged with an aerosol of viable Streptococcus pyogenes (group C), and then observed over a 15-d period for incidence of mortality. Exposure to O3 at 196 micrograms/m3 (0.1 ppm) or 590 micrograms/m3 (0.3 ppm) while exercising yielded mortality rates that were significantly higher than those observed in the O3 groups that were not exercised. With exposure to NO2 at 5640 micrograms/m3 (3 ppm), exercise produced a significant enhancement in mortality over the other treatment groups. These studies show that exercise can affect the mortality observed in this model system and indicate the need for establishing safe exposure levels of pollutants as a function of the activity level of the exposed population.

Abstract  Previous studies of 2 h of exposure to NO2 at high urban atmospheric levels (i.e., 0.50-1.0 ppm), utilizing light-to-moderate exercise for up to 1 h have failed to demonstrate significant pulmonary dysfunction in healthy humans. To test the hypothesis that heavy sustained exercise would elicit pulmonary dysfunction on exposure to 0.60 ppm NO2 and/or enhance the effects of exposure to 0.30 ppm O3, 40 aerobically trained young adults (20 males and 20 females) completed 1 h of continuous exercise at work rates eliciting a mean minute ventilation of 70 and 50 l/min for the males and females, respectively. Exposures to filtered air, 0.60 ppm NO2, 0.30 ppm O3, and 0.60 ppm NO2 plus 0.30 ppm O3 were randomly delivered via an obligatory mouthpiece inhalation system. Treatment effects were assessed by standard pulmonary function tests and exercise ventilatory and subjective symptoms response. Two-way analysis of variance with repeated measures and post hoc analyses revealed a statistically significant (P less than 0.05) effect of O3 on forced expiratory parameters, specific airway resistance, exercise ventilatory response, and reported subjective symptoms of respiratory discomfort. In contrast, no significant effect of NO2 was observed nor was there any significant interaction of NO2 and O3 in combination. There were no significant differences between male and female responses to gas mixture treatments. It was concluded that inhalation of 0.60 ppm NO2 for 1 h while engaged in heavy sustained exercise does not elicit effects evidenced by measurement techniques used in this study nor evoke additive effects beyond those induced by 0.30 ppm O3 in healthy young adults.

Abstract  Nitrogen dioxide (NO2) is an important component of both outdoor and indoor air pollution. NO2 is a reactive gas that participates with sunlight, hydrocarbons, and oxygen in the formation of ozone and other photochemical oxidants. No2 may also react with aerosols to form nitrous and nitric acids. The principal source of NO2 in outdoor air is motor vehicle emissions, although power pants and fossil-fuel-burning industries also contribute lesser amounts of this gas.