Abstract  Using historical observations and model simulations, we investigate ozone trends prior to the mid-1970s onset of halogen-induced ozone depletion. Though measurements are quite limited, an analysis based on multiple, independent data sets (direct and indirect) provides better constraints than any individual set of observations. We find that three data sets support an apparent long-term stratospheric ozone trend of -7.2 ± 2.3 DU during 1957-1975, which modeling attributes primarily to water vapor increases. The results suggest that stratospheric ozone depletion may have been roughly 50% more than is generally supposed. Similarly, three data sets support tropospheric ozone increases over polluted Northern Hemisphere continental regions of 8.2 ± 2.1 DU during this period, which are mutually consistent with the stratospheric trends. As with paleoclimate data, which is also based on indirect proxies and/or limited spatial coverage, these results must be interpreted with caution. However, they provide the most thorough estimates presently available of ozone changes prior to the coincident onset of satellite data and halogen dominated ozone changes. If these apparent trends were real, the radiative forcing by stratospheric ozone since the 1950s would then have been -0.15 ± 0.05 W/m2, and -0.2 W/m2 since the preindustrial. For tropospheric ozone, it would have been 0.38 ± 0.10 W/m2 since the 1950s, larger than current estimates since 1850 which are derived from models that are even less well constrained. Going back to the preindustrial, the radiative forcing would have been +0.7 W/m2, roughly double what is generally assumed, although even more uncertain than the late twentieth century trends. These calculations demonstrate the importance of gaining a better understanding of historical ozone changes.

Abstract  Recent model calculations of the global mean radiative forcing from tropospheric ozone since preindustrial times fall in a relatively narrow range, from 0.3 to 0.5 W m−2. These calculations use preindustrial ozone fields that overestimate observations available from the turn of the nineteenth century. Although there may be calibration problems with the observations, uncertainties in model estimates of preindustrial natural emissions must also be considered. We show that a global three-dimensional model of tropospheric chemistry with reduced NOx emissions from lightning (1–2 Tg N yr−1) and soils (2 Tg N yr−1) and increased emissions of biogenic hydrocarbons can better reproduce the nineteenth century observations. The resulting global mean radiative forcing from tropospheric ozone since preindustrial times is 0.72–0.80 W m−2, amounting to about half of the estimated CO2 forcing. Reduction in the preindustrial lightning source accounts for two thirds of the increase in the ozone forcing. Because there is near-total titration of OH by isoprene in the continental boundary layer of the preindustrial atmosphere, isoprene and other biogenic hydrocarbons represent significant ozone sinks. The weak or absent spring maximum in the nineteenth century observations of ozone is difficult to explain within our understanding of the natural ozone budget. Our results indicate that the uncertainty in computing radiative forcing from tropospheric ozone since preindustrial times is larger than is usually acknowledged.

Abstract  The U.S. Environmental Protection Agency has established a federal reference method (FRM) for ozone (O3) and allowed for designation of federal equivalent methods (FEMs). However, the ethylene-chemiluminescence FRM for O3 has been replaced by the UV photometric FEM by most state and local monitoring agencies because of its relative ease of operation. Accumulating evidence indicates that the FEM is prone to bias under the hot, humid, and stagnant conditions conducive to high O3 formation. This bias may lead to overreporting hourly O3 concentrations by as much as 20-40 ppb. Measurement bias is caused by contamination of the O3 scrubber, a problem that is not detected by dry air calibration. An adequate wet test has not been codified, although a procedure has been proposed for agency consideration. This paper includes documentation of laboratory tests quantifying specific interferant responses, collocated ambient FRM/FEM monitoring results, and smog chamber comparisons of the FRM and FEMs with alternative scrubber designs. As the numbers of reports on monitor interferences have grown, interested parties have called for agency recognition and correction of these biases.

Abstract  Health Effects Institute, contract 91-6-2.#In order to test the hypothesis that ozone (O3)-induced changes in lung function and respiratory tract injury/inflammation are greater in subjects with asthma than in normal subjects, we exposed 18 asthmatic subjects, on separate days, to O3 (0.2 ppm) and filtered air for 4 h during exercise. Symptom questionnaires were administered before and after exposure, and pulmonary function tests (FEV1, FVC, and specific airway resistance [SRaw]) were performed before, during, and immediately after each exposure. Fiberoptic bronchoscopy, with proximal airway lavage (PAL) of the isolated left main bronchus and bronchoalveolar lavage (BAL; bronchial fraction, the first 10 ml of fluid recovered) of the right middle lobe, was performed 18 h after each exposure. The PAL, bronchial fraction, and BAL fluids were analyzed for the following endpoints: total and differential cell counts; total protein, lactate dehydrogenase (LDH), fibronectin, interleukin-8 (IL-8), granulocyte-macrophage colony-stimulating factor (GM-CSF), myeloperoxidase (MPO), and transforming growth factor-beta (TGF beta 2) concentrations. We found a significant O3 effect on FEV1, FVC, SRaw (p < 0.04) and lower respiratory symptoms (p < 0.001) for the asthmatic subjects. Ozone exposure also significantly increased the percent neutrophils in PAL (p < 0.01); percent neutrophils, total protein, and IL-8 in the bronchial fraction (p < 0.001, p < 0.05, and p < 0.01, respectively); and the percent neutrophils, total protein, LDH, fibronectin, IL-8, GM-CSF, and MPO in BAL (p < 0.001, p < 0.01, p < 0.01, p < 0.001, p < 0.05, p < 0.01, and p < 0.001, respectively) for the asthmatic subjects. There were no significant differences in the lung function responses of the asthmatic subjects in comparison with a group of normal subjects (n = 81) previously studied using an identical protocol, although there was a trend toward a greater O3-induced increase in SRaw in the asthmatic subjects (p < 0.13). In contrast, the asthmatic subjects showed significantly greater (p < 0.05) O3-induced increases in several inflammatory endpoints (percent neutrophils and total protein concentration) in BAL as compared with normal subjects who underwent bronchoscopy (n = 20). Our results indicate that asthmatic persons may be at risk of developing more severe O3-induced respiratory tract injury/inflammation than normal persons, and may help explain the increased asthma morbidity associated with O3 pollution episodes observed in epidemiologic studies.

Abstract  Ozone (O3) adaptation is a well-known, but poorly understood phenomenon that has been demonstrated in humans and laboratory animals. This study examined pulmonary function and bronchoalveolar lavage fluid (BALF) parameters in O3-adapted F-344 rats to explore possible mechanisms of adaptation. Of particular interest was ascorbic acid (AA), an antioxidant reported to be protective against O3 injury and found to be increased in O3-adapted rats. Adaptation was induced by exposure to 0.25 ppm O3, 12 hr/day for 6 or 14 weeks and evaluated with a challenge test, one that reexposed rats to 1.0 ppm O3 and measured attenuation in the O3 effect on frequency of breathing. Pulmonary function was assessed 1 day postexposure and adaptation and BALF were evaluated 1, 3, and 7 days postexposure. Results showed that forced vital capacity increased over time but decreased due to exposure and that the 14-week, O3-exposed rats had an increase in forced expiratory flow rate. All of the O3-exposed rats that were tested demonstrated adaptation on Postexposure Days 1, 3, and 7, but it was diminished on Day 7. Adaptation was also more pronounced in rats exposed for 14 weeks. Except for AA, BALF levels of total protein, potassium, lysozyme, uric acid, and alpha-tocopherol were unaffected by O3 exposure. Lactic acid dehydrogenase, alkaline phosphatase, glucose-6-phosphate dehydrogenase, and total glutathione were also assayed but were always below detectable limits. Ascorbic acid concentrations were elevated on Days 1, 3, and 7, showing postexposure patterns similar to those found for adaptation. Significant correlation was found between AA concentration and the magnitude of adaptation (r = 0.91, p < 0.002). We conclude that AA may play an important role in mechanisms associated with O3 adaptation in rats.

Abstract  We examined the associations between gaseous pollutants and hospitalization for chronic obstructive pulmonary diseases (COPD) among elderly people living in Vancouver, British Columbia, Canada, a city in which ambient air pollution levels are relatively low. We regressed the logarithm of daily counts of acute COPD hospitalization during the 5-year period from 1994 to 1998 on the daily mean levels of each pollutant, after accounting for seasonal and subseasonal fluctuations, non-Poisson dispersion, and weather variables. Nitrogen dioxide and carbon monoxide were significantly associated with hospitalization for COPD, and the magnitude of effects was increased slightly with increasing days of exposure averaging, with the relative risk for a 7-day average being 1.11 (95%CI: 1.04, 1.20) and 1.08 (1.02, 1.13) for nitrogen dioxide and carbon monoxide, respectively. There was no significant association between either sulfur dioxide or ozone and COPD hospitalization. The combined relative risk for all four gaseous pollutants on COPD hospitalization was 1.21. The effects of gaseous pollutants on COPD hospitalization were not significant after adjustment for PM10, although its inclusion did not have a marked effect on the point estimates for relative risks. Nitrogen dioxide has a significant impact on COPD hospitalization. Further studies are needed to separate the effects of single pollutants from the combined effects of the complex mixture of air pollutants in urban atmospheres.

Abstract  Two studies at three sites in the UK provided confirmation that systematic positive bias in NO2 diffusion tube measurement occurred because of changes to "within-tube" chemistry, rather than eddy diffusion at the mouth of the tube. In the first study in Cambridge, UK, sampler overestimation for 1 and 2 week exposures was compared to corresponding time-averaged monitor measurements (NO-NO2-NOx, O3) and weather variables. Noninearity between sampler and monitor NO2 measurements was interpreted in terms of spatial and temporal variations in relative and absolute availability of NO, NO2 and O3 at the site. A maximum overestimation occurred for an exposure mean NO2/NOx approximately 0.5. The separate contributions of reduced NO2 photolysis and eddy diffusion were compared in Study II using samplers of two materials, acrylic and quartz, and of different lengths (40, 55, 71 and 120 mm) at three sites: Norwich background, Cambridge intermediate, London kerbside. For compared sites, NO2 measured by acrylic samplers was significantly higher than for equivalent quartz samplers. For quartz samplers [NO2]mean was only just above the monitor at Norwich and London; sampler/monitor NO2 = 1.04 (P = 0.59) and 1.01(P = 0.76), respectively. For acrylic samplers the order of [NO2]mean was 40 mm > 120 mm > 71 mm > or = 55 mm. Excepting 40 mm samplers, this accords with a chemical bias where co-diffusing NO and 03 molecules in longer tubes have more time to react to form excess NO2. Bias in 40 mm samplers is discussed. Eddy diffusion is negligible for standard samplers because [NO2]mean was equivalent for 55 mm and 71 mm acrylic samplers and close to monitor NO2 for 71 mm quartz tubes. Both studies showed that sampler accuracy was dependent on location. Significantly, overestimation was greatest (approximately 3-4 ppb) where the NO2 annual mean was approximately 20 ppb, close to the UK and EU air quality standard of 21 ppb.

Abstract  BACKGROUND: The Democratic National Convention (DNC) in Boston, Massachusetts in 2004 provided an opportunity to evaluate the impacts of a localized and short-term but potentially significant change in traffic patterns on air quality, and to determine the optimal monitoring approach to address events of this nature. It was anticipated that the road closures associated with the DNC would both influence the overall air pollution level and the distribution of concentrations across the city, through shifts in traffic patterns. METHODS: To capture these effects, we placed passive nitrogen dioxide badges at 40 sites around metropolitan Boston before, during, and after the DNC, with the goal of capturing the array of hypothesized impacts. In addition, we continuously measured elemental carbon at three sites, and gathered continuous air pollution data from US EPA fixed-site monitors and traffic count data from the Massachusetts Highway Department. RESULTS: There were significant reductions in traffic volume on the highway with closures north of Boston, with relatively little change along other highways, indicating a more isolated traffic reduction rather than an across-the-board decrease. For our nitrogen dioxide samples, while there was a relatively small change in mean concentrations, there was significant heterogeneity across sites, which corresponded with our a priori classifications of road segments. The median ratio of nitrogen dioxide concentrations during the DNC relative to non-DNC sampling periods was 0.58 at sites with hypothesized traffic reductions, versus 0.88 for sites with no changes hypothesized and 1.15 for sites with hypothesized traffic increases. Continuous monitors measured slightly lower concentrations of elemental carbon and nitrogen dioxide during road closure periods at monitors proximate to closed highway segments, but not for PM2.5 or further from major highways. CONCLUSION: We conclude that there was a small but measurable influence of DNC-related road closures on air quality patterns in the Boston area, and that a low-cost monitoring study combining passive badges for spatial heterogeneity and continuous monitors for temporal heterogeneity can provide useful insight for community air quality assessments.

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  A lack of data on responses of mature tree growth and water use to ambient ozone (O3 ) concentrations has been a major limitation in efforts to understand and model responses of forests to current and future changes in climate. ò Here, hourly to seasonal patterns of stem growth and sap flow velocity were examined in mature trees from a mixed deciduous forest in eastern Tennessee (USA) to evaluate the effects of variations in ambient O3 exposure and climate on patterns of stem growth and water use. ò Ambient O3 caused a periodic slowdown in seasonal growth patterns that was attributable in part to amplification of diurnal patterns of water loss in tree stems. This response was mediated by statistically significant increases in O3 -induced daily sap flow and led to seasonal losses in stem growth of 30-50% for most species in a high-O3 year. ò Decreased growth and increased water use of mature forest trees under episodically high ambient O3 concentrations suggest that O3 will amplify the adverse effects of increasing temperatures on forest growth and forest hydrology.

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  There is mounting evidence that maternal exposure to ambient air pollution during pregnancy is associated with adverse birth outcomes. We examined birth weight and small for gestational age (SGA <10th percentile for age and gender) among 26,617 singleton full-term births in Brisbane, Australia (July 2000-June 2003), in relation to ambient pollution during pregnancy. We also examined head circumference (HC) and crown-heel length (CHL) among a sub-sample (n=21,432) of the term neonates. Maternal exposure to PM(10), visibility reducing particles (bsp), O(3) and NO(2) was assessed by calculating average exposure estimates over months and trimesters of pregnancy based on a citywide average of the pollutants. Linear and logistic regression models were employed to examine the effect of these pollutants on the birth outcomes after adjusting for potential confounders and season of birth. The regression coefficients were based on an inter-quartile range (IQR) increase in exposure as well as quartiles of exposure with the lowest used as a reference category. Trimester- and monthly specific exposures to all pollutants were not significantly associated with a reduction in either birth weight or HC, or an increased risk of SGA. An IQR increase in NO(2) during the third trimester was associated with a reduction in CHL (beta=-0.15cm, 95% CI -0.25 to -0.05cm) and this was concentrated around exposure during month nine. No other pollutants were associated with a reduction in CHL. In conclusion, there was no strong evidence suggesting that ambient air pollution during pregnancy is associated with sub-optimal fetal growth in Brisbane.

Abstract  OBJECTIVES: To evaluate the relationship between exposure to gaseous air pollutants (ozone [O3], carbon monoxide [CO], nitrogen dioxide [NO2], and sulfur dioxide [SO2]) socioeconomic status and the prevalence of symptoms of asthma, rhinitis and atopic eczema in adolescents. SUBJECTS AND METHODS: A sample of 16 209 adolescents from Sao Paulo West (SPW), Sao Paulo South (SPS), Santo Andre (SA), Curitiba (CR), and Porto Alegre (PoA) were enrolled. Data on air pollutants and socioeconomic status were compared to prevalence of symptoms with the Spearman correlation coefficient. RESULTS: Socioeconomic status was quite similar in all cities. The levels of O3 in SPW, SPS, and SA, and of CO in SA were higher than the acceptable ones. In relation to O3 and CO exposures, adolescents from SPW and SA had a significant risk of current wheezing, whereas living in SPW was associated with a high risk of rhinoconjunctivitis, eczema, and flexural eczema and living in CR to rhinitis. Exposure to NO2 was associated with a high risk of current wheezing in SPW and SA, and of severe asthma in SPW and PoA. Exposure to SO2 was associated with a high risk of current wheezing in SPW and SA, severe asthma in SPW and PoA, and nighttime cough, eczema, flexural eczema and severe eczema in SPW. Living in SPW, CR, or PoA was associated with a high risk of rhinitis, rhinoconjunctivitis, and severe rhinitis. CONCLUSIONS: Although we did not detect a characteristic pattern for all symptoms evaluated or a specific air pollutant, our data suggest a relationship between higher exposure to photochemical pollutants and high prevalence or risk of symptoms of asthma, rhinitis, and atopic eczema.

Abstract  Ozone (O3) is known to induce lung function impairment and airways inflammation during episodes of photochemical smog. The aim of the present study was to assess the inflammatory effect of ambient O3 in healthy children using nitric oxide in exhaled air (eNO) as a noninvasive test. The study was performed on 6 groups of children (n = 11-15), aged 6.5 to 15 yr, who attended summer camps in rural areas of the south of Belgium in 2002. Ambient O3 concentrations continuously monitored in the camps ranged from 48 to 221 microg/m3 (1-h maximal concentration). Children remained outdoors during the experimental days, doing various recreational activities but no sports. Lung function tests (forced expiratory volume in 1 s [FEV1] and forced vital capacity [FVC]) and eNO were measured twice in each child in the morning and in the evening. While lung function tests did not show any consistent pattern of decrease at these O3 levels, a highly significant increase in eNO was found in all subjects from an ambient 1-h O3 level of 167 microg/m3. A multivariate analysis did not reveal any influence of age, gender, height, weight, and body mass index (BMI) of the children. The threshold for this O3-induced increase in eNO estimated benchmark dose analysis was 135 microg/m3 for 1-h exposure and 110 microg/m3 for 8-h exposure. These observations suggest that ambient ozone produces early inflammatory changes in the airways of children at levels slightly below current air quality standards.

Abstract  AIM: The aim of the present study was to analyze the respiratory and cardiovascular functions among smoking and nonsmoking girls attending two schools situated in regions with different levels of air pollution. The characteristic of air pollution is based on the data gathered by stations 1 and 2 belonging to the Uniform National System for Monitoring the Air Pollution in Bulgaria. The participants (n=108, 16.07+/-0.80 years) were separated in two groups: smokers (S1 - from school 1, S2 - from school 2) and nonsmokers (NS1 - from school 1, NS2 - from school 2). All of them performed pulmonary function testing and .cardiopulmonary exercise testing on a treadmill using our modification of the Balke protocol (Marinov et al., 2000). Reference values for European children, previously validated for the Bulgarian population, were used. RESULTS: There are no significant differences in mean levels of VC, IC, FEV1, MEF50 and MEF25 (as a percentage from the predicted value as well). The average level of the Tiffneau index is noticeably higher among nonsmokers from the two regions and is the lowest among smokers from the more polluted area, but a significant difference exists between S2 (88.7+/-5.9) and NS2 (92.6+/-4.7), p=0.047; T(L,CO)%pred: S1 (85.4+/-7.2) vs. S2 (86.7+/-8.2), p=0.048 and NS1 (88.3+/-8.2) vs. NS2 (92.8+/-14.5), p=0.037; V(E)%pred: S1 (127.5+/-9.6) vs. S2 (123.7+/-6.1), p=0.035; higher levels of total lung capacity (TLC%pred), S1 (107.3+/-9.2) vs. NS2 (104.3+/-9.1), p=0.009 and alveolar ventilation (VA), S1 (5.0+/-0.6) vs. NS2 (4.6+/-0.5), p=0.008. CONCLUSIONS: 1. The negative effects of the combined influence of tobacco smoking and air pollution on some respiratory and cardiovascular functions of adolescent girls are more pronounced than each influence alone. 2. The cardiopulmonary exercise test gives adequate information about the combined effect of air pollution and smoking and using it for preventive purposes is an advisable method.

Abstract  OBJECTIVES: Nitrogen dioxide (NO2) has been inconsistently associated with gradual decreases in lung function. Here, we studied the effects of NO2 exposure in asthmatics by examining the association between changes in lung function and concentrations of NO2 which were personally measured. METHODS: Peak expiratory flow (PEF) and daily personal exposures to NO2 were recorded on 28 patients with asthma (confirmed by methacholine provocation test) over 4 weeks. We used generalized estimating equations to assess the relationship between personal NO2 exposure and PEF, adjusting for potential confounders such as age, gender, outdoor particulate matter, temperature, humidity, and exposure to environmental tobacco smoke. RESULTS: The personal NO2 exposures were higher than the corresponding ambient levels. The mean personal: ambient ratio for NO2 was 1.48. The personal NO2 exposures were not associated with the morning PEF, evening PEF, or the diurnal PEF variability. However, environmental tobacco smoke was negatively associated with both the morning and evening PEF. CONCLUSIONS: Among the asthmatic adults who participated in this study, we found no apparent impact of personal NO2 exposures on the peak expiratory flow.

Abstract  #PURPOSE OF REVIEW: There is evidence for an association between asthma and air pollutants, including ozone, NO2 and particulate matter. Since these pollutants are ubiquitous in the urban atmosphere and typically correlated with each other it has been difficult to ascertain the specific sources of air pollution responsible for the observed effects. Similarly, uncertainty in determining a causal agent, or multiple agents, has complicated efforts to identify the mechanisms involved in pollution-mediated asthma events and whether air pollution may cause asthma as well as exacerbate preexisting cases. RECENT FINDINGS: Numerous studies have examined specific sources of air pollution and their relationship to asthma. This review summarizes recent work conducted, specifically, on traffic pollution and presents results that elucidate several plausible biological mechanisms for the observed effects. Of note are studies linking susceptibility to several genetic polymorphisms. Together, these studies suggest that remaining uncertainties in the asthma-air pollution association may be addressed through enhanced assessment of both exposures and outcomes. SUMMARY: Air-pollution research is evolving rapidly; in the near future, clinicians and public health agencies may be able to use this new information to provide recommendations for asthmatics that go beyond only paying attention to the air-pollution forecast.

Abstract  Global 3-D tropospheric chemistry models in the literature show large differences in global budget terms for tropospheric ozone. The ozone production rate in the troposphere, P(Ox ), varies from 2300 to 5300 Tg yr-1 across models describing the present-day atmosphere. The ensemble mean of P(Ox ) in models from the post-2000 literature is 35% higher than that compiled in the Intergovernmental Panel on Climate Change (IPCC) Third Assessment Report (TAR). Simulations conducted with the GEOS-Chem model using two different assimilated meteorological data sets for 2001 (GEOS-3 and GEOS-4), as well as 3 years of GISS GCM meteorology, show P(Ox ) values in the range 4250-4700 Tg yr-1; the differences appear mostly because of clouds. Examination of the evolution of P(Ox ) over the GEOS-Chem model history shows major effects from changes in heterogeneous chemistry, the lightning NOx source, and the yield of organic nitrates from isoprene oxidation. Multivariate statistical analysis of model budgets in the literature indicates that 74% of the variance in P(Ox ) across models can be explained by differences in NOx emissions, inclusion of nonmethane volatile organic compounds (NMVOCs, mostly biogenic isoprene), and ozone influx from stratosphere-troposphere exchange (STE). Higher NOx emissions, more widespread inclusion of NMVOC chemistry, and weaker STE in the more recent models increase ozone production; however, the effect of NMVOCs does not appear generally sensitive to the magnitude of emissions within the range typically used in models (500-900 Tg C yr-1). We find in GEOS-Chem that P(Ox ) saturates when NMVOC emissions exceed 200 Tg C yr-1 because of formation of organic nitrates from isoprene oxidation, providing an important sink for NOx.

Abstract  The relationships between glutathione S-transferase (GST) M1, GSTT1, and GSTP1 genotypes and acute respiratory illness were investigated in a cohort of fourth grade school children aged 9-11 years who resided in 12 southern California communities. We used respiratory illness-related absences as a measure of respiratory illness occurrence. We ascertained respiratory illness-related school absences using an active surveillance system from January 1996 through June 1996. Genotypes for GSTM1 (null versus present), GSTT1 (null versus present), and GSTP1 (lle 105Val) were determined using genomic DNA from buccal cell specimens. The effects of GST genotypes on respiratory illness were assessed using stratified absence incidence rates and Poisson regression models. GSTP1 genotype was associated with risk for respiratory illness severe enough to result in a school absence. Children who were homozygous for the Val105 variant allele had lower incidence rates of upper and lower respiratory illnesses than did children who were homozygous for the Val105 allele. Children inheriting at least one Val105 allele were protected from respiratory illnesses (relative risk, 0.80; 95% confidence interval, 0.65-0.99). GSTM1 and T1 genotypes were not associated with respiratory illness. We conclude that GSTP1 genotype influences the risk or severity of respiratory infections in school-aged children.

Abstract  Background Polymorphisms at the glutathione S-transferase (GST) P1 locus were associated with asthma-related phenotypes and bronchial hyper-responsiveness. Objective This study investigated whether GSTP1 genotypes and outdoor air pollution were interactive risk factors on childhood asthma. Methods Four hundred and thirty-six subjects were recruited for oral mucosa samplings from 2853 fourth- to ninth-grade schoolchildren from three districts with different air pollution levels in southern Taiwan. PCR-based assays were performed by oral mucosa DNA to determine GSTP1 genotypes. We also conducted a nested case-control study comprising 61 asthmatic children and 95 controls confirmed by International Study of Asthma and Allergies in Childhood questionnaire results and methacholine challenge test. Multiple logistic regression was used to adjust for potential confounding factors. Results All participants were homozygous at the Ala-114 locus. Although only a marginally significant association existed between the frequency of homozygosity at the Ile-105 locus and asthma when air pollution was not considered, we found a significant gene-environmental interaction between GSTP1-105 alleles and air pollution after adjusting for confounders (P=0.035). Specifically, we found that compared with participants carrying any Val-105 allele in low air pollution, those who are Ile-105 homozygotes in high air pollution district had a significantly increased risk of asthma (adjusted odds ratio (AOR)=5.52, 95% confidence interval (CI)=1.64-21.25). Compared with participants carrying any Val-105 allele, in high air pollution district, children with Ile-105 homozygotes had a significantly increased risk of asthma (AOR=3.79, 95% CI=1.01-17.08), but those who carried two Ile-105 alleles in low or moderate air pollution districts did not show similar tendencies. The risk of asthma also revealed a clear dose-response relationship with outdoor air pollution in children with Ile-105 homozygotes. Conclusion Our result suggests a gene-environmental interaction between GSTP1-105 genotypes and outdoor air pollution on childhood asthma.

Abstract  Measurements of NO and NO2 are reported using a highly modified photofragmentation two-photon laser-induced fluorescence (PF-TP-LIF) instrument. Available evidence suggests that the changes made substantially reduced wall decomposition of labile NOy species. In sharp contrast to the results reported from NASA's 1991 PEM-West A program where the median value for the ratio (NO2)(meas)/(NO2)(calc) was 3.36, the PEM-Tropics A observations produced a value for this ratio of 0.93. This represents the first time that remote upper tropospheric NO-NO2 data have shown a high degree of correspondence with current photochemical mechanisms.

Abstract  Oxides of nitrogen in fresh traffic exhaust are known to scavenge ambient ozone. However, there has only been little study of local variation in ozone resulting from variation in vehicular traffic patterns within communities. Homes of 78 children were selected from a sample of participants in 3 communities in the southern California Children's Health Study. Twenty-four hour ozone measurements were made simultaneously at a home and at a community central site monitor on two occasions between February and November 1994. Homes were geo-coded, and local residential nitrogen oxides (NOx) above regional background due to nearby traffic at each participant's home were estimated using a line source dispersion model. Measured home ozone declined in a predictable manner as modeled residential NOx increased. NOx modeled from local traffic near homes accounted for variation in ozone concentrations of as much as 17 parts per billion. We conclude that residential ozone concentrations may be over- or underestimated by measurements at a community monitor, depending on the variation in local traffic in the community. These findings may have implications for studies of health effects of traffic-related pollutants.