Previous studies have reported adverse effects of either regional or near-roadway air pollution (NRAP) on lung function. However, there has been little study of the joint effects of these exposures.
Objectives
To assess the joint effects of NRAP and regional pollutants on childhood lung function in the Children9s Health Study.
Methods
Lung function was measured on 1811 children from eight Southern Californian communities. NRAP exposure was assessed based on (1) residential distance to the nearest freeway or major road and (2) estimated near-roadway contributions to residential nitrogen dioxide (NO2), nitric oxide (NO) and total nitrogen oxides (NOx). Exposure to regional ozone (O3), NO2, particulate matter with aerodynamic diameter <10 µm (PM10) and 2.5 µm (PM2.5) was measured continuously at community monitors.
Results
An increase in near-roadway NOx of 17.9 ppb (2 SD) was associated with deficits of 1.6% in forced vital capacity (FVC) (p=0.005) and 1.1% in forced expiratory volume in 1 s (FEV1) (p=0.048). Effects were observed in all communities and were similar for NO2 and NO. Residential proximity to a freeway was associated with a reduction in FVC. Lung function deficits of 2–3% were associated with regional PM10 and PM2.5 (FVC and FEV1) and with O3 (FEV1), but not NO2 across the range of exposure between communities. Associations with regional pollution and NRAP were independent in models adjusted for each. The effects of NRAP were not modified by regional pollutant concentrations.
Conclusions
The results indicate that NRAP and regional air pollution have independent adverse effects on childhood lung function.
To assess the short-term respiratory effects of photochemical oxidant pollution in children, 66 volunteers—33 boys and 33 girls aged 8 to 11—were exposed in a movable laboratory to polluted Los Angeles area ambient air and to purified air as a control. Exposures lasted one hour, during which subjects exercised continuously at roughly 50 percent of maximal oxygen consumption. Forced expiratory function and symptoms were evaluated prior to and at the end of exposure. The mean ozone concentration in ambient exposures was 0.113 ppm, reflecting an unusually mild pollution season. As a group, the subjects showed no statistically significant untoward responses to ambient air in comparison to purified air, and no significant differences in response between sexes. Nevertheless, regression analyses of individual data indicated a significant (p < 0.05) trend toward forced expiratory dysfunction with increasing ambient ozone concentrations. When the regression analyses were expanded to include older children and adults studied here previously, these children’s reactivity to ambient oxidants appeared similar to the older groups’. However, definitive comparisons among age groups were not possible because their exposure levels differed.
Ozone exposure induces airway neutrophilia and modifies innate immune monocytic cell-surface phenotypes in healthy individuals. High-dose inhaled corticosteroids can reduce O(3)-induced airway inflammation, but their effect on innate immune activation is unknown.We used a human O(3) inhalation challenge model to examine the effectiveness of clinically relevant doses of inhaled corticosteroids on airway inflammation and markers of innate immune activation in healthy volunteers.Seventeen O(3)-responsive subjects [>10% increase in the percentage of polymorphonuclear leukocytes (PMNs) in sputum, PMNs per milligram vs. baseline sputum] received placebo, or either a single therapeutic dose (0.5 mg) or a high dose (2 mg) of inhaled fluticasone proprionate (FP) 1 hr before a 3-hr O(3) challenge (0.25 ppm) on three separate occasions at least 2 weeks apart. Lung function, exhaled nitric oxide, sputum, and systemic biomarkers were assessed 1-5 hr after the O(3) challenge. To determine the effect of FP on cellular function, we assessed sputum cells from seven subjects by flow cytometry for cell-surface marker activation.FP had no effect on O(3)-induced lung function decline. Compared with placebo, 0.5 mg and 2 mg FP reduced O(3)-induced sputum neutrophilia by 18% and 35%, respectively. A similar effect was observed on the airway-specific serum biomarker Clara cell protein 16 (CCP16). Furthermore, FP pretreatment significantly reduced O(3)-induced modification of CD11b, mCD14, CD64, CD16, HLA-DR, and CD86 on sputum monocytes in a dose-dependent manner.This study confirmed and extended data demonstrating the protective effect of FP against O(3)-induced airway inflammation and immune cell activation.
Mechanisms for the adverse respiratory effects of traffic-related air pollution (TRAP) have yet to be established. We evaluated the acute effects of TRAP exposure on proximal and distal airway inflammation by relating indoor nitric oxide (NO), a marker of TRAP exposure in the indoor microenvironment, to airway and alveolar sources of exhaled nitric oxide ( F eNO ). F eNO was collected online at four flow rates in 1635 schoolchildren (aged 12–15 years) in southern California (USA) breathing NO-free air. Indoor NO was sampled hourly and linearly interpolated to the time of the F eNO test. Estimated parameters quantifying airway wall diffusivity ( D awNO ) and flux ( J′ awNO ) and alveolar concentration ( C ANO ) sources of F eNO were related to exposure using linear regression to adjust for potential confounders. We found that TRAP exposure indoors was associated with elevated alveolar NO. A 10 ppb higher indoor NO concentration at the time of the F eNO test was associated with 0.10 ppb higher average C ANO (95% CI 0.04–0.16) (equivalent to a 7.1% increase from the mean), 4.0% higher J′ awNO (95% CI −2.8–11.3) and 0.2% lower D awNO (95% CI −4.8–4.6). These findings are consistent with an airway response to TRAP exposure that was most marked in the distal airways.
We exposed groups of healthy and asthmatic volunteers to sulfuric acid aerosols with volume median droplet diameters of approximately 20, 10, and 1 µm, at nominal concentrations of 2,000 µg/m2, and exposed them similarly to aerosols of purified water as a control. Exposures lasted 1 h each, and included three 10-min periods of exercise (ventilation rate typically 40 to 45 L/min). Exposures occurred in randomized order 7 days apart. Temperature was 10° C, relative humidity was ∼ 100% in 20- and 10-µm (fog) exposures, and ∼ 75 to 80% in 1-µm aerosol exposures. Healthy subjects showed no statistically significant changes in lung function or in bronchial reactivity to methacholine attributable to acid exposures. They showed significant increases in lower and upper respiratory irritant symptoms when exposed to 20- or 10-µm acid fog, but not when exposed to 1-µm acid aerosol. Asthmatics showed significant excess decreases in forced expiratory performance, increases in airway resistance, and increases in irritant symptoms during acid exposures, relative to control conditions. Lung function changes in asthmatics tended to increase with time during exposure; they did not vary significantly with acid droplet size. Symptoms in asthmatics were slightly worse with 10- or 20-µm fog as compared with 1-µm aerosol. In a few instances, symptoms and lung function decrements necessitated stopping exercise or terminating the exposure early. Thus, asthma is a risk factor for unfavorable physiologic response to sulfuric acid at occupational exposure concentrations. Large droplet size (i.e., fog) tends to exacerbate short-term symptomatic response, but we have not been able to demonstrate a consistent effect of droplet size on physiologic response.
ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTStereochemistry of additions of allenes. I. Methoxymercuration and halogenation of 1,3-dimethylalleneWilliam L. Waters, William S. Linn, and Marjorie C. CaserioCite this: J. Am. Chem. Soc. 1968, 90, 24, 6741–6749Publication Date (Print):November 1, 1968Publication History Published online1 May 2002Published inissue 1 November 1968https://doi.org/10.1021/ja01026a032Request reuse permissionsArticle Views417Altmetric-Citations68LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InReddit PDF (1 MB) Get e-Alertsclose Get e-Alerts
Abstract We tested responses to ozone (O3) under simulated “worst-case” ambient exposure conditions. Subjects included 9 men who had severe chronic obstructive pulmonary disease (COPD) with subnormal carbon monoxide diffusing capacity (i.e., an emphysemic component) and 10 age-matched healthy men. Each subject was exposed to 0.24 ppm O3 and to clean air (control) in an environmentally controlled chamber at 24 °C and 40% relative humidity. Exposures were randomized, they occurred 1 wk apart, and they lasted 4 h. During each half-hour interval, light exercise occurred (i.e., average ventilation 20 l/min) for 15 min. During both control and O3 exposures, group mean symptom intensity and specific airway resistance (SRaw) increased, whereas forced expiratory performance decreased. The healthy subgroup's mean arterial oxygen saturation (SaO2) rose slightly, and the COPD subgroup's mean SaO2 declined slightly, during exercise. Group mean forced expiratory volume in 1 s (FEV1.0) declined significantly in O3 exposures, compared with controls (p =.01). Mean excess FEV1.0 loss after 4 h in O3 (relative to control) was 8% of the preexposure value in the COPD subgroup, compared with 3% in the healthy subgroup (p > .05 [nonsignificant]). Overall FEV1.0 loss during O3 exposures, including exercise effects, averaged 19% in the COPD subgroup, compared with 2% in the healthy subgroup (p < .001). Symptoms, SRaw, and SaO2 responses, as well as healthy subjects' postexposure bronchial reactivity, differed little between O3-exposed and control subjects. We therefore concluded that in older men with or without severe COPD, O3 causes lung dysfunction under “worst-case” ambient exposure conditions, despite older subjects' comparative unresponsiveness to O3. The combined effect of O3 and exercise on lung dysfunction is markedly greater with COPD. It is still unclear whether COPD causes an increased response to O3 per se.
