Impact of a pollution breach at a coke oven factory on asthma control in nearby vulnerable adults.

BACKGROUND: Previous studies have related sulfur dioxide (SO2) exposure to asthma exacerbations. We utilized the University of Pittsburgh Asthma Institute registry to study associations of asthma exacerbations between 2 geographically distinct populations of adults with asthma. OBJECTIVE: Our objective was to examine whether asthma symptoms worsened following a significant fire event that destroyed pollution control equipment at the largest coke works in the United States. METHODS: Two groups of patients with asthma, namely, those residing within 10 miles of the coke works fire (the proximal group [n = 39]) and those residing beyond that range (the control group [n = 44]), were geocoded by residential address. Concentrations of ambient air SO2 were generated by using local University of Pittsburgh Asthma Institute registry air monitoring data. Factory emissions were also evaluated. Data from a patient historical acute exposure survey and in-person follow-up data were evaluated. Inferential statistics were used to compare the groups. RESULTS: In the immediate postfire period (6-8 weeks), the level of emissions of SO2 from the factory emissions increased to 25 times more than the typical level. Following the pollution control breach, the proximal cohort self-reported an increase in medication use (risk ratio = 1.76; 95% CI = 1.1-2.8; P < .01) and more exacerbations. In a small subset of the follow-up cohort of those who completed the acute exposure survey only, asthma control metrics improved. CONCLUSIONS: Real-world exposure to a marked increase in ambient levels of SO2 from a pollution control breach was associated with worsened asthma control in patients proximal to the event, with the worsened control improving following repair of the controls. Improved spatial resolution of air pollutant measurements would enable better examination of exposures and subsequent health impacts.

Pediatric asthma and ambient pollutant levels in industrializing nations.

Asthma is one of the most common chronic diseases in childhood and its prevalence has been increasing within industrializing nations. The contribution of ambient pollutants to asthma symptomatology has been explored in some countries through epidemiological investigations, molecular analysis and monitoring functional outcomes. The health effects of rising environmental pollution have been of increasing concern in industrializing nations with rising urbanization patterns. This review article provides an overview of the link between pediatric asthma and exposure to rising sources of urban air pollution. It primarily focuses on the asthma-specific effects of sulfur dioxide, nitrogen dioxide, ozone and particulate matter. Worldwide trends of asthma prevalence are also provided which detail the prominent rise in asthma symptoms in many urban areas of Africa, Latin America and Asia. The molecular and functional correlation of ambient pollutants with asthma-specific airway inflammation in the pediatric population are also highlighted. The final aspect of the review considers the correlation of motor vehicle, industrial and cooking energy sources, ascribed as the major emitters among the pollutants in urban settings, with asthma epidemiology in children.

Inhaled environmental allergens and toxicants as determinants of the asthma phenotype.

The driving environmental factors behind the development of the asthma phenotype remain incompletely studied and understood. Here, we present an overview of inhaled allergic/atopic and mainly nonallergic/nonatopic or toxicant shapers of the asthma phenotype, which are present in both the indoor and outdoor environment around us. The inhaled allergic/atopic factors include fungus, mold, animal dander, cockroach, dust mites, and pollen; these allergic triggers and shapers of the asthma phenotype are considered in the context of their ability to drive the immunologic IgE response and potentially induce interactions between the innate and adaptive immune responses, with special emphasis on the NADPH-dependent reactive oxygen-species-associated mechanism of pollen-associated allergy induction. The inhaled nonallergic/nonatopic, toxicant factors include gaseous and volatile agents, such as sulfur dioxide, ozone, acrolein, and butadiene, as well as particulate agents, such as rubber tire breakdown particles, and diesel exhaust particles. These toxicants are reviewed in terms of their relevant chemical characteristics and hazard potential, ability to induce airway dysfunction, and potential for driving the asthma phenotype. Special emphasis is placed on their interactive nature with other triggers and drivers, with regard to driving the asthma phenotype. Overall, both allergic and nonallergic environmental factors can interact to acutely exacerbate the asthma phenotype; some may also promote its development over prolonged periods of untreated exposure, or possibly indirectly through effects on the genome. Further therapeutic considerations should be given to these environmental factors when determining the best course of personalized medicine for individuals with asthma.

A review on human health perspective of air pollution with respect to allergies and asthma.

The increase in cases of asthma and allergies has become an important health issue throughout the globe. Although these ailments were not common diseases a few short decades ago, they are now affecting a large part of the population in many regions. Exposure to environmental (both outdoor and indoor) pollutants may partially account for the prevalence of such diseases. In this review, we provide a multidisciplinary review based on the most up-to-date survey of literature regarding various types of airborne pollutants and their associations with asthma-allergies. The major pollutants in this respect include both chemical (nitrogen dioxide, ozone, sulfur dioxide, particulate matter, and volatile organic compounds) and biophysical parameters (dust mites, pet allergens, and mold). The analysis was extended further to describe the development of these afflictions in the human body and the subsequent impact on health. This publication is organized to offer an overview on the current state of research regarding the significance of air pollution and its linkage with allergy and asthma.

Prior SO2 exposure promotes airway inflammation and subepithelial fibrosis following repeated ovalbumin challenge.

BACKGROUND: Exposure to allergens or air pollutants often leads to asthma exacerbations associated with aggravation of airway inflammation. Although, repeated allergen challenge often induces chronic allergic airway inflammation (CAAI) and airway remodelling, yet, the effects of brief exposure to air pollutants such as SO(2) on development of CAAI and airway remodelling remain to be clarified. OBJECTIVE: The aim of the experiment was to investigate the effects of acute neutrophilic airway inflammation induced by brief exposure to SO(2) on development of CAAI and subepithelial fibrosis (SEF) in a murine model of asthma. METHODS: Acute airway inflammation was induced by brief exposure to 50 p.p.m. SO(2) (1 h/d, 3 days). CAAI and SEF in BALB/c mice were induced by repeated challenge with ovalbumin (OVA) for 5 or 9 weeks with or without prior exposure to SO(2). Bronchoalveolar lavage fluid (BALF) eosinophilia as index of CAAI, BALF endothelin-1 (ET-1) and TGF-beta1 levels, morphometric evaluation of fibrotic area beneath subbasement membrane and lung hydroxyproline content (Hyp) as indexes of SEF were monitored. RESULTS: Exposure to SO(2) led to acute neutrophilic inflammation and epithelial sloughing with profound elevation of BALF ET-1. Repeated OVA challenge resulted in CAAI and SEF along with elevation of Hyp, increase of fibrotic area beneath subbasement membrane and elevation of BALF TGF-beta1. Preceding SO(2) exposure exaggerated BALF eosinophilia, facilitated and enhanced SEF with more significant elevation of BALF ET-1 and TGF-beta1 levels compared with OVA-challenged mice without prior exposure to SO(2). The increase of Hyp was positively correlated with elevation of BALF TGF-beta1 during CAAI (r=0.842, P<0.01). CONCLUSION: This data demonstrated that SEF developed in parallel with severity and time course of CAAI following repeated OVA challenge. SO(2)-induced acute epithelial injury and neutrophilic inflammation could enhance CAAI and promote SEF, probably through overexpression of ET-1 and TGF-beta1.

Effect of sulfur dioxide inhalation on cytokine levels in lungs and serum of mice.

In order to elucidate the immunotoxic mechanism exerted by sulfur dioxide (SO(2)), we investigated the effect of SO(2), a major air pollutant, on the cytokine levels in lungs and serum of male mice. Levels of interlukin-6(IL-6), tumor necrosis factor-alpha (TNF-alpha), and transforming growth factor-beta1 (TGF-beta1) in lungs and serum from male mice exposed to SO(2) at various concentrations were measured by the enzyme-linked immunosorbent assay. Sixty Kunming albino male mice were divided randomly into six equal groups: three groups exposed to SO(2) (14.00 +/- 1.25, 28.00 +/- 1.98, and 56.00 +/- 3.11 mg/m(3), which are 5 +/- 0.45, 10 +/- 0.71, and 20 +/- 1.11 ppm) and their respective control groups. The results were as follows: (1) For lung tissues of male mice, exposure to SO(2) at 14 mg/m(3) (5 ppm) caused statistically significant increase of levels of IL-6 and TNF-alpha (p < .05) compared with the control group; exposure at 28 mg/m(3) (10 ppm) caused a statistically highly significant increase of level of IL-6 (p < .01) and a significant increase of TNF-alpha (p < .05); and exposure at 56 mg/m(3) (20 ppm) caused no any significant increase of levels of IL-6 and TNF-alpha. SO(2) at all concentrations tested could not cause significant change of level of TGF-beta1 in lungs. (2) For serum from male mice, after exposure to SO(2) at 14 mg/m(3) (5 ppm), the level of TNF-a was significantly increased (p < .05) compared with the control group, but the changes of levels of IL-6 and TGF-beta1 were not significant. After exposure to SO(2) at 28 mg/m(3) (10 ppm) and 56 mg/m(3) (20 ppm), levels of IL-6 and TNF-alpha were increased nonsignificantly, but the level of TGF-beta1 was decreased nonsignificantly. These results imply that inflammation reaction could be induced in lung tissue by SO(2) inhalation and the inflammation reaction might relate to these cytokines. And determination of cytokines in lung may be more valuable than in serum when lung injury caused by SO(2).

Effects of subchronic exposure to a mixture of O3, SO2, and (NH4)2SO4 on host defenses of mice.

Mice exposed 5 h/d, 5 d/wk up to 103 d, to 0.2 mg O3/m3 or to a mixture of O3, 13.2 mg SO2/m3, and 1.04 mg (NH4)2SO4 aerosol/m3 showed significantly greater susceptibility to group C streptococcal aerosol infection relative to filtered air controls. Pulmonary bactericidal activity by alveolar macrophages was significantly enhanced in the lungs of mice exposed to the mixture relative to those inhaling filtered air or O3 alone. The total number and distribution of the free cells lavaged from the lungs, as well as cellular ATP levels, did not change due to the pollutant exposures. In vitro cytostasis in tumor target cells cocultured with peritoneal macrophages from the exposed mice was significantly enhanced in the O3-exposed and in the mixture-exposed treatment groups relative to controls and also in the mixture-exposed relative to the O3-exposed group when a target-to-effector-cell ratio of 1:10 was used; no such effects were observed when this ratio was 1:20. Splenic T-lymphocyte function, as measured by blastogenesis to mitogens and alloantigens, was affected by exposure to O3 and/or the mixture, although the patterns of effects were qualitatively different. Splenic B-cell function and macrophage antigen processing, as measured by the generation of antibody plaque-forming cells, was unaffected by exposure.

Bronchoconstrictor responses to sulfur dioxide or sulfur dioxide plus sodium chloride droplets in allergic, nonasthmatic adolescent.

Eight atopic adolescent subjects without diagnosis of clinical asthma but with signs of hyperactive airways were studied. The subjects were exposed for 30 min at rest followed by 10 min during moderate exercise on a treadmill to the following: (1) filtered air, (2) 1 mg/m3 NaCl droplet aerosol, (3) 1 ppm SO2 and NaCl droplet aerosol, or (4) 1 ppm SO2. All exposures were at 75% relative humidity and 22 degrees C. Exposures to either SO2 mode produced statistically significant changes in pulmonary function, whereas sham exposures to air on NaCl did not. These results are similar to those seen earlier in a group of extrinsic asthmatic adolescent subjects and are three to 22 times greater than changes we saw in a group of normal adolescent subjects. The changes seen after inhalation of SO2 were not statistically different from those seen after inhalation of SO2 and NaCl droplet aerosol. Our results indicate that inhalation of 1 ppm SO2 by a group of atopic adolescents can produce exercise-induced bronchospasm at a level of exercise that has no effect by itself.

Cigarette smoking, air pollution, and immunity: a model system.

BALB/c mice were exposed to fresh cigarette smoke, a mixture of SO(2) (5 ppm) and CO (50 ppm), or both for periods up to 18 weeks. After varying exposure times, animals were intratracheally inoculated with 10(8) sheep erythrocytes and sacrificed 7 days later, during which time the various exposure regimes were continued. Plaque-forming-cell responses were measured in spleens and a pool of the cervical and mediastinal lymph nodes, together with serum hemagglutinating and hemolytic responses, and compared with those of age-matched control animals. Both the organ and serum responses exhibited stimulation in the early phase of exposure, before a depression with prolonged exposure. The greatest depression was seen in animals that had been chronically exposed to both fresh cigarette smoke and the gas mixture.