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.

Respiratory immune system and consequences due to particulate matter in air pollution / Sistema inmune respiratorio y consecuencias de contaminación aérea por materia particulada

The respiratory system is commonly known for being responsible for gaseous exchange. However, chronic exposure to air born pollution increases each year the number of asthma, chronic obstructive pulmonary disease (COPD), and lung cancer cases, which compels us to view the lung as a vulnerable organ due to the fact that because of its nature it enters in contact with substances present in the environment. Fortunately, the immune response mechanism acts locally in the lung in order to modulate the inflammatory response and to facilitate the clearance of inhaled pathogens, as well as volatile organic compounds (VOCs), metals, sulphur and nitrogen oxides, ozone and particulate matter (PM). Expanding our understanding of the molecular mechanisms underlying inflammation and pathology induced by airborne contaminant particles in the long term can help to develop strategies to reduce the risks of exposure to some of the most hazardous air pollutants, as well as to reduce the toxicity of nanomaterials and may also help to identify therapeutic targets to be used in the preventive treatment of susceptible groups.

El sistema respiratorio es comúnmente conocido por ocuparse del intercambio gaseoso; sin embargo, la exposición crónica a contaminantes del aire aumenta cada año el número de casos nuevos de asma, enfermedad pulmonar obstructiva crónica (EPOC) y cáncer de pulmón, lo que nos obliga a ver el pulmón como un órgano vulnerable, ya que por su naturaleza entra en contacto con sustancias presentes en el medio ambiente. Afortunadamente, el mecanismo de respuesta inmune actúa localmente en el pulmón para modular respuestas inflamatorias y para facilitar el aclaramiento de patógenos inhalados, así como de compuestos orgánicos volátiles (VOCs, por sus siglas en inglés), metales, óxidos de azufre y nitrógeno, ozono y materia particulada (PM, por sus siglas en inglés). Ampliar nuestra comprensión de los mecanismos moleculares que subyacen a la inflamación y a la patología inducida por partículas contaminantes en las vías respiratorias a largo plazo puede ayudar a desarrollar estrategias para reducir los riesgos de exposición a algunos de los contaminantes atmosféricos más peligrosos, así como a reducir la toxicidad de los nanomateriales y quizás pueda también ayudar a identificar objetivos terapéuticos que se puedan utilizar en el tratamiento preventivo de grupos susceptibles.

[Sensitization to aeroallergens in patients with allergic rhinitis in Aguascalientes, Mexico]. / Sensibilización a aeroalérgenos en pacientes con rinitis alérgica en Aguascalientes, México.

BACKGROUND: Allergic rhinitis is the most common allergic disease worldwide and it is caused by a reaction of hypersensitivity to aeroallergens. To our knowledge, there aren't any previous studies of aeroallergenic sensitization in Aguascalientes, Mexico. OBJECTIVE: To describe the sensitization to aeroallergens in patients with allergic rhinitis who have been treated at a private clinic in Aguascalientes, Mexico. METHODS: A descriptive, cross-sectional and retrospective study was done in which patients diagnosed with allergic rhinitis were included. Skin prick tests with 32 allergenic extracts were carried out and the frequencies at each were determined. RESULTS: In total, 350 patients were analyzed. The most frequent aeroallergens were grass pollens (74.8%), followed by tree pollens (64.8%) and dust mites Dermatophagoides pteronyssinus (64%). The group of patients under 20 years of age was predominant (67.1%), followed by the group of 21 to 40 years old (22.5%). CONCLUSIONS: This research provides information about regional patterns of sensitization, which shall facilitate diagnostic tests in the region and the best practices of specific immunotherapy.

Antecedentes: La rinitis alérgica es la enfermedad alérgica más común en el mundo y es causada por hipersensibilidad a los aeroalérgenos. Hasta donde sabemos, no hay estudios previos de sensibilización aeroalergénica en Aguascalientes, México. Objetivo: Describir la sensibilización a aeroalérgenos en pacientes con rinitis alérgica tratados en una clínica privada en Aguascalientes, México. Métodos: Estudio descriptivo, transversal y retrospectivo; se incluyeron pacientes diagnosticados con rinitis alérgica. Se realizaron pruebas cutáneas con 32 extractos alergénicos y se determinaron las frecuencia de reacción a cada uno. Resultados: En total se analizaron 350 pacientes. Los aeroalérgenos más frecuentes fueron los pólenes de pastos (74.8%), seguidos por los pólenes de árboles (64.8%) y Dermatophagoides pteronyssinus (64%). El grupo de edad predominante fue el menor de 20 años (67.1%), seguido del grupo de 21 a 40 años (22.5%). Conclusión: La investigación proporciona información sobre los patrones regionales de sensibilización, que facilitará las pruebas de diagnóstico en la región y las mejores prácticas de inmunoterapia específica.

Molecular-based diagnosis of respiratory allergic diseases in children from Curitiba, a city in Southern Brazil.

BACKGROUND: Prevalence of respiratory allergic diseases has increased worldwide. Identification of the aeroallergens involved in allergenic sensitisation is important for diagnosis, treatment and prevention. OBJECTIVE: To verify the molecular pattern of sensitisation to aeroallergens in patients with allergic respiratory diseases using microarray technique for specific IgE antibody detection. METHODS: Cross-sectional study of 101 children with allergic rhinitis was followed in an outpatient clinic. All patients had positive skin prick tests (SPT) to at least one of the following antigens: Dermatophagoides pteronyssinus, Blomia tropicalis, Blattella germanica, Lolium multiflorum, and dog and cat epithelium. Serum specific IgE antibodies (sIgE) to mites, animal epithelia, fungi, cockroach and pollens components were determined by ImmunoCAP ISAC. RESULTS: sIgE to group 1 and 2 mite allergens showed higher positive rates: Der p 1 (74.2%), Der p 2 (73.3%), Der f 1 (74.2%), Der f 2 (72.3%). sIgE to animal epithelia were less frequent, Can f 1, Can f 2, Can f 3 in 4.9%, 2.9%, 1.9% respectively and Fel d 1, Fel d 2, Fel d 4 in 16.8%, 0.9% and 1.9%. respectively. Sensitisation to fungi and cockroach were rare, except for Bla g 7, to which 16.8% were positive. There was no significant recognition for tree pollens group. For grass, sIgE were detected to Cyn d 1 in 16.8%, Phl p 1 and Phl p 4 in 14.8% and 12.9%, respectively. CONCLUSION: Knowing that the pattern of allergic sensitisation varies according to environment and population, our results reinforce the need for local studies, using molecular-based diagnosis.

Lacrimal Cytokines Assessment in Subjects Exposed to Different Levels of Ambient Air Pollution in a Large Metropolitan Area.

BACKGROUND: Air pollution is one of the most environmental health concerns in the world and has serious impact on human health, particularly in the mucous membranes of the respiratory tract and eyes. However, ocular hazardous effects to air pollutants are scarcely found in the literature. DESIGN: Panel study to evaluate the effect of different levels of ambient air pollution on lacrimal film cytokine levels of outdoor workers from a large metropolitan area. METHODS: Thirty healthy male workers, among them nineteen professionals who work on streets (taxi drivers and traffic controllers, high pollutants exposure, Group 1) and eleven workers of a Forest Institute (Group 2, lower pollutants exposure compared to group 1) were evaluated twice, 15 days apart. Exposure to ambient PM2.5 (particulate matter equal or smaller than 2.5 µm) was 24 hour individually collected and the collection of tears was performed to measure interleukins (IL) 2, 4, 5 and 10 and interferon gamma (IFN-γ) levels. Data from both groups were compared using Student's t test or Mann- Whitney test for cytokines. Individual PM2.5 levels were categorized in tertiles (lower, middle and upper) and compared using one-way ANOVA. Relationship between PM2.5 and cytokine levels was evaluated using generalized estimating equations (GEE). RESULTS: PM2.5 levels in the three categories differed significantly (lower: ≤22 µg/m3; middle: 23-37.5 µg/m3; upper: >37.5 µg/m3; p<0.001). The subjects from the two groups were distributed unevenly in the lower category (Group 1 = 8%; Group 2 = 92%), the middle category (Group 1 = 89%; Group 2 = 11%) and the upper category (Group 1 = 100%). A significant relationship was found between IL-5 and IL-10 and PM2.5 levels of the group 1, with an average decrease of 1.65 pg/mL of IL-5 level and of 0.78 pg/mL of IL-10 level in tear samples for each increment of 50 µg/m3 of PM2.5 (p = 0.01 and p = 0.003, respectively). CONCLUSION: High levels of PM2.5 exposure is associated with decrease of IL-5 and IL-10 levels suggesting a possible modulatory action of ambient air pollution on ocular surface immune response.

A curated review of recent literature of biomarkers used for assessing air pollution exposures and effects in humans.

This is a cross-sectional review of biomarkers used in air pollution research from January 2009 through December 2012. After an initial keyword search in PubMed retrieving 426 articles, a comprehensive abstract review identified 54 articles of experimental design that used biomarkers of exposure or effect in human studies in the area of air pollution research during this specified time period. A thorough bibliographic search of the included articles retrieved an additional 65 articles meeting the inclusion criteria. This review presents these 119 studies and the 234 biomarkers employed in these air pollution research investigations. Data presented are 70 biomarkers of exposure with 54% relating to polycyclic aromatic hydrocarbons, 36% volatile organic carbons, and 10% classified as other. Of the 164 biomarkers of effect, 91 and 130 were used in investigating effects of short-term and chronic exposure, respectively. Results of biomarkers used in short-term exposure describe different lag times and pollutant components such as primary and secondary pollutants, and particle number associated with corresponding physiological mechanisms including airway inflammation, neuroinflammation, ocular, metabolic, early endothelial dysfunction, coagulation, atherosclerosis, autonomic nervous system, oxidative stress, and DNA damage. The review presents three different exposure scenarios of chronic, occupational, and extreme exposure scenarios (indoor cooking) with associated biomarker findings presented in three broad categories of (1) immune profile, (2) oxidative stress, and (3) DNA damage. This review offers a representation of the scope of data being explored by air pollution researchers through the use of biomarkers and has deliberately been restricted to this particular subject rather than an extensive or in-depth review. This article provides a contextualization of air pollution studies conducted with biomarkers in human subjects in given areas while also integrating this complex body of information to offer a useful review for investigators in this field of study.

Residual oil fly ash worsens pulmonary hyperreactivity in chronic allergic mice.

BALB/c mice received saline (SAL groups) or ovalbumin (OVA groups) intraperitoneally (days 1, 3, 5, 7, 9, 11 and 13). After 27 days, a burst of intratracheal OVA or SAL (days 40, 43 and 46) was performed. Animals were then divided into four groups (N=8, each) and intranasally instilled with saline (SAL-SAL and OVA-SAL) or residual oil fly ash (SAL-ROFA and OVA-ROFA). 24h later, total, initial and difference resistances (Rtot, Rinit, Rdiff) and static elastance (Est) were measured. Lung responsiveness to methacholine was assessed as slope and sensitivity of Est, Rtot, Rinit, and Rdiff. Lung morphometry (collapsed and normal areas and bronchoconstriction index) and cellularity (polymorphonuclear, mononuclear and mast cells) were determined. OVA or ROFA similarly impaired lung mechanics and increased the amount of polymorphonuclear cells and collapsed areas. OVA-ROFA showed even higher hyperresponsiveness, bronchoconstriction and mast cell infiltration. Thus, we concluded that ROFA exposure may add an extra burden to hyperresponsive lungs.

Air pollution in autoimmune rheumatic diseases: a review.

Air pollution consists of a heterogeneous mixture of gasses and particles that include carbon monoxide, nitrates, sulfur dioxide, ozone, lead, toxic by-product of tobacco smoke and particulate matter. Oxidative stress and inflammation induced by inhaled pollutants may result in acute and chronic disorders in the respiratory system, as well as contribute to a state of systemic inflammation and autoimmunity. This paper reviews the mechanisms of air contaminants influencing the immune response and autoimmunity, and it focuses on studies of inhaled pollutants triggering and/or exacerbating rheumatic diseases in cities around the world. Remarkably, environmental factors contribute to the onset of autoimmune diseases, especially smoking and occupational exposure to silica in rheumatoid arthritis and systemic lupus erythematosus. Other diseases such as scleroderma may be triggered by the inhalation of chemical solvents, herbicides and silica. Likewise, primary vasculitis associated with anti-neutrophil cytoplasmic antibody (ANCA) may be triggered by silica exposure. Only few studies showed that air pollutants could trigger or exacerbate juvenile idiopathic arthritis and systemic lupus erythematosus. In contrast, no studies of tropospheric pollution triggering inflammatory myopathies and spondyloarthropathies were carried out. In conclusion, air pollution is one of the environmental factors involved in systemic inflammation and autoimmunity. Further studies are needed in order to evaluate air pollutants and their potentially serious effects on autoimmune rheumatic diseases and the mechanisms involved in the onset and the exacerbation of these diseases.

Sensitization to airborne ascospores, basidiospores, and fungal fragments in allergic rhinitis and asthmatic subjects in San Juan, Puerto Rico.

BACKGROUND: Fungal spores are the predominant biological particulate in the atmosphere of Puerto Rico, yet their potential as allergens has not been studied in subjects with respiratory allergies. The purpose of this study was to determine the level of sensitization of subjects with respiratory allergies to these particles. METHODS: Serum samples were drawn from 33 subjects with asthma, allergic rhinitis, or nonallergic rhinitis and 2 controls with different skin prick test reactivity. An MK-3 sampler was used to collect air samples and the reactivity of the sera to fungal particles was detected with a halogen immunoassay. RESULTS: All subjects reacted to at least 1 fungal particle. Thirty-one subjects reacted to ascospores, 29 to basidiospores, 19 to hyphae/fungal fragments, and 12 to mitospores. The median percentage of haloes in allergic rhinitis subjects was 4.82% while asthma or nonallergic rhinitis subjects had values of 1.09 and 0.39%, respectively. Subjects with skin prick tests positive to 3, 2, 1, or no extract had 5.24, 1.09, 1.61, and, 0.57% of haloed particles, respectively. If skin prick tests were positive to basidiomycetes, pollen, animals, or deuteromycetes, the percentages of haloes were 4.72, 4.15, 3.63, and 3.31%, respectively. Of all haloed particles, 46% were unidentified, 25% ascospores, 20% basidiospores, 7% hyphae/fungal fragments, and 2% mitospores. IgE levels and the number of positive skin prick test extracts correlated with the percentage of haloes. CONCLUSION: In tropical environments, sensitization to airborne basidiomycetes, ascomycetes, and fungal fragments seems to be more prevalent than sensitization to mitospores in subjects with active allergies, suggesting a possible role in exacerbations of respiratory allergies.

Sensitisation to aeroallergens among asthmatic and non-asthmatic adolescents living in a poor region in the Northeast of Brazil.

OBJECTIVES: To assess the kind and frequency of sensitisation to aeroallergens (skin prick test - SPT) of asthmatic and non-asthmatic adolescents (13-14 years old) living in the city of Caruaru, Northeast of Brazil, and to analyse their exposure to some environmental factors. METHOD: A case-control study was conducted with asthmatic (50) and non-asthmatic (150) adolescents diagnosed by the International Study of Asthma and Allergies in Childhood (ISAAC) written questionnaire. All were submitted to SPT with aeroallergens (house dust mites, cat and dog epithelium, cockroaches, moulds and grass) and completed a questionnaire to evaluate their environmental exposure. RESULTS: There were no significant differences between groups regarding gender, age, number of siblings and environmental exposure. Asthmatic subjects exhibited a higher frequency of positive SPTs than non-asthmatic subjects (54.0% vs 33.3%, p=0.009) mainly due to Periplaneta americana (34.0% vs 12.7%, p=0.0007 respectively) and Canis familiaris (20.0% vs 8.7%, p=0.029). CONCLUSION: Although sensitisation to aeroallergens was high among non-asthmatic adolescents, asthma was associated with parental history of atopic disease and sensitisation to P. americana and Canis familiaris but not to D. pteronyssinus showing that local studies are mandatory for the tailoring of appropriate management of allergic diseases.

Aeroallergen sensitization in healthy children: racial and socioeconomic correlates.

OBJECTIVE: Allergic sensitization is very prevalent and often precedes the development of allergic disease. This study examined the association of race with allergic sensitization among healthy children with no family history of atopy. STUDY DESIGN: Two hundred seventy-five children, predominantly from lower socioeconomic strata, from Cincinnati, Ohio, ages 2 to 18 years without a family or personal history of allergic diseases, underwent skin prick testing to 11 allergen panels. The Pediatric Allergic Disease Quality of Life Questionnaire (PADQLQ) was used to examine the impact of sensitization on quality of life. RESULTS: Thirty-nine percent of healthy children were sensitized to 1 or more allergen panels. Multivariate logistic regression showed increased risk among African-American children for any sensitization (OR, 2.17; [95% CI: 1.23, 3.84]) and sensitization to any outdoor allergen (OR, 2.96 [95% CI: 1.52, 5.74]). Eighty-six percent of children had PADQLQ scores of 1 or less (0 to 6 scale). CONCLUSIONS: Allergic sensitization is prevalent even among children who do not have a personal or family history of asthma, allergic rhinitis, or atopic dermatitis and who have no evidence of current, even subtle effects from this sensitization on allergic disease-related quality of life. African-American children are at greater risk for presence of sensitization, especially to outdoor allergens.

Lung inflammation induced by concentrated ambient air particles is related to particle composition.

The objectives of this study were (1) to determine whether short-term exposures to concentrated air particles (CAPs) cause pulmonary inflammation in normal rats and rats with chronic bronchitis (CB); (2) to identify the site within the lung parenchyma where CAPs-induced inflammation occurs; and (3) to characterize the component(s) of CAPs that is significantly associated with the development of the inflammatory reaction. Four groups of animals were studied: (1) air treated, filtered air exposed (air-sham); (2) sulfur dioxide treated (CB), filtered air exposed (CB-sham); (3) air treated, CAPs exposed (air-CAPs); and (4) sulfur dioxide treated, CAPs exposed (CB-CAPs). CB and normal rats were exposed by inhalation either to filtered air or CAPs during 3 consecutive days (5 hours/day). Pulmonary inflammation was assessed by bronchoalveolar lavage (BAL) and by measuring the numerical density of neutrophils (Nn) in the alveolar walls at the bronchoalveolar junction and in more peripheral alveoli. CAPs (as a binary exposure term) and CAPs mass (in regression correlations) induced a significant increase in BAL neutrophils and in normal and CB animals. Nn in the lung tissue significantly increased with CAPs in normal animals only. Greater Nn was observed in the central compared with peripheral regions of the lung. A significant dose-dependent association was found between many CAPs components and BAL neutrophils or lymphocytes, but only vanadium and bromine concentrations had significant associations with both BAL neutrophils and Nn in CAPs-exposed groups analyzed together. Results demonstrate that short-term exposures to CAPs from Boston induce a significant inflammatory reaction in rat lungs, with this reaction influenced by particle composition.

Induction of the lung myofibroblast PDGF receptor system by urban ambient particles from Mexico City.

Platelet-derived growth factor (PDGF) and its receptor system regulate mesenchymal cell proliferation. We recently reported that emission-source fly-ash particles and asbestos fibers induce the PDGF alpha-receptor through a macrophage-dependent pathway, and upregulation of this receptor greatly enhances the mitogenic response of lung myofibroblasts to PDGF (Lindroos and colleagues, Am. J. Respir. Cell Mol. Biol. 1997;16:283-292). In the present study we investigated the effect of particulate matter <= 10 micrometers in size (PM10) from the southern, central, and northern regions of Mexico City on PDGF receptor induction and compared these urban, ambient particles with Mt. St. Helen's volcanic ash particles as a negative control. All Mexico City PM10 samples, but not volcanic ash, stimulated rat alveolar macrophages to secrete a soluble, upregulatory factor(s) for the PDGF alpha-receptor on early passage rat lung myofibroblasts. The macrophage-derived upregulatory activity was blocked by the interleukin (IL)-1 receptor antagonist. The ability of PM10 to stimulate IL-1beta release was blocked in part by a recombinant endotoxin neutralizing protein (rENP). Lipopolysaccharide/endotoxin (LPS) and vanadium, both constituents that were present within these PM10 samples, also stimulated macrophages to secrete factor(s) that upregulated PDGF-Ralpha on lung myofibroblasts. Direct exposure of myofibroblasts to PM10 also elicited upregulation of the PDGF alpha-receptor, and this effect was blocked by rENP and mimicked by LPS, but not vanadium. These findings suggest that PM10 particles induce expression of the PDGF receptor system through macrophage-dependent and -independent mechanisms involving endotoxin and metals.