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Air pollutants enhance rhinoconjunctivitis symptoms in pollen-allergic individuals
Michael Riediker et al, Zurich, Switzerland
Background: Little is known about the relationship of airborne pollen allergens to nasal and ocular symptoms in combination with air pollutants.
Objective: The hypothesis was that air pollutants exacerbate allergic symptoms of the nose and eyes during the pollen season. In addition, the use of allergen measurements instead of pollen counts should be tested.
Methods: Fifteen pollen-allergic, nonsmoking subjects with weak reactivity of the airways recorded rhinoconjunctival symptoms and medication every morning and evening throughout the pollen season. Symptoms were compared with air pollutants (Nitrogen oxide [NOx], particulate matter smaller than 10 micrometer, and ozone) and birch and grass pollen counts or, alternatively, to airborne birch and grass allergens determined using ELISA-techniques. A multiple linear regression model was used which controlled for autocorrelation of the residuals of the time series (Cochrane-Orcutt approach). This model was applied to each subject individually, followed by calculations of summary scores for the group.
Results: Air pollution levels were moderate, often meeting air quality standards. Effect estimates (increase of score with 10-fold increase of concentration) were NOx = 1.06, P<0.01; ozone = 1.59, P<0.001. Using allergen concentrations instead of pollen counts resulted in similar effect estimates. Using particulate matter smaller than 10 micrometer instead of NOx gave comparable but less consistent results.
Conclusion: Symptoms were related to moderate levels of pollutants, suggesting that rhinoconjunctival tissue is very sensitive to irritant stimuli during an ongoing allergic inflammation, and that susceptibility toward allergens might be increased in areas with increased levels of air pollutants. Allergen measurements seem equally usable as pollen counts to investigate rhinoconjunctivitis.
Reference: Ann Allergy Asthma Immunol 2001 ; 87: 311 - 318
Allergic inflammation enhances bacterial sinusitis Christopher Blair et al, Section of ENT & Clinical Microbiology, University of Chicago
Background: Although it is not proven, one factor considered important in the development of sinusitis is allergic rhinitis.
Objective: The purpose of the study was to determine whether ongoing allergic rhinitis enhances the infection and inflammation associated with Streptococcus pneumoniae acute sinus infection.
Methods: BALB/c mice were sensitised to ovalbumin by intraperitoneal injection. After infection of the sinuses by S. pneumoniae, either with or without concomitant administration of ovalbumin to induce allergic inflammation, mice were killed at various times and the heads were prepared for histologic evaluation of the sinuses.
Results: Mice became allergic to ovalbumin and developed eosinophilia in the sinus and lung cavities. In comparison with controls, the mice with ongoing nasal allergic inflammation that were inoculated with S pneumoniae had significantly more bacteria recovered at sacrifice and had significantly more inflammation, as indicated by neutrophil, eosinophil, and mononuclear influx into the sinus mucosa. The percentage of the sinus area occupied by neutrophil clusters was also increased after infection in the allergic mice in comparison with the control mice.
Conclusion: Their data demonstrate that mice can be sensitised to ovalbumin and develop a localized allergic reaction in the skin, nose, or lung. An ongoing local allergic response augments bacterial infection in these animals. They also demonstrate that allergic sensitisation alone, allergen exposure alone, or an allergic response at a distant site, the lung, does not augment the sinus infection.
Reference:
The risk of adenoid hypertrophy (enlargement) in children with allergic rhinitis
Shih-Wen Huang and Carla Giannoni, Dept of Pediatrics, University of Florida
Background: Adenoid hypertrophy (AH) may cause significant suffering in children but its relationship to allergic rhinitis (AR) has not been studied.
Objective: To determine the risk factor of AH in patients with AR.
Methods: They studied 315 children (ages 1 to 18 years) who had AH and AR. They compared with 315 age-matched controls who had AR alone. To identify risk factors, they were divided into four groups according to age and clinical parameters, including the prevalence of otitis media, sinusitis, lower respiratory infection, exposure to smoking, sleep disorders, use of antihistamine/decongestants, and results of allergy skin testing.
Results: The prevalence of upper and lower respiratory infections was higher in the group with AR and AH, but not in all age groups. A high prevalence of exposure to smoking and skin test reactivity to house dust mites was found in both groups. However, the prevalence of positive reactivity to moulds was significantly higher in the group with AH and AR (P ranged from 0.013 to <0.0001 and the relative risk ranged from 1.609 to 2.375). Further, the risk of AH was positively correlated with number of skin test reactivity to mould spores (P ranged from 0.035 to 0.0001). Positive skin test reactivity to animal danders or seasonal allergens failed to predict the risk of AH.
Conclusion: Sensitivity to mould allergens is an important risk factor for AH in children with AR; therefore, early prevention of exposure to moulds may help to reduce the occurrence of AH.
Reference: Ann Allergy Asthma Immunol 2001; 87: 350-355
Different expression of cytokine and membrane molecules by circulating lymphocytes on acute mental stress in patients with atopic dermatitis in comparison with healthy controls
Gerhard Schmid-Ott et al, Depts of Psychosomatic Medicine and Dermatology and Allergology, Hanover Medical School
Background: Mental stress is believed to induce an exacerbation of atopic dermatitis (AD). Until now, however, only few psychoneuroendocrinologic mechanisms underlying the link between psychologic stress and exacerbation or maintenance of AD have been described.
Objective: Their purpose was to conduct an investigation of immunologic parameters in the form of membrane molecules and cytokines with potential relevance for the cutaneous inflammation in an established psychological laboratory stress model.
Methods: Patients with AD (n =15) and healthy controls (n = 15) were exposed to mental stress, as described in a previous report. In vitro analyses were compared 1 hour before, immediately after, and 1 hour after mental stress exposure. Lymphocyte subpopulations, the cutaneous lymphocyte-associated antigen (CLA), the membrane molecule CD69+ (early activation antigen), and intracellular IL-4, IL-5, and IFN-gamma in blood-derived lymphocytes were analysed by flow cytometry. IL-4 in the supernatant of concanavalin-A-stimulated PBMCs were determined by ELISA.
Results: An increase in heart rate and blood pressure was demonstrated during psychological stress in patients with AD and healthy volunteers. They found significantly stress-induced increase of CLA+ lymphocytes, T helper cells expressing IL-5, and both CD4+ and CD8+ lymphocytes expressing IFN-gamma on mitogenic stimulation in patients with AD in comparison with healthy controls. In addition, they observed an earlier increase in the secretion of IL-4 in the supernatant of mitogen-stimulated lymphocytes during psychological stress in patients with AD in comparison with healthy volunteers.
Conclusion: A higher stress-induced increase of CLA+ cells in the circulation in patients with AD compared to healthy controls might indicate an increased ability of T lymphocytes in AD to migrate to the skin during this psychological condition. In addition, the data of this study suggest a different stress-induced cytokine profile in circulating lymphocytes in patients with AD compared to healthy controls.
Reference: J Allergy Clin Immunol 2001; 108: 455-62
Can the increase in body mass index explain the rising trend in asthma in children?
S Chinn & R J Rona, Dept. Public Health Sciences, King's College, London
Background: The reported association between asthma and obesity and the documented rise in each over time have led to suggestions that rising obesity might explain the increase in the prevalence of asthma. Trends in British children participating in the National Study of Health and Growth were marked from 1982 to 1994.
Methods: Odd ratios for trends in asthma and symptoms in 8 and 9 year old children were calculated with and without adjustment for body mass index (BMI).
Results: In a representative sample of white children the odds ratio per year of asthma was 1.09 (95% CI 1.07 to 1.11) before and after adjustment for BMI for boys and 1.09 (95% CI 1.07 to 1.12) and 1.09 (95% CI 1.05 to 1.12), respectively, for girls. Unadjusted and adjusted odds ratios were also virtually identical for wheeze and "asthma or bronchitis". The lack of effect of adjustment was due to a change in the association between BMI and symptoms with time.
Conclusions: Trends in overweight and obesity do not explain the increase in asthma. The evidence points towards the association between asthma and obesity being of recent origin. This may be explained by obesity being a marker of recent lifestyle differences now associated with both asthma and overweight.
References: Thorax 2001; 56: 845-850 (November)
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