Article

Endotoxin exposure is a risk factor for asthma—The National Survey of Endotoxin in United States Housing

Department of Occupational and Environmental Health, College of Public Health, University of Iowa, 100 Oakdale Campus, 176 IREH, Iowa City, IA 52242-5000, USA.
American Journal of Respiratory and Critical Care Medicine (Impact Factor: 11.99). 01/2006; 172(11):1371-7. DOI: 10.1164/rccm.200505-758OC
Source: PubMed

ABSTRACT Although research has shown that early life exposure to household endotoxin protects against development of allergies, studies are less clear on the relationship between household endotoxin exposure and prevalence of wheezing and asthma. We assayed 2,552 house dust samples in a representative nationwide sam- ple to explore relationships between endotoxin exposures and risk factors for asthma, asthma symptoms, and medication use.
House dust was vacuum-sampled from five locations within homes and assayed for endotoxin. Health, demographic, and housing information was assessed through questionnaire and on-site evaluation of 2,456 residents of 831 homes selected to represent the demographics of the United States.
Endotoxin concentration (EU/mg) and load (EU/m(2)) were highly correlated (r = 0.73-0.79). Geometric mean endotoxin concentrations were as follows (in EU/mg): bedroom floors, 35.3 (5th-95th percentile, 5.0-260); bedding, 18.7 (2.0-142); family room floors, 63.9 (11.5-331); sofas, 44.8 (6.4-240); and kitchen floors, 80.5 (9.8-512). Multivariate analysis demonstrated significant relationships between increasing endotoxin levels and diagnosed asthma, asthma symptoms in the past year, current use of asthma medications, and wheezing among residents of the homes. These relationships were strongest for bedroom floor and bedding dust and were observed in adults only. Modeling the joint effect of bedding and bedroom floor endotoxin on recent asthma symptoms yielded an adjusted odds ratio of 2.83 (95% confidence interval, 1.01-7.87). When stratified by allergy status, allergic subjects with higher endotoxin exposure were no more likely to have diagnosed asthma or asthma symptoms than nonallergic subjects.
This study demonstrates that household endotoxin exposure is a significant risk factor for increased asthma prevalence.

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Available from: Katarina Kulhankova, Aug 28, 2015
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    • "Some well known environmental triggers of asthma are smoke, particulate matters, pollutants and bacterial or viral infections [2]. LPS a major component of the outer membrane of gram-negative bacteria and its exposure is a major risk factor for asthma as studies have shown strong relationship between levels of household LPS and asthma exacerbations [3]. Gram negative bacterial infections like Chlamydia, Mycoplasma, and Haemophilus influenzae are most frequently associated with asthmatic exacerbations. "
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    ABSTRACT: Lipopolysaccharide (LPS) is ubiquitous in the environment and can therefore, exacerbate allergic responses. Studies have suggested immunoregulatory effects of LPS according to route, dose and stage of exposure. Present study has examined whether dose and stage of LPS exposure (during sensitization and challenge with OVA) exacerbates airway inflammations, antigen specific-IgE level, histamine release, Th1/Th2 cytokine response. Further, anti-asthmatic potential of curcumin, through intranasal route has been evaluated for the first time in LPS induced airway inflammation in an ovalbumin (OVA)-challenged mouse asthma model. Balb/c mice were first sensitized with OVA on 1st and 8th day and exposed to two LPS doses (0.1/1.0μg) separately on 2nd day and then further exposed to LPS with OVA-aerosol (from 9 to 14day). Further, lower LPS dose (0.1μg) was chosen for OVA exposed mouse model of asthma exacerbation study. Intranasal curcumin was administered from 9th to 14th day before every LPS exposure. Exposure to LPS (0.1μg) exacerbates airway inflammations in terms of IgE level, Th2-cytokine response (IL-4 and IL-5), histamine release, EPO and MPO activities and oxidative stress. Intranasal curcumin has effectively ameliorated airway exacerbations whereas dexamethasone, a known glucocorticosteroid, was not promising as compared to intranasal curcumin. Schedule and dose of LPS exposure determines asthma exacerbations and intranasal curcumin could be better immunomodulatory agent in LPS exposed asthma exacerbations. Copyright © 2015. Published by Elsevier Ltd.
    Cytokine 07/2015; DOI:10.1016/j.cyto.2015.07.022 · 2.87 Impact Factor
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    • "Epidemiological studies suggest that endotoxin levels in samples from children’s mattress were inversely related to the occurrence of atopic asthma [13]. On the other hand, some other studies have shown that endotoxin exposure is positively associated with an increased risk of asthma and asthma severity in both adults and children [14,15]. The results of animal studies are also somewhat contradictory. "
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    ABSTRACT: Background A previous study has shown that the aggravation of Asian sand dust (ASD) on ovalbumin (OVA)-induced lung eosinphilia was more severe in lipopolysaccharide (LPS)-rich ASD than in SiO2-rich ASD. Therefore, the effects of different LPS contamination levels in ASD on the aggravation of OVA-induced lung eosinophilia were investigated in the present study. Methods Before beginning the in vivo experiment, we investigated whether the ultra-pure LPS would act only on TLR4 or not using bone marrow-derived macrophages (BMDMs) of wild–type, TLR2-/-, TLR4-/- and MyD88-/- BALB/c mice. ASD collected from the desert was heated to remove toxic organic substances (H-ASD). BALB/c mice were instilled intratracheally with 12 different testing samples prepared with LPS (1 ng and 10 ng), H-ASD, and OVA in a normal saline solution. The lung pathology, cytological profiles in the bronchoalveolar lavage fluid (BALF), the levels of inflammatory cytokines/chemokines in BALF and OVA-specific immunoglobulin in serum were investigated. Results The LPS exhibited no response to the production of TNF-α and IL-6 in BMDMs from TLR4-/-, but did from TLR2-/-. H-ASD aggravated the LPS-induced neutrophilic lung inflammation. In the presence of OVA, LPS increased the level of eosinophils slightly and induced trace levels of Th2 cytokines IL-5 and IL-13 at the levels of 1 ng and 10 ng. In the presence of OVA and H-ASD, LPS induced severe eosinophil infiltration and proliferation of goblet cells in the airways as well as remarkable increases in Th2 cytokines IL-5 and IL-13 in BALF. The mixture containing LPS (1 ng) showed adjuvant activity on OVA-specific IgE and IgG1 production. Conclusions The results suggest that H-ASD with naturally-occurring levels of LPS enhances OVA-induced lung eosinophilia via increases in Th2-mediated cytokines and antigen-specific immunoglobulin. These results indicate that LPS is a strong candidate for being a major aggravating substance in ASD.
    Allergy Asthma and Clinical Immunology 06/2014; 10(1):30. DOI:10.1186/1710-1492-10-30
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    • "They are adsorbed on the surface of particles and are found to be mostly associated with coarse PM (Soukup and Becker, 2001; Schins et al., 2004). When inhaled, endotoxin can contribute to asthma exacerbation in children (Rizzo et al., 1997), and increased prevalence and severity of asthma in adults (Michel et al., 1996; Thorne et al., 2005). A number of studies have demonstrated the association of endotoxin exposure with proinflammatory cytokine production (Monn and Becker, 1999; Becker and Soukup, 1999), increased lung inflammation, airway responsiveness and systemic immune cell populations (Michel et al., 1996), and lung function modification by CD14/À260 genotype (Bakolis et al., 2012). "
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    ABSTRACT: Exposure to coarse particulate matter (PM), i.e., particles with an aerodynamic diameter between 2.5 and 10 μm (PM10-2.5), is of increasing interest due to the potential for health effects including asthma, allergy and respiratory symptoms. Limited information is available on indoor and outdoor coarse PM and associated endotoxin exposures. Seven consecutive 24-h samples of indoor and outdoor coarse PM were collected during winter and summer 2010 using Harvard Coarse Impactors in a total of 74 Edmonton homes where no reported smoking took place. Coarse PM filters were subsequently analyzed for endotoxin content. Data were also collected on indoor and outdoor temperature, relative humidity, air exchange rate, housing characteristics and occupants’ activities. During winter, outdoor concentrations of coarse PM (median = 6.7 µg/m3, interquartile range, IQR = 3.4–12 µg/m3) were found to be higher than indoor concentrations (median 3.4 µg/m3, IQR = 1.6–5.7 µg/m3); while summer levels of indoor and outdoor concentrations were similar (median 4.5 µg/m3, IQR = 2.3–6.8 µg/m3, and median 4.7 µg/m3, IQR = 2.1–7.9 µg/m3, respectively). Similar predictors were identified for indoor coarse PM in both seasons and included corresponding outdoor coarse PM concentrations, whether vacuuming, sweeping or dusting was performed during the sampling period, and number of occupants in the home. Winter indoor coarse PM predictors also included the number of dogs and indoor endotoxin concentrations. Summer median endotoxin concentrations (indoor: 0.41 EU/m3, outdoor: 0.64 EU/m3) were 4-fold higher than winter concentrations (indoor: 0.12 EU/m3, outdoor: 0.16 EU/m3). Other than outdoor endotoxin concentrations, indoor endotoxin concentration predictors for both seasons were different. Winter endotoxin predictors also included presence of furry pets and whether the vacuum had a high efficiency particulate air (HEPA) filter. Summer endotoxin predictors were problems with mice in the previous 12 months and mean indoor relative humidity levels.
    Atmospheric Environment 04/2014; 92. DOI:10.1016/j.atmosenv.2014.04.025 · 3.28 Impact Factor
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