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      Temporal and Spatial Patterns of Ambient Endotoxin Concentrations in Fresno, California

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          Abstract

          Background

          Endotoxins are found in indoor dust generated by human activity and pets, in soil, and adsorbed onto the surfaces of ambient combustion particles. Endotoxin concentrations have been associated with respiratory symptoms and the risk of atopy and asthma in children.

          Objective

          We characterized the temporal and spatial variability of ambient endotoxin in Fresno/Clovis, California, located in California’s Central Valley, to identify correlates and potential predictors of ambient endotoxin concentrations in a cohort of children with asthma [Fresno Asthmatic Children’s Environment Study (FACES)].

          Methods

          Between May 2001 and October 2004, daily ambient endotoxin and air pollutants were collected at the central ambient monitoring site of the California Air Resources Board in Fresno and, for shorter time periods, at 10 schools and indoors and outdoors at 84 residences in the community. Analyses were restricted to May–October, the dry months during which endotoxin concentrations are highest.

          Results

          Daily endotoxin concentration patterns were determined mainly by meteorologic factors, particularly the degree of air stagnation. Overall concentrations were lowest in areas distant from agricultural activities. Highest concentrations were found in areas immediately downwind from agricultural/pasture land. Among three other measured air pollutants [fine particulate matter, elemental carbon (a marker of traffic in Fresno), and coarse particulate matter (PM c)], PM c was the only pollutant correlated with endotoxin. Endotoxin, however, was the most spatially variable.

          Conclusions

          Our data support the need to evaluate the spatial/temporal variability of endotoxin concentrations, rather than relying on a few measurements made at one location, in studies of exposure and and respiratory health effects, particularly in children with asthma and other chronic respiratory diseases.

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          Most cited references35

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          Toll-like receptor signaling pathways.

          Members of the Toll-like receptor (TLR) family recognize conserved microbial structures, such as bacterial lipopolysaccharide and viral double-stranded RNA, and activate signaling pathways that result in immune responses against microbial infections. All TLRs activate MyD88-dependent pathways to induce a core set of stereotyped responses, such as inflammation. However, individual TLRs can also induce immune responses that are tailored to a given microbial infection. Thus, these receptors are involved in both innate and adaptive immune responses. The mechanisms and components of these varied responses are only partly understood. Given the importance of TLRs in host defense, dissection of the pathways they activate has become an important emerging research focus. TLRs and their pathways are numerous; Science's Signal Transduction Knowledge Environment's TLR Connections Map provides an immediate, clear overview of the known components and relations of this complex system.
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            Cytotoxicity and induction of proinflammatory cytokines from human monocytes exposed to fine (PM2.5) and coarse particles (PM10-2.5) in outdoor and indoor air.

            Increased incidence of mortality and morbidity due to cardiopulmonary complications has been found to associate with elevated levels of particulate air pollution (particulate matter with an aerodynamic diameter < 10 microm, PM10 and <2.5 microm, PM2. 5). Lung injury and an imbalance of inflammatory mediators are proposed causative mechanisms, while the toxic constituents may be acidity, transition metals, organic, and biogenic materials. To compare the ability of inhalable fine particles (PM2.5), and coarse particles (PM10-2.5) to cause cell injury and cytokine production in monocytes, dichotomous Andersen samplers were used to collect size-fractionated PM10 for in vitro testing of the particle extracts. Particles from both outdoor and indoor air were collected onto Teflon filters, on nine separate occasions. Each filter was water extracted and each extract assessed for ability to cause cell death, as well as interleukin (IL)-6 and IL-8 production in human monocytes. Significant toxicity and cytokine production was induced by outdoor PM10-2.5, but not by outdoor PM2.5 or the particles collected indoors. Outdoor PM10-2.5 induced 20 times the amounts of IL-6 and IL-8 than the fine particles. Cytotoxicity was inhibited by deferoxamine, a chelator of transition metals, while cytokine production was not. On the other hand, lipopolysaccharide binding protein (LBP) completely inhibited cytokine induction by PM10-2.5, suggesting that gram-negative bacteria and/or endotoxins are components of PM10-2.5. The effective proinflammatory effects of endotoxin on macrophages may upset lung homeostasis while metals-induced cytotoxicity/necrosis may set up inflammation independent of macrophage-derived cytokines. Copyright 1999 Academic Press.
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              Severity of asthma is related to endotoxin in house dust.

              In sensitized subjects, exposure to the mite allergen appears to be only one of several factors leading to asthma. We hypothesized that in association with allergen exposure, endotoxin, a proinflammatory agent present in house dust (HD), influences the severity of asthma. Using a cross-sectional study design, we investigated a group of 69 consecutive dust mite (HDM)-sensitized subjects defined as having rhinitis (n = 20) or asthma (n = 49); the latter were evaluated functionally and clinically by three different scores and by their need for daily medication. Concentrations of Dermatophagoides pteronyssinus p I allergen (Der p I) (by two-site monoclonal antibody enzyme-linked immunosorbent assay [ELISA]), guanine (by high-pressure liquid chromatography [HPLC]), and endotoxin (by modified Limulus. amebocyte lysate assay) were measured in HD collected in duplicate from the mattresses and floors in each subject's home. The concentrations of Der p I and of guanine in HD collected from mattresses were significantly higher in asthmatic subjects than in those with rhinitis (p or = 10 micrograms/g HD and/or guanine > or = 0.10 mg/100 mg HD), the severity of asthma was unrelated to mite allergen concentration in HD. On the contrary, the severity of asthma was related to concomitant exposure to endotoxin in HD, since the concentration of HD endotoxin was significantly and inversely correlated with FEV1 (p < 0.05), FEV1/FVC (p < 0.02), daily need for oral (p < 0.01) and inhaled (p < 0.01) corticosteroids, daily need for beta 2 agonists (p < 0.001) and xanthines (p < 0.01), and clinical scores such as the modified Aas score (p < 0.01). In HDM-sensitized subjects exposed to a high level of allergen, the concentration of endotoxin measured in HD is an important determinant of asthma severity.
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                Author and article information

                Journal
                Environ Health Perspect
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                1552-9924
                October 2010
                21 May 2010
                : 118
                : 10
                : 1490-1496
                Affiliations
                [1 ] Division of Epidemiology, School of Public Health, University of California, Berkeley, California, USA
                [2 ] Sonoma Technology, Inc., Petaluma, California, USA
                [3 ] Division of Environmental Health Science, School of Public Health, University of California, Berkeley, California, USA
                Author notes
                Address correspondence to I.B. Tager, University of California, Berkeley, 101 Haviland Hall, Berkeley, CA 94720 USA. Telephone: (510) 642-9533. Fax: (510) 643-5163. E-mail: ibt@ 123456berkeley.edu

                F.W.L., S.A., and B.P. are employed by Sonoma Technology, Inc., Petaluma, CA, an employee-owned for-profit scientific consulting firm. None of the other authors or staff who contributed to this project have any actual or potential competing financial interests.

                Article
                ehp-118-1490
                10.1289/ehp.0901602
                2957934
                20494854
                bb350629-5d92-454a-8d92-ea592b715f56
                This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.
                History
                : 21 October 2009
                : 21 May 2010
                Categories
                Research
                Children's Health

                Public health
                endotoxin,bioaerosols
                Public health
                endotoxin, bioaerosols

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