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Extreme wildfire events are becoming more common and while the immediate risks of particulate exposures to susceptible populations (i.e., elderly, asthmatics) are appreciated, the long-term health effects are not known. In 2017, the Seeley Lake (SL), MT area experienced unprecedented levels of wildfire smoke from July 31 to September 18, with a daily average of 220.9 μg/m3. The aim of this study was to conduct health assessments in the community and evaluate potential adverse health effects. The study resulted in the recruitment of a cohort (n = 95, average age: 63 years), for a rapid response screening activity following the wildland fire event, and two follow-up visits in 2018 and 2019. Analysis of spirometry data found a significant decrease in lung function (FEV1/FVC ratio: forced expiratory volume in first second/forced vital capacity) and a more than doubling of participants that fell below the lower limit of normal (10.2% in 2017 to 45.9% in 2018) one year following the wildfire event, and remained decreased two years (33.9%) post exposure. In addition, observed FEV1 was significantly lower than predicted values. These findings suggest that wildfire smoke can have long-lasting effects on human health. As wildfires continue to increase both here and globally, understanding the health implications is vital to understanding the respiratory impacts of these events as well as developing public health strategies to mitigate the effects.
Ava Orr; Cristi A. L. Migliaccio; Mary Buford; Sarah Ballou; Christopher T. Migliaccio. Sustained Effects on Lung Function in Community Members Following Exposure to Hazardous PM2.5 Levels from Wildfire Smoke. Toxics 2020, 8, 53 .
AMA StyleAva Orr, Cristi A. L. Migliaccio, Mary Buford, Sarah Ballou, Christopher T. Migliaccio. Sustained Effects on Lung Function in Community Members Following Exposure to Hazardous PM2.5 Levels from Wildfire Smoke. Toxics. 2020; 8 (3):53.
Chicago/Turabian StyleAva Orr; Cristi A. L. Migliaccio; Mary Buford; Sarah Ballou; Christopher T. Migliaccio. 2020. "Sustained Effects on Lung Function in Community Members Following Exposure to Hazardous PM2.5 Levels from Wildfire Smoke." Toxics 8, no. 3: 53.
The purpose of this chapter is to provide an overview of macrophage subtype and multinucleated giant cell classification with a specific discussion of their role(s) in response to particulates and other foreign bodies. Topics covered for the different subtypes include the following: environmental factors involved in their generation, functional characterization, disease associations, and interactions with particulates. This chapter is separated into three major parts. The first portion describes the normal structure and functions of the macrophage. Second, the currently published macrophage subsets are outlined. The classifications included in the discussion are based on function (“M” polarization) rather than anatomical position (tissue-specific macrophages – Kupffer cells, alveolar macrophages, etc.). As shown in Fig. 1.1, the ontogeny of the various types of macrophages being discussed in this chapter depends on the pathway of activation. The third major section focuses on multinucleated giant cells, which are formed by fusion of individual macrophages. The ontogeny of each subset will be discussed and the current literature regarding particulate/foreign-body interaction will be reviewed.
Kevin Trout; Forrest Jessop; Christopher T. Migliaccio. Macrophage and Multinucleated Giant Cell Classification. Current Topics in Environmental Health and Preventive Medicine 2016, 1 -26.
AMA StyleKevin Trout, Forrest Jessop, Christopher T. Migliaccio. Macrophage and Multinucleated Giant Cell Classification. Current Topics in Environmental Health and Preventive Medicine. 2016; ():1-26.
Chicago/Turabian StyleKevin Trout; Forrest Jessop; Christopher T. Migliaccio. 2016. "Macrophage and Multinucleated Giant Cell Classification." Current Topics in Environmental Health and Preventive Medicine , no. : 1-26.
Epidemiological studies have shown a correlation between chronic biomass smoke exposure and increased respiratory infection. Pulmonary macrophages are instrumental in both the innate and the adaptive immune responses to respiratory infection. In the present study, in vitro systems were utilized where alveolar macrophages (AM) and bone marrow-derived macrophages (BMdM) were exposed to concentrated wood smoke-derived particulate matter (WS-PM) and mice were exposed in vivo to either concentrated WS-PM or inhaled WS. In vivo studies demonstrated that WS-exposed mice inoculated with Streptococcus pneumoniae had a higher bacterial load 24 h post-exposure, and corresponding AM were found to have decreased lymphocyte activation activity. Additionally, while classic markers of inflammation (cellular infiltration, total protein, neutrophils) were not affected, there were changes in pulmonary macrophages populations, including significant decreases in macrophages expressing markers of activation in WS-exposed mice. The lymphocyte activation activity of WS-PM-exposed AM was significantly suppressed, but the phagocytic activity appeared unchanged. In an effort to determine a pathway for WS-induced suppression, RelB activation, assessed by nuclear translocation, was observed in AM exposed to either inhaled WS or instilled WS-PM. Finally, an analysis of WS-PM fractions determined the presence of 4–5 polycyclic aromatic hydrocarbons (PAHs), and preliminary work suggests a potential role for these PAHs to alter macrophage functions. These studies show a decreased ability of WS-exposed pulmonary macrophages to effectively mount a defense against infection, the effect lasts at least a week post-exposure, and appears to be mediated via RelB activation.
Christopher T. Migliaccio; Emily Kobos; Quinton O. King; Virginia Porter; Forrest Jessop; Tony Ward. Adverse effects of wood smoke PM2.5exposure on macrophage functions. Inhalation Toxicology 2013, 25, 67 -76.
AMA StyleChristopher T. Migliaccio, Emily Kobos, Quinton O. King, Virginia Porter, Forrest Jessop, Tony Ward. Adverse effects of wood smoke PM2.5exposure on macrophage functions. Inhalation Toxicology. 2013; 25 (2):67-76.
Chicago/Turabian StyleChristopher T. Migliaccio; Emily Kobos; Quinton O. King; Virginia Porter; Forrest Jessop; Tony Ward. 2013. "Adverse effects of wood smoke PM2.5exposure on macrophage functions." Inhalation Toxicology 25, no. 2: 67-76.
The International Biomass Smoke Health Effects (IBSHE) conference was convened in Missoula, MT, to define our current knowledge of smoke exposure and the potential health effects. In an effort to ascertain the relative health effects of an exposure to biomass smoke, numerous studies have utilized either animal or in vitro systems. A wide variety of systems that have been employed ranged from more mainstream animal models (i.e., rodents) and transformed cell lines to less common animal (piglets and dogs) and explant models. The Toxicology and Animal Study Design Workgroup at IBSHE was tasked with an analysis of the use of animal models in the assessment of the health effects of biomass smoke exposure. The present article contains a mini-review of models utilized historically, in addition to the adverse health effects assessed, and an overview of the discussion within the breakout session. The most common question that arose in discussions at the IBSHE conference was from local and federal health departments: What level of smoke is unhealthy? The present workgroup determined categories of exposure, common health concerns, and the availability of animal models to answer key health questions.
Christopher T. Migliaccio; Joe L. Mauderly. Biomass smoke exposures: toxicology and animal study design. Inhalation Toxicology 2009, 22, 104 -107.
AMA StyleChristopher T. Migliaccio, Joe L. Mauderly. Biomass smoke exposures: toxicology and animal study design. Inhalation Toxicology. 2009; 22 (2):104-107.
Chicago/Turabian StyleChristopher T. Migliaccio; Joe L. Mauderly. 2009. "Biomass smoke exposures: toxicology and animal study design." Inhalation Toxicology 22, no. 2: 104-107.
Various techniques have been utilized historically to generate acute pulmonary inflammation in the murine system. Crystalline silica exposure results in acute inflammation followed by pulmonary fibrosis. Methods of exposure are varied in their techniques, as well as types of anesthesia. Therefore, the current study sought to compare the effects of two major anesthesia (isoflurane and ketamine) and three routes of instillation, intranasal (IN), intratracheal (IT), and trans-oral (TO), on markers of inflammation. Mice were anesthetized with isoflurane or ketamine and instilled IN with silica or phosphate-buffered saline (PBS). Mice were sacrificed and lavaged after 3 days. To assess inflammation, alveolar cells were assessed by cytospin and lavage fluid was analyzed for inflammatory cytokines and total protein. While all parameters were increased in silica-exposed groups, regardless of anesthesia type, there were significant increases in neutrophils and total protein in mice anesthetized with ketamine, compared to isoflurane. In comparing instillation techniques, mice were anesthetized with isoflurane and instilled IN, IT, or TO with silica. Increases were observed in all parameters, except tumor necrosis factor-α, following IT silica instillation as compared to the IN and TO instillation groups. In addition, fluorescent microsphere uptake by alveolar macrophages supported the notion that all methods of instillation were uniform, but IT had significantly greater dispersion. Taken together, these data show that each method of exposure tested generated significant inflammation among the silica groups, and any differences in parameters or techniques should be taken into consideration when developing an animal model to study pulmonary diseases.
Sarah E. Lacher; Corbin Johnson; Forrest Jessop; Andrij Holian; Christopher T. Migliaccio. Murine pulmonary inflammation model: a comparative study of anesthesia and instillation methods. Inhalation Toxicology 2009, 22, 77 -83.
AMA StyleSarah E. Lacher, Corbin Johnson, Forrest Jessop, Andrij Holian, Christopher T. Migliaccio. Murine pulmonary inflammation model: a comparative study of anesthesia and instillation methods. Inhalation Toxicology. 2009; 22 (1):77-83.
Chicago/Turabian StyleSarah E. Lacher; Corbin Johnson; Forrest Jessop; Andrij Holian; Christopher T. Migliaccio. 2009. "Murine pulmonary inflammation model: a comparative study of anesthesia and instillation methods." Inhalation Toxicology 22, no. 1: 77-83.
Crystalline silica exposure can result in pulmonary fibrosis, where the pulmonary macrophage is key as a result of its ability to react to silica particles. In the mouse silicosis model, there is initial Th1-type inflammation, characterized by TNF-α and IFN-γ. Previous studies determined that Th2 mediators (i.e., IL-13) are vital to development of pulmonary fibrosis. The present study, using in vivo and in vitro techniques, compares silica exposures between Balb/c and Th2-deficient mice in an effort to determine the link between Th2 immunity and silicosis. In long-term experiments, a significant increase in fibrosis and activated interstitial macrophages was observed in Balb/c but not IL-4Rα−/− mice. Additionally, a significant increase in Ym1 mRNA levels, a promoter of Th2 immunity, was determined in the interstitial leukocyte population of silica-exposed Balb/c mice. To elucidate the effects of silica on macrophage function, bone marrow-derived macrophages (BMdM) were exposed to particles and assayed for T cell (TC) stimulation activity. As a control, Ym1 mRNA expression in Balb/c BMdM was determined using IL-4 stimulation. In the in vitro assay, a significant increase in TC activation, as defined by surface markers and cytokines, was observed in the cultures containing the silica-exposed macrophages in wild-type and IL-4Rα−/− mice, with one exception: IL-4Rα−/− BMdM were unable to induce an increase in IL-13. These results suggest that crystalline silica alters cellular functions of macrophages, including activation of TC, and that the increase in Th2 immunity associated with silicosis is via the IL-4Rα-Ym1 pathway.
Christopher T. Migliaccio; Mary C. Buford; Forrest Jessop; Andrij Holian. The IL-4Rα pathway in macrophages and its potential role in silica-induced pulmonary fibrosis. Journal of Leukocyte Biology 2007, 83, 630 -639.
AMA StyleChristopher T. Migliaccio, Mary C. Buford, Forrest Jessop, Andrij Holian. The IL-4Rα pathway in macrophages and its potential role in silica-induced pulmonary fibrosis. Journal of Leukocyte Biology. 2007; 83 (3):630-639.
Chicago/Turabian StyleChristopher T. Migliaccio; Mary C. Buford; Forrest Jessop; Andrij Holian. 2007. "The IL-4Rα pathway in macrophages and its potential role in silica-induced pulmonary fibrosis." Journal of Leukocyte Biology 83, no. 3: 630-639.
Silica inhalation results in chronic lung inflammation and fibrosis. While the role of the alveolar macrophage (AM) is considered key to the effects of silica on lung pathology, the etiology is not completely understood. Evidence suggests an increase in antigen presenting cell (APC) activity as a contributing factor to this process, as well as potential roles for both AM and interstitial macrophages (IM) in silicosis. In order to study the effects of crystalline silica on the APC activity of pulmonary macrophages, mice were exposed intranasally and changes in pulmonary macrophage populations were assessed using flow cytometry. Following intranasal instillation of silica, a significant increase in the APC activity of AM was observed, as well as a significant increase in a subset of IM expressing classic APC markers (MHC class II, CD11c). In addition, an in vitro system using bone marrow-derived macrophages (BMDM) was generated to assess the effects of silica on the APC activity of macrophages in vitro. Data using BMDM in the in vitro APC assay demonstrated a significant increase in APC activity following silica exposure, but not following exposure to saline or a control particle (TiO2). Using a combination of in vivo and in vitro experiments, the current study describes a significant increase in an interstitial macrophage subset with an APC phenotype, as well as an increase in the APC activity of both AM and BMDM, as a direct result of exposure to crystalline silica. These studies suggest a specific mechanism, macrophage subset activation, by which crystalline silica exposure results in chronic pulmonary inflammation and, eventually, fibrosis.
C Migliaccio; R Hamiltonjr; Andrij Holian. Increase in a distinct pulmonary macrophage subset possessing an antigen-presenting cell phenotype and in vitro APC activity following silica exposure. Toxicology and Applied Pharmacology 2005, 205, 168 -176.
AMA StyleC Migliaccio, R Hamiltonjr, Andrij Holian. Increase in a distinct pulmonary macrophage subset possessing an antigen-presenting cell phenotype and in vitro APC activity following silica exposure. Toxicology and Applied Pharmacology. 2005; 205 (2):168-176.
Chicago/Turabian StyleC Migliaccio; R Hamiltonjr; Andrij Holian. 2005. "Increase in a distinct pulmonary macrophage subset possessing an antigen-presenting cell phenotype and in vitro APC activity following silica exposure." Toxicology and Applied Pharmacology 205, no. 2: 168-176.