Does Breathing Wood Smoke Make the Flu Worse? Sex Might Matter.
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ABSTRACT:
SUBMITTER: Frampton MW
PROVIDER: S-EPMC6467314 | biostudies-literature | 2019 Apr
REPOSITORIES: biostudies-literature
Publications
Does Breathing Wood Smoke Make the Flu Worse? Sex Might Matter.
American journal of respiratory and critical care medicine 20190401 8
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Project description:Wood burning is a major source of ambient particulate matter (PM) and has been epidemiologically linked to adverse pulmonary health effects, however the impact of fuel and burning conditions on PM properties has not been investigated systematically. Here, we employed our recently developed integrated methodology to characterize the physicochemical and biological properties of emitted PM as a function of three common hardwoods (oak, cherry, mesquite) and three representative combustion conditions (flaming, smoldering, incomplete). Differences in PM and off-gas emissions (aerosol number/mass concentrations; carbon monoxide; volatile organic compounds) as well as inorganic elemental composition and organic carbon functional content of PM0.1 were noted between wood types and combustion conditions, although the combustion scenario exerted a stronger influence on the emission profile. More importantly, flaming combustion PM0.1 from all hardwoods significantly stimulated the promoter activity of Sterile Alpha Motif (SAM) pointed domain containing ETS (E-twenty-six) Transcription Factor (SPDEF) in human embryonic kidney 293 (HEK-293 T) cells, a biomarker for mucin gene expression associated with mucus production in pulmonary diseases. However, no bioactivity was observed for smoldering and incomplete combustion, which was likely driven by differences in the organic composition of PM0.1. Detailed chemical speciation of organic components of wood smoke is warranted to identify the individual compounds that drive specific biological responses.
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| S-EPMC6899763 | biostudies-literature
Project description:Previous studies have reported associations between ambient fine particle concentrations and preeclampsia; however, the impact of particulate pollution on early- and late-onset preeclampsia is understudied. Furthermore, few studies have examined the association between source-specific particles such as markers of traffic pollution or wood combustion on adverse pregnancy outcomes. Electronic medical records and birth certificate data were linked with land-use regression models in Monroe County, New York for 2009 to 2013 to predict monthly pollutant concentrations for each pregnancy until the date of clinical diagnosis during winter (November-April) for 16 116 births. Up to 30% of ambient wintertime fine particle concentrations in Monroe County, New York is from wood combustion. Multivariable logistic regression was used to separately estimate the odds of preeclampsia (all, early-, and late-onset) associated with each interquartile range increase in fine particles, traffic pollution, and woodsmoke concentrations during each gestational month, adjusting for maternal characteristics, birth hospital, temperature, and relative humidity. Each 3.64 µg/m3 increase in fine particle concentration was associated with an increased odds of early-onset preeclampsia during the first (odds ratio, 1.35 [95% CI, 1.08-1.68]), second (odds ratio, 1.51 [95% CI, 1.23-1.86]), and third (odds ratio, 1.25 [95% CI, 1.06-1.46]) gestational months. Increases in traffic pollution and woodsmoke during the first gestational month were also associated with increased odds of early-onset preeclampsia. Increased odds of late-onset preeclampsia were not observed. Our findings suggest that exposure to wintertime particulate pollution may have the greatest effect on maternal cardiovascular health during early pregnancy.
| S-EPMC7035201 | biostudies-literature
Project description:The majority of terrestrial biomass is wood, but the elemental composition of its potential consumers, xylophages, differs hugely from that of wood. This causes a severe nutritional imbalance. We studied the stoichiometric relationships of 11 elements (C, N, P, K, Ca, Mg, Fe, Zn, Mn, Cu, Na) in three species of pine-xylem-feeding insects, Stictoleptura rubra, Arhopalus rusticus (Coleoptera, Cerambycidae) and Chalcophora mariana (Coleoptera, Buprestidae), to elucidate their mechanisms of tissue growth and to match their life histories to their dietary constraints. These beetles do not differ from other Coleoptera in their absolute elemental compositions, which are approximately 1000 (N), 100 (P, Cu) and 50 (K, Na) times higher than in dead but undecayed pine wood. This discrepancy diminishes along the wood decay gradient, but the elemental concentrations remain higher by an order of magnitude in beetles than in highly decayed wood. Numerical simulation of the life history of S. rubra shows that feeding on nutrient-poor undecayed wood would extend its development time to implausible values, whereas feeding on highly decomposed wood (heavily infected with fungi) would barely balance its nutritional budget during the long development period of this species. The changes in stoichiometry indicate that the relative change in the nutrient levels in decaying wood cannot be attributed solely to carbon loss resulting from decomposer respiration: the action of fungi substantially enriches the decaying wood with nutritional elements imported from the outside of the system, making it a suitable food for wood-eating invertebrates.
| S-EPMC4275229 | biostudies-literature
Project description:Healthy human subjects were exposed to wood smoke particulate matter and filtered air on separate occasions. Alveolar leukocytes (predominantly macrophages) were then obtained and analysed by microarray to assess the impact of wood smoke on transcription in the airway.
2010-10-12 | E-MEXP-2813 | biostudies-arrayexpress
Project description:RationaleExposure to particulates from burning biomass is an increasing global health issue. Burning biomass, including wood smoke, is associated with increased lower respiratory infections.ObjectivesTo determine whether acute exposure to wood smoke modifies nasal inflammatory responses to influenza.MethodsHealthy young adults (n = 39) were randomized to a 2-hour controlled chamber exposure to wood smoke, where exposure levels were controlled to particulate number (wood smoke particles [WSP]; 500 μg/cm3) or filtered air, followed by nasal inoculation with a vaccine dose of live attenuated influenza virus (LAIV). Nasal lavage was performed before exposure (Day 0) and on Days 1 and 2 after exposure. Nasal lavage fluid cells were analyzed for inflammatory gene expression profiles, and cell-free fluid was assayed for cytokines.Measurements and main resultsOnly IP-10 protein levels were affected, suppressed, by WSP exposure in aggregate analysis. Subsequent analysis indicated an exposure × sex interaction, prompting additional analyses of WSP- and LAIV-induced changes in males and females. Inflammation-related gene expression profiles differed between the sexes, at baseline (males greater than females), after LAIV inoculation (females greater than males), and after WSP exposure (increase in males and decrease in females), demonstrating that WSP- and LAIV-induced changes in antiviral defense responses in the nasal mucosa occur in a sex-specific manner.ConclusionsWSP exposure resulted in minimal modification of LAIV-induced responses in aggregate analysis. In contrast, analyzing WSP-induced modification of LAIV responses in the sexes separately unmasked sex-specific differences in response to exposure. These data highlight the need for additional studies to understand sex-specific pollutant-induced effects. Clinical trial registered with www.clinicaltrials.gov (NCT02183753).
| S-EPMC6467301 | biostudies-literature
Project description:Cigarette smoking is associated with a higher risk of ICU admissions among patients with flu. However, the etiological mechanism by which cigarette smoke (CS) exacerbates flu remains poorly understood. Here, we show that a mild dose of influenza A virus promotes a severe lung injury in mice preexposed to CS but not room air for 4 weeks. Real-time intravital (in vivo) lung imaging revealed that the development of acute severe respiratory dysfunction in CS- and flu-exposed mice was associated with the accumulation of platelet-rich neutrophil-platelet aggregates (NPAs) in the lung microcirculation within 2 days following flu infection. These platelet-rich NPAs formed in situ and grew larger over time to occlude the lung microvasculature, leading to the development of pulmonary ischemia followed by the infiltration of NPAs and vascular leakage into the alveolar air space. These findings suggest, for the first time to our knowledge, that an acute onset of platelet-driven thrombo-inflammatory response in the lung contributes to the development of CS-induced severe flu.
| S-EPMC10906226 | biostudies-literature
Project description:Household air pollution from wood smoke (WS), contributes to adverse health effects in both low- and high-income countries. However, measurement of WS exposure has been limited to expensive in-home monitoring and lengthy face-to-face interviews. This paper reports on the development and testing of a novel, self-report nine-item measure of WS exposure, called the Household Exposure to Wood Smoke (HEWS). A sample of 149 individuals using household wood stoves for heating from western states in the U.S., completed the HEWS during the winter months (November to March) of 2013 through 2016 with 30 subjects having in-home particle monitoring. Hard copy or online surveys were completed. Cronbach's alpha (α), intraclass correlations (ICC), exploratory factor analysis (EFA) and tests of associations were done to evaluate reliability and validity of the HEWS. Based on initial analysis, only 9 of the 12 items were retained and entered in the EFA. The EFA did not support a unitary scale as the 9 items demonstrated a 3-factor solution (WS exposure duration, proximity, and intensity) with Cronbach's α of 0.79, 0.91, and 0.62, respectively. ICC was 0.86 of the combined items with single items ranging from 0.46 to 0.95. WS intensity was associated with symptoms and levoglucosan levels, while WS duration was associated with stove and flume maintenance. The three-dimensional HEWS demonstrated internal consistency and test-retest reliability, structural validity, and initial criterion and construct validity.
| S-EPMC10022189 | biostudies-literature
Project description:BackgroundSmoke from combustion of biomass fuels is a major risk factor for respiratory disease, but the underlying mechanisms are poorly understood. The aim of this study was to determine whether exposure to wood smoke from incomplete combustion would elicit airway inflammation in humans.MethodsFourteen healthy subjects underwent controlled exposures on two separate occasions to filtered air and wood smoke from incomplete combustion with PM1 concentration at 314 μg/m(3) for 3 h in a chamber. Bronchoscopy with bronchial wash (BW), bronchoalveolar lavage (BAL) and endobronchial mucosal biopsies was performed after 24 h. Differential cell counts and soluble components were analyzed, with biopsies stained for inflammatory markers using immunohistochemistry. In parallel experiments, the toxicity of the particulate matter (PM) generated during the chamber exposures was investigated in vitro using the RAW264.7 macrophage cell line.ResultsSignificant reductions in macrophage, neutrophil and lymphocyte numbers were observed in BW (p < 0.01, <0.05, <0.05, respectively) following the wood smoke exposure, with a reduction in lymphocytes numbers in BAL fluid (<0.01. This unexpected cellular response was accompanied by decreased levels of sICAM-1, MPO and MMP-9 (p < 0.05, <0.05 and <0.01). In contrast, significant increases in submucosal and epithelial CD3+ cells, epithelial CD8+ cells and submucosal mast cells (p < 0.01, <0.05, <0.05 and <0.05, respectively), were observed after wood smoke exposure. The in vitro data demonstrated that wood smoke particles generated under these incomplete combustion conditions induced cell death and DNA damage, with only minor inflammatory responses.ConclusionsShort-term exposure to sooty PAH rich wood smoke did not induce an acute neutrophilic inflammation, a classic hallmark of air pollution exposure in humans. While minor proinflammatory lymphocytic and mast cells effects were observed in the bronchial biopsies, significant reductions in BW and BAL cells and soluble components were noted. This unexpected observation, combined with the in vitro data, suggests that wood smoke particles from incomplete combustion could be potentially cytotoxic. Additional research is required to establish the mechanism of this dramatic reduction in airway leukocytes and to clarify how this acute response contributes to the adverse health effects attributed to wood smoke exposure.Trial registrationNCT01488500.
| S-EPMC4625445 | biostudies-literature
Project description:BackgroundExposure to particulate matter (PM) from wood combustion represents a global health risk, encompassing diverse exposure sources; indoor exposures due to cooking in developing countries, ambient PM exposures from residential wood combustion in developed countries, and the predicted increasing number of wildfires due to global warming. Although physicochemical properties of the PM, as well as the exposure levels vary considerably between these sources, controlled human exposure studies may provide valuable insight to the harmful effects of wood smoke (WS) exposures in general. However, no previous review has focused specifically on controlled human exposure studies to WS.ResultsThe 22 publications identified, resulting from 12 controlled human studies, applied a range of combustion conditions, exposure levels and durations, and exercise components in their WS exposure. A range of airway, cardiovascular and systemic endpoints were assessed, including lung function and heart rate measures, inflammation and oxidative stress. However, the possibility for drawing general conclusions was precluded by the large variation in study design, resulting in differences in physicochemical properties of WS, effective dose, as well as included endpoints and time-points for analysis. Overall, there was most consistency in reported effects for airways, while oxidative stress, systemic inflammation and cardiovascular physiology did not show any clear patterns.ConclusionBased on the reviewed controlled human exposure studies, conclusions regarding effects of acute WS exposure on human health are premature. Thus, more carefully conducted human studies are needed. Future studies should pay particular attention to the applied WS exposure, to assure that both exposure levels and PM properties reflect the research question.
| S-EPMC7530963 | biostudies-literature