Predictors and respiratory depositions of airborne endotoxin in homes using biomass fuels and LPG gas for cooking
Recent studies have highlighted the presence of endotoxin in indoor air and its role in respiratory morbidities. Burning of household fuels including unprocessed wood and dried animal dung could be a major source of endotoxin in homes. We measured endotoxin levels in different size fractions of airb...
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Published in | Journal of exposure science & environmental epidemiology Vol. 27; no. 1; pp. 112 - 117 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
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New York
Nature Publishing Group US
01.01.2017
Nature Publishing Group |
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Abstract | Recent studies have highlighted the presence of endotoxin in indoor air and its role in respiratory morbidities. Burning of household fuels including unprocessed wood and dried animal dung could be a major source of endotoxin in homes. We measured endotoxin levels in different size fractions of airborne particles (PM10, PM2.5, and PM1), and estimated the deposition of particle-bound endotoxin in the respiratory tract. The study was carried out in homes burning solid biomass fuel (
n
=35) and LPG (
n
=35). Sample filters were analyzed for endotoxin and organic carbon (OC) content. Household characteristics including temperature, relative humidity, and carbon dioxide levels were also recorded. Multivariate regression models were used to estimate the contributing factors for airborne endotoxin. Respiratory deposition doses were calculated using a computer-based model. We found a higher endotoxin concentration in PM2.5 fractions of the particle in both LPG (median: 110, interquartile range (IQR) 100–120 EU/m
3
) and biomass (median: 350, IQR: 315–430 EU/m
3
) burning homes. In the multivariate-adjusted model, burning of solid biomass fuel (
β
: 67; 95% CI: 10.5–124) emerged as the most significant predictor followed by OC (
β
: 4.7; 95% CI: 2.7–6.8), RH (
β
: 1.6; 95% CI: 0.76–2.4), and PM2.5 (
β
: 0.45; 95% CI: 0.11–0.78) for airborne endotoxin (
P
<0.05). We also observed an interaction between PM organic carbon content and household fuel in predicting the endotoxin levels. The model calculations showed that in biomass burning homes, total endotoxin deposition was higher among infants (59%) than in adult males (47%), of which at least 10% of inhaled endotoxin is deposited in the alveolar region of the lung. These results indicate that fine particles are significant contributors to the deposition of endotoxin in the alveolar region of the lung. Considering the paramount role of endotoxin exposure, and the source and timing of exposure on respiratory health, additional studies are warranted to guide evidence-based public health interventions. |
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AbstractList | Recent studies have highlighted the presence of endotoxin in indoor air and its role in respiratory morbidities. Burning of household fuels including unprocessed wood and dried animal dung could be a major source of endotoxin in homes. We measured endotoxin levels in different size fractions of airborne particles (PM10, PM2.5, and PM1), and estimated the deposition of particle-bound endotoxin in the respiratory tract. The study was carried out in homes burning solid biomass fuel (n=35) and LPG (n=35). Sample filters were analyzed for endotoxin and organic carbon (OC) content. Household characteristics including temperature, relative humidity, and carbon dioxide levels were also recorded. Multivariate regression models were used to estimate the contributing factors for airborne endotoxin. Respiratory deposition doses were calculated using a computer-based model. We found a higher endotoxin concentration in PM2.5 fractions of the particle in both LPG (median: 110, interquartile range (IQR) 100-120 EU/m[sup.3]) and biomass (median: 350, IQR: 315-430 EU/m[sup.3]) burning homes. In the multivariate-adjusted model, burning of solid biomass fuel ([beta]: 67; 95% CI: 10.5-124) emerged as the most significant predictor followed by OC ([beta]: 4.7; 95% CI: 2.7-6.8), RH ([beta]: 1.6; 95% CI: 0.76-2.4), and PM2.5 ([beta]: 0.45; 95% CI: 0.11-0.78) for airborne endotoxin (P [less than] 0.05). We also observed an interaction between PM organic carbon content and household fuel in predicting the endotoxin levels. The model calculations showed that in biomass burning homes, total endotoxin deposition was higher among infants (59%) than in adult males (47%), of which at least 10% of inhaled endotoxin is deposited in the alveolar region of the lung. These results indicate that fine particles are significant contributors to the deposition of endotoxin in the alveolar region of the lung. Considering the paramount role of endotoxin exposure, and the source and timing of exposure on respiratory health, additional studies are warranted to guide evidence-based public health interventions. Recent studies have highlighted the presence of endotoxin in indoor air and its role in respiratory morbidities. Burning of household fuels including unprocessed wood and dried animal dung could be a major source of endotoxin in homes. We measured endotoxin levels in different size fractions of airborne particles (PM10, PM2.5, and PM1), and estimated the deposition of particle-bound endotoxin in the respiratory tract. The study was carried out in homes burning solid biomass fuel (n=35) and LPG (n=35). Sample filters were analyzed for endotoxin and organic carbon (OC) content. Household characteristics including temperature, relative humidity, and carbon dioxide levels were also recorded. Multivariate regression models were used to estimate the contributing factors for airborne endotoxin. Respiratory deposition doses were calculated using a computer-based model. We found a higher endotoxin concentration in PM2.5 fractions of the particle in both LPG (median: 110, interquartile range (IQR) 100-120 EU/m[sup.3]) and biomass (median: 350, IQR: 315-430 EU/m[sup.3]) burning homes. In the multivariate-adjusted model, burning of solid biomass fuel ([beta]: 67; 95% CI: 10.5-124) emerged as the most significant predictor followed by OC ([beta]: 4.7; 95% CI: 2.7-6.8), RH ([beta]: 1.6; 95% CI: 0.76-2.4), and PM2.5 ([beta]: 0.45; 95% CI: 0.11-0.78) for airborne endotoxin (P [less than] 0.05). We also observed an interaction between PM organic carbon content and household fuel in predicting the endotoxin levels. The model calculations showed that in biomass burning homes, total endotoxin deposition was higher among infants (59%) than in adult males (47%), of which at least 10% of inhaled endotoxin is deposited in the alveolar region of the lung. These results indicate that fine particles are significant contributors to the deposition of endotoxin in the alveolar region of the lung. Considering the paramount role of endotoxin exposure, and the source and timing of exposure on respiratory health, additional studies are warranted to guide evidence-based public health interventions. Journal of Exposure Science and Environmental Epidemiology (2017) 27, 112-117; doi: 10.1038/jes.2016.5; published online 9 March 2016 Keywords: endotoxin, household air pollution (HAP), LUDEP, particulate matter, respiratory deposition Recent studies have highlighted the presence of endotoxin in indoor air and its role in respiratory morbidities. Burning of household fuels including unprocessed wood and dried animal dung could be a major source of endotoxin in homes. We measured endotoxin levels in different size fractions of airborne particles (PM10, PM2.5, and PM1), and estimated the deposition of particle-bound endotoxin in the respiratory tract. The study was carried out in homes burning solid biomass fuel (n=35) and LPG (n=35). Sample filters were analyzed for endotoxin and organic carbon (OC) content. Household characteristics including temperature, relative humidity, and carbon dioxide levels were also recorded. Multivariate regression models were used to estimate the contributing factors for airborne endotoxin. Respiratory deposition doses were calculated using a computer-based model. We found a higher endotoxin concentration in PM2.5 fractions of the particle in both LPG (median: 110, interquartile range (IQR) 100-120 EU/m3) and biomass (median: 350, IQR: 315-430 EU/m3) burning homes. In the multivariate-adjusted model, burning of solid biomass fuel (β: 67; 95% CI: 10.5-124) emerged as the most significant predictor followed by OC (β: 4.7; 95% CI: 2.7-6.8), RH (β: 1.6; 95% CI: 0.76-2.4), and PM2.5 (β: 0.45; 95% CI: 0.11-0.78) for airborne endotoxin (P<0.05). We also observed an interaction between PM organic carbon content and household fuel in predicting the endotoxin levels. The model calculations showed that in biomass burning homes, total endotoxin deposition was higher among infants (59%) than in adult males (47%), of which at least 10% of inhaled endotoxin is deposited in the alveolar region of the lung. These results indicate that fine particles are significant contributors to the deposition of endotoxin in the alveolar region of the lung. Considering the paramount role of endotoxin exposure, and the source and timing of exposure on respiratory health, additional studies are warranted to guide evidence-based public health interventions. Recent studies have highlighted the presence of endotoxin in indoor air and its role in respiratory morbidities. Burning of household fuels including unprocessed wood and dried animal dung could be a major source of endotoxin in homes. We measured endotoxin levels in different size fractions of airborne particles (PM10, PM2.5, and PM1), and estimated the deposition of particle-bound endotoxin in the respiratory tract. The study was carried out in homes burning solid biomass fuel (n=35) and LPG (n=35). Sample filters were analyzed for endotoxin and organic carbon (OC) content. Household characteristics including temperature, relative humidity, and carbon dioxide levels were also recorded. Multivariate regression models were used to estimate the contributing factors for airborne endotoxin. Respiratory deposition doses were calculated using a computer-based model. We found a higher endotoxin concentration in PM2.5 fractions of the particle in both LPG (median: 110, interquartile range (IQR) 100-120 EU/m3 ) and biomass (median: 350, IQR: 315-430 EU/m3 ) burning homes. In the multivariate-adjusted model, burning of solid biomass fuel (β: 67; 95% CI: 10.5-124) emerged as the most significant predictor followed by OC (β: 4.7; 95% CI: 2.7-6.8), RH (β: 1.6; 95% CI: 0.76-2.4), and PM2.5 (β: 0.45; 95% CI: 0.11-0.78) for airborne endotoxin (P<0.05). We also observed an interaction between PM organic carbon content and household fuel in predicting the endotoxin levels. The model calculations showed that in biomass burning homes, total endotoxin deposition was higher among infants (59%) than in adult males (47%), of which at least 10% of inhaled endotoxin is deposited in the alveolar region of the lung. These results indicate that fine particles are significant contributors to the deposition of endotoxin in the alveolar region of the lung. Considering the paramount role of endotoxin exposure, and the source and timing of exposure on respiratory health, additional studies are warranted to guide evidence-based public health interventions. Recent studies have highlighted the presence of endotoxin in indoor air and its role in respiratory morbidities. Burning of household fuels including unprocessed wood and dried animal dung could be a major source of endotoxin in homes. We measured endotoxin levels in different size fractions of airborne particles (PM10, PM2.5, and PM1), and estimated the deposition of particle-bound endotoxin in the respiratory tract. The study was carried out in homes burning solid biomass fuel (n=35) and LPG (n=35). Sample filters were analyzed for endotoxin and organic carbon (OC) content. Household characteristics including temperature, relative humidity, and carbon dioxide levels were also recorded. Multivariate regression models were used to estimate the contributing factors for airborne endotoxin. Respiratory deposition doses were calculated using a computer-based model. We found a higher endotoxin concentration in PM2.5 fractions of the particle in both LPG (median: 110, interquartile range (IQR) 100-120 EU/m super(3)) and biomass (median: 350, IQR: 315-430 EU/m super(3)) burning homes. In the multivariate-adjusted model, burning of solid biomass fuel ( beta : 67; 95% CI: 10.5-124) emerged as the most significant predictor followed by OC ( beta : 4.7; 95% CI: 2.7-6.8), RH ( beta : 1.6; 95% CI: 0.76-2.4), and PM2.5 ( beta : 0.45; 95% CI: 0.11-0.78) for airborne endotoxin (P<0.05). We also observed an interaction between PM organic carbon content and household fuel in predicting the endotoxin levels. The model calculations showed that in biomass burning homes, total endotoxin deposition was higher among infants (59%) than in adult males (47%), of which at least 10% of inhaled endotoxin is deposited in the alveolar region of the lung. These results indicate that fine particles are significant contributors to the deposition of endotoxin in the alveolar region of the lung. Considering the paramount role of endotoxin exposure, and the source and timing of exposure on respiratory health, additional studies are warranted to guide evidence-based public health interventions. Recent studies have highlighted the presence of endotoxin in indoor air and its role in respiratory morbidities. Burning of household fuels including unprocessed wood and dried animal dung could be a major source of endotoxin in homes. We measured endotoxin levels in different size fractions of airborne particles (PM10, PM2.5, and PM1), and estimated the deposition of particle-bound endotoxin in the respiratory tract. The study was carried out in homes burning solid biomass fuel ( n =35) and LPG ( n =35). Sample filters were analyzed for endotoxin and organic carbon (OC) content. Household characteristics including temperature, relative humidity, and carbon dioxide levels were also recorded. Multivariate regression models were used to estimate the contributing factors for airborne endotoxin. Respiratory deposition doses were calculated using a computer-based model. We found a higher endotoxin concentration in PM2.5 fractions of the particle in both LPG (median: 110, interquartile range (IQR) 100–120 EU/m 3 ) and biomass (median: 350, IQR: 315–430 EU/m 3 ) burning homes. In the multivariate-adjusted model, burning of solid biomass fuel ( β : 67; 95% CI: 10.5–124) emerged as the most significant predictor followed by OC ( β : 4.7; 95% CI: 2.7–6.8), RH ( β : 1.6; 95% CI: 0.76–2.4), and PM2.5 ( β : 0.45; 95% CI: 0.11–0.78) for airborne endotoxin ( P <0.05). We also observed an interaction between PM organic carbon content and household fuel in predicting the endotoxin levels. The model calculations showed that in biomass burning homes, total endotoxin deposition was higher among infants (59%) than in adult males (47%), of which at least 10% of inhaled endotoxin is deposited in the alveolar region of the lung. These results indicate that fine particles are significant contributors to the deposition of endotoxin in the alveolar region of the lung. Considering the paramount role of endotoxin exposure, and the source and timing of exposure on respiratory health, additional studies are warranted to guide evidence-based public health interventions. Recent studies have highlighted the presence of endotoxin in indoor air and its role in respiratory morbidities. Burning of household fuels including unprocessed wood and dried animal dung could be a major source of endotoxin in homes. We measured endotoxin levels in different size fractions of airborne particles (PM10, PM2.5, and PM1), and estimated the deposition of particle-bound endotoxin in the respiratory tract. The study was carried out in homes burning solid biomass fuel (n=35) and LPG (n=35). Sample filters were analyzed for endotoxin and organic carbon (OC) content. Household characteristics including temperature, relative humidity, and carbon dioxide levels were also recorded. Multivariate regression models were used to estimate the contributing factors for airborne endotoxin. Respiratory deposition doses were calculated using a computer-based model. We found a higher endotoxin concentration in PM2.5 fractions of the particle in both LPG (median: 110, interquartile range (IQR) 100-120 EU/m ) and biomass (median: 350, IQR: 315-430 EU/m ) burning homes. In the multivariate-adjusted model, burning of solid biomass fuel (β: 67; 95% CI: 10.5-124) emerged as the most significant predictor followed by OC (β: 4.7; 95% CI: 2.7-6.8), RH (β: 1.6; 95% CI: 0.76-2.4), and PM2.5 (β: 0.45; 95% CI: 0.11-0.78) for airborne endotoxin (P<0.05). We also observed an interaction between PM organic carbon content and household fuel in predicting the endotoxin levels. The model calculations showed that in biomass burning homes, total endotoxin deposition was higher among infants (59%) than in adult males (47%), of which at least 10% of inhaled endotoxin is deposited in the alveolar region of the lung. These results indicate that fine particles are significant contributors to the deposition of endotoxin in the alveolar region of the lung. Considering the paramount role of endotoxin exposure, and the source and timing of exposure on respiratory health, additional studies are warranted to guide evidence-based public health interventions. Recent studies have highlighted presence of endotoxin in indoor air and its role in respiratory morbidities. Burning of household fuels including unprocessed wood and dried animal dung could be a major source of endotoxin in homes. We measured endotoxin levels in different size fractions of airborne particles (PM10, PM2.5, and PM1), and estimated the deposition of particle-bound endotoxin in the respiratory tract. The study was carried out in homes burning solid biomass fuel (n = 35) and LPG (n = 35). Sample filters were analyzed for endotoxin and organic carbon (OC) content. Household characteristics including temperature, relative humidity, and carbon dioxide levels were also recorded. Multivariate regression models were used to estimate the contributing factors for airborne endotoxin. Respiratory deposition doses were calculated using a computer-based model. We found a higher endotoxin concentration in PM2.5 fractions of the particle in both LPG (median: 110, interquartile range, (IQR): 100-120 EU/m 3 ) and biomass (median: 350, IQR: 315-430 EU/m3) burning homes. In the multivariate-adjusted model, burning of solid biomass fuel (β: 67; 95%CI: 10.5-124) emerged as the most significant predictor followed by OC (β: 4.7; 95%CI: 2.7-6.8), RH (β: 1.6; 95%CI: 0.76-2.4) and PM2.5 (β: 0.45; 95%CI: 0.11-0.78) for airborne endotoxin (p < 0.05). We also observed an interaction between PM organic carbon content and household fuel in predicting the endotoxin levels. The model calculations showed that in biomass burning homes, total endotoxin deposition was higher among infants (59%) than in adult males (47%), of which at least 10% of inhaled endotoxin is deposited in the alveolar region of the lung. These results indicate that fine particles are significant contributors to the deposition of endotoxin in the alveolar region of the lung. Considering the paramount role of endotoxin exposure, and the source and timing of exposure on respiratory health, additional studies are warranted to guide evidence-based public health interventions. |
Audience | Academic |
Author | Satapathy, Prakasini Chandel, Dinesh Patra, Alok K Padhi, Bijaya K Adhikari, Atin Panigrahi, Pinaki |
AuthorAffiliation | 3 Department of Biotechnology, Ravenshaw University, Cuttack, India 4 Regional Medical Research Center, Bhubaneswar, Indian Council of Medical Research, Odisha, India 1 Center for Environmental and Occupational Health, Asian Institute of Public Health, Bhubaneswar, India 5 Center for Global Health and Development, College of Public Health, University of Nebraska Medical Center, USA 2 Department of Environmental Health Sciences, Jiann-Ping Hsu College of Public Health, Georgia Southern University, PO Box 8015, Statesboro, Georgia 30460, USA |
AuthorAffiliation_xml | – name: 5 Center for Global Health and Development, College of Public Health, University of Nebraska Medical Center, USA – name: 4 Regional Medical Research Center, Bhubaneswar, Indian Council of Medical Research, Odisha, India – name: 1 Center for Environmental and Occupational Health, Asian Institute of Public Health, Bhubaneswar, India – name: 2 Department of Environmental Health Sciences, Jiann-Ping Hsu College of Public Health, Georgia Southern University, PO Box 8015, Statesboro, Georgia 30460, USA – name: 3 Department of Biotechnology, Ravenshaw University, Cuttack, India |
Author_xml | – sequence: 1 givenname: Bijaya K surname: Padhi fullname: Padhi, Bijaya K organization: Center for Environmental and Occupational Health, Asian Institute of Public Health – sequence: 2 givenname: Atin surname: Adhikari fullname: Adhikari, Atin organization: Department of Environmental Health Sciences, Jiann-Ping Hsu College of Public Health, Georgia Southern University – sequence: 3 givenname: Prakasini surname: Satapathy fullname: Satapathy, Prakasini organization: Department of Biotechnology, Ravenshaw University, Regional Medical Research Center, Indian Council of Medical Research – sequence: 4 givenname: Alok K surname: Patra fullname: Patra, Alok K organization: Center for Global Health and Development, College of Public Health, University of Nebraska Medical Center – sequence: 5 givenname: Dinesh surname: Chandel fullname: Chandel, Dinesh organization: Center for Global Health and Development, College of Public Health, University of Nebraska Medical Center – sequence: 6 givenname: Pinaki surname: Panigrahi fullname: Panigrahi, Pinaki email: ppanigrahi@unmc.edu organization: Center for Global Health and Development, College of Public Health, University of Nebraska Medical Center |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26956936$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1016_j_apr_2018_08_013 crossref_primary_10_1111_ina_12370 crossref_primary_10_3390_ijerph16193594 crossref_primary_10_1016_j_scitotenv_2022_160881 crossref_primary_10_1007_s11356_021_15584_w crossref_primary_10_3390_atmos12111523 crossref_primary_10_1016_j_scs_2019_101537 crossref_primary_10_1111_ina_12858 crossref_primary_10_1016_j_scitotenv_2018_01_224 crossref_primary_10_1016_j_apgeochem_2022_105398 crossref_primary_10_1016_j_envpol_2017_01_045 crossref_primary_10_1513_AnnalsATS_201708_674PS |
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Snippet | Recent studies have highlighted the presence of endotoxin in indoor air and its role in respiratory morbidities. Burning of household fuels including... Recent studies have highlighted presence of endotoxin in indoor air and its role in respiratory morbidities. Burning of household fuels including unprocessed... |
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SubjectTerms | 692/699/1785 692/700/478 704/172/169/895 Adolescent Adult Air Pollutants - adverse effects Air Pollutants - analysis Air Pollution, Indoor - adverse effects Air Pollution, Indoor - analysis Airborne microorganisms Airborne sensing Alveoli Animal manures Animals Biomass Biomass burning Biomass energy Burning Carbon Carbon content Carbon dioxide Cooking Deposition Dung Endotoxins Endotoxins - adverse effects Endotoxins - analysis Environmental aspects Environmental Monitoring Epidemiology Female Fuels Health aspects Health promotion Housing Humans Humidity India Indoor air pollution Indoor environments Infant Liquefied petroleum gas LPG Lungs Male Medicine Medicine & Public Health Middle Aged Multivariate analysis Organic carbon original-article Particle Size Particulate matter Particulate Matter - adverse effects Particulate Matter - analysis Propane Public health Regression Analysis Regression models Relative humidity Respiratory tract Respiratory Tract Absorption Respiratory tract diseases Respiratory Tract Diseases - etiology Seasons |
Title | Predictors and respiratory depositions of airborne endotoxin in homes using biomass fuels and LPG gas for cooking |
URI | https://link.springer.com/article/10.1038/jes.2016.5 https://www.ncbi.nlm.nih.gov/pubmed/26956936 https://www.proquest.com/docview/1849289215 https://www.proquest.com/docview/2615530657 https://search.proquest.com/docview/1826657314 https://search.proquest.com/docview/1855081804 https://pubmed.ncbi.nlm.nih.gov/PMC5017895 |
Volume | 27 |
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