Effects of asphalt fume condensate exposure on acute pulmonary responses
The present study was carried out to characterize the effects of in vitro exposure to paving asphalt fume condensate (AFC) on alveolar macrophage (AM) functions and to monitor acute pulmonary responses to in vivo AFC exposure in rats. For in vitro studies, rat primary AM cultures were incubated with...
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| Veröffentlicht in: | Archives of toxicology 2000-10, Vol.74 (8), p.452-459 |
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| creator | MA, J. Y. C BARGER, M. W KRIECH, A. J CASTRANOVA, V |
| description | The present study was carried out to characterize the effects of in vitro exposure to paving asphalt fume condensate (AFC) on alveolar macrophage (AM) functions and to monitor acute pulmonary responses to in vivo AFC exposure in rats.
For in vitro studies, rat primary AM cultures were incubated with various concentrations of AFC for 24 h at 37 degrees C. AM-conditioned medium was collected and assayed for lactate dehydrogenase (LDH) as a marker of cytotoxicity. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) production were assayed in AM-conditioned medium to monitor AM function. The effect of AFC on chemiluminescence (CL) generated by resting AM or AM in response to zymosan or PMA stimulation was also determined as a marker of AM activity. For in vivo studies, rats received either (1) a single intratracheal (IT) instillation of saline, or 0.1 mg or 0.5 mg AFC and were killed 1 or 3 days later; or (2) IT instillation of saline, or 0.1, 0.5, or 2 mg AFC for three consecutive days and were killed the following day. Differential counts of cells harvested by bronchoalveolar lavage were measured to monitor inflammation. Acellular LDH and protein content in the first lavage fluid were measured to monitor damage. CL generation, TNF-alpha and IL-1 production by AM were assayed to monitor AM function.
In vitro AFC exposure at |
| doi_str_mv | 10.1007/s002040000145 |
| format | Article |
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For in vitro studies, rat primary AM cultures were incubated with various concentrations of AFC for 24 h at 37 degrees C. AM-conditioned medium was collected and assayed for lactate dehydrogenase (LDH) as a marker of cytotoxicity. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) production were assayed in AM-conditioned medium to monitor AM function. The effect of AFC on chemiluminescence (CL) generated by resting AM or AM in response to zymosan or PMA stimulation was also determined as a marker of AM activity. For in vivo studies, rats received either (1) a single intratracheal (IT) instillation of saline, or 0.1 mg or 0.5 mg AFC and were killed 1 or 3 days later; or (2) IT instillation of saline, or 0.1, 0.5, or 2 mg AFC for three consecutive days and were killed the following day. Differential counts of cells harvested by bronchoalveolar lavage were measured to monitor inflammation. Acellular LDH and protein content in the first lavage fluid were measured to monitor damage. CL generation, TNF-alpha and IL-1 production by AM were assayed to monitor AM function.
In vitro AFC exposure at <200 microg/ml did not induce cytotoxicity, oxidant generation, or IL-1 production by AM, but it did cause a small but significant increase in TNF-alpha release from AM. In vitro exposure of AM to AFC resulted in a significant decline of CL in response to zymosan or PMA stimulation. The in vivo studies showed that AFC exposure did not induce significant neutrophil infiltration or alter LDH or protein content in acellular lavage samples. Macrophages obtained from AFC-exposed rats did not show significant differences in oxidant production or cytokine secretion at rest or in response to LPS in comparison with control macrophages.
These results suggest that: (1) in vitro AFC exposure did not adversely affect cell viability or induce the release of high levels of inflammatory cytokines or oxidants; and (2) exposure of rats to AFC did not cause acute pulmonary inflammation or injury, and did not significantly alter AM functions.</description><identifier>ISSN: 0340-5761</identifier><identifier>EISSN: 1432-0738</identifier><identifier>DOI: 10.1007/s002040000145</identifier><identifier>PMID: 11097382</identifier><identifier>CODEN: ARTODN</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Animals ; asphalt ; Biological and medical sciences ; Cells, Cultured ; Chemical and industrial products toxicology. Toxic occupational diseases ; Gas, fumes ; Hydrocarbons - toxicity ; In Vitro Techniques ; Interleukin-1 - biosynthesis ; Luminescent Measurements ; Lung - drug effects ; Lung - pathology ; Macrophages, Alveolar - drug effects ; Macrophages, Alveolar - physiology ; Male ; Medical sciences ; Occupational Exposure ; Polycyclic Aromatic Hydrocarbons - toxicity ; Rats ; Rats, Sprague-Dawley ; Toxicology ; Tumor Necrosis Factor-alpha - biosynthesis</subject><ispartof>Archives of toxicology, 2000-10, Vol.74 (8), p.452-459</ispartof><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-b6031423551212b978a86013cb846e2ae30b7f52a7dd4c958185ebc72b47350a3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1522651$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11097382$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MA, J. Y. C</creatorcontrib><creatorcontrib>BARGER, M. W</creatorcontrib><creatorcontrib>KRIECH, A. J</creatorcontrib><creatorcontrib>CASTRANOVA, V</creatorcontrib><title>Effects of asphalt fume condensate exposure on acute pulmonary responses</title><title>Archives of toxicology</title><addtitle>Arch Toxicol</addtitle><description>The present study was carried out to characterize the effects of in vitro exposure to paving asphalt fume condensate (AFC) on alveolar macrophage (AM) functions and to monitor acute pulmonary responses to in vivo AFC exposure in rats.
For in vitro studies, rat primary AM cultures were incubated with various concentrations of AFC for 24 h at 37 degrees C. AM-conditioned medium was collected and assayed for lactate dehydrogenase (LDH) as a marker of cytotoxicity. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) production were assayed in AM-conditioned medium to monitor AM function. The effect of AFC on chemiluminescence (CL) generated by resting AM or AM in response to zymosan or PMA stimulation was also determined as a marker of AM activity. For in vivo studies, rats received either (1) a single intratracheal (IT) instillation of saline, or 0.1 mg or 0.5 mg AFC and were killed 1 or 3 days later; or (2) IT instillation of saline, or 0.1, 0.5, or 2 mg AFC for three consecutive days and were killed the following day. Differential counts of cells harvested by bronchoalveolar lavage were measured to monitor inflammation. Acellular LDH and protein content in the first lavage fluid were measured to monitor damage. CL generation, TNF-alpha and IL-1 production by AM were assayed to monitor AM function.
In vitro AFC exposure at <200 microg/ml did not induce cytotoxicity, oxidant generation, or IL-1 production by AM, but it did cause a small but significant increase in TNF-alpha release from AM. In vitro exposure of AM to AFC resulted in a significant decline of CL in response to zymosan or PMA stimulation. The in vivo studies showed that AFC exposure did not induce significant neutrophil infiltration or alter LDH or protein content in acellular lavage samples. Macrophages obtained from AFC-exposed rats did not show significant differences in oxidant production or cytokine secretion at rest or in response to LPS in comparison with control macrophages.
These results suggest that: (1) in vitro AFC exposure did not adversely affect cell viability or induce the release of high levels of inflammatory cytokines or oxidants; and (2) exposure of rats to AFC did not cause acute pulmonary inflammation or injury, and did not significantly alter AM functions.</description><subject>Animals</subject><subject>asphalt</subject><subject>Biological and medical sciences</subject><subject>Cells, Cultured</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Gas, fumes</subject><subject>Hydrocarbons - toxicity</subject><subject>In Vitro Techniques</subject><subject>Interleukin-1 - biosynthesis</subject><subject>Luminescent Measurements</subject><subject>Lung - drug effects</subject><subject>Lung - pathology</subject><subject>Macrophages, Alveolar - drug effects</subject><subject>Macrophages, Alveolar - physiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Occupational Exposure</subject><subject>Polycyclic Aromatic Hydrocarbons - toxicity</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Toxicology</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><issn>0340-5761</issn><issn>1432-0738</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpV0EFLw0AQBeBFFFurR6-yB_EWndnNZpOjlGqFghc9h81mgpUkGzMJ6L830kBxLgPDx2N4Qlwj3COAfWAABTFMg7E5EUuMtYrA6vRULEHHEBmb4EJcMH9ORKWZPhcLRMgmopZiu6kq8gPLUEnH3YerB1mNDUkf2pJadgNJ-u4Cjz3J0Ernx-nSjXUTWtf_yJ64Cy0TX4qzytVMV_Neifenzdt6G-1en1_Wj7vI6wyGqEhAY6y0MahQFZlNXZoAal-kcULKkYbCVkY5W5axz0yKqaHCW1XEVhtweiXuDrldH75G4iFv9uyprl1LYeQcrTUIaCcYHaDvA3NPVd71-2b6OUfI_6rL_1U3-Zs5eCwaKo967moCtzNw7F1d9a71ez46o1RiUP8CGLd0kQ</recordid><startdate>20001001</startdate><enddate>20001001</enddate><creator>MA, J. Y. C</creator><creator>BARGER, M. W</creator><creator>KRIECH, A. J</creator><creator>CASTRANOVA, V</creator><general>Springer</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20001001</creationdate><title>Effects of asphalt fume condensate exposure on acute pulmonary responses</title><author>MA, J. Y. C ; BARGER, M. W ; KRIECH, A. J ; CASTRANOVA, V</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-b6031423551212b978a86013cb846e2ae30b7f52a7dd4c958185ebc72b47350a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>asphalt</topic><topic>Biological and medical sciences</topic><topic>Cells, Cultured</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Gas, fumes</topic><topic>Hydrocarbons - toxicity</topic><topic>In Vitro Techniques</topic><topic>Interleukin-1 - biosynthesis</topic><topic>Luminescent Measurements</topic><topic>Lung - drug effects</topic><topic>Lung - pathology</topic><topic>Macrophages, Alveolar - drug effects</topic><topic>Macrophages, Alveolar - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Occupational Exposure</topic><topic>Polycyclic Aromatic Hydrocarbons - toxicity</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Toxicology</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MA, J. Y. C</creatorcontrib><creatorcontrib>BARGER, M. W</creatorcontrib><creatorcontrib>KRIECH, A. J</creatorcontrib><creatorcontrib>CASTRANOVA, V</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Archives of toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MA, J. Y. C</au><au>BARGER, M. W</au><au>KRIECH, A. J</au><au>CASTRANOVA, V</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of asphalt fume condensate exposure on acute pulmonary responses</atitle><jtitle>Archives of toxicology</jtitle><addtitle>Arch Toxicol</addtitle><date>2000-10-01</date><risdate>2000</risdate><volume>74</volume><issue>8</issue><spage>452</spage><epage>459</epage><pages>452-459</pages><issn>0340-5761</issn><eissn>1432-0738</eissn><coden>ARTODN</coden><abstract>The present study was carried out to characterize the effects of in vitro exposure to paving asphalt fume condensate (AFC) on alveolar macrophage (AM) functions and to monitor acute pulmonary responses to in vivo AFC exposure in rats.
For in vitro studies, rat primary AM cultures were incubated with various concentrations of AFC for 24 h at 37 degrees C. AM-conditioned medium was collected and assayed for lactate dehydrogenase (LDH) as a marker of cytotoxicity. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) production were assayed in AM-conditioned medium to monitor AM function. The effect of AFC on chemiluminescence (CL) generated by resting AM or AM in response to zymosan or PMA stimulation was also determined as a marker of AM activity. For in vivo studies, rats received either (1) a single intratracheal (IT) instillation of saline, or 0.1 mg or 0.5 mg AFC and were killed 1 or 3 days later; or (2) IT instillation of saline, or 0.1, 0.5, or 2 mg AFC for three consecutive days and were killed the following day. Differential counts of cells harvested by bronchoalveolar lavage were measured to monitor inflammation. Acellular LDH and protein content in the first lavage fluid were measured to monitor damage. CL generation, TNF-alpha and IL-1 production by AM were assayed to monitor AM function.
In vitro AFC exposure at <200 microg/ml did not induce cytotoxicity, oxidant generation, or IL-1 production by AM, but it did cause a small but significant increase in TNF-alpha release from AM. In vitro exposure of AM to AFC resulted in a significant decline of CL in response to zymosan or PMA stimulation. The in vivo studies showed that AFC exposure did not induce significant neutrophil infiltration or alter LDH or protein content in acellular lavage samples. Macrophages obtained from AFC-exposed rats did not show significant differences in oxidant production or cytokine secretion at rest or in response to LPS in comparison with control macrophages.
These results suggest that: (1) in vitro AFC exposure did not adversely affect cell viability or induce the release of high levels of inflammatory cytokines or oxidants; and (2) exposure of rats to AFC did not cause acute pulmonary inflammation or injury, and did not significantly alter AM functions.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>11097382</pmid><doi>10.1007/s002040000145</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals asphalt Biological and medical sciences Cells, Cultured Chemical and industrial products toxicology. Toxic occupational diseases Gas, fumes Hydrocarbons - toxicity In Vitro Techniques Interleukin-1 - biosynthesis Luminescent Measurements Lung - drug effects Lung - pathology Macrophages, Alveolar - drug effects Macrophages, Alveolar - physiology Male Medical sciences Occupational Exposure Polycyclic Aromatic Hydrocarbons - toxicity Rats Rats, Sprague-Dawley Toxicology Tumor Necrosis Factor-alpha - biosynthesis |
| title | Effects of asphalt fume condensate exposure on acute pulmonary responses |
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