Experimental PVC Material Challenge in Subjects with Occupational PVC Exposure

Background: Polyvinyl chloride (PVC) materials have been linked to asthma in several epidemiologic studies, but the possible causal factors remain unknown. Participants: We challenged 10 subjects experimentally to degraded PVC products under controlled conditions. All of the subjects had previously...

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Published inEnvironmental health perspectives Vol. 114; no. 9; pp. 1409 - 1413
Main Authors Tuomainen, Anneli, Stark, Harri, Seuri, Markku, Hirvonen, Maija-Riitta, Linnainmaa, Markku, Sieppi, Anne, Tukiainen, Hannu
Format Journal Article
LanguageEnglish
Published United States National Institute of Environmental Health Sciences. National Institutes of Health. Department of Health, Education and Welfare 01.09.2006
National Institute of Environmental Health Sciences
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Online AccessGet full text
ISSN0091-6765
1552-9924
DOI10.1289/ehp.8965

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Abstract Background: Polyvinyl chloride (PVC) materials have been linked to asthma in several epidemiologic studies, but the possible causal factors remain unknown. Participants: We challenged 10 subjects experimentally to degraded PVC products under controlled conditions. All of the subjects had previously experienced respiratory symptoms suspected to be caused by this kind of exposure in their work place. Five subjects had doctor-diagnosed asthma. Methods: The subjects were exposed to degraded PVC material in an exposure chamber; a challenge with ceramic tile was used as the control test. We followed exhaled nitric oxide, nasal NO, lung functions, cytokines [tumor necrosis factor-α (TNF-α), interleukin-4 (IL-4), IL-6, and IL-12] and NO in nasal lavage fluid (NAL) during and after the exposures. We also measured 2-ethylhexanol in exhaled breath samples and NAL. Results: On the morning after the PVC exposure, subjects reported respiratory tract symptoms significantly more often than they did after the control test (50% vs. 0%, respectively; p = 0.029; n = 10). We did not detect any changes in lung functions or levels of exhaled NO, nasal NO, or NO in NAL after PVC challenge compared with the control test. Cytokine levels increased after both exposures, with no statistically significant difference between situations. All of the exhaled breath samples collected during the PVC exposure contained 2-ethylhexanol. Conclusions: PVC flooring challenge can evoke respiratory tract symptoms in exposed subjects. Our results do not support the hypothesis that PVC materials themselves evoke immediate asthmatic reactions. The chamber test used is well suited to this type of exposure study.
AbstractList Background: Polyvinyl chloride (PVC) materials have been linked to asthma in several epidemiologic studies, but the possible causal factors remain unknown. Participants: We challenged 10 subjects experimentally to degraded PVC products under controlled conditions. All of the subjects had previously experienced respiratory symptoms suspected to be caused by this kind of exposure in their work place. Five subjects had doctor-diagnosed asthma. Methods: The subjects were exposed to degraded PVC material in an exposure chamber; a challenge with ceramic tile was used as the control test. We followed exhaled nitric oxide, nasal NO, lung functions, cytokines [tumor necrosis factor-α (TNF-α), interleukin-4 (IL-4), IL-6, and IL-12] and NO in nasal lavage fluid (NAL) during and after the exposures. We also measured 2-ethylhexanol in exhaled breath samples and NAL. Results: On the morning after the PVC exposure, subjects reported respiratory tract symptoms significantly more often than they did after the control test (50% vs. 0%, respectively; p = 0.029; n = 10). We did not detect any changes in lung functions or levels of exhaled NO, nasal NO, or NO in NAL after PVC challenge compared with the control test. Cytokine levels increased after both exposures, with no statistically significant difference between situations. All of the exhaled breath samples collected during the PVC exposure contained 2-ethylhexanol. Conclusions: PVC flooring challenge can evoke respiratory tract symptoms in exposed subjects. Our results do not support the hypothesis that PVC materials themselves evoke immediate asthmatic reactions. The chamber test used is well suited to this type of exposure study.
Polyvinyl chloride (PVC) materials have been linked to asthma in several epidemiologic studies, but the possible causal factors remain unknown.BACKGROUNDPolyvinyl chloride (PVC) materials have been linked to asthma in several epidemiologic studies, but the possible causal factors remain unknown.We challenged 10 subjects experimentally to degraded PVC products under controlled conditions. All of the subjects had previously experienced respiratory symptoms suspected to be caused by this kind of exposure in their work place. Five subjects had doctor-diagnosed asthma.PARTICIPANTSWe challenged 10 subjects experimentally to degraded PVC products under controlled conditions. All of the subjects had previously experienced respiratory symptoms suspected to be caused by this kind of exposure in their work place. Five subjects had doctor-diagnosed asthma.The subjects were exposed to degraded PVC material in an exposure chamber ; a challenge with ceramic tile was used as the control test. We followed exhaled nitric oxide, nasal NO, lung functions, cytokines [tumor necrosis factor-alpha (TNF-alpha) , interleukin-4 (IL-4) , IL-6, and IL-12] and NO in nasal lavage fluid (NAL) during and after the exposures. We also measured 2-ethylhexanol in exhaled breath samples and NAL.METHODSThe subjects were exposed to degraded PVC material in an exposure chamber ; a challenge with ceramic tile was used as the control test. We followed exhaled nitric oxide, nasal NO, lung functions, cytokines [tumor necrosis factor-alpha (TNF-alpha) , interleukin-4 (IL-4) , IL-6, and IL-12] and NO in nasal lavage fluid (NAL) during and after the exposures. We also measured 2-ethylhexanol in exhaled breath samples and NAL.On the morning after the PVC exposure, subjects reported respiratory tract symptoms significantly more often than they did after the control test (50% vs. 0%, respectively ; p = 0.029 ; n = 10) . We did not detect any changes in lung functions or levels of exhaled NO, nasal NO, or NO in NAL after PVC challenge compared with the control test. Cytokine levels increased after both exposures, with no statistically significant difference between situations. All of the exhaled breath samples collected during the PVC exposure contained 2-ethylhexanol.RESULTSOn the morning after the PVC exposure, subjects reported respiratory tract symptoms significantly more often than they did after the control test (50% vs. 0%, respectively ; p = 0.029 ; n = 10) . We did not detect any changes in lung functions or levels of exhaled NO, nasal NO, or NO in NAL after PVC challenge compared with the control test. Cytokine levels increased after both exposures, with no statistically significant difference between situations. All of the exhaled breath samples collected during the PVC exposure contained 2-ethylhexanol.PVC flooring challenge can evoke respiratory tract symptoms in exposed subjects. Our results do not support the hypothesis that PVC materials themselves evoke immediate asthmatic reactions. The chamber test used is well suited to this type of exposure study.CONCLUSIONSPVC flooring challenge can evoke respiratory tract symptoms in exposed subjects. Our results do not support the hypothesis that PVC materials themselves evoke immediate asthmatic reactions. The chamber test used is well suited to this type of exposure study.
Experimental polyvinyl chloride (PVC) material challenge in subjects with occupational PVC exposure was discussed. It was observed that 10 subjects were challenged experimentally to degraded PVC products under controlled conditions. All of the subjects had previously experienced respiratory symptoms caused by this kind of exposure in the work place. Five subjects had doctor-diagnosed asthma. The subjects were exposed to degraded PC material in an exposure chamber; a challenge with ceramic tile was used as the control test. On the morning after the PVC exposure, subjects reported respiratory tract symptoms significantly more often than they did after the control test. PVC flooring challenge could evoke respiratory tract symptoms in exposed subjects.
BACKGROUND: Polyvinyl chloride (PVC) materials have been linked to asthma in several epidemiologic studies, but the possible causal factors remain unknown. PARTICIPANTS: We challenged 10 subjects experimentally to degraded PVC products under controlled conditions. All of the subjects had previously experienced respiratory symptoms suspected to be caused by this kind of exposure in their work place. Five subjects had doctor-diagnosed asthma. METHODS: The subjects were exposed to degraded PVC material in an exposure chamber ; a challenge with ceramic tile was used as the control test. We followed exhaled nitric oxide, nasal NO, lung functions, cytokines [tumor necrosis factor-alpha (TNF-alpha) , interleukin-4 (IL-4) , IL-6, and IL-12] and NO in nasal lavage fluid (NAL) during and after the exposures. We also measured 2-ethylhexanol in exhaled breath samples and NAL. RESULTS: On the morning after the PVC exposure, subjects reported respiratory tract symptoms significantly more often than they did after the control test (50% vs. 0%, respectively ; p = 0.029 ; n = 10) . We did not detect any changes in lung functions or levels of exhaled NO, nasal NO, or NO in NAL after PVC challenge compared with the control test. Cytokine levels increased after both exposures, with no statistically significant difference between situations. All of the exhaled breath samples collected during the PVC exposure contained 2-ethylhexanol. CONCLUSIONS: PVC flooring challenge can evoke respiratory tract symptoms in exposed subjects. Our results do not support the hypothesis that PVC materials themselves evoke immediate asthmatic reactions. The chamber test used is well suited to this type of exposure study.
Polyvinyl chloride (PVC) materials have been linked to asthma in several epidemiologic studies, but the possible causal factors remain unknown. We challenged 10 subjects experimentally to degraded PVC products under controlled conditions. All of the subjects had previously experienced respiratory symptoms suspected to be caused by this kind of exposure in their work place. Five subjects had doctor-diagnosed asthma. The subjects were exposed to degraded PVC material in an exposure chamber ; a challenge with ceramic tile was used as the control test. We followed exhaled nitric oxide, nasal NO, lung functions, cytokines [tumor necrosis factor-alpha (TNF-alpha) , interleukin-4 (IL-4) , IL-6, and IL-12] and NO in nasal lavage fluid (NAL) during and after the exposures. We also measured 2-ethylhexanol in exhaled breath samples and NAL. On the morning after the PVC exposure, subjects reported respiratory tract symptoms significantly more often than they did after the control test (50% vs. 0%, respectively ; p = 0.029 ; n = 10) . We did not detect any changes in lung functions or levels of exhaled NO, nasal NO, or NO in NAL after PVC challenge compared with the control test. Cytokine levels increased after both exposures, with no statistically significant difference between situations. All of the exhaled breath samples collected during the PVC exposure contained 2-ethylhexanol. PVC flooring challenge can evoke respiratory tract symptoms in exposed subjects. Our results do not support the hypothesis that PVC materials themselves evoke immediate asthmatic reactions. The chamber test used is well suited to this type of exposure study.
BACKGROUND: Polyvinyl chloride (PVC) materials have been linked to asthma in several epidemio-logic studies, but the possible causal factors remain unknown. PARTICIPANTS: We challenged 10 subjects experimentally to degraded PVC products under controlled conditions. All of the subjects had previously experienced respiratory symptoms suspected to be caused by this kind of exposure in their work place. Five subjects had doctor-diagnosed asthma. METHODS: The subjects were exposed to degraded PVC material in an exposure chamber; a challenge with ceramic tile was used as the control test. We followed exhaled nitric oxide, nasal NO, lung functions, cytokines [tumor necrosis factor- alpha (TNF- alpha ), interleukin-4 (IL-4), IL-6, and IL-12] and NO in nasal lavage fluid (NAL) during and after the exposures. We also measured 2-ethyl-hexanol in exhaled breath samples and NAL. RESULTS: On the morning after the PVC exposure, subjects reported respiratory tract symptoms significantly more often than they did after the control test (50% vs. 0%, respectively; p = 0.029; n = 10). We did not detect any changes in lung functions or levels of exhaled NO, nasal NO, or NO in NAL after PVC challenge compared with the control test. Cytokine levels increased after both exposures, with no statistically significant difference between situations. All of the exhaled breath samples collected during the PVC exposure contained 2-ethylhexanol. CONCLUSIONS: PVC flooring challenge can evoke respiratory tract symptoms in exposed subjects. Our results do not support the hypothesis that PVC materials themselves evoke immediate asthmatic reactions. The chamber test used is well suited to this type of exposure study.
Polyvinyl chloride (PVC) materials have been linked to asthma in several epidemiologic studies, but the possible causal factors remain unknown. We challenged 10 subjects experimentally to degraded PVC products under controlled conditions. All of the subjects had previously experienced respiratory symptoms suspected to be caused by this kind of exposure in their work place. Five subjects had doctor-diagnosed asthma. The subjects were exposed to degraded PVC material in an exposure chamber ; a challenge with ceramic tile was used as the control test. We followed exhaled nitric oxide, nasal NO, lung functions, cytokines [tumor necrosis factor-alpha (TNF-alpha) , interleukin-4 (IL-4) , IL-6, and IL-12] and NO in nasal lavage fluid (NAL) during and after the exposures. We also measured 2-ethylhexanol in exhaled breath samples and NAL. On the morning after the PVC exposure, subjects reported respiratory tract symptoms significantly more often than they did after the control test (50% vs. 0%, respectively ; p = 0.029 ; n = 10) . We did not detect any changes in lung functions or levels of exhaled NO, nasal NO, or NO in NAL after PVC challenge compared with the control test. Cytokine levels increased after both exposures, with no statistically significant difference between situations. All of the exhaled breath samples collected during the PVC exposure contained 2-ethylhexanol. PVC flooring challenge can evoke respiratory tract symptoms in exposed subjects. Our results do not support the hypothesis that PVC materials themselves evoke immediate asthmatic reactions. The chamber test used is well suited to this type of exposure study.
Audience Academic
Author Hirvonen, Maija-Riitta
Stark, Harri
Linnainmaa, Markku
Sieppi, Anne
Tukiainen, Hannu
Tuomainen, Anneli
Seuri, Markku
AuthorAffiliation 4 Department of Environmental Health, National Public Health Institute, Kuopio, Finland
1 Technology Centre Teknia Ltd., Kuopio, Finland
3 Occupational Health Services, Atria Ltd., Nurmo, Finland
5 Department of Occupational Hygiene and Toxicology, Finnish Institute of Occupational Health, Kuopio, Finland
6 Medivire Occupational Health Centre, Kuopio, Finland
2 Department of Respiratory Medicine, Kuopio University Hospital, Kuopio, Finland
AuthorAffiliation_xml – name: 5 Department of Occupational Hygiene and Toxicology, Finnish Institute of Occupational Health, Kuopio, Finland
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– name: 4 Department of Environmental Health, National Public Health Institute, Kuopio, Finland
– name: 1 Technology Centre Teknia Ltd., Kuopio, Finland
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– name: 2 Department of Respiratory Medicine, Kuopio University Hospital, Kuopio, Finland
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  givenname: Anneli
  surname: Tuomainen
  fullname: Tuomainen, Anneli
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  givenname: Harri
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  surname: Tukiainen
  fullname: Tukiainen, Hannu
BackLink https://www.ncbi.nlm.nih.gov/pubmed/16966097$$D View this record in MEDLINE/PubMed
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The authors declare they have no competing financial interests.
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Snippet Background: Polyvinyl chloride (PVC) materials have been linked to asthma in several epidemiologic studies, but the possible causal factors remain unknown....
Polyvinyl chloride (PVC) materials have been linked to asthma in several epidemiologic studies, but the possible causal factors remain unknown. We challenged...
Polyvinyl chloride (PVC) materials have been linked to asthma in several epidemiologic studies, but the possible causal factors remain unknown. We challenged...
Experimental polyvinyl chloride (PVC) material challenge in subjects with occupational PVC exposure was discussed. It was observed that 10 subjects were...
BACKGROUND: Polyvinyl chloride (PVC) materials have been linked to asthma in several epidemio-logic studies, but the possible causal factors remain unknown....
BACKGROUND: Polyvinyl chloride (PVC) materials have been linked to asthma in several epidemiologic studies, but the possible causal factors remain unknown....
Polyvinyl chloride (PVC) materials have been linked to asthma in several epidemiologic studies, but the possible causal factors remain...
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StartPage 1409
SubjectTerms Adult
Air
Asthma
Asthma - chemically induced
Asthma - diagnosis
Asthma - epidemiology
Breath Tests
Cytokines
Cytokines - analysis
Cytokines - metabolism
Environmental health
Environmental Medicine
Environmental Monitoring
Epidemiological Monitoring
Exposure
Exposure chambers
Hexanols - toxicity
Humans
Inhalation Exposure
Lung - drug effects
Lung - pathology
Lungs
Material degradation
Middle Aged
Nasal Lavage Fluid - immunology
Nitric oxide
Nitric Oxide - analysis
Nitric Oxide - metabolism
Occupational Diseases - chemically induced
Occupational Diseases - diagnosis
Occupational Diseases - epidemiology
Occupational Exposure
Oxides
Peak expiratory flow rate
Polyvinyl chloride
Polyvinyl Chloride - toxicity
Respiratory function
Respiratory tract
Vinyl polymers
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Title Experimental PVC Material Challenge in Subjects with Occupational PVC Exposure
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