Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD

Exposure to fine particulate matter (PM2.5) is associated with worse morbidity in individuals with COPD. Inhaled PM is phagocytosed by airway macrophages (AM), and black carbon measured in AM may serve as a biomarker of air pollution exposure. As there is little data on how indoor PM exposure may influence AM black carbon content in those with respiratory disease, we investigated the association of indoor PM2.5 concentration to AM black carbon content in adults with COPD. Former smokers (>10 pack-years smoking history, quit date >1 year prior to enrollment) older than 40 years of age with moderate-severe COPD were eligible. Indoor air PM2.5 concentrations were measured over 5-7 days at baseline, 3 month, and 6 month intervals. Sputum induction was performed during clinic visits concordant with home monitoring. A total of 50 macrophages per sputum specimen were photographed and quantified using appropriate software by trained staff blinded to PM concentrations. Longitudinal analyses using generalized estimating equations were used to assess the relationship between indoor PM exposure and AM black carbon content. Participants (n=20) were older (mean (SD) age 67 (4) years), predominantly Caucasian (85%) and male (70%), with an average smoking history of 52 pack-years and mean (SD) quit date of 13 (9) years prior to enrollment. The majority of daily time was reported to be spent indoors (>23h). Mean indoor PM2.5 concentration was 12.8 (13.5)µg/m(3). The mean area of black carbon quantified in airway macrophages was 1.2 (0.7)µm(2). In multivariate cross-sectional and longitudinal analyses, each 10µg/m(3) increase in indoor PM2.5 was significantly associated with a 0.26µm(2) and 0.19µm(2) increase in airway macrophage black carbon total area, respectively (p<0.05). Higher indoor PM2.5 concentration is associated with an increase in black carbon content of AM in individuals with COPD. These data support the potential for AM black carbon content to be a useful non-invasive biomarker of exposure to indoor PM. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Belli, Andrew J [verfasserIn] Bose, Sonali Aggarwal, Neil DaSilva, Christopher Thapa, Sritika Grammer, Laura Paulin, Laura M Hansel, Nadia N

Format:	Artikel
Sprache:	Englisch

Erschienen:	2016

Rechteinformationen:	Nutzungsrecht: Copyright © 2016 Elsevier Inc. All rights reserved.

Übergeordnetes Werk:	Enthalten in: Environmental research - San Diego, Calif. : Elsevier, 1967, 150(2016), Seite 398-402
Übergeordnetes Werk:	volume:150 ; year:2016 ; pages:398-402

Links:	Volltext Link aufrufen

DOI / URN:	10.1016/j.envres.2016.06.025

Katalog-ID:	OLC1981274448

Internformat


LEADER	01000caa a2200265 4500
001	OLC1981274448
003	DE-627
005	20230515184127.0
007	tu
008	161013s2016 xx \|\|\|\|\| 00\| \|\|eng c
024	7		\|a 10.1016/j.envres.2016.06.025 \|2 doi
028	5	2	\|a PQ20161012
035			\|a (DE-627)OLC1981274448
035			\|a (DE-599)GBVOLC1981274448
035			\|a (PRQ)c924-427504d473fe51f2a018a1c6eeb9dd7b54e89177ff158a789b641a5b8fbf75670
035			\|a (KEY)0017066620160000150000000398indoorparticulatematterexposureisassociatedwithinc
040			\|a DE-627 \|b ger \|c DE-627 \|e rakwb
041			\|a eng
082	0	4	\|a 610 \|a 333.7 \|q DNB
084			\|a 44.13 \|2 bkl
100	1		\|a Belli, Andrew J \|e verfasserin \|4 aut
245	1	0	\|a Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD
264		1	\|c 2016
336			\|a Text \|b txt \|2 rdacontent
337			\|a ohne Hilfsmittel zu benutzen \|b n \|2 rdamedia
338			\|a Band \|b nc \|2 rdacarrier
520			\|a Exposure to fine particulate matter (PM2.5) is associated with worse morbidity in individuals with COPD. Inhaled PM is phagocytosed by airway macrophages (AM), and black carbon measured in AM may serve as a biomarker of air pollution exposure. As there is little data on how indoor PM exposure may influence AM black carbon content in those with respiratory disease, we investigated the association of indoor PM2.5 concentration to AM black carbon content in adults with COPD. Former smokers (>10 pack-years smoking history, quit date >1 year prior to enrollment) older than 40 years of age with moderate-severe COPD were eligible. Indoor air PM2.5 concentrations were measured over 5-7 days at baseline, 3 month, and 6 month intervals. Sputum induction was performed during clinic visits concordant with home monitoring. A total of 50 macrophages per sputum specimen were photographed and quantified using appropriate software by trained staff blinded to PM concentrations. Longitudinal analyses using generalized estimating equations were used to assess the relationship between indoor PM exposure and AM black carbon content. Participants (n=20) were older (mean (SD) age 67 (4) years), predominantly Caucasian (85%) and male (70%), with an average smoking history of 52 pack-years and mean (SD) quit date of 13 (9) years prior to enrollment. The majority of daily time was reported to be spent indoors (>23h). Mean indoor PM2.5 concentration was 12.8 (13.5)µg/m(3). The mean area of black carbon quantified in airway macrophages was 1.2 (0.7)µm(2). In multivariate cross-sectional and longitudinal analyses, each 10µg/m(3) increase in indoor PM2.5 was significantly associated with a 0.26µm(2) and 0.19µm(2) increase in airway macrophage black carbon total area, respectively (p<0.05). Higher indoor PM2.5 concentration is associated with an increase in black carbon content of AM in individuals with COPD. These data support the potential for AM black carbon content to be a useful non-invasive biomarker of exposure to indoor PM.
540			\|a Nutzungsrecht: Copyright © 2016 Elsevier Inc. All rights reserved.
700	1		\|a Bose, Sonali \|4 oth
700	1		\|a Aggarwal, Neil \|4 oth
700	1		\|a DaSilva, Christopher \|4 oth
700	1		\|a Thapa, Sritika \|4 oth
700	1		\|a Grammer, Laura \|4 oth
700	1		\|a Paulin, Laura M \|4 oth
700	1		\|a Hansel, Nadia N \|4 oth
773	0	8	\|i Enthalten in \|t Environmental research \|d San Diego, Calif. : Elsevier, 1967 \|g 150(2016), Seite 398-402 \|w (DE-627)12948864X \|w (DE-600)205699-9 \|w (DE-576)014881454 \|x 0013-9351 \|7 nnns
773	1	8	\|g volume:150 \|g year:2016 \|g pages:398-402
856	4	1	\|u http://dx.doi.org/10.1016/j.envres.2016.06.025 \|3 Volltext
856	4	2	\|u http://www.ncbi.nlm.nih.gov/pubmed/27372063
912			\|a GBV_USEFLAG_A
912			\|a SYSFLAG_A
912			\|a GBV_OLC
912			\|a SSG-OLC-UMW
912			\|a SSG-OLC-FOR
912			\|a SSG-OLC-IBL
912			\|a SSG-OLC-PHA
912			\|a SSG-OLC-DE-84
912			\|a GBV_ILN_21
912			\|a GBV_ILN_22
912			\|a GBV_ILN_70
936	b	k	\|a 44.13 \|q AVZ
951			\|a AR
952			\|d 150 \|j 2016 \|h 398-402

Indexfelder

author_variant	a j b aj ajb
matchkey_str	article:00139351:2016----::noratcltmteepsriascaewticesdlccrocnetniwyar
hierarchy_sort_str	2016
bklnumber	44.13
publishDate	2016
allfields	10.1016/j.envres.2016.06.025 doi PQ20161012 (DE-627)OLC1981274448 (DE-599)GBVOLC1981274448 (PRQ)c924-427504d473fe51f2a018a1c6eeb9dd7b54e89177ff158a789b641a5b8fbf75670 (KEY)0017066620160000150000000398indoorparticulatematterexposureisassociatedwithinc DE-627 ger DE-627 rakwb eng 610 333.7 DNB 44.13 bkl Belli, Andrew J verfasserin aut Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Exposure to fine particulate matter (PM2.5) is associated with worse morbidity in individuals with COPD. Inhaled PM is phagocytosed by airway macrophages (AM), and black carbon measured in AM may serve as a biomarker of air pollution exposure. As there is little data on how indoor PM exposure may influence AM black carbon content in those with respiratory disease, we investigated the association of indoor PM2.5 concentration to AM black carbon content in adults with COPD. Former smokers (>10 pack-years smoking history, quit date >1 year prior to enrollment) older than 40 years of age with moderate-severe COPD were eligible. Indoor air PM2.5 concentrations were measured over 5-7 days at baseline, 3 month, and 6 month intervals. Sputum induction was performed during clinic visits concordant with home monitoring. A total of 50 macrophages per sputum specimen were photographed and quantified using appropriate software by trained staff blinded to PM concentrations. Longitudinal analyses using generalized estimating equations were used to assess the relationship between indoor PM exposure and AM black carbon content. Participants (n=20) were older (mean (SD) age 67 (4) years), predominantly Caucasian (85%) and male (70%), with an average smoking history of 52 pack-years and mean (SD) quit date of 13 (9) years prior to enrollment. The majority of daily time was reported to be spent indoors (>23h). Mean indoor PM2.5 concentration was 12.8 (13.5)µg/m(3). The mean area of black carbon quantified in airway macrophages was 1.2 (0.7)µm(2). In multivariate cross-sectional and longitudinal analyses, each 10µg/m(3) increase in indoor PM2.5 was significantly associated with a 0.26µm(2) and 0.19µm(2) increase in airway macrophage black carbon total area, respectively (p<0.05). Higher indoor PM2.5 concentration is associated with an increase in black carbon content of AM in individuals with COPD. These data support the potential for AM black carbon content to be a useful non-invasive biomarker of exposure to indoor PM. Nutzungsrecht: Copyright © 2016 Elsevier Inc. All rights reserved. Bose, Sonali oth Aggarwal, Neil oth DaSilva, Christopher oth Thapa, Sritika oth Grammer, Laura oth Paulin, Laura M oth Hansel, Nadia N oth Enthalten in Environmental research San Diego, Calif. : Elsevier, 1967 150(2016), Seite 398-402 (DE-627)12948864X (DE-600)205699-9 (DE-576)014881454 0013-9351 nnns volume:150 year:2016 pages:398-402 http://dx.doi.org/10.1016/j.envres.2016.06.025 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27372063 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-UMW SSG-OLC-FOR SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_21 GBV_ILN_22 GBV_ILN_70 44.13 AVZ AR 150 2016 398-402
spelling	10.1016/j.envres.2016.06.025 doi PQ20161012 (DE-627)OLC1981274448 (DE-599)GBVOLC1981274448 (PRQ)c924-427504d473fe51f2a018a1c6eeb9dd7b54e89177ff158a789b641a5b8fbf75670 (KEY)0017066620160000150000000398indoorparticulatematterexposureisassociatedwithinc DE-627 ger DE-627 rakwb eng 610 333.7 DNB 44.13 bkl Belli, Andrew J verfasserin aut Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Exposure to fine particulate matter (PM2.5) is associated with worse morbidity in individuals with COPD. Inhaled PM is phagocytosed by airway macrophages (AM), and black carbon measured in AM may serve as a biomarker of air pollution exposure. As there is little data on how indoor PM exposure may influence AM black carbon content in those with respiratory disease, we investigated the association of indoor PM2.5 concentration to AM black carbon content in adults with COPD. Former smokers (>10 pack-years smoking history, quit date >1 year prior to enrollment) older than 40 years of age with moderate-severe COPD were eligible. Indoor air PM2.5 concentrations were measured over 5-7 days at baseline, 3 month, and 6 month intervals. Sputum induction was performed during clinic visits concordant with home monitoring. A total of 50 macrophages per sputum specimen were photographed and quantified using appropriate software by trained staff blinded to PM concentrations. Longitudinal analyses using generalized estimating equations were used to assess the relationship between indoor PM exposure and AM black carbon content. Participants (n=20) were older (mean (SD) age 67 (4) years), predominantly Caucasian (85%) and male (70%), with an average smoking history of 52 pack-years and mean (SD) quit date of 13 (9) years prior to enrollment. The majority of daily time was reported to be spent indoors (>23h). Mean indoor PM2.5 concentration was 12.8 (13.5)µg/m(3). The mean area of black carbon quantified in airway macrophages was 1.2 (0.7)µm(2). In multivariate cross-sectional and longitudinal analyses, each 10µg/m(3) increase in indoor PM2.5 was significantly associated with a 0.26µm(2) and 0.19µm(2) increase in airway macrophage black carbon total area, respectively (p<0.05). Higher indoor PM2.5 concentration is associated with an increase in black carbon content of AM in individuals with COPD. These data support the potential for AM black carbon content to be a useful non-invasive biomarker of exposure to indoor PM. Nutzungsrecht: Copyright © 2016 Elsevier Inc. All rights reserved. Bose, Sonali oth Aggarwal, Neil oth DaSilva, Christopher oth Thapa, Sritika oth Grammer, Laura oth Paulin, Laura M oth Hansel, Nadia N oth Enthalten in Environmental research San Diego, Calif. : Elsevier, 1967 150(2016), Seite 398-402 (DE-627)12948864X (DE-600)205699-9 (DE-576)014881454 0013-9351 nnns volume:150 year:2016 pages:398-402 http://dx.doi.org/10.1016/j.envres.2016.06.025 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27372063 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-UMW SSG-OLC-FOR SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_21 GBV_ILN_22 GBV_ILN_70 44.13 AVZ AR 150 2016 398-402
allfields_unstemmed	10.1016/j.envres.2016.06.025 doi PQ20161012 (DE-627)OLC1981274448 (DE-599)GBVOLC1981274448 (PRQ)c924-427504d473fe51f2a018a1c6eeb9dd7b54e89177ff158a789b641a5b8fbf75670 (KEY)0017066620160000150000000398indoorparticulatematterexposureisassociatedwithinc DE-627 ger DE-627 rakwb eng 610 333.7 DNB 44.13 bkl Belli, Andrew J verfasserin aut Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Exposure to fine particulate matter (PM2.5) is associated with worse morbidity in individuals with COPD. Inhaled PM is phagocytosed by airway macrophages (AM), and black carbon measured in AM may serve as a biomarker of air pollution exposure. As there is little data on how indoor PM exposure may influence AM black carbon content in those with respiratory disease, we investigated the association of indoor PM2.5 concentration to AM black carbon content in adults with COPD. Former smokers (>10 pack-years smoking history, quit date >1 year prior to enrollment) older than 40 years of age with moderate-severe COPD were eligible. Indoor air PM2.5 concentrations were measured over 5-7 days at baseline, 3 month, and 6 month intervals. Sputum induction was performed during clinic visits concordant with home monitoring. A total of 50 macrophages per sputum specimen were photographed and quantified using appropriate software by trained staff blinded to PM concentrations. Longitudinal analyses using generalized estimating equations were used to assess the relationship between indoor PM exposure and AM black carbon content. Participants (n=20) were older (mean (SD) age 67 (4) years), predominantly Caucasian (85%) and male (70%), with an average smoking history of 52 pack-years and mean (SD) quit date of 13 (9) years prior to enrollment. The majority of daily time was reported to be spent indoors (>23h). Mean indoor PM2.5 concentration was 12.8 (13.5)µg/m(3). The mean area of black carbon quantified in airway macrophages was 1.2 (0.7)µm(2). In multivariate cross-sectional and longitudinal analyses, each 10µg/m(3) increase in indoor PM2.5 was significantly associated with a 0.26µm(2) and 0.19µm(2) increase in airway macrophage black carbon total area, respectively (p<0.05). Higher indoor PM2.5 concentration is associated with an increase in black carbon content of AM in individuals with COPD. These data support the potential for AM black carbon content to be a useful non-invasive biomarker of exposure to indoor PM. Nutzungsrecht: Copyright © 2016 Elsevier Inc. All rights reserved. Bose, Sonali oth Aggarwal, Neil oth DaSilva, Christopher oth Thapa, Sritika oth Grammer, Laura oth Paulin, Laura M oth Hansel, Nadia N oth Enthalten in Environmental research San Diego, Calif. : Elsevier, 1967 150(2016), Seite 398-402 (DE-627)12948864X (DE-600)205699-9 (DE-576)014881454 0013-9351 nnns volume:150 year:2016 pages:398-402 http://dx.doi.org/10.1016/j.envres.2016.06.025 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27372063 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-UMW SSG-OLC-FOR SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_21 GBV_ILN_22 GBV_ILN_70 44.13 AVZ AR 150 2016 398-402
allfieldsGer	10.1016/j.envres.2016.06.025 doi PQ20161012 (DE-627)OLC1981274448 (DE-599)GBVOLC1981274448 (PRQ)c924-427504d473fe51f2a018a1c6eeb9dd7b54e89177ff158a789b641a5b8fbf75670 (KEY)0017066620160000150000000398indoorparticulatematterexposureisassociatedwithinc DE-627 ger DE-627 rakwb eng 610 333.7 DNB 44.13 bkl Belli, Andrew J verfasserin aut Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Exposure to fine particulate matter (PM2.5) is associated with worse morbidity in individuals with COPD. Inhaled PM is phagocytosed by airway macrophages (AM), and black carbon measured in AM may serve as a biomarker of air pollution exposure. As there is little data on how indoor PM exposure may influence AM black carbon content in those with respiratory disease, we investigated the association of indoor PM2.5 concentration to AM black carbon content in adults with COPD. Former smokers (>10 pack-years smoking history, quit date >1 year prior to enrollment) older than 40 years of age with moderate-severe COPD were eligible. Indoor air PM2.5 concentrations were measured over 5-7 days at baseline, 3 month, and 6 month intervals. Sputum induction was performed during clinic visits concordant with home monitoring. A total of 50 macrophages per sputum specimen were photographed and quantified using appropriate software by trained staff blinded to PM concentrations. Longitudinal analyses using generalized estimating equations were used to assess the relationship between indoor PM exposure and AM black carbon content. Participants (n=20) were older (mean (SD) age 67 (4) years), predominantly Caucasian (85%) and male (70%), with an average smoking history of 52 pack-years and mean (SD) quit date of 13 (9) years prior to enrollment. The majority of daily time was reported to be spent indoors (>23h). Mean indoor PM2.5 concentration was 12.8 (13.5)µg/m(3). The mean area of black carbon quantified in airway macrophages was 1.2 (0.7)µm(2). In multivariate cross-sectional and longitudinal analyses, each 10µg/m(3) increase in indoor PM2.5 was significantly associated with a 0.26µm(2) and 0.19µm(2) increase in airway macrophage black carbon total area, respectively (p<0.05). Higher indoor PM2.5 concentration is associated with an increase in black carbon content of AM in individuals with COPD. These data support the potential for AM black carbon content to be a useful non-invasive biomarker of exposure to indoor PM. Nutzungsrecht: Copyright © 2016 Elsevier Inc. All rights reserved. Bose, Sonali oth Aggarwal, Neil oth DaSilva, Christopher oth Thapa, Sritika oth Grammer, Laura oth Paulin, Laura M oth Hansel, Nadia N oth Enthalten in Environmental research San Diego, Calif. : Elsevier, 1967 150(2016), Seite 398-402 (DE-627)12948864X (DE-600)205699-9 (DE-576)014881454 0013-9351 nnns volume:150 year:2016 pages:398-402 http://dx.doi.org/10.1016/j.envres.2016.06.025 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27372063 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-UMW SSG-OLC-FOR SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_21 GBV_ILN_22 GBV_ILN_70 44.13 AVZ AR 150 2016 398-402
allfieldsSound	10.1016/j.envres.2016.06.025 doi PQ20161012 (DE-627)OLC1981274448 (DE-599)GBVOLC1981274448 (PRQ)c924-427504d473fe51f2a018a1c6eeb9dd7b54e89177ff158a789b641a5b8fbf75670 (KEY)0017066620160000150000000398indoorparticulatematterexposureisassociatedwithinc DE-627 ger DE-627 rakwb eng 610 333.7 DNB 44.13 bkl Belli, Andrew J verfasserin aut Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Exposure to fine particulate matter (PM2.5) is associated with worse morbidity in individuals with COPD. Inhaled PM is phagocytosed by airway macrophages (AM), and black carbon measured in AM may serve as a biomarker of air pollution exposure. As there is little data on how indoor PM exposure may influence AM black carbon content in those with respiratory disease, we investigated the association of indoor PM2.5 concentration to AM black carbon content in adults with COPD. Former smokers (>10 pack-years smoking history, quit date >1 year prior to enrollment) older than 40 years of age with moderate-severe COPD were eligible. Indoor air PM2.5 concentrations were measured over 5-7 days at baseline, 3 month, and 6 month intervals. Sputum induction was performed during clinic visits concordant with home monitoring. A total of 50 macrophages per sputum specimen were photographed and quantified using appropriate software by trained staff blinded to PM concentrations. Longitudinal analyses using generalized estimating equations were used to assess the relationship between indoor PM exposure and AM black carbon content. Participants (n=20) were older (mean (SD) age 67 (4) years), predominantly Caucasian (85%) and male (70%), with an average smoking history of 52 pack-years and mean (SD) quit date of 13 (9) years prior to enrollment. The majority of daily time was reported to be spent indoors (>23h). Mean indoor PM2.5 concentration was 12.8 (13.5)µg/m(3). The mean area of black carbon quantified in airway macrophages was 1.2 (0.7)µm(2). In multivariate cross-sectional and longitudinal analyses, each 10µg/m(3) increase in indoor PM2.5 was significantly associated with a 0.26µm(2) and 0.19µm(2) increase in airway macrophage black carbon total area, respectively (p<0.05). Higher indoor PM2.5 concentration is associated with an increase in black carbon content of AM in individuals with COPD. These data support the potential for AM black carbon content to be a useful non-invasive biomarker of exposure to indoor PM. Nutzungsrecht: Copyright © 2016 Elsevier Inc. All rights reserved. Bose, Sonali oth Aggarwal, Neil oth DaSilva, Christopher oth Thapa, Sritika oth Grammer, Laura oth Paulin, Laura M oth Hansel, Nadia N oth Enthalten in Environmental research San Diego, Calif. : Elsevier, 1967 150(2016), Seite 398-402 (DE-627)12948864X (DE-600)205699-9 (DE-576)014881454 0013-9351 nnns volume:150 year:2016 pages:398-402 http://dx.doi.org/10.1016/j.envres.2016.06.025 Volltext http://www.ncbi.nlm.nih.gov/pubmed/27372063 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-UMW SSG-OLC-FOR SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_21 GBV_ILN_22 GBV_ILN_70 44.13 AVZ AR 150 2016 398-402
language	English
source	Enthalten in Environmental research 150(2016), Seite 398-402 volume:150 year:2016 pages:398-402
sourceStr	Enthalten in Environmental research 150(2016), Seite 398-402 volume:150 year:2016 pages:398-402
format_phy_str_mv	Article
institution	findex.gbv.de
dewey-raw	610
isfreeaccess_bool	false
container_title	Environmental research
authorswithroles_txt_mv	Belli, Andrew J @@aut@@ Bose, Sonali @@oth@@ Aggarwal, Neil @@oth@@ DaSilva, Christopher @@oth@@ Thapa, Sritika @@oth@@ Grammer, Laura @@oth@@ Paulin, Laura M @@oth@@ Hansel, Nadia N @@oth@@
publishDateDaySort_date	2016-01-01T00:00:00Z
hierarchy_top_id	12948864X
dewey-sort	3610
id	OLC1981274448
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a2200265 4500</leader><controlfield tag="001">OLC1981274448</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230515184127.0</controlfield><controlfield tag="007">tu</controlfield><controlfield tag="008">161013s2016 xx \|\|\|\|\| 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.envres.2016.06.025</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">PQ20161012</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)OLC1981274448</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)GBVOLC1981274448</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(PRQ)c924-427504d473fe51f2a018a1c6eeb9dd7b54e89177ff158a789b641a5b8fbf75670</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(KEY)0017066620160000150000000398indoorparticulatematterexposureisassociatedwithinc</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="a">333.7</subfield><subfield code="q">DNB</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.13</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Belli, Andrew J</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2016</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">ohne Hilfsmittel zu benutzen</subfield><subfield code="b">n</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Band</subfield><subfield code="b">nc</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Exposure to fine particulate matter (PM2.5) is associated with worse morbidity in individuals with COPD. Inhaled PM is phagocytosed by airway macrophages (AM), and black carbon measured in AM may serve as a biomarker of air pollution exposure. As there is little data on how indoor PM exposure may influence AM black carbon content in those with respiratory disease, we investigated the association of indoor PM2.5 concentration to AM black carbon content in adults with COPD. Former smokers (>10 pack-years smoking history, quit date >1 year prior to enrollment) older than 40 years of age with moderate-severe COPD were eligible. Indoor air PM2.5 concentrations were measured over 5-7 days at baseline, 3 month, and 6 month intervals. Sputum induction was performed during clinic visits concordant with home monitoring. A total of 50 macrophages per sputum specimen were photographed and quantified using appropriate software by trained staff blinded to PM concentrations. Longitudinal analyses using generalized estimating equations were used to assess the relationship between indoor PM exposure and AM black carbon content. Participants (n=20) were older (mean (SD) age 67 (4) years), predominantly Caucasian (85%) and male (70%), with an average smoking history of 52 pack-years and mean (SD) quit date of 13 (9) years prior to enrollment. The majority of daily time was reported to be spent indoors (>23h). Mean indoor PM2.5 concentration was 12.8 (13.5)µg/m(3). The mean area of black carbon quantified in airway macrophages was 1.2 (0.7)µm(2). In multivariate cross-sectional and longitudinal analyses, each 10µg/m(3) increase in indoor PM2.5 was significantly associated with a 0.26µm(2) and 0.19µm(2) increase in airway macrophage black carbon total area, respectively (p<0.05). Higher indoor PM2.5 concentration is associated with an increase in black carbon content of AM in individuals with COPD. These data support the potential for AM black carbon content to be a useful non-invasive biomarker of exposure to indoor PM.</subfield></datafield><datafield tag="540" ind1=" " ind2=" "><subfield code="a">Nutzungsrecht: Copyright © 2016 Elsevier Inc. All rights reserved.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bose, Sonali</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Aggarwal, Neil</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">DaSilva, Christopher</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Thapa, Sritika</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Grammer, Laura</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Paulin, Laura M</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hansel, Nadia N</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Environmental research</subfield><subfield code="d">San Diego, Calif. : Elsevier, 1967</subfield><subfield code="g">150(2016), Seite 398-402</subfield><subfield code="w">(DE-627)12948864X</subfield><subfield code="w">(DE-600)205699-9</subfield><subfield code="w">(DE-576)014881454</subfield><subfield code="x">0013-9351</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:150</subfield><subfield code="g">year:2016</subfield><subfield code="g">pages:398-402</subfield></datafield><datafield tag="856" ind1="4" ind2="1"><subfield code="u">http://dx.doi.org/10.1016/j.envres.2016.06.025</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">http://www.ncbi.nlm.nih.gov/pubmed/27372063</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_OLC</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-UMW</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-FOR</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-IBL</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-DE-84</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_21</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.13</subfield><subfield code="q">AVZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">150</subfield><subfield code="j">2016</subfield><subfield code="h">398-402</subfield></datafield></record></collection>
author	Belli, Andrew J
spellingShingle	Belli, Andrew J ddc 610 bkl 44.13 Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD
authorStr	Belli, Andrew J
ppnlink_with_tag_str_mv	@@773@@(DE-627)12948864X
format	Article
dewey-ones	610 - Medicine & health 333 - Economics of land & energy
delete_txt_mv	keep
author_role	aut
collection	OLC
remote_str	false
illustrated	Not Illustrated
issn	0013-9351
topic_title	610 333.7 DNB 44.13 bkl Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD
topic	ddc 610 bkl 44.13
topic_unstemmed	ddc 610 bkl 44.13
topic_browse	ddc 610 bkl 44.13
format_facet	Aufsätze Gedruckte Aufsätze
format_main_str_mv	Text Zeitschrift/Artikel
carriertype_str_mv	nc
author2_variant	s b sb n a na c d cd s t st l g lg l m p lm lmp n n h nn nnh
hierarchy_parent_title	Environmental research
hierarchy_parent_id	12948864X
dewey-tens	610 - Medicine & health 330 - Economics
hierarchy_top_title	Environmental research
isfreeaccess_txt	false
familylinks_str_mv	(DE-627)12948864X (DE-600)205699-9 (DE-576)014881454
title	Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD
ctrlnum	(DE-627)OLC1981274448 (DE-599)GBVOLC1981274448 (PRQ)c924-427504d473fe51f2a018a1c6eeb9dd7b54e89177ff158a789b641a5b8fbf75670 (KEY)0017066620160000150000000398indoorparticulatematterexposureisassociatedwithinc
title_full	Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD
author_sort	Belli, Andrew J
journal	Environmental research
journalStr	Environmental research
lang_code	eng
isOA_bool	false
dewey-hundreds	600 - Technology 300 - Social sciences
recordtype	marc
publishDateSort	2016
contenttype_str_mv	txt
container_start_page	398
author_browse	Belli, Andrew J
container_volume	150
class	610 333.7 DNB 44.13 bkl
format_se	Aufsätze
author-letter	Belli, Andrew J
doi_str_mv	10.1016/j.envres.2016.06.025
dewey-full	610 333.7
title_sort	indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with copd
title_auth	Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD
abstract	Exposure to fine particulate matter (PM2.5) is associated with worse morbidity in individuals with COPD. Inhaled PM is phagocytosed by airway macrophages (AM), and black carbon measured in AM may serve as a biomarker of air pollution exposure. As there is little data on how indoor PM exposure may influence AM black carbon content in those with respiratory disease, we investigated the association of indoor PM2.5 concentration to AM black carbon content in adults with COPD. Former smokers (>10 pack-years smoking history, quit date >1 year prior to enrollment) older than 40 years of age with moderate-severe COPD were eligible. Indoor air PM2.5 concentrations were measured over 5-7 days at baseline, 3 month, and 6 month intervals. Sputum induction was performed during clinic visits concordant with home monitoring. A total of 50 macrophages per sputum specimen were photographed and quantified using appropriate software by trained staff blinded to PM concentrations. Longitudinal analyses using generalized estimating equations were used to assess the relationship between indoor PM exposure and AM black carbon content. Participants (n=20) were older (mean (SD) age 67 (4) years), predominantly Caucasian (85%) and male (70%), with an average smoking history of 52 pack-years and mean (SD) quit date of 13 (9) years prior to enrollment. The majority of daily time was reported to be spent indoors (>23h). Mean indoor PM2.5 concentration was 12.8 (13.5)µg/m(3). The mean area of black carbon quantified in airway macrophages was 1.2 (0.7)µm(2). In multivariate cross-sectional and longitudinal analyses, each 10µg/m(3) increase in indoor PM2.5 was significantly associated with a 0.26µm(2) and 0.19µm(2) increase in airway macrophage black carbon total area, respectively (p<0.05). Higher indoor PM2.5 concentration is associated with an increase in black carbon content of AM in individuals with COPD. These data support the potential for AM black carbon content to be a useful non-invasive biomarker of exposure to indoor PM.
abstractGer	Exposure to fine particulate matter (PM2.5) is associated with worse morbidity in individuals with COPD. Inhaled PM is phagocytosed by airway macrophages (AM), and black carbon measured in AM may serve as a biomarker of air pollution exposure. As there is little data on how indoor PM exposure may influence AM black carbon content in those with respiratory disease, we investigated the association of indoor PM2.5 concentration to AM black carbon content in adults with COPD. Former smokers (>10 pack-years smoking history, quit date >1 year prior to enrollment) older than 40 years of age with moderate-severe COPD were eligible. Indoor air PM2.5 concentrations were measured over 5-7 days at baseline, 3 month, and 6 month intervals. Sputum induction was performed during clinic visits concordant with home monitoring. A total of 50 macrophages per sputum specimen were photographed and quantified using appropriate software by trained staff blinded to PM concentrations. Longitudinal analyses using generalized estimating equations were used to assess the relationship between indoor PM exposure and AM black carbon content. Participants (n=20) were older (mean (SD) age 67 (4) years), predominantly Caucasian (85%) and male (70%), with an average smoking history of 52 pack-years and mean (SD) quit date of 13 (9) years prior to enrollment. The majority of daily time was reported to be spent indoors (>23h). Mean indoor PM2.5 concentration was 12.8 (13.5)µg/m(3). The mean area of black carbon quantified in airway macrophages was 1.2 (0.7)µm(2). In multivariate cross-sectional and longitudinal analyses, each 10µg/m(3) increase in indoor PM2.5 was significantly associated with a 0.26µm(2) and 0.19µm(2) increase in airway macrophage black carbon total area, respectively (p<0.05). Higher indoor PM2.5 concentration is associated with an increase in black carbon content of AM in individuals with COPD. These data support the potential for AM black carbon content to be a useful non-invasive biomarker of exposure to indoor PM.
abstract_unstemmed	Exposure to fine particulate matter (PM2.5) is associated with worse morbidity in individuals with COPD. Inhaled PM is phagocytosed by airway macrophages (AM), and black carbon measured in AM may serve as a biomarker of air pollution exposure. As there is little data on how indoor PM exposure may influence AM black carbon content in those with respiratory disease, we investigated the association of indoor PM2.5 concentration to AM black carbon content in adults with COPD. Former smokers (>10 pack-years smoking history, quit date >1 year prior to enrollment) older than 40 years of age with moderate-severe COPD were eligible. Indoor air PM2.5 concentrations were measured over 5-7 days at baseline, 3 month, and 6 month intervals. Sputum induction was performed during clinic visits concordant with home monitoring. A total of 50 macrophages per sputum specimen were photographed and quantified using appropriate software by trained staff blinded to PM concentrations. Longitudinal analyses using generalized estimating equations were used to assess the relationship between indoor PM exposure and AM black carbon content. Participants (n=20) were older (mean (SD) age 67 (4) years), predominantly Caucasian (85%) and male (70%), with an average smoking history of 52 pack-years and mean (SD) quit date of 13 (9) years prior to enrollment. The majority of daily time was reported to be spent indoors (>23h). Mean indoor PM2.5 concentration was 12.8 (13.5)µg/m(3). The mean area of black carbon quantified in airway macrophages was 1.2 (0.7)µm(2). In multivariate cross-sectional and longitudinal analyses, each 10µg/m(3) increase in indoor PM2.5 was significantly associated with a 0.26µm(2) and 0.19µm(2) increase in airway macrophage black carbon total area, respectively (p<0.05). Higher indoor PM2.5 concentration is associated with an increase in black carbon content of AM in individuals with COPD. These data support the potential for AM black carbon content to be a useful non-invasive biomarker of exposure to indoor PM.
collection_details	GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-UMW SSG-OLC-FOR SSG-OLC-IBL SSG-OLC-PHA SSG-OLC-DE-84 GBV_ILN_21 GBV_ILN_22 GBV_ILN_70
title_short	Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD
url	http://dx.doi.org/10.1016/j.envres.2016.06.025 http://www.ncbi.nlm.nih.gov/pubmed/27372063
remote_bool	false
author2	Bose, Sonali Aggarwal, Neil DaSilva, Christopher Thapa, Sritika Grammer, Laura Paulin, Laura M Hansel, Nadia N
author2Str	Bose, Sonali Aggarwal, Neil DaSilva, Christopher Thapa, Sritika Grammer, Laura Paulin, Laura M Hansel, Nadia N
ppnlink	12948864X
mediatype_str_mv	n
isOA_txt	false
hochschulschrift_bool	false
author2_role	oth oth oth oth oth oth oth
doi_str	10.1016/j.envres.2016.06.025
up_date	2024-07-04T04:36:57.191Z
_version_	1803621831479918592
fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a2200265 4500</leader><controlfield tag="001">OLC1981274448</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230515184127.0</controlfield><controlfield tag="007">tu</controlfield><controlfield tag="008">161013s2016 xx \|\|\|\|\| 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.envres.2016.06.025</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">PQ20161012</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)OLC1981274448</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)GBVOLC1981274448</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(PRQ)c924-427504d473fe51f2a018a1c6eeb9dd7b54e89177ff158a789b641a5b8fbf75670</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(KEY)0017066620160000150000000398indoorparticulatematterexposureisassociatedwithinc</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="a">333.7</subfield><subfield code="q">DNB</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.13</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Belli, Andrew J</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2016</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">ohne Hilfsmittel zu benutzen</subfield><subfield code="b">n</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Band</subfield><subfield code="b">nc</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Exposure to fine particulate matter (PM2.5) is associated with worse morbidity in individuals with COPD. Inhaled PM is phagocytosed by airway macrophages (AM), and black carbon measured in AM may serve as a biomarker of air pollution exposure. As there is little data on how indoor PM exposure may influence AM black carbon content in those with respiratory disease, we investigated the association of indoor PM2.5 concentration to AM black carbon content in adults with COPD. Former smokers (>10 pack-years smoking history, quit date >1 year prior to enrollment) older than 40 years of age with moderate-severe COPD were eligible. Indoor air PM2.5 concentrations were measured over 5-7 days at baseline, 3 month, and 6 month intervals. Sputum induction was performed during clinic visits concordant with home monitoring. A total of 50 macrophages per sputum specimen were photographed and quantified using appropriate software by trained staff blinded to PM concentrations. Longitudinal analyses using generalized estimating equations were used to assess the relationship between indoor PM exposure and AM black carbon content. Participants (n=20) were older (mean (SD) age 67 (4) years), predominantly Caucasian (85%) and male (70%), with an average smoking history of 52 pack-years and mean (SD) quit date of 13 (9) years prior to enrollment. The majority of daily time was reported to be spent indoors (>23h). Mean indoor PM2.5 concentration was 12.8 (13.5)µg/m(3). The mean area of black carbon quantified in airway macrophages was 1.2 (0.7)µm(2). In multivariate cross-sectional and longitudinal analyses, each 10µg/m(3) increase in indoor PM2.5 was significantly associated with a 0.26µm(2) and 0.19µm(2) increase in airway macrophage black carbon total area, respectively (p<0.05). Higher indoor PM2.5 concentration is associated with an increase in black carbon content of AM in individuals with COPD. These data support the potential for AM black carbon content to be a useful non-invasive biomarker of exposure to indoor PM.</subfield></datafield><datafield tag="540" ind1=" " ind2=" "><subfield code="a">Nutzungsrecht: Copyright © 2016 Elsevier Inc. All rights reserved.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bose, Sonali</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Aggarwal, Neil</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">DaSilva, Christopher</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Thapa, Sritika</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Grammer, Laura</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Paulin, Laura M</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hansel, Nadia N</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Environmental research</subfield><subfield code="d">San Diego, Calif. : Elsevier, 1967</subfield><subfield code="g">150(2016), Seite 398-402</subfield><subfield code="w">(DE-627)12948864X</subfield><subfield code="w">(DE-600)205699-9</subfield><subfield code="w">(DE-576)014881454</subfield><subfield code="x">0013-9351</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:150</subfield><subfield code="g">year:2016</subfield><subfield code="g">pages:398-402</subfield></datafield><datafield tag="856" ind1="4" ind2="1"><subfield code="u">http://dx.doi.org/10.1016/j.envres.2016.06.025</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="u">http://www.ncbi.nlm.nih.gov/pubmed/27372063</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_OLC</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-UMW</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-FOR</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-IBL</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-DE-84</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_21</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_22</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.13</subfield><subfield code="q">AVZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">150</subfield><subfield code="j">2016</subfield><subfield code="h">398-402</subfield></datafield></record></collection>
score	7.4012003

Nicht das Richtige dabei?

Schreiben Sie uns!

Indoor particulate matter exposure is associated with increased black carbon content in airway macrophages of former smokers with COPD

Nicht das Richtige dabei?

Zugang & Verfügbarkeit

Vorhandene Bände

Nicht das Richtige dabei?