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Air Pollution, Change in Retinal Vas...

Young, Michael T.

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Air Pollution, Change in Retinal Vascular Caliber, and Cellular Adhesion in the Multi-Ethnic Study of Atherosclerosis (MESA).

Record Type:	Electronic resources : Monograph/item
Title/Author:	Air Pollution, Change in Retinal Vascular Caliber, and Cellular Adhesion in the Multi-Ethnic Study of Atherosclerosis (MESA)./
Author:	Young, Michael T.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2018,
Description:	137 p.
Notes:	Source: Dissertations Abstracts International, Volume: 79-11, Section: B.
Contained By:	Dissertations Abstracts International79-11B.
Subject:	Environmental Health. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10750970
ISBN:	9780355850628

Air Pollution, Change in Retinal Vascular Caliber, and Cellular Adhesion in the Multi-Ethnic Study of Atherosclerosis (MESA).
Young, Michael T.

Air Pollution, Change in Retinal Vascular Caliber, and Cellular Adhesion in the Multi-Ethnic Study of Atherosclerosis (MESA). - Ann Arbor : ProQuest Dissertations & Theses, 2018 - 137 p.

Source: Dissertations Abstracts International, Volume: 79-11, Section: B.

Thesis (Ph.D.)--University of Washington, 2018.

This item is not available from ProQuest Dissertations & Theses.

Research strongly suggests an association between acute air pollution exposure and cardiovascular events, and there is growing evidence that long-term exposure to air pollution may be associated with cardiovascular disease development. Further research on possible biologic pathways relating air pollution and cardiovascular pathology is needed to support a causal relationship and provide evidence for stricter federal air quality standards. Vascular changes and cellular adhesion processes are important pathways in cardiovascular disease, and preliminary evidence suggests they may be related to air pollution exposure. We investigated whether air pollution is associated with several markers of vascular change and cellular adhesion. Further, we estimated whether these associations might mediate the relationship between air pollution exposure and coronary artery calcium, a clinical measure of atherosclerotic plaque. All analyses were performed in a longitudinal cohort study, the Multi-ethnic Study of Atherosclerosis (MESA), which was designed to measure subclinical cardiovascular disease as well as cardiovascular events. We performed a longitudinal analysis of exposure to air pollutants PM2.5 and NOX with respect to change in vascular diameters measured in the retina (centralized retinal arteriolar equivalents or CRAE). We then performed analyses of the cross-sectional relationship between both long-term and acute exposure to air pollutants (PM2.5 and NOX) with fifteen different cellular adhesion proteins measured in blood or serum. Finally, we tested whether retinal vascular diameter and several adhesion proteins statistically mediate the relationship between air pollution and coronary artery calcium. Our results indicated that greater PM2.5 exposure was associated with more narrowing of CRAE. Comparing individuals differing by 5 µg/m 3 of PM2.5 exposure averaged over a 7.8 year follow-up period, adjusted change in CRAE differed on average by -1.41 µm (95% CI: -3.40, 0.58, p=0.17). This estimate of -1.41 corresponds to approximately half the average change in individual CRAE values over the 7.8 years of follow-up in MESA, although this estimate of 1.41 was for a 5 µg/m3 of PM2.5 whereas the interquartile range of exposure for this follow-up period in MESA was 1.9 µg/m3. We also found strong associations between greater air pollution exposure and higher levels of three specific adhesion proteins. We found that year-prior exposure to PM2.5 and NOX were both positively associated with the chemokine CCL21, that both pollutants had strong positive associations with the adhesion protein ICAM-1, and that PM2.5 had a strong association with the inhibitor of matrix metalloproteinase TIMP-2. For a 5 µg/m3 interval of PM2.5, the strengths of these associations were all roughly equivalent to 20% of the interquartile variability observed in MESA for each respective adhesion protein. The strengths of the associations between acute PM2.5 exposure and adhesion proteins were generally weak or null. Finally, we found evidence suggesting that CCL21 and TIMP-2 may statistically mediate the relationship between PM2.5 and coronary artery calcium, but due to the possibility of unknown confounders between the adhesion proteins and coronary artery calcium, we cannot necessarily conclude that these proteins are causal mediators. Overall, our results are consistent with the hypothesis that air pollution exposure may cause vascular and adhesion changes, but further research is needed to verify these results and determine whether these specific pathways could explain the relationship between air pollution and cardiovascular disease.

ISBN: 9780355850628Subjects--Topical Terms:

578282
Environmental Health.
Subjects--Index Terms:

Adhesion

Air Pollution, Change in Retinal Vascular Caliber, and Cellular Adhesion in the Multi-Ethnic Study of Atherosclerosis (MESA).
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520 $a Research strongly suggests an association between acute air pollution exposure and cardiovascular events, and there is growing evidence that long-term exposure to air pollution may be associated with cardiovascular disease development. Further research on possible biologic pathways relating air pollution and cardiovascular pathology is needed to support a causal relationship and provide evidence for stricter federal air quality standards. Vascular changes and cellular adhesion processes are important pathways in cardiovascular disease, and preliminary evidence suggests they may be related to air pollution exposure. We investigated whether air pollution is associated with several markers of vascular change and cellular adhesion. Further, we estimated whether these associations might mediate the relationship between air pollution exposure and coronary artery calcium, a clinical measure of atherosclerotic plaque. All analyses were performed in a longitudinal cohort study, the Multi-ethnic Study of Atherosclerosis (MESA), which was designed to measure subclinical cardiovascular disease as well as cardiovascular events. We performed a longitudinal analysis of exposure to air pollutants PM2.5 and NOX with respect to change in vascular diameters measured in the retina (centralized retinal arteriolar equivalents or CRAE). We then performed analyses of the cross-sectional relationship between both long-term and acute exposure to air pollutants (PM2.5 and NOX) with fifteen different cellular adhesion proteins measured in blood or serum. Finally, we tested whether retinal vascular diameter and several adhesion proteins statistically mediate the relationship between air pollution and coronary artery calcium. Our results indicated that greater PM2.5 exposure was associated with more narrowing of CRAE. Comparing individuals differing by 5 µg/m 3 of PM2.5 exposure averaged over a 7.8 year follow-up period, adjusted change in CRAE differed on average by -1.41 µm (95% CI: -3.40, 0.58, p=0.17). This estimate of -1.41 corresponds to approximately half the average change in individual CRAE values over the 7.8 years of follow-up in MESA, although this estimate of 1.41 was for a 5 µg/m3 of PM2.5 whereas the interquartile range of exposure for this follow-up period in MESA was 1.9 µg/m3. We also found strong associations between greater air pollution exposure and higher levels of three specific adhesion proteins. We found that year-prior exposure to PM2.5 and NOX were both positively associated with the chemokine CCL21, that both pollutants had strong positive associations with the adhesion protein ICAM-1, and that PM2.5 had a strong association with the inhibitor of matrix metalloproteinase TIMP-2. For a 5 µg/m3 interval of PM2.5, the strengths of these associations were all roughly equivalent to 20% of the interquartile variability observed in MESA for each respective adhesion protein. The strengths of the associations between acute PM2.5 exposure and adhesion proteins were generally weak or null. Finally, we found evidence suggesting that CCL21 and TIMP-2 may statistically mediate the relationship between PM2.5 and coronary artery calcium, but due to the possibility of unknown confounders between the adhesion proteins and coronary artery calcium, we cannot necessarily conclude that these proteins are causal mediators. Overall, our results are consistent with the hypothesis that air pollution exposure may cause vascular and adhesion changes, but further research is needed to verify these results and determine whether these specific pathways could explain the relationship between air pollution and cardiovascular disease.
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