東華大學圖書館 |

Persistent Environmental Pollutants and Risk of Cardiovascular Disease.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Persistent Environmental Pollutants and Risk of Cardiovascular Disease./
作者:	Schillemans, Tessa.
面頁冊數:	1 online resource (74 pages)
附註:	Source: Dissertations Abstracts International, Volume: 84-11, Section: B.
Contained By:	Dissertations Abstracts International84-11B.
標題:	Cardiovascular disease. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=30450276click for full text (PQDT)
ISBN:	9798379480653

Persistent Environmental Pollutants and Risk of Cardiovascular Disease.
Schillemans, Tessa.

Persistent Environmental Pollutants and Risk of Cardiovascular Disease. - 1 online resource (74 pages)

Source: Dissertations Abstracts International, Volume: 84-11, Section: B.

Thesis (Ph.D.)--Karolinska Institutet (Sweden), 2023.

Includes bibliographical references

Persistent chemicals emitted in the environment can have a considerable impact onecosystems and human health, now and in the future. One notorious group of persistentorganic pollutants (POPs) is the per- and polyfluoroalkyl substances (PFAS). Since theirproduction in 1940s for household and consumer products, they have accumulated in theenvironment and in humans via consumption of contaminated drinking water and food.They are hypothesized to induce metabolic disturbances, due to shared chemicalsimilarities with fatty acids. Consequently, PFAS may have high societal and economicimpact by increasing risk of obesity, type 2 diabetes (T2D) and cardiovascular disease(CVD). However, reports on these associations are scarce, and the underlying molecularpathways are still unclear. Therefore, in this PhD project, we aimed to i) investigateassociations between PFAS and risk of several cardiometabolic diseases and ii) explorepotential underlying pathways.In Paper I, we investigated cross-sectional associations between PFAS mixtures and bodymass index (BMI) in European teenagers using meta-regression. Results showed atendency for inverse associations between PFAS and BMI and indicated a potential fordiverging contributions between PFAS compounds. In Paper II, using a nested casecontrol study on T2D including metabolomics data in Swedish adults, we found that PFAScorrelated positively with glycerophospholipids and diacylglycerols. But whilstglycerophospholipids associated with lower T2D risk, diacylglycerols associated withhigher T2D risk. This indicates a potential for diverging effects on disease risk. In Paper III,we investigated whether genetic polymorphisms in peroxisome proliferator-activatedreceptor gamma coactivator-1 alpha (PPARGC1A), which encodes a master regulator ofpathways potentially disrupted by PFAS exposure, associated with secondarycardiovascular events in a large consortium study. However, we did not find clearevidence for such associations. In Paper IV, we assessed associations of PFAS with bloodlipids and incident CVD using case-control studies nested in two Swedish adult cohorts.We observed overall null associations with stroke, but a tendency for inverse associationswith myocardial infarction as well as associations with higher HDL-cholesterol and lowertriglycerides, but also with higher LDL-cholesterol. In Paper V, we included OMICs data(metabolites, proteins and genes), which linked PFAS to lower myocardial infarction riskvia lipid and inflammatory pathways. Likewise, a group of 'old POPs', the organochlorinecompounds (OCs), were linked to higher myocardial infarction risk via the same pathwaysand to higher stroke risk via mitochondrial pathways.Thus, although we found no evidence for associations between PFAS and increasedcardiometabolic disease risk, the overall findings indicate associations of PFAS withmetabolic disturbances, particularly lipid metabolism. This is a potential adverse effect onhuman physiology and warrants further attention.

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2023

Mode of access: World Wide Web

ISBN: 9798379480653Subjects--Topical Terms:

3564561
Cardiovascular disease.
Index Terms--Genre/Form:

542853
Electronic books.

Persistent Environmental Pollutants and Risk of Cardiovascular Disease.
LDR:04342nmm a2200361K 4500 001 2362889
005 20231109093755.5
006 m o d
007 cr mn ---uuuuu
008 241011s2023 xx obm 000 0 eng d
020 $a 9798379480653
035 $a (MiAaPQ)AAI30450276
035 $a (MiAaPQ)Karolinska_1061648496
035 $a AAI30450276
040 $a MiAaPQ $b eng $c MiAaPQ $d NTU
100 1 $a Schillemans, Tessa. $3 3703633
245 1 0 $a Persistent Environmental Pollutants and Risk of Cardiovascular Disease.
264 0 $c 2023
300 $a 1 online resource (74 pages)
336 $a text $b txt $2 rdacontent
337 $a computer $b c $2 rdamedia
338 $a online resource $b cr $2 rdacarrier
500 $a Source: Dissertations Abstracts International, Volume: 84-11, Section: B.
500 $a Advisor: Akesson, Agneta;Brunius, Carl;Leander, Karin;Donat-Vargas, Carolina.
502 $a Thesis (Ph.D.)--Karolinska Institutet (Sweden), 2023.
504 $a Includes bibliographical references
520 $a Persistent chemicals emitted in the environment can have a considerable impact onecosystems and human health, now and in the future. One notorious group of persistentorganic pollutants (POPs) is the per- and polyfluoroalkyl substances (PFAS). Since theirproduction in 1940s for household and consumer products, they have accumulated in theenvironment and in humans via consumption of contaminated drinking water and food.They are hypothesized to induce metabolic disturbances, due to shared chemicalsimilarities with fatty acids. Consequently, PFAS may have high societal and economicimpact by increasing risk of obesity, type 2 diabetes (T2D) and cardiovascular disease(CVD). However, reports on these associations are scarce, and the underlying molecularpathways are still unclear. Therefore, in this PhD project, we aimed to i) investigateassociations between PFAS and risk of several cardiometabolic diseases and ii) explorepotential underlying pathways.In Paper I, we investigated cross-sectional associations between PFAS mixtures and bodymass index (BMI) in European teenagers using meta-regression. Results showed atendency for inverse associations between PFAS and BMI and indicated a potential fordiverging contributions between PFAS compounds. In Paper II, using a nested casecontrol study on T2D including metabolomics data in Swedish adults, we found that PFAScorrelated positively with glycerophospholipids and diacylglycerols. But whilstglycerophospholipids associated with lower T2D risk, diacylglycerols associated withhigher T2D risk. This indicates a potential for diverging effects on disease risk. In Paper III,we investigated whether genetic polymorphisms in peroxisome proliferator-activatedreceptor gamma coactivator-1 alpha (PPARGC1A), which encodes a master regulator ofpathways potentially disrupted by PFAS exposure, associated with secondarycardiovascular events in a large consortium study. However, we did not find clearevidence for such associations. In Paper IV, we assessed associations of PFAS with bloodlipids and incident CVD using case-control studies nested in two Swedish adult cohorts.We observed overall null associations with stroke, but a tendency for inverse associationswith myocardial infarction as well as associations with higher HDL-cholesterol and lowertriglycerides, but also with higher LDL-cholesterol. In Paper V, we included OMICs data(metabolites, proteins and genes), which linked PFAS to lower myocardial infarction riskvia lipid and inflammatory pathways. Likewise, a group of 'old POPs', the organochlorinecompounds (OCs), were linked to higher myocardial infarction risk via the same pathwaysand to higher stroke risk via mitochondrial pathways.Thus, although we found no evidence for associations between PFAS and increasedcardiometabolic disease risk, the overall findings indicate associations of PFAS withmetabolic disturbances, particularly lipid metabolism. This is a potential adverse effect onhuman physiology and warrants further attention.
533 $a Electronic reproduction. $b Ann Arbor, Mich. : $c ProQuest, $d 2023
538 $a Mode of access: World Wide Web
650 4 $a Cardiovascular disease. $3 3564561
650 4 $a Perfluoroalkyl & polyfluoroalkyl substances. $3 3695333
650 4 $a Insulin resistance. $3 1016456
650 4 $a Lipids. $3 558980
650 4 $a Body mass index. $3 3562858
650 4 $a Metabolites. $3 683644
650 4 $a Apolipoproteins. $3 2156915
650 4 $a Chronic illnesses. $3 3550688
650 4 $a Obesity. $3 525736
650 4 $a Health sciences. $3 3168359
650 4 $a Medicine. $3 641104
650 4 $a Pharmaceutical sciences. $3 3173021
650 4 $a Public health. $3 534748
655 7 $a Electronic books. $2 lcsh $3 542853
690 $a 0566
690 $a 0564
690 $a 0572
690 $a 0573
710 2 $a ProQuest Information and Learning Co. $3 783688
710 2 $a Karolinska Institutet (Sweden). $3 3557748
773 0 $t Dissertations Abstracts International $g 84-11B.
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=30450276 $z click for full text (PQDT)