Eosinophil Count Is a Common Factor for Complex Metabolic and Pulmonary Traits and Diseases: The LifeLines Cohort Study
There is ongoing debate on the association between eosinophil count and diseases, as previous studies were inconsistent. We studied the relationship of eosinophil count with 22 complex metabolic, cardiac, and pulmonary traits and diseases. From the population-based LifeLines Cohort Study (N = 167,72...
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| Vydané v: | PloS one Ročník 11; číslo 12; s. e0168480 |
|---|---|
| Hlavní autori: | , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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United States
Public Library of Science
15.12.2016
Public Library of Science (PLoS) |
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| ISSN: | 1932-6203, 1932-6203 |
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| Abstract | There is ongoing debate on the association between eosinophil count and diseases, as previous studies were inconsistent. We studied the relationship of eosinophil count with 22 complex metabolic, cardiac, and pulmonary traits and diseases. From the population-based LifeLines Cohort Study (N = 167,729), 13,301 individuals were included. We focused on relationship of eosinophil count with three classes of metabolic (7 traits, 2 diseases), cardiac (6 traits, 2 diseases), and pulmonary (2 traits, 2 diseases) outcomes. Regression analyses were applied in overall, women and men, while adjusted for age, sex, BMI and smoking. A p-value of <0.00076 was considered statistically significant. 58.2% of population were women (mean±SD 51.3±11.1 years old). In overall, one-SD higher of ln-eosinophil count was associated with a 0.04 (±SE ±0.002;p = 6.0×10-6) SD higher levels in ln-BMI, 0.06 (±0.007;p = 3.1×10-12) SD in ln-TG, 0.04 (±0.003;p = 7.0×10-6) SD in TC, 0.04 (±0.004;p = 6.3×10-7) SD in LDL, 0.04 (±0.006;p = 6.0×10-6) SD in HbA1c; and with a 0.05 (±0.004;p = 1.7×10-8) SD lower levels in HDL, 0.05 (±0.007;p = 3.4×10-23) SD in FEV1, and 0.09 (±0.001;p = 6.6×10-28) SD in FEV1/FVC. A higher ln-eosinophil count was associated with 1.18 (95%CI 1.09-1.28;p = 2.0×10-5) odds ratio of obesity, 1.29 (1.19-1.39;p = 1.1×10-10) of metabolic syndrome, 1.40 (1.25-1.56;p = 2.7×10-9) of COPD and 1.81 (1.61-2.03;p = 1.0×10-23) of asthma. Similar results were found in women. We found no association between ln-eosinophil count either with blood pressure indices in overall, women and men; or with BMI, LDL, HbA1c and obesity in men. In a large population based cohort, we confirmed eosinophil count as a potential factor implicated in metabolic and pulmonary outcomes. |
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| AbstractList | There is ongoing debate on the association between eosinophil count and diseases, as previous studies were inconsistent. We studied the relationship of eosinophil count with 22 complex metabolic, cardiac, and pulmonary traits and diseases. From the population-based LifeLines Cohort Study (N = 167,729), 13,301 individuals were included. We focused on relationship of eosinophil count with three classes of metabolic (7 traits, 2 diseases), cardiac (6 traits, 2 diseases), and pulmonary (2 traits, 2 diseases) outcomes. Regression analyses were applied in overall, women and men, while adjusted for age, sex, BMI and smoking. A p-value of <0.00076 was considered statistically significant. 58.2% of population were women (mean±SD 51.3±11.1 years old). In overall, one-SD higher of ln-eosinophil count was associated with a 0.04 (±SE ±0.002;p = 6.0x10.sup.-6) SD higher levels in ln-BMI, 0.06 (±0.007;p = 3.1x10.sup.-12) SD in ln-TG, 0.04 (±0.003;p = 7.0x10.sup.-6) SD in TC, 0.04 (±0.004;p = 6.3x10.sup.-7) SD in LDL, 0.04 (±0.006;p = 6.0x10.sup.-6) SD in HbA1c; and with a 0.05 (±0.004;p = 1.7x10.sup.-8) SD lower levels in HDL, 0.05 (±0.007;p = 3.4x10.sup.-23) SD in FEV1, and 0.09 (±0.001;p = 6.6x10.sup.-28) SD in FEV1/FVC. A higher ln-eosinophil count was associated with 1.18 (95%CI 1.09-1.28;p = 2.0x10.sup.-5) odds ratio of obesity, 1.29 (1.19-1.39;p = 1.1x10.sup.-10) of metabolic syndrome, 1.40 (1.25-1.56;p = 2.7x10.sup.-9) of COPD and 1.81 (1.61-2.03;p = 1.0x10.sup.-23) of asthma. Similar results were found in women. We found no association between ln-eosinophil count either with blood pressure indices in overall, women and men; or with BMI, LDL, HbA1c and obesity in men. In a large population based cohort, we confirmed eosinophil count as a potential factor implicated in metabolic and pulmonary outcomes. There is ongoing debate on the association between eosinophil count and diseases, as previous studies were inconsistent. We studied the relationship of eosinophil count with 22 complex metabolic, cardiac, and pulmonary traits and diseases. From the population-based LifeLines Cohort Study (N = 167,729), 13,301 individuals were included. We focused on relationship of eosinophil count with three classes of metabolic (7 traits, 2 diseases), cardiac (6 traits, 2 diseases), and pulmonary (2 traits, 2 diseases) outcomes. Regression analyses were applied in overall, women and men, while adjusted for age, sex, BMI and smoking. A p-value of <0.00076 was considered statistically significant. 58.2% of population were women (mean±SD 51.3±11.1 years old). In overall, one-SD higher of ln-eosinophil count was associated with a 0.04 (±SE ±0.002;p = 6.0×10−6) SD higher levels in ln-BMI, 0.06 (±0.007;p = 3.1×10−12) SD in ln-TG, 0.04 (±0.003;p = 7.0×10−6) SD in TC, 0.04 (±0.004;p = 6.3×10−7) SD in LDL, 0.04 (±0.006;p = 6.0×10−6) SD in HbA1c; and with a 0.05 (±0.004;p = 1.7×10−8) SD lower levels in HDL, 0.05 (±0.007;p = 3.4×10−23) SD in FEV1, and 0.09 (±0.001;p = 6.6×10−28) SD in FEV1/FVC. A higher ln-eosinophil count was associated with 1.18 (95%CI 1.09–1.28;p = 2.0×10−5) odds ratio of obesity, 1.29 (1.19–1.39;p = 1.1×10−10) of metabolic syndrome, 1.40 (1.25–1.56;p = 2.7×10−9) of COPD and 1.81 (1.61–2.03;p = 1.0×10−23) of asthma. Similar results were found in women. We found no association between ln-eosinophil count either with blood pressure indices in overall, women and men; or with BMI, LDL, HbA1c and obesity in men. In a large population based cohort, we confirmed eosinophil count as a potential factor implicated in metabolic and pulmonary outcomes. There is ongoing debate on the association between eosinophil count and diseases, as previous studies were inconsistent. We studied the relationship of eosinophil count with 22 complex metabolic, cardiac, and pulmonary traits and diseases. From the population-based LifeLines Cohort Study (N = 167,729), 13,301 individuals were included. We focused on relationship of eosinophil count with three classes of metabolic (7 traits, 2 diseases), cardiac (6 traits, 2 diseases), and pulmonary (2 traits, 2 diseases) outcomes. Regression analyses were applied in overall, women and men, while adjusted for age, sex, BMI and smoking. A p-value of <0.00076 was considered statistically significant. 58.2% of population were women (mean±SD 51.3±11.1 years old). In overall, one-SD higher of ln-eosinophil count was associated with a 0.04 (±SE ±0.002;p = 6.0×10-6) SD higher levels in ln-BMI, 0.06 (±0.007;p = 3.1×10-12) SD in ln-TG, 0.04 (±0.003;p = 7.0×10-6) SD in TC, 0.04 (±0.004;p = 6.3×10-7) SD in LDL, 0.04 (±0.006;p = 6.0×10-6) SD in HbA1c; and with a 0.05 (±0.004;p = 1.7×10-8) SD lower levels in HDL, 0.05 (±0.007;p = 3.4×10-23) SD in FEV1, and 0.09 (±0.001;p = 6.6×10-28) SD in FEV1/FVC. A higher ln-eosinophil count was associated with 1.18 (95%CI 1.09-1.28;p = 2.0×10-5) odds ratio of obesity, 1.29 (1.19-1.39;p = 1.1×10-10) of metabolic syndrome, 1.40 (1.25-1.56;p = 2.7×10-9) of COPD and 1.81 (1.61-2.03;p = 1.0×10-23) of asthma. Similar results were found in women. We found no association between ln-eosinophil count either with blood pressure indices in overall, women and men; or with BMI, LDL, HbA1c and obesity in men. In a large population based cohort, we confirmed eosinophil count as a potential factor implicated in metabolic and pulmonary outcomes. There is ongoing debate on the association between eosinophil count and diseases, as previous studies were inconsistent. We studied the relationship of eosinophil count with 22 complex metabolic, cardiac, and pulmonary traits and diseases. From the population-based LifeLines Cohort Study (N = 167,729), 13,301 individuals were included. We focused on relationship of eosinophil count with three classes of metabolic (7 traits, 2 diseases), cardiac (6 traits, 2 diseases), and pulmonary (2 traits, 2 diseases) outcomes. Regression analyses were applied in overall, women and men, while adjusted for age, sex, BMI and smoking. A p -value of <0.00076 was considered statistically significant. 58.2% of population were women (mean±SD 51.3±11.1 years old). In overall, one-SD higher of ln-eosinophil count was associated with a 0.04 (±SE ±0.002;p = 6.0×10 −6 ) SD higher levels in ln-BMI, 0.06 (±0.007;p = 3.1×10 −12 ) SD in ln-TG, 0.04 (±0.003;p = 7.0×10 −6 ) SD in TC, 0.04 (±0.004;p = 6.3×10 −7 ) SD in LDL, 0.04 (±0.006;p = 6.0×10 −6 ) SD in HbA1c; and with a 0.05 (±0.004;p = 1.7×10 −8 ) SD lower levels in HDL, 0.05 (±0.007;p = 3.4×10 −23 ) SD in FEV1, and 0.09 (±0.001;p = 6.6×10 −28 ) SD in FEV1/FVC. A higher ln-eosinophil count was associated with 1.18 (95%CI 1.09–1.28;p = 2.0×10 −5 ) odds ratio of obesity, 1.29 (1.19–1.39;p = 1.1×10 −10 ) of metabolic syndrome, 1.40 (1.25–1.56;p = 2.7×10 −9 ) of COPD and 1.81 (1.61–2.03;p = 1.0×10 −23 ) of asthma. Similar results were found in women. We found no association between ln-eosinophil count either with blood pressure indices in overall, women and men; or with BMI, LDL, HbA1c and obesity in men. In a large population based cohort, we confirmed eosinophil count as a potential factor implicated in metabolic and pulmonary outcomes. There is ongoing debate on the association between eosinophil count and diseases, as previous studies were inconsistent. We studied the relationship of eosinophil count with 22 complex metabolic, cardiac, and pulmonary traits and diseases. From the population-based LifeLines Cohort Study (N = 167,729), 13,301 individuals were included. We focused on relationship of eosinophil count with three classes of metabolic (7 traits, 2 diseases), cardiac (6 traits, 2 diseases), and pulmonary (2 traits, 2 diseases) outcomes. Regression analyses were applied in overall, women and men, while adjusted for age, sex, BMI and smoking. A p-value of <0.00076 was considered statistically significant. 58.2% of population were women (mean plus or minus SD 51.3 plus or minus 11.1 years old). In overall, one-SD higher of ln-eosinophil count was associated with a 0.04 ( plus or minus SE plus or minus 0.002; p = 6.010-6) SD higher levels in ln-BMI, 0.06 ( plus or minus 0.007; p = 3.110-12) SD in ln-TG, 0.04 ( plus or minus 0.003; p = 7.010-6) SD in TC, 0.04 ( plus or minus 0.004; p = 6.310-7) SD in LDL, 0.04 ( plus or minus 0.006; p = 6.010-6) SD in HbA1c; and with a 0.05 ( plus or minus 0.004; p = 1.710-8) SD lower levels in HDL, 0.05 ( plus or minus 0.007; p = 3.410-23) SD in FEV1, and 0.09 ( plus or minus 0.001; p = 6.610-28) SD in FEV1/FVC. A higher ln-eosinophil count was associated with 1.18 (95%CI 1.09-1.28; p = 2.010-5) odds ratio of obesity, 1.29 (1.19-1.39; p = 1.110-10) of metabolic syndrome, 1.40 (1.25-1.56; p = 2.710-9) of COPD and 1.81 (1.61-2.03; p = 1.010-23) of asthma. Similar results were found in women. We found no association between ln-eosinophil count either with blood pressure indices in overall, women and men; or with BMI, LDL, HbA1c and obesity in men. In a large population based cohort, we confirmed eosinophil count as a potential factor implicated in metabolic and pulmonary outcomes. There is ongoing debate on the association between eosinophil count and diseases, as previous studies were inconsistent. We studied the relationship of eosinophil count with 22 complex metabolic, cardiac, and pulmonary traits and diseases. From the population-based LifeLines Cohort Study (N = 167,729), 13,301 individuals were included. We focused on relationship of eosinophil count with three classes of metabolic (7 traits, 2 diseases), cardiac (6 traits, 2 diseases), and pulmonary (2 traits, 2 diseases) outcomes. Regression analyses were applied in overall, women and men, while adjusted for age, sex, BMI and smoking. A p-value of <0.00076 was considered statistically significant. 58.2% of population were women (mean±SD 51.3±11.1 years old). In overall, one-SD higher of ln-eosinophil count was associated with a 0.04 (±SE ±0.002;p = 6.0×10-6) SD higher levels in ln-BMI, 0.06 (±0.007;p = 3.1×10-12) SD in ln-TG, 0.04 (±0.003;p = 7.0×10-6) SD in TC, 0.04 (±0.004;p = 6.3×10-7) SD in LDL, 0.04 (±0.006;p = 6.0×10-6) SD in HbA1c; and with a 0.05 (±0.004;p = 1.7×10-8) SD lower levels in HDL, 0.05 (±0.007;p = 3.4×10-23) SD in FEV1, and 0.09 (±0.001;p = 6.6×10-28) SD in FEV1/FVC. A higher ln-eosinophil count was associated with 1.18 (95%CI 1.09-1.28;p = 2.0×10-5) odds ratio of obesity, 1.29 (1.19-1.39;p = 1.1×10-10) of metabolic syndrome, 1.40 (1.25-1.56;p = 2.7×10-9) of COPD and 1.81 (1.61-2.03;p = 1.0×10-23) of asthma. Similar results were found in women. We found no association between ln-eosinophil count either with blood pressure indices in overall, women and men; or with BMI, LDL, HbA1c and obesity in men. In a large population based cohort, we confirmed eosinophil count as a potential factor implicated in metabolic and pulmonary outcomes.There is ongoing debate on the association between eosinophil count and diseases, as previous studies were inconsistent. We studied the relationship of eosinophil count with 22 complex metabolic, cardiac, and pulmonary traits and diseases. From the population-based LifeLines Cohort Study (N = 167,729), 13,301 individuals were included. We focused on relationship of eosinophil count with three classes of metabolic (7 traits, 2 diseases), cardiac (6 traits, 2 diseases), and pulmonary (2 traits, 2 diseases) outcomes. Regression analyses were applied in overall, women and men, while adjusted for age, sex, BMI and smoking. A p-value of <0.00076 was considered statistically significant. 58.2% of population were women (mean±SD 51.3±11.1 years old). In overall, one-SD higher of ln-eosinophil count was associated with a 0.04 (±SE ±0.002;p = 6.0×10-6) SD higher levels in ln-BMI, 0.06 (±0.007;p = 3.1×10-12) SD in ln-TG, 0.04 (±0.003;p = 7.0×10-6) SD in TC, 0.04 (±0.004;p = 6.3×10-7) SD in LDL, 0.04 (±0.006;p = 6.0×10-6) SD in HbA1c; and with a 0.05 (±0.004;p = 1.7×10-8) SD lower levels in HDL, 0.05 (±0.007;p = 3.4×10-23) SD in FEV1, and 0.09 (±0.001;p = 6.6×10-28) SD in FEV1/FVC. A higher ln-eosinophil count was associated with 1.18 (95%CI 1.09-1.28;p = 2.0×10-5) odds ratio of obesity, 1.29 (1.19-1.39;p = 1.1×10-10) of metabolic syndrome, 1.40 (1.25-1.56;p = 2.7×10-9) of COPD and 1.81 (1.61-2.03;p = 1.0×10-23) of asthma. Similar results were found in women. We found no association between ln-eosinophil count either with blood pressure indices in overall, women and men; or with BMI, LDL, HbA1c and obesity in men. In a large population based cohort, we confirmed eosinophil count as a potential factor implicated in metabolic and pulmonary outcomes. |
| Audience | Academic |
| Author | Wijmenga, Cisca Koppelman, Gerard H. Franke, Lude Wolffenbuttel, Bruce H. R. Snieder, Harold Navis, Gerjan Vonk, Judith Stolk, Ronald P. Alizadeh, Behrooz Z. Corpeleijn, Eva Amini, Marzyeh Bashirova, Dinara Harst, Pim van der Prins, Bram P. Postma, Dirkje S. Bruinenberg, Marcel Boezen, H. Marike |
| AuthorAffiliation | 4 Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands 1 Department of Epidemiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands 2 LifeLines Cohort Study, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands 5 Department of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands 6 Department of Endocrinology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands Tulane University School of Public Health and Tropical Medicine, UNITED STATES 3 Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands 7 Department of Pulmonology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands 8 Groningen Research Institute for Asthma and COPD, University Medical Center Groningen, University of Groni |
| AuthorAffiliation_xml | – name: 7 Department of Pulmonology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands – name: 8 Groningen Research Institute for Asthma and COPD, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands – name: Tulane University School of Public Health and Tropical Medicine, UNITED STATES – name: 2 LifeLines Cohort Study, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands – name: 9 Department of Pediatric Pulmonology and Pediatric Allergology, Beatrix Children’s Hospital, Groningen, The Netherlands – name: 3 Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands – name: 6 Department of Endocrinology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands – name: 1 Department of Epidemiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands – name: 4 Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands – name: 5 Department of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands |
| Author_xml | – sequence: 1 givenname: Marzyeh orcidid: 0000-0002-0123-9510 surname: Amini fullname: Amini, Marzyeh – sequence: 2 givenname: Dinara surname: Bashirova fullname: Bashirova, Dinara – sequence: 3 givenname: Bram P. surname: Prins fullname: Prins, Bram P. – sequence: 4 givenname: Eva surname: Corpeleijn fullname: Corpeleijn, Eva – sequence: 5 givenname: Marcel surname: Bruinenberg fullname: Bruinenberg, Marcel – sequence: 6 givenname: Lude surname: Franke fullname: Franke, Lude – sequence: 7 givenname: Pim van der surname: Harst fullname: Harst, Pim van der – sequence: 8 givenname: Gerjan surname: Navis fullname: Navis, Gerjan – sequence: 9 givenname: Bruce H. R. surname: Wolffenbuttel fullname: Wolffenbuttel, Bruce H. R. – sequence: 10 givenname: Ronald P. surname: Stolk fullname: Stolk, Ronald P. – sequence: 11 givenname: Cisca surname: Wijmenga fullname: Wijmenga, Cisca – sequence: 12 givenname: Dirkje S. surname: Postma fullname: Postma, Dirkje S. – sequence: 13 givenname: Gerard H. surname: Koppelman fullname: Koppelman, Gerard H. – sequence: 14 givenname: H. Marike surname: Boezen fullname: Boezen, H. Marike – sequence: 15 givenname: Judith surname: Vonk fullname: Vonk, Judith – sequence: 16 givenname: Harold surname: Snieder fullname: Snieder, Harold – sequence: 17 givenname: Behrooz Z. surname: Alizadeh fullname: Alizadeh, Behrooz Z. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27978545$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | COPYRIGHT 2016 Public Library of Science 2016 Amini et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2016 Amini et al 2016 Amini et al |
| Copyright_xml | – notice: COPYRIGHT 2016 Public Library of Science – notice: 2016 Amini et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. – notice: 2016 Amini et al 2016 Amini et al |
| CorporateAuthor | LifeLines Cohort Study |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Competing Interests: The authors have declared that no competing interests exist. Conceptualization: BZA HS.Data curation: MA BZA.Formal analysis: MA BZA DB BPP.Funding acquisition: BZA.Investigation: MA BZA.Methodology: MA BZA.Project administration: MA BZA.Resources: LF PH GN BHRW RPS CW HMB MB.Supervision: BZA.Validation: HS JV DSP GHK EC.Visualization: MA BZA.Writing – original draft: MA BZA.Writing – review & editing: HS JV DSP GHK. Membership of the LifeLines Cohort Study is listed in the Acknowledgments. |
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| SubjectTerms | Adult Aged Asthma Asthma - blood Asthma - metabolism Biology and Life Sciences Blood pressure Body mass Body Mass Index Chronic obstructive pulmonary disease Cohort analysis Cohort Studies Coronary artery disease Diagnosis Diseases Eosinophils Eosinophils - physiology Epidemiology Female Glycated Hemoglobin A - metabolism Heart diseases High density lipoprotein Humans Leukocyte Count Leukocytes (eosinophilic) Lipoproteins (high density) Lipoproteins (low density) Lipoproteins, HDL - blood Logistic Models Low density lipoprotein Lung diseases Male Measurement Medicine and Health Sciences Men Mens health Metabolic diseases Metabolic disorders Metabolic syndrome Metabolic Syndrome - blood Metabolic Syndrome - metabolism Middle Aged Multivariate Analysis Obesity Obesity - blood Obesity - metabolism Pediatrics Physiological aspects Population Population studies Pulmonary Disease, Chronic Obstructive - blood Pulmonary Disease, Chronic Obstructive - metabolism Regression Analysis Respiratory tract diseases Sex Factors Smoking Statistical analysis Womens health |
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| Title | Eosinophil Count Is a Common Factor for Complex Metabolic and Pulmonary Traits and Diseases: The LifeLines Cohort Study |
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