Adhesion molecules, endothelin-1 and lung function in seven population-based cohorts

E. C. Oelsner, T. D. Pottinger, K. M. Burkart, M. Allison, S. G. Buxbaum, N. N. Hansel, R. Kumar, E. K. Larkin, L. A. Lange, L. R. Loehr, S. J. London, G. T. O'Connor, G. Papanicolaou, M. F. Petrini, D. Rabinowitz, S. Raghavan, S. Redline, B. Thyagarajan, R. P. Tracy, J. B. WilkW. B. White, S. S. Rich, R. G. Barr

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


Context: Endothelial function is abnormal in chronic obstructive pulmonary disease (COPD); whether endothelial dysfunction causes COPD is unknown. Objective: Test associations of endothelial biomarkers with FEV1 using instrumental variables. Methods: Among 26907 participants with spirometry, ICAM-1, P-selectin, E-selectin and endothelin-1 were measured in subsets. Results: ICAM-1 and P-selectin were inversely associated with FEV1 among European-Americans (-29mL and-34mL per standard deviation of log-transformed biomarker, p<0.001), as was endothelin-1 among African-Americans (-22mL, p=0.008). Genetically-estimated ICAM-1 and P-selectin were not significantly associated with FEV1. The instrumental variable for endothelin-1 was non-informative. Conclusion: Although ICAM-1, P-selectin and endothelin-1 were inversely associated with FEV1, associations for ICAM-1 and P-selectin do not appear causal.

Original languageEnglish (US)
Pages (from-to)196-203
Number of pages8
Issue number3
StatePublished - May 2013

Bibliographical note

Funding Information:
The authors report no declarations of interest with the following exception: Dr. Barr was reimbursed for conference travel by Boehringer Ingelheim, and Cenetra Health provided in-kind donation for an NIH-sponsored clinical trial. Dr. London is supported by the Division of Intramural Research, NIEHS, NIH, DHHS. Infrastructure was partly supported by Grant Number UL1RR025005, a component of the National Institutes of Health and NIH Roadmap for Medical Research. The NHLBI cohorts were funded by contracts from NIH/NHLBI: ARIC: HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN 268201100008C, HHSN268201100009C, HHSN26820 1100010C, HHSN268201100011C, and HHSN268201 100012C, R01-HL-087641, R01-HL-059367 and R01-HL-086694; NIH/NHGRI contract U01-HG-004402 and National Institutes of Health contract HHSN 268200625226C; carotid MRI data was funded by U01-HL-075572-01; neurocognitive data is collected by U01-HL-096812, HL-096814, HL-096899, HL-096902 and HL-096917, with previous brain MRI examinations funded by R01-HL-70825; CARDIA: HHS-N2-68201200036-C, N01-HC-48047, N01-HC-48048, N01-HC-48049, N01-HC-48050, N01-HC-95095, N01-HC-45204, N01-HC-45205, N01-HC-05187, N01-HC-45134, N01-HC-95100; the Young Adult Longitudinal Trends in Antioxidants (YALTA) ancillary study was funded by R01-HL-53560; CFS: R01-HL-46380-01-16; CHS: N01-HC-85239, N01-HC-85079, N01-HC-85080, N01-HC-85081, N01-HC-85082, N01-HC-85083, N01-HC-85084, N01-HC-85085, N01-HC-85086, N01-HC-35129, N01-HC-15103, N01-HC-75150, N01-HC-45133, N01-HC-55222, U01-HL-080295; AG-023629, AG-15928, AG-20098 and AG-027058; FHS: N01-HC-25195; JHS: N01-HC-95170, N01-HC-95171, N01-HC-95172; MESA: N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, N01-HC-95169, N01-HC-65226, RC1-HL-100543, R01-HL-077612, N01-HC-95159-HC-95169 and RR-024156. R01-HL-071051, R01-HL-071205, R01-HL-071250, R01-HL-071251, R01-HL-071252, R01-HL-071258, R01-HL-071259, EPA grant RD-831697.


  • Genetic polymorphisms
  • Growth factors/cytokines/inflammatory mediators
  • Respiratory disease


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