title: Passive smoking increases experimental atherosclerosis in cholesterol-fed rabbits.
abstract: OBJECTIVE
  We evaluated the influence of passive smoking on experimental atherosclerosis in cholesterol-fed rabbits.
  
  
  BACKGROUND
  Exposure to environmental tobacco smoke (ETS) has been epidemiologically linked to death from ischemic heart disease in nonsmokers.
  
  
  METHODS
  New Zealand male rabbits were randomly divided into three groups after 2 weeks of a 0.3% cholesterol diet. Sixteen rabbits were exposed to a high and 16 rabbits to a low dose of ETS; 32 rabbits located in another room served as an unexposed control group. After 10 weeks of ETS exposure, all rabbits were killed, and the percent of aortic and pulmonary artery endothelial surfaces covered by lipid lesions was measured by staining and planimetry.
  
  
  RESULTS
  Average air nicotine, carbon monoxide and total particulate concentrations were 1,040 micrograms/m3, 60.2 ppm and 32.8 mg/m3 for the high dose ETS group, 30 micrograms/m3, 18.8 ppm and 4.0 mg/m3 for the low dose ETS group and < 1 microgram/m3, 3.1 ppm and 0.13 mg/m3 for the control group. The percent atherosclerotic involvement of the aorta and pulmonary artery increased significantly with ETS exposure (for the aorta, 30 +/- 19% [mean +/- SD] for the control group, 36 +/- 14% for the low dose ETS group and 52 +/- 21% for the high dose ETS group, p < 0.001; for the pulmonary artery, 22 +/- 15% for the control group, 29 +/- 25% for the low dose ETS group, and 45 +/- 12% for the high dose ETS group, p < 0.001). Bleeding time was significantly shorter in the two ETS groups than in the control group (86 +/- 17 vs. 68 +/- 15, 68 +/- 18 s, p < 0.001). There were no significant differences in serum triglycerides, cholesterol and high density lipoprotein cholesterol at the end of the study.
  
  
  CONCLUSIONS
  Environmental tobacco smoke affects platelet function and increases aortic and pulmonary artery atherosclerosis. This increase of atherosclerosis was independent of changes in serum lipids and exhibited a dose-response relation. These results are consistent with data from epidemiologic studies demonstrating that ETS increases the risk of death due to heart disease.
authors.affiliation: Department of Medicine, University of California, San Francisco.
authors.forename: B Q
authors.initials: BQ
authors.lastname: Zhu
authors.forename: Y P
authors.initials: YP
authors.lastname: Sun
authors.forename: R E
authors.initials: RE
authors.lastname: Sievers
authors.forename: W M
authors.initials: WM
authors.lastname: Isenberg
authors.forename: S A
authors.initials: SA
authors.lastname: Glantz
authors.forename: W W
authors.initials: WW
authors.lastname: Parmley
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001161:Arteriosclerosis / Q000097:blood / Q000150:complications* / Q000453:epidemiology / Q000473:pathology; D002791:Cholesterol, Dietary / Q000008:administration & dosage*; D004305:Dose-Response Relationship, Drug; D008055:Lipids / Q000097:blood; D008297:Male; D010316:Particle Size; D011817:Rabbits; D012044:Regression Analysis; D013997:Time Factors; D014028:Tobacco Smoke Pollution / Q000009:adverse effects* / Q000032:analysis / Q000706:statistics & numerical data; D015430:Weight Gain / Q000187:drug effects
chemical_list: D002791:Cholesterol, Dietary; D008055:Lipids; D014028:Tobacco Smoke Pollution