Influence of worksite environmental tobacco smoke on serum lipoprotein profiles of female nonsmokers

Metabolism. 1995 Dec;44(12):1536-9. doi: 10.1016/0026-0495(95)90071-3.

Abstract

The purpose of this study was to examine the influence of environmental tobacco smoke (ETS) in the workplace on high-density lipoprotein cholesterol (HDL-C), HDL-C subfractions, and apolipoprotein (apo) A-I and apo B in female workers. Premenopausal women free from factors known to influence HDL-C (cigarette smoking, vigorous physical exercise, etc) who were not taking oral contraceptives, were moderate consumers of alcohol, caffeine, and dietary fat, and were between the ages of 21 and 50 years participated in one of two groups: (1) nonsmokers who had never smoked cigarettes and were generally free from ETS exposure (nonsmokers), and (2) nonsmokers who had never smoked but were subjected to concentrated doses of ETS at least 6 hours per day, 4 days per week, for at least 6 consecutive months (ETS-exposed). A third group consisting of current cigarette smokers who smoked a minimum of 20 cigarettes per day for at least the past 5 consecutive years served as smoking control (smokers). Subjects were matched by group as closely as possible with regard to criteria that can influence blood lipoprotein levels. Participants were solicited from taverns and restaurants where they were employed. It was hypothesized that individuals chronically exposed to ETS would demonstrate unfavorable lipoprotein profiles. Results showed that HDL-C, HDL2, and apo A-I were significantly (P < .05) depressed for ETS-exposed and smokers as compared with nonsmokers. Values for ETS-exposed were not different from those for smokers. Total cholesterol, triglycerides, HDL3, and apo B did not differ among the three groups. It was concluded that excessive exposure to ETS in female workers can have deleterious effects on HDL-C, HDL2, and apo A-I in nonsmokers that are similar to effects observed in cigarette smokers. It is possible that these effects increase coronary artery disease (CAD) risk.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Apolipoprotein A-I / blood
  • Carbon Monoxide
  • Cholesterol, HDL / blood
  • Female
  • Humans
  • Lipoproteins / blood*
  • Middle Aged
  • Respiration
  • Smoking
  • Tobacco Smoke Pollution*

Substances

  • Apolipoprotein A-I
  • Cholesterol, HDL
  • Lipoproteins
  • Tobacco Smoke Pollution
  • Carbon Monoxide