Rj. Moffatt et al., INFLUENCE OF WORKSITE ENVIRONMENTAL TOBACCO-SMOKE ON SERUM-LIPOPROTEIN PROFILES OF FEMALE NONSMOKERS, Metabolism, clinical and experimental, 44(12), 1995, pp. 1536-1539
The purpose of this study was to examine the influence of environmenta
l tobacco smoke (ETS) in the workplace on high-density lipoprotein cho
lesterol (HDL-C), HDL-C subfractions, and apolipoprotein (ape) 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 an
d 50 years participated in one of two groups: (1) nonsmokers who had n
ever smoked cigarettes and were generally free from ETS exposure (nons
mokers), 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 the past 6 consecutive months (ETS-exposed). A third grou
p consisting of current cigarette smokers who smoked a minimum of 20 c
igarettes per day for at least the past 5 consecutive years served as
smoking controls (smokers). Subjects were matched by group as closely
as possible with regard to criteria that can influence blood lipoprote
in levels. Participants were solicited from taverns and restaurants wh
ere they were employed. It was hypothesized that individuals chronical
ly exposed to ETS would demonstrate unfavorable lipoprotein profiles.
Results showed that HDL-C, HDL(2), 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. To
tal cholesterol, triglycerides, HDL(3), 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, HDL(2), and apo
A-l in nonsmokers that are similar to effects observed in cigarette sm
okers. It is possible that these effects increase coronary artery dise
ase (CAD) risk. Copyright (C) 1995 by W.B. Saunders Company