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Passive smoking and atherosclerosis - IESC/UFRJ

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Crude <strong>and</strong> adjusted estimates of the differences in mean carotid wall thickness in never<br />

active smokers according to exposure to environmental tobacco smoke are shown in table 2.<br />

Table 2. Differences in mean carotid wall thickness (mm) between never smokers exposed <strong>and</strong><br />

those unexposed to environmental tobacco smoke, unadjusted <strong>and</strong> adjusted for combinations of<br />

selected factors in participants of the ARIC study baseline visit, excluding persons with<br />

prevalent clinical cardiovascular disease¤<br />

Difference in mean carotid<br />

wall thickness (mm)<br />

between never smokers<br />

exposed <strong>and</strong> those<br />

Adjusted for:<br />

unexposed to ETS<br />

(p-value)<br />

No factors (crude) 0.012§<br />

Age, race <strong>and</strong> gender<br />

Age, race, gender plus life style factors (education, physical<br />

activity, fat intake, alcohol intake, body mass index)<br />

Age, race, gender, life style factors plus diabetes, hypertension<br />

<strong>and</strong> low density lipoprotein cholesterol<br />

¤ Myocardial infarction, angina pectoris, stroke, intermittent claudication<br />

Environmental tobacco smoke<br />

§ From table 1 (0.705 – 0.693 = 0.012)<br />

0.019 (p0.001)<br />

0.018 (p=0.003)<br />

0.016 (p=0.001)<br />

(12) Why is it important to examine the association between passive <strong>smoking</strong> <strong>and</strong><br />

carotid wall thickness adjusting for different combinations of risk factors (as<br />

opposed to using a single model in which all potential confounders are<br />

simultaneously adjusted)? What is the reason why the adjusted values are<br />

larger than the unadjusted ones?<br />

(13) What is the main shortcoming of assessing environmental tobacco smoke as a<br />

dichotomous variable, as done in tables 1 <strong>and</strong> 2, <strong>and</strong> Figure 3?<br />

E8-7

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