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TABLE 12–1 Urinary Cotinine (ng/ml) in Nonsmokers According to Number of Reported Hours of Exposure to Other People’s Tobacco Smoke Within the Past 7 Days (Including Day Urine Sample Was Collected)

Duration of Exposure

 

Urinary Cotinine, mean±SDa

Quintile

Limits (h)

No.

1st

0.0–1.5

43

2.8±3.0

2nd

1.5–4.5

47

3.4±2.7

3rd

4.5–8.6

43

5.3±4.3

4th

8.6–20.0

43

14.7±19.5

5th

20.0–80.0

45

29.6±73.7

All

0.0–80.0

221

11.2±35.6

aTrend with increasing exposure was significant (p<0.001).

SOURCE: Wald et al. (1984).

USING BIOLOGICAL MARKERS TO ESTIMATE RISK

Cotinine, a metabolite of nicotine, while of itself not considered a carcinogen, is a useful marker of exposure to tobacco smoke, whether through active or passive smoking. Table 12–1 shows that the mean urinary cotinine concentration increases with the estimated exposure to other people’s tobacco smoke over the past 7 days. Much of these data, collected in the United Kingdom (Wald et al., 1984), showed that nonsmokers had, on average, about 0.4% of the concentration of urinary cotinine found in active smokers. Similar work done in Japan suggested that nonsmokers had relatively high cotinine levels, about one-seventh the levels in average Japanese smokers (Matsukara et al., 1984). The reason for this difference is not known and it needs to be investigated. However, in both countries studies showed increasing urinary cotinine levels in proportion to the estimated increasing ETS exposure.

In most of the epidemiologic studies that assessed the relationship of lung cancer to ETS-exposed nonsmokers, the measure of exposure used was “living with a smoking spouse.” The observed risks of lung cancer for nonsmokers were compared for those living with a smoking spouse and those living with nonsmokers. While it is reasonable to believe that people living with smokers would be more heavily exposed to ETS than people living with nonsmokers,



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