Comparison of nonsmoker serum cotinine concentrations acquired from NHANES over a period of 14 years clearly demonstrates a substantial decline, averaging approximately 70% overall, during this time. This decrease in serum cotinine concentrations suggests a substantial reduction in the exposure of the U.S. population to SHS over this period. For example, during NHANES III, approximately 65% of nonsmokers had serum cotinine concentrations > 0.1 ng/mL (DHHS 2000b
). On that basis, a Healthy People 2010 objective was established stating that, by the year 2010, no more than 45% of nonsmokers should have cotinine levels > 0.1 ng/mL (DHHS 2000c
). Our present results suggest that this goal was met during 1999–2000. However, children and non-Hispanic blacks had consistently higher serum cotinine concentrations than did other segments of the population and thus remain at relatively elevated risk from exposure to SHS.
The most likely explanations for this decrease in serum cotinine concentrations are the increased restrictions on smoking that have been widely instituted at work and in other public places during this time period, and further efforts to reduce the exposure of nonsmokers in the home. Using data from the Current Population Survey, Shopland et al. (2001)
found that between 1993 and 1999 the percentage of indoor workers reporting smoke-free policies in the workplace increased from less than 46% to nearly 70%. In 1993, only two states had at least 60% of indoor workers reporting that smoke-free policies were in place; by 1999, 47 states (and the District of Columbia) had at least that level of coverage. In general, women reported more workplace smoke-free policies than did men, although the sex difference narrowed somewhat by 1999. Smoke-free workplaces are also known to contribute to a reduction in smoking prevalence among workers (Farrelly et al. 1999
; Fichtenberg and Glantz 2002
). Increases in smoke-free policies and reductions in smoking prevalence may both have contributed to the decline in exposure of non-smokers to SHS. The role of restrictions, however, is presumably more important because the prevalence of adult smoking in the United States did not decrease substantially during the 1990s: between 1990 and 1999, the national median decreased only slightly from 25.5% to 22.7% (CDC 2000
). In general, smoke-free environmental policies are regarded as the most effective means of reducing exposure to SHS (Task Force on Community Preventive Services 2001
Certain subgroups, when characterized by age, sex, or race/ethnicity, had consistently higher cotinine concentrations during each time period. A major source of SHS exposure in young children is from parents or other adults smoking at home, and exposure of non-smokers to SHS in homes with children also declined during the 1990s. Comparing data from the 1992 and 2000 National Health Interview Surveys, Soliman et al. (2004)
found that reported SHS exposure declined from 36% to approximately 25%, more than would be expected from declines in adult smoking prevalence alone. This decrease occurred across all groups, although home SHS exposures remained most prevalent among non-Hispanic whites in that study, and we found that cotinine concentrations were higher in non-Hispanic children than in adults during all NHANES survey periods.
In the present study, Mexican-American nonsmokers generally had lower serum cotinine levels than did the other two race/ethnicity groups, whereas mean serum cotinine concentrations in non-Hispanic blacks were consistently higher in each time period. The higher cotinine concentrations found in non-Hispanic blacks presumably reflect greater exposure to SHS within this population, although the interpretation of these results is complicated by possible metabolic influences. Among active smokers, blacks have consistently higher serum cotinine concentrations per cigarette smoked than do whites (Caraballo et al. 1998
; Wagenknecht et al. 1990
), and this has been attributed, at least in part, to differences between blacks and whites in the metabolism of nicotine, cotinine, and their glucuronides (Benowitz et al. 1999
). Thus, metabolic factors might also account for at least part of the ethnic/racial differences seen in serum cotinine levels among nonsmokers. In a study of children with asthma, Wilson et al. (2005)
reported finding significantly higher serum cotinine concentrations for African-American children even after adjusting for self-reported SHS exposure. However, Wagenknecht et al. (1993)
found that SHS exposure assessed by either self-report or serum cotinine measurements among 3,300 nonsmokers in the CARDIA study was significantly higher for blacks than for whites, but that the difference in serum cotinine did not persist after adjustment for self-reported exposure to SHS. Sexton et al. (2004)
also found that questionnaires, time–activity data, and cotinine measurements all indicated higher SHS exposure among African-American children. Thus, the consistently higher serum cotinine levels for black nonsmokers in NHANES appear to reflect higher SHS exposure, although the extent to which differences in metabolism may confound these estimates remains uncertain.
Exposure of nonsmokers to SHS also appears to have declined in other countries besides the United States during this time period, at least based on self-report. For example, Borland et al. (1999)
described annual surveys of approximately 2,500 adults conducted in Victoria, Australia, from 1989 to 1997. The percentage of respondents reporting that they did not smoke in the presence of children and that visitors were discouraged from smoking in the home both approximately doubled during this time. In addition, the percentage of indoor workers in Victoria protected by restrictions on smoking in the workplace increased from 17% to 66% between 1988 and 1995. Within 1 year after Finland passed its Tobacco Control Act in 1995 prohibiting smoking in the workplace in all joint and public premises, workers reporting no ETS exposure in the workplace increased almost 3-fold, from 19.2% to 54.2% (Heloma et al. 2001
Most studies finding decreased exposure to SHS over time have relied on self-reports. However, Jarvis et al. (2000)
have reported a substantial decrease during the 1990s in the exposure of British school children to SHS as assessed by salivary cotinine measurements. They monitored secondary school children 11–15 years of age from 1988 through 1996 and found that their salivary cotinine levels decreased by almost 50% during that time. They attributed the decline to both the decrease in prevalence of smoking among young adults with children and the increased restrictions in Great Britain on smoking in public places. However, Jarvis et al. (2000)
found only small declines among children whose parents smoked, suggesting that cessation rather than smokers simply avoiding exposure of children in the home was the primary factor driving the decline.
Our study has several strengths and some limitations. The data were taken from several large surveys conducted over a period of 14 years, evaluating national samples of individuals who were representative of the entire U.S. civilian, noninstitutionalized population, and included a total of nearly 30,000 nonsmokers. We used a sensitive and specific method for serum cotinine analysis, and all assays were conducted under uniform and rigorously controlled conditions. Repetitive analyses of common samples over time confirmed the absence of any unusual variations or drift in the analytic method. Thus, the substantial decreases in serum cotinine we observed over time most likely reflect corresponding decreases in exposure of nonsmokers to SHS. Nevertheless, serum cotinine has limitations as an exposure marker because it can monitor exposures only over the previous few days, and because nicotine metabolic differences among groups may influence the concentrations observed. However, despite the relatively short half-life of cotinine, measures of central tendency among groups based on large numbers of individuals should provide reasonable estimates of group steady-state levels. Although the differences we observed among ethnic/racial groups most likely reflect differences in exposure, metabolic influences cannot be excluded, and additional work is needed to evaluate the relative contributions of exposure and metabolism. Finally, a few occasional smokers could possibly have been included inadvertently among the more highly exposed participants in our study, because some infrequent smokers may have serum cotinine levels < 10 ng/mL. This factor is unlikely to have been significant among adults, and it is even less likely to have been influential among young children because few children in the 4–11 age group are active smokers.