This study reports updated findings using the latest available NHANES data between 2001 and 2006. Overall, our results suggest that the long-term trend of declining exposure to SHS among nonsmokers, as reported by Pirkle et al. [6
], have stabilized since 2002. While the work of Pirkle et al. provided evidence to show the progress and impact of antismoking policies and public health efforts over the last decade, our current findings reveal that declines in SHS exposure seem to have leveled off.
Despite the stabilizing downward trend in national exposure, the demographic and racial/ethnic differences noted by Pirkle et al. [6
] persist today, with the young (children and adolescents age 4-19 years), males, and non-Hispanic Blacks experiencing higher levels of SHS exposure. While male nonsmokers were consistently exposed to higher cotinine levels than female nonsmokers, their overall cotinine levels remained consistently below 0.1 ng/mL over time. Children and adolescents age 4-19 years of non-Hispanic Black descent had consistently higher cotinine levels than their comparison groups across the 3 time periods examined. During 2005 to 2006, overall cotinine levels in children age 4-11 years fell below 0.1 ng/mL. While there is no direct evidence from this study to address the possibility of a declining trend in children's exposure, this finding is consistent with the Healthy People 2010 objective calling for no more than 45% of nonsmokers to have cotinine levels >0.1 ng/mL [6
In children, our findings are consistent with previous Centers for Disease Control and Prevention publications concluding that children are more heavily exposed to SHS than nonsmoking adults. Specifically, children's measured cotinine levels have been twice that of adults [9
]. The reasons for this are multifactorial. Children have a ventilation rate that is higher, proportional to their body size, than that seen in adults. The toxicity level in SHS is in effect amplified in children as they inhale many of the same cancer-causing substances as current smokers [10
]. In addition, children get most of their smoke exposure in private homes and vehicles [11
]. Children can not choose who they live with, whereas nonsmoking adults can choose to live with nonsmokers or have people smoke outside the home. There is currently little data to inform on the specific impact of controlling private household or vehicle exposure.
Concerning racial and ethnic differences in exposure, our findings are consistent with previous studies concluding that Black nonsmokers have higher serum cotinine levels than do White or Mexican American nonsmokers [6
]. It is also consistent with previous studies that documented differences between Black and White smokers [12
One question that these data raise is whether ethnic/demographic differences in African Americans, males, and children are due to their differences in nicotine metabolism. In 1998, Pérez-Stable et al. [12
] reported that African Americans take in more nicotine per cigarette than whites, which may explain why African Americans have a higher incidence of lung cancer. In general, African Americans have a slower rate of nicotine metabolism than Caucasians, resulting in greater accumulation of cotinine.
The results from the 2-way interaction between age and gender are notable, showing the highest exposure levels in children and adolescents age 4-19 years of non-Hispanic Black descent as compared with other comparison groups over time. This finding is consistent with previous studies linking a lower socioeconomic status to a greater probability of SHS exposure in children. Previous research has suggested that persons with low income are more likely to be exposed in the home than are other income groups. Specifically, 58% of children in households with annual incomes under $10,000 per year experience SHS exposure, as compared with 30% of children in households with annual incomes greater than $40,000 [14
]. It has been previously documented that African Americans earn less money per year and have the highest poverty rates as compared with other race/ethnicity groups [15
Our study has some strengths and limitations that should be noted. The data used in this analysis comes from a large national sample of individuals who are representative of the United States civilian non-institutionalized population. To validate the differences and/or similarities that are observed over time, consistent methodology was utilized across all time periods examined. One important caveat to consider in understanding the current study findings is the tool being used to characterize exposures over time. While cotinine represents the most widely used biomarker (primarily due to its specificity, half-life, and ease of measurement), questionnaire reports remain the primary tool to track exposures over a certain time period. Previous findings from questionnaire reports have been compared with biomarker data and have demonstrated high degrees of correlation between the two ways of exposure assessment [16
]. In addition, this study is currently missing an in-depth analysis of chronic conditions (e.g., asthma attacks and lung cancer) given infrequent observations within a single wave of data. Such information would better inform and substantiate our understanding of the relationship between serum cotinine levels and impact on various health risks.
Important GAPS and research questions remain concerning the progress and impact of reducing SHS exposure. Despite the relatively widespread implementation of smoke-free laws in the US, there are opportunities for states to implement greater protection. We now know that only 100% smoke-free indoor air laws can effectively protect the public from secondhand smoke. Yet, as of the end of 2008, only 16 states have provided 100% smoke-free indoor air laws for bars, restaurants, government worksites, and private worksites [17
]. The extent of smoke-free legislation was likely even less comprehensive two years prior, during which the data for the current analysis was captured (2001 - 2006). It is possible that an analysis using post-2006 data may demonstrate improvements though these data were not available at the time of the current study. In addition, indoor spaces such as homes and vehicles represent another critical area of focus with regard to reducing a major location of exposure.
Finally, it is possible that the measurement of secondhand smoke exposure using serum cotinine analysis is approaching its limits of detection and possibly introducing challenges to demonstrate further declines in exposure. Further efforts of continuous method improvements could lead to more sensitive instruments that will serve to be even more effective in monitoring and detecting further exposure declines.