Trends in Exposure of Nonsmokers
Trends in Exposure of Nonsmokers
The objective of this study was to describe the exposure of nonsmokers in the U.S. population to secondhand smoke (SHS) using serum cotinine concentrations measured over a period of 14 years, from October 1988 through December 2002. This study consists of a series of National Health and Nutrition Examination Surveys (NHANES) measuring serum cotinine as an index of SHS exposure of participants. Study participants were individuals representative of the U.S. civilian, noninstitutionalized population, ≥ 4 years of age. We analyzed serum cotinine and interview data from NHANES obtained during surveys conducted during four distinct time periods. Our results document a substantial decline of approximately 70% in serum cotinine concentrations in nonsmokers during this period. This decrease was reflected in all groups within the population regardless of age, sex, or race/ethnicity. The large decrease that we observed in serum cotinine concentrations suggests a substantial reduction in the exposure of the U.S. population to SHS during the 1990s. The exposure of nonsmokers to SHS represents an important public health concern. Our findings suggest that recent public health efforts to reduce such exposures have had an important effect, although children and non-Hispanic black nonsmokers show relatively higher levels of serum cotinine.
Health risks associated with the active use of tobacco have been documented extensively over many years. After the first Surgeon General's report on smoking and health in 1964, the prevalence of cigarette smoking in the United States began a gradual decline [Department of Health and Human Services (DHHS) 2000a], although the use of tobacco continues to be an important problem and remains the leading preventable cause of death and disability in the United States (DHHS 2004). In addition to mainstream smoke that is inhaled by the smoker, burning cigarettes also generate secondhand smoke [SHS; also sometimes referred to as environmental tobacco smoke (ETS)] that is formed from smoke emitted into the environment from the smoldering tip of the cigarette, mixed with smoke exhaled by the smoker [National Research Council (NRC) 1986]. Involuntary smoking results when nonsmokers are exposed to SHS, and health risks for nonsmokers posed by involuntary smoking were gradually realized. As early as 1972, the topic of SHS and the potential risk faced by nonsmokers exposed to SHS were noted in a Surgeon General's report addressing the use of tobacco (DHHS 1972). An important further impetus for investigations regarding adverse health effects from SHS exposure resulted from the 1986 Surgeon General's report (DHHS 1986), which for the first time focused on the health risks of SHS, and also from two influential reports by the National Research Council (NRC 1986) and the U.S. Environmental Protection Agency (U.S. EPA 1992). Both reports concluded that exposure to SHS causes lung cancer in nonsmokers and has other adverse effects in both adults and children. Several subsequent reports have confirmed and extended this link between SHS and adverse health effects (Jaakola and Samet 1999; National Cancer Institute 1999), which may include cancer, asthma, respiratory infections, decreased pulmonary function, and cardiovascular disease.
Despite the increasing awareness that SHS represents an important public health concern, the extent of the problem was initially difficult to measure because data on the exposure of nonsmokers were limited and often depended solely on self-reported exposure or on inferences, such as living with a smoker, rather than on direct measurements. However, objective biomarkers of exposure to tobacco have been identified and validated (Benowitz 1983, 1996; Jarvis et al. 1988), and an expert panel convened to review the prospects for biomarker measurements as an index of SHS exposure concluded that plasma cotinine was the marker of choice (Watts et al. 1990). Cotinine, the primary proximate metabolite of nicotine, is specific for exposure to tobacco, and it is preferred as a marker over nicotine itself partly because the half-life of cotinine in the body of about 18 hr (Benowitz 1983; Jarvis et al. 1988) is much longer than that of nicotine. Serum cotinine can mark the exposure of an individual to tobacco only over the previous few days, and it is subject to interindividual variations in the metabolism of nicotine. However, these limitations are not substantial drawbacks when comparing mean values from groups of people, and in a review, Benowitz (1996) concluded that the evidence supports cotinine measurements providing "a valid and quantitative measure of average human ETS exposure over time."
The first national survey of SHS exposure of the entire U.S. population based on serum cotinine measurements was conducted as part of the Third National Health and Nutrition Examination Survey (NHANES III) that covered the time period of 1988-1994. NHANES III consisted of two phases, and we previously reported the results of cotinine measurements conducted with > 10,000 participants ≥ 4 years of age from phase 1, extending from 1988 through 1991 (Pirkle et al. 1996). Our results at that time indicated widespread exposure of the population to tobacco smoke. Overall, 88% of nonsmokers in the U.S. population in that study were found to have detectable levels (≥ 0.050 ng/mL) of cotinine in their blood, and certain groups of nonsmokers, including blacks, males, and children, were found to be at elevated risk of exposure based on their serum cotinine levels (Pirkle et al. 1996).
After phase 1, additional data were acquired during the continuation of NHANES III in phase 2, which extended from 1991 through 1994. No further studies were conducted during 1995-1998, but NHANES resumed in 1999 and has been continuous from that time onward, providing a new sampling of the U.S. population every 2 years. Serum cotinine was measured in NHANES III (1988-1994), in NHANES 1999-2000, and NHANES 2001-2002. Thus, we now have acquired data from NHANES for > 10 years that represent exposures after our initial report from the time period 1988-1991 (Pirkle et al. 1996). We report here the analysis of these data extending from 1988 through 2002, which indicates a decreasing trend in SHS exposure of nonsmokers in the United States, most likely reflecting extensive efforts made by the public health community during this time to reduce smoking in the home and the exposure of nonsmokers in public places. However, our results also indicate that two groups in the population, blacks and children, show relatively higher levels of SHS exposure during this time, suggesting that further work should provide special focus on these at-risk groups.
Abstract and Introduction
Abstract
The objective of this study was to describe the exposure of nonsmokers in the U.S. population to secondhand smoke (SHS) using serum cotinine concentrations measured over a period of 14 years, from October 1988 through December 2002. This study consists of a series of National Health and Nutrition Examination Surveys (NHANES) measuring serum cotinine as an index of SHS exposure of participants. Study participants were individuals representative of the U.S. civilian, noninstitutionalized population, ≥ 4 years of age. We analyzed serum cotinine and interview data from NHANES obtained during surveys conducted during four distinct time periods. Our results document a substantial decline of approximately 70% in serum cotinine concentrations in nonsmokers during this period. This decrease was reflected in all groups within the population regardless of age, sex, or race/ethnicity. The large decrease that we observed in serum cotinine concentrations suggests a substantial reduction in the exposure of the U.S. population to SHS during the 1990s. The exposure of nonsmokers to SHS represents an important public health concern. Our findings suggest that recent public health efforts to reduce such exposures have had an important effect, although children and non-Hispanic black nonsmokers show relatively higher levels of serum cotinine.
Introduction
Health risks associated with the active use of tobacco have been documented extensively over many years. After the first Surgeon General's report on smoking and health in 1964, the prevalence of cigarette smoking in the United States began a gradual decline [Department of Health and Human Services (DHHS) 2000a], although the use of tobacco continues to be an important problem and remains the leading preventable cause of death and disability in the United States (DHHS 2004). In addition to mainstream smoke that is inhaled by the smoker, burning cigarettes also generate secondhand smoke [SHS; also sometimes referred to as environmental tobacco smoke (ETS)] that is formed from smoke emitted into the environment from the smoldering tip of the cigarette, mixed with smoke exhaled by the smoker [National Research Council (NRC) 1986]. Involuntary smoking results when nonsmokers are exposed to SHS, and health risks for nonsmokers posed by involuntary smoking were gradually realized. As early as 1972, the topic of SHS and the potential risk faced by nonsmokers exposed to SHS were noted in a Surgeon General's report addressing the use of tobacco (DHHS 1972). An important further impetus for investigations regarding adverse health effects from SHS exposure resulted from the 1986 Surgeon General's report (DHHS 1986), which for the first time focused on the health risks of SHS, and also from two influential reports by the National Research Council (NRC 1986) and the U.S. Environmental Protection Agency (U.S. EPA 1992). Both reports concluded that exposure to SHS causes lung cancer in nonsmokers and has other adverse effects in both adults and children. Several subsequent reports have confirmed and extended this link between SHS and adverse health effects (Jaakola and Samet 1999; National Cancer Institute 1999), which may include cancer, asthma, respiratory infections, decreased pulmonary function, and cardiovascular disease.
Despite the increasing awareness that SHS represents an important public health concern, the extent of the problem was initially difficult to measure because data on the exposure of nonsmokers were limited and often depended solely on self-reported exposure or on inferences, such as living with a smoker, rather than on direct measurements. However, objective biomarkers of exposure to tobacco have been identified and validated (Benowitz 1983, 1996; Jarvis et al. 1988), and an expert panel convened to review the prospects for biomarker measurements as an index of SHS exposure concluded that plasma cotinine was the marker of choice (Watts et al. 1990). Cotinine, the primary proximate metabolite of nicotine, is specific for exposure to tobacco, and it is preferred as a marker over nicotine itself partly because the half-life of cotinine in the body of about 18 hr (Benowitz 1983; Jarvis et al. 1988) is much longer than that of nicotine. Serum cotinine can mark the exposure of an individual to tobacco only over the previous few days, and it is subject to interindividual variations in the metabolism of nicotine. However, these limitations are not substantial drawbacks when comparing mean values from groups of people, and in a review, Benowitz (1996) concluded that the evidence supports cotinine measurements providing "a valid and quantitative measure of average human ETS exposure over time."
The first national survey of SHS exposure of the entire U.S. population based on serum cotinine measurements was conducted as part of the Third National Health and Nutrition Examination Survey (NHANES III) that covered the time period of 1988-1994. NHANES III consisted of two phases, and we previously reported the results of cotinine measurements conducted with > 10,000 participants ≥ 4 years of age from phase 1, extending from 1988 through 1991 (Pirkle et al. 1996). Our results at that time indicated widespread exposure of the population to tobacco smoke. Overall, 88% of nonsmokers in the U.S. population in that study were found to have detectable levels (≥ 0.050 ng/mL) of cotinine in their blood, and certain groups of nonsmokers, including blacks, males, and children, were found to be at elevated risk of exposure based on their serum cotinine levels (Pirkle et al. 1996).
After phase 1, additional data were acquired during the continuation of NHANES III in phase 2, which extended from 1991 through 1994. No further studies were conducted during 1995-1998, but NHANES resumed in 1999 and has been continuous from that time onward, providing a new sampling of the U.S. population every 2 years. Serum cotinine was measured in NHANES III (1988-1994), in NHANES 1999-2000, and NHANES 2001-2002. Thus, we now have acquired data from NHANES for > 10 years that represent exposures after our initial report from the time period 1988-1991 (Pirkle et al. 1996). We report here the analysis of these data extending from 1988 through 2002, which indicates a decreasing trend in SHS exposure of nonsmokers in the United States, most likely reflecting extensive efforts made by the public health community during this time to reduce smoking in the home and the exposure of nonsmokers in public places. However, our results also indicate that two groups in the population, blacks and children, show relatively higher levels of SHS exposure during this time, suggesting that further work should provide special focus on these at-risk groups.
