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Disparities in Secondhand Smoke Exposure --- United States, 1988--1994 and 1999--2004

No level of exposure to secondhand smoke (SHS) is safe (1). Breathing SHS can cause heart disease and lung cancer in nonsmoking adults and increases the risk for sudden infant death syndrome, acute respiratory infections, middle-ear disease, and exacerbation of asthma in children (1--3). In the United States, exposure to SHS declined approximately 70% from the late 1980s through 2002, most likely reflecting widespread implementation of laws and policies prohibiting smoking in indoor workplaces and public places during this period (1,4). Although the major sources of SHS exposure for nonsmoking adults are the home and workplace, the primary source of SHS exposure for children is the home (1); therefore, eliminating smoking in workplaces and public places is less likely to reduce children's exposure to SHS. This report examines changes in the prevalence of self-reported SHS exposure at home and changes in any exposure, as measured by serum cotinine (a biologic indicator of SHS exposure), in nonsmoking children, adolescents, and adults. The analysis was conducted using data from the 1988--1994 and 1999--2004 National Health and Nutrition Examination Surveys (NHANES). The results indicated that self-reported SHS exposure at home and SHS exposure as measured by serum cotinine declined significantly (i.e., by 51.2% and 44.7%, respectively) in the U.S. population from 1988--1994 to 1999--2004; however, the decline was smaller for persons aged 4--11 years and 12--19 years. These results underscore the need to continue surveillance of SHS exposure and to focus on strategies to reduce children's SHS exposure.

NHANES consists of a series of cross-sectional surveys designed to monitor the health and nutritional status of the U.S. civilian, noninstitutionalized population. Participants were selected through a complex, multistage probability design and completed a household interview and standardized physical examination in specially equipped mobile examination centers. Subgroups of the population, including blacks and Mexican Americans, were oversampled to provide reliable estimates for these groups. For persons aged >4 years in 1988--1994 and aged >3 years in 1999--2004, blood was collected by venipuncture and serum cotinine levels were measured in blood samples using a high performance liquid chromatography mass spectrometry method at CDC. Serum cotinine levels indicate exposure to nicotine during the past 3--4 days (4).

The study sample was limited to nonsmokers aged >4 years. Nonsmokers were defined as respondents with serum cotinine <10 ng/mL. Respondents aged >12 years were excluded if, at the examination, they reported tobacco or nicotine use during the past 5 days. Serum cotinine measures were available for 83.7% (N = 22,377) of examined persons aged >4 years in 1988--1994 and for 89.9% (N = 22,994) in 1999--2004.

The final sample size for nonsmokers was 17,261 in 1988--1994 and 17,931 in 1999--2004. Exposure to SHS in nonsmokers was defined as a detectable serum cotinine level of >0.05 ng/mL (i.e., the laboratory limit of detection during 1988--1994 and 1999--2000). Serum cotinine was not used as a continuous variable because approximately 50% of results were below the laboratory limit of detection in the study population during 1999--2000. Exposure to SHS inside the home was defined as the presence of at least one household member who smoked cigarettes inside the home.*

The percentage of persons with self-reported home SHS exposure, the percentage with detectable serum cotinine, stratified by age group (4--11 years, 12--19 years, and >20 years), race/ethnicity (non-Hispanic white, non-Hispanic black, and Mexican American), and other demographic characteristics were calculated. Data analyses accounted for the complex survey design, differential probabilities of sample selection, nonresponse, and sample noncoverage. Differences between population subgroups and between periods were evaluated using a univariate t-statistic. All significance tests were two-sided using p<0.05 as the level of statistical significance.

The percentage of the U.S. nonsmoking population aged >4 years with self-reported home SHS exposure declined from 20.9% in 1988--1994 to 10.2% in 1999--2004 (Table). Similarly, the percentage of the nonsmoking population with detectable serum cotinine declined significantly, from 83.9% in 1988--1994 to 46.4% in 1999--2004. The decline was statistically significant within all subgroups of the study population for both measures of exposure.

The percentage of nonsmokers with detectable serum cotinine was uniformly high for all age groups during 1988--1994. The percentage decreased for all age groups during 1999--2004, and remained highest for those aged 4--11 years (60.5%) and those aged 12--19 years (55.4%) compared with those aged >20 years (42.2%). The decline in the prevalence of detectable serum cotinine was 28.1% for those aged 4--11 years, 35.1% for those aged 12--19 years, and 49.5% for those aged >20 years.

During 1988--1994, non-Hispanic blacks were more likely than non-Hispanic whites and Mexican Americans to have detectable serum cotinine (93.7%, 83.2%, and 77.7%, respectively). However, by 1999--2004, the gap had increased between non-Hispanic blacks with detectable serum cotinine (70.5%) and non-Hispanic whites (43.0%) and Mexican Americans (40.0%). The percentage of nonsmokers with detectable serum cotinine was inversely associated with family income in both periods, and the decline over time was smaller for the lowest income group compared with the higher income groups.

Although the percentage decrease in home SHS exposure from 1988--1994 to 1999--2004 was seen for persons of all ages, it was smaller in children, especially those aged 4--11 years, compared with those aged >20 years. For SHS exposure in the home, the declines were 37.7%, 44.9%, and 59.8% among those aged 4--11 years, 12--19 years, and >20 years, respectively.

During both periods, prevalence of SHS exposure in the home was highest among non-Hispanic blacks and for persons with lower incomes. For both periods, self-reported home SHS exposure was not significantly different in males than in females, but a higher percentage of males had detectable serum cotinine than did females.

Reported by: SE Schober PhD, C Zhang, DJ Brody, MPH, Div for National Health and Nutrition Examination Survey, National Center for Health Statistics; C Marano, DrPH, EIS Officer, CDC.

Editorial Note:

This report assesses changes in exposure to SHS among nonsmokers from self-reported information about cigarette smoke exposure in the home and by serum cotinine levels. Based on both measures, SHS exposure decreased markedly from 1988--1994 to 1999--2004 for the total U.S. population and major population subgroups. However, despite the decreases in SHS exposure, 46.4% of U.S. nonsmokers still had detectable levels of serum cotinine during 1999--2004, indicating that SHS exposure remains an important public health problem.

Documented reductions in SHS exposure since the late 1980s have been attributed to widespread implementation of laws and policies restricting or eliminating exposure in workplaces and public places during this period (4,5). Additionally, the prevalence of cigarette smoking has decreased during this period, from 28% in 1988 to 21% in 2004 (6), which likely reduced SHS exposure, particularly in the home.

A recent study reported that the proportion of households that have rules against smoking in the home has increased since the early 1990s, from 43% in 1992--1993 to 72% in 2003 (7). That parallels the decline in the prevalence of SHS exposure in the home reported in this study. However, a higher prevalence of SHS exposure was still evident in the groups aged 4--11 years and 12--19 years compared with the group aged >20 years during 1999--2004, a pattern that has been noted previously (4). Additionally, the disparity in exposure between those aged 4--11 years and 12--19 years compared with those aged >20 years has widened since the early 1990s. The major source of SHS exposure for those aged 4--11 years is from parental smoking in the home (8).

This analysis determined that the decrease in home SHS exposure from 1988--1994 to 1999--2004 was similar for non-Hispanic blacks and non-Hispanic whites. For SHS exposure as measured by serum cotinine, however, the relative decline was nearly twice as large for non-Hispanic whites compared with non-Hispanic blacks. Previous studies have noted that non-Hispanic blacks have higher serum cotinine levels than non-Hispanic whites, both for smokers and nonsmokers, and that differences in nicotine metabolism might partially explain this disparity (4). At least one study that assessed multiple sources of SHS exposure reported that among nonsmokers, non-Hispanic blacks had higher levels of SHS exposure than other groups, which explained the higher serum cotinine levels in non-Hispanic blacks (9). Information about other sources of exposure to SHS is needed to interpret the disparity between non-Hispanic whites and non-Hispanic blacks in the percentage with detectable serum cotinine in the NHANES surveys.

The findings in this report are subject to at least three limitations. First, the assessment of self-reported home SHS exposure is based only on information about household members who smoke inside the home. Information about smoking inside the home by visitors was not collected. Second, information is not available about potential SHS exposure in locations outside of the home, including automobiles, workplaces, public places, and other homes. Information about smoker behaviors to protect nonsmokers from SHS exposure in the home also was not obtained. Finally, measurement of serum cotinine levels in nonsmokers only provides a measure of overall SHS exposure, regardless of the sources of exposure.

The U.S. Surgeon General has concluded that protecting nonsmokers from SHS exposure can only be accomplished by completely eliminating smoking in indoor places (1). SHS exposure among nonsmokers has declined markedly during the past 2 decades, largely through implementation of laws and policies that prohibit smoking in workplaces and public places (4,6). Despite this success in reducing SHS exposure, the results of this study underscore the need for ongoing prevention efforts to reduce SHS exposure with strategies that focus on protection for those at greatest risk (10).

References

  1. US Department of Health and Human Services. The health consequences of involuntary exposure to tobacco smoke: a report of the Surgeon General. Atlanta, GA: US Department of Health and Human Services, CDC; 2006. Available at http://www.cdc.gov/tobacco/data_statistics/sgr/sgr_2006/index.htm.
  2. California Environmental Protection Agency. Proposed identification of environmental tobacco smoke as a toxic air contaminant. Sacramento, CA: Office of Environmental Health Hazard Assessment; 2005. Available at http://www.arb.ca.gov/regact/ets2006/ets2006.htm.
  3. World Health Organization International Agency for Research on Cancer. Monographs on the evaluation of carcinogenic risks to humans. Volume 83: tobacco smoke and involuntary smoking. Lyon, France: IARC Press; 2004.
  4. Pirkle JL, Bernert JT, Caudill SP, Sosnoff CS, Pechacek TF. Trends in the exposure of nonsmokers in the U.S. population to secondhand smoke. Environ Health Perspect 2006;114:853--8.
  5. Pickett MS, Schober SE, Brody DJ, Curtin LR, Giovino GA. Smoke-free laws and secondhand smoke exposure in US non-smoking adults, 1999--2002. Tob Control 2006;15:302--7.
  6. National Center for Health Statistics. Health, United States, 2006. With chartbook on trends in the health of Americans. Hyattsville, MD: US Department of Health and Human Services, CDC, National Center for Health Statistics; 2006. Available at http://www.cdc.gov/nchs/data/hus/hus06.pdf.
  7. CDC. State-specific prevalence of smoke-free home rules---United States, 1992--2003. MMWR 2007;56:501--4.
  8. Jarvis MJ, Goddard E, Higgins V, Feyerabend C, Bryant A, Cook DG. Children's exposure to passive smoking in England since the 1980s: cotinine evidence from population surveys. BMJ 2000;321:343--5.
  9. Wagenknecht LE, Manolio TA, Sidney S, Burke GL, Haley NJ. Environmental tobacco smoke exposure as determined by cotinine in black and white young adults: the CARDIA study. Environ Res 1993;63: 39--46.
  10. CDC. Best practices for comprehensive tobacco control programs---2007. Atlanta, GA: US Department of Health and Human Services, CDC; 2007. Available at http://www.cdc.gov/tobacco/tobacco_control_programs/stateandcommunity/best_practices.

* As determined by responses to questions in NHANES 1988--1994 ("Does anyone who lives here smoke cigarettes in the home?") and NHANES 1999--2004 ("Does anyone who lives here smoke cigarettes, cigars, or pipes anywhere inside this home?" and for each household member who smokes: "How many cigarettes per day do you/does [PERSON] usually smoke anywhere inside the home?").

Table

TABLE. Percentage of nonsmoking persons* who had home exposure to secondhand smoke† and who had detectable serum
cotinine levels (>0.05 ng/mL) — National Health and Nutrition Examination Survey (NHANES), United States, 1988–1994 and 1999–2004§
Sample size Home exposure Detectable serum cotinine
NHANES NHANES NHANES NHANES NHANES
1988– 1999– 1988–1994 1999–2004 Decrease 1988–1994 1999–2004 Decrease
Characteristic 1994 2004 % (95% CIΆ) % (95% CI) (%) % (95% CI) % (95% CI) (%)
Total 17,261 17,931 20.9 (19.1–22.8) 10.2 (9.2–11.2) 51.2 83.9 (81.4–86.2) 46.4 (43.0–50.0) 44.7
Sex
Male 7,734 8,203 21.0 (19.0–23.3) 10.5 (9.5–11.5) 50.0 87.1 (84.8–89.1)Ά 51.2 (47.4–54.9)Ά 41.2
Female 9,527 9,728 20.8 (18.7–23.1) 10.0 (8.9–11.2) 51.9 81.3 (78.1–84.1)Ά 42.5 (39.1–46.0)Ά 47.7
Age group (yrs)
4–11 3,926 3,395 38.2 (34.4–42.2)** 23.8 (20.7–27.2)** 37.7 84.5 (81.0–87.5) 60.5 (55.7–65.2)** 28.1
12–19 2,508 5,127 35.4 (31.8–39.2)** 19.5 (17.2–22.0)** 44.9 85.4 (81.3–88.7) 55.4 (50.6–60.0)** 35.1
>20 (referent) 10,827 9,409 14.7 (13.2–16.4) 5.9 (5.3–6.7) 59.8 83.5 (80.8–85.9) 42.2 (38.7–45.7) 49.5
Race/Ethnicity††
Mexican American 5,595 5,415 21.9 (19.1–25.0)** 6.8 (5.4–8.6)** 68.5 77.7 (72.7–82.1)** 40.0 (35.1–45.1) 48.5
White, non-Hispanic
(referent) 6,171 6,860 18.6 (16.3–21.1) 9.8 (8.6–11.2) 47.3 83.2 (80.3–85.7) 43.0 (38.8–47.3) 48.3
Black, non-Hispanic 4,710 4,206 30.7 (28.2–33.3)** 15.4 (13.7–17.2)** 49.8 93.7 (92.1–95.0)** 70.5 (67.0–73.7)** 24.8
PIR§§
0–1.3 (referent) 5,911 5,841 31.5 (27.8–35.5) 17.9 (15.2–21.0) 43.2 87.6 (84.6–90.0) 62.7 (57.2–67.8) 28.4
1.3–3.0 5,671 5,274 22.7 (20.0–25.7)** 11.7 (10.3–13.4)** 48.4 84.0 (80.8–86.8) 48.7 (44.6–53.0)** 42.0
>3.0 4,143 5,582 14.0 (11.7–16.6)** 5.9 (5.1–7.0)** 57.9 81.8 (78.2–84.3)** 37.4 (34.0–41.0)** 54.3
* Respondents with serum cotinine <10 ng/mL, and for respondents aged >12 years, those who at the time of venipuncture reported no tobacco or nicotine product use in the
past 5 days.
† The presence of at least one household member who smokes in the home.
§ The differences between 1988–1994 and 1999–2004 in the percentage with home exposure to tobacco smoke and the percentage with detectable serum cotinine levels were
statistically significant for the total population and all population subgroups shown in the table.
Ά Confidence interval.
** p<0.05, by t-test for difference from referent.
†† Estimates for persons of other racial/ethnic groups are not included here but are included in all other estimates in the table.
§§ Poverty income ratio, defined as the ratio of family income to the U.S. Census Bureau poverty threshold accounting for family size; it was classified as low income (<1.3),
middle income (1.3–3.0), and high income (>3.0).
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Date last reviewed: 7/9/2008

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