Trends in the Exposure of Nonsmokers in the U.S. Population to Secondhand Smoke: 1988–2002

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 non-smokers 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.

Passive smoking and the use of noncigarette tobacco products in association with risk for pancreatic cancer: A case‐control study

“…Our control recruitment excluded individuals who were accompanying patients who had cancers that were associated strongly with cigarette smoking, eg, lung cancer and head and neck cancer. Consequently, the prevalence of passive smoking exposure among noncigarette-smoking controls was comparable to that reported for United States adults by Pirkle et al 15 and in other population-based studies. 35,36 Previous studies conducted in this country and in Europe have reported positive associations between the use of pipes, smokeless tobacco, and cigars and pancreatic cancer.…”

“…The greatest prevalence of exposure was reported among African Americans. 15 Previous studies demonstrated that passive smoking is associated positively with an increased risk for lung cancer and breast cancers. [16][17][18][19] The relation between passive smoking and pancreatic cancer previously had been investigated in only 1 study.…”

Analysis of [3′,3′-d2]-nicotine and [3′,3′-d2]-cotinine by capillary liquid chromatography–electrospray tandem mass spectrometry

“…In both tobacco users and individuals using nicotine replacement therapies greater than 70% of the nicotine dose is converted to cotinine, which is subsequently oxidized to trans-3′-hydroxycotinine [3]. Plasma cotinine concentrations are routinely used to assess both tobacco use and environmental tobacco smoke exposure (ETS) [6][7][8]. However, plasma cotinine levels vary as much as two fold due to individual differences in nicotine metabolism [3].…”

Tobacco Industry Efforts Undermining Evidence Linking Secondhand Smoke With Cardiovascular Disease

“…The urinary cotinine levels of nonsmokers in nonsmoking households were 8.6Ϯ10.8 (SD) ng/mL, indicating substantial SHS exposure, which is not surprising in Germany, which has no meaningful public smoking restrictions. 101 (Serum cotinine is detectable at 0.05 ng/mL, 104 with urine levels Ϸ6 times higher than serum; 105 a serum cotinine level of 0.7 ng/mL indicates enough SHS exposure to have effects on CVD events. 9 ) More important, Smith's interpretation that thromboxane release did not differ between active smokers and nonsmokers because of large smoke exposures may reflect the fact that the nonsmoker platelets were already sensitized to SHS because of high SHS exposure outside the home.…”

“…The average serum cotinine for the nonsmokers not exposed to SHS was 0.2Ϯ0.6 (SD) ng/mL, 91 indicating substantial SHS exposure. 104 Reviewers 125 of the manuscript for Toxicological Sciences questioned the variation in the thromboxane levels because the nonsmokers not exposed to SHS had a higher level of urinary thromboxane than the nonsmokers exposed to SHS. In the final published article, 91 Smith acknowledged that these results were not consistent with previous literature 94,95 suggesting that thromboxane was released with active smoking but suggested that the higher levels were due to an unknown stress (although Smith did not find that oxidative or hormonal stress was significantly associated).…”