We detected concentrations of free plus conjugated species of triclosan in urine in 74.6% of the samples examined. This high frequency of detection is most likely associated with daily use by the U.S. general population of consumer products that contain triclosan, including at least one toothpaste brand (Food and Drug Administration 1997), skin-care products (e.g., soap, deodorant, skin cleanser), and other household products (e.g., pet care, cleaners) (National Library of Medicine 2007). In humans, triclosan can be absorbed through skin (Moss et al. 2000) and through the mucosa in the mouth and intestinal tract (Lin 2000; Sandborgh-Englund et al. 2006). The detection of triclosan in blood (Hovander et al. 2002; Sandborgh-Englund et al. 2006), urine (Sandborgh-Englund et al. 2006; Wolff et al. 2007; Ye et al. 2005), and milk (Allmyr et al. 2006) collected from small groups of persons in the United States and Sweden suggests that the general population is exposed to triclosan.
The range of urinary concentrations of triclosan in the NHANES 2003-2004 sample was wide, with 25% of persons examined having concentrations < 2.3 µg/L, and 5% of the participants having concentrations > 363.8 µg/g creatinine ( Table 1 ). A wide distribution of concentrations of triclosan has also been reported for 10 healthy Swedish volunteers, five of whom related using personal-hygiene products that contained triclosan (Sandborgh-Englund et al. 2006). In the Swedish study, the baseline urinary excretion of triclosan (determined from 24-hr urine samples) was 0.1-743 µg/day among people not using triclosan-containing products, and 21-218 µg/day among users of triclosan-containing products. In another Swedish study involving a group of 36 nursing women, triclosan concentrations were higher in both plasma and milk among the women who used personal care products containing triclosan than in the women who did not (Allmyr et al. 2006). These data suggest that personal care products may be a principal source of exposure to triclosan in humans. The wide range of concentrations of triclosan may be attributable to differences in exposure, as well as to individual variations in distribution kinetics and metabolism (Sandborgh-Englund et al. 2006).
Data are limited on the urinary concentrations of triclosan in human populations. In a pilot study, triclosan was detected in 67.8% of 90 prepubertal girls, with mean age of 7.77 years, from New York City, New York; Cincinnati, Ohio; and Northern California (Wolff et al. 2007). The median concentration (5.9 µg/L) was comparable to the median concentration of triclosan for the 341 children 6-11 years of age in this NHANES 2003-2004 population (7.2 µg/L).
As is true for other nonpersistent chemicals (Fenske et al. 2005; Hauser et al. 2004; Hoppin et al. 2002; Meeker et al. 2005), within-person variability in urinary concentrations of triclosan exists. Despite this variability, results from one recent study suggest that triclosan concentrations in a single urine sample can be used to categorize the 6-month average exposure to triclosan among a group of 35 children (Teitelbaum et al. 2007). More important, concentrations based on one spot sample per person can be useful in calculating mean population concentration estimates in cross-sectional studies such as NHANES.
We observed a curvilinear-increased relation between age and triclosan LSGM concentration for people ≥ 6 years of age. For people ≥ 20 years of age, concentrations appeared to decline as age increases (Figure 1 and Table 2 ). These data suggest that the concentrations of urinary species of triclosan peak around the third decade of life and then slowly decrease. This relation between age and triclosan concentration is not clearly understood, and these differences might reflect differences in lifestyle choices affecting exposure and/or pharmacokinetic factors based on age.
We did not observe differences in the adjusted LSGM concentrations of triclosan based on race/ethnicity or sex. LSGM triclosan concentrations were significantly higher among people in the high household income category than among people in the medium (p = 0.04) and low (p < 0.01) income categories. These differences might reflect differences in lifestyle choices (e.g., use of personal care products) that affect exposure to triclosan.
In summary, these NHANES 2003-2004 triclosan data can be used to establish a nationally representative baseline assessment of exposure, a baseline to which the triclosan concentrations in future populations can be compared to identify exposure trends. The reported high frequency of detection of triclosan and the differences in urinary concentrations based on age and socioeconomic status highlight the importance of additional research to identify the sources and potential routes of human exposure to triclosan. In addition, these data provide exposure information that can be useful for risk assessment if toxicologic or epidemiologic studies so indicate.
We thank J. Ekong for technical assistance, and J. Osterloh and J. Pirkle for useful comments.Reprint Address
A.M. Calafat, Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, 4770 Buford Hwy., NE, Mailstop F53, Atlanta, GA 30341. Telephone: (770) 488-7891. Fax: (770) 488-4609. E-mail: Acalafat@cdc.gov .
Environ Health Perspect. 2008;116(3):303-307. © 2008 National Institute of Environmental Health Sciences
Cite this: Urinary Concentrations of Triclosan in the U.S. Population: 2003-2004 - Medscape - Mar 01, 2008.