Triclosan and prescription antibiotic exposures and enterolactone production in adults

• Published in: Environmental research Vol. 142; pp. 66 - 71
• Main Authors: Adgent, Margaret A., Rogan, Walter J.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 01.10.2015
• Subjects: 4-Butyrolactone - analogs & derivatives; 4-Butyrolactone - analysis; 4-Butyrolactone - biosynthesis; Adjustment; Adult; Anti-Bacterial Agents - adverse effects; Anti-Bacterial Agents - urine; Antibiotics; Antiinfectives and antibacterials; Antimicrobial; Bacteria; Derivatives; Enterolactone; Exposure; Female; Gastrointestinal Microbiome - drug effects; Gastrointestinal Microbiome - physiology; Humans; Intestinal metabolite; Lignans; Lignans - analysis; Lignans - biosynthesis; Male; Middle Aged; NHANES; Nutrition; Prescription Drugs; Triclosan; Triclosan - adverse effects; Triclosan - urine; Young Adult; Antimicrobial; NHANES; Triclosan; Enterolactone; Intestinal metabolite
• ISSN: 0013-9351; 1096-0953
• DOI: 10.1016/j.envres.2015.06.017

The gut microbiome plays an important role in the development of disease. The composition of the microbiome is influenced by factors such as mode of delivery at birth, diet and antibiotic use, yet the influence of environmental chemical exposures is largely unknown. The antimicrobial compound triclosan, found in many personal care products and widely detected in human urine, is an environmental exposure for which systemic microbiotic effects may be of particular interest. To investigate the relationship between triclosan and gut microflora, we assessed the association between triclosan and enterolactone, an intestinal metabolite that is produced via bacterial transformation of dietary lignans (seeds, nuts) and has known susceptibility to oral antibiotics. We examined urinary triclosan and enterolactone for 2005-2008 U.S. National Health and Nutrition Examination Survey subjects, aged ≥20 years (n=3041). We also examined the association between prescription antibiotic use and enterolactone to confirm its susceptibility to changes in bacterial composition of the body. Associations between natural log-transformed enterolactone and (1) detected vs. not detected (<2.3ng/mL) triclosan, (2) triclosan quintiles (Q1–Q5), and (3) any vs. no antibiotics were estimated with multiple linear regression, adjusting for sex, age, race, body mass index, poverty income ratio, education, fiber intake, bowel movement frequency, cotinine and creatinine (n=2441). Triclosan was detected in 80% of subjects (range: <2.3–3620ng/mL), while enterolactone was detected in >99% of subjects (range: <0.1–122,000ng/mL). After adjustment, enterolactone was not associated with triclosan (detect vs. non-detect: β= 0.07 (95% CI: −0.15, 0.30); Q5 (≥104.5ng/mL) vs. Q1 (none): β= 0.06 (95% CI: −0.21, 0.34)). In sex-stratified analyses, triclosan was associated with higher enterolactone in women (detect vs. non-detect: β= 0.31 (95% CI: −0.07, 0.70), but not men β= −0.18 (95% CI: −0.47, 0.11). However, any antibiotic use (n=112), as compared to no antibiotic use, was associated with significantly lower enterolactone (β=−0.78 (95%CI: −1.22, −0.36)), with no sex-specific effects. This association was driven by inverse associations with the following antibiotic classes: macrolide derivatives, quinolones, sulfonamides, and lincomycin derivatives. Antibiotics, but not triclosan, are negatively associated with urinary enterolactone. Antibiotics may reduce enterolactone by killing certain gut bacteria. At levels detected in the U.S., triclosan does not appear to be acting similarly, despite broad antimicrobial properties. Additional study of determinants of triclosan exposure and enterolactone production may be needed to better understand positive associations among women. •Human exposure to antimicrobial triclosan is widespread.•Enterolactone is made by bacterial conversion of dietary lignans in the human gut.•Enterolactone decreases with antibiotic use, but not in association with triclosan.•Antibiotics and triclosan may not be acting similarly upon intestinal microflora.