Warning: mkdir(): Permission denied in /home/virtual/lib/view_data.php on line 81

Warning: fopen(upload/ip_log/ip_log_2024-11.txt): failed to open stream: No such file or directory in /home/virtual/lib/view_data.php on line 83

Warning: fwrite() expects parameter 1 to be resource, boolean given in /home/virtual/lib/view_data.php on line 84
Relationship between triclosan exposure and thyroid hormones: the Second Korean National Environmental Health Survey (2012–2014)
Skip Navigation
Skip to contents

Ann Occup Environ Med : Annals of Occupational and Environmental Medicine

OPEN ACCESS
SEARCH
Search

Articles

Page Path
HOME > Ann Occup Environ Med > Volume 31; 2019 > Article
Research Article Relationship between triclosan exposure and thyroid hormones: the Second Korean National Environmental Health Survey (2012–2014)
Na-Young Haorcid, Dae Hwan Kimorcid, Ji Young Ryuorcid
Annals of Occupational and Environmental Medicine 2019;31:e22.
DOI: https://doi.org/10.35371/aoem.2019.31.e22
Published online: September 5, 2019

Department of Occupational and Environmental Medicine, Inje University Haeundae Paik Hospital, Busan, Korea.

Correspondence: Ji Young Ryu. Department of Occupational and Environmental Medicine, Inje University Haeundae Paik Hospital, 875 Haeundae-ro, Haeundae-gu, Busan 48108, Korea. lyou77@paik.ac.kr
• Received: July 8, 2019   • Accepted: August 23, 2019

Copyright © 2019 Korean Society of Occupational & Environmental Medicine

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

  • 196 Views
  • 0 Download
  • 13 Web of Science
  • 14 Crossref
  • 15 Scopus
prev next
  • Background
    5-chloro-2-(2,4-dichlorophenoxy)phenol (triclosan) is used as an antiseptic and is a potential endocrine-disrupting chemical that can affect thyroid hormone levels. This study evaluated the relationship between triclosan exposure and thyroid hormones.
  • Methods
    Data from the second Korean National Environmental Health Survey (2012–2014) were analyzed. Triclosan exposure was evaluated using urinary triclosan concentrations and classified into 2 groups: ‘below detection (< limit of detection [LOD])’ vs. ‘detected (≥ LOD).’ Multiple linear regression analysis was conducted to determine the relationship between triclosan exposure and the serum thyroid hormone concentrations, adjusting for age, body mass index, urinary creatinine, and smoking status.
  • Results
    When grouped by sex, triclosan exposure was positively associated with the serum thyroid-stimulating hormone (TSH) concentrations in females with marginal significance (β = 0.066, p = 0.058). However, no significant association was identified between triclosan exposure and serum total triiodothyronine and thyroxine in both males and females, and TSH in males.
  • Conclusions
    This study is the first human study to evaluate the relationship between triclosan exposure and serum thyroid hormone concentrations in the Korean population. There was suggestive positive association between triclosan exposure and the serum TSH in females. Further studies need to evaluate the relationship between long-term exposure to low-dose triclosan and thyroid hormones.
5-chloro-2-(2,4-dichlorophenoxy)phenol (triclosan) is a synthetic compound that has broad antimicrobial action. It is used as an antiseptic in personal hygiene products, such as soaps, body cleansers, hand sanitizers, deodorants, and cosmetics, as well as in textiles, including carpets, socks, underwear, and sportswear [1,2,3]. With dermal application, 10% or less of the triclosan is absorbed into the body, while almost 100% is absorbed with oral ingestion [4]. Once in the body, triclosan is metabolized into glucuronide and sulfate conjugates and excreted mainly in urine [5]. The median excretion half-life of triclosan after oral intake in humans is 11 hours [6].
The toxic effects of triclosan have been studied. There have been several cases of contact dermatitis after using personal hygiene products containing triclosan, such as toothpaste and deodorant [7]. Triclosan may also increase the risk of allergy sensitization [8]. Some studies have suggested that triclosan is a potential endocrine-disrupting chemical that can affect estrogen, testosterone, and thyroid hormone levels [9,10,11,12,13]. In a cohort study, birth outcomes such as birth weight, length, head circumference, and gestational age were inversely related to maternal urinary triclosan levels [14].
Triclosan and thyroxine (T4) have similar molecular structures. Previous studies suggested that triclosan inhibits thyroid function because of this structural similarity [1,15]. A recent meta-analysis of rodent studies showed that the T4 concentration decreased in a dose-dependent manner with postnatal triclosan administration [13]. Triclosan decreased circulating serum total T4 [9,16,17,18] and total triiodothyronine (T3) [17] in rats. Compared to the animal studies that showed a distinct negative association between triclosan exposure and thyroid hormone levels, the results of previous human studies were inconsistent. A U.S. study found a positive association between triclosan and total T3 levels in adolescents [12]. There was a negative correlation between triclosan and serum free T4 in obese women [19]. In a study of pregnant women in the third trimester, triclosan levels were inversely associated with free T4 levels [20]. However, some studies did not show any significant relationship between triclosan exposure and thyroid function [21,22].
Although a few studies have evaluated the effects of triclosan exposure on thyroid function in humans, the results of these studies are inconsistent and, thus, the effect on thyroid hormones in human remains unclear. In this study, we investigated the relationship between triclosan exposure and thyroid hormones in Korean population.
Study participants
Data from The Second Korean National Environmental Health Survey (KoNEHS), which was conducted by the National Institute of Environmental Research under the Ministry of Environment from 2012 to 2014, were analyzed. The survey examined 6,478 subjects from 400 districts who were selected through stratified multistage cluster sampling in proportion to the population distribution. Data were collected through personal interviews, physical examinations, and laboratory tests. We excluded subjects who were pregnant (n = 30) or had thyroid diseases (n = 160). Subjects with missing values (n = 232) or thyroid hormone extremes (n = 66) were also excluded. Finally, 5,990 subjects were included in the analysis.
Covariates
Age, sex, body mass index (BMI), and smoking status were included as variables. BMI was divided into 4 groups: underweight (< 18.50 kg/m2), normal (18.50–22.99 kg/m2), overweight (23.00–24.99 kg/m2), and obese (≥ 25.00 kg/m2). Smoking status was grouped into 2 conditions based on questionnaire: smoker and current non-smoker.
Triclosan exposure and urinary triclosan levels
Triclosan exposure was evaluated using urinary triclosan concentrations. Analytic method for urinary triclosan levels, which was detailed in KoNEHS laboratory manual, is as following. After spot urine specimens were collected, they were transferred to the laboratory in an ice box and stored frozen at −20°C until analysis. The urine samples were hydrolyzed with β-glucuronidase/aryl sulfatase and extracted with ethyl ether for measurement. The urinary triclosan concentrations were analyzed using ultra-performance liquid chromatography-mass spectrometry. The triclosan concentrations were determined using a calibration curve prepared by the standard addition method. The limit of detection (LOD) was 0.5 μg/L. The values below the LOD were treated with the LOD divided by the square root of 2.
Because 59.6% of the urinary triclosan concentrations were below the LOD, we classified triclosan into 2 groups: ‘below detection (< LOD)’ vs. ‘detected (≥ LOD).’
Serum thyroid hormones
The thyroid profile measured included serum total T3, total T4, and thyroid-stimulating hormone (TSH or thyrotropin). Serum thyroid hormones were measured using chemiluminescence immunoassays (CLIA). Thyroid hormone concentrations were skewed and natural-log transformed before analysis.
Statistical analyses
Because the KoNEHS has been sampled by stratified multistage cluster method, a general linear model including stratum, cluster, and sample weights was used in analyses. The unweighted and weighted geometric mean of the serum total T3, total T4, and TSH and weighted percentage for urinary triclosan above the LOD were calculated according to the demographic characteristics. The serum thyroid hormone concentrations were compared with the t-test and ANOVA by demographic factors. The χ2 test was used to analyze the difference in the proportions of detected triclosan exposure group by each variable. Multiple linear regression analysis was performed to determine the relationship between triclosan exposure (dichotomous variable: ‘below detection’ and ‘detected’) and serum thyroid hormone concentrations adjusting for age, BMI, urinary creatinine, and smoking status. SPSS (ver. 25; IBM, Armonk, NY, USA) was used for all statistical analyses.
Ethics statement
This study was approved by the Institutional Review Board of Haeundae Paik Hospital (IRB No. 2018-12-002).
Table 1 lists the geometric means and percentiles of serum thyroid hormone levels and urinary triclosan concentrations among the participants. The geometric means of serum total T3, total T4, and TSH were 98.55 ng/dL, 7.95 μg/dL, and 1.93 μIU/mL. The proportion of urinary triclosan concentrations below the LOD was 59.6% (61.6% in males and 58.1% in females). The geometric mean of urinary triclosan was not calculated. The 75th and 95th percentile of the urinary triclosan concentrations were 1.21 μg/L and 41.73 μg/L, respectively.
Table 1

Distribution of serum thyroid hormone levels and urinary triclosan concentrations among the participants (n = 5,990)

Variable % < LOD* GM Percentile
5th 10th 25th 50th 75th 90th 95th
Total T3 (ng/dL) 0.0%
Total 98.55 74.00 79.00 87.00 99.00 111.00 124.00 132.00
Male 101.63 76.00 81.00 90.00 102.00 114.00 127.00 136.00
Female 96.22 73.00 78.00 86.00 96.00 108.00 120.00 128.00
Total T4 (µg/dL) 0.0%
Total 7.95 5.70 6.30 7.10 8.10 9.00 9.90 10.40
Male 7.93 5.60 6.20 7.10 8.10 9.00 9.89 10.40
Female 7.96 5.70 6.30 7.20 8.10 9.00 9.90 10.40
TSH (µIU/mL) 0.0%
Total 1.93 0.66 0.86 1.29 1.95 2.92 4.29 5.43
Male 1.81 0.64 0.81 1.20 1.83 2.74 3.96 4.92
Female 2.03 0.69 0.91 1.36 2.04 3.05 4.56 5.77
Triclosan (µg/L)
Total 59.6% NC - - - - 1.21 7.89 41.73
Male 61.6% NC - - - - 1.10 6.37 41.29
Female 58.1% NC - - - - 1.34 9.25 42.89
LOD: limit of detection; GM: geometric mean; T3: triiodothyronine; T4: thyroxine; TSH: thyroid-stimulating hormone; Triclosan: 5-chloro-2-(2,4-dichlorophenoxy)phenol; NC: not calculated; -, below limit of detection.
*LOD = 0.5 μg/L.
Table 2 shows the geometric means of the serum thyroid hormone concentrations and percentages of urinary triclosan detection categorized by demographic characteristics. In females, the total T3 concentration was significantly lower (p < 0.001) and the TSH concentration was significantly higher (p < 0.001) than in males. The geometric mean of TSH increased with age (p for trend < 0.001). The geometric mean of total T3 (p for trend < 0.001) and the geometric mean of TSH (p for trend < 0.001) were significantly higher as BMI increased. The smoker group had a significantly higher geometric mean of total T3 (p < 0.001) and total T4 (p = 0.003), and lower geometric mean of TSH (p < 0.001) than the current non-smoker group.
Table 2

Geometric mean with 95% CI of serum thyroid hormone levels and percentage for urinary triclosan above the detection limit by demographic characteristics

Variable Category No. (weighted %) Total T3 (ng/dL) Total T4 (µg/dL) TSH (µIU/mL) Triclosan detected*
Unweighted GM (95% CI) Weighted GM (95% CI) Unweighted GM (95% CI) Weighted GM (95% CI) Unweighted GM (95% CI) Weighted GM (95% CI) No. (weighted %)
Sex Male 2,630 (50.3) 101.63 (100.93–102.32) 102.08 (100.91–103.28) 7.93 (7.88–7.99) 7.96 (7.88–8.04) 1.81 (1.76–1.85) 1.77 (1.72–1.82) 1,010 (41.5)
Female 3,360 (49.7) 96.22 (95.65–96.79) 95.62 (94.60–96.64) 7.96 (7.91–8.01) 7.96 (7.88–8.04) 2.03 (1.98–2.07) 1.96 (1.91–2.02) 1,409 (43.9)
p-value < 0.001 < 0.001 0.534 0.991 < 0.001 < 0.001 0.158
Age (years) 19–29 499 (17.7) 98.36 (96.88–99.84) 98.35 (96.38–100.35) 8.01 (7.88–8.15) 7.98 (7.82–8.14) 1.53 (1.46–1.62) 1.53 (1.45–1.62) 255 (49.4)
30–39 981 (20.0) 98.06 (96.95–99.19) 99.13 (97.43–100.87) 7.93 (7.84–8.01) 7.97 (7.85–8.09) 1.82 (1.75–1.88) 1.77 (1.69–1.85) 422 (43.8)
40–49 1,153 (21.5) 98.47 (97.50–99.46) 98.35 (96.71–100.00) 7.94 (7.86–8.02) 7.96 (7.84–8.07) 1.97 (1.90–2.04)§ 1.94 (1.86–2.02)§ 508 (45.1)
50–59 1,325 (19.3) 99.49 (98.53–100.47) 100.33 (98.95–101.74) 7.90 (7.82–7.98) 7.92 (7.81–8.03) 2.04 (1.97–2.12)§ 2.03 (1.93–2.13)§ 549 (42.9)
60–69 1,232 (11.0) 99.67 (98.67–100.69) 98.98 (97.43–100.55) 7.99 (7.90–8.08) 7.95 (7.83–8.07) 2.00 (1.93–2.08)§ 2.05 (1.95–2.15)§ 435 (35.5)
≥ 70 800 (10.4) 96.14 (94.94–97.36) 97.03 (95.28–98.81) 7.94 (7.83–8.04) 7.98 (7.84–8.12) 1.98 (1.88–2.08)§ 2.05 (1.92–2.18)§ 250 (31.6)
p-value < 0.001 0.073 0.629 0.985 < 0.001 < 0.001 < 0.001
p for trend 0.331 0.794 0.616 0.766 < 0.001 < 0.001
BMI (kg/m2) < 18.50 142 (3.0) 93.51 (90.41–96.72) 93.07 (89.26–97.04) 8.01 (7.75–8.28) 8.19 (7.88–8.51) 1.58 (1.42–1.75) 1.44 (1.26–1.63) 58 (40.9)
18.50–22.99 2,040 (36.4) 95.51 (94.77–96.24) 95.71 (94.57–96.85) 7.95 (7.89–8.01) 7.93 (7.83–8.02) 1.84 (1.79–1.90) 1.80 (1.74–1.86) 832 (42.4)
23.00–24.99 1,491 (23.1) 98.67 (97.81–99.53) 99.08 (97.72–100.45) 7.89 (7.82–7.97) 7.90 (7.79–8.01) 1.96 (1.90–2.03) 1.86 (1.79–1.93) 606 (43.3)
≥ 25.00 2,317 (37.5) 101.57 (100.83–102.31)§ 102.26 (101.00–103.53)§ 7.97 (7.91–8.03) 8.01 (7.92–8.10) 2.00 (1.95–2.06) 1.97 (1.91–2.04)§ 923 (42.8)
p-value < 0.001 < 0.001 0.403 0.088 < 0.001 < 0.001 0.962
p for trend < 0.001 < 0.001 0.656 0.480 < 0.001 < 0.001
Smoking status Smoker 1,090 (22.0) 104.19 (103.06–105.33) 104.57 (102.87–106.31) 8.09 (8.00–8.18) 8.10 (7.98–8.21) 1.60 (1.54–1.65) 1.60 (1.53–1.67) 408 (40.7)
Current non-smoker 4,900 (78.0) 97.34 (96.86–97.82) 97.25 (96.27–98.23) 7.91 (7.87–7.95) 7.92 (7.84–7.99) 2.01 (1.97–2.05) 1.95 (1.90–1.99) 2,011 (43.3)
p-value < 0.001 < 0.001 < 0.001 0.003 < 0.001 < 0.001 0.230
Total 5,990 (100) 98.55 (98.11–99.00) 98.82 (97.83–99.81) 7.95 (7.91–7.98) 7.96 (7.89–8.03) 1.93 (1.89–1.96) 1.86 (1.83–1.90) 2,419 (42.7)
BMI: body mass index; T3: triiodothyronine; T4: thyroxine; TSH: thyroid-stimulating hormone; Triclosan: 5-chloro-2-(2,4-dichlorophenoxy)phenol; GM: geometric mean; CI: confidence interval; LOD: limit of detection.
*Sample size and weighted percentage for urinary triclosan above the detection limit (≥ LOD, 0.5 μg/L); Post hoc analysis ( < < §).
Table 3 describes the results of the multiple linear regression analysis using dichotomous variables adjusting for age, BMI, urinary creatinine, and smoking status. When grouped by sex, detection of triclosan was positively associated with the serum TSH concentrations in females with marginal significance (β = 0.066, p = 0.058). However, no significant association was identified between triclosan exposure and serum total T3 and T4 in both males and females, and TSH in males.
Table 3

Weighted adjusted* regression coefficients and estimated mean with 95% CI between serum thyroid hormones and triclosan exposure group

Triclosan exposure group ln total T3 (ng/dL) Total T3 (ng/dL) ln total T4 (µg/dL) Total T4 (µg/dL) ln TSH (µIU/mL) TSH (µIU/mL)
β (95% CI) Estimated mean (95% CI) β (95% CI) Estimated mean (95% CI) β (95% CI) Estimated mean (95% CI)
Male
Detected (≥ LOD) 0.000 (−0.019, 0.018) 103.11 (101.36, 104.88) −0.011 (−0.033, 0.010) 7.95 (7.82, 8.08) 0.028 (−0.035, 0.091) 1.76 (1.68, 1.85)
Below detection (< LOD) 0 (reference) 103.13 (101.85, 104.43) 0 (reference) 8.04 (7.94, 8.15) 0 (reference) 1.71 (1.65, 1.78)
p-value 0.984 0.298 0.379
Female
Detected (≥ LOD) −0.010 (−0.028, 0.007) 94.79 (92.02, 97.64) −0.010 (−0.028, 0.008) 7.93 (7.70, 8.16) 0.066 (−0.002, 0.134) 1.86 (1.71, 2.02)
Below detection (< LOD) 0 (reference) 95.78 (92.82, 98.84) 0 (reference) 8.01 (7.80, 8.22) 0 (reference) 1.74 (1.60, 1.89)
p-value 0.251 0.288 0.058
T3: triiodothyronine; T4: thyroxine; TSH: thyroid-stimulating hormone; Triclosan: 5-chloro-2-(2,4-dichlorophenoxy)phenol; CI: confidence interval; LOD: limit of detection.
*Adjusted for age, body mass index, urinary creatinine, and smoking status; Coded as a dichotomous variable, regression coefficient represents change in serum thyroid measure in relation to having a detectable urinary triclosan concentration; LOD = 0.5 μg/L.
This study assessed the relationship between triclosan exposure and thyroid hormones in the Korean population. In this study, there was suggestive positive association between triclosan exposure and the serum TSH in females, but not in males. There was no statistically significant association between triclosan exposure and serum total T3 and T4 in both males and females.
In a meta-analysis of rodent studies, the T4 concentration decreased in a dose-dependent manner with postnatal triclosan administration [13]. In several in vivo studies of adult rats, triclosan increased the elimination of thyroid hormone via hepatic catabolism, causing decreases in the serum T4 and T3 concentrations, with increased T4 glucuronidation and upregulation of phase II enzymes in the liver [17,23]. In other in vitro and in vivo studies, triclosan also affected thyroid hormone metabolism by inhibiting sulfotransferase or deiodinase activity, which plays an important role in thyroid hormone synthesis [24,25,26].
While animal studies have shown that there is a distinct association between triclosan and thyroid hormone levels, the results of human studies evaluating the relationship between triclosan and thyroid hormones have shown conflicting findings. In a study of U.S. population, triclosan exposure and total T3 concentrations were positively associated in adolescents [12]. On the other hand, several studies have found that the thyroid function may be hindered by triclosan. There was a negative association of urinary triclosan with serum free T4 in obese women [19] and urinary triclosan levels were negatively correlated with the serum free T4 in the pregnant women of the third trimester [20]. In a prospective preconception cohort, there was an inverse relationship between urinary triclosan concentrations and serum free T3 among women [27]. In another cohort study of pregnant women, urinary triclosan had a significant association with a decrease in total T3 [28]. However, some studies did not show statistically significant outcomes between triclosan exposure and thyroid function. There was no significant difference in thyroid function in patients with coronary heart disease using 0.3% triclosan toothpaste for more than 4 years compared with a control group [21]. Random intervention of personal hygiene products (e.g., toothpaste and soap) containing a triclosan in pregnant women showed no significant results in thyroid function during pregnancy or in the body measurements of babies at delivery [22].
The finding of our study is not consistent with the previous researches, but it also suggests that triclosan may have an effect that interferes with thyroid function. Our study showed a positive association between triclosan exposure and serum TSH concentrations in females with marginal significance. This might be due to the negative feedback of serum free T4, which was not included in KoNEHS, although there were no significant correlations between triclosan exposure and the serum total T4 or T3.
Previous animal studies have shown that triclosan has a significant effect on thyroid hormones. However, in this study, there was a suggestive association with TSH among females only. This result appears to be related to the difference in the triclosan exposure level. Animal studies identified the effects of high-dose triclosan exposure on thyroid hormones, while the level of triclosan exposure in the current study is considered to be low. The 95th percentile of the urinary triclosan concentrations among the participants in current study was 41.73 μg/L. The German Human Biomonitoring Commission has stated that there is no risk of adverse health effects on the human body with up to 3,000 µg/L of urinary triclosan for adults based on animal study [29]. Nevertheless, it is necessary to evaluate the effect of long-term exposure to low-concentration of triclosan on thyroid hormone levels.
In our study, the proportion of urinary triclosan concentrations which was below the LOD among the participants was 59.6%. The 75th and 95th percentile of the urinary triclosan concentrations among the study population were 1.21 μg/L and 41.73 μg/L. The detection rate and the 75th and 95th percentile concentrations were highly low compared with U.S. and Canada data [30,31]. This may be related to the difference in overall national consumption of personal hygiene products containing triclosan, such as toothpaste, soap, body cleanser, hand sanitizer, and deodorant. When a product containing triclosan is used, triclosan can be rapidly absorbed into the skin or into the mucous membrane of the mouth and excreted mainly in urine [4,5]. Therefore, if products containing triclosan are frequently used, the detection rate of triclosan in urine can also increase.
This is the first human study to assess the relationship between triclosan exposure and thyroid hormones in the Korean population. The few reported human studies have produced inconsistent results. In addition to the previous studies, our study provides data on the effect of triclosan exposure on thyroid hormones. However, there are some limitations in our study. First, the serum free T4 concentrations, which are used to evaluate essential thyroid functions and diagnose thyroid diseases, were not included in the laboratory tests. We could not evaluate the relationship between serum free T4 and triclosan exposure. Second, the long-term effect of triclosan exposure on thyroid hormones could not be identified because KoNEHS is a cross-sectional observational study. Third, spot urine specimens were collected in this study. A single urine sample of triclosan might not be representative of the subject's body burden due to the short half-life of triclosan. However, Smith et al. [32] suggested that a single urine specimen may reasonably indicate an individual's exposure over several months.
Thyroid hormones play an important role in human metabolism and normal fetal development. In Korea, triclosan was banned in the domestic market for toothpastes and mouthwashes in 2015. However, triclosan can still be used in other household products, such as antimicrobial wash products, plastics, and fibers. Therefore, further studies need to evaluate the relationship between long-term exposure to low-dose triclosan and thyroid hormones. Because the survey used in this study was conducted before triclosan was banned in 2015, further studies using the third KoNEHS (2015–2017) are also required.
This study was the first to evaluate the relationship between triclosan exposure and serum thyroid hormone concentrations in the Korean population. There was suggestive positive association between triclosan exposure and the serum TSH in females. Further studies that complement the limitations of this study are needed.
This study used data from the Second Korean National Environmental Health Survey (2012–2014), which was conducted by National Institute of Environmental Research. The Authors gratefully acknowledge their effort.

Competing interests: The authors declare that they have no competing interests.

Availability of data and materials: The datasets analyzed during the current study are available on request at the National Institute of Environmental Research, Environmental Health Research Department, http://www.nier.go.kr/NIER/kor/openapi/getAsub.do?menuNo=14010.

Author Contributions:

  • Formal analysis: Ha NY, Ryu JY.

  • Funding acquisition: Ryu JY.

  • Investigation: Kim DH.

  • Supervision: Ryu JY.

  • Writing - original draft: Ha NY, Ryu JY.

BMI

body mass index

CLIA

chemiluminescence immunoassay

GM

geometric mean

CI

confidence interval

KoNEHS

Korean National Environmental Health Survey

LOD

limit of detection

T3

triiodothyronine

T4

thyroxine

TSH

thyroid-stimulating hormone

Triclosan

5-chloro-2-(2,4-dichlorophenoxy)phenol
  • 1. Dann AB, Hontela A. Triclosan: environmental exposure, toxicity and mechanisms of action. J Appl Toxicol 2011;31(4):285–311. 21462230.ArticlePubMed
  • 2. Lu S, Yu Y, Ren L, Zhang X, Liu G, Yu Y. Estimation of intake and uptake of bisphenols and triclosan from personal care products by dermal contact. Sci Total Environ 2018;621:1389–1396. 29054660.ArticlePubMed
  • 3. Singer H, Müller S, Tixier C, Pillonel L. Triclosan: occurrence and fate of a widely used biocide in the aquatic environment: field measurements in wastewater treatment plants, surface waters, and lake sediments. Environ Sci Technol 2002;36(23):4998–5004. 12523412.ArticlePubMed
  • 4. Rodricks JV, Swenberg JA, Borzelleca JF, Maronpot RR, Shipp AM. Triclosan: a critical review of the experimental data and development of margins of safety for consumer products. Crit Rev Toxicol 2010;40(5):422–484. 20377306.ArticlePubMed
  • 5. Krishnan K, Gagné M, Nong A, Aylward LL, Hays SM. Biomonitoring equivalents for triclosan. Regul Toxicol Pharmacol 2010;58(1):10–17. 20541577.ArticlePubMed
  • 6. Sandborgh-Englund G, Adolfsson-Erici M, Odham G, Ekstrand J. Pharmacokinetics of triclosan following oral ingestion in humans. J Toxicol Environ Health A 2006;69(20):1861–1873. 16952905.ArticlePubMed
  • 7. Robertshaw H, Leppard B. Contact dermatitis to triclosan in toothpaste. Contact Dermat 2007;57(6):383–384.Article
  • 8. Savage JH, Matsui EC, Wood RA, Keet CA. Urinary levels of triclosan and parabens are associated with aeroallergen and food sensitization. J Allergy Clin Immunol 2012;130(2):453–460.e7. 22704536.ArticlePubMedPMC
  • 9. Stoker TE, Gibson EK, Zorrilla LM. Triclosan exposure modulates estrogen-dependent responses in the female Wistar rat. Toxicol Sci 2010;117(1):45–53. 20562219.ArticlePubMed
  • 10. Kumar V, Chakraborty A, Kural MR, Roy P. Alteration of testicular steroidogenesis and histopathology of reproductive system in male rats treated with triclosan. Reprod Toxicol 2009;27(2):177–185. 19118620.ArticlePubMed
  • 11. Zorrilla LM, Gibson EK, Jeffay SC, Crofton KM, Setzer WR, Cooper RL, et al. The effects of triclosan on puberty and thyroid hormones in male Wistar rats. Toxicol Sci 2009;107(1):56–64. 18940961.ArticlePubMed
  • 12. Koeppe ES, Ferguson KK, Colacino JA, Meeker JD. Relationship between urinary triclosan and paraben concentrations and serum thyroid measures in NHANES 2007–2008. Sci Total Environ 2013;445-446:299–305. 23340023.ArticlePubMedPMC
  • 13. Johnson PI, Koustas E, Vesterinen HM, Sutton P, Atchley DS, Kim AN, et al. Application of the navigation guide systematic review methodology to the evidence for developmental and reproductive toxicity of triclosan. Environ Int 2016;92-93:716–728. 27156197.ArticlePubMedPMC
  • 14. Etzel TM, Calafat AM, Ye X, Chen A, Lanphear BP, Savitz DA, et al. Urinary triclosan concentrations during pregnancy and birth outcomes. Environ Res 2017;156:505–511. 28427038.ArticlePubMedPMC
  • 15. Allmyr M, Panagiotidis G, Sparve E, Diczfalusy U, Sandborgh-Englund G. Human exposure to triclosan via toothpaste does not change CYP3A4 activity or plasma concentrations of thyroid hormones. Basic Clin Pharmacol Toxicol 2009;105(5):339–344. 19686543.ArticlePubMed
  • 16. Crofton KM, Paul KB, Devito MJ, Hedge JM. Short-term in vivo exposure to the water contaminant triclosan: evidence for disruption of thyroxine. Environ Toxicol Pharmacol 2007;24(2):194–197. 21783810.ArticlePubMed
  • 17. Paul KB, Hedge JM, DeVito MJ, Crofton KM. Short-term exposure to triclosan decreases thyroxine in vivo via upregulation of hepatic catabolism in young long-evans rats. Toxicol Sci 2010;113(2):367–379. 19910387.ArticlePubMedPMC
  • 18. Axelstad M, Boberg J, Vinggaard AM, Christiansen S, Hass U. Triclosan exposure reduces thyroxine levels in pregnant and lactating rat dams and in directly exposed offspring. Food Chem Toxicol 2013;59:534–540. 23831729.ArticlePubMed
  • 19. Geens T, Dirtu AC, Dirinck E, Malarvannan G, Van Gaal L, Jorens PG, et al. Daily intake of bisphenol A and triclosan and their association with anthropometric data, thyroid hormones and weight loss in overweight and obese individuals. Environ Int 2015;76:98–105. 25575039.ArticlePubMed
  • 20. Wang X, Ouyang F, Feng L, Wang X, Liu Z, Zhang J. Maternal urinary triclosan concentration in relation to maternal and neonatal thyroid hormone levels: a prospective study. Environ Health Perspect 2017;125(6):067017. 28669941.ArticlePubMedPMC
  • 21. Cullinan MP, Palmer JE, Carle AD, West MJ, Seymour GJ. Long term use of triclosan toothpaste and thyroid function. Sci Total Environ 2012;416:75–79. 22197412.ArticlePubMed
  • 22. Ley C, Pischel L, Parsonnet J. Triclosan and triclocarban exposure and thyroid function during pregnancy-a randomized intervention. Reprod Toxicol 2017;74:143–149. 28939492.ArticlePubMedPMC
  • 23. Paul KB, Hedge JM, Bansal R, Zoeller RT, Peter R, DeVito MJ, et al. Developmental triclosan exposure decreases maternal, fetal, and early neonatal thyroxine: a dynamic and kinetic evaluation of a putative mode-of-action. Toxicology 2012;300(1-2):31–45. 22659317.ArticlePubMedPMC
  • 24. Butt CM, Stapleton HM. Inhibition of thyroid hormone sulfotransferase activity by brominated flame retardants and halogenated phenolics. Chem Res Toxicol 2013;26(11):1692–1702. 24089703.ArticlePubMedPMC
  • 25. Butt CM, Wang D, Stapleton HM. Halogenated phenolic contaminants inhibit the in vitro activity of the thyroid-regulating deiodinases in human liver. Toxicol Sci 2011;124(2):339–347. 21565810.ArticlePubMedPMC
  • 26. Shimizu R, Yamaguchi M, Uramaru N, Kuroki H, Ohta S, Kitamura S, et al. Structure-activity relationships of 44 halogenated compounds for iodotyrosine deiodinase-inhibitory activity. Toxicology 2013;314(1):22–29. 24012475.ArticlePubMed
  • 27. Skarha J, Mínguez-Alarcón L, Williams PL, Korevaar TIM, de Poortere RA, Broeren MAC, et al. Cross-sectional associations between urinary triclosan and serum thyroid function biomarker concentrations in women. Environ Int 2019;122:256–262. 30477815.ArticlePubMedPMC
  • 28. Aker AM, Johns L, McElrath TF, Cantonwine DE, Mukherjee B, Meeker JD. Associations between maternal phenol and paraben urinary biomarkers and maternal hormones during pregnancy: a repeated measures study. Environ Int 2018;113:341–349. 29366524.ArticlePubMedPMC
  • 29. Apel P, Angerer J, Wilhelm M, Kolossa-Gehring M. New HBM values for emerging substances, inventory of reference and HBM values in force, and working principles of the German human biomonitoring commission. Int J Hyg Environ Health 2017;220(2 Pt A):152–166. 27914867.ArticlePubMed
  • 30. Calafat AM, Ye X, Wong LY, Reidy JA, Needham LL. Urinary concentrations of triclosan in the U.S. population: 2003–2004. Environ Health Perspect 2008;116(3):303–307. 18335095.ArticlePubMedPMC
  • 31. Haines DA, Saravanabhavan G, Werry K, Khoury C. An overview of human biomonitoring of environmental chemicals in the Canadian health measures survey: 2007–2019. Int J Hyg Environ Health 2017;220(2 Pt A):13–28. 27601095.ArticlePubMed
  • 32. Smith KW, Braun JM, Williams PL, Ehrlich S, Correia KF, Calafat AM, et al. Predictors and variability of urinary paraben concentrations in men and women, including before and during pregnancy. Environ Health Perspect 2012;120(11):1538–1543. 22721761.ArticlePubMedPMC

Figure & Data

REFERENCES

    Citations

    Citations to this article as recorded by  
    • Relationship between endocrine disrupting chemicals (phthalate metabolites, triclosan and bisphenols) and vitamin D in female subjects: An exploratory pilot study
      Edwina Brennan, Alexandra E. Butler, Manjula Nandakumar, Kristie Thompson, Thozhukat Sathyapalan, Stephen L. Atkin
      Chemosphere.2024; 349: 140894.     CrossRef
    • Conceptualizing the Role of the Microbiome as a Mediator and Modifier in Environmental Health Studies: A Scoping Review of Studies of Triclosan and the Microbiome
      Hannah E. Laue, Aislinn J. Gilmour, Valerie M. Tirado, Megan E. Romano
      Current Environmental Health Reports.2024; 11(1): 30.     CrossRef
    • Critical review on the environmental behaviors and toxicity of triclosan and its removal technologies
      Yanhong Jiang, Liangying Liu, Biao Jin, Yi Liu, Xiaoliang Liang
      Science of The Total Environment.2024; 932: 173013.     CrossRef
    • Triclosan and its alternatives, especially chlorhexidine, modulate macrophage immune response with distinct modes of action
      Stefanie Raps, Laura Bahr, Isabel Karkossa, Manuela Rossol, Martin von Bergen, Kristin Schubert
      Science of The Total Environment.2024; 914: 169650.     CrossRef
    • “The issues still persist”: a roundtable discussion of perpetual crisis, the massification of grief and joyful black futures
      Lwanda Maqwelane, Abongile Nkamisa, Candice Sehoma, Kharnita Mohamed, Gcobani Qambela
      Anthropology Southern Africa.2024; 47(1): 85.     CrossRef
    • Associations of Maternal Urinary Concentrations of Phenols, Individually and as a Mixture, with Serum Biomarkers of Thyroid Function and Autoimmunity: Results from the EARTH Study
      Glen McGee, Maximilien Génard-Walton, Paige L. Williams, T. I. M. Korevaar, Jorge E. Chavarro, John D. Meeker, Joseph M. Braun, Maarten A. Broeren, Jennifer B. Ford, Antonia M. Calafat, Irene Souter, Russ Hauser, Lidia Mínguez-Alarcón
      Toxics.2023; 11(6): 521.     CrossRef
    • Sustainable Conversion of Biowaste to Energy to Tackle the Emerging Pollutants: A Review
      Yue Li, Karthikeyan Meenatchisundaram, Karthik Rajendran, Nisarg Gohil, Vinay Kumar, Vijai Singh, Manoj Kumar Solanki, Sharareh Harirchi, Zengqiang Zhang, Raveendran Sindhu, Mohammad J. Taherzadeh, Mukesh Kumar Awasthi
      Current Pollution Reports.2023; 9(4): 660.     CrossRef
    • The Influence of Triclosan on the Thyroid Hormone System in Humans - A Systematic Review
      Mai Homburg, Åse Krogh Rasmussen, Louise Ramhøj, Ulla Feldt-Rasmussen
      Frontiers in Endocrinology.2022;[Epub]     CrossRef
    • Obesogens in Foods
      Iva Kladnicka, Monika Bludovska, Iveta Plavinova, Ludek Muller, Dana Mullerova
      Biomolecules.2022; 12(5): 680.     CrossRef
    • Effectiveness of hand sanitizers in the prevention of COVID-19 and related public health concerns: A review
      Jerikias Marumure, Zakio Makuvara, Richwell Alufasi, Lazarus Chapungu, Claudious Gufe
      Cogent Public Health.2022;[Epub]     CrossRef
    • Triclosan and Its Consequences on the Reproductive, Cardiovascular and Thyroid Levels
      Ana C. Marques, Melissa Mariana, Elisa Cairrao
      International Journal of Molecular Sciences.2022; 23(19): 11427.     CrossRef
    • Effect of Maternal Triclosan Exposure on Neonatal Thyroid‐Stimulating Hormone Levels: A Cross‐Sectional Study
      Elham Attarian, Karim Ebrahimpour, Mohammadreza Maracy, Seyede Shahrbanoo Daniali, Bahareh Shoshtari-Yeganeh, Malihe Moazeni, Afshin Ebrahimi, Roya Kelishadi, Gabriella Galluccio
      Journal of Environmental and Public Health.2022;[Epub]     CrossRef
    • Evaluation of triclosan exposures on secretion of pro-inflammatory cytokines from human immune cells
      Wendy J. Wilburn, Sara Jamal, Farah Ismail, Dylan Brooks, Margaret Whalen
      Environmental Toxicology and Pharmacology.2021; 83: 103599.     CrossRef
    • Comprehensive insight into triclosan—from widespread occurrence to health outcomes
      Maja Milanović, Larisa Đurić, Nataša Milošević, Nataša Milić
      Environmental Science and Pollution Research.2021; 30(10): 25119.     CrossRef

    • PubReader PubReader
    • ePub LinkePub Link
    • Cite
      CITE
      export Copy Download
      Close
      Download Citation
      Download a citation file in RIS format that can be imported by all major citation management software, including EndNote, ProCite, RefWorks, and Reference Manager.

      Format:
      • RIS — For EndNote, ProCite, RefWorks, and most other reference management software
      • BibTeX — For JabRef, BibDesk, and other BibTeX-specific software
      Include:
      • Citation for the content below
      Relationship between triclosan exposure and thyroid hormones: the Second Korean National Environmental Health Survey (2012–2014)
      Ann Occup Environ Med. 2019;31:e22  Published online September 5, 2019
      Close
    • XML DownloadXML Download
    Related articles
    Relationship between triclosan exposure and thyroid hormones: the Second Korean National Environmental Health Survey (2012–2014)
    Relationship between triclosan exposure and thyroid hormones: the Second Korean National Environmental Health Survey (2012–2014)
    Variable% < LOD*GMPercentile
    5th10th25th50th75th90th95th
    Total T3 (ng/dL)0.0%
    Total98.5574.0079.0087.0099.00111.00124.00132.00
    Male101.6376.0081.0090.00102.00114.00127.00136.00
    Female96.2273.0078.0086.0096.00108.00120.00128.00
    Total T4 (µg/dL)0.0%
    Total7.955.706.307.108.109.009.9010.40
    Male7.935.606.207.108.109.009.8910.40
    Female7.965.706.307.208.109.009.9010.40
    TSH (µIU/mL)0.0%
    Total1.930.660.861.291.952.924.295.43
    Male1.810.640.811.201.832.743.964.92
    Female2.030.690.911.362.043.054.565.77
    Triclosan (µg/L)
    Total59.6%NC----1.217.8941.73
    Male61.6%NC----1.106.3741.29
    Female58.1%NC----1.349.2542.89
    VariableCategoryNo. (weighted %)Total T3 (ng/dL)Total T4 (µg/dL)TSH (µIU/mL)Triclosan detected*
    Unweighted GM (95% CI)Weighted GM (95% CI)Unweighted GM (95% CI)Weighted GM (95% CI)Unweighted GM (95% CI)Weighted GM (95% CI)No. (weighted %)
    SexMale2,630 (50.3)101.63 (100.93–102.32)102.08 (100.91–103.28)7.93 (7.88–7.99)7.96 (7.88–8.04)1.81 (1.76–1.85)1.77 (1.72–1.82)1,010 (41.5)
    Female3,360 (49.7)96.22 (95.65–96.79)95.62 (94.60–96.64)7.96 (7.91–8.01)7.96 (7.88–8.04)2.03 (1.98–2.07)1.96 (1.91–2.02)1,409 (43.9)
    p-value< 0.001< 0.0010.5340.991< 0.001< 0.0010.158
    Age (years)19–29499 (17.7)98.36 (96.88–99.84)98.35 (96.38–100.35)8.01 (7.88–8.15)7.98 (7.82–8.14)1.53 (1.46–1.62)1.53 (1.45–1.62)255 (49.4)
    30–39981 (20.0)98.06 (96.95–99.19)99.13 (97.43–100.87)7.93 (7.84–8.01)7.97 (7.85–8.09)1.82 (1.75–1.88)1.77 (1.69–1.85)422 (43.8)
    40–491,153 (21.5)98.47 (97.50–99.46)98.35 (96.71–100.00)7.94 (7.86–8.02)7.96 (7.84–8.07)1.97 (1.90–2.04)§1.94 (1.86–2.02)§508 (45.1)
    50–591,325 (19.3)99.49 (98.53–100.47)100.33 (98.95–101.74)7.90 (7.82–7.98)7.92 (7.81–8.03)2.04 (1.97–2.12)§2.03 (1.93–2.13)§549 (42.9)
    60–691,232 (11.0)99.67 (98.67–100.69)98.98 (97.43–100.55)7.99 (7.90–8.08)7.95 (7.83–8.07)2.00 (1.93–2.08)§2.05 (1.95–2.15)§435 (35.5)
    ≥ 70800 (10.4)96.14 (94.94–97.36)97.03 (95.28–98.81)7.94 (7.83–8.04)7.98 (7.84–8.12)1.98 (1.88–2.08)§2.05 (1.92–2.18)§250 (31.6)
    p-value< 0.0010.0730.6290.985< 0.001< 0.001< 0.001
    p for trend0.3310.7940.6160.766< 0.001< 0.001
    BMI (kg/m2)< 18.50142 (3.0)93.51 (90.41–96.72)93.07 (89.26–97.04)8.01 (7.75–8.28)8.19 (7.88–8.51)1.58 (1.42–1.75)1.44 (1.26–1.63)58 (40.9)
    18.50–22.992,040 (36.4)95.51 (94.77–96.24)95.71 (94.57–96.85)7.95 (7.89–8.01)7.93 (7.83–8.02)1.84 (1.79–1.90)1.80 (1.74–1.86)832 (42.4)
    23.00–24.991,491 (23.1)98.67 (97.81–99.53)99.08 (97.72–100.45)7.89 (7.82–7.97)7.90 (7.79–8.01)1.96 (1.90–2.03)1.86 (1.79–1.93)606 (43.3)
    ≥ 25.002,317 (37.5)101.57 (100.83–102.31)§102.26 (101.00–103.53)§7.97 (7.91–8.03)8.01 (7.92–8.10)2.00 (1.95–2.06)1.97 (1.91–2.04)§923 (42.8)
    p-value< 0.001< 0.0010.4030.088< 0.001< 0.0010.962
    p for trend< 0.001< 0.0010.6560.480< 0.001< 0.001
    Smoking statusSmoker1,090 (22.0)104.19 (103.06–105.33)104.57 (102.87–106.31)8.09 (8.00–8.18)8.10 (7.98–8.21)1.60 (1.54–1.65)1.60 (1.53–1.67)408 (40.7)
    Current non-smoker4,900 (78.0)97.34 (96.86–97.82)97.25 (96.27–98.23)7.91 (7.87–7.95)7.92 (7.84–7.99)2.01 (1.97–2.05)1.95 (1.90–1.99)2,011 (43.3)
    p-value< 0.001< 0.001< 0.0010.003< 0.001< 0.0010.230
    Total5,990 (100)98.55 (98.11–99.00)98.82 (97.83–99.81)7.95 (7.91–7.98)7.96 (7.89–8.03)1.93 (1.89–1.96)1.86 (1.83–1.90)2,419 (42.7)
    Triclosan exposure groupln total T3 (ng/dL)Total T3 (ng/dL)ln total T4 (µg/dL)Total T4 (µg/dL)ln TSH (µIU/mL)TSH (µIU/mL)
    β (95% CI)Estimated mean (95% CI)β (95% CI)Estimated mean (95% CI)β (95% CI)Estimated mean (95% CI)
    Male
    Detected (≥ LOD)0.000 (−0.019, 0.018)103.11 (101.36, 104.88)−0.011 (−0.033, 0.010)7.95 (7.82, 8.08)0.028 (−0.035, 0.091)1.76 (1.68, 1.85)
    Below detection (< LOD)0 (reference)103.13 (101.85, 104.43)0 (reference)8.04 (7.94, 8.15)0 (reference)1.71 (1.65, 1.78)
    p-value0.9840.2980.379
    Female
    Detected (≥ LOD)−0.010 (−0.028, 0.007)94.79 (92.02, 97.64)−0.010 (−0.028, 0.008)7.93 (7.70, 8.16)0.066 (−0.002, 0.134)1.86 (1.71, 2.02)
    Below detection (< LOD)0 (reference)95.78 (92.82, 98.84)0 (reference)8.01 (7.80, 8.22)0 (reference)1.74 (1.60, 1.89)
    p-value0.2510.2880.058
    Table 1 Distribution of serum thyroid hormone levels and urinary triclosan concentrations among the participants (n = 5,990)

    LOD: limit of detection; GM: geometric mean; T3: triiodothyronine; T4: thyroxine; TSH: thyroid-stimulating hormone; Triclosan: 5-chloro-2-(2,4-dichlorophenoxy)phenol; NC: not calculated; -, below limit of detection.

    *LOD = 0.5 μg/L.

    Table 2 Geometric mean with 95% CI of serum thyroid hormone levels and percentage for urinary triclosan above the detection limit by demographic characteristics

    BMI: body mass index; T3: triiodothyronine; T4: thyroxine; TSH: thyroid-stimulating hormone; Triclosan: 5-chloro-2-(2,4-dichlorophenoxy)phenol; GM: geometric mean; CI: confidence interval; LOD: limit of detection.

    *Sample size and weighted percentage for urinary triclosan above the detection limit (≥ LOD, 0.5 μg/L); Post hoc analysis ( < < §).

    Table 3 Weighted adjusted* regression coefficients and estimated mean with 95% CI between serum thyroid hormones and triclosan exposure group†

    T3: triiodothyronine; T4: thyroxine; TSH: thyroid-stimulating hormone; Triclosan: 5-chloro-2-(2,4-dichlorophenoxy)phenol; CI: confidence interval; LOD: limit of detection.

    *Adjusted for age, body mass index, urinary creatinine, and smoking status; Coded as a dichotomous variable, regression coefficient represents change in serum thyroid measure in relation to having a detectable urinary triclosan concentration; LOD = 0.5 μg/L.


    Ann Occup Environ Med : Annals of Occupational and Environmental Medicine
    Close layer
    TOP