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Park, Yelim,Lee, Aram,Choi, Kyungho,Kim, Hai-Joong,Lee, Jeong Jae,Choi, Gyuyeon,Kim, Sungjoo,Kim, Su Young,Cho, Geum Joon,Suh, Eunsook,Kim, Sung Koo,Eun, So-Hee,Eom, Soyong,Kim, Seunghyo,Kim, Gun-Ha,M Elsevier 2018 Science of the Total Environment Vol.612 No.-
<P><B>Abstract</B></P> <P>Mercury and lead are naturally occurring toxicants and are responsible for various health issues including neurobehavioral and developmental disorders. Because of crucial synchronized developmental processes occurring at the early stage of life, infancy and childhood are considered as among the most susceptible windows to the exposure to these metals. Breastmilk is often the only source of nutrition during the first months of life. As breastmilk can be contaminated with these metals, breastfeeding may serve as a significant route of heavy metal exposure among infants. In order to understand current levels of exposure to mercury and lead through breastfeeding, and their associated risks, a total of 157 lactating mothers were recruited from Children's Health and Environmental Chemicals of Korea (CHECK) cohort, and breastmilk samples were collected at 15 and 30days after delivery (<I>n</I> =207). Mercury was detected from 100% of breastmilk with a median concentration of 0.59μg/L, and lead was detected in 77% of the samples with a median at 4.71μg/L. Higher concentrations of lead were found in the 30- day breastmilk than in the 15-day. Up to 45% of the breastmilk samples exceeded the normal range of the breastmilk lead suggested by WHO. Based on Monte Carlo simulation, about 71% of 15days old infants and 56% of 30days old infants were estimated at risk due to lead exposure through breastfeeding. Considering vulnerability of infants and well-known neurological toxicity of these metals, further studies to identify major exposure sources that contribute the lead concentration in breastmilk and health implication of early life stage exposure to lead among the breastfed infants are warranted.</P> <P><B>Highlights</B></P> <P> <UL> <LI> We analyzed mercury and lead in 207 breastmilk collected at 15 and 30days after delivery. </LI> <LI> Mercury was detected from 100% of breastmilk with the median of 0. 59μg/L. </LI> <LI> Lead was detected in 77 % of breastmilk with the median of 4.71μg/L. </LI> <LI> The hazard quotient of lead exceeded 1.0 for 71% of 15days and for 56% for 30days old infants from breastfeeding. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
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Kim, Sunmi,Park, Jeongim,Kim, Hai-Joong,Lee, Jeong Jae,Choi, Gyuyeon,Choi, Sooran,Kim, Sungjoo,Kim, Su Young,Lee, Duk Hee,Moon, Hyo-Bang,Kim, Sungkyoon,Choi, Kyungho American Chemical Society 2015 Environmental science & technology Vol.49 No.13
<P>Exposure to several persistent organic pollutants (POPs) has been linked to alteration of lipid metabolism. Adipokines, such as leptin and adiponectin, are hormones that play roles in lipid metabolism, and have been suggested as markers of health effects that may lead to obesity. To date, only serum adipokines have been associated with POPs exposure. In the present study, for the first time, the associations between leptin and adiponectin in breast milk, and several POPs in serum were investigated among 82 lactating Korean women between 25 and 46 years of age. Breast milk adipokines are important because adipokine intake of infant through breastfeeding may influence the growth of infants. The median concentrations of leptin and adiponectin in skimmed milk of the Korean lactating women were 17.9 ng/L and 16.5 μg/L, respectively. Leptin concentrations in breast milk were negatively associated with ∑hexachlorohexane (HCH), oxychlordane, ∑chlordane, or 2,2′,4,4′,5,5′-hexachlorobiphenyl (CB 153) levels in maternal serum. Linear relationships between adiponectin and POPs concentrations were not observed, however, nonmonotonic relationship which showed generally positive associations was suggested for <I>p</I>,<I>p</I>′-dichlorodiphenyltrichloroethane (DDT) and ∑chlordane in quartile analysis. Our observations show that POPs at the current level of exposure may be associated with the alteration of lipid metabolism among lactating women. Implication of adipokine transfer to breastfed infants is of concern and deserves further investigation.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/esthag/2015/esthag.2015.49.issue-13/acs.est.5b00520/production/images/medium/es-2015-00520t_0003.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/es5b00520'>ACS Electronic Supporting Info</A></P>
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Lee, Sunggyu,Kim, Sunmi,Park, Jeongim,Kim, Hai-Joong,Choi, Gyuyeon,Choi, Sooran,Kim, Sungjoo,Kim, Su Young,Kim, Sungkyoon,Choi, Kyungho,Moon, Hyo-Bang Elsevier 2018 Science of the Total Environment Vol.612 No.-
<P><B>Abstract</B></P> <P>Breastfeeding is an important exposure pathway to perfluoroalkyl substances (PFASs) for newborn infants. Nevertheless, reports are limited on the occurrence and time-course of PFASs in breast milk, and most studies have focused on the analysis of perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA). In this study, 16 PFASs were analyzed in breast milk samples (<I>n</I> =293) collected from 128 mothers in Korea during various lactation periods to assess maternal exposure levels, contamination profiles, time-course variations, and infant health risks. The total concentrations of PFASs (ΣPFAS) ranged from 31.7 to 1004 (median: 188) ng/L, which was within the ranges recently reported for Asian and European populations. After a month of nursing, the concentrations of PFOS, PFOA, perfluorononanoic acid (PFNA), and ΣPFAS significantly increased. This could be due to changes in the dietary and behavior patterns of the mothers after the first month of lactation. The concentrations of PFOS and PFOA were significantly correlated with maternal age, body mass index, and parity. Certain types of diet (e.g. consuming snacks and milk) and eating-out frequency were significantly associated with increasing levels of PFAS. Significant correlations and similar time-course trends were found between PFASs and PCBs/DDTs, implying similar exposure sources and biokinetics for these contaminants. The estimated daily intakes of PFOS and PFOA via the consumption of breast milk were below the tolerable daily intakes for infants suggested by the European Food Safety Authority (EFSA).</P> <P><B>Highlights</B></P> <P> <UL> <LI> PFOS, PFOA, PFUnDA, and PFNA were the predominant compounds in breast milk. </LI> <LI> Concentrations of PFASs were significantly correlated with maternal age, BMI, and parity. </LI> <LI> Increased levels of PFASs were found in breast milk after the first month of nursing. </LI> <LI> Snack consumption and frequency of eating-out were significantly associated with increased PFAS levels. </LI> <LI> The infant exposure levels of PFOS and PFOA via breast milk were lower than the TDI. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
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Kim, Jin Hee,Park, Hyunkyung,Lee, Jangwoo,Cho, Geumjoon,Choi, Sooran,Choi, Gyuyeon,Kim, Su Young,Eun, So-Hee,Suh, Eunsook,Kim, Sung Koo,Kim, Hai-Joong,Kim, Gun-Ha,Lee, Jeong Jae,Kim, Young Don,Eom, So BMJ Publishing Group 2016 Journal of epidemiology & community health Vol.70 No.5
<P><B>Background</B></P><P>Several studies have suggested potential links of phthalates to obesity in children and adults. Limited evidence, however, has been available for the relations between diethylhexyl phthalate (DEHP) and obesity-related markers or body mass change in early life.</P><P><B>Methods</B></P><P>128 healthy pregnant women were recruited and, after delivery, their newborns’ first urine and umbilical cord blood samples were collected. We measured urinary levels of two DEHP metabolites, mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP). We also measured the levels of leptin, total cholesterol and triglyceride (TG) in cord serum, and used them along with weight, length, head circumference and ponderal index (PI, 100 g/cm<SUP>3</SUP>) at birth, as obesity-related markers, and estimated the relations between DEHP metabolites and obesity-related markers using generalised linear models. For the evaluation of body mass increase by early life DEHP exposure, body mass index (BMI) z-score change during 3 months after birth by DEHP metabolites in the first urine samples of the newborns were evaluated using logistic regression.</P><P><B>Results</B></P><P>DEHP exposure was associated with decrease of PI and increase of TG (PI, β=−0.11, p=0.070 and TG, β=0.14, p=0.027), especially for boys (PI, β=−0.13, p=0.021; and TG, β=0.19, p=0.025). Moreover, DEHP exposure was positively associated with body mass increase during 3 months after birth (change of BMI z-scores, OR=4.35, p=0.025).</P><P><B>Conclusions</B></P><P>Our findings suggest that DEHP exposure may affect body mass change in early life through changes of obesity-related markers.</P>
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Kim, Sunmi,Lee, Jangwoo,Park, Jeongim,Kim, Hai-Joong,Cho, Geum Joon,Kim, Gun-Ha,Eun, So-Hee,Lee, Jeong Jae,Choi, Gyuyeon,Suh, Eunsook,Choi, Sooran,Kim, Sungjoo,Kim, Sung Koo,Kim, Young Don,Kim, Su You Elsevier 2017 The Science of the total environment Vol.607 No.-
<P><B>Abstract</B></P> <P>Phthalates are important group of endocrine disruptors. Infants and young children are susceptible to phthalate exposure. However, information on the phthalate exposure during the early stages of life is very limited. This study was conducted to understand the temporal trend of exposure to major phthalates among infants of Korea during the first 15months after birth, and to estimate associated risks. A total of 286 urine samples were collected from 171 children at 3, 9, 12, or 15months of age, with 77 children sampled for two or more times. Four phthalates, i.e., di(2-ethylhexyl) phthalate (DEHP), di-isobutyl phthalate (DiBP), di-n-butyl phthalate (DnBP), and diethyl phthalate (DEP) were chosen, and their major metabolites were analyzed in the urine. The DEHP metabolites were detected in 100% of the urine samples at relatively higher levels compared to those reported in other countries. The levels of mono-ethyl phthalate (MEP) were generally lower. Urinary concentrations of most phthalate metabolites, especially DEHP metabolites, increased as children grew older. Intra-class correlation coefficients (ICCs) calculated for DEHP metabolites over time were high (0.7–0.8), suggesting persistence of consistent exposure sources during this sensitive period of life. Hazard quotient (HQ) and hazard index (HI) were calculated from daily intake estimates divided by recommended toxicity thresholds. Among the study population, 4, 16, and 26% of the children showed HI >1 at 9, 12, and 15months of age, respectively. DEHP exposure explained most of the risk estimates. Considering vulnerability of young children to endocrine disruption, efforts to identify sources of exposure and to develop appropriate mitigation options are warranted.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Multiple urines were collected at 3, 9, 12, or 15months of age from 171 children. </LI> <LI> High intra-individual correlation and age-dependent increase were observed. </LI> <LI> Up to 26% of children showed hazard index >1 by exposure to target phthalates. </LI> <LI> Estimated risks are mostly due to the exposure to DEHP and DnBP. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
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Lee, Jangwoo,Choi, Kyungho,Park, Jeongim,Moon, Hyo-Bang,Choi, Gyuyeon,Lee, Jeong Jae,Suh, Eunsook,Kim, Hai-Joong,Eun, So-Hee,Kim, Gun-Ha,Cho, Geum Joon,Kim, Sung Koo,Kim, Sungjoo,Kim, Su Young,Kim, Se Elsevier 2018 Science of the Total Environment Vol.626 No.-
<P><B>Abstract</B></P> <P>Bisphenol A (BPA) exposure during the perinatal and postnatal periods increases the susceptibility to disease over the life cycle. However, information on the BPA delivered to fetuses or infants via the placenta and breastfeeding is limited. We determined the BPA exposure levels in various bodily fluids and tissues of pregnant women and described fetus and infant exposures to BPA based on associations and BPA ratios in mother–neonate paired samples. Maternal serum, urine, placenta, breast milk, cord serum, and neonatal urine samples were collected from 318 mother–neonate pairs at six university hospitals in Korea. BPA levels were detected using liquid chromatography tandem mass spectrometry. The ratios of the BPA levels in the other sample types to the levels in maternal serum were calculated. BPA was detected in 79.5–100% of the maternal and fetal samples. The median BPA concentration in the samples decreased in the order of neonatal urine (4.75ng/mL), maternal urine (2.86ng/mL), cord serum (1.71ng/mL), maternal serum (1.56ng/mL), breast milk (0.74ng/mL), and the placenta (0.53ng/g). We estimated the ratios of BPA levels in the other sample types to those in maternal serum. The median (95th percentile) cord serum-to-maternal serum ratio was 1.12 (15.2) for 160 mother–fetal pairs, in which BPA was detected in both samples. The placenta-, maternal urine-, neonatal urine-, and breast milk-to-maternal serum ratios were 0.28 (5.31), 1.79 (29.9), 1.98 (28.2), and 0.51 (10.5), respectively. In addition, the median (95th percentile) cord serum-to-placenta ratio was 4.03 (45.8), and the neonatal urine-to-cord serum ratio was 1.95 (25.6). The 95th percentile values were 14–20-fold greater than the medians. Urine contained the highest BPA concentrations, followed by serum, breast milk, and the placenta. The variations of BPA ratio show individual differences in the amounts of BPA delivered from mother to fetus.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Not enough data on tissue distribution of BPA in mother‑neonate (or fetus) pair </LI> <LI> The order of BPA concentrations in examined tissue or bio-samples are urine in mother and neonates>cord serum>maternal serum>breast milk>placenta. </LI> <LI> BPA in cord serum, significantly associated with in maternal serum and urine but not in others. </LI> <LI> The variations of BPA ratio show individual differences in the amounts of BPA delivered from mother to fetus. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
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Lee, Inae,Kim, Sunmi,Park, Suhyeon,Mok, Sori,Jeong, Yunsun,Moon, Hyo-Bang,Lee, Jangwoo,Kim, Sungkyoon,Kim, Hai-Joong,Choi, Gyuyeon,Choi, Sooran,Kim, Su Young,Lee, Aram,Park, Jeongim,Choi, Kyungho Elsevier BV 2019 Science of the Total Environment Vol.688 No.-
<P><B>Abstract</B></P> <P>Chemicals such as phthalates and phenolics have been associated with metabolic markers in humans. However, most studies have only looked at a limited number of chemicals, and little is known about their potential effects on adipokines in humans. In the present study, the associations between dozens of urinary chemicals, including phthalate metabolites and phenolics, and markers related to insulin resistance as well as major adipokines, were assessed among the women of reproductive age (<I>n</I> = 459, between 20 and 48 years of age) recruited from major cities in Korea between 2015 and 2016. Adipokines such as adiponectin and leptin, and insulin resistance related markers such as glucose and insulin, were analyzed in serum. Associations between urinary chemicals and the adipokines or insulin resistance related markers were assessed in two steps. First, ordinary least squares (OLS) regression was used to assess the association of each urinary chemical with the adipokines or insulin resistance related markers (single-pollutant model). Second, several chemicals were selected using elastic net regression and were subsequently analyzed with OLS regression model (multi-pollutant model), considering simultaneous exposure to multiple chemicals. In both single- and multi-pollutant models, several urinary chemicals consistently showed significant associations with adipokines or the insulin resistance related markers. The sum of di-(2-ethylhexyl) phthalate metabolites (ΣDEHPm) and ethyl paraben (EtP) were associated with increased serum adiponectin levels. Urinary ΣDEHPm levels also showed positive associations with fasting glucose. Moreover, urinary mono-methyl phthalate (MMP), mono-isobutyl phthalate (MiBP), and bisphenol S (BPS) levels showed positive associations with the homeostasis model assessment for insulin resistance (HOMA-IR). Interestingly, urinary propyl paraben (PrP) levels showed a negative association with HOMA-IR, in both models. Our observations show that among many consumer chemicals, phthalates may affect serum adipokines, and thus glucose, and insulin resistance in adult females. Further confirmation is warranted in other populations.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Urinary chemicals and metabolism related markers were measured in women of reproductive age. </LI> <LI> Multiple chemicals were considered in statistical models for adipokines and insulin resistance. </LI> <LI> Sum of DEHP metabolites and EtP were positively associated with serum adiponectin levels. </LI> <LI> Sum of DEHP metabolites was significantly associated with increased fasting glucose. </LI> <LI> MiBP was significantly associated with for increased HOMA-IR. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
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