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Biomedical subjects

Antonia M Calafat

Publications and source records attributed to Antonia M Calafat.

At least 19 recordsLinked to original sources
PubMed2006

Uses and issues of biomonitoring.

In the last two decades, an explosion in information and literature on human biomonitoring data has occurred. Symposia, workshops, and workgroups have been formed to discuss all issues surrounding biomonitoring. One such workgroup, formed by the International Life Sciences Institute's Health and Environmental Sciences Institute (HESI), developed a wheel which has biomonitoring at its hub; its spokes depict the uses of biomonitoring. As it rolls and picks up speed, the biomonitoring wheel will no doubt gain additional spokes. In this manuscript, we describe and give examples of these biomonitoring uses and some of their further applications as well as some of the issues surrounding biomonitoring. Special emphasis is placed on the uses and limitations of large-scale representative cross sectional studies such as the National Health and Nutrition Examination Surveys in the United States. Priority setting, improved modeling methods for interpreting the biomonitoring data, and an increase in studies designed to associate health indicators and health risks to selected environmental chemicals are needed to increase the power of biomonitoring.

Biomarkers↗
PubMed2006

Gestational PFOA exposure of mice is associated with altered mammary gland development in dams and female offspring.

Perfluorooctanoic acid (PFOA), with diverse and widespread commercial and industrial applications, has been detected in human and wildlife sera. Previous mouse studies linked prenatal PFOA exposure to decreased neonatal body weights (BWs) and survival in a dose-dependent manner. To determine whether effects were linked to gestational time of exposure or to subsequent lactational changes, timed-pregnant CD-1 mice were orally dosed with 5 mg PFOA/kg on gestation days (GD) 1-17, 8-17, 12-17, or vehicle on GD 1-17. PFOA exposure had no effect on maternal weight gain or number of live pups born. Mean pup BWs on postnatal day (PND) 1 in all PFOA-exposed groups were significantly reduced and decrements persisted until weaning. Mammary glands from lactating dams and female pups on PND 10 and 20 were scored based on differentiation or developmental stages. A significant reduction in mammary differentiation among dams exposed GD 1-17 or 8-17 was evident on PND 10. On PND 20, delays in normal epithelial involution and alterations in milk protein gene expression were observed. All exposed female pups displayed stunted mammary epithelial branching and growth at PND 10 and 20. While control litters at PND 10 and 20 had average scores of 3.1 and 3.3, respectively, all treated litters had scores of 1.7 or less, with no progression of duct epithelial growth evident over time. BW was an insignificant covariate for these effects. These findings suggest that in addition to gestational exposure, abnormal lactational development of dams may play a role in early growth retardation of developmentally exposed offspring.

Administration, Oral↗
PubMed2006

Developmental toxicity of perfluorooctanoic acid in the CD-1 mouse after cross-foster and restricted gestational exposures.

Perfluorooctanoic acid (PFOA) is a persistent pollutant and is detectable in human serum (5 ng/ml in the general population of the Unites States). PFOA is used in the production of fluoropolymers which have applications in the manufacture of a variety of industrial and commercial products (e.g., textiles, house wares, electronics). PFOA is developmentally toxic and in mice affects growth, development, and viability of offspring. This study segregates the contributions of gestational and lactational exposures and considers the impact of restricting exposure to specific gestational periods. Pregnant CD-1 mice were dosed on gestation days (GD) 1-17 with 0, 3, or 5 mg PFOA/kg body weight, and pups were fostered at birth to give seven treatment groups: unexposed controls, pups exposed in utero (3U and 5U), lactationally (3L and 5L), or in utero + lactationally (3U + L and 5U + L). In the restricted exposure (RE) study, pregnant mice received 5 mg PFOA/kg from GD7-17, 10-17, 13-17, or 15-17 or 20 mg on GD15-17. In all PFOA-treated groups, dam weight gain, number of implantations, and live litter size were not adversely affected and relative liver weight increased. Treatment with 5 mg/kg on GD1-17 increased the incidence of whole litter loss and pups in surviving litters had reduced birth weights, but effects on pup survival from birth to weaning were only affected in 5U + L litters. In utero exposure (5U), in the absence of lactational exposure, was sufficient to produce postnatal body weight deficits and developmental delay in the pups. In the RE study, birth weight and survival were reduced by 20 mg/kg on GD15-17. Birth weight was also reduced by 5 mg/kg on GD7-17 and 10-17. Although all PFOA-exposed pups had deficits in postnatal weight gain, only those exposed on GD7-17 and 10-17 also showed developmental delay in eye opening and hair growth. In conclusion, the postnatal developmental effects of PFOA are due to gestational exposure. Exposure earlier in gestation produced stronger responses, but further study is needed to determine if this is a function of higher total dose or if there is a developmentally sensitive period.

Animals↗
PubMed2006

Quantifying phthalate metabolites in human meconium and semen using automated off-line solid-phase extraction coupled with on-line SPE and isotope-dilution high-performance liquid chromatography--tandem mass spectrometry.

We developed an analytical method using off-line solid-phase extraction (SPE) coupled with on-line SPE and isotope-dilution high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS) to determine the concentrations of phthalate metabolites in human meconium and in semen. First, we used off-line SPE to remove interfering proteins and other biomolecules from the samples. Then, we preconcentrated the phthalate metabolites in the extract using on-line SPE before measuring them by HPLC-MS/MS. For most of the analytes, the limits of detection ranged between 0.2 and 0.7 ng/g for meconium and between 0.3 and 0.7 ng/mL for semen. The recovery after off-line SPE varied for most analytes between 65 and 99% at concentrations ranging from 3.0 to 30.0 ng/mL in semen and between 67 and 103% at concentrations ranging from 2.0 to 10.0 ng/mL in meconium. Precision measured by the relative standard deviation ranged from 3.2 to 19.1% for intraday and from 3.9 to 18.6% for interday. We validated this novel approach--which is applicable to other biological matrixes, including serum and breast milk--on spiked samples and on five meconium samples and one pooled semen sample from people with no known occupational exposure to phthalates.

Animals↗
PubMed2006

Quantification of the urinary concentrations of parabens in humans by on-line solid phase extraction-high performance liquid chromatography-isotope dilution tandem mass spectrometry.

Parabens (alkyl esters of p-hydroxybenzoic acid) are widely used as antimicrobial preservatives in cosmetic products, pharmaceuticals, and food processing. However, weak estrogenicity of some parabens has been revealed from several studies. Human exposure to parabens may be assessed by measuring the conjugated or free species of these compounds or their metabolites in urine. We have developed a method using on-line solid phase extraction-high performance liquid chromatography-isotope dilution tandem mass spectrometry with peak focusing to measure the urinary concentrations of methyl, ethyl, propyl, n- and iso- butyl, and benzyl parabens. This method has good reproducibility and accuracy with detection limits for all analytes below 0.2ng/mL in 100microL of urine, and permits quick and accurate analysis of a large number of samples in epidemiologic studies for assessing the prevalence of human exposure to parabens. Using this method, we detected methyl, ethyl, and propyl parabens, mostly as conjugated species, in 22 urine samples collected from anonymous adults.

Calibration↗
PubMed2006

Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002.

Manufacturers have used perfluorochemicals (PFCs) since the 1950s in many industrial and consumer products, including protective coatings for fabrics and carpet, paper coatings, insecticide formulations, and surfactants. Some PFCs are persistent ubiquitous contaminants in the environment and in humans. Exposures to PFCs result in potential developmental and other adverse effects in animals. The sources of human exposure to PFCs and the potential health risks associated with exposure are still unclear, and differences in patterns of human exposure may vary. We measured the serum concentrations of perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA; C8), perfluorohexane sulfonic acid (PFHxS), and 8 other PFCs in 54 pooled serum samples collected from 1832 participants of the 2001-2002 National Health and Nutrition Examination Survey. Participants were 12 years of age and older. The pools represented three major racial groups/ethnicities (non-Hispanic blacks, non-Hispanic whites, and Mexican Americans), four age categories (12-19 years, 20-39 years, 40-59 years, and 60 years and older), and both genders. PFCs were extracted from 100 microL of serum using on-line solid-phase extraction coupled to isotope dilution-high performance liquid chromatography-tandem mass spectrometry. The limits of detection ranged from 0.05 ng/mL to 0.2 ng/mL. The concentrations of most PFCs were similar among the four age groups. For PFOS, the estimated least-squares mean (LSM) concentrations among non-Hispanic white males (40.19 ng/mL) and females (23.97 ng/mL) were greater than among non-Hispanic black males (18.27 ng/mL) and females (17.93 ng/mL) or Mexican American males (13.71 ng/mL) and females (10.40 ng/ mL). Similarly, for PFOA, the LSM concentrations among non-Hispanic white males (6.98 ng/mL) and females (3.97 ng/ mL) were greater than among non-Hispanic black males (3.62 ng/mL) and females (2.85 ng/mL) or Mexican American males (2.89 ng/mL) and females (2.08 ng/mL). Non-Hispanic whites had also greater LSM concentrations of PFHxS than non-Hispanic blacks and Mexican Americans. These findings indicate different patterns of human exposure to PFCs among the population groups examined and stress the importance of conducting research to identify the environmental sources and pathways of human exposure to PFCs.

Chromatography, High Pressure Liquid↗
PubMed2006

Urinary biomarkers of di-isononyl phthalate in rats.

Commercial di-isononyl phthalate (DiNP) is a mixture of various branched-chain dialkyl phthalates mainly containing nine-carbon alkyl isomers. At high doses in rodents, DiNP is a carcinogen, and a developmental toxicant. After exposure, the diester isomers are de-esterified to form hydrolytic monoesters, monoisononyl phthalates (MiNP), which subsequently metabolize to form oxidative metabolites. These metabolites can be excreted in urine or feces. The urinary excretion of DiNP metabolites was monitored in adult female Sprague-Dawley rats after oral administration of a single dose (300 mg/kg) of commercial DiNP. The metabolites were extracted from urine, resolved with high performance liquid chromatography, analyzed by mass spectrometry, and tentatively identified based on their chromatographic separation and mass spectrometric fragmentation pattern. Because DiNP is an isomeric mixture, its metabolites were also isomeric mixtures that eluted from the HPLC column with close retention times. Mono(carboxy-isooctyl)phthalate (MCiOP) was identified as the major metabolite of DiNP; in addition, mono(hydroxy-isononyl)phthalate (MHiNP) and mono(oxo-isononyl)phthalate (MOiNP) were present. Furthermore, metabolites of di-isooctyl phthalate (DiOP) and di-isodecyl phthalate (DiDP) were also detected. Excretion toxicokinetics of the DiNP metabolites in urine followed a biphasic pattern with initial rapid decay in concentration. Despite potential differences in the metabolism of DiNP among species, MCiOP, MHiNP and MOiNP were detected in humans with no known exposure to DiNP at levels significantly higher than MiNP suggesting that these oxidative metabolites may be better urinary biomarkers of human exposure to DiNP than is MiNP.

Administration, Oral↗
PubMed2006

Impact of urine preservation methods and duration of storage on measured levels of environmental contaminants.

Collection of urine samples in human studies involves choices regarding shipping, sample preservation, and storage that may ultimately influence future analysis. As more studies collect and archive urine samples to evaluate environmental exposures in the future, we were interested in assessing the impact of urine preservative, storage temperature, and time since collection on nonpersistent contaminants in urine samples. In spiked urine samples stored in three types of urine vacutainers (no preservative, boric acid, and chlorhexidine), we measured five groups of contaminants to assess the levels of these analytes at five time points (0, 24, 48, and 72 h, and 1 week) and at two temperatures (room temperature and 4 degrees C). The target chemicals were bisphenol A (BPA), metabolites of organophosphate (OP), carbamate, and pyrethroid insecticides, chlorinated phenols, and phthalate monoesters, and were measured using five different mass spectrometry-based methods. Three samples were analyzed at each time point, with the exception of BPA. Repeated measures analysis of variance was used to evaluate effects of storage time, temperature, and preservative. Stability was summarized with percent change in mean concentration from time 0. In general, most analytes were stable under all conditions with changes in mean concentration over time, temperature, and preservative being generally less than 20%, with the exception of the OP metabolites in the presence of boric acid. The effect of storage temperature was less important than time since collection. The precision of the laboratory measurements was high allowing us to observe small differences, which may not be important when categorizing individuals into broader exposure groups.

Environmental Exposure↗
PubMed2006

Mono-(3-carboxypropyl) phthalate, a metabolite of di-n-octyl phthalate.

Di-n-octyl phthalate (DnOP) is found as a component of mixed C6-C10 linear-chain phthalates used as plasticizers in various polyvinyl chloride applications, including flooring and carpet tiles. Following exposure and absorption, DnOP is metabolized to its hydrolytic monoester, mono-n-octyl phthalate (MnOP), and other oxidative products. The urinary levels of one of these oxidative metabolites, mono-(3-carboxypropyl) phthalate (MCPP), were about 560-fold higher than MnOP in Sprague-Dawley rats dosed with DnOP by gavage. Furthermore, MCPP was also found in the urine of rats dosed with di-isooctyl phthalate (DiOP), di-isononyl phthalate (DiNP), di-isodecyl phthalate (DiDP), di-(2-ethylhexyl) phthalate, and di-n-butyl phthalate (DBP), although at concentrations considerably lower than in rats given similar concentrations of DnOP. The comparatively much higher urinary concentrations of MCPP than of the hydrolytic monoesters of the high-molecular-weight phthalates DiOP, DiNP, and DiDP in the exposed rats suggest that these monoesters may be poor biomarkers of exposure to their precursor phthalates and may explain the relatively low frequency of detection of these monoester metabolites in human populations. MCPP and MnOP were also measured in 267 human urine samples. The frequent detection and higher urinary concentrations of MCPP than MnOP suggest that exposure to DnOP might be higher than previously thought based on the measurements of MnOP alone. However, because MCPP is also a minor metabolite of DBP and other phthalates in rats, and the metabolism of phthalates in rodents and humans may differ, additional data on the absorption, distribution, metabolism, and elimination of MCPP are needed to completely understand the extent of human exposure to DnOP from the urinary concentrations of MCPP.

Animals↗
PubMed2006

Altered semen quality in relation to urinary concentrations of phthalate monoester and oxidative metabolites.

BACKGROUND: Phthalates are multifunctional chemicals used in a variety of consumer, medical, and personal care products. Previously, we reported dose-response associations of decreased semen quality with urinary concentrations of monobutyl phthalate (MBP) and monobenzyl (MBzP) phthalate, which are metabolites of dibutyl phthalate and butylbenzyl phthalate, respectively. The present study extends our work in a larger sample of men and includes measurements of di(2-ethylhexyl) phthalate (DEHP) oxidative metabolites. METHODS: Between January 2000 and May 2004, we recruited 463 male partners of subfertile couples who presented for semen analysis to the Massachusetts General Hospital. Semen parameters were dichotomized based on World Health Organization reference values for sperm concentration (<20 million/mL) and motility (<50% motile) and the Tygerberg Kruger Strict criteria for morphology (<4% normal). The comparison group was men with all 3 semen parameters above the reference values. In a single spot urine sample from each man, phthalate metabolites were measured using solid-phase extraction coupled to high-performance liquid chromatography isotope-dilution tandem mass spectrometry. RESULTS: There were dose-response relationships of MBP with low sperm concentration (odds ratio per quartile adjusted for age, abstinence time, and smoking status = 1.00, 3.1, 2.5, 3.3; P for trend = 0.04) and motility (1.0, 1.5, 1.5, 1.8; P for trend = 0.04). There was suggestive evidence of an association between the highest MBzP quartile and low sperm concentration (1.00, 1.1, 1.1, 1.9; P for trend = 0.13). There were no relationships of monoethyl phthalate, monomethyl phthalate, and the DEHP metabolites with these semen parameters. CONCLUSION: The present study confirms previous results on the relationship of altered semen quality with exposure to MBP at general population levels. We did not find associations between semen parameters and 3 DEHP metabolites.

Adult↗
PubMed2006

Human exposure assessment to environmental chemicals using biomonitoring.

In modern societies, humans may be exposed to a wide spectrum of environmental chemicals. Although the health significance of this exposure for many chemicals is unknown, studies to investigate the prevalence of exposure are warranted because of the chemicals' potential harmful health effects, as often indicated in animal studies. Three tools have been used to assess exposure: exposure history/questionnaire information, environmental monitoring, and biomonitoring (i.e. measuring concentrations of the chemicals, their metabolites, or their adducts in human specimens). We present an overview on the use of biomonitoring in exposure assessment using phthalates, bisphenol A and other environmental phenols, and perfluorinated chemicals as examples. We discuss some factors relevant for interpreting and understanding biomonitoring data, including selection of both biomarkers of exposure and human matrices, and toxicokinetic information. The use of biomonitoring in human risk assessment is not discussed.

Biomarkers↗
PubMed2006

Estimated daily phthalate exposures in a population of mothers of male infants exhibiting reduced anogenital distance.

Phthalate diesters have been shown to be developmental and reproductive toxicants in animal studies. A recent epidemiologic study showed certain phthalates to be significantly associated with reduced anogenital distance in human male infants, the first evidence of subtle developmental effects in human male infants exposed prenatally to phthalates. We used two previously published methods to estimate the daily phthalate exposures for the four phthalates whose urinary metabolites were statistically significantly associated with developmental effects in the 214 mother-infant pairs [di-n-butyl phthalate (DnBP) , diethyl phthalate (DEP) , butylbenzyl phthalate (BBzP) , diisobutyl phthalate (DiBP) ] and for another important phthalate [di-2-ethylhexyl phthalate (DEHP) ]. We estimated the median and 95th percentile of daily exposures to DBP to be 0.99 and 2.68 microg/kg/day, respectively ; for DEP, 6.64 and 112.3 microg/kg/day ; for BBzP, 0.50 and 2.47 microg/kg/day ; and for DEHP, 1.32 and 9.32 microg/kg/day. The U.S. Environmental Protection Agency (EPA) reference doses for these chemicals are 100 (DBP) , 800 (DEP) , 200 (BBzP) , and 20 (DEHP) microg/kg/day. The median and 95th percentile exposure estimates for the phthalates associated with reduced anogenital distance in the study population are substantially lower than current U.S. EPA reference doses for these chemicals and could be informative to any updates of the hazard assessments and risk assessments for these chemicals.

Cohort Studies↗
PubMed2006

Oxidative metabolites of diisononyl phthalate as biomarkers for human exposure assessment.

Diisononyl phthalate (DINP) is a complex mixture of predominantly nine-carbon branched-chain dialkyl phthalate isomers. Similar to di(2-ethylhexyl) phthalate, a widely used phthalate, DINP causes antiandrogenic effects on developing rodent male fetuses. Traditionally, assessment of human exposure to DINP has been done using monoisononyl phthalate (MINP) , the hydrolytic metabolite of DINP, as a biomarker. However, MINP is only a minor urinary metabolite of DINP. Oxidative metabolites, including mono(carboxyisooctyl) phthalate (MCIOP) , mono(oxoisononyl) phthalate (MOINP) , and mono(hydroxyisononyl) phthalate (MHINP) are the major urinary metabolites in DINP-dosed rats. The urinary concentrations of MINP, MCIOP, MOINP, and MHINP were measured in 129 adult anonymous human volunteers with no known exposure to DINP. Although MINP was not present at detectable levels in any of the samples analyzed, MCIOP, MHINP, and MOINP were detected in 97, 100, and 87% of the urine samples at geometric mean levels equal to 8.6, 11.4, and 1.2 ng/mL, respectively. The concentrations of all three oxidative metabolites were highly correlated with each other (p<0.0001), which confirms a common precursor. MCIOP was excreted predominantly as a free species, whereas MOINP was excreted mostly in its glucuronidated form. The percentage of MHINP excreted either glucuronidated or in its free form was similar. The significantly higher frequency of detection and urinary concentrations of oxidative metabolites than of MINP suggest that these oxidative metabolites are better biomarkers of exposure assessment of DINP than is MINP. Therefore, we concluded that the prevalence of human exposure to DINP is underestimated by using MINP as the sole DINP urinary biomarker.

Adult↗
PubMed2006

Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.

OBJECTIVE: We previously demonstrated that among 54 infants in neonatal intensive care units, exposure to polyvinyl chloride plastic medical devices containing the plasticizer di(2-ethylhexyl) phthalate (DEHP) is associated with urinary concentrations of mono(2-ethylhexyl) phthalate (MEHP) , a DEHP metabolite. In this follow-up report, we studied the neonates' exposure to DEHP-containing devices in relation to urinary concentrations of two other DEHP metabolites, and to urinary concentrations of metabolites of dibutyl phthalate (DBP) and benzylbutyl phthalate (BzBP) , phthalates found in construction materials and personal care products. MEASUREMENTS: A priori, we classified the intensiveness of these 54 infants' exposure to DEHP-containing medical products. We measured three metabolites of DEHP in infants' urine: MEHP and two of its oxidative metabolites, mono(2-ethyl-5-hydroxylhexyl) phthalate (MEHHP) and mono(2-ethyl-5-oxohexyl) phthalate (MEOHP) . We also measured monobutyl phthalate (MBP) , a metabolite of DBP, and monobenzyl phthalate (MBzP), a metabolite of BzBP. RESULTS: Intensiveness of DEHP-containing product use was monotonically associated with all three DEHP metabolites. Urinary concentrations of MEHHP and MEOHP among infants in the high-DEHP-intensiveness group were 13-14 times the concentrations among infants in the low-intensiveness group (p</= 0.007). Concentrations of MBP were somewhat higher in the medium- and high-DEHP-intensiveness group; MBzP did not vary by product use group. Incorporating all phthalate data into a structural equation model confirmed the specific monotonic association between intensiveness of product use and biologic measures of DEHP. CONCLUSION: Inclusion of the oxidative metabolites MEHHP and MEOHP strengthened the association between intensiveness of product use and biologic indices of DEHP exposure over that observed with MEHP alone.

Age Factors↗
PubMed2006

Integrating biomonitoring exposure data into the risk assessment process: phthalates [diethyl phthalate and di(2-ethylhexyl) phthalate] as a case study.

The probability of nonoccupational exposure to phthalates is high given their use in a vast range of consumables, including personal care products (e.g., perfumes, lotions, cosmetics), paints, industrial plastics, and certain medical devices and pharmaceuticals. Phthalates are of high interest because of their potential for human exposure and because animal toxicity studies suggest that some phthalates affect male reproductive development apparently via inhibition of androgen biosynthesis. In humans, phthalates are rapidly metabolized to their monoesters, which can be further transformed to oxidative products, conjugated, and eliminated. Phthalate metabolites have been used as biomarkers of exposure. Using urinary phthalate metabolite concentrations allows accurate assessments of human exposure because these concentrations represent an integrative measure of exposure to phthalates from multiple sources and routes. However, the health significance of this exposure is unknown. To link biomarker measurements to exposure, internal dose, or health outcome, additional information (e.g., toxicokinetics, inter- and intraindividual differences) is needed. We present a case study using diethyl phthalate and di(2-ethylhexyl) phthalate as examples to illustrate scientific approaches and their limitations, identify data gaps, and outline research needs for using biomonitoring data in the context of human health risk assessment, with an emphasis on exposure and dose. Although the vast and growing literature on phthalates research could not be covered comprehensively in this article, we made every attempt to include the most relevant publications as of the end of 2005.

Animals↗
PubMed2006

Parabens as urinary biomarkers of exposure in humans.

BACKGROUND: Parabens appear frequently as antimicrobial preservatives in cosmetic products, in pharmaceuticals, and in food and beverage processing. In vivo and in vitro studies have revealed weak estrogenic activity of some parabens. Widespread use has raised concerns about the potential human health risks associated with paraben exposure. OBJECTIVES: Assessing human exposure to parabens usually involves measuring in urine the conjugated or free species of parabens or their metabolites. In animals, parabens are mostly hydrolyzed to p-hydroxybenzoic acid and excreted in the urine as conjugates. Still, monitoring urinary concentrations of p-hydroxybenzoic acid is not necessarily the best way to assess exposure to parabens. p-hydroxybenzoic acid is a nonspecific biomarker, and the varying estrogenic bioactivities of parabens require specific biomarkers. Therefore, we evaluated the use of free and conjugated parent parabens as new biomarkers for human exposure to these compounds. RESULTS: We measured the urinary concentrations of methyl, ethyl, n-propyl, butyl (n- and iso-), and benzyl parabens in a demographically diverse group of 100 anonymous adults. We detected methyl and n-propyl parabens at the highest median concentrations (43.9 ng/mL and 9.05 ng/mL, respectively) in nearly all (> 96%) of the samples. We also detected other parabens in more than half of the samples (ethyl, 58%; butyl, 69%). Most important, however, we found that parabens in urine appear predominantly in their conjugated forms. CONCLUSIONS: The results, demonstrating the presence of urinary conjugates of parabens in humans, suggest that such conjugated parabens could be used as exposure biomarkers. Additionally, the fact that conjugates appear to be the main urinary products of parabens may be important for risk assessment.

Biomarkers↗