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Bisphenol A (BPA) is an endocrine-disrupting chemical (EDC) that has been associated with various human disorders. Human exposure is ubiquitous. The primary route of exposure is ingestion, as BPA can leach from plastic food packaging and the epoxy resin lining of cans into food. Restrictions on the use of BPA in consumer products due to its health concerns have resulted in the development and introduction of new BPA alternatives. These compounds are likely to have health effects comparable to those of BPA. However, data on the type and amount of substitutes used in consumer products are difficult to obtain, and studies on their prevalence of use and impact on health in human populations are sparse. The aim of the present study was to evaluate the urinary concentrations of BPA and its analogues after the consumption of soda from cans compared to polyethylene terephthalate (PET) bottles and glass bottles. Additionally, we investigated blood pressure levels before and after soda consumption from cans, PET bottles, and glass bottles. We conducted a randomized crossover trial with 103 female participants between 30 and 65 years of age. The participants were assigned to drink soda (Coca-Cola light) from cans, PET bottles and glass bottles on two days of an intervention week. Urine samples were collected two to three hours after the intervention. Blood pressure levels were measured before and two to three hours after the intervention. Urinary bisphenol concentrations were measured via GC-AEI-MS/MS. The associations between the intervention and log10-transformed bisphenol concentrations and blood pressure levels were evaluated via a mixed models approach. For comparisons of the interventions, we used Tukey tests. We found significantly higher BPA concentrations in the urine samples of our study participants after soda consumption from cans than after soda consumption from PET bottles (+ 22.3%, 95% CI 3.37;44.64, P value 0.014). There was no difference compared to glass bottles. In addition to BPA, we detected BPF, BPS and BPE in some of the urine samples, but to a lesser extent, and independent of beverage packaging. Systolic and diastolic blood pressure increased across all interventions independent of whether soda was consumed from cans, PET bottles, or glass bottles. This study suggests that canned soda may increase the amount of BPA excreted in the urine of humans. The increase in blood pressure, independent of beverage packaging, may be due to the caffeine content of the consumed beverage. Given the potential of bisphenol exposure from canned food and beverage consumption, as well as the availability of alternatives in the epoxy resin lining of cans, complete removal of BPA from cans is an attractive option for mitigating human exposure to bisphenols. Universal Trial Number/ DRKS-ID: U1111-1244-7033/ DRKS00019922 (Registration Date 29/11/2019).

Diet is a primary source of exposure for high-molecular-weight phthalates and bisphenol A (BPA), but little is known about the efficacy of various interventions to reduce exposures. We conducted a randomized trial with 10 families to test the efficacy of a 5-day complete dietary replacement (Arm 1; n =21) versus written recommendations to reduce phthalate and BPA exposures (Arm 2; n =19). We measured phthalate and BPA concentrations in urine samples at baseline, intervention, and post-intervention periods. We used Wilcoxon paired signed-rank tests to assess change in concentrations across time and multi-level mixed effects regression models to assess differences between Arms 1 and 2. Urinary di(2-ethylhexyl) phthalate (DEHP) metabolite concentrations increased unexpectedly from a median of 283.7 nmol/g at baseline to 7027.5 nmol/g during the intervention ( P <0.0001) among Arm 1 participants, and no significant changes were observed for Arm 2 participants. We observed a statistically significant increase in total BPA concentration between baseline and intervention periods in Arm 1 but no significant changes in Arm 2. Arm 1 food ingredient testing for DEHP revealed concentrations of 21,400 ng/g in ground coriander and 673 ng/g in milk. Food contamination with DEHP led to unexpected increases in urinary phthalate concentrations in a trial intended to minimize exposure. In the absence of regulation to reduce phthalate and BPA concentrations in food production, it may be difficult to develop effective interventions that are feasible in the general population. An estimate of DEHP daily intake for children in the dietary replacement Arm was above the US Environmental Protection Agency oral reference dose and the European Food Safety Authority’s tolerable daily intake, suggesting that food contamination can be a major source of DEHP exposure.

IntroductionPhthalates and bisphenols, chemicals commonly used in the production of plastic products, exhibit endocrine disrupting properties linked to obesity and systemic inflammation. Given the ubiquitous use of plastic chemicals, their adverse impact on human health is of great importance. In this protocol, we describe a randomised controlled trial aimed at testing whether minimising exposure to plastics and plastic-associated chemicals (PACs) in community-dwelling adults with cardiometabolic risk factors can reduce urinary excretion of PACs and improve cardiometabolic health.Methods and analysisThe study will recruit (n=60) community-dwelling adults (18–60 years) with cardiometabolic risk factors, characterised by a body mass index of ≥30 kg/m2 and waist circumference of ≥88 cm in women and ≥102 cm in men. Participants will be randomised to a control (n=30) or an intervention group (n=30) receiving a 4-week diet and lifestyle modification designed to reduce plastic exposure, which includes the replacement of all food, kitchen utensils and equipment, personal care and cleaning products. The primary outcome is a reduction in urinary excretion of bisphenols after the 4-week intervention compared with the control arm. The secondary outcomes are the reduction in urinary excretion of low and high molecular weight phthalates. Finally, tertiary outcomes investigate improvements to cardiometabolic biomarkers, body composition, waist circumference and blood pressure. Participants will self-collect urine, stool and nasal lavage samples a day before beginning the intervention and at the end of each week. Fasting blood samples and health assessments will be collected during clinic visits: at baseline, mid-point and a day after the intervention period. Urinary PAC excretion and cardiometabolic health outcomes will be compared between the intervention and control groups.Ethics and disseminationThe PERTH Trial has ethics approval from the University of Western Australia Human Research Ethics Committee; 2021-ET001118. Results will be submitted for publication in peer-reviewed journals and presented at conferences.Trial registration numberNCT06571994.

Modafinil has been reported to reduce cocaine use in a clinical sample of infrequent users (2 days/week), but the effects of modafinil on cocaine self-administration in the laboratory have not been studied. The present study investigated the effects of modafinil maintenance on cocaine self-administration by frequent users (4 days/week) under controlled laboratory conditions. During this 48-day double-blind, crossover design study, the effects of modafinil maintenance (0, 200, and 400 mg/day) on response to smoked cocaine (0, 12, 25, and 50 mg) were examined in nontreatment-seeking cocaine-dependent individuals ( n =8). Cocaine significantly increased self-administration, subjective-effect ratings, and cardiovascular measures; modafinil at both doses (200 and 400 mg/day) markedly attenuated these effects. These findings agree with data from previous human laboratory and clinical investigations of modafinil as a potential cocaine abuse treatment medication. Thus, our data support the potential of modafinil as a pharmacotherapy for cocaine dependence.

Bisphenol A (BPA) is an endocrine disruptor. To evaluate the effect of canned food consumption on internal BPA dose, urinary BPA concentrations were measured before and after intake of canned foods. This study applied a randomized crossover design, recruited 20 healthy volunteers, and divided them into two groups. One group consumed canned food; the other group consumed fresh food. After a 1-day washout, the dietary interventions were reversed. In each period, urine samples were collected immediately before meals and then 2 h, 4 h, and 6 h after meals. A mixed-effects model was used to assess BPA changes over time. Our results showed urinary BPA concentrations increased after consumption of canned food. Specifically, urinary BPA concentrations significantly differed between consumption of canned food and fresh food at 2 h, 4 h, and 6 h after intake ( p values of 0.001, < 0.001, and < 0.001, respectively). Mean BPA concentrations at 2 h, 4 h, and 6 h after meals were 152%, 206%, and 79% higher, respectively, than mean BPA concentrations before meals. Urine concentration profiles of canned food intake showed that peaks were at 4 h, the increase diminished at 6 h, and returned to baseline levels at 24 h after intake. Therefore, dietary intervention and a 1-day washout period are effective for limiting internal BPA burden. This study provides convincing evidence of a human exposure route to BPA and a basis for designing interventions to mitigate exposure.

Bisphenol A (BPA) is a high-production-volume chemical associated with a wide range of health outcomes in animal and human studies. BPA is used as a developer in thermal paper products, including cash register receipt paper; however, little is known about exposure of cashiers to BPA and alternative compounds in receipt paper. We determined whether handling receipt paper results in measurable absorption of BPA or the BPA alternatives bisphenol S (BPS) and 4-hydroxyphenyl 4-isoprooxyphenylsulfone (BPSIP). Cashiers (n = 77) and non-cashiers (n = 25) were recruited from the Raleigh-Durham-Chapel Hill region of North Carolina during 2011-2013. Receipts were analyzed for the presence of BPA or alternatives considered for use in thermal paper. In cashiers, total urine and serum BPA, BPS, and BPSIP levels in post-shift samples (collected ≤ 2 hr after completing a shift) were compared with pre-shift samples. Levels of these compounds in urine from cashiers were compared to levels in urine from non-cashiers. Each receipt contained 1-2% by weight of the paper of BPA, BPS, or BPSIP. The post-shift geometric mean total urinary BPS concentration was significantly higher than the pre-shift mean in 33 cashiers who handled receipts containing BPS. The mean urine BPA concentrations in 31 cashiers who handled BPA receipts were as likely to decrease as to increase after a shift, but the mean post-shift concentrations were significantly higher than those in non-cashiers. BPSIP was detected more frequently in the urine of cashiers handling BPSIP receipts than in the urine of non-cashiers. Only a few cashiers had detectable levels of total BPA or BPS in serum, whereas BPSIP tended to be detected more frequently. Thermal receipt paper is a potential source of occupational exposure to BPA, BPS, and BPSIP. Thayer KA, Taylor KW, Garantziotis S, Schurman SH, Kissling GE, Hunt D, Herbert B, Church R, Jankowich R, Churchwell MI, Scheri RC, Birnbaum LS, Bucher JR. 2016. Bisphenol A, bisphenol S, and 4-hydro​xyphenyl 4-isopro​oxyphenyl​sulfone (BPSIP) in urine and blood of cashiers. Environ Health Perspect 124:437-444; http://dx.doi.org/10.1289/ehp.1409427.

Exposure to environmental chemicals may be a modifiable risk factor for progression of chronic kidney disease (CKD). The purpose of this study was to examine the impact of serially assessed exposure to bisphenol A (BPA) and phthalates on measures of kidney function, tubular injury, and oxidative stress over time in a cohort of children with CKD. Samples were collected between 2005 and 2015 from 618 children and adolescents enrolled in the Chronic Kidney Disease in Children study, an observational cohort study of pediatric CKD patients from the US and Canada. Most study participants were male (63.8%) and white (58.3%), and participants had a median age of 11.0 years (interquartile range 7.6 to 14.6) at the baseline visit. In urine samples collected serially over an average of 3.0 years (standard deviation [SD] 1.6), concentrations of BPA, phthalic acid (PA), and phthalate metabolites were measured as well as biomarkers of tubular injury (kidney injury molecule-1 [KIM-1] and neutrophil gelatinase-associated lipocalin [NGAL]) and oxidative stress (8-hydroxy-2'-deoxyguanosine [8-OHdG] and F2-isoprostane). Clinical renal function measures included estimated glomerular filtration rate (eGFR), proteinuria, and blood pressure. Linear mixed models were fit to estimate the associations between urinary concentrations of 6 chemical exposure measures (i.e., BPA, PA, and 4 phthalate metabolite groups) and clinical renal outcomes and urinary concentrations of KIM-1, NGAL, 8-OHdG, and F2-isoprostane controlling for sex, age, race/ethnicity, glomerular status, birth weight, premature birth, angiotensin-converting enzyme inhibitor use, angiotensin receptor blocker use, BMI z-score for age and sex, and urinary creatinine. Urinary concentrations of BPA, PA, and phthalate metabolites were positively associated with urinary KIM-1, NGAL, 8-OHdG, and F2-isoprostane levels over time. For example, a 1-SD increase in ∑di-n-octyl phthalate metabolites was associated with increases in NGAL (β = 0.13 [95% CI: 0.05, 0.21], p = 0.001), KIM-1 (β = 0.30 [95% CI: 0.21, 0.40], p < 0.001), 8-OHdG (β = 0.10 [95% CI: 0.06, 0.13], p < 0.001), and F2-isoprostane (β = 0.13 [95% CI: 0.01, 0.25], p = 0.04) over time. BPA and phthalate metabolites were not associated with eGFR, proteinuria, or blood pressure, but PA was associated with lower eGFR over time. For a 1-SD increase in ln-transformed PA, there was an average decrease in eGFR of 0.38 ml/min/1.73 m2 (95% CI: -0.75, -0.01; p = 0.04). Limitations of this study included utilization of spot urine samples for exposure assessment of non-persistent compounds and lack of specific information on potential sources of exposure. Although BPA and phthalate metabolites were not associated with clinical renal endpoints such as eGFR or proteinuria, there was a consistent pattern of increased tubular injury and oxidative stress over time, which have been shown to affect renal function in the long term. This raises concerns about the potential for clinically significant changes in renal function in relation to exposure to common environmental toxicants at current levels.

This study examined the associations between exposure to heavy metals, bisphenol A (BPA), and phthalates and precocious or delayed puberty. This study was a cross-sectional study using the data obtained from the Korea Environmental Exposure and Health Survey in Children and Adolescents. Blood samples were collected to measure lead, mercury, and cadmium levels, whereas spot urine samples were analyzed for BPA, phthalate metabolites, and creatinine levels. Sexual maturation status was assessed using self-measured Tanner stages. Our analyses involved single- and multi-exposure binomial logistic regression models adjusted for age, body mass index, presence of siblings, urban residence, and socioeconomic status. In the multi-exposure models, we applied quantile g-computation mixture analysis to calculate odds ratios (ORs) for precocious and delayed puberty. In the study cohort of 1,424 individuals, precocious puberty was identified in 50 (3.5%) individuals, whereas delayed puberty was identified in 54 (3.8%) individuals. In the single-exposure models, a higher mono-benzyl phthalate concentration was associated with a higher risk of delayed puberty in girls (OR = 2.75, 95% confidence interval: 1.34, 5.66). In the mixture exposure models, exposure to a mixture of BPA and phthalate metabolites was associated with precocious puberty in boys and delayed puberty in both sexes, although the risk estimates were imprecise. Our findings add to the increasing evidence suggesting that exposure to environmental chemicals may contribute to delayed puberty.

Early-life adversity increases the risk for psychopathology in later life. The underlying mechanism(s) is unknown, but epigenetic variation represents a plausible candidate. Early-life exposures can disrupt epigenetic programming in the brain, with lasting consequences for gene expression and behavior. This evidence is primarily derived from animal studies, with limited study in humans due to inaccessibility of the target brain tissue. In humans, although there is evidence for DNA methylation changes in the peripheral blood of psychiatric patients, a fundamental question remains as to whether epigenetic markers in the blood can predict epigenetic changes occurring in the brain. We used in utero bisphenol A (BPA) exposure as a model environmental exposure shown to disrupt neurodevelopment and exert long-term effects on behavior in animals and humans. We show that prenatal BPA induces lasting DNA methylation changes in the transcriptionally relevant region of theBdnfgene in the hippocampus and blood of BALB/c mice and that these changes are consistent withBDNFchanges in the cord blood of humans exposed to high maternal BPA levels in utero. Our data suggest thatBDNFDNA methylation in the blood may be used as a predictor of brainBDNFDNA methylation and gene expression as well as behavioral vulnerability induced by early-life environmental exposure. BecauseBDNFexpression and DNA methylation are altered in several psychiatric disorders that are associated with early-life adversity, including depression, schizophrenia, bipolar disorder, and autism, BDNF DNA methylation in the blood may represent a novel biomarker for the early detection of psychopathology.

Several studies indicate that bisphenol A (BPA) and phthalates may have a role in the development of metabolic diseases using different molecular pathways, including epigenetic regulatory mechanisms. However, it is unclear whether exposure to these chemicals modifies serum levels of miRNAs associated with gestational diabetes mellitus (GDM) risk. In the present study, we evaluated the serum levels of miRNAs associated with GDM (miR-9-5p, miR-16-5p, miR-29a-3p and miR-330-3p) and urinary levels of phthalate metabolites (mono-n-butyl phthalate (MBP), mono-isobutyl phthalate (MiBP), mono-benzyl phthalate (MBzP) and mono(2-ethyl hexyl) phthalate (MEHP)) and bisphenol A in GDM patients and women without GDM during the second trimester of gestation. We observed higher levels of miR-9-5p, miR-29a-3p and miR-330-3p in sera of patients with GDM compared to non-diabetic subjects. Phthalates were detected in 97–100% of urine samples, while BPA only in 40%. Urinary MEHP and BPA concentrations were remarkably higher in both study groups compared to previously reported data. Unadjusted MEHP levels and adjusted BPA levels were higher in non-diabetics than in GDM patients (p = 0.03, p = 0.02). We found positive correlations between adjusted urinary MBzP levels and miR-16-5p expression levels (p < 0.05), adjusted MEHP concentrations and miR-29a-3p expression levels (p < 0.05). We also found negative correlations between unadjusted and adjusted MBP concentrations and miR-29a-3p expression levels (p < 0.0001, p < 0.05), unadjusted MiBP concentrations and miR-29a-3p expression levels (p < 0.01). Urinary MEHP levels reflect a striking exposure to di(2-ethylhexyl) phthalate (DEHP) in pregnant Mexican women. This study highlights the need for a regulatory strategy in the manufacture of several items containing endocrine disruptors in order to avoid involuntary ingestion of these compounds in the Mexican population.