Urinary Bisphenol A (BPA) Concentrations among Workers in Industries that Manufacture and Use BPA in the USA

Abstract

Background Bisphenol A (BPA) toxicity and exposure risk to humans has been the subject of considerable scientific debate; however, published occupational exposure data for BPA are limited. Methods In 2013–2014, 77 workers at six US companies making BPA, BPA-based resins, or BPA-filled wax provided seven urine samples over two consecutive work days (151 worker-days, 525 samples). Participant information included industry, job, tasks, personal protective equipment used, hygiene behaviors, and canned food/beverage consumption. Total (free plus conjugated) BPA, quantified in urine by mass spectrometry, was detected in all samples. Results The geometric mean (GM) creatinine-adjusted total BPA (total BPACR) concentration was 88.0 μg g−1 (range 0.78–18 900 μg g−1), ~70 times higher than in US adults in 2013–2014 (1.27 μg g−1). GM total BPACR increased during Day 1 (26.6–127 μg g−1), decreased by pre-shift Day 2 (84.4 μg g−1) then increased during Day 2 to 178 μg g−1. By industry, baseline and post-baseline total BPACR was highest in BPA-filled wax manufacturing/reclaim (GM = 111 μg g−1) and lowest in phenolic resin manufacturing (GM = 6.56 μg g−1). By job, total BPACR was highest at baseline in maintenance workers (GM = 157 μg g−1) and post-baseline in those working with molten BPA-filled wax (GM = 441 μg g−1). Workers in the job of flaking a BPA-based resin had the lowest concentrations at baseline (GM = 4.81 μg g−1) and post-baseline (GM = 23.2 μg g−1). In multiple regression models, at baseline, industry significantly predicted increased total BPACR (P = 0.0248); post-baseline, handling BPA containers (P = 0.0035), taking ≥3 process/bulk samples with BPA (P = 0.0002) and wearing a Tyvek® coverall (P = 0.0042) significantly predicted increased total BPACR (after adjusting for total BPACR at baseline, time point, and body mass index). Conclusion Several work-related factors, including industry, job, and certain tasks performed, were associated with increased urinary total BPACR concentrations in this group of manufacturing workers. The potential for BPA-related health effects among these workers is unknown.

Protein Kinase D1 (PKD1) Is a New Functional Non-Genomic Target of Bisphenol A in Breast Cancer Cells

“…Among the most common endocrine disruptors, bisphenol A (BPA), used in epoxy resins and polycarbonate plastics, has been detected in biological fluids of most of the population worldwide, essentially due to oral contamination by ingestion of BPAcontaining food and drinks (Pirard et al, 2012;Galloway et al, 2018). Epidemiological and experimental studies show that human BPA serum concentrations generally vary from 0.2 to 1.6 ng/mL −1 (0.88 to 7 nM), but may reach higher values in workers who manipulate high amounts of BPA (thermal paper or plastics industries) (Hines et al, 2017). Many adverse health effects, such as hyperactivity, obesity, fertility problems, enamel defects, and cardiac arrhythmia have been associated with exposure to BPA, especially during the perinatal period of life (Jedeon et al, 2013) (reviewed in Giulivo et al, 2016).…”

Early life bisphenol A exposure and neurobehavior at 8 years of age: Identifying windows of heightened vulnerability

“…Exposure to BPA is almost universal in the United States; over 90% of the U.S. population has detectable levels of urinary BPA (Calafat et al 2008). Diet is the primary route of exposure, although exposure may also occur via inhalation and dermal absorption, particularly in occupational settings (Ehrlich et al 2014; Hehn 2016; Li et al 2010; Hines et al 2017; Thayer et al 2015b; Von Goetz et al 2010; Zalko et al 2011). BPA is capable of binding to the membrane and nuclear estrogen receptors and can affect gonadal hormone signaling, which play critical roles in the developing brain, influencing pathways that lead to sex-specific development and behavior (Henrichs et al 2013; Schug et al 2015).…”

Bisphenol A aggravates renal ischemia–reperfusion injury by disrupting mitochondrial homeostasis and N‐acetylcysteine mitigates the injurious outcomes

“…The 5 mg/kg BPA is chosen as a starting dose, since it is a no‐observed‐adverse‐effect level (NOAEL) . In view of the high dose, BPA as high as 250–500 mg/kg were used in several animal studies and BPA detectable level in occupational individuals were reported to be 70 times higher than in general population . In the present study, however, BPA at the maximum of 50 mg/kg is selected as it has been reported to induce oxidative and mitochondrial injury to a certain extent .…”

“…16 In view of the high dose, BPA as high as 250-500 mg/kg were used in several animal studies 10,17 and BPA detectable level in occupational individuals were reported to be 70 times higher than in general population. 18 In the present study, however, BPA at the maximum of 50 mg/kg is selected as it has been reported to induce oxidative and mitochondrial injury to a certain extent. 3 A dose and regimen of NAC is based on a study showing its potential to restore cognitive dysfunction and oxidative stress induced by BPA.…”