A review of dietary and non-dietary exposure to bisphenol-A

Geens, Tinne; Aerts, Dominique; Berthot, Carl; Bourguignon, Jean-Pierre; Goeyens, Léo; Lecomte, Philippe; Maghuin‐Rogister, Guy; Pironnet, Anne-Madeleine; Pussemier, Luc; Scippo, Marie‐Louise; Loco, Joris Van; Covaci, Adrian

doi:10.1016/j.fct.2012.07.059

Cited by 835 publications

(542 citation statements)

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“…4, 80 The estimated exposure from food is 0.01–13 µg kg –1 BW day –1 for children, and less than 4.2 µg kg –1 BW day –1 for adults 4. Canned food is the primary source of human BPA exposure 17.…”

Section: Sources and Routes Of Bpa Exposure In Everyday Settingsmentioning

confidence: 99%

Low‐Dose Bisphenol A Exposure: A Seemingly Instigating Carcinogenic Effect on Breast Cancer

2016

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Breast cancer is the fifth most common cause of cancer death in the world and the second most common fatal cancer in women. Epidemiological studies and clinical data have indicated that hormones, including estrogen, progesterone, and prolactin, play important roles in the initiation and progression of breast cancer. Bisphenol A (BPA) is one of the most commonly used and thoroughly studied endocrine disruptors. It can be released from consumer products and deposited in the environment, thus creating potential for human exposure through oral, inhaled, and dermal routes. Some recent reviews have summarized the known mechanisms of endocrine disruptions by BPA in human diseases, including obesity, reproductive disorders, and birth defects. However, large knowledge gaps still exist on the roles BPA may play in cancer initiation and development. Evidence from animal and in vitro studies has suggested an association between increased incidence of breast cancer and BPA exposure at doses below the safe reference doses that are the most environmentally relevant. Most current studies have paid little attention to the cancer‐promoting properties of BPA at low doses. In this review, recent findings on the carcinogenic effects of low‐dose BPA on breast cancer and discussed possible biologic mechanisms are summarized.

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Section: Sources and Routes Of Bpa Exposure In Everyday Settingsmentioning

confidence: 99%

Low‐Dose Bisphenol A Exposure: A Seemingly Instigating Carcinogenic Effect on Breast Cancer

2016

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“…The use of BPA in food packaging, along with the ability of BPA to leach into the food (7) , has led many to believe that diet is a major route of human BPA exposure (7)(8)(9)(10)(11)(12) . BPA has also been found in products made from recycled paper (21) , dust particles (22)(23)(24) , thermal receipt paper (25,26) , soil, tap water and surface water (27)(28)(29)(30)(31)(32) .…”

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confidence: 99%

Bisphenol A exposure and associations with obesity among adults: a critical review

Oppeneer

Robien

2014

Public Health Nutr.

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Objective: To review the literature on bisphenol A (BPA) exposure and obesity in human populations. Design: Systematic review of the literature via searches of PubMed, EMBASE, Web of Science and reference lists for articles published to 1 August 2014. Setting: China, Italy, Japan, Republic of Korea, Sweden, UK, USA. Subjects: Adults (≥18 years). Results: Eighteen articles were identified and included in the review. Twelve studies included secondary evaluations of BPA exposure and BMI, and six studies evaluated body composition as the primary outcome. All analyses were crosssectional and no study included in the review received a positive quality rating (twelve negative, six neutral). Eight studies observed a statistically significant positive association between urinary or serum BPA levels and BMI, and ten studies observed no association. Studies where BMI was a primary outcome and studies of neutral quality were more likely to observe an association. Conclusions: Study results are conflicting and significant methodological issues limit the ability to draw conclusions from these studies. Prospective studies that measure BPA exposure and changes in body weight and composition are needed to establish temporality, causality and the direction of any observed associations.

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“…Despite current literature suggesting canned foods and diet as a primary source of exposure, there is increasing debate as to whether diet is the primary source of BPA exposure given the lack of paired dietary intake data and data on urinary or serum BPA concentrations (59,87,108,111) . While current data indicate that other known sources of exposure likely contribute only minimally to exposure levels (59,73,87,88) , diet has long been assumed to be the primary source of BPA exposure in the general population and this may have led to limited investigation of other potential dietary and non-dietary sources of exposure. BPA is also used in cigarette filters, but smokers were excluded from the present study (59,87,112) .…”

Section: Discussionmentioning

confidence: 97%

“…Microwave meals and restaurant meals have previously been shown to be additional sources of BPA exposure, possibly due to use of canned food items in preparation or contact with non-BPA-free storage containers; thus, microwave and restaurant meals are included in the score (42,57) . While receipt paper handling is not a dietary source of exposure, we chose to include this variable because we wanted to account for all the potential major contributing factors to the variability in urinary BPA levels and frequent handling of thermal receipt paper is a known source of BPA exposure (72)(73)(74)(75) . The score was weighted to account for reported variation in BPA content of foods.…”

Section: Measurement Of Urinary Bisphenol Amentioning

confidence: 99%

Estimating bisphenol A exposure levels using a questionnaire targeting known sources of exposure

Nomura

Harnack

Robien

2015

Public Health Nutr.

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Objective: To develop a BPA Exposure Assessment Module (BEAM) for use in large observational studies and to evaluate the ability of the BEAM to estimate bisphenol A (BPA) exposure levels. Design: The BEAM was designed by modifying an FFQ with questions targeting known sources of BPA exposure. Frequency of intake of known dietary sources of BPA was assessed using the BEAM and three 24 h food records as a reference diet measurement tool. Urinary BPA (uBPA) levels were measured as the criterion tool in a pooled urine sample (nine spot samples per participant). Spearman correlations, linear regression and weighted kappa analysis were used to evaluate the ability of the BEAM and food records to estimate BPA exposure levels. Setting: Minneapolis/Saint Paul, MN, USA. Subjects: Sixty-eight healthy adult (20-59 years) volunteers. Results: Dietary BPA intake assessed by the BEAM was not associated with uBPA levels and was unable to predict participants' rank by uBPA levels. BEAM models with all a priori predictors explained 25 % of the variability in uBPA levels. Canned food intake assessed by food records was associated with uBPA levels, but was unable to rank participants by uBPA levels. Multivariable-adjusted food record models with a priori predictors explained 41 % of the variability in uBPA levels. Conclusions: Known dietary sources of BPA exposure explained less than half the variability in uBPA levels, regardless of diet assessment method. Findings suggest that a questionnaire approach may be insufficient for ranking BPA exposure level and additional important sources of BPA exposure likely exist.Bisphenol A (BPA), used in the manufacture of polycarbonate plastics and epoxy resins, is one of the highest-volume chemicals produced worldwide (1,2) and production is predicted to reach more than 4·09 Mt (9 billion lb) by 2020 (3) . Biomonitoring data indicate widespread, chronic low-level exposure to BPA (2,(4)(5)(6) . Animal and in vitro data indicate exposure adversely affects health, but limited and conflicting human epidemiological data is often cited as a barrier for risk assessment by regulatory agencies (7)(8)(9) . While recent epidemiological data suggest that BPA may be associated with alterations in sex and thyroid hormone levels (10)(11)(12)(13)(14)(15)(16)(17)(18) , infertility and polycystic ovary syndrome (19)(20)(21) , obesity (18,(22)(23)(24)(25)(26)(27)(28)(29) , pre-diabetes/type 2 diabetes (23,(30)(31)(32) and CVD (23,31,(33)(34)(35) , most are crosssectional analyses with important limitations, such as lack of long-term exposure data which are more relevant for chronic disease risk (36) . Diet has been considered the primary source of BPA exposure (37)(38)(39)(40)(41)(42)(43) and previous studies support diet as the major route of human BPA exposure (44)(45)(46)(47)(48)(49)(50) . The use of polycarbonate plastics in the production of food and beverage storage containers has been largely phased out in the USA. However, BPA is still used in epoxy resin linings of metal cans and lids (1,2,6,51...

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A review of dietary and non-dietary exposure to bisphenol-A

Cited by 835 publications

References 120 publications

Low‐Dose Bisphenol A Exposure: A Seemingly Instigating Carcinogenic Effect on Breast Cancer

Low‐Dose Bisphenol A Exposure: A Seemingly Instigating Carcinogenic Effect on Breast Cancer

Bisphenol A exposure and associations with obesity among adults: a critical review

Estimating bisphenol A exposure levels using a questionnaire targeting known sources of exposure

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