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Critical Reviews in Food Science and... 2022Endocrine-disrupting compounds (EDCs) are ubiquitous substances that are found in our everyday lives, including pesticides, plasticizers, pharmaceutical agents, personal...
BACKGROUND
Endocrine-disrupting compounds (EDCs) are ubiquitous substances that are found in our everyday lives, including pesticides, plasticizers, pharmaceutical agents, personal care products, and also in food products and food packaging. Increasing epidemiological evidence suggest that EDCs may affect the development or progression of breast cancer and consequently lead to lifelong harmful health consequences, especially when exposure occurs during early life in humans. Yet so far no appraisal of the available evidence has been conducted on this topic.
OBJECTIVE
To systematically review all the available epidemiological studies about the association of the levels of environmental exposures of EDCs with breast cancer risk.
METHODS
The search was performed in accordance with the PRISMA guidelines. We retrieved articles from PubMed (MEDLINE) until 10 March 2021. The key words used in this research were: "Endocrine disruptor(s)" OR "Endocrine disrupting chemical(s)" OR any of the EDCs mentioned below AND "Breast cancer" to locate all relevant articles published. We included only cohort studies and case-control studies. All relevant articles were accessed in full text and were evaluated and summarized in tables.
RESULTS
We identified 131 studies that met the search criteria and were included in this systematic review. EDCs reviewed herein included pesticides (e.g. p,p'-dichlorodiphenyltrichloroethane (DDT), p,p'-dichlorodiphenyldichloroethylene (DDE), atrazine, 2,3,7,8-tetrachloridibenzo-p-dioxin (TCDD or dioxin)), synthetic chemicals (e.g. bisphenol A (BPA), phthalates, per- and polyfluoroalkyl substances (PFAS), parabens, polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs), contraceptive pills), phytoestrogens (e.g. genistein, resveratrol), and certain mycotoxins (e.g. zearalenone). Most studies assessed environmental EDCs exposure via biomarker measurements.
CONCLUSION
We identified certain EDC exposures could potentially elevate the risk of breast cancer. As majority of EDCs are highly persistent in the environment and bio-accumulative, it is essential to assess the long-term impacts of EDC exposures, especially multi-generational and transgenerational. Also, since food is often a major route of exposure to EDCs, well-designed exposure assessments of potential EDCs in food and food packing are necessary and their potential link to breast cancer development need to be carefully evaluated for subsequent EDC policy making and regulations.
Topics: Case-Control Studies; Endocrine Disruptors; Environmental Exposure; Environmental Pollutants; Epidemiologic Studies; Humans; Neoplasms; Pesticides
PubMed: 33819127
DOI: 10.1080/10408398.2021.1903382 -
The Science of the Total Environment Aug 2021Tetrabromobisphenol A (TBBPA) is a type of brominated flame retardant widely detected in the environment and organisms. It has been reported to cause cytotoxicity and... (Meta-Analysis)
Meta-Analysis Review
Tetrabromobisphenol A (TBBPA) is a type of brominated flame retardant widely detected in the environment and organisms. It has been reported to cause cytotoxicity and disrupt endocrine system of animals. However, the effect of TBBPA on the reproductive system of male rodents is still controversial. Hence, this meta-analysis aims to determine whether TBBPA exposure damage to the reproductive system of male rodents. In this study, a thorough search of literatures was undertaken to select papers published before December 1st, 2020. The standard mean difference (SMD) and 95% confidence interval (CI) were calculated by random model. The results showed a statistically significant association between TBBPA exposure and the reproductive system health of male rodents (SMD = -0.35, 95% CI -0.50 to -0.19). The SMD for the reproductive system index organ weight, sperm quality, hormone levels, and gene expression were 0.03 (95% CI -0.18 to 0.23), -0.47 (95% CI -0.78 to -0.16), -0.51 (95% CI -0.75 to -0.27), and -0.98 (95% CI -1.36 to -0.60), respectively. There was a significant dose-effect relationship between TBBPA exposure and the reproductive health of male rodents, with the SMD values of low, medium, and high doses -0.20 (95% CI -0.34 to -0.05), -0.24 (95% CI -0.56 to 0.07), and -0.48 (95% CI -0.83 to -0.13), respectively. For exposure duration of TBBPA, an exposure time of >10 weeks (SMD = -0.33, 95% CI -0.54 to -0.12) showed more significant effect than an exposure time of ≤10 weeks (SMD = -0.22, 95% CI -0.43 to -0.02). Moreover, TBBPA exposure exhibited significant negative effects on sperm count (SMD = -0.49, 95% CI -0.82 to -0.17) while also reduced the content of triiodothyronine (T3), thyroxine (T4), and thyroid stimulating hormone (TSH) hormones. To summarize, our meta-analysis indicated that TBBPA had a toxicity effect to the reproductive system of male rodents.
Topics: Animals; Flame Retardants; Male; Polybrominated Biphenyls; Reproductive Health; Rodentia
PubMed: 33794456
DOI: 10.1016/j.scitotenv.2021.146745 -
Human Reproduction Update Feb 2021Despite increasing regulation, exposure to persistent organic pollutants (POPs) remains a serious public health concern due to their accumulation in the environment and...
BACKGROUND
Despite increasing regulation, exposure to persistent organic pollutants (POPs) remains a serious public health concern due to their accumulation in the environment and ability to biomagnify up the food chain. POPs are associated with endocrine-disrupting effects including adverse reproductive outcomes that could affect fecundability, i.e. the capacity to conceive a pregnancy, quantified as time to pregnancy (TTP).
OBJECTIVE AND RATIONALE
Results of epidemiologic studies that examine the impact of various chemical classes of POPs on TTP have not been synthesised. We undertook a systematic review to summarise the strength of evidence for associations of four common groups of POPs with couple fecundability and to identify gaps and limitations in the literature in order to inform policy decisions and future research.
SEARCH METHODS
We performed an electronic search of literature published between 1 January 2007 and 6 August 2019 in MEDLINE, EMBASE.com, Global Health, DART/TOXLINE and POPLINE. We included empirical research papers that examined human exposure to organochlorine (OC) pesticides, brominated flame retardants, polychlorinated organic compounds and/or per- and polyfluoroalkyl substances (PFAS) and considered TTP or fecundability as an outcome. Standardised forms for screening, data extraction and study quality were developed using DistillerSR software, and all reviews were completed in duplicate. We used the Newcastle-Ottawa Scale to assess risk of bias and devised additional quality metrics based on specific methodological features of fecundability studies.
OUTCOMES
The search returned 4573 articles, and 28 papers from 19 different studies met inclusion criteria. Among them, four studies measured TTP prospectively, three had data on participants' prenatal exposure, three examined associations in both male and female partners and one focused exclusively on males. Analyses varied widely in terms of exposure characterisation, precluding a meta-analytic approach. Evidence was strongest for adverse associations of female exposure to polychlorinated biphenyls with TTP, with some additional support for associations of female exposure to polybrominated diphenyl ethers and PFAS with longer TTP. Our review provided little or no support for associations between female exposure to OC pesticides or male exposure to any of the POP groups and TTP.
WIDER IMPLICATIONS
Evidence suggests that female exposure to at least some POPs may reduce fecundability. Although many of these chemicals are no longer in production, they are still detectable in human biosamples because of their persistence in the environment. Replacement chemicals that are being introduced as older ones are restricted may have similar reproductive consequences. Future studies should examine these newer POPs, assess interactions between POPs and other chemical and non-chemical exposures, investigate how POPs are distributed in and metabolised by the human body and focus on populations that may be disproportionately exposed.
Topics: Environmental Pollutants; Female; Halogenated Diphenyl Ethers; Humans; Male; Persistent Organic Pollutants; Pesticides; Polychlorinated Biphenyls; Pregnancy; Time-to-Pregnancy
PubMed: 33147335
DOI: 10.1093/humupd/dmaa037 -
BMJ Open Jun 2020Endocrine-disrupting chemicals (EDCs) are viewed as a major potential link between the environment and obesity development. We did a systematic review and meta-analysis... (Meta-Analysis)
Meta-Analysis
OBJECTIVE
Endocrine-disrupting chemicals (EDCs) are viewed as a major potential link between the environment and obesity development. We did a systematic review and meta-analysis to examine the association between exposure to EDCs and obesity.
DATA SOURCES, DESIGN AND ELIGIBILITY CRITERIA
PubMed, Scopus and Web of Science were searched from inception to 6 June 2018 for studies primarily addressing the association between exposure to EDCs after the age of 2 years and anthropometric measures of obesity or body fat. The Newcastle-Ottawa scale was used to assess the risk of bias.
DATA EXTRACTION AND SYNTHESIS
Two independent reviewers screened and conducted data extraction and synthesis. A third reviewer resolved disagreements.
RESULTS
A total of 73 studies investigating bisphenol A (32 286 individuals), organochlorine compounds (34 567 individuals), phthalates (21 401 individuals), polybrominated biphenyls (2937 individuals), polycyclic aromatic hydrocarbons (5174 individuals), parabens (4097 individuals), benzoic acid (3671 individuals) and polyfluoroalkyl substances (349 individuals) met our inclusion criteria. Most had a cross-sectional design and low or medium risk of bias. In qualitative analysis, bisphenol A and phthalates were consistently associated with general and abdominal obesity, in children and adults, and some studies suggested this association was age-dependent and gender-dependent. Meta-analysis indicated a significant association between exposure to bisphenol A and overweight (OR 1.254, 95% CI 1.005 to 1.564), obesity (OR 1.503, 95% CI 1.273 to 1.774) and increased waist circumference (OR 1.503, 95% CI 1.267 to 1.783) in adults, and between exposure to 2,5-dichlorophenol and obesity in children (OR 1.8, 95% CI 1.1018 to 3.184).
CONCLUSION
Most observational studies supported a positive association between obesity and exposure to EDCs. Although causality cannot be determined from these data, they underscore the need to limit human exposure to EDCs in light of the evidence from animal and cell-based studies indicating the effects of these chemicals on adiposity.
PROSPERO REGISTRATION NUMBER
CRD42018074548.
Topics: Anthropometry; Endocrine Disruptors; Environmental Exposure; Humans; Obesity
PubMed: 32565448
DOI: 10.1136/bmjopen-2019-033509 -
Journal of Applied Toxicology : JAT Jun 2018A no-significant-risk-level of 20 mg day was derived for tetrabromobisphenol A (TBBPA). Uterine tumors (adenomas, adenocarcinomas, and malignant mixed Müllerian)...
A no-significant-risk-level of 20 mg day was derived for tetrabromobisphenol A (TBBPA). Uterine tumors (adenomas, adenocarcinomas, and malignant mixed Müllerian) observed in female Wistar Han rats from a National Toxicology Program 2-year cancer bioassay were identified as the critical effect. Studies suggest that TBBPA is acting through a non-mutagenic mode of action. Thus, the most appropriate approach to derivation of a cancer risk value based on US Environmental Protection Agency guidelines is a threshold approach, akin to a cancer safe dose (RfD ). Using the National Toxicology Program data, we utilized Benchmark dose software to derive a benchmark dose lower limit (BMDL ) as the point of departure (POD) of 103 mg kg day . The POD was adjusted to a human equivalent dose of 25.6 mg kg day using allometric scaling. We applied a composite adjustment factor of 100 to the POD to derive an RfD of 0.26 mg kg day . Based on a human body weight of 70 kg, the RfD was adjusted to a no-significant-risk-level of 20 mg day . This was compared to other available non-cancer and cancer risk values, and aligns well with our understanding of the underlying biology based on the toxicology data. Overall, the weight of evidence from animal studies indicates that TBBPA has low toxicity and suggests that high doses over long exposure durations are needed to induce uterine tumor formation. Future research needs include a thorough and detailed vetting of the proposed adverse outcome pathway, including further support for key events leading to uterine tumor formation and a quantitative weight of evidence analysis.
Topics: Animals; Body Weight; Carcinogenicity Tests; Carcinogens; Dose-Response Relationship, Drug; Female; Flame Retardants; Humans; Models, Biological; Polybrominated Biphenyls; Rats, Wistar; Risk Assessment; Species Specificity; Time Factors; Uterine Neoplasms
PubMed: 29441599
DOI: 10.1002/jat.3594 -
Environmental Toxicology and... Oct 2016Structural analogs of bisphenol A are commonly used as its alternatives in industrial and commercial applications. Nevertheless, the question arises whether the use of... (Review)
Review
Structural analogs of bisphenol A are commonly used as its alternatives in industrial and commercial applications. Nevertheless, the question arises whether the use of other bisphenols is justified as replacements for bisphenol A in mass production of plastic materials. To evaluate the influence of metabolic reactions on endocrine activities of bisphenols, we conducted a systematic review of the literature. Knowledge about the metabolic pathways and enzymes involved in metabolic biotransformations is essential for understanding and predicting mechanisms of toxicity. Bisphenols are metabolized predominantly by the glucuronidation reaction, which is considered their most important detoxification pathway, as based on current knowledge, glucuronides do not have activity on endocrine receptors. In contrast, several oxidative metabolites of bisphenols with enhanced endocrine activities are presented, and these findings indicate that oxidative metabolites of bisphenols can still have endocrine activities in humans.
Topics: Animals; Benzhydryl Compounds; Endocrine Disruptors; Humans; Phenols; Polybrominated Biphenyls; Sulfones
PubMed: 27771500
DOI: 10.1016/j.etap.2016.09.014 -
The Lancet. Neurology Mar 2014Neurodevelopmental disabilities, including autism, attention-deficit hyperactivity disorder, dyslexia, and other cognitive impairments, affect millions of children... (Review)
Review
Neurodevelopmental disabilities, including autism, attention-deficit hyperactivity disorder, dyslexia, and other cognitive impairments, affect millions of children worldwide, and some diagnoses seem to be increasing in frequency. Industrial chemicals that injure the developing brain are among the known causes for this rise in prevalence. In 2006, we did a systematic review and identified five industrial chemicals as developmental neurotoxicants: lead, methylmercury, polychlorinated biphenyls, arsenic, and toluene. Since 2006, epidemiological studies have documented six additional developmental neurotoxicants-manganese, fluoride, chlorpyrifos, dichlorodiphenyltrichloroethane, tetrachloroethylene, and the polybrominated diphenyl ethers. We postulate that even more neurotoxicants remain undiscovered. To control the pandemic of developmental neurotoxicity, we propose a global prevention strategy. Untested chemicals should not be presumed to be safe to brain development, and chemicals in existing use and all new chemicals must therefore be tested for developmental neurotoxicity. To coordinate these efforts and to accelerate translation of science into prevention, we propose the urgent formation of a new international clearinghouse.
Topics: Animals; Brain; Developmental Disabilities; Environmental Exposure; Humans; Methylmercury Compounds; Neurotoxicity Syndromes; Polychlorinated Biphenyls
PubMed: 24556010
DOI: 10.1016/S1474-4422(13)70278-3