Uterine fibroid growth activated by chemicals found in everyday products
"“These toxic pollutants are everywhere, including food packaging, hair
and makeup products, and more, and their usage is not banned,” said
corresponding study author Dr. Serdar Bulun,
chair of the department of obstetrics and gynecology at Northwestern
University Feinberg School of Medicine and a Northwestern Medicine
physician. “These are more than simply environmental pollutants. They
can cause specific harm to human tissues.”
"Up to 80% of all women may develop a fibroid tumor during their lifetime, Bulun said. One-quarter of these women become symptomatic with excessive and uncontrolled uterine bleeding, anemia, miscarriages, infertility and large abdominal tumors necessitating technically difficult surgeries."
"Prior epidemiological studies have consistently indicated an association between phthalate exposure and uterine fibroid growth, but this study explains the mechanisms behind that link. The scientists discovered exposure to DEHP may activate a hormonal pathway that activates an environmentally responsive receptor (AHR) to bind to DNA and cause increased growth of fibroid tumors."
Critical Overview on Endocrine Disruptors in Diabetes Mellitus
"Diabetes mellitus is a major public health problem in all countries due
to its high human and economic burden. Major metabolic alterations are
associated with the chronic hyperglycemia that characterizes diabetes
and causes devastating complications, including retinopathy, kidney
failure, coronary disease and increased cardiovascular mortality."
Endocrine disruptors in plastics alter β-cell physiology and increase the risk of diabetes mellitus
"Here we review epidemiological, animal, and cellular studies linking
exposure to BPs and phthalates to altered glucose regulation, with
emphasis on the role of pancreatic β-cells. Epidemiological studies
indicate that exposure to BPs and phthalates is associated with diabetes
mellitus. Studies in animal models indicate that treatment with doses
within the range of human exposure decreases insulin sensitivity and
glucose tolerance, induces dyslipidemia, and modifies functional β-cell
mass and serum levels of insulin, leptin, and adiponectin. These studies
reveal that disruption of β-cell physiology by EDCs plays a key role in
impairing glucose homeostasis by altering the mechanisms used by
β-cells to adapt to metabolic stress such as chronic nutrient excess.
Studies at the cellular level demonstrate that BPs and phthalates modify
the same biochemical pathways involved in adaptation to chronic excess
fuel. These include changes in insulin biosynthesis and secretion,
electrical activity, expression of key genes, and mitochondrial
function. The data summarized here indicate that BPs and phthalates are
important risk factors for diabetes mellitus and support a global effort
to decrease plastic pollution and human exposure to EDCs."
Phthalate exposure and risk of diabetes mellitus: Implications from a systematic review and meta-analysis
"Our
results showed that urinary concentrations of phthalates were
positively associated with risk of DM. In literature review, most
studies showed positive correlations of
phthalates, especially ∑DEHP, with homeostasis model assessment of
insulin resistance and fasting glucose."
Association between phthalate exposure and insulin resistance: a systematic review and meta-analysis update
"The
majority of included studies revealed positive relationships of
insulin resistance with different phthalate metabolites exposure. The
results of sensitivity analyses stratified by age, sex, and site of
study remained stable, suggesting the robustness of these
meta-analyses."
Urinary
phthalate metabolites and metabolic syndrome in U.S. adolescents:
Cross-sectional results from the National Health and Nutrition
Examination Survey (2003-2014) data
"Relationships between MiBP
concentrations and odds of MetS varied by
sex. Males with higher concentrations of MnBP and MiBP had greater odds
of having a higher number of MetS components. Relationships between
phthalate metabolites and MetS did not vary by economic adversity."
(MetS is metabolic syndrome, and MnBP and MiBP are types of phthalates)
Association of Early Life Exposure to Phthalates With Obesity and Cardiometabolic Traits in Childhood: Sex Specific Associations
"Prenatal phthalate exposure was not consistently associated with child
adiposity and cardiometabolic measures. Our findings suggest that early
life phthalate exposure may affect child growth and adiposity in a
sex-specific manner and depends on the timing of exposure."
Exposure to endocrine-disrupting compounds such as phthalates and bisphenol A is associated with an increased risk for obesity
"Increasing evidence from epidemiological, animal and in vitro studies
suggests that the increased production of synthetic chemicals that
interfere with the proper functioning of the hormonal system, so-called
endocrine-disrupting compounds (EDCs), might be involved in the
development and rapid spread of obesity, coined the obesity epidemic.
Recent findings have demonstrated that EDCs may interfere with hormonal
receptors that regulate adipogenesis and metabolic pathways.
Furthermore, prenatal exposure to EDCs has been shown to influence the
metabolism of the developing embryo through epigenetic mechanisms and to
promote obesity in subsequent generations."
Diabetes mellitus: Plasticizers and nanomaterials acting as endocrine-disrupting chemicals (Review)
"Various plasticizers and nanomaterials have been linked to endocrine
disruptors or endocrine-disrupting chemicals (EDCs) which represent a
large, heterogeneous, yet incompletely understood group of structures
acting on normal and pathological body pathways such as hormonal
production, secretion, transport and receptor binding."
Bisphenol A and Phthalates in Diet: An Emerging Link with Pregnancy Complications
"Bisphenol A (BPA) and phthalates contaminate food and water and have
been largely studied as obesogenic agents. They might contribute to
weight gain, insulin resistance and pancreatic β-cell dysfunction in
pregnancy, potentially playing a role in the development of pregnancy
complications, such as gestational diabetes mellitus (GDM), and adverse
outcomes. Pregnancy and childhood are sensitive windows of
susceptibility, and, although with not univocal results, preclinical and
clinical studies have suggested that exposure to BPA and phthalates at
these stages of life might have an impact on the development of
metabolic diseases even many years later. The molecular mechanisms
underlying this association are largely unknown, but adipocyte and
pancreatic β-cell dysfunction are suspected to be involved. Remarkably,
transgenerational damage has been observed, which might be explained by
epigenetic changes."
Bisphenol A is a carcinogen that induces lipid accumulation, peroxisome proliferator‑activated receptor‑γ expression and liver disease
"Bisphenol (BP) A is an exogenous endocrine disruptor that mimics
hormones closely associated with health complications, e.g., obesity and
cancers."
"The present study revealed that BPA served as a carcinogen, enhanced tumorigenesis susceptibility and may induce other types of liver disease."
Pathogenesis of Male Reproductive Tract Lesions from Gestation ThroughAdulthood Following in Utero Exposure to Di(n-butyl) Phthalate
Human 'testicular dysgenesis syndrome': a possible model using in-utero exposure of the rat to dibutyl phthalate
"
Abnormal development of Sertoli cells, leading to abnormalities in
other cell types, is our hypothesized explanation for the abnormal
changes in DBP-exposed animals. As the testicular and other changes in
DBP-exposed rats have all been reported in human TDS, DBP exposure in
utero may provide a useful model for defining the cellular pathways in
TDS."
Disruption of reproductive development in male rat offspring following in utero exposure to phthalate esters
"Certain Phthalate esters have been shown to produce reproductive
toxicity in male rodents with an age dependent sensitivity in effects
with foetal animals being more sensitive than neonates which are in turn
more sensitive than pubertal and adult animals. While the testicular
effects of phthalates in rats have been known for more than 30 years,
recent attention has been focused on the ability of these agents to
produce effects on reproductive development in male offspring after in
utero exposure. These esters and in particular di-butyl,
di-(2-ethylhexyl) and butyl benzyl phthalates have been shown to produce
a syndrome of reproductive abnormalities characterized by malformations
of the epididymis, vas deferens, seminal vesicles, prostate, external
genitalia (hypospadias), cryptorchidism and testicular injury together
with permanent changes (feminization) in the retention of
nipples/areolae (sexually dimorphic structures in rodents) and
demasculinization of the growth of the perineum resulting in a reduced
anogenital distance (AGD). Critical to the induction of these effects is
a marked reduction in foetal testicular testosterone production at the
critical window for the development of the reproductive tract normally
under androgen control. A second Leydig cell product, insl3, is
also significantly down regulated and is likely responsible for the
cryptorchidism commonly seen in these phthalate-treated animals. The
testosterone decrease is mediated by changes in gene expression of a
number of enzymes and transport proteins involved in normal testosterone
biosynthesis and transport in the foetal Leydig cell. Alterations in
the foetal seminiferous cords are also noted after in utero phthalate
treatment with the induction of multinucleate gonocytes that contribute
to lowered spermatocyte numbers in postnatal animals. The phthalate
syndrome of effects on reproductive development has parallels with the
reported human testicular dysgenesis syndrome, although no cause and
effect relationship exists after exposure of humans to phthalate esters.
However humans are exposed to and produce the critical phthalate
metabolites that have been detected in blood of the general population,
in children and also human amniotic fluid."
