nm l Shahidehnia, J Environ Anal Toxicol 2016, 6:4

Overview

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Key numbers

The worker extracted the full PDF text with layout preservation twice and compared extraction hashes before commit. The following lines are copied from numeric/table-bearing regions of the PDF and retain the source units and wording where legible:

Introduction about 10% of the whole male population of the world. This increase
consumption. Endocrine disruption is a secondary outcome of toxic Table 1 describes the classifications of endocrine disrupting
Health Organization (WHO). In this table, EDCs are grouped into 11
Table 1: Classification of EDCs.
The genome of inner cell mass is hyper-methylated for about 20% have been suggested to be the main causal effects for these changes. In
of the CpG sites but in sperm 90% and in oocyte 40% of CpG sites majority of developed countries, the amount of early pubertal onsets
up to 15% of different populations. Part of all these infertilities among This process is the most studied epigenetic modification as a
organisms from yeast to human being (15). 0.1%, but this is much lower than the prevalence of subfertility and
MicroRNAs and epigenetics be >90% and it can occur in both sons and daughters. The reproductive
boys whereas it was very high in the in utero exposed boys (3.57%).
Exposure to DES in the mouse model can cause abnormalities such for adverse outcomes of DES. Table 2 shows the comparisons between
dysplasia of ventral penis and urethra. Often several surgeries are pregnant women as referent group, the odd ratio (OR) with 95%
is 1 in 150 new male births. The increased risk of hypospadias due was estimated to be OR=2.3 (95% CI 0.7-7.9) (19). Another study
transgenerational inheritance in humans. When the baby is a girl exposed mothers to DES was more than 3% (27).
structural abnormalities, vaginal and cervical cell adenocarcinoma, risk of breast cancer from 1% up to 1.4% among the exposed mothers.
defects and cardiac disease elevations among sons of up to 1.53% and
Exposure to DES can cause vaginal cancer in both exposed for daughters up to 2.35% in prenatal maternal DES exposed cohort
generation of DES exposed females, menstrual irregularities are defects. Table 3, indicates the type of malformations caused by DES (29).
In an epidemiological cohort follow up study on five hundred (0.7 and 0.6 respectively%), but among the exposed females 0.8%,
Second generation (0% hypospadic*) (0% genital malformation) (3.5% hypospadic, n=16) (28.4% mullerian abnormalities, n=157)
Skeletal anomalies single dose, 6 mg/kg/day is assumed to be the safe dose for acute oral
Kidney, renal agenesis and dysgenesis or even born adverse effect level (LOAEL) for rat is estimated to be 11.5 mg/kg/day.
eyes are observed at the LOAEL of 2.3 mg/kg/day in rat in a chronic
anomalies or ear and hearing anomalies, learning disabilities, blood disorders, determined to be 1.2 mg/kg/day (33).
Table 3: The association between mothers DES exposure during pregnancy and polycystic ovary disease and primary ovarian in-sufficiency, which is
up to untreated foods and vegetables as well as treated ones. Vinclozolin also other tissues for at least three generations. 75% of the exposed
This compound has been widely used in agriculture since 1984. It is still adulthood. Moreover, 34% had two or more diseases caused by daily
in limited use for commercial and industrial purposes. This compound intraperitoneal injection of 100 mg/kg vinclozolin per day (35).
spermatogenic defect, infertility among male rats, breast cancer in When gestating female rats were exposed to 100-200 mg/kg
more anxiety and behavioral changes in their mating (32). mg/kg/day for female of child bearing age and 0.000078 mg/kg/day for
High incidence of defect which was up to 90% of vinclozolin exposed Exposure Dose (mg/kg/day) Endpoint Study
health risk assessment are indicated in Table 4. According to Table 4
the overall anti-androgenic effects of vinclozolin has a NOAEL of 1.2 Table 4: Health risk assessment of vinclozolin.
of 0.025 mg/kg/day for oral exposure to vinclozolin (EPA 2007).
Acceptable daily intake (ADI) of vinclozolin in food is assumed 0.005 Scheme 3: Bisphenol-A (BPA).
and composition. In general, early life exposure to BPA promotes a mice (5 mg/kg diet) spent more time sitting next to each other than
decrease uterine receptivity and increases the risk of implantation is around 300 µg/l. The colloids are assumed to have less bioavailability
failure in animals and because of these effects, BPA is a known uterine in the body. The solubility of DEHP is 15% in well water and 42% in
works as a testicular toxicant and can affect male reproductive system About 51% of total phthalate used as plasticizer in different products
Table 5: Human exposure to BPA. exposure occurs via food or medical products (41).
in a chronic >90 days toxicity study, 1,000 ppm of DEHP produced a
ppm DEHP in the diet for 13 weeks and the result was minimal to mild

Methods (brief)

sugar and mineral homeostasis, heart rate and digestion are some of the decreased sperm quality and increased incidence of testicular cancer.
mechanism of airway hyper-responsiveness to nicotine challenge was maternal active smoking. 1,062 infant cord blood samples were also

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Update history

The five most recent substantive edits to this page, classified major (evidence or structure moved), correction (a published value or statement was wrong and has been fixed), or minor (narrative rewritten without changing the underlying evidence). Each description is derived from what the edit did to this page; the linked commit is the authoritative record, routine regeneration passes are excluded, and the full version history lives in git. When DOI minting comes online (see schema docs), each entry below will also link to a version-pinned DataCite DOI.

Commit	Date	Change	Description
b01ec52c	2026-08-04	major	2 sections added
d49e450f	2026-08-03	major	5 sections added; narrative text revised