3/5/2021 Abnormal Development - Chemicals - Embryology

Abnormal Development - Chemicals

Embryology - 4 Mar 2021           Expand to Translate   [Expand]

Contents
1 Introduction
2 Some Recent Findings
3 United Nations - Globally Harmonized System of Classification and Labelling of Chemicals
3.1 GHS08 Health Hazard
4 Chemical Terms
4.1 Acute Toxicity
4.2 Carcinogen
4.3 Effective Dose
4.4 Lethal Dose
4.5 Material Safety Data Sheet
4.6 Mutagen
4.7 Reproductive Toxicity
4.8 Risk
4.9 Safety Data Sheet
4.10 Solvents
4.11 Threshold Limit Value
5 Persistent Organic Pollutants
5.1 Stockholm Convention on Persistent Organic Pollutants
5.2 Annex A (Elimination)
5.3 Annex B (Restriction)
5.4 Annex C (Unintentional production)
5.5 Polychlorinated Biphenyls
5.6 Endosulfan
5.7 Dioxin 20XX
5.8 Styrene
5.9 Formaldehyde
6 Carbon Monoxide
7 USA - National Toxicology Program
7.1 Center for the Evaluation of Risks to Human Reproduction
8 Australia
8.1 Therapeutic Goods Administration
8.2 Safe Work Australia
8.3 Food Standards Australia
8.4 National Measurement Institute
8.5 National Research Centre for Environmental Toxicology (Queensland)
9 Poison Control Centres
9.1 Australian Poison Control Centres
10 Toxicogenomics
11 Biological Toxins
11.1 Domoic Acid
12 References
12.1 Reviews
12.2 Articles
12.3 Search Pubmed
13 External Links
14 Glossary Links

Introduction
Effects due to environmental chemicals on development, both pre- and post-natal are difficult to quantify. There are also chemical
hazards to development covered elsewhere in these notes, Metals, Fetal Alcohol Syndrome, smoking, illicit drugs. Postnatally some
chemicals can be also transferred through milk or contamination of milk formulas. Several environmental chemicals, or their products,
have been identified as endocrine disruptors.

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The specific effects of chemicals is detailed in chemical Safety and Data Sheets (SDS).
These sheets are now generally required to be supplied along with the chemical
purchased from a supplier and give a standardised description of the chemical, its
physical properties, handling and health effects/toxicity. The information relating to
chemical safety is continuously changing and the most current source of Safety Data
Sheet (SDS) should be used for accurate information. Note the original term for this
associated information sheet was a Material Safety Data Sheet (MSDS). There are also
several internet sites that have searchable databases of SDS information. Note that
handling chemical safety has previously varied from country to country.
Stockholm Convention on Persistent Organic
Recently the WHO has developed an internationally agreed-upon system Globally Pollutants
Map showing worldwide ratification status
Harmonized System of Classification and Labeling of Chemicals (GHS) that will eventually
23/10/2010
standardise this information.

In addition, there is much information about chemicals in relation to food safety and
poisoning.

Environmental Links: Introduction | low folic acid | iodine deficiency | Nutrition | Drugs | Australian Drug Categories | USA Drug
Categories | thalidomide | herbal drugs | Illegal Drugs | smoking | Fetal Alcohol Syndrome | TORCH | viral infection | bacterial infection |
fungal infection | zoonotic infection | toxoplasmosis | Malaria | maternal diabetes | maternal hypertension | maternal hyperthermia |
Maternal Inflammation | Maternal Obesity | hypoxia | biological toxins | chemicals | heavy metals | air pollution | radiation | Prenatal
Diagnosis | Neonatal Diagnosis | International Classification of Diseases | Fetal Origins Hypothesis

Some Recent Findings

Environmental Influences and Template:Polycystic Ovary Syndrome[2]
"Polycystic ovarian syndrome (PCOS) is a complex endocrine-metabolic disorder
whose pathogenesis is not well-understood. While genetic insults have been
hypothesized as possible causes, there are a large number of environmental
chemicals known to have detrimental effects on the endocrine system and may be
irreversible, especially when exposure occurs early in development. Many of these
chemicals have been investigated as causes of PCOS by measuring serum and
urinary levels of common endocrine disruptors in women and adolescents with Endocrine disrupting chemicals historical
timeline[1]
PCOS as well as using animal models for PCOS induction with chemical exposures."

The Impact of Di-2-Ethylhexyl Phthalate on Sperm Fertility[3] "A growing

number of studies point to reduced fertility upon chronic exposure to endocrine-
disrupting chemicals (EDCs) such as phthalates and plasticizers. These toxins are
ubiquitous and are often found in food and beverage containers, medical devices, as
well as in common household and personal care items. Animal studies with EDCs,
such as phthalates and bisphenol A have shown a dose-dependent decrease in
fertility and embryo toxicity upon chronic exposure. However, limited research has
been conducted on the acute effects of these EDCs on male fertility. Here we used a
murine model to test the acute effects of four ubiquitous environmental toxins:
bisphenol A (BPA), di-2-ethylhexyl phthalate (DEHP), diethyl phthalate (DEP), and
dimethyl phthalate (DMP) on sperm fertilizing ability and pre-implantation embryo
development. The most potent of these toxins, di-2-ethylhexyl phthalate (DEHP),
was further evaluated for its effect on sperm ion channel activity, capacitation status,
acrosome reaction and generation of reactive oxygen species (ROS). DEHP
demonstrated a profound hazardous effect on sperm fertility by producing an
altered capacitation profile, impairing the acrosome reaction, and, interestingly, also
increasing ROS production. These results indicate that in addition to its known
chronic impact on reproductive potential, DEHP also imposes acute and profound
damage to spermatozoa, and thus, represents a significant risk to male fertility."

Prenatal exposure to organophosphate pesticides and functional neuroimaging

in adolescents living in proximity to pesticide application[4] "We have reported
consistent associations of prenatal organophosphate pesticide (OP) exposure with
poorer cognitive function and behavior problems in our Center for the Health
Assessment of Mothers and Children of Salinas (CHAMACOS), a birth cohort of
Mexican American youth in California's agricultural Salinas Valley. However, there is
little evidence on how OPs affect neural dynamics underlying associations. We used
functional near-infrared spectroscopy (fNIRS) to measure cortical activation during
tasks of executive function, attention, social cognition, and language comprehension
in 95 adolescent CHAMACOS participants. We estimated associations of residential
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proximity to OP use during pregnancy with cortical activation in frontal, temporal,

and parietal regions using multiple regression models, adjusting for
sociodemographic characteristics. OP exposure was associated with altered brain
activation during tasks of executive function. For example, with a 10-fold increase in
total OP pesticide use within 1 km of maternal residence during pregnancy, there
was a bilateral decrease in brain activation in the prefrontal cortex during a cognitive
flexibility task (β = -4.74; 95% CI: -8.18, -1.31 and β = -4.40; 95% CI: -7.96, -0.84 for
the left and right hemispheres, respectively). We also found that prenatal OP
exposure was associated with sex differences in brain activation during a language
comprehension task. This first functional neuroimaging study of prenatal OP
exposure suggests that pesticides may impact cortical brain activation, which could
underlie previously reported OP-related associations with cognitive and behavioral
function. Use of fNIRS in environmental epidemiology offers a practical alternative
to neuroimaging technologies and enhances our efforts to assess the impact of
chemical exposures on neurodevelopment." neural abnormalities

Review - A mechanism for the effect of endocrine disrupting chemicals on

placentation[5] "Numerous recent studies have shown that endocrine disrupting
chemicals (EDCs) in the body of pregnant women can pass through the placenta and
be exposed to the fetus, leading to fetal development and cognitive impairment.
Placentation through invasion of trophoblast cells and vascular remodeling is
essential to maintaining maternal and fetal health throughout the pregnancy.
Abnormal placentation can lead to pregnancy disorders such as preeclampsia (PE)
and intrauterine growth retardation (IUGR). However, many studies have not been
conducted on whether EDCs can inhibit the development and function of the
placenta. Isolating placental tissues to analyze the effect of EDCs on placentation has
several limitations. In this review, we discussed the types of EDCs that can pass
through the placental barrier and accumulate in the placenta with relative outcome.
EDCs can be released from a variety of products including plasticizers, pesticides,
and retardant. We also discussed the development and dysfunction of the placenta
when EDCs were treated on trophoblast cells or pregnant rodent models. The effects
of EDCs on the placenta of livestock are also discussed, together with the molecular
mechanism of EDCs acting in trophoblast cells. We describe how EDCs cross the
membrane of trophoblasts to regulate signaling pathways, causing genetic and
epigenetic changes that lead to changes in cell viability and invasiveness. Further
studies on the effects of EDCs on placenta may draw attention to the correct use of
products containing EDCs during pregnancy." placenta

Toxicokinetics of bisphenol A, bisphenol S, and bisphenol F in a pregnancy

sheep model[6] "Bisphenol A (BPA), S (BPS), and F (BPF) are among the most
abundant bisphenols detected in humans, yet pregnancy toxicokinetics for BPS or
BPF remain unknown. Because gestational BPS can disrupt placental function and
result in reproductive and metabolic disorders in the progeny, the aim of the study
was to investigate BPS and BPF toxicokinetics during pregnancy using an in vivo
approach. Fetal catheterizations were conducted in pregnant sheep (n = 6) at mid-
pregnancy and injected with either a single dose of BPS (n = 3, 0.5 mg/kg, s.c.), or a
combination of BPS, BPF, and BPA (n = 3, 0.5 mg/kg for each chemical, s.c.). Maternal
and fetal blood and urine and amniotic fluid were collected over 72 h and analyzed
for bisphenols by HPLC-MS/MS. We observed significant differences in half-life,
maximum concentration, and total body clearance in maternal circulation among
bisphenols. Longer half-lives were observed in fetal vs. maternal circulation for all
bisphenols. Fetal toxicokinetics differed among bisphenols with BPS having the
longest fetal half-life. All bisphenols reached basal levels at 48 h in maternal plasma,
but were still detectable in amniotic fluid, fetal urine, and fetal plasma at 72 h. In this
first pregnancy toxicokinetic study of BPS and BPF we have demonstrated maternal
and fetal toxicokinetic differences among all three bisphenols. Higher BPS
persistence in the fetal compartment warrants studies into progeny adverse
outcomes following gestational exposure. Additionally, toxicokinetic differences
among bisphenols call for a more careful approach when extrapolating kinetic
information from one bisphenol chemical to another."

Endocrine Disrupting Chemicals: An Occult Mediator of Metabolic Disease[1]

"Endocrine disrupting chemicals (EDCs), a heterogeneous group of exogenous

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chemicals that can interfere with any aspect of endogenous hormones, represent an
emerging global threat for human metabolism. There is now considerable evidence
that the observed upsurge of metabolic disease cannot be fully attributed to
increased caloric intake, physical inactivity, sleep deficit, and ageing. Among
environmental factors implicated in the global deterioration of metabolic health,
EDCs have drawn the biggest attention of scientific community, and not
unjustifiably. EDCs unleash a coordinated attack toward multiple components of
human metabolism, including crucial, metabolically-active organs such as
hypothalamus, adipose tissue, pancreatic beta cells, skeletal muscle, and liver.
Specifically, EDCs' impact during critical developmental windows can promote the
disruption of individual or multiple systems involved in metabolism, via inducing
epigenetic changes that can permanently alter the epigenome in the germline,
enabling changes to be transmitted to the subsequent generations. The clear effect
of this multifaceted attack is the manifestation of metabolic disease, clinically
expressed as obesity, metabolic syndrome, diabetes mellitus, and non-alcoholic fatty
liver disease."

Chlorothalonil inhibits mouse ovarian development through endocrine

disruption[7] "Although many studies have investigated the toxic effects and even
the reproductive toxicity of chlorothalonil, almost no studies have focused on the
ovary, the organ of oocyte development. Puberty is a critical window for
development of the female reproductive system. Therefore, this investigation aimed
to explore the effects and underlying mechanisms of chlorothalonil at low doses on
peripubertal mouse ovarian development. Chlorothalonil is frequently used in
horticulture with short intervals between applications, therefore, vegetables and
fruits may be potential sources of chlorothalonil contamination. For the first time,
this study demonstrated that chlorothalonil inhibited ovarian development during
puberty in mice, and at levels currently assumed to have no adverse health
consequences for humans. Chlorothalonil exposure inhibited mouse ovarian
development by increasing the number of primary follicles and decreasing the
number of mature follicles. It acted by decreasing the levels of hormone production
proteins, such as FSH receptor and estrogen receptor alpha, while increasing the
levels of DNA repairing marker RAD51 and cell apoptosis. These results suggest that
chlorothalonil may disrupt endocrine function and inhibit murine ovarian
development. Therefore it may pose a potential health risk to female reproductive
systems in other species, especially to the ovary." Chlorothalonil is an organic
compound mainly used as a broad spectrum, non-systemic fungicide.

Perinatal exposure to an environmentally relevant mixture of phthalates results

in a lower number of neurons and synapses in the medial prefrontal cortex and
decreased cognitive flexibility in adult male and female rats[8] "The growth and
organization of the developing brain is known to be influenced by hormones, but
little is known about whether disruption of hormones affects cortical regions, like
the medial prefrontal cortex (mPFC). This region is particularly important given its
involvement in executive functions and implication in the pathology of many
neuropsychiatric disorders. Here, we examine the long-term effects of perinatal
exposure to endocrine-disrupting compounds, the phthalates, on the mPFC and
associated behavior. This investigation is pertinent as humans are ubiquitously
exposed to phthalates through a variety of consumer products and phthalates can
readily cross the placenta and be delivered to offspring via lactation. Pregnant dams
orally consumed an environmentally relevant mixture of phthalates at 0, 200, or
1000 μg/kg/day through pregnancy and for 10 days while lactating. As adults,
offspring were tested in an attentional set-shifting task, which assesses cognitive
flexibility. Brains were also examined in adulthood for stereological quantification of
the number of neurons, glia, and synapses within the mPFC. We found that,
independent of sex, perinatal phthalate exposure at either dose resulted in a
reduction in neuron number, synapse number, and size of the mPFC and a deficit in
cognitive flexibility. Interestingly, the number of synapses was correlated with
cognitive flexibility, such that rats with fewer synapses were less cognitively flexible
than those with more synapses. These results demonstrate that perinatal phthalate
exposure can have long-term effects on the cortex and behavior of both male and
female rats. SIGNIFICANCE STATEMENT Humans globally are exposed on a daily
basis to a variety of phthalates, which are endocrine-disrupting chemicals. The

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effects of phthalate exposure on the developing brain, especially on cognitively

relevant regions like the medial prefrontal cortex (mPFC), is not known. Here, we use
a rat model of human prenatal exposure to an environmentally relevant mixture of
phthalates and find there is an appreciable reduction in neuron number, synapse
number, and size of the mPFC and a deficit in cognitive flexibility. These results may
have serious implications for humans given the mPFC is involved in executive
functions and is implicated in the pathology of many neuropsychiatric disorders."

Genotoxic and mutagenic studies of teratogens in developing rat and mouse[9]

"In this review, genotoxic and mutagenic effects of teratogenic chemical agents in
both rat and mouse have been reviewed. Of these chemicals, 97 are drugs and 33
are pesticides or belong to other groups. Large literature searches were conducted
to determine the effects of chemicals on chromosome abnormalities, sister
chromatid exchanges, and micronucleus formation in experimental animals such as
rats and mice. In addition, studies that include unscheduled DNA synthesis, DNA
adduct formations, and gene mutations, which help to determine the genotoxicity or
mutagenicity of chemicals, have been reviewed. It has been estimated that 46.87%
of teratogenic drugs and 48.48% of teratogenic pesticides are positive in all tests.
So, all of the teratogens involved in this group have genotoxic and mutagenic
effects. On the other hand, 36.45% of the drugs and 21.21% of the pesticides have
been found to give negative results in at least one test, with the majority of the tests
giving positive results. However, only 4.16% of the drugs and 18.18% of the
pesticides were determined to give negative results in the majority of the tests.
Among tests with major negative results, 12.50% of the teratogenic drugs and
12.12% of the teratogenic pesticides were negative in all conducted tests."

More recent papers   [Expand]

Older papers  [Expand]

United Nations - Globally Harmonized System of Classification and Labelling of

Chemicals
(GHS) The new system, which was called "Globally Harmonized System of Classification and Labelling of
Chemicals (GHS)", addresses classification of chemicals by types of hazard and proposes harmonized hazard
communication elements, including labels and safety data sheets. It aims at ensuring that information on
physical hazards and toxicity from chemicals be available in order to enhance the protection of human health
and the environment during the handling, transport and use of these chemicals. The GHS also provides a basis
for harmonization of rules and regulations on chemicals at national, regional and worldwide level, an
important factor also for trade facilitation.

(Text from UN Website)

GHS08 Health Hazard

Of the 9 pictogram codes, this relates to systemic health hazard as well as reproductive and developmental
Globally Harmonized
effects.
System of Classification
and Labelling of
Germ cell mutagenicity (State route of exposure if it is conclusively proven that no other routes of exposure
Chemicals
cause the hazard)

Category 1A - Danger - H340 - May cause genetic defects

Category 1B - Danger - H340 - May cause genetic defects
Category 2 - Warning - H341 - Suspected of causing genetic defects

Carcinogenicity (State route of exposure if it is conclusively proven that no other routes of exposure cause
the hazard)

Category 1A - Danger - H350 - May cause cancer

Category 1B - Danger - H350 - May cause cancer GHS08 Health Hazard
Category 2 - Warning - H351 - Suspected of causing cancer

Reproductive toxicity (state specific effect if known)(state route of exposure if it is conclusively proven that
no other routes of exposure cause the hazard)

Category 1A - Danger
H360 - May damage fertility or the unborn child.
H360F - May damage fertility. GHS08 Health Hazard
H360D - May damage the unborn child.
H360FD - May damage fertility. May damage the unborn child.
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Category 1B - Danger
H360Fd - May damage fertility. Suspected of causing damage the unborn child.
H360Df - May damage the unborn child. Suspected of damaging fertility.
Category 2 - Warning
H361 - Suspected of damaging fertility or the unborn child.
H361f - Suspected of damaging fertility.
H361d - Suspected of damaging the unborn child.
H361fd - Suspected of damaging fertility. Suspected of damaging the unborn child.
Additional category for effects on or via lactation (no pictogram)
H362 - May cause harm to breast-fed children.

Links: United Nations - GHS (http://www.unece.org/trans/danger/publi/ghs/ghs_welcome_e.html) | Safe Work Australia - GHS (htt
p://www.safeworkaustralia.gov.au/SafetyInYourWorkplace/HazardousSubstancesAndDangerousGoods/GHS/Pages/GHS.aspx)

Chemical Terms
Below are listed some terms which relate to a chemicals harmful effects.

Acute Toxicity
Adverse effects occurring following oral or dermal administration of a single dose of a substance, or multiple doses given within 24
hours, or an inhalation exposure of 4 hours. This is further classified by five toxicity categories based upon exposure route.

Carcinogen
A chemical known or believed to cause cancer in humans. The number of known carcinogens is comparatively small, but many more
chemicals are suspected to be carcinogenic.

Effective Dose
(ED50) The amount of material required to produce a specified effect in 50% of an animal population. (See qualification in the definition
of LD50).

Lethal Dose
(LD50) The dose of a chemical which kills 50% of a sample population. In full reporting, the dose, treatment and observation period
should be given. Further, LD50 and ED50 values are strictly only comparable when the age, sex and nutritional state of the animals is
specified. Nevertheless, LD50 values are widely reported as a measure of the potential toxicity of chemicals.

Material Safety Data Sheet

(MSDS) A defined set of information about a specific chemical's properties, risks, hazards and toxicity. This term in Australia is being
replaced by Safety Data Sheet (SDS), under the United Nations Globally Harmonized System of Classification and Labelling of Chemicals
(GHS) program to standardise chemical data around the world.

Mutagen
An agent that changes the hereditary genetic material which is a part of every living cell. Such a mutation is probably an early step in the
sequence of events that ultimately leads to the development of cancer.

Reproductive Toxicity
Adverse effects on sexual function and fertility in adult males and females, as well as developmental toxicity in the offspring.

Risk
The probability that a hazard will give rise to an adverse effect at a level in a specified period and is normally indicated in descriptive
terms; high, modest, negligible. A hazard is the potential for physical harm to life, health or property.

Safety Data Sheet

(SDS) Under the United Nations "Globally Harmonized System of Classification and Labelling of Chemicals" (GHS) program to
standardise chemical data around the world.

Solvents
Are liquids which can dissolve substances. Organic solvents (examples) are also used in paints and adhesives and include aromatic
solvents (xylene and toluene), aliphatic hydrocarbons (kerosene and n-heptane), alcohols (ethanol and isopropanol), glycols (ethylene
glycol), esters (iso-propyl acetate), chlorohydrocarbons (methylene chloride), ethers (diethylene glycol), ketones and aldehydes
(acetone).

Threshold Limit Value

(TLV) The maximum permissible concentration of a material, generally expressed in parts per million in air for some defined period of
time (often 8 hours). These values, which may differ from country to country, are often backed up by regulation and are therefore often
legally enforceable.

Persistent Organic Pollutants

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(POPs) These are organic (carbon-based) chemical substances with a combination of physical and chemical properties that once
released into the environment:

1. remain intact for exceptionally long periods of time (many years)

2. become widely distributed throughout the environment as a result of natural processes involving soil, water and, most notably, air
3. accumulate in the fatty tissue of living organisms including humans, and are found at higher concentrations at higher levels in the
food chain
4. are toxic to both humans and wildlife

Stockholm Convention on Persistent Organic Pollutants

The Stockholm Convention on Persistent Organic Pollutants is a global treaty to protect
human health and the environment from chemicals that remain intact in the
environment for long periods, become widely distributed geographically, accumulate in
the fatty tissue of humans and wildlife, and have adverse effects to human health or to
the environment. The text of the Stockholm Convention on Persistent Organic Pollutants
was adopted 22 May 2001 and entered into force ninety days after the deposit of the
fiftieth instrument of ratification, acceptance, approval or accession by a country to the
Convention, 17 May 2004.

Twelve persistent organic pollutants were initially recognized as causing adverse effects
on humans and the ecosystem. These have been placed in 3 categories.
Map showing worldwide ratification status
1. Pesticides: aldrin, chlordane, DDT, dieldrin, endrin, heptachlor, hexachlorobenzene, 23/10/2010

mirex, toxaphene;
2. Industrial chemicals: hexachlorobenzene, polychlorinated biphenyls (PCBs); and
3. By-products: hexachlorobenzene; polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/PCDF), and PCBs.

Annex A (Elimination)
Parties must take measures to eliminate the production and use of the chemicals listed under Annex A. Specific exemptions for use or
production are listed in the Annex and apply only to Parties that register for them.

Aldrin, Chlordane, Chlordecone, Dieldrin, Endrin, Heptachlor, Hexabromobiphenyl, Hexabromodiphenyl ether and heptabromodiphenyl
ether, Hexachlorobenzene (HCB), Alpha hexachlorocyclohexane, Beta hexachlorocyclohexane, Lindane, Mirex, Pentachlorobenzene,
Polychlorinated biphenyls (PCB), Tetrabromodiphenyl ether and pentabromodiphenyl ether, Toxaphene

Annex B (Restriction)
Parties must take measures to restrict the production and use of the chemicals listed under Annex B in light of any applicable acceptable
purposes and/or specific exemptions listed in the Annex.

DDT, Perfluorooctane sulfonic acid, its salts and perfluorooctane sulfonyl fluoride

Annex C (Unintentional production)

Parties must take measures to reduce the unintentional releases of chemicals listed under Annex C with the goal of continuing
minimization and, where feasible, ultimate elimination.

Polychlorinated dibenzo-p-dioxins (PCDD), Polychlorinated dibenzofurans (PCDF), Hexachlorobenzene (HCB), Pentachlorobenzene,

Polychlorinated biphenyls (PCB)

Links: Stockholm Convention on Persistent Organic Pollutants (http://chm.pops.int/default.aspx) | What are POPs? (http://chm.pops.i
nt/Convention/The%20POPs/tabid/673/language/en-US/Default.aspx)

Polychlorinated Biphenyls
A recent study using rat model showed effects on fetal cerebral cortex development through radial neuronal migration in the fetal
cortex.[13]

An example of the effects of polychlorinated biphenyls (PCBs) can be seen following contaminated rice oil consumption in Taiwan
between 1978-1979.[17][18]

"Yucheng "oil-disease" victims were Taiwanese people exposed to polychlorinated biphenyls (PCBs) and their heat-degradation
products, mainly polychlorinated dibenzofurans (PCDFs), from the ingestion of contaminated rice oil in 1978-1979. Serial studies in
Yucheng offspring born between 1978 and 1992 are summarized. Children of the exposed women were born with retarded growth,
with dysmorphic physical findings, and, during development, with delayed cognitive development, increased otitis media, and more
behavioral problems than unexposed children. Recently, examination of the reproductive system has suggested that prenatal
exposure exerts late effects on semen parameters in young men after puberty. Results of the investigation in Yucheng children will
provide important information about the human health effects and toxicology of PCB/PCDF exposure. Prenatal exposure to these
environmental chemicals causes the fetus to be sensitive to the toxic effects of persistent organic pollutants." [17]

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Groups of chemicals Level of Acton

polychlorinated biphenyl (PCB) and polychlorinated dibenzodioxins (PCDD) 5, 7
polybrominated diphenyl ethers (PBDEs) 5, 6, 7, 8
pesticides 4, 5, 7
perfluoroalkyl substances (PFASs) 5, 6; NIS: 3
bisphenol A (BPA) 2, 7
phthalates 1, 2, 5, 8.

Table Data[19]
Links: thyroid | chemicals | endocrine abnormalities

Thyroid Signaling Pathway and Endocrine-disrupting Chemicals

Links: endocrine abnormalities

Endosulfan
Endosulfan is commercial name for a chemical (6,7,8,9,10,10-hexachloro-1,5,5a,6,9,9a-hexahydro- 6,9-methano-2,4,3-benzodioxathiepin-
3-oxide) broad-spectrum insecticide and acaricide to control agricultural insect and mite pests in crops. Technical-grade endosulfan is
composed of two stereochemical isomers, alpha-endosulfan (70%) and beta-endosulfan (30%), at high levels chemical has acute toxicity
and neurological effects.

Endosulfan environmental breakdown

An Indian study has suggested that it acts as an endocrine disruptor, exposure in male children may delay sexual maturity and interfere
with sex hormone synthesis.[20] There has been some criticism of the data used in this particular study.[21][22]

Links: Endocrine System - Abnormalities

Dioxin 20XX
Dioxin 20XX is a non-profit organization founded by the International Advisory Board of the International Symposium on Halogenated
Persistent Organic Pollutants (POPs) for the purpose of promoting scientific education and research on POPs. Dioxin20XX facilitates the
organization of the annual International "Dioxin" Symposium and publishes "Organohalogen Compounds".

Links: Dioxin 20XX (http://www.dioxin20xx.org/) | Organohalogen Compound Database (http://www.dioxin20xx.org/ohc_database_se

arch.htm)

Styrene
In 2008 as part of the US National Toxicology Program a report "Final Report on Carcinogens Background Document for Styrene"[23]
looking into the potential carcinogenic effects of styrene. The following text has been modified from that report.

Styrene Properties - viscous, highly flammable liquid used worldwide in the production of polymers.

Styrene Uses - incorporated into many products in our environment (rubber, plastic, insulation, fiberglass, pipes, automobile parts, food
containers, and carpet backing).

Absorption - absorbed through inhalation, ingestion, or skin contact. Most important route of exposure in humans in occupational
settings is by inhalation, which results in rapid absorption

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Distribution - highest tissue concentrations (60% to 70%) of inhaled styrene are in subcutaneous fat.

Formaldehyde
In 2010 as part of the US National Toxicology Program a report "Final Report on Carcinogens Background Document for
Formaldehyde"[24] looking into the potential carcinogenic effects of formaldehyde.

Carbon Monoxide
(CO) A colourless and odorless gas formed mainly as a by-product of incomplete combustion of hydrocarbons and can cause
cytotoxicity by tissue hypoxia. Smoking tobacco is also a source of carbon monoxide. A recent study has identified in a newborn mouse
model, effects on neurodevelopment of even sub-clinical levels of carbon monoxide.[25]

Carbon monoxide:

enters circulation though the respiratory system

binding to haemoglobin to form carboxy-haemoglobin (COHb)
haemoglobin affinity is 240 times greater than for oxygen
fetal haemoglobin binds with even greater affinity
tissue hypoxia occurs when COHb levels are greater than 70%

Links: Smoking - Carbon Monoxide

USA - National Toxicology Program

The following information is an excerpt from the website background information (February 17, 2005).

The NTP is an interagency program whose mission is to evaluate agents of public health concern by developing and applying tools
of modern toxicology and molecular biology. The program maintains an objective, science-based approach in dealing with critical
issues in toxicology and is committed to using the best science available to prioritize, design, conduct, and interpret its studies. To
that end, the NTP is continually evolving to remain at the cutting edge of scientific research and to develop and apply new
technologies.
More than 80,000 chemicals are registered for use in the United States. Each year, an estimated 2,000 new ones are introduced for
use in such everyday items as foods, personal care products, prescription drugs, household cleaners, and lawn care products. We do
not know the effects of many of these chemicals on our health, yet we may be exposed to them while manufacturing, distributing,
using, and disposing of them or when they become pollutants in our air, water, or soil. Relatively few chemicals are thought to pose
a significant risk to human health. However, safeguarding public health depends on identifying both what the effects of these
chemicals are and at what levels of exposure they may become hazardous to humans—that is, understanding their toxicology.

Center for the Evaluation of Risks to Human Reproduction

The National Toxicology Program (NTP) Center for the Evaluation of Risks to Human
Reproduction (CERHR) was established in 1998 to serve as an environmental health
resource to the public and regulatory and health agencies. CERHR publishes
monographs that assess the evidence that environmental chemicals, physical substances,
or mixtures (collectively referred to as "substances") cause adverse effects on
reproduction and development and provide opinion on whether these substances are
hazardous for humans.

Links: National Toxicology Program (http://ntp.niehs.nih.gov) | Center for the

Evaluation of Risks to Human Reproduction (http://cerhr.niehs.nih.gov/) Center for the Evaluation of Risks to Human
Reproduction
Australia
Therapeutic Goods Administration
Standard for the Uniform Scheduling of Drugs and Poisons (SUSDP) - produced by the National Health and Medical Research
Council (NHMRC) is the basis for State and Territory Poisons Act legislation (which may differ between regions in detail). The legislation
applies restrictions at the point of sale. There are nine Poisons Schedules listing substances or types of substances which require certain
labelling and description, packaging (inner and outer), controls on advertising and supply, storage, and for some, the permitted level of
impurities.

Revised medicines and chemicals scheduling arrangements (23 Nov 2010)

the National Drugs and Poisons Schedule Committee (NDPSC) will be replaced by the Secretary of the Department of Health and
Ageing (DoHA) - or her delegate - as the decision maker for the scheduling of medicines and chemicals.
two new expert advisory committees, the Advisory Committee on Medicines Scheduling and the Advisory Committee on Chemicals
Scheduling, will be established to provide advice and make recommendations to the Secretary (or delegate) on medicines and
chemicals scheduling decisions.
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a single Secretariat, supporting both Advisory Committees, will ensure ongoing consistency and cohesiveness of processes and
decisions.
closer integration of the revised scheduling arrangements with existing Commonwealth evaluation and product registration
schemes.

Links: Poisons Standard 2010 (http://www.comlaw.gov.au/Details/F2010L02386) | TGA - About The Poisons Standard (http://www.tg
a.gov.au/ndpsc/susdp.htm) | Therapeutic Goods Administration (http://www.tga.gov.au/index.htm) | Revised Scheduling Nov 2010 (h
ttp://www.tga.gov.au/ndpsc/scheduling-revised.htm)

Safe Work Australia

An independent statutory agency responsible to improve occupational health and safety and workers' compensation arrangements
across Australia.

Links: [Work Australia (http://www.safeworkaustralia.gov.au) | Hazardous Substances Information System (http://hsis.ascc.gov.au/Def

ault.aspx) | PDF - Approved Criteria for Classifying Hazardous Substances [NOHSC: 1008 (2004) (http://www.safeworkaustralia.gov.a
u/AboutSafeWorkAustralia/WhatWeDo/Publications/Documents/258/ApprovedCriteria_Classifying_Hazardous_Substances_NOHSC1
008-2004_PDF.pdf)

Food Standards Australia

This government body's responsibility is to develop and administer the Australia New Zealand Food Standards Code (the Code), which
lists requirements for foods such as additives, food safety, labelling and GM foods. Enforcement and interpretation of the Code is the
responsibility of State/Territory departments and food agencies within Australia and New Zealand.

National Measurement Institute

National Measurement Institute (NMI) is Australia's peak measurement body responsible for biological, chemical, legal, physical and
trade measurement.

National Research Centre for Environmental Toxicology (Queensland)

(EnTox) This centre is a Joint Venture of the University of Queensland and the Queensland Department of Health.

Links: Food Standards Australia (http://www.foodstandards.gov.au) | Food Standards Code (http://www.foodstandards.gov.au/foodst

andards/foodstandardscode/) | Standard 1.4.1 - Contaminants and Natural Toxicants PDF (http://www.foodstandards.gov.au/_srcfile
s/Standard_1_4_1_Contaminants_v113.pdf) | Standard 1.4.2 Maximum Residue Limits (Australia Only) (http://www.foodstandards.gov.
au/foodstandards/foodstandardscode/standard142maximumre4244.cfm) | National Measurement Institute (http://www.measuremen
t.gov.au/Pages/default.aspx) | Persistent Organic Pollutants (http://www.measurement.gov.au/ScienceTechnology/Pages/PersistentOr
ganicPollutants.aspx) | EnTox (http://www.entox.uq.edu.au/)

Poison Control Centres

Generally throughout the world at national, state and hospital levels are centres available
to provide information on poisons. These centres advise on, or assists with, the
prevention, diagnosis and management of poisoning. The structure and function of
poisons centres varies around the world. At a minimum a poisons centre is an
information service. Some poisons centres may also include a toxicology laboratory
and/or a clinical treatment unit.

Australian Poison Control Centres

Australians should initially telephone 13 11 26 and they will be directed to their local
Poisons Information Centre.

Links: WHO - International Programme on Chemical Safety (http://www.who.int/ipcs/

WHO International Programme on Chemical
en/) | WHO - World directory of poisons centres (http://www.who.int/ipcs/poisons/ce Safety (IPCS) Regions
ntre/directory/en/) | IPCS - Chemicals in food (http://www.who.int/ipcs/food/en/) |
IPCS directory of poison centres - Western Pacific Region (http://www.who.int/ipcs/p
oisons/centre/directory/wpro/en/)

Toxicogenomics
This term is a combination of toxicology associated with chemicals and the effects on our genome. It is thought that molecular-based
approaches, such as transcriptomics, proteomics and metabolomics for studying the impact of chemicals on human and wildlife
populations will have an important role in hazard and risk assessment. There have subsequently been several Organisation for Economic
Co-operation and Development (OECD) and the International Programme on Chemical Safety (IPCS) co-operatively organised
workshops to explore the potential regulatory applications of toxicogenomics.

Links: USA - Toxicogenomics Research Consortium (http://www.niehs.nih.gov/research/supported/centers/trc)

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Biological Toxins
There are a variety of toxins produced by organisms that may impact upon development.
A single toxin example and study is show below, text has been modified from the rat
development study.[26]

Domoic Acid
A marine toxin domoic acid (DA) is produced
by the cosmopolitan diatom species
Pseudonitzchia and known to form harmful
algal blooms. The toxin has been shown to
affect numerous organisms in the wild
through trophic transfer including: sea birds,
manatees, dolphins, sea lions, as well as
humans. In human causes the illness amnesic
Toxicogenomics Research Consortium
shellfish poisoning.
acts as excitotoxin that binds to kainate
subtypes of ionotropic glutamate
receptors as a high affinity partial agonist
that prevents normal channel
inactivation.
behavioral effects of DA exposure, such
Domoic acid as scratching, ataxia, tremors, and
seizures.
identified as potential cause of cause
fatal loss in stranded pregnant sea lions.
single injection into maternal rat led to
detectable levels in amniotic fluid and
embryonic brain tissue within 1 hour.

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Mariana M & Cairrao E. (2020). Phthalates Implications in the Cardiovascular System. J Cardiovasc Dev Dis , 7, . PMID: 32707888 (https://
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PCDDs/PCDFs and dioxin-like PCBs in relation to birth weight. Environ. Res. , 109, 906-13. PMID: 19683226 (https://www.ncbi.nlm.nih.go
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Search Pubmed
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Search Pubmed: chemicals in pregnancy (http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=chemicals%20i

n%20pregnancy) | Persistent Organic Pollutants (http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=Persisten
t%20Organic%20Pollutants) | Biological Toxin (http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=search&term=Biological%2
0Toxin)

NCBI - Policies and Guidelines (https://www.ncbi.nlm.nih.gov/home/about/policies.shtml) | PubMed (https://www.ncbi.nlm.nih.gov/pubm

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longer works search the web with the link text or name. Links to any external commercial sites are provided for information purposes
only and should never be considered an endorsement. UNSW Embryology is provided as an educational resource with no clinical
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Globally Harmonized System of Classification and Labeling of Chemicals (GHS (http://www.unece.org/trans/danger/publi/ghs/ghs_w

elcome_e.html)) | Implementation (http://www.unece.org/trans/danger/publi/ghs/implementation_e.html) | USA - Department of
Labor (https://www.osha.gov/dsg/hazcom/ghs.html) | Australia - Safe Work Australia (http://www.safeworkaustralia.gov.au/sites/sw
a/whs-information/hazardous-chemicals/ghs/pages/ghs)
Stockholm Convention on Persistent Organic Pollutants (http://chm.pops.int/default.aspx) | What are POPs? (http://chm.pops.int/Con
vention/The%20POPs/tabid/673/language/en-US/Default.aspx)
USA - National Toxicology Program (http://ntp.niehs.nih.gov/) | Reports (http://www.ncbi.nlm.nih.gov/pubmed?term=%22National%
20Toxicology%20Program%22%5BCorporate%20Author%5D)
USA - Center for the Evaluation of Risks to Human Reproduction (http://cerhr.niehs.nih.gov/)
USA - Toxicogenomics Research Consortium (http://www.niehs.nih.gov/research/supported/centers/trc)
Dioxin 20XX (http://www.dioxin20xx.org/) | Organohalogen Compound Database (http://www.dioxin20xx.org/ohc_database_search.h
tm)
WHO - International Programme on Chemical Safety WHO - International Programme on Chemical Safety (http://www.who.int/ipcs/
en/) | WHO - World directory of poisons centres (http://www.who.int/ipcs/poisons/centre/directory/en/) | IPCS directory of poison
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