Abnormal Development - Chemicals

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Stockholm Convention on Persistent Organic Pollutants
Map showing worldwide ratification status 23/10/2010

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.

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.

Recently the WHO has developed an internationally agreed-upon system Globally Harmonized System of Classification and Labeling of Chemicals (GHS) that will eventually 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 | radiation | Prenatal Diagnosis | Neonatal Diagnosis | International Classification of Diseases | Fetal Origins Hypothesis

Some Recent Findings

  • 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[1] "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 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[2] "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."
  • Effects of environmental Bisphenol A exposures on germ cell development and Leydig cell function in the human fetal testis[3] "Using an organotypic culture system termed human Fetal Testis Assay (hFeTA) we previously showed that 0.01 μM BPA decreases basal, but not LH-stimulated, testosterone secreted by the first trimester human fetal testis. The present study was conducted to determine the potential for a long-term antiandrogenic effect of BPA using a xenograft model, and also to study the effect of BPA on germ cell development using both the hFETA and xenograft models. ... Exposure to BPA at environmentally relevant concentrations impairs germ cell development in first trimester human fetal testis, whilst gonadotrophin-stimulated testosterone production was unaffected in both first and second trimester testis. Studies using first trimester human fetal testis demonstrate the complementarity of the FeTA and xenograft models for determining the respective short-term and long term effects of environmental exposures."
More recent papers  
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This table shows an automated computer PubMed search using the listed sub-heading term.

  • Therefore the list of references do not reflect any editorial selection of material based on content or relevance.
  • References appear in this list based upon the date of the actual page viewing.

References listed on the rest of the content page and the associated discussion page (listed under the publication year sub-headings) do include some editorial selection based upon both relevance and availability.

Links: References | Discussion Page | Pubmed Most Recent | Journal Searches

Search term: Chemical Teratology Teresa Dodd-Butera, Penelope J E Quintana, Martha Ramirez-Zetina, Ana C Batista-Castro, Maria M Sierra, Carolyn Shaputnic, Maura Garcia-Castillo, Sonja Ingmanson, Stacy Hull Placental biomarkers of PAH exposure and glutathione-S-transferase biotransformation enzymes in an obstetric population from Tijuana, Baja California, Mexico. Environ. Res.: 2016; PubMed 27567517

Asher Ornoy, Liza Weinstein-Fudim, Zivanit Ergaz Genetic Syndromes, Maternal Diseases and Antenatal Factors Associated with Autism Spectrum Disorders (ASD). Front Neurosci: 2016, 10;316 PubMed 27458336

Katarina Dathe, Evelin Beck, Christof Schaefer Pregnancy outcome after chelation therapy in Wilson disease. Evaluation of the German Embryotox Database. Reprod. Toxicol.: 2016; PubMed 27350316

Zivanit Ergaz, Meytal Neeman-Azulay, Liza Weinstein-Fudim, Sarah Weksler-Zangen, Dana Shoshani-Dror, Moshe Szyf, Asher Ornoy Diabetes in the Cohen Rat Intensifies the Fetal Pancreatic Damage Induced by the Diabetogenic High Sucrose Low Copper Diet. Birth Defects Res. B Dev. Reprod. Toxicol.: 2016; PubMed 26748987

Thijs R A Vandenbroucke, Poul Emsbo, Axel Munnecke, Nicolas Nuns, Ludovic Duponchel, Kevin Lepot, Melesio Quijada, Florentin Paris, Thomas Servais, Wolfgang Kiessling Metal-induced malformations in early Palaeozoic plankton are harbingers of mass extinction. Nat Commun: 2015, 6;7966 PubMed 26305681

Search term: Persistent Organic Pollutant Teratology

Older papers  
  • Low-dose exposure to bisphenol A (BPA) and replacement bisphenol S induces precocious hypothalamic neurogenesis in embryonic zebrafish[4] "Here, we used zebrafish to link BPA mechanistically to disease etiology. Strikingly, treatment of embryonic zebrafish with very low-dose BPA (0.0068 μM, 1,000-fold lower than the accepted human daily exposure) and bisphenol S (BPS), a common analog used in BPA-free products, resulted in 180% and 240% increases, respectively, in neuronal birth (neurogenesis) within the hypothalamus, a highly conserved brain region involved in hyperactivity. Furthermore, restricted BPA/BPS exposure specifically during the neurogenic window caused later hyperactive behaviors in zebrafish larvae. Unexpectedly, we show that BPA-mediated precocious neurogenesis and the concomitant behavioral phenotype were not dependent on predicted estrogen receptors but relied on androgen receptor-mediated up-regulation of aromatase. Although human epidemiological results are still emerging, an association between high maternal urinary BPA during gestation and hyperactivity and other behavioral disturbances in the child has been suggested. Our studies here provide mechanistic support that the neurogenic period indeed may be a window of vulnerability and uncovers previously unexplored avenues of research into how endocrine disruptors might perturb early brain development. Furthermore, our results show that BPA-free products are not necessarily safer and support the removal of all bisphenols from consumer merchandise." zebrafish
  • Preconception Maternal and Paternal Exposure to Persistent Organic Pollutants and Birth Size: The LIFE Study[5] "Parental serum concentrations of 9 organochlorine pesticides, 1 polybrominated biphenyl (PBB), 7 perfluoroalkyl chemicals (PFCs), 10 polybrominated diphenyl ethers (PBDEs) and 36 polychlorinated biphenyls (PCBs) were measured prior to conception for 234 couples. ...Among girls (n = 117) birth weight was significantly lower in association with 1-SD increase in ln-transformed maternal serum concentrations of DDT, PBDE congeners 28 and 183 and paternal serum concentrations of PBDE-183 and PCB-167. Among boys (n = 113), maternal (PCBs: 138, 153, 167, 170, 195, and 209, PFOSA) and paternal (PCBs: 172 and 195) serum concentrations of several POPs were statistically associated with lower birth weight (range: 98-170 grams), while paternal concentrations of PBDEs (66, 99) were associated with higher birth weight. Differences in offspring head circumference, length, and ponderal index were also associated with parental exposures. Conclusions: Preconceptional maternal and paternal concentrations of several POPs were associated with statistically significant differences in birth size among offspring."
  • Alteration of rat fetal cerebral cortex development after prenatal exposure to polychlorinated biphenyls[6] "Perinatal exposure to these endocrine disruptors causes cognitive deficits and learning disabilities in children. ... Exposure to Aroclor 1254 increased cell cycle exit of the neuronal progenitors and delayed radial neuronal migration in the fetal cortex. Progenitor cell proliferation, cell death and differentiation rate were not altered by prenatal exposure to PCBs. Given that PCBs remain ubiquitous, though diminishing, contaminants in human systems, it is important that we further understand their deleterious effects in the brain."
  • Developmental and reproductive outcomes in humans and animals after glyphosate exposure: a critical analysis[7] "Glyphosate is the active ingredient of several widely used herbicide formulations. Glyphosate targets the shikimate metabolic pathway, which is found in plants but not in animals. ... To estimate potential human exposure concentrations to glyphosate as a result of working directly with the herbicide, available biomonitoring data were examined. These data demonstrated extremely low human exposures as a result of normal application practices. Furthermore, the estimated exposure concentrations in humans are >500-fold less than the oral reference dose for glyphosate of 2 mg/kg/d set by the U.S. Environmental Protection Agency (U.S. EPA 1993). In conclusion, the available literature shows no solid evidence linking glyphosate exposure to adverse developmental or reproductive effects at environmentally realistic exposure concentrations.
  • In utero exposure to dioxin causes neocortical dysgenesis through the actions of p27Kip1[8] "Dioxins have been reported to exert various adverse effects, including cell-cycle dysregulation in vitro and impairment of spatial learning and memory after in utero exposure in rodents. Furthermore, children born to mothers who are exposed to dioxin analogs polychlorinated dibenzofurans or polychlorinated biphenyls have developmental impairments in cognitive functions. Here, we show that in utero exposure to dioxins in mice alters differentiation patterns of neural progenitors and leads to decreased numbers of non-GABAergic neurons and thinner deep neocortical layers. This reduction in number of non-GABAergic neurons is assumed to be caused by accumulation of cyclin-dependent kinase inhibitor p27(Kip1) in nuclei of neural progenitors. Lending support to this presumption, mice lacking p27(Kip1) are not susceptible to in utero dioxin exposure. These results show that environmental pollutants may affect neocortical histogenesis through alterations of functions of specific gene(s)/protein(s) (in our case, dioxins), exerting adverse effects by altering functions of p27(Kip1)."
  • The Pine River statement: human health consequences of DDT use[9] "Dichlorodiphenyltrichloroethane (DDT) was used worldwide until the 1970s, when concerns about its toxic effects, its environmental persistence, and its concentration in the food supply led to use restrictions and prohibitions. In 2001, more than 100 countries signed the Stockholm Convention on Persistent Organic Pollutants (POPs), committing to eliminate the use of 12 POPs of greatest concern. However, DDT use was allowed for disease vector control. In 2006, the World Health Organization and the U.S. Agency for International Development endorsed indoor DDT spraying to control malaria."

United Nations - Globally Harmonized System of Classification and Labelling of Chemicals

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

GHS08 Health Hazard
GHS08 Health Hazard
GHS08 Health Hazard

Of the 9 pictogram codes, this relates to systemic health hazard as well as reproductive and developmental effects.

Germ cell mutagenicity (State route of exposure if it is conclusively proven that no other routes of exposure 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
  • 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.
    • H360D - May damage the unborn child.
    • H360FD - May damage fertility. May damage the unborn child.
  • 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 | Safe Work Australia - GHS

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.


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.


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.


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.


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

(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

Map showing worldwide ratification status 23/10/2010

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.

  1. Pesticides: aldrin, chlordane, DDT, dieldrin, endrin, heptachlor, hexachlorobenzene, 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 | What are POPs?

Polychlorinated Biphenyls

A recent study using rat model showed effects on fetal cerebral cortex development through radial neuronal migration in the fetal cortex.[6]

An example of the effects of polychlorinated biphenyls (PCBs) can be seen following contaminated rice oil consumption in Taiwan between 1978-1979.[10][11]

"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." [10]
Links: Endocrine System - Abnormalities


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.jpg

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.[12] There has been some criticism of the data used in this particular study.[13][14]

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 | Organohalogen Compound Database


In 2008 as part of the US National Toxicology Program a report "Final Report on Carcinogens Background Document for Styrene"[15] 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

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


In 2010 as part of the US National Toxicology Program a report "Final Report on Carcinogens Background Document for Formaldehyde"[16] 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.[17]

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

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 | Center for the Evaluation of Risks to Human Reproduction


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.
  • 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 | TGA - About The Poisons Standard | Therapeutic Goods Administration | Revised Scheduling Nov 2010

Safe Work Australia

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

Links: [Work Australia | Hazardous Substances Information System | PDF - Approved Criteria for Classifying Hazardous Substances [NOHSC: 1008 (2004)

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 | Food Standards Code | Standard 1.4.1 - Contaminants and Natural Toxicants PDF | Standard 1.4.2 Maximum Residue Limits (Australia Only) | National Measurement Institute | Persistent Organic Pollutants | EnTox

Poison Control Centres

WHO International Programme on Chemical Safety (IPCS) Regions

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 | WHO - World directory of poisons centres | IPCS - Chemicals in food | IPCS directory of poison centres - Western Pacific Region


Toxicogenomics Research Consortium

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

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.[18]

Domoic Acid

Domoic acid.jpg

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 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 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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