Endocrine disrupting chemicals in Tasmania

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Eco-toxicology of endocrine disruption in wildlife

The first published mention of endocrine disruption per se appears in a 1992 book entitled: Chemically-Induced Alterations in Sexual and Functional Development: the Wildlife/Human Connection.[1] This early work covers examples of endocrine disruption in wildlife such as the effects of pulp-mill effluent on the sexuality of fish; thyroid abnormalities in Great Lakes salmon, abnormal sexual development in North American birds, organotin (tributyl tin) related sex anomalies in molluscs and hormone dysfunction in marine mammals.

Synthetic substances with endocrine action had been known since the 1930s, for example estrogenic activity of diethylstilbestrol (DES). The new concept in the early 1990’s was an attempt to explain many pathologies and other abnormalities in wildlife and humans in terms of endocrine interference through hormone mimicry and other mechanisms.

Despite the growing scientific literature, the idea that synthetic substances with only slight or no resemblance to hormones or their known antagonists, could be causing widespread biological effects in the natural world through interference with endocrine systems are still given limited recognition. Furthermore, the effects on wildlife populations of discharges of naturally occurring hormonally active substances had only been studied to a limited extent.[2] The catalyst meeting on endocrine distruption took place at the Wingspread Conference Centre, Racine, Wisconsin in July 1991 organised by Theo Colborn and co-workers.[1]

Endocrine disruption is dismissed as primarily of academic interest (or even as self-interest), with little if any relevance for ecosystem health. This follows a long tradition employed by critics with various axes to grind, who either deliberately or accidentally overlook the abundance or significance of evidence for particular phenomena.[2] There is now an overwhelming body of science which shows not only that endocrine disruption (ED) in some wildlife is a widespread reality, but that it can cause both population-level or community-level damage given the right combination of conditions.[2] There is certainly debate about the extent of such damage, however, the quantity and quality of available literature now make it clear that ED is a common mechanism whereby a range of man-made pollutants is able to cause effects in wildlife.[3]

Probably the best-known example of an assemblage of eco-toxicological knowledge is Rachel Carson’s book Silent Spring, published in 1962. It publicly exposed the impacts on wildlife caused by the organochlorine (OC) pesticides.[4] Carson drew attention to the ability of certain OCs to interfere with reproduction, although at that time the endocrine-disrupting mechanisms were unclear. Partly because Carson attacked our unsustainable exploitation of nature, and partly because Silent Spring was written as a highly readable polemic rather than as a scientific treatise, Carson was heavily criticized by a variety of chemical manufacturers. However time has proved her largely correct, both about OCs and adverse consequences of ED mimicry on the health of whole ecosystems.[2]

Carson prepared the ground for Colborn and others, who demonstrated and furthered the understanding of human-induced endocrine disruption. Crucially, they prepared the discipline of ecotoxicology, demonstrating that certain substances - in extremely small concentrations - could have far-reaching biological effects which were completely unrelated to a possible high-dose, acute toxicity.

Since 1991 good evidence for population-level impacts of endocrine disruption is still limited to a few groups of wildlife taxa. These include the feminization of fish by natural and synthetic oestrogens in sewage and pulp-mill effluents; abnormal renal function leading to weakening of the stress response in fish exposed to a range of contaminants[5]; and altered sex determination and differentiation in alligators and other reptiles[6] which, in some contaminated locations, has caused population declines. Dr Lou Guilllette after hearing a talk by comparative endocrinologist, Howard Bern from University of California (Berkeley) recognized similarities between the developmental disruptions induced by diethylstilbestrol (DES) in birds and the observed reproductive dysfunction seen in alligators in a Florida lake called Lake Apopka. In 1980 a chemical spill from the Tower Chemical Company had discharged dicofol, an organochlorine pesticide with endocrine disrupting activity. In Lake Apopka, the male alligators showed small penises and female alligators had abnormalities in egg development and hatching rates associated with abnormal sex hormone ratios. In addition, red-eared turtles in Lake Apopka were declining due to a loss of normal male turtles from the population; with genetic males becoming non-functional intersex individuals.[7] This retrospective unravelling of the 1980 chemical spill on Lake Apopka and the consequent impact on the lake’s food web only happened because wildlife officials had been asked to supply alligator eggs from various Everglades location for commercial alligator farms[3]; they found most eggs from Lake Apopka did not hatch. Linking man-made chemicals to severe endocrine disruption activity would have gone undetected without this monitoring.[3]

There is also some evidence that limb deformities in amphibians may be caused by a form of ED related to environmental retinoids and laboratory studies show that amphibians can be feminized or demasculinized by endocrine-active substances such as atrazine.

Several studies have provided support for the hypothesis that oestrogenic actions could be due to increased aromatase activity. For example, the feminizing effect of atrazine on some species has been hypothesized to be caused by its ability to alter aromatase-induced conversion of androgens to oestrogens.[8][9] Although many contaminant-induced oestrogenic actions described to date appear to be caused by receptor-mediated interactions, mechanisms exist whereby xenobiotics alter steroid action via alterations in the synthesis of these hormones by modification in the enzymatic pathways, either by direct changes in enzyme synthesis or in enzyme activity levels.[10]

Dramatic declines in the populations of numerous bird species occurred during the post-World War II decades after the wide-scale use of DDT for insect control. The major metabolite of DDT, p,p´-DDE [1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene] was associated with altering the physiological process of egg shell formation that subsequently led to shell thinning and population declines of numerous avian species, particularly raptors and shorebirds.[11] These studies indicate that this organochlorine contaminant disrupts calcium transport within the eggshell gland. In addition, prostaglandins (PGs) have been implicated in eggshell thinning because DDE disrupts PG synthesis, which reduces bicarbonate transport in the duck shell gland lumen, thereby reducing calcium transport.

Given the important roles of various PGs during ovulation, pregnancy, and parturition in a wide array of vertebrate species[10], it is surprising that few investigators have examined the disruption of this important class of hormones. Like steroidogenesis, PG synthesis is controlled by a pathway of enzymes. Steroids, particularly oestrogens, regulate the expression of a number of these enzymes. Thus, with a wide range of chemicals capable of altering the “estrogenic milieu,” it could be hypothesized that PG synthesis is altered in the reproductive system of any vertebrate, as described previously for the avian reproductive tract.[10] Recent studies have suggested that PGs could work through perinuclear receptors as well as through the established membrane–G protein receptors[12]. If this is the case, disruption at the level of transcription could occur via several mechanisms leading to different outcomes. Finally, it is important to recognize that PGs are not just reproductive hormones, they play essential roles in the immune response, including inflammation and arthritis, cardiovascular regulation encompassing hypertension, and respiration including asthma. These are just some of the roles that ubiquitous PG hormones play in vertebrates. Moreover, PGs are evolutionarily ancient and are also important in reproduction and development in invertebrates.[13] In brief, a major research effort is needed to examine the possible linkages between the wide-ranging alterations seen in organisms living in contaminated environments and alterations in prostaglandin synthesis.

An emerging feature of endocrine disruption and ecotoxicology is the close collaboration between wildlife scientists and clinicians or medical scientists.[14] Endocrine disruption represents less a new field, and more an integration of many fields, including biology, chemistry, epidemiology, and atmospheric and earth sciences. It is a new synthesis of science to begin to understand the complexity of the world around us and our human impact on it. New understanding of the effect of contamination has been gained because comparative endocrinologists, developmental biologists, ecologists and evolutionary biologists have exchanged ideas, knowledge, and hypotheses with physicians, epidemiologists, toxicologists and biochemists. Understanding the complex interactions between the plethora of environmental contaminants and the organisms living in contaminated environments will require many approaches. The most important is a broad, creative approach to the science and its interpretation.[10]

In 1991, a group of expert scientists at a Wingspread work session on endocrine-disrupting chemicals (EDCs) concluded that 'Many compounds introduced into the environment by human activity are capable of disrupting the endocrine system of animals, including fish, wildlife, and humans. Endocrine disruption can be profound because of the crucial role hormones play in controlling development'.'[15] Fifteen years later in 2007, there are a growing number of documented examples of adverse effects of EDCs in invertebrates, fish, wildlife, domestic animals, and humans. Hormonal systems can be disrupted by numerous different anthropogenic chemicals including anti-androgens, androgens, oestrogens, AhR agonists, inhibitors of steroid hormone synthesis, anti-thyroid substances, and retinoid agonists. In addition, pathways and targets for endocrine disruption extend beyond the traditional oestrogen/ androgen/thyroid receptor–mediated reproductive and developmental systems. New concerns include complex endocrine alterations induced by mixtures of chemicals, an issue broadened due to the growing awareness that EDCs present in the environment include a variety of potent human and veterinary pharmaceutical products, personal care products, nutraceuticals and phytosterols.[16]

Among the detected pharmaceuticals in the environment are potent, long-lasting oestrogens, antibiotics, beta-blockers, anti-epileptics, androgenic steroids, and lipid regulating agents. Some pharmaceuticals have been linked to dramatic effects in wildlife, including death in bald eagles [4], threatened extinction of at least three species of vulture in Asia [17] and sex reversal and infertility in several species of fish (WHO, 2002).

Recent in situ caged and laboratory-based exposures of fish confirm that sewage effluent is responsible for the observed increases in vitellogenin [see Biomarkers for Endocrine Disruption] and reproductive failure.[18] Although no single chemical has been identified as the culprit, chemical fractionation studies of sewage effluent have shown that synthetic and natural estrogens are often present in biologically significant quantities.[19][20] These oestrogenic compounds include synthetic pharmaceuticals and natural hormones in wastewater, such as ethinyl estradiol and 17 beta-estradiol. Various laboratory studies have shown that exposure to relatively low levels of these steroids will induce vitellogenin and can cause the development of intersex gonads (ovotestis) in fish and amphibians.[21] Furthermore, another recently published study showed that levels of ethinyl oestradiol in water was sufficient to induce vitellogenin along with a substantial decrease in the sustainability of the wild fish populations.[22]

There is still only moderate evidence for a direct causal linkage between persistent organic pollutants (PCBs, Dioxins, Furans, and PBDEs) exposure and effects in wildlife; for example, polychlorinated biphenyl-induced reproductive and immune dysfunction in Baltic seals and St Lawrence River Belugas and increased suspectibility to infectious disease, degenerative disease and cancers. The North American Great Lakes’ trout populations were adversely affected by PCB and dioxin exposures in the 1960-1970s, PCB-contaminated cormorants displayed crossed-bills; great blue herons were infertile, and mink fed PCB contaminated fish from the Great Lakes either died after high exposures or were infertile at lower exposure levels. Other wildlife case studies involving synthetic chemical exposures include reproductive and developmental anomalies in frogs exposed to atrazine and cryptorchidism in Florida panthers attributed to agrichemical exposure.[16][23][24]

Triazine herbicides

Atrazine - a member of the triazine herbicide group - is a common agricultural herbicide with endocrine disruptor activity. There is evidence that this triazine interferes with reproduction and development, and may promote cancer. The United States Environmental Protection Agency approved its continued use in October 2003, yet in the same month the European Union (EU) announced a ban of atrazine because of ubiquitous and unpreventable water contamination.[25]

Atrazine is probably the most widely used herbicide in the world and one of the most common contaminants in ground and surface waters.[26] Since it first went on the U.S. market over 50 years ago, atrazine has become one of the most widely used herbicides in the United State and is one of the most common pesticide contaminants in U.S. surface and groundwater. In the Midwest states most farmers and other rural residents get their drinking water directly from private wells that tap into groundwater, they and their families are particularly vulnerable to atrazine contamination in water. Between 1998 and 2003, an estimated seven million people were exposed to atrazine in their treated drinking water at levels above the US health-based limits. In October 2009, US EPA officially re-opened an examination of atrazine, despite the fact that it had previously been reviewed and approved for continued use in 2003. The EPA will spend the 2010 reviewing the health and environmental risks of the chemical.[27]

Human health effects of Atrazine

Birth Defects

A recent study showed a significant correlation between peaks in drinking water contamination with atrazine and small-for-gestational age and pre-term delivery with the effective dose of ≥ 0.1ug/L.[28] Another recent study shows that birth defects in humans are highly correlated with atrazine exposure in surface waters.[29]

Prostate cancer

A study was conducted in Syngenta’s (then known as Novartis) atrazine-production facility in San Gabriel Louisiana.[30] The results revealed an 8.4 times increase in prostate cancer amongst workers who had worked for the company for ten or more years who were exposed to atrazine (without ventilation) were compared to unexposed workers.

Breast cancer

At least one study (from Kentucky, USA) has shown an increase in the incidence of breast cancer in women with atrazine-contaminated well water (P < 0.0001).[31]

Other cancers

There is also some earlier published data that exposure to atrazine may be associated with other cancers in humans (lung, bladder, non-Hodgkin’s lymphoma, leukemia, multiple myeloma, ovarian cancer, colon cancer).[32][33] In addition to the endocrine effects, there is some evidence that atrazine may induce non- Hodgkin’s lymphoma (NHL) cancer through a cytogenic mechanism; one study reported an elevated risk of NHL associated with atrazine use only in cases with a particular chromosomal translocation.[34]

Male fertility

At least one study has shown a correlation between urine concentrations of atrazine and impaired male fertility. Men from Columbia, Missouri USA with low sperm count, poor semen quality and fertility problems had significantly more atrazine in their urine than men without fertility problems.[35]

Cell biology - Aromatase induction

Aromatase is induced in multiple human cell lines when exposed to atrazine.[36][37]Heneweer, M., M. van den Berg and J. Sanderson A comparison of human H295R and rat R2C cell lines as in vitro screening tools for effects on aromatase. Toxicological Letters 2004, Volume 146, pages 183-194</ref>[38][39][40][41] Though some studies have used aromatase constructs to examine this effect, some human cancer cell lines respond to atrazine exposure without any manipulation.

Atrazine in laboratory animal studies


US EPA studies showed that atrazine exposure induced abortion in at least four strains of rats.[42][43]

Cancers - general

Atrazine exposure is associated with cancer induction in laboratory rats (mammary, uterine, combined leukemia and lymphoma).[44]

Mammary Cancer

Several studies conducted by the industry (Ciba/Novartis/Syngenta) have demonstrated that atrazine exposure increases the incidence of mammary cancer relative to controls in age-matched rats.[45][46][47][48][49] The authors claim that the incidence is not increased, despite a P value <0.05;justification is that the incidence observed in atrazine-exposed rats at the age of examination was not higher than the incidence observed in older unexposed rats. Thus, they claim that the incidence was not increased, but rather the age of onset was lower in atrazine-exposed rats.

Prostatitis and prostate cancer

Atrazine induced prostate cancer in rats in at least one published study,[50] and prostate disease in male pups of atrazine-exposed mothers.[51][52]

Reproductive Development

Exposure to atrazine is associated with delayed reproductive development in male and female laboratory rodents,[53][54]. Decreased testosterone in rats has been demonstrated in independent laboratories in rats, including one EPA laboratory.[55] Several mechanisms for declining androgens have been proposed, including increased degradation of testosterone.[56][57][58][59][60][61][62][63]

Several studies, mostly published by the manufacturer have demonstrated increased oestrogen production in rats exposed to atrazine. The increased oestrogen is consistent with the increase in mammary tumour incidence in rats, especially given that atrazine-induced mammary tumours tend to be oestrogen receptor positive/ oestrogen sensitive.[64].

Atrazine exposure in pregnant rats also results in severely impaired mammary development in the female offspring of the exposed rat.[65][66][67]

The disruptive effects of atrazine on endocrine activity has been suggested to occur via multiple mechanisms, including inhibition of androgen receptors in mammals,[68] disruption of the hypothalamic control of pituitary–ovarian function in mammals,[69] and alteration of corticosterone and thyroid hormones in amphibians,[70] and by induction of aromatase that results in an increased conversion of androgen to estrogen in human cell lines,[71][72] in amphibians[73][74] and potentially in reptiles.[75]

Atrazine and amphibians

Male hermaphroditism and impaired immune system function leading to increased susceptibility to infection are reported. Atrazine-exposure (at 21 ppb) for as little as 48 hours resulted in severe gonadal dysgenesis in African clawed frogs (Xenopus laevis).[76] At concentrations of only 0.1 ppb atrazine induced hermaphrodite amphibians when administered throughout larval (egg & tadpole) development.[74]

Most water sources in the United States of America (a major user of atrazine), including rainwater, can exceed the effective concentrations in these laboratory studies.[74] The concentration of atrazine associated with hermaphroditism in frogs was 30 times lower than the United States drinking water standard of 3 ppb.[77] These reported effects were in African clawed frogs, however, further testing of the effects of atrazine at 0.1 ppb resulted in retarded gonadal development (gonadal dysgenesis) and testicular oogenesis (hermaphroditism) in the endemic North American leopard frogs (Rana pipiens).[73][78] Gonadal dysgenesis and hermaphroditism was observed in free-ranging frogs collected from atrazine-contaminated sites across the United States. Such toxicological laboratory experiments combined with field studies demonstrated the biological impact of atrazine contamination in the environment and raises concern about the effects of atrazine on amphibians in general and the potential role of atrazine and other endocrine disrupting pesticides in amphibian declines.[73]

The association of pesticides and amphibian declines has been most intensely examined by Garry Fellers and his coworkers in North America.[79][80] They have published research on the detection of organophosphate insecticides and the herbicide atrazine.[81] In August 2009 another study found that insecticides used in the highly populated agricultural areas of California’s Central Valley affected amphibians that breed in the Sierra Nevada mountains to the east. Several Californian frogs have declined disproportionately from sites that are downwind from areas with agricultural activity.[82] This study adds to the increasing evidence that pesticides impact areas and wildlife species that are miles from sources of pesticide application.[83][84] Each year, approximately 700 tonnes of pesticides are applied to crops in the California Central Valley (figures for 2000), a portion of which is carried by winds into the seemingly pristine areas of the Sierra Nevada.[85] Rainwater brings drifting pesticides back to earth, where they are absorbed through the frogs’ moist skin. At the time Gary Fellers of the U.S. Geological Survey (USGS) characterized frogs as ‘essentially environmental sponges, soaking up chemicals from water.[86] Exposure to agricultural chemicals have been linked to adverse affects on developing larval amphibians, increasing their vulnerablity to parasites and predators.[87]

Increased susceptibility to parasitic infections in amphibian exposed to atrazine are reported.[88]

Atrazine and fish

Endocrine-active compounds are associated with intersex and reproductive effects in fish. These chemicals have the ability to adversely affect endocrine systems and include some pesticides, PCBs, certain heavy metals, certain household products, and many pharmaceuticals specifically designed to interact with endocrine function. Atrazine, one of the most commonly used herbicides in the world, has been shown to affect reproduction of fish. According to a 2010 U.S. Geological Survey (USGS) study[89] at concentrations commonly found in agricultural streams and rivers caused reduced reproduction and spawning, as well as tissue abnormalities in laboratory studies with fish. In announcing its publication the lead author Donald Tillitt said: ‘The reproductive effects observed in this study warrant further investigation and evaluation of the potential risks posed by atrazine, particularly in wild populations of fish from streams in agricultural areas with high use of this herbicide.’ Fathead minnows were exposed to atrazine at the USGS Columbia Environmental Research Center in Columbia, Mo., and observed for effects on egg production, tissue abnormalities and hormone levels. Fish were exposed to concentrations ranging from 0 to 50 micrograms per liter [50ppb] of atrazine for up to 30 days. All tested levels of exposure are less than the US EPA Office of Pesticides Aquatic Life Benchmark of 65 micrograms per liter for chronic exposure of fish. Substantial reproductive effects were observed in this study at concentrations below the USEPA water-quality guideline. Study results show that normal reproductive cycling was disrupted by atrazine and fish did not spawn as much or as well when exposed to atrazine. Researchers found that total egg production was lower in all atrazine-exposed fish, as compared to the non-exposed fish, within 17 to 20 days of exposure. In addition, atrazine-exposed fish spawned less and there were abnormalities in reproductive tissues of both males and females.

Tasmania and the use of Triazine herbicides

Usage & Detection in water catchments

Documented evidence of persistent triazine contamination of Tasmanian surface and ground waters has been known since at least 1994.[90] ‘Contamination of Tasmanian streams with triazine herbicides is a frequent occurrence wherever they are used. It is also apparent that atrazine may persist in streams for up to 16 months after single spraying events…the data are insufficient to allow comments on long-term effects of low-level contamination on stream communities…the present study shows that triazine contamination occurs frequently in streams draining catchments where triazines are used. Contamination occurred more frequently, and at higher concentrations, with the use of atrazine and simazine in forestry operations than it did in cropped catchments where other triazines were used.’[90]

‘Twenty of 29 streams (69%) sampled intensively from 1989 to 1992 contained detectable residues of triazines. The most commonly used triazines, atrazine and simazine, had mean contaminations of 2.85 and 1.05 ug/L (ppb) but astonishingly the triazine herbicide concentrations ranged widely - up to 53 mg/L (ppm). Atrazine contamination of one catchment [Big Creek, near Wynyard, NW Tasmania] after aerial spraying of plantation coupes led to a detection of 22mg/L in water.[90] The authors reported persistence of atrazine contamination over 12 to 16 months; it is estimated that contamination of groundwater with triazines will take up to 20 years to be cleared from water catchments from the time when the herbicide is no longer used. Atrazine has a longer half-life in cool Tasmanian climates compared to warmer climates [a half-life of over 200 days in Tasmania compared to 12 days in northern Queensland]. Spraying during saturated soil conditions with soil and runoff after rain events are considered the main sources of surface water contamination.[90] Atrazine is a very mobile, long-lived pollutant that can migrate readily down catchments from source runoff to surface water and groundwater supplies.[91]

Atrazine has reported water solubilities of 70 mg/L at 20C [92]. Davies cites the marked differences in Tasmanian operational practices for triazine applications between forestry and agricultural uses. ‘Forestry spraying is carried out by helicopter with relatively high application rates, in contrast to the ground-spraying of triazines on crops’, he attributes the high concentrations of triazine residues detected in streams draining aerial sprayed forestry areas to this.[90]

According to Tasmanian hydrologist, Dr David Leaman[93] Tasmanian drinking water is derived from river catchments where chemical use from forestry and agricultural land-use activities compromises water quality. Catchments supplying drinking water to the city of Burnie (population ~50,000) are exposed to chemical residues from substantial land-use for farming and silviculture.[93] In eastern Tasmania water from the Prosser River have consistently recorded triazine residues sufficient to trigger public health concerns since 2003.[93] Despite the frequent detections of these triazine residues, no attempt to determine the source of the contaminations has been undertaken by the State water authorities. ’Since there have been several recurrences we may conclude that no proper investigation has ever been done’.[93] A characteristic of the water-soluble triazines is their ability to migrate considerable distances from the site of use. Forestry plantations a considerable distance from the Rubicon River in Northern Tasmania were acknowledged as the source of simazine contamination in water samples.[93] ‘It seems that no one with any responsibility has any knowledge of the transmission characteristics of of polluted groundwater’, Dr Leaman states.[93] Leaman concludes,'Tasmanian chemical use rules are lax on approaches and policing, so it may not be known which land owners have been recent users of the [identified] chemicals’.

In 1992 the Lorinna (NW Tasmania) drinking water was heavily polluted with atrazine, as was the drinking water of Derby in 1994. In 1994 the Hellyer River, the Great Forester River, the South George River was polluted with simazine, the Cattley River and the Rubicon River with atrazine, and the Little Henty River and the Lisle Creek with hexazinone.

Simazine pollution was recorded in 1995 in the Great Forester catchment, in 2003 in the Mt Leslie treated water and the West Tamar untreated and treated water, and in 2004 in the West Tamar untreated water (Launceston water supply). In 2004 at a helicopter crash site (aerial spraying) in the South George catchment - alphacypermethrin, atrazine, simazine, chlorothalonil, and terbacil was found at the helicopter crash site. In September 2004 at Wyena, the Carpenter family discovered their groundwater and drinking water had been polluted with atrazine from forestry spraying operations. In 2005 the Prosser River was found to be polluted with simazine from forestry operations.[94]

In 2005, the Tasmanian Government started a Pesticide Monitoring Programme for tasmanian rivers - see Water pollution in Tasmania for results and comments.[95]

In April 2009 the drinking water for Tasmania’s capital city, Hobart was contaminated with the triazine, hexazinone at levels up to 1.02 ppb; it was the third detection in recent years, the other two were atrazine in 2006 (0.05 ppb)and September 2008 (0.08 ppb).[96]

Currently under National Health & Medical Research Council, Australian Drinking Water Guideline health value for atrazine is set at 40 ppb (40 ng/mL; 40 ug/L)[97]; in USA, the value is set at 3 ppb. The Australian authorities are currently reviewing this benchmark. 'Atrazine should not be detected in drinking water. If present in drinking water, atrazine would not be a health concern [unless the concentration exceeded 0.04 mg/L [40 ppb].] If it is detected, then remedial action should be taken to stop contamination.' The practical limit of detection (LOD) is 0.00005 mg/L [0.05 ppb].[98]

"Australia is allowing 400 times the amount of atrazine contamination that we found castrated amphibians and fish - there's now way I would be drinking the water'.[99]

The first tests of Tasmania ground waters commenced in April/May 2009; they detected atrazine at 2 sites at levels of 1.2 and 1.5 ppb. [[5]]

In Tasmania as atrazine is persistent and seemingly cannot be used without contaminating nearby waterways, and is also an endocrine disrupting chemical and a reproductive toxin; it should not be used in water catchments.

In October 2009 the Tasmanian Greens attempted to introduce a Bill into the Tasmanian parliament to ban the use of triazine herbicides in Tasmania.[100][pdf here] The Tasmanian Greens also raised the implications of low dose exposure of atrazine to wild fish stocks.[101]pdf here based on the 2010 USGS atrazine study on flathead minnows.[89]

Tracing cryptic sources of persistent EDCs in the environment

Polychlorinated biphenyls (PCBs)

Commercial production of polychlorinated biphenyls (PCBs) started in the late 1920s. Since 1929, it is estimated that 2 billion kilograms of PCBs were produced commercially. In 2003, about 200 million kilograms of PCBs remain freely mobile within environmental systems and biotic reservoirs.[102]

PCB pollution may be generated during the incineration of municipal waste. PCB concentrations of 0.01–1.5 mg/kg were detected in fly ash from five municipal incinerators operating under different technological and working conditions. Aersol effluents from several municipal refuse and sewage incinerators in the mid-western USA contained PCB concentrations of 0.3–3.0 μg/m3. The total PCB concentration measured in the flue gas effluent from a municipal waste incinerator in Ohio, USA, was 0.26 μg/m3. PCB levels of 2–10 ng/m3 [w/v] were detected in effluents from coal and refuse combustion in Ames, Iowa, USA (US EPA, 1988a). An additional and potentially substantial source of PCB pollution is volatilization from landfills containing transformers, capacitors, and other PCB waste and from contaminated bodies of water, such as the Great Lakes in North America. Because of environmental health and human health impacts, the use and production of PCBs has been severely restricted or banned in many countries. Sweden restricted their use and production in 1972, the USA in 1977, Norway in 1980, Finland in 1985, and Denmark in 1986.[102] In 1985, the US EPA issued a final rule requiring the removal of PCB fluids or electrical transformers containing PCBs from all buildings by October 1, 1990.[103] PCBs remains the only chemical specifically banned by a vote of the United States Congress by an amendement to the U.S. Toxic Substances Control Act.[104]

In 1968 about 1,800 people in Yusho, Japan were poisoned when PCBs leaked from a heat exchanger at a company processing rice-bran cooking oil. Many people became seriously unwell, babies were born dead and approximately 300 people died. A range of horrific skin sores typical of chloracne erupted on the faces and bodies of PCB-contamined individuals. Dark skin colourations were reported in newborn children of affected mothers and hypertropy & hypersecretion from the glands in the eyelids; respiratory and neurological diseases were also reported.[105] A similar mass poisoning incident occurred in Taiwan in 1979.[104] A combination of the growing evidence of persistent biaccumulation of PCBs in natural ecosystems and the horrific acute poisonings and fatalaties in Yusho and Taiwan were the catalyst for governments all over the world to phase out and then ban outright the manufacture and use of PCBs.[104]

PCBs were manufactured and sold as complex mixtures of the 209 theoretically possible chlorobiphenyl congeners; 132 congeners are found in the commercial PCB preparations Aroclor 1016, 1221, 1242, 1254 and 1260 and Clophen A30, A40, A50 and A60[106] under a variety of trade names. Commercial formulations were traded under Aroclor (Monsanto, USA), Pyranol, Pyroclor (USA), Phenochlor, Pyralene (Prodolec, France), Clophen (Bayer, Germany), Elaol (Germany), Kanechlor (Kanegafuchi, Japan), Santotherm (Mitsubishi, Japan), Fenchlor, Apirolio (Italy), and Sovol (USSR).[102]

Of the 209 possible PCB molecules, approximately 30 to 60 congeners are detected in the tissues of terrestrial and aquatic mammals.[107] Twenty of these detectable congeners lack a chlorine substitution in the ortho positions and can assume a planar configuration, making them structurally similar to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) - the most toxic of the polyhalogenated dibenzo-p-dioxins (PCDDs). The toxic potencies of PCB congeners have been categorized in comparison to TCDD according to their toxic equivalence factor (TEFs).[108][109] The toxic potencies of non-ortho, planar PCBs act through the aryl hydrocarbon (Ah) receptor to cause thymic atrophy, immune immunosuppression, reproductive impairment and weight loss.[107] Three non-ortho, planar PCBs - congeners 126, 169 and 77 are recognised as the most potent inducers of the 3-methylchloranthrene enzyme [3-MC] with TEFs of 0.1, 0.03 and 0.0001 respectively.

As man-made chlorinated hydrocarbon compounds that consist of two benzene rings linked by a single carbon–carbon bond, with from 1 to all 10 of the hydrogen atoms replaced with chlorines, they have been used in plasticizers, surface coatings, inks, adhesives, flame retardants, pesticide extenders, paints, and microencapsulation of dyes for carbonless duplicating paper. Because PCBs resist both acids and alkalis and are relatively heat-stable, they have been used in dielectric fluids in transformers and capacitors. Further environmental contamination may occur from the disposal of old electrical equipment containing PCBs. The pyrolysis of PCB mixtures produces hydrogen chloride and polychlorinated dibenzofurans (PCDFs), and pyrolysis of mixtures containing chlorobenzenes also produces polychlorinated dibenzodioxins (PCDDs).

Although PCBs are not pesticides they were added to synthetic pesticide formulations such as organochlorines to extend their ‘kill effect’; apparently the addition of PCBs to biocide formulations increased their ‘kill-life’.[103] Not being the active ingredients, PCB additives were not identified on product labels.

In May 2009 the international officials to the Stockholm Convention on Persistent Organic Pollutants met in Geneva to advance global efforts to rid the world of some of the most hazardous chemicals produced by humankind. One of the specific challenges discussed at the 2009 convention was: Challenge #4: ‘continuing to ensure the Convention meets its goal of protecting human health and the environment from POPs; how to strengthen the efforts to phase out PCB use. A vital next step will be to consider the endorsement of a PCB elimination club to establish key data and to evaluate whether the use of PCBs is indeed declining.’ The meeting also considered further steps for promoting the use of best available techniques, best available practices and best environmental practices to reduce or eliminate the unintentional releases of unintentionally produced POPs.

The 12 initial POPs covered by the Convention include nine pesticides (aldrin, chlordane, DDT, dieldrin, endrin, heptachlor, hexachlorobenzene, mirex and toxaphene); two industrial chemical groups (PCBs as well as hexachlorobenzenes, also used as a pesticide); and the unintentional by-products, most importantly the dioxins and furans.[110]

Polybrominated biphenyls (PBBs)

Polybrominated biphenyl (PBBs) are another group of persistent halogenated aromatic hydrocarbons (not to be confused with polybrominated dipheyl ethers [PBDEs]) used predominantly for their flame/fire retardant properties; they are incorporated into a range of domestic plastics subject to heat including electrical appliances. In May and June 1973 approximately 500 to 1000 lbs of PBBs was mistakenly sent to a Michigan livestock feed mill in place of magnesium oxide. This incident was nicknamed 'Cattlegate' and invlved the mix up on Firemaster - the PBB additive produced at the Michigan Chemical Corporation with Nutrimaster - the MgO additive for stock feed.[111] The PBBs was mixed into the grain-based feed for cattle and other farm animals. The contaminated feed was used on dairy farms, fed to hens producing eggs and used to feed pigs, chickens and cattle destined for slaughter. The acute PBB toxicity caused dramatic collapse in egg and milk production, severe skin disease, hoof deformities and generalised kidney and liver damage as well as birth defects. Once the cause of the catastrophic accident was understood it necessitated the slaughter of 35,000 cattle, 1.6 million chickens and thousands of pigs on approximately 100 Michigan farms.[112]

Except for a remarkable combination of circumstances and some good luck, the precise chemical cause of this disaster might have remained a mystery.[111] One affected daity farmer, Frederic Halbert - a former chemical engineer at Dow Chemical Company - was exceptionally resourceful and perserving in ensuring that the PBB contaminant in his dairy cattle feed was discovered.[104] Through Halbert's dogged determination and direct contact with a chemist, George Fries, at the USDA Animal Research Centre in Beltsville, Maryland the critical mix-up between Firemaster and Nutrimaster at the Michigan Chemical Company was uncovered....but it took over 2 years to prove.[111]

Polybrominated diphenyl ethers (PBDEs)

Fish, as a food source, are the highest in PBDE contaminants on a whole weight basis, followed by dairy products and meat. In English-speaking countries (UK, US, Canada, Australia, New Zealand), meat represents the largest contributor to PBDE accumulation after young infants cease breastfeeding, followed by fish and dairy products. Farm-grown salmon and other aquacultured fish tend to have higher PBDE concentrations than wild fish; the exception was wild-caught sardines - a common fish-meal ingredient for farmed fish rations - with 3.7ng/g wet weight (or 3.7 ppb) total PBDEs.[113]

The daily PBDE intake from dietary sources for adult Americans is ~0.9-1.2 ng/kg BWt compared to 1.2-1.4 ng/kg for Spaniards, 1.5ng/kg for Britons and 0.58-0.63 ng/km for Swedes.[114][115][116] According to a comprehensive PBDE residue audit of an expanded basket of foods consumed in the United Stateseven accounting for age group and gender, the contribution of PBDEs from food cannot account for the 10- to 20-fold higher levels in the blood and breast milk from the general population compared with European Union countries and Canada.

Question: Is the PBDE accumulation in humans via food under-estimated or are there are sources of PBDE contaminations contributing to their annual bioaccumulation?

Scheter et al (2006) concluded that ‘it was unlikely that diet was the sole or even the major source of exposure of PBDEs’; in contrast the US EPA recognizes that 95% of the PCB and dioxin accumulation in the US general population is via food intake.[113] Some PBDE congeners reported in human blood - 47, 99, 100, 153 and 154 and in some cases 209 are considered sourced from food,[117] Other toxicologists have also concluded that routes of PBDE exposure besides food such as house dust ingestion and inhalation are likely to be important pathways of PBDE intake for children as well as adults.[118]


Organo-tins are associated with endocrine-mediated dysfunction in fish populations.[16] Exposure to the biocide tributyl-tin (TBT) causes imposex, or pseudohermaphroditism in female prosobranch gastropods[119][120] Imposex is the imposition of male sex organs, including penis and vas deferens, into female molluscs and can lead to reproductive failure in some species.[121] It is an reproductive abnormality documented worldwide in approximately 150 species.[121]

There are several potential mechanisms for inducing this effect, including aromatase inhibition, altered metabolism of testosterone, disruption of neuropeptide signaling and activation of the retinoid X receptor (RXR); a definitive mechanism of action has yet to be fully confirmed.[121][122][123]

Phthalates - plasticizer chemicals

The global phthalate production is estimated to be in excess of 8.1 million tonnes annually.[104] Phthalates look like clear vegetable oils and their very greasiness has them being used in commercial applications - in toys for infants and toddlers, lures for fishers and sex devices for adult humans. As ‘plasticizers’, incorporated in polyvinyl chloride products, phthalates make products soft and rubbery when they would otherwise be hard and brittle. About 60% of the world’s manufactured phthalates is used to plasticize vinyl. Unlike the other persistent organic pollutants like, OCs, PCBS, Dioxins and PBDEs, absorbed phthalates are detoxified quickly by mammals and in the environment; the exception being in deep sediments of oceans and lakes.[104] The residue issue is that they are in so many plastic products and phthalate exposure and intake occurs on a daily basis.[104]

Scientific concern and research on the adverse effects of phthalates has been growing since the 1990s. Studies in laboratory rodents linked fetal exposure to phthalates with morphological changes in the these mammals - a decrease in the distance between the anus and the base of the penis in male rodents, incomplete testicular descent and a specific defect in the penis called hypospadias, a deformity where the urethra doesn’t open at the tip of the penis but anywhere long its length. Exposure of rat mothers to phthalates is correlated to increased risk of testicular cancer and decreased sperm quality in male offspring when they reach adulthood.[124][125] Similarly researchers studying humans have noted a pattern of male sexual abnormalities labeled, ‘testicular dysgenesis syndrome’ (TDS). This syndrome includes hypospadias, impaired sperm quality, testicular cancer and cryptorchidism (failure of one or testicles to descend into the scrotum). One of the leading theories for the cause of TDS amongst humans in the 21st century are EDCs like phthalates.[126][127]

In 2005 Dr Shanna Swan and her co-researchers published the results of human study that confirmed the rodent studies. They offer compelling evidence that the quantities of phthalates in the environment and continual exposure was very likely to be linked to impaired reproductive development in male babies’ and testicular dysfunction. They identified smaller penis size, incomplete testicle descent (crytorchidism) and male babies with small undifferentiated scrotums. Demasculinisation was the term used by Swan et al.[128]. According to Smith & Lourie[104] the release of Swan’s research was the catalyst for the American chemical industry to label her work flawed, remature and based manipulated data. A measure of the impact of this research was that Dr Swan was the only researcher specially mentioned in the chemical industries Media Information Kit on their propaganda website.[129]

In August 2008, President George Bush signed the most significant pieces of comsumer protectio legislation in a generation. It permanently prohibited the sale of children's toys or childcare products that contain more than 0.1% diethylhexyl phthalate (DEHP), dibutyl phthalate (DBP) and benzyl butyl phthalate (BBP), and three other phthalates - di-isononyl phthalate (DINP) di-isodecyl phthalate (DIDP) and di-n-octyl phthalate (DNOP) were placed on an interim ban subject to safety evaluation. The Comsumer Product Safety Commission Improvement Act ensures that the manufacturers of phthalates demonstrate that these phthalates are safe before they are allowed to be commercially used. This is the first time in a piece of United States legislation that the burden of proof in respect of toxic pollutants has been to prove 'safety' rather than for the US EPA to prove a chemical is harming health.[104]

Bispenol A (BPA) and its xeno-oestrogen analogues

Bispenol A (BPA) is a synthetic oestrogen that was at one time investigated for potential use in birth control pill but was instead favoured as a 'plastizer' for use in polycarbonate plastics, in dental sealants and the linings of fod cans. Both BPA and 4-nonylphenol, a derived product of non-ionc surfactant used in many commercial detergents, pesticides and cleaning products, have been shown to activate the eostrogen receptor alpha, induce oestrogen-dependent gene expression and stimulate the growth of oestrogen-responsive MCF7 breast cancer cells.[130][131] The wide use of several alkyphenols such as BPA, nonylphenol and octylphenol as 'wetting agents' in detergents and pesticide concentrates is reported.[131] Epigenetic effects of these xenobiotics have been reported to activate interleukin-4 responsive T-cells by stimulating a gene-protein signaling pathway that enhances IL-4 T-cell allergic responses.[132][133]

In 2007 the United States National Institures for Health (NIH) funded a meeting the the world’s top 38 scientists currently working on Bisphenol A (BPA). The prepared a Chapel Hill Bisphenol A Expert Panel Consensus Statement.[134] It stated: ‘The wide range of adverse effects of low doses of Bisphenol A in laboratory animals exposed during development and in adulthood is a great cause for concern with regard to the potential for similar adverse effects in humans.’ Specific human illnesses these experts believe may be linked to BPA exposure include increases in prostate and breast cancer; uro-genital abnormalities in male babies; a decline in sperm quality in men; early onset of puberty in girls; metabolic disorders, including insulin-resistant diabetes and obesity; and neurobehavioural problems such as attention deficit hyperactivity disorder (ADHD).[135]

A surprisingly diverse range of chemicals can be agonists or antagonists for cellular oestrogen receptors to produce 'feminising' or 'masculinising' effects; these include o,p'-DDE, PCBSc, PCDDs, PCDFs, alkylphenols and naturally occurring phyto- and myco-oestrogens [136] At the core of the BPA-endocrine disrution debate is the question of whether low levels of the chemical cause a biological effect; many governments the world over and the chemical industry say absolutely not.[135] Dr Pete Myers, co-author of the Chapel Hill concensus statement explained the low dose effect this way: 'Picture a drop of water in which Bisphenol A is present in a concentration of 1 part per billion, now how many individual molecules of BPA would be in that one water drop. A few thousand?, a few hundred thousand? not even close, try 132 billion, and each one of those molecules is able to turn cell receptors on or off just like [endogenous] hormones do'.[135]

The latest review evaluating human health risks from endocrine disruptors such a Bisphenol A has recently been published.[137] After the US Endocrine Society and the American Medical Association called for greater government oversight and centralised regulation of the EDCs, the Food and Drug Administration has been asked to finalise its position on the safety of Bisphenol A used in food containers by the end of 2009. In addition the US EPA has announced it will review the health effects of Bisphenol A, the molecule used in polycarbonate manufacture. The Obama Administration has asked the US Congeress to draft new legislation allowing for greater scrutiny and regulation of chemicals.

Mechanisms through which endocrine-disrupting effects transmit to subsequent generations are not well understood, but emerging evidence indicates that these epigenetic mechanisms might be primary. Modifications in gene expression patterns without modifying the gene sequences through DNA methylation and histone modifications are mechanisms being investigated. This newly discovered and evolving area of research has once again challenged 20th century toxicology and introduced novel ways that synthetic chemicals and other toxicants affect not only pathological disease processes but also affect vertebrate physiology and behaviour.[137]

Biomarkers for Endocrine Disruption

Biomarkers of exposure are now being used as diagnostic tools for environmental risk assessment of endocrine-disrupting chemicals (EDCs).[138]

The integrated use of biomarkers for endocrine disruption - such as plasma steroid hormones, vitellogenin and gonad histology - has advanced the understanding of fish reproductive toxicology and provide diagnostic alerts for other aquatic biota (e.g., amphibians, echinoderms, and molluscs) that may share similar reproductive hormone systems.[138]

Vitellogenin (VTG) is an estrogen-responsive egg yolk protein precursor not normally expressed in male fish. The protein’s induction in male fish - as a biomarker of adverse EDC effect - has been repeatedly used in both field and laboratory-based data.[16][138] Such ‘standardised’ biomarkers are now playing an important role in the design of adverse effect tests for EDCs in tracking single substances and mixtures of concern.[138] Currently there are some constraints at applying these biomarkers as diagnostic tests and predictive risk assessments at the population or ecosystem level. Nevertheless these biomarkers have been used to investigate gradients of adverse effect using sentinel fish at distances from esturarine or river human sewage outflows.[139][140][141]

The single most significant source of abnormal vitellogenin expression in male fish and the occurrence of intersex in wild fish comes from exposure to human sewage effluent.[142][143]

Articles and resources

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  82. Davidson C., H.B. Shaffer, and M.R. Jennings Declines of the California red-legged frog: Climate, UV-B, habitat, and pesticides hypotheses Ecological Applications 2001, Volume 11, pages 464-479
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