Technical ReportPDF Available

Fluoridation of Port Macquarie Hastings District-a case study of novel environmental risk taking on a grand scale involving microorganism metabolism of Fluoride

Authors:

Abstract and Figures

The people of Port Macquarie Hastings in the state New South Wales, Australia, voted overwhelmingly against Fluoridation of their drinking water but their wishes were ignored due to political pressure to aid the disposal of industrial waste from the Phosphate Fertilizer industry. The water supply is drawn from the Hastings River and the project is unusual due to storage of unfiltered Fluoridated water in interconnected earth dams exposed to sunlight. No environmental impact assessment was performed before the project despite the presence of threatened, vulnerable and endangered wildlife in the catchment area. Risks to public health from organic molecules containing Fluorine manufactured by bacteria and algae appear never to have been considered.
Content may be subject to copyright.
Fluoridation of Port Macquarie Hastings District a case study of novel environmental
risk taking on a grand scale involving microorganism metabolism of Fluoride
Geoff Pain
November 2017
Abstract
The people of Port Macquarie Hastings in the state New South Wales, Australia, voted overwhelmingly against
Fluoridation of their drinking water but their wishes were ignored due to political pressure to aid the disposal of
industrial waste from the Phosphate Fertilizer industry. The water supply is drawn from the Hastings River and the
project is unusual due to storage of unfiltered Fluoridated water in interconnected earth dams exposed to sunlight.
No environmental impact assessment was performed before the project despite the presence of threatened,
vulnerable and endangered wildlife in the catchment area. Risks to public health from organic molecules containing
Fluorine manufactured by bacteria and algae appear never to have been considered.
Keywords: Actinomycetes, Actinomycetoma , Cancer, Fluoride, Fluoridation, Fluorinase, Fluoroacetaldehyde,
Fluoroacetate (1080), Fluorocitrate, Fluorothreonine, Geosmin, GMO, Gudgeon, Methylisoborneol, Mutation,
Mycetoma, Neurotoxin, Nocardia, Organofluorine, Oyster, PFAS, Photochemistry, Politics, Preeclampsia,
Streptomyces, Warfare
Introduction
Port Macquarie Hastings is a coastal community of about 70,000 people dependent on the Hastings River for its
drinking water.
Raw water is pumped from the Hastings River at Koree Island (5 km south-west of Wauchope). The three Koree
Island river intake pumping stations have a combined capacity to pump 120 ML per day via rising mains into nearby
Rosewood Reservoirs.
Water can’t be drawn at certain times of year due to insufficient flow and algal blooms [Thompson 2001, NSWOW
2009, Ryder 2017]. As a result the local water authority monitors indicators of biological activity including the foul
smelling and tasting molecules Geosmin and Methylisoborneol [Giglio 2009]. These molecules are produced by a
number of biota including Actinomycetes Streptomyces. They cause earthy taint, with a taste and odour threshold of
approximately 0.00001 mg/L (10 ng/L) [Young 1996].
Use of other organisms to destroy the Actinomycetes has been proposed, however it is worth noting that Fluoride is
toxic to many of the organisms that are supposed to degrade the noxious cyanobacteria [Ho 2009].
Due to scarcity of water three reservoirs are used with the facility to back pump between them. The Hastings District
Water Supply Augmentation Scheme [HDWS], built at a cost of over $65M includes the Cowarra 10GL off-creek
storage dam. The raw water is treated in the rising mains at the Wauchope Water Treatment plant with lime and
carbon dioxide to increase alkalinity and stabilise the pH of the raw water (Figure 1).
Figure 1 The Hastings River at Koree Island, Rosewood Quarry and Wauchope Water Treatment Plant
Figure 2 Cowarra Off-Creek Dam with capacity of 10GL
Figure 3 Port Macquarie Off-Creek Storage Dam (Rosendahl Reservoir)
Fluoridation of the Water Supply
About $1.8M was spent on the Fluoridation facility (Figure 4). Fluoridation and chlorination are completed at the
Rosewood Reservoir site, prior to the water being stored in Rosewood #2 and #3 Reservoirs. The unfiltered water in
Rosewood Reservoirs #2 and #3 is then gravity fed to the 10,000 ML Cowarra Off-Creek Storage (Figure 2) and 2,500
ML Port Macquarie (Rosendahl Reservoir, Figure 3) Dams [PMHC 2016]. Hydrofluorosilicic (HFSA) waste is supplied
to Port Macquarie Hastings Council by IXOM Operations Pty Ltd (formerly Orica) at the rate of about 600 kg per
pumping day. Fluoride is a bioaccumulative endocrine disruptor with no nutritional value [Pain 2015a, Pain 2017a].
HFSA is known to increase plumbosolvency, the leaching of Lead from brass [Pain 2015b] which leads to all the
diseases caused by Lead poisoning, including damaged teeth. Blood lead concentrations in pregnant women are a
major risk factor for preeclampsia, with an increase of 1 μg/dL Lead/blood associated with a 1.6% increase in
likelihood of preeclampsia, the strongest risk factor for preeclampsia yet reported [Poropat 2017].
Figure 4 The Fluoridation equipment at Rosewood Road Fluoridation plant which cost $1.8 million
The HFSA is contaminated with light and heavy metals, further increasing the toxic load to residents and local
produce including oysters in the estuary (Figure 5). The oysters also accumulate Fluoride.
Figure 5 The estuary of Hastings River that receives all the toxins of Fluoridation
According to a project manager, who provides an interesting account of the design, construction and politics behind
the Fluoridation plant [Randall 2014], “The issue of fluoridation of the Port Macquarie-Hastings District Water Supply
was first addressed by the former Port Macquarie Municipal and Hastings Shire Councils prior to amalgamation in
1980. The councils resolved to defer a decision on fluoridation for the newly constituted Hastings Municipal Council.
Fluoridation was not considered again until 1985 when a series of reports and discussions on the issue over several
years resulted in the decision to hold a community poll on the issue at the September 1991 Local Government
election.
The community poll asked: “Are you in favour of having Sodium Fluoride or Sodium Silicofluoride, as appropriate,
added to the Hastings District Water Supply to fluoride ion levels recommended by the NSW Department of Health?”
The poll results reported to the November 1991 Council meeting were 20,533 votes “No” to fluoridation and 8,198
Yes. (emphasis added)
Based on these results, Council resolved not to fluoridate but acknowledged the dental health benefits provided by
fluoride and resolved to lobby NSW DOH for an upgrade of dental services in the area.
In early 2004, the Mid North Coast Area Health Service convened a meeting of council to address the claimed dental
decay crisis on the Mid North Coast. On August 6, 2004 NSW Health directed the addition of fluoride to the Port
Macquarie-Hastings District Water Supply.
A series of fluoridation workshops and meetings were held. Council received letters supporting fluoridation from the
NSW Cancer Council, Australian Dental Association and local State Government members.
After 6 years of haggling over costs and design, in May 2010, Council signed a $1.78 million funding agreement with
NSW DOH for the construction of the fluoridation plant. The conditions of this funding agreement require Council to
refund this amount if fluoridation is discontinued within a period of 15 years.
Under Section 6B of the Act, a water supply authority cannot discontinue fluoridation unless directed by NSW DOH.
Port Macquarie Hastings Council held a Forum on Fluoridation on 15 February 2012 addressed by Colgate Professor
of Dentistry W Evans with NSW Health Fluoridation Advisory Committee representative Dr S Sivaneswaran in
attendance [Lusk 2016]. Members of the public reiterated their opposition, however fluoridation of water
commenced that year with a “target” value of 1ppm, interestingly much more than the 0.7 ppm target currently
used in Australia’s capital city, Canberra.
Residents in Port Macquarie Hastings receive different Fluoride doses depending where they live.
A centralised fluoridation dosing plant at the Rosewood Road Reservoir resulted in a gradual increase in the level of
fluoride due to the initial dilution of the fluoridated water (1 mg/L of fluoride target) which is piped into the Port
Macquarie Off-Creek Storage Dam. The pre-existing stored water in the dam had a natural level of fluoride of
approximately 0.1 mg/L. Because the dams are open, rainfall and evaporation impacts on the actual concentration at
any time, removing effective control of the target.
Residents in Wauchope including Beechwood, Rawdon Island, Sancrox and Thrumster areas, who receive water
directly from the Rosewood Road Reservoir, immediately received a fluoride content of 1 mg/L.
Effect of Fluoride on Algae and Cyanobacteria
As discussed in recent reviews [Wolk 1973, Bhatnagar 2000, Agalakova 2011], Fluoride can suppress [Vennesland
1966, Zurita 2007] or intensify growth of populations of algae and cyanobacteria depending on its concentration,
time of exposure, and alga species.
Some species can tolerate relatively high concentrations of Fluoride [Jonker 2013] and low pH makes the Fluoride
more toxic due to formation of HF. Some species actively metabolize Fluoride ion.
Naturally fluorinated compounds are extremely rare in nature. They have been studied for their potential as toxic
drugs in medicine [Eustáquio 2010, Waler 2013] as well as chemical warfare [Rivett 1953].
The extreme toxicity of organofluoride compounds requires them to be handled as special wastes [Environment
Agency 1999]. About 20% of licensed toxic drugs contain a fluorine atom [Deng 2008].
Nucleocidin (4’-α-fluoro-5’-O-sulfamoyl adenosine, Figure 6) was first isolated from Streptomyces calvus [Hewitt
1956].
Figure 6 The structure of Nucleocidin.
Fluorinase, 5'-fluoro-5'-deoxyadenosine synthase, was the first enzyme identified and isolated from the soil
bacterium Streptomyces cattleya [O’Hagan 2002]. Subsequently Fluorinase was identified in Streptomyces sp. MA37,
Actinoplanes sp. N902-109 and Nocardia brasiliensis [Ma 2015 and references therein].
The success of enzymes that Fluorinate organic substrates is known to be due to the removal of solvation water
molecules inside the organic structure [Zhu 2007]. It has been shown that the Fluorine atom has attached hydrogen
bonds inside the Fluorinase enzymes [Cobb 2006].
This provides interesting insights into where Fluoride goes when it enters the human body.
Much of the Fluoride circulating in the blood of humans exposed to the toxin is not available to the ion selective
electrode. In other words, analysis of whole blood shows much higher Fluorine content than is sensed by an
electrode [Pain 2017c].
We can be confident that the “hidden” Fluoride circulating in our bodies is strongly held in a hydrophobic
environment, enhancing its reactivity and toxicity.
Human Disease Risk from natural Organofluorine compounds
Amputation or death can result from Actinomycetoma, a chronic, granulomatous and subcutaneous tissue infection
caused by Actinomycetes. Nocardia brasiliensis is the major causative pathogen of the Actinomycetoma (Mycetoma)
infections in Mexico.
It has been suggested that the toxicity of Actinomycetes might be due to conversion of serum Fluoride to
Fluoroacetate and Fluorocitrate [Wang 2014]. Endemic Fluorosis and Mycetoma cases overlap in Africa, Mexico and
India, where Actinomycetoma infections are known as Madura foot.
Comorbidity studies are proving useful as shown by correlation between Fluorosis and Cataract [Pain 2017b].
Cases of Mycetoma due to Nocardia brasiliensis have been reported in Australia [Lucas 2000].
Fluorinase catalyses a reaction between S-adenosyl-L-Methionine (SAM) and fluoride ion to produce 5'-
fluorodeoxyadenosine (5'FDA) and L-Methionine. Formation of Fluoroacetaldehyde as an intermediate allows
synthesis of the potent toxins Fluoroacetate [Sanada 1986] and Fluorothreonine (Figure 7) [Reid 1995, Murphy 2001,
Tamura 2003, Deng 2008].
Figure 7 Formation of Toxic Organofluorine compounds by microorganisms possessing the Fluorinase enzyme
Fluoroacetate, a known neurotoxin [Grandjean 2006] can in turn be transformed into the bioaccumulative
neurotoxin Fluorocitrate which was of great interest to the Australian, British, Canadian, South African and US armed
forces [Rivett 1953].
It appears that very many organofluorine compounds are neurotoxins with outcomes including ADHD [Hoffman
2010].
Another organofluorine natural product, (2R3S4S)-5-fluoro-2,3,4-trihydroxypentanoic acid (5- FHPA), was isolated
from a Ghanaian Streptomyces isolate named Streptomyces sp. MA37 [Ma 2015].
Fluoroacetate, more commonly known as the knock-down toxin 1080 [Fairweather 2013], named after its first
commercial catalogue number, has a human lethal dose of less than 0.5 mg/kg. In dogs the lethal dose was found to
be 0.06 mg/kg [Chenowyth 1949]. Fluoroacetate can have far reaching environmental effects on ecology through
bioaccumulation in predators [Peacock 2011].
Some plants produce this toxic compound which accumulates, in concentrations as high as 3875 ppm dry weight, as
a defence mechanism against grazing by herbivores [Baunthiyal 2012]. It is also possible that bacteria present as
endophytes might produce the toxin in a suitable host plant.
Ingestion by livestock often results in fatal poisonings, causing significant economic problems to commercial farmers
in many countries including Australia. Fluoroacetate toxicity costs the Australian livestock industry around 45 million
dollars annually due to the increased death rates and associated productivity impacts [Perkins 2015, Leong 2017].
Symptoms of acute Fluoroacetate (1080) poisoning include abnormal posturing, loss of balance, urinary
incontinence, muscle spasms and convulsions, severe respiratory distress and extremely rapid heart rate, central
nervous system depression, coma followed by death. Quite rightly, the RSPA states it is not a humane poison
[Sherley 2007]. Fluoracetate is also a chronic heart poison [Santos 2016].
Fluoroacetate conversion to bioaccumulative Fluorocitrate is enhanced in animals with higher metabolic rate.
Fluorocitrate causes reduced aconitase resulting in glutamine depletion, ammonia accumulation [Gallon 1978],
termination of the tricarboxylic acid (TCA) cycle and build up of glucose. It increases citrate which leads to acidosis,
hypocalcemia and heart failure. The TCA cycle is central to cellular energy production in the mitochondria of higher
organisms (Figure 8).
Figure 8 Fluoroacetate and Fluorocitrate toxicity summary
Figure 9 shows how the toxic organofluoride compounds Fluoroacetate and Fluorocitrate, produced in legumes,
grains and leafy vegetables from Fluoride residues in phosphate fertilizer pose a serious hazard to animals.
Figure 9 Application of Fluoride contaminated Superphosphate Fertilizer contaminates vegetables that produce and
accumulate Fluoroacetate and Fluorocitrate which are toxic to mammals
Fluoroacetate is probably involved in cancer progression as it concentrates in cancerous tissue including sarcoma,
glioblastoma and the prostate [Li 2010].
Genetic Engineering and Directed Evolution of Fluorinase
Due to its importance, the complete genome sequence of Streptomyces cattleya has been determined. Gene clusters
which contain the genes encoding the fluorinase and the 5’-fluoro-5’-deoxyadenosine phosphorylase and other
related enzymes were located on the chromosomes [Barbe 2011]. The natural evolution of halogenases is a rapidly
developing field of study [Neumann 2008, Xu 2016]. Mutation of Streptomyces is easily induced by ultraviolet light
irradiation [Fukuda 2009].
The Fluorinase genes have been successfully transferred to other organisms [Deng 2008]. Due to the extreme
toxicity of naturally synthesized Fluorinated organic molecules, there has been great interest in them for drug
discovery. Large quantities are need for testing and production of toxins such as nucleocidin [Fukuda 2009, Browne
2016].The fluorinase gene has been successfully cloned and used to transform the expression hosts, E.coli BL21(DE3)
and Pichia pastoris (PichiaPink™ strains) [Browne 2016].
The focus of this paper is the risk associated with Fluoride artificially added to fresh drinking water. However, this
water is close in Fluoride concentration to that found in the oceans where various marine species of Streptomyces
are also known to produce toxic organofluorine molecules.
The Fluorinase in marine Streptomyces xinghaiensis is described as “the most efficient fluorinase by far and,
impressively, highly robust” [Ma 2016]. Thus the risk associated with deliberate mixing of drinking water with
industrial waste Fluoride can be expected to mimic the sea and help “directed evolution” [Sun 2016] of Streptomyces
and related organisms, to which humans or land based wildlife have not previously been exposed. This can be
regarded as GMO production in the wild.
Conclusion
The Fluoridation of the Port Macquarie Hastings water supplies was opposed by 71% of the resident population but
their wishes were ignored by local and state government bureaucrats and politicians.
The scarcity of water supply prompted a very risky and unusual strategy involving fluoridation of dams exposed to
soil, air and sunlight that represents an ecological threat to humans and wildlife through metabolism of Fluoride by
microorganisms. It appears a similar risk was taken in Prospect NSW and there is an urgent need to identify all
locations with similar problems of biological activity, not usually encountered in Fluoride contaminated
groundwater.
It is likely that soil and water organisms are manufacturing known extremely toxic organofluorine compounds that
are bioaccumulative toxins affecting numerous organs. These organisms are subject to possible photochemical
mutation that could lead to formation of previously unknown organofluoride compounds in the water.
Fluoridation of the dams will prevent repeat of previous creek flushing due to the impact of Fluoride in the dam
water on endangered species known to be present, including the Southern Purple Spotted Gudgeon, frogs, birds of
prey and numerous species of bats. Bioaccumulation of organofluorine toxins will occur up the food chain.
It is not necessary to have more than one Fluoride atom in an organofluorine molecule, as found for example in
perfluoroalklyl substances (PFAS), for it to be bioaccumulative and extremely toxic.
Fluoridation will increase the toxic metal and Fluoride load of humans and estuarine oyster production.
Fluoridation severely restricts recycling of water, which is judged to be essential to the future of Port Macquarie
Hastings Council plans [Thompson 2005].
Immediate cessation of Fluoridation at Port Macquarie Hastings with thorough investigation of environmental
damage must be followed by a protracted period requiring dam emptying to sea and refilling, creating severe water
shortages until residents have potable water supplies restored.
References
Agalakova NI, Gusev GP. 2011. Effect of inorganic fluoride on living organisms of different phylogenetic level. Journal
of Evolutionary Biochemistry and Physiology 47(5):393-406.
Barbe V, Bouzon M, Mangenot S, Badet B, Poulain J, Segurens B, Vallenet D, Marlie`re P, Weissenbach J. 2011.
Complete Genome Sequence of Streptomyces cattleya NRRL 8057, a Producer of Antibiotics and Fluorometabolites.
Journal of Bacteriology 193(18):5055-5056.
Baunthiyal M, Pandey A. 2012. Organofluorine metabolism in plants. Fluoride 45(2):78-85.
Bhatnagar M, Bhatnagar A. 2000. Algal and Cyanobacterial Responses to Fluoride. Fluoride 55-65.
Browne LE, Rumbold D. 2016. High Level Expression of Fluorinase in Escherichia Coli and Pichia Pastoris.
International Journal of Bioengineering and Life Sciences 3(2) Abstract 36807.
Camargo JA. 2003. Fluoride Toxicity to Aquatic Organisms: a Review. Chemosphere 50:251-264.
Chenoweth MB. 1949. Monofluoroacetic acid and related compounds. Pharmacological Reviews 1:383-424.
Cobb SL, Deng H, McEwan AR, Naismith JH, O’Hagan D, Robinson DA. 2006. Substrate specificity in enzymatic
fluorination. The fluorinase from Streptomyces cattleya accepts 2-deoxyadenosine substrates. Org Biomol Chem.
4(8):1458-1460.
Deng H, O’Hagan D, Schaffrath C. 2004. Fluorometabolite Biosynthesis and the Fluorinase from Streptomyces
cattleya. Nat. Prod. Rep. 21:773-784.
Deng H, Cobb SL, McEwan AR, McGlinchey RP, Naismith JH, O’Hagan D, Robinson DA, Spencer JB. 2006. The
Fluorinase from Streptomyces cattleya is also a Chlorinase. Angew Chem Int Ed Engl. 45(5):759-762.
Deng H, Cross SM, McGlinchey RP, Hamilton JTG, O’Hagan D. 2008. In Vitro Reconstituted Biotransformation of 4-
Fluorothreonine from Fluoride Ion: Application of the Fluorinase. Chemistry & Biology 15:1268-1276.
Dong C, Huang F, Deng H, Schaffrath C, Spencer JB, O’Hagan D, Naismith JH. 2004. Crystal structure and mechanism
of a bacterial fluorinating enzyme. Nature 427:561-565.
Environment Agency. 1999. Special Wastes: A technical guidance note on their definition and classification.
Eustáquio AS, O’Hagan D, Moore BS. 2010. Engineering fluorometabolite production: fluorinase expression in
Salinispora tropica yields fluorosalinosporamide. J Nat Prod. 73:378-382.
Fairweather AAC, Broome KG, Fisher P. 2013. Sodium Fluoroacetate Pesticide Information Review. Department of
Conservation, Hamilton, New Zealand.
Fukuda A, Tamura K, Segawa Y, Mutaguchi Y, Inagaki K. 2009. Enhanced Production of the Fluorinated Nucleoside
Antibiotic Nucleocidin by a rifR-Resistant Mutant of Streptomyces calvus IFO13200. Actinomycetologica 23:51-55.
Gallon JR, Ul-Haque MI, Chaplin AE. Fluoroacetate Metabolism in Gloeocapsa sp. LB795 and its Relationship to
Acetylene Reduction (Nitrogen Fixation). Journal of General Microbiology. 106:329-336.
Giglio S, Jiang J, Saint C, Cane D, Monis P. 2009. Isolation and characterisation of the gene associated with geosmin
production in cyanobacteria. Abstract. Cyanobacterial Bloom Management - Current and Future Options. See
NSWOW.
Grandjean P, Landrigan PJ. 2006. The Lancet. Developmental neurotoxicity of industrial chemicals A silent
pandemic. 368(9553):2167-2178.
Hewitt R, Gumble A, Taylor L, Wallace W. 1956. The activity of a new antibiotic, nucleocidin, in experimental
infections with Trypanosoma equiperdum. Antibiot. Annu. 722-729.
Ho L, Hoefel D, Smith M, Saint S, Newcombe G. 2009. Biological degradation of cyanobacterial toxins. Abstract.
Cyanobacterial Bloom Management - Current and Future Options. See NSWOW.
Hoffman K, Webster TF, Weisskopf MG, Weinberg J, Vieira VM. 2010. Exposure to polyfluoroalkyl chemicals and
attention deficit/hyperactivity disorder in US children, 12 to 15 years of age. Environ. Health Perspect. 118:176267.
Huang S, Ma L, Tong MH, Yu Y, Deng H, O’Hagan D. 2014. Fluoroacetate from the marine-derived bacterium
Streptomyces xinghaiensis NRRL B-24674. Organic & Biomolecular Chemistry. 12(217):4828-4831.
Jonker CZ, van Ginkel C, Olivier J. 2013. Association between physical and geochemical characteristics of thermal
springs and algal diversity in Limpopo Province, South Africa. Water S.A. 95-103.
Leong LEX, Khan S, Davis CK, Denman SE, Mc Sweeney CS. 2017. Fluoroacetate in plants - a review of its distribution,
toxicity to livestock and microbial detoxification. Journal of Animal Science and Biotechnology. 8:55-65.
Li X-G, Domarkas J, O’Hagan D. 2010. Fluorinase mediated chemoenzymatic synthesis of [18F]-fluoroacetate. Chem.
Commun. 46:7819-7821.
Lucas RE, Armstrong PK. 2000. Two cases of mycetoma due to Nocardia brasiliensis in central Australia. Med J Aust
172(4):167-9.
Lusk J. 2016. Public consultation on NHMRC Draft Information Paper: Effects of water fluoridation on dental and
other health outcomes - A Personal Response. Available from the NHMRC website.
Ma L, Bartholome A, Tong MH, Qin Z, Yu Y, Shepherd T, Kyeremeh K, Deng H, O’Hagan D. 2015. Identification of a
fluorometabolite from Streptomyces sp. MA37: (2R3S4S)-5-fluoro- 2,3,4-trihydroxypentanoic acid Chem. Sci. 6:1414-
1419.
Ma L, Li Y, Meng L, Deng H, Li Y, Zhang Q, Diao A. 2016. Biological fluorination from the sea: discovery of a SAM-
dependent nucleophilic fluorinating enzyme from the marine-derived bacterium Streptomyces xinghaiensis NRRL
B24674. RSC Adv. 6:27047-27051.
Murphy CD, Moss SJ, O’Hagan D. 2001. Isolation of an aldehyde dehydrogenase involved in the oxidation of
fluoroacetaldehyde to fluoroacetate in Streptomyces cattleya. Appl. Environ. Microbiol. 67:4919-4921.
Neumann CS, Fujimori DC, Walsh CT. 2008. Halogenation Strategies in Natural Product Biosynthesis. Chemistry &
Biology 15:99-109.
NSW. 2009. Fluoridation of Public Water Supplies Advisory Committee. Minutes.
NSWOW. 2009. Office of Water, NSW Department of Environment, Climate Change and Water. Cyanobacterial
Bloom Management - Current and Future Options.
O’Hagan D, Schaffrath C, Cobb S L, Hamilton JTG, Murphy CD. 2002. Biosynthesis of an organofluorine molecule. A
fluorinase enzyme has been discovered that catalyses carbon-fluorine bond formation. Nature 416:279.
Oliveira, L, Antia NJ, Bisalputra T. 1978. Culture Studies on the Effects from Fluoride Pollution on the Growth of
Marine Phytoplankters. J. Fish. Res. Board Can. 35:1500-1504.
Pain GN. 2015a. Fluoride is a bio-accumulative, endocrine disrupting, neurotoxic carcinogen not a nutrient
https://www.researchgate.net/publication/285771633_Fluoride_is_a_bioaccumulative_endocrine_disrupting_neur
otoxic_carcinogen_-_not_a_nutrient
Pain GN. 2015b. Plumbosolvency exacerbated by Water Fluoridation
https://www.researchgate.net/publication/282439972_Plumbosolvency_exacerbated_by_Water_Fluoridation
Pain GN. 2017a. A Quick Guide to Fluoride Harms
https://www.researchgate.net/publication/318876264_A_Quick_Guide_to_Fluoride_Harms
Pain GN. 2017b. Fluoride is the major Cause of Cataract Blindness
https://www.researchgate.net/publication/319164619_Fluoride_is_the_major_Cause_of_Cataract_Blindness
Pain GN. 2017c. Accounting for the missing Fluoride in ingestion and excretion studies.
Peacock DE, Christensen PE, Williams BD. 2011. Historical accounts of toxicity to introduced carnivores consuming
bronzewing pigeons (Phaps chalcoptera and P. elegans) and other vertebrate fauna in south-west Western Australia.
Australian Zoologist. 35(3):826-842.
Perkins I, Perkins TAP, Perkins N. 2015. Impact of fluoroacetate toxicity in grazing cattle. North Sydney: Meat and
Livestock Australia Limited.
PMHC. Port Macquarie Hastings Council. 2012. Fluoridation Fact Sheet.
PMHC. Port Macquarie Hastings Council. 2016. Water Supply Policy.
Poropat A, Laidlaw M, Lanphear B, Ball A, Mielke HW. 2018. Blood lead and preeclampsia: A meta-analysis and
review of implications. Environmental Research. 160:12-19.
https://www.researchgate.net/publication/319552229_Blood_lead_and_preeclampsia_A_metaanalysis_and_review
_of_implications
Randall T, Thompson M. 2014. 120ML/Day Fluoridation Dosing Plant. How to Build Your Own Hydrofluorosilicic Acid
Dosing System. 8th Annual WIOA NSW Water Industry Operations Conference, Orange, 2014.
Reid KA, Hamilton JTG, Bowden RD, O’Hagan D, Dasaradhi L, Amin MR, Harper DB. 1995. Biosynthesis of fluorinated
secondary metabolites by Streptomyces cattleya. Microbiology 141:1385-1393.
Rivett DEA. 1953. The Preparation of Fluorocitric Acid and Attempted Synthesis of Fluoropyruvic Acid. Porton
Technical paper No. 319.
Ryder D, Mika S, Vincent B, Schmidt B. 2017. Hastings and Camden Haven Catchments Ecohealth Project Assessment
of River and Estuarine Condition 2015. Final Technical Report. University of New England, Armidale.
Sanada M, Miyano T, Iwadare S. 1986. Biosynthesis of fluorothreonine and fluoroacetic acid by the thienamycin
producer Streptomyces cattleya. J. Antibiot. (Tokyo) 39:259-265.
Santos AM, Peixoto PV, D’Ávila MS, Peixoto TC, França TN, Costa SZR, Cid GC, Nogueira VA. 2016. Troponina C na
detecção imuno-histoquímica de alterações regressivas precoces no miocárdio de bovinos e ovinos intoxicados por
monofluoroacetato de sódio. Pesq. Vet. Bras. 36(2):67-72.
Sherley M. 2007. Is sodium fluoroacetate (1080) a humane poison? Animal Welfare 16:449-458.
Sun H, Yeo WL, Lin YH, Chew X, Smith DJ, Xue B, Chan KP, Robinson RC, Robins EG, Zhao H, Ang EL. 2016. Directed
Evolution of a Fluorinase for Improved Fluorination Efficiency with a Non-native Substrate. Angew. Chem. Int. Ed.
55:14277-14280.
Tamura T, Sawamoto Y, Kuriyama T, Oba K, Tanaka H, Inagaki K. 2003. Cosynthesis of monofluoroacetate and 4-
fluorothreonine by resting cells of blocked mutants of Streptomyces cattleya NRRL8057Journal of Molecular Catalysis
B: Enzymatic 23:257-263.
Tang W, Kovalsky P, He D, Waite TD. 2015. Fluoride and nitrate removal from brackish groundwaters by batch-mode
capacitive deionization. Water Research 84:342-349.
Thompson M. 2001. Protecting Environmental River Flows While Catering for Urban Water Supply Demand. Hastings
Council.
Thompson M. 2005. Port Macquarie’s Urban Reclaimed Water Supply Scheme. IPWEA NSW Division Annual
Conference.
Vennesland B, Turkington EO. 1966. The relationship of the Hill reaction to photosynthesis: studies with fluoride-
poisoned blue-green algae. Arch. Biochem. Biophys. 116:153-161.
Walker MC. 2013. Expanding the scope of organofluorine biochemistry through the study of natural and engineered
systems. Ph.D. Dissertation. University of California, Berkeley.
Wang Y, Deng Z, Qu X. 2014. Characterization of a SAM-dependent fluorinase from a latent biosynthetic pathway for
fluoroacetate and 4-fluorothreonine formation in Nocardia brasiliensis. F1000 Research 3:61.
Wolk CP. 1973. Physiology and Cytological Chemistry of Blue-Green Algae. Bacteriological Reviews. 37(1):31-101.
Xu G, Wang B-G. 2016. Independent Evolution of Six Families of Halogenating Enzymes. PLoS ONE 11(5):e0154619.
Young WF, Horth H, Crane R, Ogden T, Arnott M. 1996. Taste and odour threshold concentrations of potential
potable water contaminants. Water Research 30(2):331-340.
Zechel DL, Reid SP, Nashiru O, Mayer C, Stoll D, Jakeman DL, Warren RA, Withers SG. 2001. Enzymatic Synthesis of
Carbon-Fluorine Bonds. J. Am. Chem. Soc. 123:4350-4351.
Zhu X, Robinson DA, McEwan AR, O’Hagan D, Naismith JH. 2007. Mechanism of enzymatic fluorination in
Streptomyces cattleya. J. Am. Chem. Soc. 129:14597-14604.
Zurita JL, Jos A, Camean AM, Salguero M, Lo´pez-Artı´guez M, Repetto G. 2007. Ecotoxicological evaluation of sodium
fluoroacetate on aquatic organisms and investigation of the effects on two fish cell lines. Chemosphere 67:1-12.
News media articles
ABC News. Australian Broadcasting Corporation. 2015. 14 July. Fluoride debate returns to Port Macquarie.
Camden Haven Courier. 2010. 12 May. Hastings: Construction work begins on fluoridation plant.
Fairhurst T. 2014. Port Macquarie News. 13 January. Port Macquarie-Hastings Council: Turn the tap off fluoridation.
Jennings B. 2004. 15 September. Fluoride moratorium sought. Port Macquarie News.
Lusk J. 2013. 21 May Letter to the Editor. Come clean on fluoridation. Port Macquarie News.
Port Macquarie News. 2004. 10 May. Fluoridation to be discussed in Hastings.
Port Macquarie News. 2004. 11 June. Safe Water bites back.
Port Macquarie News. 2004. 23 June. Fluoride anger in council.
Port Macquarie News. 2012. 6 February. Port Macquarie: Fluoride added to water in two weeks.
Port Macquarie News. 2012. 24 May. Port Macquarie-Hastings. Water war: Council rejects poll plea.
Tisdell L. Port Macquarie News. 2004. 26 May. Hastings Council discusses fluoride.
Tisdell L. Port Macquarie News. 2004. 2 June. Expert panel to review fluoridation in Hastings.
Wauchope Gazette. 2012. 1 March. Port Macquarie-Hastings region: Fluoridation has started.
Wauchope Gazette. 2012. 11 April. Fluoride group wants poll.
ResearchGate has not been able to resolve any citations for this publication.
Technical Report
Full-text available
Cataract blindness affects tens of millions of people, many of whom will never have access to lens replacement surgery. Fluoride from various sources including drinking water, tea, salt and drugs, enhances and stabilizes crystal growth of Hydroxyapatite within the eye. Fluoride is identified as the major risk for cataract and contributes to risk of other eye diseases including macular degeneration.
Technical Report
Full-text available
Australia's National Health and Medical Research Council states that the only harm arising from water Fluoridation and total dietary Fluoride intake is Dental Fluorosis. This guide provides a quick reference to harms known by toxicologists to be caused by Fluoride, including those still under intensive research and recognized by other administrations.
Article
Full-text available
Fluoroacetate producing plants grow worldwide and it is believed they produce this toxic compound as a defence mechanism against grazing by herbivores. Ingestion by livestock often results in fatal poisonings, which causes significant economic problems to commercial farmers in many countries such as Australia, Brazil and South Africa. Several approaches have been adopted to protect livestock from the toxicity with limited success including fencing, toxic plant eradication and agents that bind the toxin. Genetically modified bacteria capable of degrading fluoroacetate have been able to protect ruminants from fluoroacetate toxicity under experimental conditions but concerns over the release of these microbes into the environment have prevented the application of this technology. Recently, a native bacterium from an Australian bovine rumen was isolated which can degrade fluoroacetate. This bacterium, strain MFA1, which belongs to the Synergistetes phylum degrades fluoroacetate to fluoride ions and acetate. The discovery and isolation of this bacterium provides a new opportunity to detoxify fluoroacetate in the rumen. This review focuses on fluoroacetate toxicity in ruminant livestock, the mechanism of fluoroacetate toxicity, tolerance of some animals to fluoroaceate, previous attempts to mitigate toxicity, aerobic and anaerobic microbial degradation of fluoroacetate, and future directions to overcome fluoroacetate toxicity.
Article
Full-text available
Halogenated natural products are widespread in the environment, and the halogen atoms are typically vital to their bioactivities. Thus far, six families of halogenating enzymes have been identified: cofactor-free haloperoxidases (HPO), vanadium-dependent haloperoxidases (V-HPO), heme iron-dependent haloperoxidases (HI-HPO), non-heme iron-dependent halogenases (NI-HG), flavin-dependent halogenases (F-HG), and S-adenosyl-L-methionine (SAM)-dependent halogenases (S-HG). However, these halogenating enzymes with similar biological functions but distinct structures might have evolved independently. Phylogenetic and structural analyses suggest that the HPO, V-HPO, HI-HPO, NI-HG, F-HG, and S-HG enzyme families may have evolutionary relationships to the α/β hydrolases, acid phosphatases, peroxidases, chemotaxis phosphatases, oxidoreductases, and SAM hydroxide adenosyltransferases, respectively. These halogenating enzymes have established sequence homology, structural conservation, and mechanistic features within each family. Understanding the distinct evolutionary history of these halogenating enzymes will provide further insights into the study of their catalytic mechanisms and halogenation specificity.
Article
Full-text available
Sodium monofluoroacetate (MF) is the toxic principle of several plants that cause "sudden death" of cattle in Brazil. Groups of cardiomyocites with high cytoplasmic eosinophilia are sometimes observed in animals poisoned by MF. However, this cardiac alteration is difficult to interpret, as there is no inflammatory reaction and it must be differentiated from artifacts. The present study had the objective to detect the presence of early regressive lesions in the myocardium of sheep and cattle experimentally poisoned by MF through immunohistochemistry with troponin C (cTnC). Fragments of the heart muscle from six cattle (three received, orally, single doses of 0.5mg/kg and the others, single doses of 1.0mg/kg) and five sheep (one received, orally, single dose of 0.5mg/kg, the other two received single doses of 1.0mg/kg, one received sublethal daily doses of 0.1mg/kg for four days, and another received daily sublethal doses of 0.2mg/kg for six days) were submitted to immunohistochemistry with antibody anti-cTnC. In the cardiomyocites of cattle and sheep, it was possible to observe reduction of the expression levels for cTnC in the cytoplasm of groups of cardiac muscle fibers. Significant reduction of immunoreactivity ocurred overall in cardiomyocites that presented high cytoplasmic eosinophilia. The decrease or absence of expression for cTnC in animals poisoned by MF allowed to estabilish the difference between coagulative necrosis of cardiomyocites and artifacts caused by fixation. This indicates that this method can be used safely to identify any lesions, early regressive or not, in the myocardium independently of the cause. It is also possible to affirm that poisoning by MF as well as the one caused by "sudden death" causing plants can progress with necrotizing myocardial lesions.
Technical Report
Full-text available
Fluoride, Asbestos, Uranium, Lead and Tobacco (FAULT) are multibillion dollar industries that have caused immeasurable harm to humans who have recently discovered that decades of propaganda claims that the products are “safe and effective” are demonstrably false. Each of these industries has a history of denial of harm, suppression of evidence, attempts to avoid litigation and compensation of victims. In a last ditch attempt to retain public drinking water as a conduit for disposal of Fluoride, an industrial waste product, myth-mongers are attempting to promulgate the “Big Lie” that Fluoride is a nutrient.
Article
Background Multiple cross-sectional studies suggest that there is an association between blood lead and preeclampsia. Objectives We performed a systematic review and meta-analysis to summarize information on the association between preeclampsia and lead poisoning. Methods Searches of Medline, Web of Science, Scopus, Pubmed, Science Direct and ProQuest (dissertations and theses) identified 2089 reports, 46 of which were downloaded after reviewing the abstracts, and 11 studies were evaluated as meeting the selection criteria. Evaluation using the ROBINS-I template (Sterne, et al., 2016), indicated moderate risk of bias in all studies. Results We found that blood lead concentrations were significantly and substantially associated with preeclampsia (k = 12; N = 6069; Cohen’s d = 1.26; odds ratio = 9.81; odds ratio LCL = 8.01; odds ratio UCL = 12.02; p = 0.005). Eliminating one study produced a homogeneous meta-analysis and stronger estimates, despite the remaining studies coming from eight separate countries and having countervailing risks of bias. Conclusions Blood lead concentrations in pregnant women are a major risk factor for preeclampsia, with an increase of 1 μg/dL lead/blood associated with a 1.6% increase in likelihood of preeclampsia, which appears to be the strongest risk factor for preeclampsia yet reported. Pregnant women with historical lead exposure should routinely have blood lead concentrations tested, especially after mid-term. Women with concentrations higher than 5 μg/dL should be actively monitored for preeclampsia and be advised to take prophylactic calcium supplementation. All pregnant women should be advised to actively avoid lead exposure.
Article
Fluorinases offer an environmentally friendly alternative for selective fluorination under mild conditions. However, their diversity is limited in nature and they have yet to be engineered through directed evolution. Herein, we report the directed evolution of the fluorinase FlA1 for improved conversion of the non-native substrate 5′-chloro-5′-deoxyadenosine (5′-ClDA) into 5′-fluoro-5′-deoxyadenosine (5′-FDA). The evolved variants, fah2081 (A279Y) and fah2114 (F213Y, A279L), were successfully applied in the radiosynthesis of 5′-[18F]FDA, with overall radiochemical conversion (RCC) more than 3-fold higher than wild-type FlA1. Kinetic studies of the two-step reaction revealed that the variants show a significantly improved kcat value in the conversion of 5′-ClDA into S-adenosyl-l-methionine (SAM) but a reduced kcat value in the conversion of SAM into 5′-FDA.
Article
The Hastings District Water Supply Augmentation Scheme [HDWS] includes a 10GL off-creek storage dam and a 120ML/day river pumping station, which are currently under construction and due for completion in December 2002. The Cowarra off-creek storage dam is required to meet predicted long-term urban growth demands for water supply and to ensure the long-term protection of environmental flows in the Hastings River. Since 1985 the Hastings Council has progressively developed a major strategy for the sustainable augmentation of the water supply scheme including a very successful ongoing consultation process with both the local community, aboriginal land Council and key government agencies. The premise was: "That the impact upon aquatic flora and fauna in the Hastings River should be minimised and appropriate safeguards developed by maintaining minimum river flows to ensure that the river habitat is not adversely affected". The subsequent H D W S Environmental Impact Statement, 1995 was one of the first in Australia to recognise the importance of environmental river flows in the assessment of the aquatic ecological effects of water supply schemes. The adopted water supply scheme includes an innovative operation and environmental monitoring strategy for river abstraction activities, which is being implemented to fill and operate the off-creek dam storages and a long-term demand management program to reduce water usage.
Article
This review summarizes the principal studies on biochemical and genetic aspects of the metabolism of organofluorine compounds (organoFs) in plants. Only a few plants are known to biosynthesize the C-F bond and thus form this rare class of fluorinated natural products. Most studies have been done on Streptomyces cattleya, which possesses the ability to synthesize organoFs such as fluoroacetate and 4-fluorothreonine from inorganic fluorides. The biosynthetic pathway for the formation of these organoFs in S. cattleya and the enzymes involved in their synthesis have been identified and characterized. A gene cluster in S. cattleya encodes enzymes involved in the formation of organoFs.