Environmental Health in Australia and New Zealand:
Case Studies in Environmental Health Risk Assessment
N.J. CROMAR, J.S. HEYWORTH & J.P. RALPH
Case Study 1: Accidental release of copper into reticulated
drinking water supplies
Tutor Notes and Teaching Aids
Table of Contents
Scenario
Chronology
Resources
1.
Hazard Identification
2.
Exposure Assessment
3.
Dose Response Relationship
4.
Risk Characterisation
5.
Risk Management
6.
Risk Communication
SCENARIO
Potteroo, a country town in central South Australia (population approximately 2000)
receives its water supply from a small reservoir (volume = 100 ML). Last spring, the
reservoir experienced a cyanobacterial bloom, which the local water authority decides
to treat by the addition of copper sulphate to the water. Unfortunately, the company
contracted to dose the reservoir miscalculates the volume to be treated resulting in a
massive overdose of copper sulphate (CuSO4.5H2O) equivalent to 100 mg l-1. The
bloom in the reservoir is subsequently analysed by mouse bioassay and found to be
non-toxic. Following the incident, local inhabitants begin to complain of blue
coloured water with a metallic bitter taste, and staining of laundry. The local GP
reports an elevated number of consultations from patients suffering from vomiting,
diarrhoea and headaches.
OUTLINE OF PROCEDURE / CHRONOLOGY OF EVENTS
The reservoir was dosed on Monday and complaints from members of the public
started on the following day (Tuesday). The dosage error was recognised on Thursday
and the Health Department was notified on Friday.
It is now the following Monday. You are a group of scientists from the local
Department of Health who have been called in by the local water authority and
council to provide expert guidance on how to proceed.
The water authority informs you that there is no alternative supply of water. You are
given the task of performing a risk assessment and suggesting a management and
communication strategy that will minimise the public health concern of the incident.
You have the full cooperation of the local authorities and of your colleagues in the
Health Department. Your assessment has to be made as swiftly as possible as the local
authority is awaiting your judgement on how to proceed.
You will find the risk assessment protocol set out in this document helpful in
completing this project. Preliminary reading will be provided. Literature, data and
reference personnel will be available to the project group for the duration of the
course. A structured timetable for project activities will assist you to plan your final
report, which will be presented at the completion of the project.
RESOURCES
1.
These will be made available on a stage by stage basis. This process will
attempt to simulate the normal/desirable chronology of questions and answers.
It will also mirror the progress of the course’s schedule of presentations.
2.
(a)
An assortment of scientific papers, books and reports will be available
for consultation. Extra references will be given. It is not necessary,
however, for the purposes of this project to review the literature
comprehensively.
(b)
Information on local, national and international recommendations,
standards and monitoring procedures will be provided
TUTOR NOTES
This case study introduces the student to the process of assessing and managing
public and environmental health risks. This exercise presents a hypothetical scenario
in which the health of a community is adversely affected by copper in reticulated
drinking water. The task of the student is to develop a risk assessment protocol to
assess and manage this situation.
Most of the questions are provided with suggested answers. The answers are intended
as a guide only.
1.
HAZARD IDENTIFICATION
(A ‘hazard’ is a latent cause of adverse health effect(s))
Generic Questions:
(a)
‘Is the reticulated water supply associated with adverse health effects?’
OR
(b)
‘Does exposure to the reticulated water supply - which we know from
prior evidence can be a vehicle for potentially hazardous substances pose a hazard to the health of this population?’
Students should review the available literature on the effects of copper in
drinking water on human health
Why is copper found in water?
In the environment, copper is commonly found in drinking water. It is present in the
natural mineral content of water, from industrial pollution, algicide treatment and
dissolution from copper plumbing. The treatment of surface waters with copper
sulphate to disperse algal blooms is commonly practised, and can significantly elevate
copper levels. Concentrations in drinking water can also increase in distribution
systems containing copper plumbing. Increases are mainly due to interactions with
copper pipe and water chemistry, particularly the pH and aggressivity. Changes in
water pH change the speciation and concentration of copper in water. Decreasing
water pH levels will increase the proportion of soluble copper in the unbound ionic
form, and increase the corrosion of pipes. The aggressivity of water can be quantified
by the Langeliers Index (LI). The LI index is the ability of water to form or dissolve a
protective calcium carbonate scale on internal pipe surfaces, and is related to pH,
hardness, alkalinity and conductivity. Aggressive water (LI below –2) is considered
corrosive and leads to high aqueous copper concentrations.
Copper exists in water predominantly in the cupric form (Cu2+) and readily complexes
with both inorganic and organic ligands, such as ammonium, chloride ions and humic
acids. Concentrations of copper in ground water can be high due to natural mineral
deposits, and levels in excess of 3 mg/L have been reported. Concentrations in surface
freshwaters are usually very low, found at levels below 0.1 mg/L. Concentrations of
copper in drinking water supplied to households are generally below 0.5 mg/L.
Does exposure to copper in reticulated water supplies affect human health?
Copper in drinking water can have significant effects on human health. Although it is
an essential element for normal human functioning, at high concentrations copper can
cause adverse gastrointestinal symptoms including nausea and vomiting.
What type of evidence exists - human, animal, and other?
Several studies have documented adverse health effects from the consumption of
copper in drinking water. Knobeloch et al. (1998) investigated effects from the
consumption of copper contaminated household tap water. Water containing copper at
concentrations up to 3.7 mg/L caused gastrointestinal symptoms including nausea,
diarrhoea, abdominal cramps and vomiting in humans. Symptoms were more common
among new houses containing copper plumbing, and supplied with naturally corrosive
water. Spitalny et al. (1984) reported high rates of vomiting and abdominal pains in a
family consuming water with median copper levels of 3.1 mg/L. Morning water
concentrations after overnight stagnation in copper pipes up to 7.8 mg/L were
documented. Additionally, the symptoms of residents ceased when the water supply
was changed, suggesting copper was the causative agent. Nausea and vomiting in
children consuming cordial with drinking water containing up to 17mg/L of copper
has been reported (Scholz & Cavagnino, 1995). The high copper levels, attributed to
the acidity of water, would have been masked by the taste of cordial, preventing its
detection. However, in all the studies described, the actual copper concentrations at
the time of illness were only estimates. Gastrointestinal symptoms from the
consumption of accurately known copper concentrations in drinking water have only
recently been investigated. A study examining the health effects of females
consuming copper at concentrations of 0, 1, 3 and 5 mg/L, showed the consumption
of concentrations greater than 3mg/L in drinking water caused vomiting and stomach
cramps (Pizarro et al., 1999). However, there was no correlation between diarrhoea
and copper consumption, as previously suggested (Knobeloch et al., 1998). There
may also be differences in the susceptibility of copper to males and females due to
differing copper requirements between sexes, and this was not considered. The
consumption of copper in infants has been shown to cause liver damage (discussed
later). The consumption of copper in rats and mice (chronic exposure up to 640 mg/L)
caused liver damage and decreased survival.
What types of health effects have been reported - positive and negative?
Copper is an essential element for human health. It is involved in normal enzyme
functioning and in gene expression. The recommended daily intake ranges from 30
ug/kg in children to 80 ug/kg in adults and occurs mainly through the diet
Deficiencies of copper in humans in rare, and effects include anaemia and bone
abnormalities.
Copper toxication in humans is rare. The ingestion of copper induces vomiting,
preventing the intake of toxic amounts . Historically, copper was commonly used as
an emetic at doses above 100mg . The health effects of chronic copper toxication are
mainly derived through studying toxic interactions in Wilson’s disease and childhood
cirrhosis (discussed later), as the emetic effects of copper prevent chronic exposure in
normal individuals . The Long-Evans Cinnamon rat, with a genetic defect similar to
Wilson’s disease, is commonly used to study chronic copper toxication in the
laboratory. Incidences of acute copper toxication are generally associated with
accidental poisonings. Wylie (1957) reported copper toxication in humans through
alcoholic cocktails prepared in copper cocktail shakers. The consumption of an
estimated 32mg of copper caused nausea, vomiting, diarrhoea and dizziness.
However, the validity of the study due to the lack of data and scientific approach is
questionable. Additionally, the combined effect of copper and alcohol in humans is
unknown. Copper toxication via the ingestion of over 300 copper coins (97% copper)
by an adult male caused hepatic fibrosis and extensive copper deposition in hepatic
tissue (Nasan et al., 1995). The patient died, but death could be linked to surgical
complications as well as copper toxicity. Copper poisoning through the ingestion of
large quantities of copper sulphate has been shown to cause gastrointestinal upsets,
jaundice, haemoglobinuria, hypotension, coma and death in humans (Chuttani, 1965)
The lethal dose of ingested copper sulphate has been demonstrated as low as 1 gram.
Chronic copper toxication in animals has been shown to cause haemolysis and fatal
liver cirrhosis. Short term effects in animals are not known.
What are the main exposure routes to copper and what concentrations are involved?
Exposure to copper occurs mainly through consumption. Copper is found naturally in
many food sources, with high concentrations in organ meats and oysters. The
consumption of copper in drinking water is an important source of the daily intake,
especially in areas experiencing high concentrations. The concentrations involved will
depend on relative concentrations in food and water. Assuming the concentration in
drinking water is between 0.1 and 0.5 mg/L, ingestion of 2L per day will provide 1350% of acceptable daily intake. In most instances, the gastrointestinal system will
absorb 25-60% of ingested copper. Exposure to copper via inhalation and absorption
is minimal and occurs mainly in industrial occupations.
How is exposure to copper measured?
Exposure to copper is generally measured by serum copper and ceruloplasmin
concentrations. Ceruloplasmin is a liver protein used in the transportation of copper in
the body. Concentrations are dependant on age (increase with age) and gender.
Concentrations of copper in adult women (especially pregnant) are generally higher
than males due to interactions with oestrogen. Copper is an intergral part of many
enzymes, including erythrocyte superoxide dismutase and platelet cytochrome c have
recently been investigated in measuring copper exposure as they are highly sensitive
to changes in copper intake. Copper is also measured in urine. The measurement of
copper in hair can be unreliable is concentrations can vary with environmental
contamination (ie shampoos, water), and only change with prolonged exposure.
If toxication through the consumption of drinking water is suspected, concentrations
in drinking water may be indicative of exposure
Are any individuals more susceptible to environmental copper?
Individuals may have an increased susceptibility to copper through age or certain
medical conditions. Wilson’s disease is an autosomal recessive disorder causing
copper toxicosis through the excessive accumulation of copper within the body.
Clinical manifestations of Wilsons disease include damage to the nervous system,
cirrhosis of the liver and the kidneys . Wilson’s disease causes an increased
suseptibility to environmental copper, including copper in drinking water, but is
treatable with chelation therapy. Other conditions causing an increased sensitivity to
environmental copper include glucose 6 phosphate dehydrogenase deficiency,
diabetes, pregnancy and individuals with liver and kidney disease.
Recent evidence has suggested infants have an increase susceptibility to copper.
Indian childhood cirrhosis (ICC) is a disease in children linked to the consumption of
copper in drinking water. ICC is a fatal liver disease in infants causing fever,
abdominal swelling and death from micronodular liver cirrhosis. It is characterised by
the excessive accumulation of copper in hepatocytes, and differs both pathologically
and genetically from Wilson’s disease. Similar cases of childhood cirrhosis
attributable to copper have been reported in Europe, Germany and Australia. The
cause of ICC is debatable. ICC is common in non breast-fed infants exposed to copper
through cooking utensils and the consumption of copper contaminated water.
However, it is not fully understood if ICC occurs through exposure to environmental
copper or if it is a genetic disease. Hucker et al. (1998) showed that ICC is linked to
the intake of high copper levels in drinking water. The death of two siblings from
ICC, attributable to the consumption of copper contaminated drinking water were
examined. The drinking water consumed contained copper at levels up to 3 mg/L, and
was the primary source of exposure to copper. However, other family members
consuming well water were not affected, indicating an increased sensitivity in infants.
Similar results have also been found by other. In comparison, Fewtrell et al. (1996)
found children consuming copper in drinking water ranging from 3.0 to 26.0 mg/L
exhibited no adverse health effects. However, health effects were only measured by
liver complaints at a hospital paediatric unit, and other symptoms indicative of copper
toxicity were not measured. Olivares et al. (1998) showed no difference in serum and
liver enzyme copper concentrations and gastrointestinal symptoms, indicative of
copper toxicity, between infants consuming low (<0.01 mg/L) and high (2 mg/L)
copper levels in drinking water. It has been suggested that ICC isn’t solely caused by
an excessive intake, and an unidentified genetic defect causing increased copper
sensitivity is responsible. Epidemiological evidence suggests a genetic etiology for
ICC, but as yet, this has not been confirmed.
Are health effects dependent on the form of the copper?
The speciation of copper greatly affects its bioavailability in the human body. In
general, free copper ions are more bioavailable than bound copper ions. Copper ions
readily complex to organic and inorganic materials, preventing interactions in the
body. However, binding to metallotheionein, a liver protein important in preventing
toxic interactions by heavy metals, and ceruloplasmin decreases its toxicity in the
body.
How good is the evidence?
Evidence of health effects from copper in drinking water are not completely
established. Several studies have documented adverse health effects from the
consumption of high concentrations, however, the levels were only estimates and the
health effects from accurately known copper concentrations have been less well
investigated.
What is the ‘official view’ of the evidence ie. do exposure standards exist?
The Australian National Health and Medical Research Council (NH&MRC) guideline
value for copper in drinking water is 1 mg/L (NH&MRC, 1993). This guideline value
is based primarily on aesthetic considerations, including colour, taste and the potential
staining of domestic tap fittings. High concentrations of copper in drinking water can
cause a metallic taste upon consumption. Beguin-Bruhin et al. (1983) investigated the
detection of copper through the consumption of spiked drinking water. The taste
threshold for copper in distilled water was 2.4-3.2 mg/L, and 0.8-1.0 mg/L in spring
water, with the lower threshold in spring water attributable to interactions with carbon
dioxide. Copper may also have different taste thresholds with different water quality
and this has not been investigated. Copper in water can cause a blue colouration, and
the staining of domestic plumbing fittings occurs with concentrations above 1 mg/L.
Copper concentrations in drinking water, however, are not considered a risk to public
health unless concentrations exceed 2 mg/L.
The World Health Organisation guideline value for copper in drinking water is 2.0
mg/L, based primarily on health concerns (WHO, 1973). Worldwide, recommended
copper levels in drinking water range from 1.0 to 3.0 mg/L (Fitzgerald, 1998). In
South Australia, a health alert level of 3mg/L of copper in drinking water has been
proposed (GSC, 1994). There is currently no ratified standard for copper in drinking
water in Australia.
Guideline values for copper in drinking water are derived from the relationship
between the provisional mean tolerable daily intake (PMTDI), human body weight,
the proportion of the PMTDI consumed through drinking water and the volume of
water consumed per day. The recommended values, however, have been extensively
debated. Fitzgerald (1995) reported discrepancies between studies establishing the
PMTDI of copper. These studies contained misprints, leading to calculation errors,
which were used in the derivation of guideline values. Additionally, because of the
small number of studies on health effects from copper in drinking water, guideline
values may not be accurate, as adverse health effects are not completely established.
More research is necessary on the health effects of exposure to copper in drinking
water and on causes of high copper levels in household drinking water, before an
accurate, safe and achievable guideline value can be determined.
2.
EXPOSURE ASSESSMENT
Generic Question:
‘What is the level and pattern of exposure to copper within the population?’
Students will need to know how to determine daily intake
Consider:
Different consumption rates by different age groups
High number of children below 5 years
Elderly
Number of individuals exposed
Exposure to copper before and after dosing
Estimation of daily intake
Water borne concentration
Water quality- hard and non aggressive
acidic after algal treatment
Estimation of dose and bioavailability
After dosing concentrations ~ 19 mg/L. If consuming 2 L per
day, typical exposure will be ~38 mg/day.
Bioavailability will depend on the form of copper. Copper will
be more bioavailable in the free form in drinking water.
Contaminated drinking water used for cooking will have lower
bioavailability due to complexation with proteins and
carbohydrates
Students will need to review articles available on exposure
Biological exposure- normal concentrations
Environmental measurements
Are there any environmental factors that may contribute to the same health effects?
Many environmental factors can contribute to adverse health effects observed in
copper toxication. The consumption of algal toxins through contaminated water may
cause both physical and pathological effects observed with copper toxication. Clinical
effects of copper intoxication include gastrointestinal illness, similar to those
observed with food poisoning.
Assessment of Exposure to Copper in Drinking Water
Students are encouraged to familiarise themselves with the literature on exposure assessment prior to tackling this section.
You are provided here with:
1. a demographic breakdown of the population of Potteroo
2. the health status of selected groups within the Potteroo population
3. the reliance of the Potteroo population on rainwater as a source of drinking water
4. copper levels determined in the water supply.
Medical
Information supplied to you by the local GP included the following:
1. one member of the population (male - 35 years) is suffering from hepatolenticular degeneration,
2. about 15 % of the population above 55 years have elderly onset diabetes,
3. there are 83 confirmed pregnancies in women aged from 16 to 43 years, and
4. one female (22 years) is currently undergoing renal dialysis. Activated carbon is used to purify water prior to dialysis.
Rainwater Usage
The drinking water in approximately 20 % of the 650 households is supplied by on-site rainwater tanks.
Population Demographics
Age Group
0 to 12 mo
13-24 mo
25-36 mo
37-48 mo
5-9 yr
10-14 yr
15-19 yr
20-24 yr
25-29 yr
30-34 yr
35-39 yr
40-44 yr
45-49 yr
50-54 yr
55-59 yr
60-64 yr
65-69 yr
70-74 yr
75-79 yr
80-84 yr
> 84 yr
sub-total
TOTAL
Number
Male
25
20
23
27
84
65
75
60
77
87
92
88
53
49
46
40
42
43
12
10
7
Female
22
15
20
26
83
74
72
47
82
99
97
80
60
55
36
43
36
36
20
20
13
1025
1036
2061
Time line: The reservoir was dosed with copper sulphate on Monday. Copper in the reservoir and at the tap had previously
been determined (approx. 2 months ago). At that time the mean concentration of copper in 3 samples of water from the
reservoir was 0.04 mg/L (pH = 8). The levels and pH of copper at the tap are given in Table 1. Copper in the reservoir and at
the tap was reanalysed on Friday. The concentration of copper in 3 samples of water from the reservoir was 17 mg/L, 15 mg/L
and 18 mg/L, with a pH of 6. The levels and pH of copper at the tap are given in Table 2. The results of other analyses of the
water in the reservoir averaged over a five year period are given in Table 3.
ROUTINE MEASUREMENT OF COPPER LEVELS
Measurements taken from supply taps in randomly selected households in Potteroo.
2 months ago
Table 1. Copper Levels (total copper, mg / litre) at pH (range)
11 High St.
Initial flush
30 secs
1 min
2 min
5 min
6 Acacia
Ave
0.92
at 7.7
0.26
at 7.7
0.22
at 7.6
0.14
at 7.5
0.12
at 7.5
0.18
at 7.3
0.14
at 7.5
0.05
at 7.5
0.04
at 7.5
0.04
at 7.5
2 Broad St
0.25
at 7.5
0.13
at 7.5
0.08
at 7.5
0.07
at 7.5
0.07
at 7.5
19 Miller
Rd
0.93
at 7.4
0.93
at 7.4
0.18
at 7.5
0.18
at 7.5
0.12
at 7.5
Sampling Location Details
11 High St
2 years old; unoccupied for 9 months
6 Acacia Ave
10 years old
2 Broad St
10 years old; screw on filter
slow filling rate
19 Miller Rd
5 years old
35 Kings Ct
50 years old
22 Wynds Rd
copper pipe replaced 2 years ago
35 Kings Ct
0.52
at 7.5
0.08
at 7.5
0.10
at 7.5
0.08
at 7.4
0.07
at 7.4
22 Wynds
Rd
0.77
at 7.8
0.73
at 7.7
0.74
at 7.8
0.17
at 7.8
0.11
at 7.7
MEASUREMENT OF COPPER LEVELS FOLLOWING ACCIDENTAL CONTAMINATION
Measurements taken from supply taps as per routine measurement in Potteroo.
Friday
Table 2. Copper Levels (total copper, mg / litre) at pH (range)
11 High St.
Initial flush
30 secs
1 min
2 min
5 min
6 Acacia
Ave
19.0
at 5.5
18.3
at 5.5
18.2
at 5.4
18.1
at 5.4
18.1
at 5.3
0.08
at 7.4
1.03
at 7.0
6.2
at 6.4
16.6
at 5.4
16.6
at 5.3
2 Broad St
17.6
at 5.7
17.5
at 5.7
17.2
at 5.6
17.2
at 5.7
17.1
at 5.6
19 Miller
Rd
18.8
at 5.7
18.3
at 5.7
18.0
at 5.8
18.1
at 5.8
18.0
at 5.7
Sampling Location Details
11 High St
2 years old; unoccupied for 11 months
6 Acacia Ave
10 years old
2 Broad St
10 years old; screw on filter
slow filling rate
19 Miller Rd
5 years old
35 Kings Ct
50 years old
22 Wynds Rd
copper pipe replaced 2 years ago
35 Kings Ct
17.9
at 5.3
17.4
at 5.5
17.3
at 5.4
17.4
at 5.4
17.3
at 5.4
22 Wynds
Rd
17.8
at 5.7
17.5
at 5.6
17.5
at 5.8
17.4
at 5.7
17.4
at 5.7
COUNTRY WATER SUPPLIES - POTTEROO RESERVOIR
RAW WATERS
LAST 5 YEAR AVERAGE AND RANGE
Table 3. MAJOR COMPONENTS (mg /l)
Min
Max
Aver
Conduc
TDS
pH
Ca
Mg
Na
K
HCO2
SO4
Cl
F
NO3
SiO2
total
Fe
CaCO3
FeCO3
CO2
Langel.
Index
791
2000
1380
429
1160
755
7.4
8.7
8.3
32
61
48
24
69
43
94
285
171
3.8
8.4
6.0
153
317
248
33
86
60
147
490
289
0.30
0.57
0.43
0.05
2.57
0.62
6
15
10
0.01
0.83
0.19
180
434
297
40
143
83
NI
7
2
-0.11
1.17
0.79
3.
DOSE RESPONSE RELATIONSHIP
Generic Question:
‘What is the dose-response relationship between copper and any adverse
health effects?’
Review articles on adverse health effects from copper in drinking water.
Is it possible to derive a dose response relationship from the available data?
Only one study to date has examined possible dose response relationships from the
consumption of copper in drinking water. Pizarro et al. (1999) examined effects in 60
adult women consuming copper at accurately known concentrations. Copper
concentrations greater than 3 mg/L were shown to induce nausea, abdominal pain and
vomiting, however, there was no relationship with diarrhoea. However, it was not
possible to derive a dose response relationship from this study, and more research is
needed. Dose response in animals is well characterised but is species specific, with
higher sensitivity shown in sheep and dogs due to differing transport mechanisms.
Is there evidence of a threshold?
Based on the small number of studies, it is not possible to define threshold values for
gastrointestinal symptoms from copper in drinking water.
Some values have been suggested: vomiting 12 mg/L, nausea 3-4 mg/L, taste 1-5 mg/L.
Students will need to review medical status of community before and after dosing
Health of community after dosing
Vomiting and diarrhoea
Headaches (not characteristic of copper toxicity?)
4.
RISK CHARACTERISATION
Generic Questions:
‘What is the aggregate risk to public health within this population?’
‘How does this health risk compare with others accepted by the community?’
‘How much anxiety is the exposure causing?’
‘How does the exposure relate to existing standards?’
‘What are the costs of remediation? Do they represent good ‘cost-benefit’
relative to potential expenditure on other public health problems?’
Need to determine aggregate risk.
Consider: Number of individuals exposed –Proportion of community consuming water
Health effects at observed copper concentrations?
Comparison of values with reported toxications
Are there categories of people at particularly high risk?
Individuals at high risk of copper toxication include:
-
-
Individuals with a large reliance on reticulated water than other water sources (ie.
Bottled or rain)
- 20 % of Potteroo community use rainwater as drinking water
Individuals with a biologically increased risk (ie Wilsons disease, elderly,
pregnant, diabetic, pregnant or infants)
Sporting groups
Dialysis patients – activated carbon will not remove the copper
Problems will be perceived differently be different groups
Problem should be given high priority
Solution to problem obtainable
Consider: Environmental costs – changes in ecosystem in the reservoir, remediation
of sediments?
Short term costs - health care, confidence in water supply, alternate water
source, problems due to discoloured water
Long term costs - long term health effects probably minimal, damage to
plumbing pipes
Costs to health system – increased doctor and hospital demand initially,
possibly more problems for infants
Costs to local economy – industries reliant on water,
(Not specifically at specific dollar values, just estimates of "high" and "low")
5.
RISK MANAGEMENT
Generic Questions:
‘What are the options for managing this problem?’
‘How will we implement, monitor and evaluate the management strategy?’
Refer additional material:
Problem/Context – Risks – Options – Decisions – Actions – Evaluation – (cyclical process).
Removal of residual copper from drinking water
Water chemistry conditions in drinking water treatment plants are adjusted to
minimise conditions leading to increasing copper concentrations. Copper can be
removed from water by reacting with phosphates and increasing water pH to favour
the insoluble forms of copper. In distribution systems, high copper levels are
minimised by flushing pipes to remove residual copper. However, in this example
flushing will not decrease copper concentrations due to the acidic pH levels and
treatment is necessary at the reservoir.
Cost benefits
Consider different solutions
Prevention of adverse health effects
Use of other water sources for cooking and consumption
Regular testing
Public notification
Monitoring and evaluation: what can be done?
Monitoring water quality
Reservoir
Household taps
6.
RISK COMMUNICATION
Generic Questions:
‘Who are the interested parties and who need to know what is going on?’
‘How is the nature of the risk and the purpose and likely effect of the
intervention best communicated to interested parties?’
6.1
Modes of communication
Meetings
Print and other media
Letter drops
6.2
What is to be communicated?
Explaining the underlying nature and extent of the risk
Dealing with public outrage
Explaining the purpose and content of the intervention (risk management)
Explaining the expected outcomes of the intervention
6.3
To whom should the communication be targeted?
Industrial consumers
Individuals
COPPER CASE STUDY
REFERENCE LIST

Australian Food Standards Code (1994) Standards A12, Metals and contaminants
in food.

Barceloux DG. (1999) Copper. Clinical Toxicology 37(2): 217-230.

Barrett DB. (1984) An assessment of the current levels and the effects of copper in
the drinking water if the Perth metropolitan area. West Australian Health Surveyor
5: 7-15.

Beshgetoor D & Hambidge M. (1998) Clinical conditions altering copper
metabolism in humans. American Journal of Clinical Nutrition 67: 1017-1021.

Burch MD. (1990) Algicidal Control of Algal Blooms. Proceedings of the Water
Board Cyanobacteria Workshop Blue-Green Algae in Drinking and receiving
waters. pp 21-23.

Chuttani K, Gupta PS, Gulati S & Gupta DN. (1965) Acute copper sulphate
poisoning. American Journal of Medicine 39: 849-854.
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