Tài liệu Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment -

Committee on Toxicity of Chemicals in Food,

Consumer Products and the Environment

Subgroup Report on the Lowermoor

Water Pollution Incident

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Chapter 1: Executive Summary 13

Chapter 2: Introduction 21

Historical perspective 21

Terms of reference of COT Subgroup 23

Membership of Subgroup 23

Methods of working 23

Dates of meetings and visits 25

Chapter 3: The Lowermoor water pollution incident: water supply and contamination 27

Introduction 27

Lowermoor Water Treatment Works 27

The pollution incident 32

The distribution of contaminated water 33

The nature of the contamination of the water supply 33

Calculated values for the aluminium sulphate concentration in the Lowermoor Water Treatment Works 34

Collection of water samples for water quality analysis 35

Water quality data from SWWA and South West Water Ltd 36

Introduction 36

Pre-incident monitoring data 38

Results of monitoring – 7 July to 4 August 1988 41

Results of monitoring – 5 August to 31 December 1988 57

Results of monitoring – 1989 61

Monitoring data from other sources 63

Modelling of pollutant concentrations in Lowermoor treatment works and in trunk main system 64

Indications of copper concentrations in the contaminated water 72

Other water pollution incidents involving aluminium sulphate 73

Key points 73

Chapter 4: The assessment of exposure to contaminants 77

Introduction 77

Calculated estimates of exposure by the oral route 77

Water consumption data 77

Possible intakes from food 78

Water quality data 78

Estimated exposure to contaminants from 7 July to 4 August 1988 79

Estimated exposure to contaminants from 5 August 1988 to 31 December 1989 85

Modelling of exposure estimates 88

Modelling by Black and Veatch Consulting Ltd 88

Modelling by Crowther Clayton Associates Ltd 88

Dermal exposures 91

Key Points 91

Chapter 5: Evidence from individuals and population studies from the North Cornwall area 95

Introduction 95

Personal evidence 95

Population studies 95

Data from personal testimonies made by members of the public 96

Contents

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Introduction and method of working 96

General observations 97

Water quality, usage and consumption 97

Reported health effects (Adults) 99

Reported health data (Children) 101

Information provided by health professionals 101

Dr David Miles 101

General practitioners: Dr Chris Jarvis, Dr James Lunny, Dr Anthony Nash and Dr Richard Newman 105

Dr Ian Coutts 107

Mrs Jenny McArdle 108

Studies of the North Cornwall population 108

Epidemiological studies 108

Neuropsychological testing 115

Questionnaire survey 124

Homeopathic data 124

Data on Educational Assessment 125

Children with special educational needs 125

Tissue analyses 128

Taylor (1990) 128

Eastwood et al (1990) 128

McMillan et al (1993) 129

Powell et al (1995) 129

Howard (1993) 130

Ward (1989) 131

Critical appraisal of studies on tissue analysis 131

Effects on livestock and domestic animals 132

Types of Effects Reported 132

Concentrations of Contaminants in Animal Tissues 132

The concentration of aluminium in ice cream 133

Fish 133

Discussions with Mr Cooper 133

Report by Dr W. M. Allen 134

The Veterinary Investigation Centre 134

Appraisal of the effects on livestock and domestic animals 134

Key Points 135

Chapter 6: Toxicological and epidemiological data on contaminants from the scientific literature 139

Introduction 139

Aluminium 140

Introduction 140

General information 140

The chemistry, absorption and bioavailability of aluminium 141

The distribution of aluminium in the body 144

The excretion of aluminium 144

The toxicity of aluminium – acute and short-term effects 146

The neurotoxicity of aluminium 147

Effects on bone 150

Aluminium and carcinogenesis 150

Reproductive and developmental toxicity 151

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Other effects 152

Recommended upper level intakes 152

Copper 153

Introduction 153

General information 153

The absorption, distribution and excretion of copper in man 154

The toxicity of copper 154

Recommended upper level intakes 156

Zinc 156

Introduction 156

General information 156

The absorption, distribution and excretion of zinc in humans 156

The toxicity of zinc 157

Recommended upper level intakes 157

Lead 158

Introduction 158

General information 158

The absorption, distribution and excretion of lead in humans 158

The toxicity of lead 159

Recommended upper level intakes 160

Manganese 160

Introduction 160

General information 160

The absorption, distribution and excretion of manganese

in humans 161

The toxicity of manganese 161

Recommended upper level intakes 162

Iron 163

Introduction 163

General information 163

The absorption, distribution and excretion of iron in humans 164

The toxicity of iron 164

Recommended upper level intakes 165

Metal-metal interactions 165

Introduction 165

Interactions with aluminium 166

Interactions with lead 167

Interactions between the essential metals 167

Sulphate 167

Acidity (pH) 168

Key points 168

Chapter 7: Implications for health of exposure to the contaminants 173

Introduction 173

WHO Guideline Values 173

Overview of contaminant concentrations 174

Aluminium, copper and lead 174

Sulphate, zinc, manganese and iron 174

Methods used to estimate exposures 175

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Aluminium 177

Exposures 177

Toxicity 180

Discussion 181

Copper 183

Exposures 183

Toxicity 184

Discussion 185

Zinc 185

Exposures 185

Toxicity 186

Discussion 186

Lead 187

Exposures 187

Toxicity 188

Discussion 189

Manganese 190

Exposures 190

Toxicity 191

Discussion 191

Iron 192

Exposures 192

Toxicity 193

Discussion 193

Sulphate 194

Acidity (pH) 194

Additive/synergistic effects of contaminants 195

Key Points 196

Chapter 8: Evaluation of the health effects reported following the Lowermoor incident 199

Introduction 199

The exposure of individuals to contaminants 200

Symptoms experienced at the time, or months or years after the event 201

Health outcomes in the population and scientific data 202

Health effects 202

Acute effects 203

Chronic effects 203

Sensitivity to tapwater 207

Behaviour and academic performance of children 207

Chapter 9: Recommendations 209

Future monitoring and research on health 209

Future handling of similar incidents 210

References 213

Abbreviations 229

Glossary of Terms 231

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Appendices

Appendix 1: Membership of the Lowermoor Subgroup 243

Appendix 2: Membership of the Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment 245

Appendix 3: Health and other professionals who provided information 247

Appendix 4: Discussion of the quality and reliability of scientific data 249

Appendix 5: Drinking water quality – the legislative framework 255

Appendix 6*: Water quality data for the parishes of Camelford, Davidstow, Advent, St Minver Lowlands 259

and St Minver Highlands

Appendix 7*: Water quality data for the parishes of Camelford and Davidstow, 1989 259

Appendix 8*: Water quality data for the parishes of St Teath, Tintagel and Trevalga 259

Appendix 9*: Water quality data for the parishes of St Endellion, Forrabury & Minster and St Juliot 259

Appendix 10: Lowermoor water quality modelling report. Black and Veatch Consulting Ltd. August 2004 261

Appendix 11: Other water pollution incidents involving aluminium sulphate 297

Appendix 12: Report on the estimated consumption of aluminium, sulphate, copper, zinc, lead and pH following the 299

contamination incident on 6th July 1988. Crowther Clayton Associates. Report no. 91/2737

Appendix 13: Extract from “The Health of the Population”, Department of Public Health Medicine, Cornwall and 301

Isles of Scilly Health Authority, 1988

Appendix 14: Letter from DHSS to Dr CR Grainger, 24 August 1988 309

Appendix 15: Summary and critique of epidemiological studies of the North Cornwall population 317

Appendix 16: Review paper on aluminium prepared for the Lowermoor Subgroup by the 331

Department of Health Toxicology Unit, Imperial College

Appendix 17: Review paper on metal-metal interactions prepared for the Lowermoor Subgroup by the 402

Department of Health Toxicology Unit, Imperial College

Appendix 18: Current procedures for the management of chemical incidents 445

Appendix 19: Declaration of Lowermoor Subgroup members’ interests 447

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* On CD only.

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Table 1: Theoretical concentrations of aluminium and aluminium sulphate in the treated water reservoir, 35

if mixing had been complete

Table 2: Standards and guidelines for drinking water quality 39

Table 3: Water quality data from SWWA for the North Cornwall area, 6 January 1988 to 5 July 1988 – a summary 40

Table 4: Water quality data from SWWA for the Lowermoor water distribution area, 7 July 1988 to 4 August 1988 42

Table 5: Aluminium concentrations in samples taken from two locations at intervals from 9 July 1988 to 2 August 1988 52

Table 6: Number of sample results from SWWA monitoring data provided for each contaminant, 57

5 August to 31 December 1988

Table 7: Percentage of sample results between 5 August and 31 December 1988 containing more than 0.2 mg aluminium/l 58

Table 8: Number of results exceeding 1984 WHO Guideline Value, 5 August 1988 to 31 December 1988 58

Table 9: Locations and dates of samples containing high concentrations of contaminants between 5 August 61

and 31 December 1988

Table 10: Number of sample results from SWWA monitoring data provided for each contaminant in 1989 62

Table 11: Number of results exceeding 1984 WHO Guideline Value in 1989 62

Table 12: Locations and dates of samples where at least one parameter had high concentrations of contaminants in 1989 63

Table 13: Water quality data obtained from other sources 64

Table 14: Maximum modelled aluminium concentration (mg/l) for specific locations (from Black and Veatch 72

Consulting Ltd, 2004)

Table 15: Estimated worst-case exposures to aluminium (calculated using water quality data from SWWA) 80

Table 16: Estimated exposures to aluminium (calculated using water quality data from non-SWWA samples) 80

Table 17: Estimated worst-case exposures to copper (calculated using water quality data from SWWA) 82

Table 18: Estimated exposures to copper (calculated using water quality data from non-SWWA sources) 83

Table 19: Estimated exposures to zinc from the 3 samples containing concentrations in excess

of the 1984 WHO Guideline Value (calculated using water quality data from SWWA and other sources) 83

Table 20: Estimated worst-case exposures to lead (calculated using water quality data from SWWA) 84

Table 21: Estimated exposures to lead (calculated using water quality data from other sources) 84

Table 22: Estimated exposures to aluminium from the 3 samples containing the highest concentrations

in excess of the 1984 WHO Guideline Value (calculated using water quality data from SWWA) 85

Table 23: Estimated exposures to copper from the 3 samples containing the highest concentrations

in excess of the 1984 WHO Guideline Value (calculated using water quality data from SWWA) 86

Table 24: Estimated exposures to zinc from the 3 samples containing water in excess of the 1984 WHO Guideline 86

Value (calculated using water quality data from SWWA)

Table 25: Estimated exposures to lead from the 3 samples containing the highest concentrations in excess of the 87

1984 WHO Guideline Value (calculated using water quality data from SWWA)

Table 26: Estimated exposures to manganese from the 3 samples containing the highest concentrations in 87

excess of the 1984 WHO Guideline Value (calculated using water quality data from SWWA)

Table 27: Estimated exposures to iron from the 3 samples containing the highest concentrations in excess of the 1984 87

WHO Guideline Value (calculated using water quality data from SWWA)

Table 28: Estimated worst-case exposures to aluminium (calculated using results of modelling by Black and 88

Veatch Consulting Ltd)

Table 29: Commonly-reported conditions attributed to the incident by 54 individuals 100

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Table 30: Less commonly-reported conditions attributed to the incident 101

Table 31: Standardised mortality ratio (95% confidence intervals), July 1988 to December 1997 (from Owen et al, 2002) 111

Table 32: Cancer incidence, July 1988 to December 1998 (from Owen et al, unpublished report) 112

Table 33: Cancer mortality, July 1988 to December 1988 (from Owen et al, unpublished report) 112

Table 34: Leukaemia incidence, July 1988 to December 1998 (from Owen et al, unpublished report) 114

Table 35: Leukaemia mortality, July 1988 to December 1998 (from Owen et al, unpublished report) 114

Table 36: Battery of tests administered by McMillan et al (1990, 1993) 116

Table 37: Details of subjects examined by McMillan et al (1993) 117

Table 38: Tests carried out by Altmann et al, 1999 120

Table 39: Average Richmond test scores and year of administration 123

Table 40: Percentages of children with statements (SEN Stage 5), 1997 to 2001 127

Table 41: A summary of changes in metal concentrations in pig tissue from exposed animals compared to tissues 133

from non-exposed animals

Table 42: The most sensitive neurological responses observed following aluminium exposure in animals 151

Table 43: 1984 WHO Guideline Values (GV) for drinking water quality and current standards 173

Table 44: Percentage of SWWA samples (total number of samples) exceeding the relevant 1984 WHO Guideline 174

Values for aluminium, copper and lead in drinking water

Table 45: Percentage of SWWA samples (total number of samples) exceeding 1984 WHO Guideline Values for 175

manganese and iron in drinking water

Table 46: Estimated worst-case exposures to aluminium from drinking water, 7 July to 4 August 1988 177

(calculated and modelled using water quality data from SWWA)

Table 47: Estimated exposures to aluminium from drinking water, 6 to 11 July 1988 (calculated using 179

concentrations of aluminium in water samples from non-SWWA sources)z

Table 48: Estimated worst-case exposures to aluminium from drinking water, 6 July to 4 August 1988 179

(calculated using the results of modelling by Black and Veatch Consulting Ltd, Appendix 10)

Table 49: Estimated exposures to aluminium from drinking water, calculated from the 3 highest concentrations 180

recorded between 5 August 1988 and 31 December 1988 (SWWA data)

Table 50: Usual intakes of aluminium from food and water and potential intakes from medicines (mg/kg bw/day) 181

Table 51: Summary of margin of safety (MoS) for aluminium after the pollution incident 182

Table 52: Estimated worst-case exposures to copper from drinking water, 8 July 1988 to 4 August 1988 184

(calculated using water quality data from SWWA)

Table 53: Estimated exposures to copper from drinking water (calculated using water quality data from 184

non-SWWA sources)

Table 54: Usual intakes of copper from food and water and potential intakes from medicines and dietary 185

supplements (mg/kg bw/day)

Table 55: Estimated exposures to zinc from drinking water calculated forsamples taken between 186

6 July 1988 and 4 August 1988 which exceeded the 1984 WHO Guideline Value

Table 56: Usual intakes of zinc from food and water and potential intakes from dietary supplements (mg/kg bw/day) 187

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Table 57: Estimated worst-case exposures to lead from drinking water, 8 July 1988 to 4 August 1988 (calculated 188

using water quality data from SWWA)

Table 58: Estimated exposures to lead from drinking water (calculated using water quality data from non-SWWA sources) 188

Table 59: Usual intakes of lead from food, water, air and dust (mg/kg bw/day) 189

Table 60: Estimated worst-case exposure to manganese from drinking water, 6 July to 4 August 1988 190

(calculated from SWWA data)

Table 61: Usual intakes of manganese from food and water and potential intakes from dietary supplements 191

(mg/kg bw/day)

Table 62: Worst-case estimated exposures to iron from drinking water, 6 July to 4 August 1988 193

(calculated from SWWA data)

Table 63: Usual intakes of iron from food and water and potential intakes from dietary supplements 193

(mg/kg bw/day)

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Figure 1: The North Cornwall water distribution network 28

Figure 2: Schematic layout of Lowermoor Water Treatment Works at the time of the incident (after Lawrence, 1988) 30

Figure 3a: Contact tank: Plan (from Black & Veatch, 2004) 31

Figure 3b: Contact tank: 3-dimensional representation (from Black & Veatch, 2004) 31

Figure 4: Parishes served by the Lowermoor Water Treatment Works from which water quality data were available 37

Figure 5: Aluminium concentrations plotted from SWWA data (7 July to 4 August 1988) 51

Figure 6: Sulphate concentrations plotted from SWWA data (9 July to 4 August 1988) 53

Figure 7: Acidity concentrations plotted from SWWA data (7 July to 4 August 1988) 54

Figure 8: Copper concentrations plotted from SWWA data (8 July to 14 July 1988) 55

Figure 9: Lead concentrations plotted from SWWA data (8 July to 14 July 1988) 56

Figure 10: SWWA samples which exceeded the 1984 WHO Guideline Value for copper 59

(5 August 1988 to 31 December 1988)

Figure 11: SWWA samples which exceeded the 1984 WHO Guideline Value for zinc 59

(5 August 1988 to 31 December 1988)

Figure 12: SWWA samples which exceeded the 1984 WHO Guideline Value for lead 60

(5 August 1988 to 31 December 1988)

Figure 13: SWWA samples which exceded the 1984 WHO Guideline Values for manganese 60

(5 August 1988 to 31 December 1988)

Figure 14: SWWA samples which exceeded the 1984 WHO Guideline Value for iron (5 August to 31 December 1988) 61

Figure 15: Modelled dispersion of alum in the contact tank 66

Figure 16: Modelled predicted outlet concentration from the clearwater reservoir 66

Figure 17: Network – Model set-up 67

Figure 18: Camelford model and samples 68

Figure 19: St Teath model and samples 68

Figure 20: Helstone model and samples 69

Figure 21: Port Isaac and St Endellion model and samples 69

Figure 22: Delabole reservoir model and samples 70

Figure 23: Rockhead reservoir model and samples 70

Figure 24: Davidstow reservoir model and samples 71

Figure 25: Estimated worst-case exposures to aluminium (mg/day) for adults, 7 July 1988 to 4 August 1988 81

(calculated using water quality data from SWWA)

Figure 26: Estimated worst-case exposures to aluminium (mg/day) for toddlers and bottle-fed infants, 7 July 81

1988 to 4 August 1988 (calculated using water quality data from SWWA)

Figure 27: Maximum modelled intake of aluminium for 10 individuals (from Crowther Clayton Associates, 1999) 90

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Figure 28: Minimum modelled intake of aluminium for 10 individuals (from Crowther Clayton Associates, 1999) 90

Figure 29: The speciation of aluminium in water at different pH, after Martin (1991) and Priest (2001) 141

Figure 30: A summary of the fate of ingested aluminium sulphate in the body 145

Figure 31: Estimated worst-case exposures to aluminium from drinking water (mg/kg bw/day) calculated and modelled 178

from SWWA water monitoring data, 7 July to 4 August 1988: Adults

Figure 32: Estimated worst-case exposures to aluminium from drinking water (mg/kg bw/day) calculated from 178

SWWA monitoring data, 7 July to 4 August 1988: Toddlers and bottle-fed infants

Figure 33: Acidity of some common consumables and of the most acidic sample of Lowermoor water 195

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1.1 This report of the Committee on Toxicity of Chemicals in Food, Consumer Products and the Environment

(COT) considers the human health effects of the chemical exposure resulting from the water pollution

incident which occurred in July 1988 at the Lowermoor Water Treatment Works, North Cornwall. The

report was drafted by a specially convened Subgroup of the Committee which was asked to address the

following terms of reference:

“To advise on whether the exposure to chemicals resulting from the 1988 Lowermoor water pollution

incident has caused, or is expected to cause, delayed or persistent harm to human health; and

“To advise whether the existing programme of monitoring and research into the human health effects

of the incident should be augmented and, if so, to make recommendations.”

Structure of the report

1.2 The Subgroup held a total of nineteen meetings between October 2001 and December 2004. In addition,

a public meeting was held in Camelford in April 2002. The chairman and members of the Subgroup and

secretariat made four visits to Camelford between July 2002 and October 2003 to collect evidence from

people in the area affected by the pollution incident.

1.3 The information assessed by the Subgroup included:

• Personal evidence submitted in meetings with members of the Subgroup or in writing.

• Evidence from public health doctors, GPs and hospital doctors, and other experts.

• Detailed reviews of the scientific literature on the health effects of the chemicals whose

concentrations in the water supply were increased as a result of the incident.

• A visit to the Lowermoor Water Treatment Works.

• Work commissioned by the Subgroup from outside experts.

1.4 Full details of the background to the establishment of the Subgroup, its composition and methods of

working are given in Chapter 2 of the report.

1.5 Chapter 3 describes the Lowermoor water pollution incident. This occurred when 20 tonnes of aluminium

sulphate solution was discharged into the wrong tank at the treatment works, and, as a result,

contaminated water entered the distribution network to North Cornwall. The mains water, containing high

concentrations of aluminium sulphate, was sufficiently acidic to cause corrosion of metallic plumbing

materials. Flushing of the mains distribution system to remove the contaminated water also resulted in the

disturbance of old mains sediments, mainly deposits of iron and manganese oxides. Thus, a number of

contaminants could have been present at increased concentrations in the water at the tap. The chapter

describes the structure of the works, the distribution of contaminated water, the nature of the

contamination of the water supply, water quality data on the concentrations of the contaminants from

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before the incident to the end of 1990, and modelling of the aluminium sulphate concentrations in the

treatment works and mains system.

1.6 Chapter 4 discusses the potential exposures to the contaminants whose concentrations in tap water were

increased as a result of the incident i.e. aluminium, sulphate, copper, zinc, lead, manganese and iron.

Worst-case exposures have been estimated for three groups: adults, toddlers and bottle-fed infants. The

chapter also describes the modelling of exposure estimates carried out for South West Water Ltd in 1991.

1.7 Chapter 5 considers the evidence provided to the Subgroup by individuals who received contaminated

water, and the population studies carried out in the North Cornwall area. It includes a discussion of the

value and the limitations of both types of data. The personal evidence provided by individuals comprises

general observations; observations on water quality, usage and consumption; and health effects.

Information from local health professionals is summarised. The chapter then describes the studies which

have been carried out on the North Cornwall population since the incident. These include

epidemiological studies of: self-reported symptoms, pregnancy outcomes, the growth of children,

hospital discharge rates, mortality rates, and cancer incidence and mortality. The neuropsychological

testing carried out after the incident is described and critically appraised. Other subjects covered in this

chapter are: children with special education needs; homeopathic data; tissue analyses and effects on

livestock and domestic animals.

1.8 Chapter 6 consists of summaries of the toxicological and epidemiological data on the contaminants of

interest from the scientific literature. In the case of aluminium, the main contaminant, two main literature

sources were used: a published review of the scientific literature to 1997 by a group of international

experts, and a detailed update of the literature since 1995 which was commissioned by the Subgroup. For

lead, the main source of information was an international review published in 1997, updated by important

new information from the literature. For all other metals, the Subgroup used the extensive reviews of

research and the risk assessments published by the Food Standard Agency’s Expert Group on Vitamins and

Minerals in 2003. The chapter also includes an assessment of the information in the scientific literature on

biological interactions between the metals of concern.

1.9 Two chapters discuss the Subgroup’s conclusions. Chapter 7 presents an assessment of the health

implications of each contaminant at the estimated worst-case exposures given in Chapter 4. Chapter 8

addresses the question of whether exposure to the contaminants has caused, or is expected to cause,

delayed or persistent harm to human health, in the context of the symptoms and illnesses which were

either reported by individuals or were identified from epidemiological studies. In Chapter 9,

recommendations are made both for future monitoring and research on health and for the future handling

of similar incidents.

Conclusions

Who received contaminated water and how long was the water supply contaminated after the

pollution incident?

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1.10 With the exception of those locations for which monitoring data exist, it is not possible to determine

whether any particular point on the Lowermoor distribution network did or did not receive contaminated

water because of a large scale flushing exercise which was carried out by the water supplier at different

points in the distribution network. The extent and severity of the contamination can only be determined

by the analysis of samples of water taken at a particular vicinity and time. Sequential water quality data

are not available to enable a description of the progress of the aluminium sulphate as it travelled through

the distribution system.

1.11 The period of contamination with high concentrations of contaminants was short. Both water quality data

and modelling of the passage of aluminium in the trunk mains indicate that the concentrations of this

metal in the water supply fell rapidly from a high, initial peak. However, thirty per cent of samples taken

up to the end of 1988 and 6% in 1989 remained above the 1984 WHO Guideline Value for Drinking Water

Quality for aluminium. This value was set to avoid deposits in the distribution system and discolouration

of water, not because of a risk of adverse health effects above this concentration. Concentrations of

copper and lead were high for approximately a week after the contamination incident and very few water

samples exceeded the 1984 WHO Guideline Value for zinc.

1.12 Water quality data on the contaminants arising from the flushing exercises indicated that the proportion

of samples with concentrations of manganese above the relevant 1984 WHO Guideline Value increased in

the month after the incident but fell markedly thereafter. The proportion of iron samples exceeding the

relevant 1984 WHO Guideline Value rose in the month after the incident and remained high to the end of

1990.

On the basis of the toxicity data in the scientific literature and the estimated exposures, would the

contaminants be expected to cause delayed or persistent harm to human health?

1.13 This question is considered separately for each contaminant in Chapter 7. The possibility of additive or

synergistic interactions is also addressed. For each contaminant, the implications for health of the worst￾case estimated intakes are considered in the context of the toxicological and epidemiological data in the

scientific literature.

1.14 It is not anticipated that the increased exposure to aluminium would have caused, or would be expected

to cause, delayed or persistent harm to health in those who were adults or toddlers at the time of the

incident. However, the possibility of delayed or persistent harm to health, although unlikely, should be

explored further in those who were bottle-fed infants at the time of the incident (i.e. below one year

of age).

1.15 The increased concentrations of copper in the first week or thereabouts after the incident probably

contributed to acute, adverse gastrointestinal symptoms. It is not anticipated that they would have

caused, or would be expected to cause, delayed or persistent harm to health.

1.16 The occasional high concentrations of zinc which occurred after the incident may have contributed to

acute, adverse gastrointestinal symptoms. It is not anticipated that they would have caused, or would be

expected to cause, delayed or persistent harm to health.

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