Committee on Toxicity of Chemicals in Food,
Consumer Products and the Environment
Subgroup Report on the Lowermoor
Water Pollution Incident
78933-COI-Toxic-Lowermoor ch1-4 21/1/05 10:58 pm Page 1
78933-COI-Toxic-Lowermoor ch1-4 21/1/05 10:58 pm Page 2
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

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

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

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
6
COT Lowermoor Subgroup
78933-COI-Toxic-Lowermoor ch1-4 21/1/05 10:58 pm Page 6
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

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)

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
9
Consultation Report January 2005
78933-COI-Toxic-Lowermoor ch1-4 21/1/05 10:58 pm Page 9
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)
10
COT Lowermoor Subgroup
78933-COI-Toxic-Lowermoor ch1-4 21/1/05 10:58 pm Page 10

(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
11
Consultation Report January 2005
78933-COI-Toxic-Lowermoor ch1-4 21/1/05 10:58 pm Page 11
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
12
COT Lowermoor Subgroup
78933-COI-Toxic-Lowermoor ch1-4 21/1/05 10:58 pm Page 12
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

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?
14

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.
15
Consultation Report January 2005
78933-COI-Toxic-Lowermoor ch1-4 21/1/05 10:58 pm Page 15
1.17 It is unlikely that the potential brief period of increased exposure to lead, would have caused, or would
be expected to cause, delayed or persistent harm to health. However, any additional exposure of young
children to lead is undesirable and the possibility of a delayed or persistent effect should be explored
further in those who were bottle-fed infants at the time of the incident, potentially the most highly
exposed group. Inorganic lead compounds are considered to be possible carcinogens in humans and it is
not possible to say whether the small additional exposures to lead will have any effect on cancer
incidence.
1.18 It is not anticipated that concentrations of manganese after the incident would have caused, or would
be expected to cause, delayed or persistent harm to health in those who were adults at the time of
the incident, nor is it considered that there would be any substantial increased risk to health to those
who were toddlers at the time. It is unlikely that there would have been any delayed or persistent harm
to health in those who were bottle-fed infants but recommendations have been made for further
monitoring of this age group.
1.19 It is not anticipated that the concentrations of iron in drinking water after the incident would have caused
or would be expected to cause, delayed or persistent harm to health.
1.20 The sporadic high concentrations of sulphate in drinking water after the incident may have caused 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.

neurotoxic effects in adults nor in those who were children at the time of the incident. However, the
Subgroup was advised that the overall pattern of results in one of the neuropsychological studies
indicated subtle effects in the individuals tested but that it was not possible to determine whether these
effects were due to the contaminated water because of deficiencies in the design of these studies. Further
work is recommended on this endpoint.
1.26 There is no indication from the toxicological data that the estimated exposures to the contaminants
which occurred after the incident can cause effects on joints and it is not possible to conclude that there
is a causal relationship between the joint pains and/or swelling reported and exposure to the
contaminants. It should be borne in mind that arthritis and related problems occur commonly in the
population. However, the Subgroup recognised that many individuals with whom they spoke were
concerned about joint problems. Therefore, further work is recommended on this endpoint.
1.27 A consultant dermatologist who, two years after the incident, examined individuals suffering from nail and
skin problems reported that the types of nail problems seen were common and that further metabolic
investigation of the patients’ nails was not required. There is no relevant information in the
epidemiological studies nor from the toxicological data on possible effects of the contaminants on nails
which can add to this opinion.
1.28 The results of a study of cancer incidence and mortality between 1988 and 1998 in the population living
in the area which received contaminated water provide no evidence of an increased overall cancer risk
arising from the incident.
1.29 The results of an investigation of a cluster of three cases of acute leukaemia in children attending a
secondary school in the area which had received contaminated water were consistent with the hypothesis
that the incidence of leukaemia could be affected by prior exposure to infectious agents. However, the
study found that the pollution incident did not cause an increased incidence of infection.
1.30 There was no indication from the toxicological data on the contaminants of an adverse effect on the
thyroid gland. Thyroid disease is common in the population and the cases reported are considered
unlikely to be caused by exposure to the contaminants resulting from the incident.
1.31 The homeopathic report cited a sensitivity to tap water as a common finding after the incident but, from
the symptoms described, this does not appear to be the immune condition termed “sensitisation”. It has
17
Consultation Report January 2005

Monitoring of routine health statistics
1.36 The monitoring of routine health statistics for the population potentially exposed to contaminated water
after the Lowermoor pollution incident, recommended by the Lowermoor Incident Health Advisory
18
COT Lowermoor Subgroup
78933-COI-Toxic-Lowermoor ch1-4 21/1/05 10:58 pm Page 18
Group (1991), should continue. The monitoring should include analysis of overall cancer incidence and
mortality rates, and analysis of cancer subgroups. If possible, the assessment of the exposed population
should be refined to take account of the fact that some areas experienced a higher level of contamination
than others. If such a refinement is possible, it could also be applied retrospectively. It is suggested that
monitoring is continued until 2008, twenty years after the incident, and that the burden of this work is
removed from the local primary care trust and is, in future, carried out by an academic department
familiar with the analysis of routine health statistics.
B. Toxicological studies
1.37 The toxicological data on aluminium, although extensive, is insufficient to make a definitive hazard
assessment. There is a need for further work on the toxicity of aluminium, including:
• studies to identify No Observed Adverse Effect Levels for aluminum salts using both acute and chronic
exposure and a range of salts of different bioavailabilities
• mechanistic data on the neurotoxicity of aluminium and of its potential role in neurological disease and
other disorders such as macrophagic myofasciitis
• further investigations of the bioavailability of aluminium in humans, including of the reasons for the
reported interindividual variation.
C. Future handling of similar incidents
1.38 There have been considerable improvements in contingency arrangements for and the management of
any future chemical incidents since 1988. However, it is noted that the following areas may require
particular consideration in the management of a future incident of the type which occurred in Cornwall:
• the early identification of populations which may need to be monitored in any later epidemiological
studies
• rapid, widespread dissemination of clear and accurate advice. Individuals should be informed about
what has happened, the likely consequences and any action they may need to take as promptly as

result from exposures of the degree and short duration that occurred after this incident. Although the
possibility of effects due to the interaction of these chemicals cannot be wholly excluded, we can find
no supportive evidence. Increased absorption of aluminium may have occurred in some individuals who
persisted in drinking the heavily contaminated water. However, all the available evidence suggests that
such increases would have been transient, with most of the aluminium being excreted rapidly and only
trace amounts being deposited in tissue, chiefly bone. All the known toxic effects of aluminium are
associated with chronically elevated exposure and we have concluded therefore that delayed or
persistent effects following such brief exposures are unlikely. In our view it is not possible to attribute
the toxic effects of the incident except insofar as they are a consequence of the sustained anxiety
naturally felt by many people.”
2.3 The report also made a series of recommendations about the future handling and follow-up of similar
incidents (Lowermoor Incident Health Advisory Group, 1989).
2.4 In October 1990, following representations from the local community, some of whom continued to
attribute health problems to the incident, LIHAG was reconvened with the following terms of reference:
“To assess reports which have become available since July 1989 of persistent symptoms and
clinicopathological findings amongst people who were resident in the Camelford area at the time of the
Lowermoor incident; and to advise the Department of Health and the Cornwall and Isles of Scilly
District Health Authority on the implications of its findings.”
21
2. Introduction
78933-COI-Toxic-Lowermoor ch1-4 21/1/05 10:58 pm Page 21
2.5 The second report, which was published in November 1991, concluded that:
“The research reported to us does not provide convincing evidence that harmful accumulation of
aluminium has occurred, nor that there is a greater prevalence of organic abnormalities in the exposed
population. We do not expect lasting physical harm from the toxicity of the contaminated water itself
Nevertheless, the incident was unique, and the actual doses of aluminium and other contaminants
received by the residents are unknown; therefore, although we have no reason to predict any late
consequences, we cannot exclude them completely.
We still have no doubt that the accident itself and subsequent events have led to real mental and
physical suffering in the community. We emphasize that we do not believe that people in the

2.8 In 2001, in response to representations from members of the local community that the health consequences
of the incident had not been properly addressed, Health and Environment Ministers asked the Chief Medical
Officer’s independent expert advisory committee, the Committee on Toxicity of Chemicals in Food,
Consumer Products and the Environment (COT), to advise on whether the pollution incident had resulted in
delayed or persistent health effects, and on the need for additional monitoring and research (Department of
Environment, Food and Rural Affairs, 2001). The COT set up a Subgroup, the Lowermoor Subgroup (LSG),
under the Chairmanship of Professor HF Woods CBE, to undertake this task. The Subgroup held its first
meeting on 16 October 2001. However, due to delays in the appointment of the secretariat and of the local
representatives, the Subgroup could not begin substantive work until January 2002.
Terms of Reference of the COT Lowermoor Subgroup
2.9 The Subgroup had 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.”
Membership of Subgroup
2.10 The membership of the Subgroup is given in Appendix 1. Professor Woods, a clinical pharmacologist and
chairman of the COT between 1992 and 2002, chaired the Subgroup. Membership of the Subgroup
comprised a public interest representative, two local representatives, a consultant physician, a
paediatrician, and scientists with expertise in toxicology and epidemiology. The Subgroup was supported
by a secretariat from the Department of Health.
2.11 The membership of the Committee on the Toxicity of Chemicals in Food, Consumer Products and the
Environment is given in Appendix 2.
Methods of Working
2.12 Our investigation comprised:
• A reassessment of evidence previously seen by the Lowermoor Incident Health Advisory Group
(LIHAG).
• A reassessment of the data on water quality with particular attention to the concentrations of, and the
exposures to, aluminium, copper, lead, zinc, manganese, iron, sulphate and hydrogen ions.
• A consideration of background information on the prevalence and causes of symptoms and diseases

of scientific rigour with which the different types of information were collected and analysed affects the
confidence with which conclusions can be drawn. We have laid out, in the introductions to the relevant
chapters, the strengths and weaknesses of the information received in the course of our investigation and
the ways in which different data have been used. We have also considered the strengths and weaknesses
of study design and conduct when assessing the quality and reliability of particular scientific data and
papers, and have discussed these aspects in this report (see Appendix 4 for a detailed discussion of the
principles we have followed in assessing information). The review methodology used has depended upon
the nature of the data under consideration.
24
COT Lowermoor Subgroup
78933-COI-Toxic-Lowermoor ch1-4 21/1/05 10:58 pm Page 24
Dates of meetings and visits
2.14 We convened 19 committee meetings on the following dates: 16 October 2001, 22 January 2002, 3 April
2002, 29 May 2002, 16 July 2002, 30 September 2002, 19 November 2002, 27 January 2003, 10 March 2003,
19 May 2003, 7 July 2003, 15 September 2003, 24 November 2003, 9 February 2004, 29 March 2004, 7 June
2004, 26 July 2004, 6 September 2004 and 14 December 2004.
2.15 We held a public meeting in Camelford on 3 April 2002, at North Cornwall District Council Offices, in
order to introduce the work of the Subgroup to the local population. The visit to the Lowermoor Water
Treatment Works and discussion with local individuals took place on 4th April 2002. Subsequently, visits
to Camelford were made by the Chairman and members of the Subgroup and secretariat on 19 July 2002,
6 and 7 May 2003, 22 July 2003, and 27 and 28 October 2003.
2.16 The Subgroup agreed to a request by the Department of Health that the agendas and minutes of
meetings, once cleared by the Chairman, would be placed on the Department’s website
(http://www.advisorybodies.doh.gov.uk/cotnonfood/lowermoor.htm). However, where evidence was
submitted ‘in confidence’ from interested parties and groups, confidentiality was observed.
25
Consultation Report January 2005
78933-COI-Toxic-Lowermoor ch1-4 21/1/05 10:58 pm Page 25