Disturbance of cerebral function in people exposed to drinking water contaminated with aluminium sulphate: retrospective study of the Camelford water incidentBMJ 1999; 319 doi: https://doi.org/10.1136/bmj.319.7213.807 (Published 25 September 1999) Cite this as: BMJ 1999;319:807
All rapid responses
EDITOR- Altman et al1 described sequelae of the Camelford water
incident that suggest the possibility that ingestion of aluminum-
containing water causes brain damage. However, consideration of a variety
of methodological and interpretational issues raises serious questions
about the validity of their findings.
Subjects were volunteers with unverified exposure to aluminum
Since this study was commissioned by attorneys who were acting on the
behalf of plaintiff's in a lawsuit, the potential monetary gain to be
derived from claiming such exposure must be considered as a potential
influence on self classification. Moreover, the base rates of cognitive
symptoms in the general population are not insignificant.
Testing such self-selected subjects increased the probability of a
disproportionately high representation of cognitively-impaired people in
the exposure group.
The cognitive assessment suffered from several weaknesses including
the omission of an assessment of depression, and tests of symptom
validity. Depression can lead to psychomotor slowing as well as
impairment of memory, attention and executive functioning2. This is
particularly important since an earlier study of persons claiming
aluminum exposure at Camelford indicated increasing incidence of
depression over time3. In view of the monetary incentive to appear
impaired, some efforts should have been made to detect malingering.
Although there are shortcomings in such tests, they are usually effective
in discriminating the more obvious examples of symptom exaggeration4.
An additional problem was the use of the Bexley Maudsley Automated
Psychological Screening (BMAPS) as the method for evaluating cognitive
functioning. BMAPS is a screening device in which an abnormal score is
taken as the indication of the need for neuropsychological testing.
However BMAPS does not substitute for such testing3 and, as a screening
device, should not be used to diagnose impairment.
The primary distinguishing feature of the exposure group was inferior
performance on the digit- symbol test. However such abnormal results are
not specific to the effects of brain injury. Impairments on this test can
be caused by a variety of factors including, but not limited to,
depression, untreated hypertension and lack of aerobic exercise5.
The authors recorded visual evoked potentials suggesting that these
"...measurements, carefully administered, are extremely objective and not
subject to the individual's wish to underperform." Unfortunately, visual
evoked potentials are no more immune from the effects of intentional under
-performance than are neuropsychological tests and can
also be affected by emotional state and a variety of commonly used
In summary, the Altman et al1 study has several methodological
shortcomings that, considered individually, raise serious concerns.
Taken together, these weaknesses are sufficiently significant to preclude
meaningful interpretation of this study's conclusions.
Theodore I. Lidsky
head, laboratory of electrophysiology
Department of Psychobiology, New York State Institute for Basic Research
in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New
York, 10314 USA
1. Altman P, Cunningham J, Dhanesha U, Ballard M, Thompson J, Marsh
F.Disturbance of cerebral function in people exposed to aluminium sulfate:
retrospective study of the Camelford water incident. BMJ 1999:319:807-11.
2. Alexander M, Benson F, Delis DC, LaRue A, Meador K, Ponton MO, et
al. Assessment: neuropsychological testing of adults. Considerations for
neurologists. Neurol 1996:47:592-9.
3. David AS., Wessely S.C. The legend of Camelford: medical
consequences of a water pollution accident. J Psychosom Res
4. Hinnant D, Tollison CD. Impairment and disability associated with
mild head injury: medical and legal aspects. Sem in Neurol 1994:14:84-9.
5. Lezak MD. Neuropsychological Assessment. Third Edition. New York,
Oxford University Press, 1995.
Competing interests: No competing interests
Esmonde, David, Fahy and McMillan make a number of comments
about the paper in their separate letters, many of which overlap and are
Time interval between incident and our study
We strongly support Professor David's statement that incidents
like Camelford should trigger a rapid and co-ordinated response from
appropriate health professionals. Unfortunately this did not happen after
Camelford and as stated in our paper it was not until three years later
that we were asked to perform these studies, although at that time we
ourselves anticipated that such a delay would favour negative
investigation results. We were surprised by the results of our studies.
Competing interests of authors
In our paper we openly acknowledged that our study was
commissioned by lawyers acting for the plaintiffs and funded through Legal
Aid. This legal action constrained the nature of our study but we do not
believe it biased our conduct consciously or unconsciously. The legal
action affected, in particular, our own wish to study other relevant
groups of randomly selected subjects such as those affected by anxiety,
asymptomatic exposed and non-exposed (to the water contamination) control
subjects, as well as randomly selected exposed individuals irrespective of
symptoms. These suggestions were made to the lawyers. It was also as a
result of the legal action that there was delay in publishing the work.
As we had to accept the constraints imposed upon us and mindful
of previous reports concerning Camelford complainants, we tried to design
a study in which the tests were as objective as possible and could be
compared with our previous studies of dialysis patients. In this way we
hoped to obtain data of clinical and scientific interest. If we had had a
completely free hand we would have studied the additional subjects
discussed above. We have not been engaged to represent the claimants we
studied or others in subsequent legal actions.
The question of competing interests was discussed at length with
the editorial staff of the BMJ before the paper went to print. The details
regarding the commissioning and funding of the studies are explicitly
discussed in the paper and there were no competing interests according to
the guidelines published by the BMJ.
In our paper we expressed our own concerns over the possibility
of experimental bias caused by the interests of participants who alleged
they were symptomatic. We emphasised that it was the pattern of the
results obtained in the psychometric testing, combined with the results of
the visual evoked responses and the similarity of these to our previous
findings in dialysis patients which was important and suggested that the
Camelford subjects had suffered from exposure to an acute toxic insult. We
therefore suggested that "aluminium poisoning must be considered a
possibility, although other contaminants may have contributed."
One of the reasons why we had chosen the battery of tests from
the Bexley Maudsley package (following advice from clinical psychology
colleagues) was that the symbol digit coding test is particularly
sensitive to organic brain disease. In addition, the manner in which it
tests psychomotor function is subtle to the subject being tested compared
to the more overt tests of memory such as the verbal recognition and
visual spatial recognition memory tests. Both in these and our previous
studies, subjects commented, after testing, that the visual spatial
ability, visual perceptual ability, verbal recognition memory and visual
spatial recognition memory tests were far more daunting and difficult than
the symbol digit coding test. No mention regarding the sensitivity of the
tests was ever made to the subjects and none had any prior knowledge of
what type of testing was going to be done. The tests were run in a calm
but most rigorous and uniform manner, and before each test the subject was
given time to rest and it was explained that they should perform as fast
and accurately as possible. Individuals who have early organic brain
disease exhibit the pattern of abnormality exactly as described in this
Camelford group - a pattern that has been used repeatedly in other studies
of psychomotor function in a variety of contexts including potentially
psychotropic drugs. If litigation-motivated bias had been operating then
one would expect the subject to under-perform on the tasks most overtly
related to memory rather than in the symbol digit coding test. As this was
not the case there is no evidence that such bias affected these results.
The purpose of choosing unexposed siblings, who denied exposure
to neurotoxins or psychotropic drugs of any type, was to provide genetic
(phenotypic) controls as this is a standard way of establishing
abnormalities which might be acquired rather than inherited. There were
only 15 available such siblings and so this was the number that we had to
accept - it would have been wrong not to proceed with this part of the
study and, indeed, we have not been criticised for this or the statistics
thereon by medical statisticians
We did not discuss the very small number of abnormal tap water
aluminium levels as this clearly was open to bias. The samples were posted
to us by the subjects in containers that we gave them. Because we were not
in a position to sample their tap water ourselves we felt that these data
could not be regarded as 100% reliable, and as there were no elevated
serum aluminium levels, we did not follow these up except to recommend to
the patients that they have their water systems overhauled.
We addressed the issue of possible effects from anxiety not just
through the finding of relatively low levels of anxiety, but more
importantly by finding no relationship between the absolute levels of
anxiety, as measured by the SCL90 score, and the parameters we measured.
In response to Professor David's comments concerning technique we
merely wish to observe that Dr Dhanesha is a fully qualified clinical
neurophysiologist, having trained under the directorship of Professor G
Harding in the Clinical Neurophysiology Unit at Aston University,
Birmingham where she did her PhD studies on visual evoked subcortical
potentials (Aston University 1986). The wave forms were analysed in
exactly the same way as in our previous publications and in the manner
described in many publications from Professor Harding's group.
There is, as we stated, very little normative data published on
large series of visual evoked potential results, either flash stimulated
or pattern stimulated or the difference in timing between them.
It is possible that in a given subject the flash-pattern
difference may be large because of a quicker pattern latency than
"normal". However, as we have remarkably little information about what is
normal we chose to use the difference between the two types of visual
evoked potential and not the absolute measures. In many studies looking at
the relationship between severity of dementia and visual evoked
potentials, it is noteworthy that it is the flash-pattern difference that
correlates rather than absolute values.
Indeed, the magnitude of the flash-pattern difference was
significantly correlated with the magnitude of the symbol digit coding
abnormality (but not the other Bexley Maudsley tests), as in dialysis
patients where it was also related to cumulative aluminium exposure.
If there was a functional relationship between the two types of
visual evoked responses one might expect the two measurements to
correlate, whereas if they were independent of each other there should be
little or no relationship. In our studies there was a very significant
relationship between these two parameters in normals, which was nearly
absent in the Camelford "victims" and completely absent in our dialysis
How aluminium exposure might lead to this effect on visual
evoked potential is not an area that we addressed in this or previous
papers, but there is no reason to suppose that aluminium toxicity is
manifested solely by causing neuronal death.
We acknowledged the controversy about aluminium and Alzheimer's
disease, but there is no controversy about the potential for aluminium to
be neurotoxic. There are many published reports of visual evoked potential
abnormalities of the sort that we have discussed in dementias including
Alzheimer's disease, some of which were referred to in our paper.
Professor David misquotes our data in his table - we did not
quote absolute latencies for the 55 adults - the 28 cases he quotes were a
separate quality control study and he refers to SD (standard deviation)
where we used SE (standard error), and it is therefore unclear whether the
other data quoted in his table refers to means with SDs or SEs. In
addition there is no mention of the SDs or SEs in the bottom panel of the
table. Our dialysis studies included 16 patients (see reference 24 of web
version paper), and there are no descriptions of pathologically short
pattern evoked visual evoked reponses in the literature.
The ethics of medical publications
Finally, although we were concerned about the possible effects
that the publication of our paper might have on people who were involved
in the Camelford incident, it would have been wrong to withhold it. Had
our studies not been designed to provide scientifically useful information
(despite the inevitable limitations), and only been used to satisfy the
legal process, then the clinical and scientific communities would have
been deprived of results that we find interesting and worthy of debate,
and which we believe are valid.
It is unlikely that another Camelford will occur, so the
opportunity to study the effects will, we hope, not recur.
Competing interests: No competing interests
Could a chemical incident resulting in water contamination such as
Camelford happen again? We believe that the conclusions of Altmann et al
(1) about cerebral dysfunction are limited by design and experimental
technique. In addition their study does not report on the subsequent
developments to respond to or prevent a similar incident happening again.
In 1988, the domestic water supply of 20 000 people in the Lowermoor area
was contaminated with aluminium sulphate.
However much of the information on the adverse health effects arising from
the exposure were obtained from self-reported questionnaires that may not
have been completed by a representative sample of the local population
(2). In Altman’s study the 55 cases were also a self-selected group.
Differences in psychomotor tests and visually evoked potentials (VEP) were
found when they were compared to unmatched controls and the cases’
siblings but VEP were only measured in half the cases.
Amongst other issues already raised, differences in VEP have also been
observed in major depression (3) and there was no
formal psychological evaluation of the study group.
A timely response to assess the impact of any chemical incident on a
population is essential. Since 1996 health authorities have been required
to have contracts with chemical incident service provider units. The
Chemical Incident Response Service is one of the five UK providers and has
contracts with all health authorities in six of the eight English Regions.
Incident identification and
management has pointed to the need for early response with appropriate
collection of biological and environmental samples, usually within hours
of exposure. These issues are discussed by public health physicians
attending training courses and supported by relevant guidance material,
including a recent handbook (4). With continuing surveillance to monitor
response effectiveness methods are now in place to prevent the delays in
investigation identified in the Camelford incident.
All water utilities have also responded to the lessons learnt from
Camelford. Following the Camelford incident a report was written by an
independent non-executive director of the South West Water Authority which
made recommendations to prevent a similar incident occurring again in the
future. These recommendations were largely concerned with the control of
access to water treatment plant and control of chemical deliveries (5).
The Government sent copies of the report to the Chief Executives of all
water authorities, who were then obliged to inform Government of the
management and operating procedures they had put in place to implement the
recommendations. In addition, water utilities are now required to inform
health authorities immediately
about any customer health concerns or operational incidents.
Dr Virginia Murray,
Director, Chemical Incident Response Service
Research Engineer – Water, Chemical Incident Response
Medical Toxicology Unit Laboratory
Dr Richard Bogle,
Chemical Incident Response Service
Medical Toxicology Unit,
Guy’s and St Thomas’ Hospital Trust,
Avonley Road, London SE14 5ER
1. Altmann, P, Cunningham, J, Dhanesha U, Ballard M, Thompson, J,
Marsh F. BMJ 1999; 319:807-11.
2. Lowermore Incident Health Advisory Group. Water pollution at
Lowermore, North Cornwall. London: HMSO, 1989.
3. Sloan E, Fenton G. Serial visual evoked potential recordings in
geriatric psychiatry. Electroenceph Clin Neurophys. 1992; 84:325-331
4. Irwin DJ, Cromie DT, Murray V. Chemical incident management for
public health physicians. The Stationery Office, 1999
5. Lawrence, J. The Report of an Inquiry into the Lowermore Incident,
6 July 1988. Produced by South West Water
Authority for the Department of the Environment. 12/8/88.
Competing interests: No competing interests
I was interested in Altmann's article with reference to whether
neurodegenerative disease has been triggered in people exposed to the
quite elevated levels of aluminum during the accidental aluminum sulfate
Since it has been about eleven years since the incident, long term effects
may become evident.
With reference to epidemiology, has there been a greater incidence of
development of neurodegenerative disease such as Alzheimer's disease in
the people exposed? Elderly people could be particulary vulnerable to
such an aluminum exposure since it may have effects on brain free radical
status and they would be less able to compensate.
Reviewing admissions to nursing homes in the area could provide some
information with reference as to whether those exposed to aluminum
contaminated drinking water have a greater chance of developing dementia.
With reference to the neuropsychological and neurophysiological
studies referred to in the article, it appeared the studies were geared to
detecting changes in a population of people rather than individual
It is not uncommon in the clinic to see patients with complaints about
impaired memory and concentration.
Ordinarily such complaints are in the context of impairments of activities
of daily living or with reference to difficulties with employment.
Specific investigations to determine if a patient has something wrong with
them are usually performed. Neuropsychological tests certainly have value
especially when retesting can be performed over a period of time to see if
there is progressive deterioration or if there is a static condition.
Ordinarily I also find brain imaging studies such as CAT scanning or MRI
scanning can be quite valuable to see if there is cerebral atrophy,
hydrocephalus or some other anatomic abnormality. In especially difficult
cases where it is some question as to the diagnosis, PET scanning of brain
to see if there are metabolic changes compatible with Alzheimer's disease
or some other neurodegenerative condition such as frontal atrophy, can be
very helpful in determining if there is an alteration in normal brain
function and if a disease process is likely to be occurring.
It appeared the intent of the study was to determine if there were
measurable effects in a population of patients with complaints of altered
mental capacity, however individual attention to the affected patients
might provide valuable information as to whether they experienced effects
such as cerebral atrophy or perhaps even metabolic disturbances of
I am glad the editors chose to publish the study, despite the funding
from a nontraditional source. I believe the public health issues are of
such importance, publishing the article was justified. If studies of the
affected population funded through a more traditional source were
available, then I believe there would be cause for criticism, however
apparently such funding has not been forthcoming. It may be the legal
entanglements have obstructed interest in the scientific and humanitarian
aspects of the situation, however since the contamination has occurred I
believe there is an ethical obligation to investigate the effects
regardless of the outcome.
Steven Brenner MD
Dept. of Neurology,
Cochran Veterans Administration Hospital,
915 North Grand,
St.Louis, Mo. 63106,
Addendum: I do not believe I have any competing interests.
Competing interests: No competing interests
Altmann et al (1) conclude that poisoning with aluminium sulphate in
Camelford 10 years ago 'probably led to long term cerebral impairment', an
opinion which has predictably led to immediate media attention, including
speculation about damage to children and unborn foetuses at the time and
doubtless to some rekindling of psychological distress in this
population. There is a possibility that the paper by Altmann et al will
stimulate a further round of litigation (2). This should be carefully
considered because the evidence presented by Altmann et al was obtained
under instruction of plaintiffs' solicitors in the context of the earlier
round of litigation which ended in 1994, where the out of court
settlements were small (average £2,000) and despite the medias assertions,
the authors have not presented new evidence.
It is possible that some people exposed to polluted water in Cornwall
in July 1988 suffered brain damage (3). However the absence of
physiological measures of absorption of aluminium and other toxins at the
time of the accident has made it impossible for a definite conclusion to
be reached. With regard to persisting complaints attributed to the
accident, the paper by Altmann et al is unhelpful and their conclusion
unwarranted. Methodological flaws include use of a highly self-selected
group of litigants and sibling controls which is a source of bias, however
this and difficulties with interpretation of the evoked potential data
have been described already (4,5,6).
They also persist in using the
unrevised normative data for the National Adult Reading Test, a test which
is used to estimate premorbid ability. The revised norms for this test
were published in 1991 and are used throughout the UK; by using the
outdated version they overestimate IQ in the patient group increasing
the likelihood of finding a decrement in tests of current ability.
addition the authors must be criticised for failing to discuss in depth
the relatively few key papers in this area, such as the thorough review by
David and Wesseley, or implications from other disasters involving
pollution such as Braer (7,8). Perhaps it is because of this that they
rebutt possible psychological causation of symptoms oversimply on the
basis of 'anxiety' self-reporting and really fail to deal with this
Nor do they defend the use of evoked potentials given the
crticisms levelled specifically at their work in the second report of the
Clayton Committee in 1991 (9).
Finally, they do not acknowledge or explain
the absence of effect in the only study on the entire exposed population
(of children) who were compared to an age matched non-exposed group of
Cornish children on routinely administered psychometric tests of
educational attainment given before and after the accident. No evidence
for impairment in the exposed group was found-implying that severe brain
damage was unlikely to have occurred (10).
In accord with David (5) I think that it is regretable that
psychological wounds may be reopened in North Cornwall at such a late
stage and seemingly without good reason.However I do hope that plans have
been made for early systematic assessment of exposure, and any physical
and psychological sequelae in the event of future accidents.
1. Altmann P, Cunningham J, Dhanesha U et al BMJ 1999, 3, 807-811.
2. The Guardian, Friday September 24 1999, p 9 col 1-2.
3. McMillan TM, Freemont AJ, Herxheimer A et al Camelford water
Poisoning Accident: serial neuropsychological assessments and further
observation on bone aluminium. Human Exptal Toxicol 1993,12, 37-42.
4. Esmonde TFG Methodological errors BMJ letters 1999, 319,7213,807
5. David A Camelford: faulty data and faulty assumptions. BMJ
6. Fahy T Competing interests and weak study design undermine
conclusions. BMJ letters 1999, 319,7213,807
7. David A, Wessely SC. The legend of Camelford: medical consequences
of pollution accident. J Psychosom Res 1995, 39, 1-9.
8. Campbell D, Cox D, Crum J et al. Later effects of the grounding of
the tanker Braer on health. BMJ, 309, 773-774.
9. Clayton B Water pollution at Lowermoor North Cornwall. HMSO,
London 1991 pp 22-23
10. McMillan TM, Dunn G, Colwill, S.J Psychological testing on
children before and after pollution of drinking water in North Cornwall.
J. Child, Adolescent Psychiatry, 1993, 34, 1449-1459.
Competing interests: No competing interests
The valuable Camelford Aluminium report (Altmann P et
al BMJ 99:319:807-811) raises more questions than it answers. What was the
outcome of the damages claims?
Your Commentary “This Week” notes that two Inquiries dismissed
complaints. Yet by 1980, after UK-led enthusiasm for Aluminium
Hydroxide therapy in dialysis patients a decade before, we were painfully
aware of water, dialysate and oral aluminium causing neuro- and bone
toxicity, worldwide clinical disasters in dialysis units including ours in
cape Town leading us to abandon aludrox in favour of (Vital) dolomite
(calcium-magnesium carbonate vitamin D) as the ideal oral phosphate
antacid, anti-cramp, anxiolytic and supplement for needed calcium,
magnesium and carbonate.
People do not take medicines (unlike nutritional supplements) unless
ill. Mineral (alum) salts including sulfacrate are taken for symptoms –
dyspepsia, gastritis, diarrhoea etc. It is axiomatic from time
immemorial that chronic dyspepsia means hyperacidity or inflammation of
the upper gastrointestinal tract, and that while absorption of
micronutrients eg B12 may be thereby impaired, the absorption of metals
is increased. So the duplicity of the medicinal Aluminium industry (in
still claiming that their products are safe) is like that of the cigarette
industry - they both know they market
dangerous patented poisons. Like unprocessed foods, long-used naturals
including linseed, dolomite, valerian, st john's wort and perhaps even
marijhuana are safe and cheap in moderate longterm use, which is why they
are not promoted for prescription like the patented statins, margarines,
aluminium and H2 antagonist!
Non-medicinal aluminium intake may arguably now be minimal in
first-world communities, but not if oral aluminium medicines (in
antacids, antidiarrhoeals, aspirin, douches & pastes) are still
Dreisbach RH & Robertson WO, (Handbook of Poisons, 12th Ed,
Lange, Connecticut ) noted p 430-1 that alum salts have an exposure limit
of 2mg/cubic metre, toxicity including encephalopathy, weakness and
Casdorf H & Walker M, (Toxic Metal Syndrome, Avery, NewYork 1994)
notes p 126 that “toxicity of alum is aggravated by insufficiency of zinc,
and excess of arsenic, cadmium, iron, lead, manganese mercury” etc; that
“coffee is the chief source of dietary cadmium, that hyperacidity
promotes aluminium absorption; and that the director of the early FDA Dr
WH Wiley in 1929 wrote that aluminium was universally condemned as a
poison in foods”! So, apart from the controversy over “aluminium in cow's
milk, in tea, in
cooking utensils" ( perhaps harmless) , "aluminosis from air pollution,
and water purification by alum , and Alzheimer' disease”, oral Aluminium
medicines should have been banned as unnecessary years ago, but for the
tenacity of unscrupulous marketeers.
Just as the USA Secretary for Health 40 years ago was dismissed
after he produced the latest FDA report showing that (unlike the biggest
killers of all, smoking and alcohol), marijhuana never kills anyone, and
released on prescription, so cigarettes and aluminium medicines are
still heavily marketted, while marijhuana is proscribed except in a few
states of America..
In the light of the decades of knowledge about (dietary and water)
aluminium poisoning by 1988, the Camelford Commissions, and the various
Authorities that allowed, ignored, and dismissed the poisoning, were
surely prosecuted for negligence and damages?
Neil D Burman MRCP(UK)
retired renal physician,
PO Box 44285, Claremont, 7735 RSA.
Competing interests: No competing interests
The paper by Altmann and colleagues concludes with a statement that
the authors have no competing interests. However, the neuropsychological
assessments which form the basis of the report were comissioned by legal
aid on a group of prospective claimants. The study subjects have overt
competing interests in the form of financial compensation for alleged
injury. Exposed subjects who are not involved in litigation are not
included in this study. Surely this is a remarkably powerful sourse of
bias and competing interest. The small control group of siblings are
hardly a disinterested party.
Legal aid paid for the assessments, and funded the authors in
interpreting results. Were the assessments done as a private practice
arrangement? Have the authors been engaged to represent the claimants in
subsequent court actions? It seems extraordinary that these issues were
not teased out by peer review and addressed in the competing interest
section of the paper.
By publishing a paper with such a weak experimental design, without
these explicit details of competing interest, and without a critical
discussion of the paper in the editorial section, the BMJ publicises and,
in effect, endorses the litigants claims.
Dr Thomas Fahy
Competing Interests: None
Competing interests: No competing interests
Altmann and colleagues(1) have published results on a group of
litigants following a water pollution incident in Camelford almost 10
years after the event. While the authors and the BMJ in its "Editor's
Choice" section acknowledge the competing interests involved, they both
fail to emphasis the main problem, namely the bias inherent in the self
selection of the cases.
Such individuals may have already been suffering
from unexplained symptoms and cognitive problems, or may have had a
propensity to suffer them - the incident merely served to focus their (and
their legal advisers') attention on a possible cause. The results show
significant impairment on neuropsychological and neurophysiological tests
in these "exposed" cases compared to controls, which the authors can only
explain as the result of prolonged toxicity to acute exposure to aluminium
in drinking water. First of all the authors make the mistake of assuming
that neuropsychological tests are objective; automated, computerised and
quantitative though they may be, they require the conscious effort of the
subject. A subject complaining of poor memory and concentration who
wishes to demonstrate the extent of their problems is given a test which
clearly requires both - performance cannot therefore be taken at face
value. This is not to say that the subject is carrying out a deliberate
deception, it is just that their performance is bound to be influenced by
the context. We are all susceptible to this, the best example of which is
the Placebo Effect. It doesn't take much to fall short of 100% effort in a
taxing concentration test. Similarly, Altmann et al's choice of relatives
as controls is unfortunate. Competing influences will play on the them.
Out of loyalty, they will tend to give "110%" - thus widening the gulf
between cases and controls' performance.
Sensory evoked potentials are less liable to such effects. The authors
report an increased 'flash minus pattern' evoked potential latency, an
index of cognitive impairment in patients with Alzheimer's disease as well
as aluminium-related dialysis dementia. The data in the paper are totally
inadequate to enable this finding to be evaluated since neither the raw
latencies are given for the controls nor is a figure illustrating the
waveforms given for the cases. The results hang on the difference between
patterned visual evoked potentials (VEPs) and flash EPs. The VEP is also
known as the P100, since it is a positive potential which occurs reliably,
100msec after the stimulus onset. The response to flash is
characteristically longer, by around 20msec in normal subjects, more in
those with brain disorders. In studies of depressed and demented elderly
patients(3,4) and in Altmann's original 10 dialysis patients(5) the patterned
minus flash EP difference was increased. Data from the Camelford cases and
from other published reports are given below in the table for comparison.
Mean latencies for VEPs (in msecs) in published studies and
____________________________________________________________ SAMPLE Patterned EP Flash EP Difference latency (ms) latency (ms) ____________________________________________________________ Camelford cases (n=28) 93.5 (SD 0.9) 119.8 (SD 2.6) 27.3 (1.64) Controls (n=42)(1) ? ? 18.6 (1.47) ------------------------------------------------------------ Dialysis cases (n=10) 101.8 133.4 31.6 Controls (n=22)(5) ? ? 19.4 ------------------------------------------------------------ Elderly normals (n=13) 106±11 128±11 21±15 Mild memory impairment (n=12) 105±5 129±10 24±11 Dementia (n=12)(3) 110±6 137±10 26±8 ------------------------------------------------------------ Elderly normals (n=40) 100.5 140.5 40.0 Major depression (n=32) 104.3 153.0 48.7 Alzheimer's dementia (n=30)(4) 101.7 152.5 50.8 ____________________________________________________________
It is clear that the flash EP latency is not prolonged, contrary to
the basic assumption of the paradigm, but that the increased difference
between the two measures is accounted for by the apparent quickening of
the patterned VEP. The Altmann group reported P100 latencies at, on
average, 93.5msec; if it had been 100msec, the difference would have been
19.8, a normal result. The most parsimonious explanation for this
extraordinary "hypernormal" response to the patterned VEP is faulty
technique. There are no clinical neurophysiologists as co-authors on the
paper and one wonders whether the VEP equipment used met clinical
specifications. Presumably there had been some "drift" in the
measurements between the 1989 dialysis study and the subsequent
It is regrettable that the issue has been re-opened by this latest report
since there is a danger that the individuals concerned may suffer renewed
worries about their health. On reviewing the whole episode(6) we
recommended that incidents like that at Camelford should trigger a rapid
response by public health professionals, to gather data on the entire
exposed and non-exposed populations, addressing psychological and physical
factors, before litigation, media attention and understandable local fears
distort health perception. It seems that such lessons have still to be
1. Altmann P, Cunningham J, Dhanesha U, Ballard M, Thompson J, Marsh F. BMJ
2. Lowermoor Incident Health Advisory Group. Water pollution at Lowermoor,
North Cornwall, 2nd Report. London: HMSO, 1991.
3. Philpot MP, Amin D, Levy R. Visual evoked potentials in Alzheimer's
disease: correlations with age and severity. Electroenceph Clin
Neurophysiol 1990;77: 323-329.
4. Sloan EP, Fenton GW. Serial visual evoked potential recordings in
geriatric psychiatry. Electroenceph Clin Neurophys 1992;84:325-331.
5. Altmann P, Dhanesha U, Hamon C et al. Disturbance of cerebral function
by aluminium in haemodialysis patients without overt aluminium toxicity.
Lancet 1989;2: 7-12.
6. David AS, Wessely SC. The legend of Camelford: medical consequences of a
water pollution accident. J Psychosom Res, 1995;39:1-9.
Competing interests: ____________________________________________________________SAMPLE Patterned EP Flash EP Difference latency (ms) latency (ms) ____________________________________________________________ Camelford cases(n=28) 93.5 (SD 0.9) 119.8 (SD 2.6) 27.3 (1.64)Controls(n=42)(1) ? ? 18.6 (1.47) ------------------------------------------------------------Dialysis cases(n=10) 101.8 133.4 31.6 Controls(n=22)(5) ? ? 19.4------------------------------------------------------------Elderlynormals (n=13) 106±11 128±11 21±15Mild memory impairment(n=12) 105±5 129±10 24±11Dementia(n=12)(3) 110±6 137±10 26±8------------------------------------------------------------Elderly normals (n=40) 100.5 140.5 40.0Major depression(n=32) 104.3 153.0 48.7Alzheimer'sdementia(n=30)(4) 101.7 152.5 50.8____________________________________________________________
Altman et al have concluded from their retrospective study that some
individuals who lived in Camelford at the time of the incident in which
water supplies were contaminated with aluminium sulphate have suffered
"considerable damage to cerebral function". I believe this conclusion to
be erroneous for several reasons: Firstly, the design of the study is
flawed in its selection of individuals who themselves believed they had
suffered damage, and such individuals would be more prone to demonstrate
errors on psychological tests which they knew were designed to find them
abnormal. The authors then used controls who were siblings living in a
different part of the UK and presumably (though no mention is made)
unaffected by any similar poisonings or neurotoxin exposure. Why did the
authors not use siblings who had been exposed but did not complain of any
cognitive difficulties? Using only 15 sibling pairs is a small sample
size, and makes it more likely to find significant differences between the
groups, but this possible bias is not taken into account by the authors.
Great stress is laid upon the finding of a significant difference
between the cases and siblings in the absolute differences between pattern
and flash evoked visual responses. However, no absolute values of the
latencies for either method of stimulation are given, and thus it is
difficult to be certain whether the increase in difference between the two
stimuli was because of a reduction of latency with one form of
stimulation, or an increase in the other. Interpretation of a
prolongation of latency is difficult, and not attempted in the article.
If the argument is that aluminium causes direct neuronal death, why would
this lead to slowing of conduction along the axons of the optic nerves?
Would it not be more likely that a reduction in the amplitude of the
response would be the expected result? The contentious link between
Alzheimer's disease and aluminium is again raised, and yet the authors
fail to mention that no such abnormalities of visual evoked response are
observed in Alzheimer's.
There is scant comment on the level of aluminium in "current" tap
water samples form the area stated to be "high", and neither is there any
indication of what aluminium levels were like in the sibling controls or
their tap water.
The authors also dismiss the effects of underlying anxiety as a cause
of the observed phenomena, basing this on a low SCL90 score, despite the
fact that almost 35% of their study population did not attend for testing.
In summary, this paper is little more than a series of observations
in a group of people. Evidence of "considerable" cerebral damage is not
evident from the abnormalities on testing, there is no correlation with
the level of day-to-day impairment, and bias abounds in the methodology.
It would be wrong to conclude that this study substantiates the claims
that these individuals' symptoms are due to direct toxic effects of
Competing interests: No competing interests