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. 2000 May 13;320(7245):1337.

Cerebral dysfunction after water pollution incident in Camelford

Results were biased by self selection of cases

Anthony David 1
PMCID: PMC1127323  PMID: 10885914

Editor—Altmann et al's results on a group of litigants were published almost 10 years after the water pollution incident in Camelford.1 Although they acknowledge competing interests, they overlook the main problem—the bias inherent in self selection of cases.

The cases may have already had unexplained symptoms and cognitive problems, the incident serving to focus attention on a possible cause. The results show significant impairment in neuropsychological and neurophysiological tests among the cases, which the authors argue must be the result of prolonged toxicity to acute exposure to aluminium in drinking water. Neuropsychological tests are assumed to be objective, automated, computerised, and quantitative, but they do require the conscious effort of subjects. Those complaining of poor memory and concentration are given a test that requires both, so performance cannot be taken at face value. Subjects are not carrying out a deliberate deception, but their performance like everyone else's is influenced by the context. Similarly, the choice of relatives as controls is unfortunate. Out of loyalty, they will tend to give more than their best, thus widening the gulf in performance.

Sensory evoked potentials are less liable to such effects. The authors report an increased latency in “flash minus pattern” evoked potential (EP), an index of cognitive impairment in patients with Alzheimer's disease and aluminium related dialysis dementia. Their data are inadequate for evaluating this finding since neither the raw latencies for the controls nor the waveforms for the cases are given. 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 occurs reliably 100 ms after the onset of the stimulus. The response to flash is characteristically longer, by around 20 ms in normal subjects, more in those with brain disorders.2,3 The table compares results in four groups.14 It shows that the latency of the flash EP is not prolonged in the Camelford cases but that the increased difference between the two measures is accounted for by the apparent quickening of the patterned VEP. The most parsimonious explanation for this unphysiological result is a calibration error and wandering baseline.

The reopening of the Camelford case is regrettable as the people concerned may worry anew about their health. Wessely and I recommended that incidents such as these should trigger a rapid response by public health professionals to gather complete data before litigation, media attention, and local fears distort health perception.5 It seems that such lessons have still to be learnt.

Table.

Latencies (in ms) for visual evoked potentials (VEPs) in published studies. Values are means (SE) in studies by Altmann et al and means (SD) in the others

Reference Patterned EP latency Flash EP latency Difference
Altmann et al1 (Camelford):
 Cases (n=28) 93.5 (0.9) 119.8 (2.6) 27.3 (1.64)
 Controls (n=42) NK NK 18.6 (1.47)
Altmann et al4 (dialysis):
 Cases (n=10) 101.8 (3.2) 133.4 (2.4) 31.6 (4.3)
 Controls (n=22) NK NK 19.4 (2.4)
Philpot et al2:
 Elderly normal subjects (n=13) 106 (11) 128 (11) 21 (15)
 Elderly subjects with mild memory impairment (n=12) 105 (5) 129 (10) 24 (11)
 Elderly subjects with dementia (n=12) 110 (6) 137 (10) 26 (8)
Sloan et al3:
 Elderly normal subjects (n=40) 100.5 (7.5) 140.5 (13.8) 40.0*
 Elderly subjects with major depression (n=32) 104.3 (11.7) 153.0 (15.8) 48.7*
 Elderly subjects with Alzheimer's dementia (n=30) 101.7 (14.7) 152.5 (19.1) 50.8*

NK=not known. 

*

SD not given. 

References

  • 1.Altmann P, Cunningham J, Dhanesha U, Ballard M, Thompson J, Marsh F. Disturbance of cerebral function in people exposed to drinking water contaminated with aluminium sulphate: retrospective study of the Camelford water incident. BMJ. 1999;319:807–811. doi: 10.1136/bmj.319.7213.807. . (25 September.) [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2.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. doi: 10.1016/0168-5597(90)90053-g. [DOI] [PubMed] [Google Scholar]
  • 3.Sloan EP, Fenton GW. Serial visual evoked potential recordings in geriatric psychiatry. Electroenceph Clin Neurophys. 1992;84:325–331. doi: 10.1016/0168-5597(92)90085-p. [DOI] [PubMed] [Google Scholar]
  • 4.Altmann P, Dhanesha U, Hamon C, Cunningham J, Blair J, Marsh F. Disturbance of cerebral function by aluminium in haemodialysis patients without overt aluminium toxicity. Lancet. 1989;ii:7–12. doi: 10.1016/s0140-6736(89)90254-7. [DOI] [PubMed] [Google Scholar]
  • 5.David AS, Wessely SC. The legend of Camelford: medical consequences of a water pollution accident. J Psychosom Res. 1995;39:1–9. doi: 10.1016/0022-3999(94)00085-j. [DOI] [PubMed] [Google Scholar]
BMJ. 2000 May 13;320(7245):1337.

Study has several methodological errors

T F G Esmonde 1

Editor—Altmann et al conclude that some people who lived in Camelford when water supplies were contaminated with aluminium sulphate have suffered “considerable damage to cerebral function.”1-1 This conclusion is wrong for several reasons.

The design of the study is flawed in selecting as cases people who believed that they had suffered damage and who would therefore be more prone to show errors in psychological tests which they knew were designed to show abnormalities. The authors then used as controls siblings living in a different part of the United Kingdom and presumably unaffected by any similar poisonings. Why did they not use siblings who had been exposed but did not complain of any cognitive difficulties? Fifteen sibling pairs is a small sample size and means that significant differences between the groups are more likely to be found, but this possible bias is not taken into account by the authors.

The authors emphasise the finding of a significant difference between the cases and controls in the absolute differences between pattern and flash evoked visual responses. However, they do not give any absolute values for the latencies for either method of stimulation. Thus whether the increase in difference between the two stimuli was because of a reduction in latency with one form of stimulation or an increase in the other is uncertain. Interpreting a prolongation in latency is difficult and was not attempted. If aluminium causes direct neuronal death, why would this lead to slowing of conduction along the axons of the optic nerves? Would not a reduction in the amplitude of the response be more likely? They raise the contentious link between Alzheimer's disease and aluminium but do not mention that abnormalities in visual evoked response are not observed in Alzheimer's disease.

There is scant comment on the concentration of aluminium in current tap water samples from the area described as high and no indication of aluminium concentrations in the controls or their tap water.

The authors also dismiss the effects of underlying anxiety as a cause of the observed phenomena on the basis of a low SCL90 score, but almost 35% of their study population did not attend for testing.

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 methods. It would be wrong to conclude that this study substantiates the claims that these people's symptoms are due to direct toxic effects of aluminium poisoning.

References

  • 1-1.Altmann P, Cunningham J, Dhanesha U, Ballard M, Thompson J, Marsh F. Disturbance of cerebral function in people exposed to drinking water contaminated with aluminium sulphate: retrospective study of the Camelford water incident. BMJ. 1999;319:807–811. doi: 10.1136/bmj.319.7213.807. . (25 September.) [DOI] [PMC free article] [PubMed] [Google Scholar]
BMJ. 2000 May 13;320(7245):1337.

Study may prolong the agony

T M McMillan 1

Editor—Altmann et al conclude that poisoning with aluminium sulphate in Camelford 10 years ago “probably led to long term cerebral impairment.”2-1 Media attention immediately after this paper was published led to speculation about damage to children and unborn fetuses at the time and possibly a further round of litigation. The results of this paper were, however, obtained under the instruction of plaintiffs' solicitors in the earlier round of litigation, which ended in 1994 with small out of court settlements (average £2000), and they are not new evidence.

Some people exposed to polluted water in Cornwall in July 1988 may have developed brain damage,2-2 but the absence of physiological measures of absorption of aluminium and other toxins at the time of the accident 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 its conclusion unwarranted. Methodological flaws include use of a highly self selected group of litigants and sibling controls, which is a source of bias, as described by David and Esmonde (above) and by Fahy in bmj.com (bmj.com/cgi/eletters/319/7213/807/DC1#EL3).

Altmann et al persist in using the unrevised normative data for the national adult reading test, which is used to estimate premorbid ability. Revised normal values for this test were published in 1991 and are used throughout the United Kingdom; by using the outdated version Altmann et al overestimate IQ in the patient group, increasing the likelihood of finding a decrement in tests of current ability.

They must also be criticised for not discussing in depth the two key papers on such incidents.2-3,2-4 Neither do they defend the use of evoked potentials, given the criticisms levelled specifically at their work in the second report of the Clayton committee.2-5

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 with an age matched non-exposed group of Cornish children in 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.2-6

I agree with David (previous page) that it is regrettable that psychological wounds may be reopened in North Cornwall at such a late stage and seemingly without good reason. I hope, however, that plans have been made for early systematic assessment of exposure and any physical and psychological sequelae in the event of future accidents.

References

  • 2-1.Altmann P, Cunningham J, Dhanesha U, Ballard M, Thompson J, Marsh F. Disturbance of cerebral function in people exposed to drinking water contaminated with aluminium sulphate: retrospective study of the Camelford water incident. BMJ. 1999;319:807–811. doi: 10.1136/bmj.319.7213.807. . (25 September.) [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2-2.McMillan TM, Freemont AJ, Herxheimer A, et al. Camelford water poisoning accident: serial neuropsychological assessments and further observation on bone aluminium. Hum Exp Toxicol. 1993;12:37–42. doi: 10.1177/096032719301200108. [DOI] [PubMed] [Google Scholar]
  • 2-3.David AS, Wessely SC. The legend of Camelford: medical consequences of pollution accident. J Psychosom Res. 1995;39:1–9. doi: 10.1016/0022-3999(94)00085-j. [DOI] [PubMed] [Google Scholar]
  • 2-4.Campbell D, Cox D, Crum J, Riley A. Later effects of the grounding of the tanker Braer on health. BMJ. 1994;309:773–774. doi: 10.1136/bmj.309.6957.773. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2-5.Clayton B Lowermoor Incident Health Advisory Group. Water pollution at Lowermoor, North Cornwall. Second report. London: HMSO; 1991. pp. 22–23. [Google Scholar]
  • 2-6.McMillan TM, Dunn G, Colwill SJ. Psychological testing on children before and after pollution of drinking water in North Cornwall. J Child Adolesc Psychiatry. 1993;34:1449–1459. doi: 10.1111/j.1469-7610.1993.tb02102.x. [DOI] [PubMed] [Google Scholar]
BMJ. 2000 May 13;320(7245):1337.

Inappropriate study, inappropriate conclusions

Virginia Murray 1,2, Faith Goodfellow 1,2, Richard Bogle 1,2

Editor—We believe that the design and experimental technique limit the conclusions of Altmann et al about cerebral dysfunction in the Camelford incident of 1989.3-1 In addition, their study does not report on the subsequent developments to respond to or prevent a similar incident.

In 1988 the domestic water supply of 20 000 people in the Lowermoor area was contaminated with aluminium sulphate. Much of the information on the adverse health effects arising from the exposure was obtained from self reported questionnaires that may not have been completed by a representative sample of the local population.3-2 In the study of Altmann et al the 55 cases were also a self selected group. Differences in psychomotor tests and visually evoked potentials (VEP) were found when cases were compared with unmatched controls and the cases' siblings, but VEP were measured in only half of the cases. In addition to the issues raised by David, Esmonde, and McMillan in the previous letters, differences in VEP have also been observed in major depression3-3 and the study group was not formally evaluated psychologically.

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 five providers in the United Kingdom 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.3-4 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. A report was written after the Camelford incident by an independent non-executive director of the South West Water Authority which made recommendations to prevent a similar incident occurring in the future. These recommendations were largely concerned with the control of access to water treatment plant and control of chemical deliveries.3-5

The government sent copies of the report to the chief executives of all water authorities, who were then obliged to inform the 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.

Footnotes

Created by potrace 1.16, written by Peter Selinger 2001-2019 The study authors were asked to reply but did not do so in time for publication here.

References

  • 3-1.Altmann P, Cunningham J, Dhanesha U, Ballard M, Thompson J, Marsh F. Disturbance of cerebral function in people exposed to drinking water contaminated with aluminium sulphate: retrospective study of the Camelford water incident. BMJ. 1999;319:807–811. doi: 10.1136/bmj.319.7213.807. . (25 September.) [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3-2.Lowermore Incident Health Advisory Group. Water pollution at Lowermoor, North Cornwall. London: HMSO; 1989. [Google Scholar]
  • 3-3.Sloan E, Fenton G. Serial visual evoked potential recordings in geriatric psychiatry. Electroenceph Clin Neurophys. 1992;84:325–331. doi: 10.1016/0168-5597(92)90085-p. [DOI] [PubMed] [Google Scholar]
  • 3-4.Irwin DJ, Cromie DT, Murray V. Chemical incident management for public health physicians. London: Stationery Office; 1999. [Google Scholar]
  • 3-5.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. London: Department of the Environment; 1988. [Google Scholar]

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