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Acute health impact of the gas release at Lake Nyos, Cameroon, 1986
Journal o[ Volcanology and Geothermal Research, 39 ( 1989 ) 265-275
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Elsevier Science Publishers B.V., Amsterdam - - Printed in The Netherlands
Acute health impact of the gas release at Lake Nyos, Cameroon, 1986 P E T E R J. BAXTER 1 and M U K E S H KAPILA 2 1University of Cambridge Clinical School, A ddenbrooke's Hospital, Cambridge CB2 2QQ, U.K. 2Cambridge Health Authority, Fulbourn Hospital, Cambridge CBI 5EF U.K. (Received October 2, 1987, revised and accepted January 21, 1988 )
Abstract Baxter, P.J. and Kapila, M., 1989. Acute health impact of the gas release at Lake Nyos, Cameroon, 1986. In: F. Le Guern and G. Sigvaldason (Editors), The Lake Nyos Event and Natural C02 Degassing, I.J. Volcanol. Geotherm. Res., 39: 265-275. Available medical evidence on the acute health impact of the gas release at Lake Nyos is summarised, including the results of a survey of medical records of 845 survivors treated at Wum and Nkambe hospitals. The main clinical features were compatible with exposure to an asphyxiant gas such as C02 but confirmation of the identity of the gas or gases involved was not possible. Exposure to C02 over such a large inhabited area and reversible coma lasting for hours after C02 gassing do not appear to have been reported before. In some victims, blistering or ulceration of the skin was present which could not be readily explained by local injury from pressure, or burns from acid, or falling near fires. Further epidemiological studies on survivors are unlikely to be feasible, but the possibility of long-term anoxic brain damage among adults and children who had been rendered comatose by the gas should be considered, though overt evidence of major neurological or respiratory disability was not apparent in survivors in the weeks following the disaster. The inadequacy of the toxicological and forensic evidence obtained points to the need for the rapid mobilisation of medical scientists in future disasters of this kind.
Introduction Since the historic eruption at the Laki fissure in Iceland in 1783, catastrophic incidents involving human exposure to massive volcanic or natural gas emissions have not been reported to our knowledge (Baxter et al., 1982), with the exception of the gas releases at Dieng Plateau, Java, in 1979 when 146 people died (Le Guern et al., 1982) and Lake Monoun, Cameroon, in 1984 when 35 people succumbed (Sigurdsson et al., 1987). Retrospective geological studies have pointed to CO2 as being the major gas released in the latter incidents, but it is important to emphasise that autopsy and toxicological studies were not performed on the deceased in either 0377-0273/89/$03.50
event. At Dieng Plateau, the gas release was attributed to a phreatic eruption which could have involved other gases as well as CO2, but at Lake Monoun, Sigurdsson et al. (1987) suggested that C02 of volcanic origin had accumulated slowly in the lake over time and was released as a result of a sudden overturning of the stratified waters. Both of these mechanisms have been proposed to explain the catastrophe at Lake Nyos. Unlike the incidents at Dieng and Lake Monoun, the Lake Nyos disaster attracted worldwide attention, and investigative teams which included medical personnel were sent from several countries, including the United States, Israel, Japan and the United Kingdom. Despite this response, the quantity and quality
© 1989 Elsevier Science Publishers B.V.
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of medical information obtained was less than ideal; the reasons for this will be discussed. We report here a summary of our findings from the available medical evidence to assist geologists in determining the nature of the gas or gases released. The medical information is also important to aid officials in determining the needs of survivors and for emergency planning for any future gas release from Lake Nyos or other Cameroon lakes.
B a c k g r o u n d and methods The British team comprised two geologists and one author (P.J.B.) who arrived in the disaster area two weeks after the gas release. By then the emergency was over and survivors were beginning to leave hospital. We held discussions with Government officials and experts, and interviewed relief workers and survivors. The pathology reports of the United States and Japanese teams were made available to us. An environmental appraisal was made at Lake Nyos. M.K. collated the epidemiological data available at the time of his visit six weeks after the gas release, and undertook a study of the records of clinical symptoms and signs in survivors presenting to the hospitals at Wum and Nkambe in the weeks after the incident (a report was submitted to the Cameroon government in October/November 1986). We consulted the report by Dr Daniel Mfonfu (Chief of Epidemiology, Ministry of Public Health, Cameroon) on the signs and symptoms of survivors admitted to the two hospitals, together with over 60 photographs he took of the dead and survivors on August 23 and 24. Other photographic and film material was made available by Helimission, the Cameroon Ministry of Culture and Information, and the BBC. In addition, one of us (M.K.) interviewed 150 survivors over 15 years of age in 5 temporary camps six weeks after the incident, though the representativeness of this sample is not clear. No other medical studies appear to have been undertaken immediately after the disaster on sur-
P.J. BAXTER AND M. KAPILA
vivors who were not admitted to hospital. Any retrospective enquiry in the aftermath of this disaster faced almost insuperable difficulties in obtaining scientific data by interviewing survivors. Because of the numerous local dialects, important differences in meaning may have emerged when interpreters were used and there may be no exact local equivalent for some English words. The use of pidgin English, the lingua franca of Northern Cameroon, does not overcome this problem. Even more important are the profound cultural differences that exist between the scientifically trained outsider and the local people so that the use of a questionnaire, so beloved of epidemiologists, may be of little worth. Responses of the people to direct questioning are likely to be overwhelmingly biased by cultural factors and should be interpreted in the presence of a social anthropologist with considerable local experience so that the value of the responses can be assessed. The journalists and investigators first on the scene seemed to have been unaware of these pitfalls and by the time of our arrival, hospital survivors were able to reproduce suspiciously identical accounts of events and experiences. Thus the information we received via interpreters was treated guardedly and we placed much greater emphasis on the reports from relief workers and the few survivors who spoke fluent English. We did not undertake an epidemiological questionnaire survey of survivors for these reasons.
Results There was general agreement that the gas release began about 9.00-10.00 p.m. on Thursday, August 21, 1986. The precise number of casualties may never be known, but according to Government sources at least 1700 people were said to have died and an estimated 5000 people in the zone either escaped exposure to the gas or survived its effects. The best estimate of the zone affected by the gas, which we obtained from local Roman Catholic missionaries who had observed or received reports on the locations of
ACUTEHEALTH IMPACTOF THE GAS RELEASEAT LAKENYOS,CAMEROON
human and cattle corpses, was an area about 20 km long and 15 km wide (Fig. 1). There was evidence that the gas had primarily affected the valley bottoms, e.g. at Fang; no deaths occurred in that part of the settlement above the valley. It was at least 36 hours before outside help entered the zone, by which time most deaths had already occurred. Information on events during those 36 hours was very sparse. The majority of survivors began entering hospitals at Wum and Nkambe on August 23 and 24, though at Wum 10 survivors reached the hospital as early as August 22. Many of the survivors were picked up by lorry and transported to hospital, though the criteria for admission to hospital was not clear to us. It did seem that the majority, if not all, of the hospital in-patients had lost consciousness at the time of the disaster, and were in any case likely to have been the worst affected. The Israeli medical team and other foreign experts did not start to arrive in the area until one week after the gas release.
Kwana .Nkang
Fig. 1. Area of the mountainous region north of Lake Nyos where gas flowed, according to missionary reports on locations of human and cattle corpses.
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Environmental damage Environmental observations around the lake area showed little damage to vegetation or homes (Fig. 2 ). The taller vegetation had been partially flattened in a few places along the incline between the lake and Lower Nyos. There was no evidence of thermal or acidic damage. A high concentration of sulphur dioxide or its aerosols would undoubtedly have left evidence of vegetation damage and so a lethal concentration of sulphur dioxide is more or less excluded by these findings (W. Winner, pets. commun., 1986). Further away from the lake there were no reports of environmental damage either, providing no obvious clues as to how the scattered human and cattle deaths could have been caused.
Deaths from the gas Unfortunately, the locations, disposition and appearances of corpses were not systematically recorded. Relatives of the dead and emergency workers buried the corpses over the weekend following the gas release, or soon after, and no autopsies were performed at that time. Relief workers stated that numerous corpses had had the appearance of the clothes having been removed during life, presumably in an effort to breath. The insides of some houses were in disarray, indicating confusion or distress on the part of the inhabitants. Some lay dead on their beds, others had reached for torches or gone outside before losing consciousness, a few having managed to reach a short way into the bush. These appearances indicated that people had been rapidly overwhelmed and many had lost consciousness within seconds. Consciousness could have been preserved for some minutes in others while they made efforts to breathe; or lack of oxygen could have led to confusion and inability to move freely. Post mortern changes, which would have been well advanced by the time rescuers entered the zone, could account for the reports of swollen corpses.
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p.J. BAXTERAND M. KAPILA
Fig. 2. Upper Nyos settlement: decomposing cattle corpses lie near homes where six people survived. The gas flowed over the ridge from the lake beyond.
Some corpses were reported to have bled from the mouth and there were conflicting reports over whether some had bled from the nose. Pools of blood were reported close to some corpses, but whether the blood had been vomited or coughed up was not clear. The whites of eyes were mentioned to be reddened, a finding compatible with the suffused conjunctivitis of asphyxiation or inflammation from an irritant gas. Most corpses, however, looked normal, though some had skin lesions resembling burns. Available photographs of these lesions indicate the presence of blisters, in two photographs these were 5-15 cm across. Some children were reported to have defecated. Numerous animal corpses, including cattle, were also found, and some of the latter were also said to have bled from the mouth. There were no reliable data on mortality rates in different parts of the region affected by the
gas, except at Upper Nyos (i.e. the settlement located between the lake and Lower Nyos, or Nyos). Here, six out of 30 people survived. Crude estimates suggest that perhaps one third of the population in and around Subum and one fifth at Cha were killed.
Experience o[ survivors The commonest reported experience from survivors in the Nyos area was that they were going to bed or sitting around fires talking whilst others were asleep when they heard an unusual disturbance outside, such as animals moving or birds fluttering, or the sound of a strong wind. They went out to see what was happening and then smelt 'rotten eggs' or 'gunpowder' before rapidly losing consciousness. There were no feelings of irritation to the eyes and chest, no gagging, choking, coughing or chest pain. Oth-
ACUTE HEALTH IMPACT OF THE GAS RELEASE AT LAKE NYOS, CAMEROON
ers reported a feeling of warmth and difficulty in breathing, or had feelings of suffocation. The duration of unconsciousness appears to have been for hours, rather than minutes, in many survivors. At Upper Nyos one survivor, a 24 year-old Fulani who had received secondary education and spoke fluent English, recalled how, when he had recovered consciousness, it was about 10 hours after the gas release (7 a.m. by his watch) and he was lying outdoors. He helped to revive his father whilst others around him were dead. Survivors stated that people had lost consciousness or had died in the open air or indoors, and the dead and survivors had even been in the same spot when the gas struck. On recovering consciousness survivors had noticed difficulty in breathing or had tightness of the chest for a short period, but no wheeze. A male nurse, who spoke fluent English, related how he was riding on a moped into Cha at about 6 a.m. on August 22 (i.e. approximately nine hours after the gas release) when he suddenly lost consciousness; he woke 1½ hours later gasping, feeling tired and 'drunk', with a headache, and subsequently developed a cough which lasted three days. Some survivors had a mild cough with blood-stained sputum. A boy was noticed to be ill for several days after recovering consciousness, during which time he vomited blood. Over the following days survivors were dazed and many had a cough, but severe chest pains do not appear to have been common. There was no loss of smell or taste such as may occur in poisoning from hydrogen sulphide. Blurred vision or subconjunctival haemorrhages were noted, but marked eye inflammation, another feature of hydrogen sulphide poisoning, was not common.
Clinical findings in survivors Dr. Mfonfu collected data on the 548 in-patients seen in the two hospitals in the two weeks after the disaster. At one hospital 50% and 43% of patients were from Cha and Subum, respectively; at Nkambe 93% were from Subum. There
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was an approximately twofold excess of females over males in 0-4 and 20-39 age groups, a finding which was not explained. One of us (M.K.) reviewed data from patient registers on 845 people attending for treatment at the two hospitals which included the same in-patients, and was able to include information on location at the time of the disaster (Tables 1 and 2). The information recorded included the main clinical features at presentation of each patient and we believe it to be reasonably reliable, though validation is obviously impossible. Nevertheless, our data set and Dr. Mfonfu's showed a very similar pattern of illness, which was found throughout the affected zone, both near and distant to the lake, though the numbers of patients from the areas of Fang and Koskin were small, and data on age and sex were incomplete. A most notable finding was the small number of patients with serious respiratory problems. Severe difficulty in breathing, chest pain and clinical signs indicative of pulmonary oedema (fluid in the lungs caused by severe irritation of the respiratory passages) were remarkable by their absence. Shortness of breath, cough and blood-stained sputum were present in a minority of patients only, and were mild; patchy consolidation of the lungs and not severe pulmonary oedema was suggested on clinical exami nation in about 25% of patients, and these findings were associated with skin lesions (X. Pisoh, pers. commun., 1986). The patients with respiratory problems were treated with antibiotics and the worst affected, with steroids and oxygen. Only three people were diagnosed as having pneumonia and these were at Wum hospital; two of these patients died. Cough and blood-stained sputum had mostly cleared by the third day after admission, though antibiotic treatment was considered to have been important in the recovery of many patients (D. Mfonfu, pets. commun., 1987). Conjunctivitis was recorded in about 3% of patients only. Skin lesions resembling burns were recorded in 19% of the survivors overall and these were mostly redness of the skin. Unequivocal evi-
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P.J. BAXTERANDM. KAPILA
TABLE 1 Clinical symptoms of survivors attending for treatment at Nkambe and Wum Hospitals (including 548 admissions) Symptom
Pre-disaster area of residence
All areas
No. (%) Nyos No. (%)
Subum No. (%)
'Burns' Limb paralysis Limb/jointswelling Eye symptoms Cough Dyspnoea Haemoptysis Vomiting Diarrhoea Bodypains Weakness/malaise Headache Fever Palpitations
12 5 7 4 9 7 3 3 4 53 3 18 4 2
140 43 78 30 218 35 18 36 38 420 50 134 94 6
Hospital attenders (information obtained ) Hospital attenders (information missing) Total number of hospital attenders
76 (100)
(16) (7) (9) (5) (12) (9) (4) (4) (5) (70) (4) (24) (5) (3)
(24) (7) (14) (5) (38) (6) (3) (6) (7) (73) (9) (23) (16) (1)
574 (100)
Cha No. (%) 8 3 2 7 23 3 2 5 2 97 41 47 2 1
(5) (2) (1) (5) (15) (2) (1) (3) (1) (64) (27) (31) (1) (1)
151 (100)
Fang No. (%)
Koskin No. (%)
2 0 0 2 11 0 0 2 0 21 0 8 3 1
2 0 0 2 5 0 0 0 0 15 1 9 1 0
(7) (0) (0) (7) (41) (0) (0) (7) (0) (78) (0) (30) (11) (4)
27 (100)
(12) (0) (0) (12) (29) (0) (0) (0) (0) (88) (6) (53) (6) (0)
17 (100)
164 51 87 45 226 45 23 46 44 606 95 216 104 10
845 (100)
6
10
3
3
3
25
82
584
154
30
20
870
dence of blistering or ulceration of the skin was present in 36 (7%) of 548 in-patients only, according to Dr. Mfonfu's data. Virtually all of the victims with skin lesions had reported a period of unconsciousness (L. Kaptud, pers. commun., 1986). A common site for the skin lesions was over the cheekbone of the face or other likely pressure points or skin sites with poor circulation (e.g. shins and feet). Photographs showed that swelling of the adjacent skin sometimes accompanied the lesions but without other signs of inflammation. However, several photographs of corpses showed marked blistering of the skin of limbs or trunk which seemed most unlikely to be related to pressure or thermal damage. In other instances the lesions could have been burns caused by falling on to, or near fires, but it is impossible to tell from the photographic appearances alone. Comatose vic-
(19) (6) (10) (5) (31) (5) (3) (5) (5) (72) (11) (26) (12) (1)
tims might have suffered convulsions and these disturbances in body posture could have contributed to the distribution of skin lesions. Most of the lesions were superficial and had healed by 17 days after the incident; four patients, however, had full thickness skin loss and required skin grafting, but we were unable to obtain further details. Weakness or paralysis of limbs were found in 6% of survivors overall and was associated with swelling of the affected limb. Clinical examination indicated that these findings were most likely to be due to pressure on the peripheral nerves as a result of lying on the ground in prolonged coma. Most had improved by 2-3 weeks after the event. There were no patients with overt evidence of gross brain damage. Apparently none had loss of smell or taste, but several patients reported unilateral hearing loss since
ACUTEHEALTHIMPACTOFTHE GASRELEASEATLAKENYOS,CAMEROON TABLE 2 Age and sex distribution of survivors in Table 1 attending (a) Nkambe and (b)Wum hospitals (data incomplete) (a)
Age group (yrs) 0-4 5-14 15-44 45+ Total
Males No. (%) 33 67 74 24 198 (48)
Females No. (%) 36 70 89 20 215 (52)
Total No. (%) 69 137 163 44
(17) (33) (39) (11)
413" (100)
*'of 416 hospital attenders, data not recorded in three cases. (b)
Age group (yrs)
Males No. (%)
0-4 5-14 15-44 45+
11 33 26 23
Total
93 (40)
Females No. (%) 33 33 56 19 141 (60)
Total No. (%) 44 66 82 42
(19) (28) (35) (18)
234* (100)
*of 468 hospital attenders, data not recorded in 234 cases.
the disaster, suggesting an ischaemic lesion of the auditory nerve. The majority of survivors had complained of body pains and about a quarter had had headache. About 12% had fever (malaria is endemic and the disaster could have triggered clinical relapses) and around 5% had diarrhoea and/or vomiting. In the two hospitals there had been seven miscarriages (under 20 weeks gestation) and four stillbirths (one at 32 weeks gestation and three near term), whilst at Nkambe three infants had been born normally at term, in the two weeks after the disaster. Proteinuria was a common early finding in survivors at Nkambe hospital, but urine testing on survivors at Wum hospital two weeks after admission showed an unremarkable pattern (transient proteinuria may be found in survivors from asphyxiation).
Pathology
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from Nyos who had died two days after admission at Wum (the body had been embalmed). The cause of death was pneumonia. One male victim was exhumed at Subum and examined on site; despite advanced decomposition there was evidence of pulmonary congestion and oedema. The carcass of a bull was also examined at Subum but anatomical findings were non-specific. Additional material was collected by Cameroonian physicians from a 30 year-old male victim who died on August 27 and this showed congestion of the lungs but no other gross changes. These sparse findings were in keeping with death from asphyxia. Toxicological tests were performed on tissue specimens from all three of the deceased and they were found to be negative for cyanide, carboxyhaemoglobin and sulphhaemoglobin. Moderate increases in methaemoglobin were attributed to decomposition (U.S. Scientific Team, 1987). The Japanese team dissected the body of a male patient who had died in Cha village 1½ hours previously on August 30. Massive pulmonary congestion was found in the lungs; in skin samples an increased sulphate level was found compared with controls, but this could have been due to contamination of the formalin that the samples had been preserved in or the choice of inappropriate control skin in Japan (Japanese International Disaster Relief Team, 1986).
Survivors in camp Of the 150 survivors interviewed at one camp, 10 people appeared to have mild weakness of one or more limbs. There were no other gross neurological or dermatological abnormalities which could be related to the gas exposure, but about half had a history of loss of consciousness. Twenty-five (17%) had evidence of healing skin lesions.
Discussion The U.S. medical team worked in the affected areas on August 29 and 30. On August 30 they performed an autopsy on a 30 year-old male
The principal volcanic gases (Table 3) can be broadly categorised as asphyxiant or irritant
P.J. BAXTERAND M. KAPILA
272 TABLE 3 Life t h r e a t e n i n g acute exposure levels for principal volcanic gases
Irritant gases Concentration ( p p m ) Density relative to air
SO~
HC1
HF
400 2.3
1000 1.3
150 0.7
C02
CO
H2S
NOx
100 > 1.6
Asphyxiant gases Concentration (%) Density relative to air
30 1.5
0.4
0.1
1
1.2
depending upon their toxic effects, though H2S has features of both types. Asphyxiant gases interfere with the supply or utilisation of oxygen, whereas irritant gases have a direct inflammatory action on lung tissue, the mucous membranes of the respiratory tract and the skin (Henderson and Haggard, 1943). CO2 and CO are the main asphyxiant volcanic gases and hydrogeological tests of the lake water have shown that CO2 was the major if not the only gas released (Freeth and Kay, 1987). During most volcanic eruptions the gases and ejecta are released at high temperatures which, together with the height of the crater and the vertical eruption column, usually result in the dispersion of gases away from the local population. No information is available on the temperature of the gas released at Lake Nyos, but at ordinary air temperatures COe is 1½ times denser than air whereas CO has about the same density (Table 2 ) ; t h u s COe is more likely than CO to have flowed down into the valleys surrounding Lake Nyos. The main effects of CO: are sudden loss of consciousness without warning if the concentration in air is greater than 30%. At lower concentrations breathing may be markedly increased to the point of distress and at 7-10% concentration symptoms including flushing, sweating, dizziness, exhaustion with marked hyperventilation; consciousness may be lost within 10-15 minutes (Hill and Flack, 1908; Brown, 1930; Seevers, 1944). The clinical and
pathological findings noted above have all been associated previously with the actions of asphyxiant gases. However, the number of industrial incidents recorded in the literature involving C02 are few and there is no precedent for massive community exposure as probably occurred at Lake Nyos. Prolonged states of unconsciousness and skin blisters have not been recorded with C02. Carbon monoxide poisoning is, however, common throughout the world from domestic as well as industrial exposures, and both prolonged coma and skin lesions like those reported here are recognised clinical features (Meigs and Hughes, 1952; WHO, 1979). The pathogenesis of these lesions during prolonged coma states has not been adequately explained; similar lesions occur in barbiturate poisoning (Beveridge and Lawson, 1965). It is noteworthy that human skin differs in important respects from animal skin, and experimental animal models may not be applicable to man. Human skin readily blisters in response to environmental damage from agents such as heat or chemicals which is not the case for the skin of many animals, including cattle; thus the absence of blisters or other skin lesions on the cattle corpses is not surprising. Some drawbacks of this enquiry have already been mentioned. To be of value in such incidents, environmental and human samples for toxicological and forensic study must be obtained as soon as possible; systematic autopsy examinations of the respiratory tract in corpses before decomposition had become advanced would almost certainly have resolved whether exposure to a mixture of volcanic gases had occurred or not. The half life of carboxyhaemoglobin in the blood is about four hours, and cyanide one hour, and so negative results for these substances on samples taken days after exposure, as above, does not rule out the presence of carbon monoxide or cyanide in the lake gas. The explanation of the prolonged coma in survivors and no doubt amongst many of those who subsequently died in the Lake Nyos dis-
ACUTE HEALTH IMPACT OF THE GAS RELEASE AT LAKE NYOS, CAMEROON
aster may be that C02 with air mixture induces narcosis. C02 is unique in that it is the only known gas which can produce reversible narcosis in man and higher animals by an effect other than ordinary anaesthetic mechanisms (Eisele et al., 1967; Gray et al., 1980). It was used experimentally in the past as a human and animal anaesthetic in 30% concentrations with air. A sour taste is reported at this concentration and the gas mixture may be difficult to inhale (Hill and Flack, 1908). The anaesthetic state is reversible in a short time after removal to fresh air unless cerebral oedema (brain swelling) has supervened, in which case a return to consciousness may be delayed. As with CO poisoning (Beveridge and Lawson, 1965; Smith and Brandon, 1973), a minority of victims may be expected, at least on theoretical grounds, to suffer anoxic brain damage and skin blistering if coma is prolonged. Death or survival would have been governed by the concentration of C02 in the air and duration of exposure, as with all gases, as well as factors to do with individual susceptibility. The duration of exposure to narcotic levels of CO2 in the different areas remains conjectural at present, but it is likely to have been for at least several hours and considerably longer in places. We speculate that the C02 in air mixture collected in pockets in valleys and depressions and acted as an anaesthetic to cause the prolonged coma. Prolonged CO2 narcosis is seen in patients with severe respiratory disorders in hospitals, but to our knowledge it has not been reported in gassing incidents before. The main irritant volcanic gases are S02, HC1 and H2S, and these are all denser than air (Table 2). Hydrogen fluoride is normally present in volcanic gas in small concentrations, is less dense than air, but is extremely irritant and would cause burns and ulceration of the upper respiratory tract (Patty, 1963). There was no clinical evidence of exposure to nitrogen oxides {NOx) which are also minor constituents of volcanic emissions. The smell of gunpowder reported by survivors suggests the presence of
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S02. S02 and HC1 could both be readily detectable in dangerous concentrations by their irritating effects, causing coughing, tightness in the chest, difficulty in breathing and soreness of eyes, nose and throat. Without treatment deaths from pulmonary oedema due to irritant gases mostly occur within 24-36 hours, or recovery commences in about 48 hours; survivors often develop pneumonia subsequently or have breathlessness on exertion for days or even weeks afterwards. Recurrent chest infections may be a subsequent problem (Henderson and Haggard, 1943). Hydrogen sulphide, which is both an asphyxiant and irritant gas, is also denser than air and its presence is signalled by the odour of rotten eggs, as was reported by some survivors. A small amount of H2S could have been present, and it should be remembered that a concentration of < ½% in inhaled air can lead to rapid death; a single breath may be sufficient to cause unconsciousness and lethal respiratory paralysis. This may happen almost without warning as the gas causes olfactory paralysis and death occurs unless the victim is removed to fresh air within a few minutes. The irritant effects of H2S in sub-lethal concentrations include marked eye irritation with damage to the cornea, blurred vision, nausea and gastro-intestinal disturbances, coughing, pain in the nose throat and chest, and pulmonary oedema; blistering of the skin has not been reported (Patty, 1963; WHO, 1981). If irritant volcanic gas had been emitted in large quantities from Lake Nyos, we would expect eye and respiratory symptoms to have been much more in evidence even one week after the event when foreign teams arrived. The rapid recovery of the survivors is also in favour of the action of an asphyxiant gas. Nevertheless, the Japanese team was sufficiently impressed with the clinical picture to suggest that H2S and SO2 were present in addition to CO2 and in amounts sufficient to cause chemical burns of the lungs and skin (Japanese International Disaster Relief Team, 1986).
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We have considered the possible long-term implications for the health of the survivors. Residual lung damage is unlikely if CO2 was the main or only gas involved and we have not heard since our visit of any reports of marked residual respiratory disability among survivors. The need for an epidemiological study of lung function in survivors was considered but rejected on the grounds that the results were unlikely to be readily interpretable, or to be of practical value in the further management of the survivors. The presence of disabling brain damage due to anoxia in at least a proportion of the survivors who had been rendered unconscious is a real possibility even though survivors may appear outwardly unaffected. Detailed scientific testing might reveal impairment of memory or perception and difficulty in carrying out practical skills in adults, and learning difficulties in children. Unfortunately, diagnostic imaging equipment for the diagnosis of brain damage in asphyxia (e.g. computerised tomography; Sang Choi, 1983) is not available in Cameroon and is not portable; and field psychological tests applicable to illiterate populations would have uncertain validity as screening tools in addition to the problems of cultural barriers as mentioned earlier. The possibility of long-term neurological damage and consequent cognitive impairments must nevertheless be considered when resettling these people, especially the children. The disaster zone in Figure 1 needs refining so that the locations of where people died or were affected by the gas can be more clearly demarcated. It may be possible to show more precisely which areas remained unaffected because of their altitude or for other reasons and these would obviously be recommended as locations for future settlements until a warning system for a future gas release from Lake Nyos is in place. Emergency disaster planning should also be organised as another gas release without warning from Lake Nyos or other Cameroon lakes cannot be ruled out on present knowledge. As in other natural disasters, medical teams offering emergency treatment have to be
P.J. BAXTER AND M. KAPILA
in the field within hours of the incident if they are to have an impact in terms of reducing loss of life and the severity of injuries, and such teams should be trained beforehand in the methods of monitoring for volcanic gases in the environment and for the treatment of gas casualties. The Lake Nyos disaster has demonstrated the need to form a team of medical scientists to join in the disaster response so that epidemiological, toxicological and pathological investigations are begun as soon as possible. Ideally, multi-disciplinary teams of volcanologists and medical scientists should be established on an international basis to provide the emergency skills needed if we are to advance our understanding of the mechanisms and effects of large scale gas emissions of volcanic origin.
Acknowledgements We thank the Cameroon Government and Cameroon relief workers for their collaboration. The assistance of medical colleagues in Cameroon in sharing their information was indispensible; in particular we are indebted to Professor L. Kaptud, Drs. O. Nana, G. Ngufor and Pisoh, and Dr. D. Mfonfu whose photographs and epidemiological data provide a unique record of this tragedy. Our visits were made possible by the support of the U.K. Overseas Development Administration Disaster Unit with the unstinting co-operation of the staff of the British Embassy in Yaounde, in particular Ms. K. Oliver and Mr. R. Osborne. We are also grateful for the assistance provided by Mr. D. Hughes and Mr. A. Ndonyi of the Mission de la Developpement de la Province du Nord-ouest, and Mr. Gamnge, regional geologist. We thank Father F. ten Horn at the Roman Catholic Mission, Wum, for assisting us in our visits to the refuge camps and for information on the local impact of the disaster. We are indebted to numerous colleagues and organisations for their advice, in particular Prof. A. Gresham and Prof. C. Douglas (University
ACUTEHEALTHIMPACTOFTHE GASRELEASEAT LAKENYOS,CAMEROON
of Cambridge); Drs. G. Park, R. Pye and I. Wilkinson (Addenbrooke's Hospital, Cambridge), Dr. A. Newman-Taylor (Brompton Hospital, London); Dr. T. Shallice (MRC Applied Psychology Unit, Cambridge); Mr. J. Groves (Health and Safety Executive, London); Dr. I. Hymes (SRD, U.K. Atomic Energy Authority); the Ministry of Agriculture, Fisheries and Food, Weybridge and Lowestoft; the Chemical Defence Establishment, Porton Down; Dr. J. Durand (Institut Pasteur, Yaounde); Dr. W. Winner (Virginia Polytechnic Institute and State University); and Mr. D. Zeitlyn who provided valuable anthropological advice. The British Red Cross Society, London, facilitated the visit of Dr. Kapila. Photographs and film were also kindly provided by Helimission, Cameroon Television and the BBC. The manuscript was typed by Mrs. M. Ratcliffe. Finally our thanks go to our two geologist colleagues, Drs. S. Freeth and L. Kay for their invaluable collaboration. References Baxter, P.J., Stoiber, R.E. and Williams, S.N., 1982. Volcanic gases and health: Masaya volcano, Nicaragua. Lancet, 2: 150-151. Beveridge, G.W. and Lawson, A.A.H., 1965. Occurrence of bullous lesions in acute barbiturate intoxication. Br. Med. J., 1: 835-837. Brown, E.W., 1930. The physiological effects of high concentrations of carbon dioxide. U.S. Navy Med. Bull., 28: 721-734. Clark, C.J., Campbell, D. and Reid, W.H., 1981. Blood car-
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boxyhaemoglobin and cyanide levels in fire survivors. Lancet, 1: 1332-1335. Eisele, J.H., Eger, E.I. and Muallem, M., 1967. Narcotic properties of carbon dioxide in the dog. Anesthesiology, 28: 856-865. Freeth, S.J. and Kay, R.L.F., 1987. The Lake Nyos gas disaster. Nature, 325: 104-105. Gray, T.C., Nunn, J.F. and Utting, J.E., 1980. General Anaesthesia. Butterworths, London. Henderson, Y. and Haggard, H.W., 1943. Noxious Gases. Reinhold, New York, NY. Hill, L. and Flack, M., 1908. The effect of excess of CO2 and of want of oxygen upon the respiration and the circulation. J. Phys., 37: 77-111. Japanese International Disaster Relief Team, 1986. Research report on gas disaster at Lake Nyos in the United Republic of Cameroon (unpublished). Le Guern, F., Tazieff, H. and Faivre Pierret, R., 1982. Bull. Volcanol., 45 (2): 153-156. Meigs, J.W. and Hughes, J.P.W., 1952. Acute carbon monoxide poisoning. An analysis of one hundred and five cases. AMA Arch. Ind. Hygiene, 6: 344-356. Patty, F.A. (Editor), 1963. Industrial Hygiene and Toxicology, Vol. 2. Interscience, New York, NY. Saing Choi, H., 1983. Delayed neurological sequelae in carbon monoxide intoxication. Arch. Neurol., 40: 433-435. Seevers, M.H., 1944. The narcotic properties of carbon dioxide. N.Y.J. Med., 44: 597-602. Sigurdsson, H., Devine, J.D., Tchoua, F.M., Presser, T.S., Pringle, M.K.W. and Evans, W.C., 1987. Origin of the lethal gas burst from Lake Monoun, Cameroon. J. Volcanol. Geotherm. Res., 31: 1-16. Smith, J.S. and Brandon, S., 1973. Morbidity from acute carbon monoxide poisoning at three-year follow up. Br. Med. J., 1: 318-321. United States Scientific Team, 1987. The 21 August 1986 Lake Nyos gas disaster, Cameroon. Final Report. World Health Organisation, 1979. Environmental Health Criteria 13. Carbon Monoxide. WHO, Geneva. World Health Organisation, 1981. Environmental Health Criteria 19. Hydrogen Sulphide. WHO, Geneva.
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Elsevier Science Publishers B.V., Amsterdam - - Printed in The Netherlands
Acute health impact of the gas release at Lake Nyos, Cameroon, 1986 P E T E R J. BAXTER 1 and M U K E S H KAPILA 2 1University of Cambridge Clinical School, A ddenbrooke's Hospital, Cambridge CB2 2QQ, U.K. 2Cambridge Health Authority, Fulbourn Hospital, Cambridge CBI 5EF U.K. (Received October 2, 1987, revised and accepted January 21, 1988 )
Abstract Baxter, P.J. and Kapila, M., 1989. Acute health impact of the gas release at Lake Nyos, Cameroon, 1986. In: F. Le Guern and G. Sigvaldason (Editors), The Lake Nyos Event and Natural C02 Degassing, I.J. Volcanol. Geotherm. Res., 39: 265-275. Available medical evidence on the acute health impact of the gas release at Lake Nyos is summarised, including the results of a survey of medical records of 845 survivors treated at Wum and Nkambe hospitals. The main clinical features were compatible with exposure to an asphyxiant gas such as C02 but confirmation of the identity of the gas or gases involved was not possible. Exposure to C02 over such a large inhabited area and reversible coma lasting for hours after C02 gassing do not appear to have been reported before. In some victims, blistering or ulceration of the skin was present which could not be readily explained by local injury from pressure, or burns from acid, or falling near fires. Further epidemiological studies on survivors are unlikely to be feasible, but the possibility of long-term anoxic brain damage among adults and children who had been rendered comatose by the gas should be considered, though overt evidence of major neurological or respiratory disability was not apparent in survivors in the weeks following the disaster. The inadequacy of the toxicological and forensic evidence obtained points to the need for the rapid mobilisation of medical scientists in future disasters of this kind.
Introduction Since the historic eruption at the Laki fissure in Iceland in 1783, catastrophic incidents involving human exposure to massive volcanic or natural gas emissions have not been reported to our knowledge (Baxter et al., 1982), with the exception of the gas releases at Dieng Plateau, Java, in 1979 when 146 people died (Le Guern et al., 1982) and Lake Monoun, Cameroon, in 1984 when 35 people succumbed (Sigurdsson et al., 1987). Retrospective geological studies have pointed to CO2 as being the major gas released in the latter incidents, but it is important to emphasise that autopsy and toxicological studies were not performed on the deceased in either 0377-0273/89/$03.50
event. At Dieng Plateau, the gas release was attributed to a phreatic eruption which could have involved other gases as well as CO2, but at Lake Monoun, Sigurdsson et al. (1987) suggested that C02 of volcanic origin had accumulated slowly in the lake over time and was released as a result of a sudden overturning of the stratified waters. Both of these mechanisms have been proposed to explain the catastrophe at Lake Nyos. Unlike the incidents at Dieng and Lake Monoun, the Lake Nyos disaster attracted worldwide attention, and investigative teams which included medical personnel were sent from several countries, including the United States, Israel, Japan and the United Kingdom. Despite this response, the quantity and quality
© 1989 Elsevier Science Publishers B.V.
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of medical information obtained was less than ideal; the reasons for this will be discussed. We report here a summary of our findings from the available medical evidence to assist geologists in determining the nature of the gas or gases released. The medical information is also important to aid officials in determining the needs of survivors and for emergency planning for any future gas release from Lake Nyos or other Cameroon lakes.
B a c k g r o u n d and methods The British team comprised two geologists and one author (P.J.B.) who arrived in the disaster area two weeks after the gas release. By then the emergency was over and survivors were beginning to leave hospital. We held discussions with Government officials and experts, and interviewed relief workers and survivors. The pathology reports of the United States and Japanese teams were made available to us. An environmental appraisal was made at Lake Nyos. M.K. collated the epidemiological data available at the time of his visit six weeks after the gas release, and undertook a study of the records of clinical symptoms and signs in survivors presenting to the hospitals at Wum and Nkambe in the weeks after the incident (a report was submitted to the Cameroon government in October/November 1986). We consulted the report by Dr Daniel Mfonfu (Chief of Epidemiology, Ministry of Public Health, Cameroon) on the signs and symptoms of survivors admitted to the two hospitals, together with over 60 photographs he took of the dead and survivors on August 23 and 24. Other photographic and film material was made available by Helimission, the Cameroon Ministry of Culture and Information, and the BBC. In addition, one of us (M.K.) interviewed 150 survivors over 15 years of age in 5 temporary camps six weeks after the incident, though the representativeness of this sample is not clear. No other medical studies appear to have been undertaken immediately after the disaster on sur-
P.J. BAXTER AND M. KAPILA
vivors who were not admitted to hospital. Any retrospective enquiry in the aftermath of this disaster faced almost insuperable difficulties in obtaining scientific data by interviewing survivors. Because of the numerous local dialects, important differences in meaning may have emerged when interpreters were used and there may be no exact local equivalent for some English words. The use of pidgin English, the lingua franca of Northern Cameroon, does not overcome this problem. Even more important are the profound cultural differences that exist between the scientifically trained outsider and the local people so that the use of a questionnaire, so beloved of epidemiologists, may be of little worth. Responses of the people to direct questioning are likely to be overwhelmingly biased by cultural factors and should be interpreted in the presence of a social anthropologist with considerable local experience so that the value of the responses can be assessed. The journalists and investigators first on the scene seemed to have been unaware of these pitfalls and by the time of our arrival, hospital survivors were able to reproduce suspiciously identical accounts of events and experiences. Thus the information we received via interpreters was treated guardedly and we placed much greater emphasis on the reports from relief workers and the few survivors who spoke fluent English. We did not undertake an epidemiological questionnaire survey of survivors for these reasons.
Results There was general agreement that the gas release began about 9.00-10.00 p.m. on Thursday, August 21, 1986. The precise number of casualties may never be known, but according to Government sources at least 1700 people were said to have died and an estimated 5000 people in the zone either escaped exposure to the gas or survived its effects. The best estimate of the zone affected by the gas, which we obtained from local Roman Catholic missionaries who had observed or received reports on the locations of
ACUTEHEALTH IMPACTOF THE GAS RELEASEAT LAKENYOS,CAMEROON
human and cattle corpses, was an area about 20 km long and 15 km wide (Fig. 1). There was evidence that the gas had primarily affected the valley bottoms, e.g. at Fang; no deaths occurred in that part of the settlement above the valley. It was at least 36 hours before outside help entered the zone, by which time most deaths had already occurred. Information on events during those 36 hours was very sparse. The majority of survivors began entering hospitals at Wum and Nkambe on August 23 and 24, though at Wum 10 survivors reached the hospital as early as August 22. Many of the survivors were picked up by lorry and transported to hospital, though the criteria for admission to hospital was not clear to us. It did seem that the majority, if not all, of the hospital in-patients had lost consciousness at the time of the disaster, and were in any case likely to have been the worst affected. The Israeli medical team and other foreign experts did not start to arrive in the area until one week after the gas release.
Kwana .Nkang
Fig. 1. Area of the mountainous region north of Lake Nyos where gas flowed, according to missionary reports on locations of human and cattle corpses.
267
Environmental damage Environmental observations around the lake area showed little damage to vegetation or homes (Fig. 2 ). The taller vegetation had been partially flattened in a few places along the incline between the lake and Lower Nyos. There was no evidence of thermal or acidic damage. A high concentration of sulphur dioxide or its aerosols would undoubtedly have left evidence of vegetation damage and so a lethal concentration of sulphur dioxide is more or less excluded by these findings (W. Winner, pets. commun., 1986). Further away from the lake there were no reports of environmental damage either, providing no obvious clues as to how the scattered human and cattle deaths could have been caused.
Deaths from the gas Unfortunately, the locations, disposition and appearances of corpses were not systematically recorded. Relatives of the dead and emergency workers buried the corpses over the weekend following the gas release, or soon after, and no autopsies were performed at that time. Relief workers stated that numerous corpses had had the appearance of the clothes having been removed during life, presumably in an effort to breath. The insides of some houses were in disarray, indicating confusion or distress on the part of the inhabitants. Some lay dead on their beds, others had reached for torches or gone outside before losing consciousness, a few having managed to reach a short way into the bush. These appearances indicated that people had been rapidly overwhelmed and many had lost consciousness within seconds. Consciousness could have been preserved for some minutes in others while they made efforts to breathe; or lack of oxygen could have led to confusion and inability to move freely. Post mortern changes, which would have been well advanced by the time rescuers entered the zone, could account for the reports of swollen corpses.
268
p.J. BAXTERAND M. KAPILA
Fig. 2. Upper Nyos settlement: decomposing cattle corpses lie near homes where six people survived. The gas flowed over the ridge from the lake beyond.
Some corpses were reported to have bled from the mouth and there were conflicting reports over whether some had bled from the nose. Pools of blood were reported close to some corpses, but whether the blood had been vomited or coughed up was not clear. The whites of eyes were mentioned to be reddened, a finding compatible with the suffused conjunctivitis of asphyxiation or inflammation from an irritant gas. Most corpses, however, looked normal, though some had skin lesions resembling burns. Available photographs of these lesions indicate the presence of blisters, in two photographs these were 5-15 cm across. Some children were reported to have defecated. Numerous animal corpses, including cattle, were also found, and some of the latter were also said to have bled from the mouth. There were no reliable data on mortality rates in different parts of the region affected by the
gas, except at Upper Nyos (i.e. the settlement located between the lake and Lower Nyos, or Nyos). Here, six out of 30 people survived. Crude estimates suggest that perhaps one third of the population in and around Subum and one fifth at Cha were killed.
Experience o[ survivors The commonest reported experience from survivors in the Nyos area was that they were going to bed or sitting around fires talking whilst others were asleep when they heard an unusual disturbance outside, such as animals moving or birds fluttering, or the sound of a strong wind. They went out to see what was happening and then smelt 'rotten eggs' or 'gunpowder' before rapidly losing consciousness. There were no feelings of irritation to the eyes and chest, no gagging, choking, coughing or chest pain. Oth-
ACUTE HEALTH IMPACT OF THE GAS RELEASE AT LAKE NYOS, CAMEROON
ers reported a feeling of warmth and difficulty in breathing, or had feelings of suffocation. The duration of unconsciousness appears to have been for hours, rather than minutes, in many survivors. At Upper Nyos one survivor, a 24 year-old Fulani who had received secondary education and spoke fluent English, recalled how, when he had recovered consciousness, it was about 10 hours after the gas release (7 a.m. by his watch) and he was lying outdoors. He helped to revive his father whilst others around him were dead. Survivors stated that people had lost consciousness or had died in the open air or indoors, and the dead and survivors had even been in the same spot when the gas struck. On recovering consciousness survivors had noticed difficulty in breathing or had tightness of the chest for a short period, but no wheeze. A male nurse, who spoke fluent English, related how he was riding on a moped into Cha at about 6 a.m. on August 22 (i.e. approximately nine hours after the gas release) when he suddenly lost consciousness; he woke 1½ hours later gasping, feeling tired and 'drunk', with a headache, and subsequently developed a cough which lasted three days. Some survivors had a mild cough with blood-stained sputum. A boy was noticed to be ill for several days after recovering consciousness, during which time he vomited blood. Over the following days survivors were dazed and many had a cough, but severe chest pains do not appear to have been common. There was no loss of smell or taste such as may occur in poisoning from hydrogen sulphide. Blurred vision or subconjunctival haemorrhages were noted, but marked eye inflammation, another feature of hydrogen sulphide poisoning, was not common.
Clinical findings in survivors Dr. Mfonfu collected data on the 548 in-patients seen in the two hospitals in the two weeks after the disaster. At one hospital 50% and 43% of patients were from Cha and Subum, respectively; at Nkambe 93% were from Subum. There
269
was an approximately twofold excess of females over males in 0-4 and 20-39 age groups, a finding which was not explained. One of us (M.K.) reviewed data from patient registers on 845 people attending for treatment at the two hospitals which included the same in-patients, and was able to include information on location at the time of the disaster (Tables 1 and 2). The information recorded included the main clinical features at presentation of each patient and we believe it to be reasonably reliable, though validation is obviously impossible. Nevertheless, our data set and Dr. Mfonfu's showed a very similar pattern of illness, which was found throughout the affected zone, both near and distant to the lake, though the numbers of patients from the areas of Fang and Koskin were small, and data on age and sex were incomplete. A most notable finding was the small number of patients with serious respiratory problems. Severe difficulty in breathing, chest pain and clinical signs indicative of pulmonary oedema (fluid in the lungs caused by severe irritation of the respiratory passages) were remarkable by their absence. Shortness of breath, cough and blood-stained sputum were present in a minority of patients only, and were mild; patchy consolidation of the lungs and not severe pulmonary oedema was suggested on clinical exami nation in about 25% of patients, and these findings were associated with skin lesions (X. Pisoh, pers. commun., 1986). The patients with respiratory problems were treated with antibiotics and the worst affected, with steroids and oxygen. Only three people were diagnosed as having pneumonia and these were at Wum hospital; two of these patients died. Cough and blood-stained sputum had mostly cleared by the third day after admission, though antibiotic treatment was considered to have been important in the recovery of many patients (D. Mfonfu, pets. commun., 1987). Conjunctivitis was recorded in about 3% of patients only. Skin lesions resembling burns were recorded in 19% of the survivors overall and these were mostly redness of the skin. Unequivocal evi-
270
P.J. BAXTERANDM. KAPILA
TABLE 1 Clinical symptoms of survivors attending for treatment at Nkambe and Wum Hospitals (including 548 admissions) Symptom
Pre-disaster area of residence
All areas
No. (%) Nyos No. (%)
Subum No. (%)
'Burns' Limb paralysis Limb/jointswelling Eye symptoms Cough Dyspnoea Haemoptysis Vomiting Diarrhoea Bodypains Weakness/malaise Headache Fever Palpitations
12 5 7 4 9 7 3 3 4 53 3 18 4 2
140 43 78 30 218 35 18 36 38 420 50 134 94 6
Hospital attenders (information obtained ) Hospital attenders (information missing) Total number of hospital attenders
76 (100)
(16) (7) (9) (5) (12) (9) (4) (4) (5) (70) (4) (24) (5) (3)
(24) (7) (14) (5) (38) (6) (3) (6) (7) (73) (9) (23) (16) (1)
574 (100)
Cha No. (%) 8 3 2 7 23 3 2 5 2 97 41 47 2 1
(5) (2) (1) (5) (15) (2) (1) (3) (1) (64) (27) (31) (1) (1)
151 (100)
Fang No. (%)
Koskin No. (%)
2 0 0 2 11 0 0 2 0 21 0 8 3 1
2 0 0 2 5 0 0 0 0 15 1 9 1 0
(7) (0) (0) (7) (41) (0) (0) (7) (0) (78) (0) (30) (11) (4)
27 (100)
(12) (0) (0) (12) (29) (0) (0) (0) (0) (88) (6) (53) (6) (0)
17 (100)
164 51 87 45 226 45 23 46 44 606 95 216 104 10
845 (100)
6
10
3
3
3
25
82
584
154
30
20
870
dence of blistering or ulceration of the skin was present in 36 (7%) of 548 in-patients only, according to Dr. Mfonfu's data. Virtually all of the victims with skin lesions had reported a period of unconsciousness (L. Kaptud, pers. commun., 1986). A common site for the skin lesions was over the cheekbone of the face or other likely pressure points or skin sites with poor circulation (e.g. shins and feet). Photographs showed that swelling of the adjacent skin sometimes accompanied the lesions but without other signs of inflammation. However, several photographs of corpses showed marked blistering of the skin of limbs or trunk which seemed most unlikely to be related to pressure or thermal damage. In other instances the lesions could have been burns caused by falling on to, or near fires, but it is impossible to tell from the photographic appearances alone. Comatose vic-
(19) (6) (10) (5) (31) (5) (3) (5) (5) (72) (11) (26) (12) (1)
tims might have suffered convulsions and these disturbances in body posture could have contributed to the distribution of skin lesions. Most of the lesions were superficial and had healed by 17 days after the incident; four patients, however, had full thickness skin loss and required skin grafting, but we were unable to obtain further details. Weakness or paralysis of limbs were found in 6% of survivors overall and was associated with swelling of the affected limb. Clinical examination indicated that these findings were most likely to be due to pressure on the peripheral nerves as a result of lying on the ground in prolonged coma. Most had improved by 2-3 weeks after the event. There were no patients with overt evidence of gross brain damage. Apparently none had loss of smell or taste, but several patients reported unilateral hearing loss since
ACUTEHEALTHIMPACTOFTHE GASRELEASEATLAKENYOS,CAMEROON TABLE 2 Age and sex distribution of survivors in Table 1 attending (a) Nkambe and (b)Wum hospitals (data incomplete) (a)
Age group (yrs) 0-4 5-14 15-44 45+ Total
Males No. (%) 33 67 74 24 198 (48)
Females No. (%) 36 70 89 20 215 (52)
Total No. (%) 69 137 163 44
(17) (33) (39) (11)
413" (100)
*'of 416 hospital attenders, data not recorded in three cases. (b)
Age group (yrs)
Males No. (%)
0-4 5-14 15-44 45+
11 33 26 23
Total
93 (40)
Females No. (%) 33 33 56 19 141 (60)
Total No. (%) 44 66 82 42
(19) (28) (35) (18)
234* (100)
*of 468 hospital attenders, data not recorded in 234 cases.
the disaster, suggesting an ischaemic lesion of the auditory nerve. The majority of survivors had complained of body pains and about a quarter had had headache. About 12% had fever (malaria is endemic and the disaster could have triggered clinical relapses) and around 5% had diarrhoea and/or vomiting. In the two hospitals there had been seven miscarriages (under 20 weeks gestation) and four stillbirths (one at 32 weeks gestation and three near term), whilst at Nkambe three infants had been born normally at term, in the two weeks after the disaster. Proteinuria was a common early finding in survivors at Nkambe hospital, but urine testing on survivors at Wum hospital two weeks after admission showed an unremarkable pattern (transient proteinuria may be found in survivors from asphyxiation).
Pathology
271
from Nyos who had died two days after admission at Wum (the body had been embalmed). The cause of death was pneumonia. One male victim was exhumed at Subum and examined on site; despite advanced decomposition there was evidence of pulmonary congestion and oedema. The carcass of a bull was also examined at Subum but anatomical findings were non-specific. Additional material was collected by Cameroonian physicians from a 30 year-old male victim who died on August 27 and this showed congestion of the lungs but no other gross changes. These sparse findings were in keeping with death from asphyxia. Toxicological tests were performed on tissue specimens from all three of the deceased and they were found to be negative for cyanide, carboxyhaemoglobin and sulphhaemoglobin. Moderate increases in methaemoglobin were attributed to decomposition (U.S. Scientific Team, 1987). The Japanese team dissected the body of a male patient who had died in Cha village 1½ hours previously on August 30. Massive pulmonary congestion was found in the lungs; in skin samples an increased sulphate level was found compared with controls, but this could have been due to contamination of the formalin that the samples had been preserved in or the choice of inappropriate control skin in Japan (Japanese International Disaster Relief Team, 1986).
Survivors in camp Of the 150 survivors interviewed at one camp, 10 people appeared to have mild weakness of one or more limbs. There were no other gross neurological or dermatological abnormalities which could be related to the gas exposure, but about half had a history of loss of consciousness. Twenty-five (17%) had evidence of healing skin lesions.
Discussion The U.S. medical team worked in the affected areas on August 29 and 30. On August 30 they performed an autopsy on a 30 year-old male
The principal volcanic gases (Table 3) can be broadly categorised as asphyxiant or irritant
P.J. BAXTERAND M. KAPILA
272 TABLE 3 Life t h r e a t e n i n g acute exposure levels for principal volcanic gases
Irritant gases Concentration ( p p m ) Density relative to air
SO~
HC1
HF
400 2.3
1000 1.3
150 0.7
C02
CO
H2S
NOx
100 > 1.6
Asphyxiant gases Concentration (%) Density relative to air
30 1.5
0.4
0.1
1
1.2
depending upon their toxic effects, though H2S has features of both types. Asphyxiant gases interfere with the supply or utilisation of oxygen, whereas irritant gases have a direct inflammatory action on lung tissue, the mucous membranes of the respiratory tract and the skin (Henderson and Haggard, 1943). CO2 and CO are the main asphyxiant volcanic gases and hydrogeological tests of the lake water have shown that CO2 was the major if not the only gas released (Freeth and Kay, 1987). During most volcanic eruptions the gases and ejecta are released at high temperatures which, together with the height of the crater and the vertical eruption column, usually result in the dispersion of gases away from the local population. No information is available on the temperature of the gas released at Lake Nyos, but at ordinary air temperatures COe is 1½ times denser than air whereas CO has about the same density (Table 2 ) ; t h u s COe is more likely than CO to have flowed down into the valleys surrounding Lake Nyos. The main effects of CO: are sudden loss of consciousness without warning if the concentration in air is greater than 30%. At lower concentrations breathing may be markedly increased to the point of distress and at 7-10% concentration symptoms including flushing, sweating, dizziness, exhaustion with marked hyperventilation; consciousness may be lost within 10-15 minutes (Hill and Flack, 1908; Brown, 1930; Seevers, 1944). The clinical and
pathological findings noted above have all been associated previously with the actions of asphyxiant gases. However, the number of industrial incidents recorded in the literature involving C02 are few and there is no precedent for massive community exposure as probably occurred at Lake Nyos. Prolonged states of unconsciousness and skin blisters have not been recorded with C02. Carbon monoxide poisoning is, however, common throughout the world from domestic as well as industrial exposures, and both prolonged coma and skin lesions like those reported here are recognised clinical features (Meigs and Hughes, 1952; WHO, 1979). The pathogenesis of these lesions during prolonged coma states has not been adequately explained; similar lesions occur in barbiturate poisoning (Beveridge and Lawson, 1965). It is noteworthy that human skin differs in important respects from animal skin, and experimental animal models may not be applicable to man. Human skin readily blisters in response to environmental damage from agents such as heat or chemicals which is not the case for the skin of many animals, including cattle; thus the absence of blisters or other skin lesions on the cattle corpses is not surprising. Some drawbacks of this enquiry have already been mentioned. To be of value in such incidents, environmental and human samples for toxicological and forensic study must be obtained as soon as possible; systematic autopsy examinations of the respiratory tract in corpses before decomposition had become advanced would almost certainly have resolved whether exposure to a mixture of volcanic gases had occurred or not. The half life of carboxyhaemoglobin in the blood is about four hours, and cyanide one hour, and so negative results for these substances on samples taken days after exposure, as above, does not rule out the presence of carbon monoxide or cyanide in the lake gas. The explanation of the prolonged coma in survivors and no doubt amongst many of those who subsequently died in the Lake Nyos dis-
ACUTE HEALTH IMPACT OF THE GAS RELEASE AT LAKE NYOS, CAMEROON
aster may be that C02 with air mixture induces narcosis. C02 is unique in that it is the only known gas which can produce reversible narcosis in man and higher animals by an effect other than ordinary anaesthetic mechanisms (Eisele et al., 1967; Gray et al., 1980). It was used experimentally in the past as a human and animal anaesthetic in 30% concentrations with air. A sour taste is reported at this concentration and the gas mixture may be difficult to inhale (Hill and Flack, 1908). The anaesthetic state is reversible in a short time after removal to fresh air unless cerebral oedema (brain swelling) has supervened, in which case a return to consciousness may be delayed. As with CO poisoning (Beveridge and Lawson, 1965; Smith and Brandon, 1973), a minority of victims may be expected, at least on theoretical grounds, to suffer anoxic brain damage and skin blistering if coma is prolonged. Death or survival would have been governed by the concentration of C02 in the air and duration of exposure, as with all gases, as well as factors to do with individual susceptibility. The duration of exposure to narcotic levels of CO2 in the different areas remains conjectural at present, but it is likely to have been for at least several hours and considerably longer in places. We speculate that the C02 in air mixture collected in pockets in valleys and depressions and acted as an anaesthetic to cause the prolonged coma. Prolonged CO2 narcosis is seen in patients with severe respiratory disorders in hospitals, but to our knowledge it has not been reported in gassing incidents before. The main irritant volcanic gases are S02, HC1 and H2S, and these are all denser than air (Table 2). Hydrogen fluoride is normally present in volcanic gas in small concentrations, is less dense than air, but is extremely irritant and would cause burns and ulceration of the upper respiratory tract (Patty, 1963). There was no clinical evidence of exposure to nitrogen oxides {NOx) which are also minor constituents of volcanic emissions. The smell of gunpowder reported by survivors suggests the presence of
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S02. S02 and HC1 could both be readily detectable in dangerous concentrations by their irritating effects, causing coughing, tightness in the chest, difficulty in breathing and soreness of eyes, nose and throat. Without treatment deaths from pulmonary oedema due to irritant gases mostly occur within 24-36 hours, or recovery commences in about 48 hours; survivors often develop pneumonia subsequently or have breathlessness on exertion for days or even weeks afterwards. Recurrent chest infections may be a subsequent problem (Henderson and Haggard, 1943). Hydrogen sulphide, which is both an asphyxiant and irritant gas, is also denser than air and its presence is signalled by the odour of rotten eggs, as was reported by some survivors. A small amount of H2S could have been present, and it should be remembered that a concentration of < ½% in inhaled air can lead to rapid death; a single breath may be sufficient to cause unconsciousness and lethal respiratory paralysis. This may happen almost without warning as the gas causes olfactory paralysis and death occurs unless the victim is removed to fresh air within a few minutes. The irritant effects of H2S in sub-lethal concentrations include marked eye irritation with damage to the cornea, blurred vision, nausea and gastro-intestinal disturbances, coughing, pain in the nose throat and chest, and pulmonary oedema; blistering of the skin has not been reported (Patty, 1963; WHO, 1981). If irritant volcanic gas had been emitted in large quantities from Lake Nyos, we would expect eye and respiratory symptoms to have been much more in evidence even one week after the event when foreign teams arrived. The rapid recovery of the survivors is also in favour of the action of an asphyxiant gas. Nevertheless, the Japanese team was sufficiently impressed with the clinical picture to suggest that H2S and SO2 were present in addition to CO2 and in amounts sufficient to cause chemical burns of the lungs and skin (Japanese International Disaster Relief Team, 1986).
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We have considered the possible long-term implications for the health of the survivors. Residual lung damage is unlikely if CO2 was the main or only gas involved and we have not heard since our visit of any reports of marked residual respiratory disability among survivors. The need for an epidemiological study of lung function in survivors was considered but rejected on the grounds that the results were unlikely to be readily interpretable, or to be of practical value in the further management of the survivors. The presence of disabling brain damage due to anoxia in at least a proportion of the survivors who had been rendered unconscious is a real possibility even though survivors may appear outwardly unaffected. Detailed scientific testing might reveal impairment of memory or perception and difficulty in carrying out practical skills in adults, and learning difficulties in children. Unfortunately, diagnostic imaging equipment for the diagnosis of brain damage in asphyxia (e.g. computerised tomography; Sang Choi, 1983) is not available in Cameroon and is not portable; and field psychological tests applicable to illiterate populations would have uncertain validity as screening tools in addition to the problems of cultural barriers as mentioned earlier. The possibility of long-term neurological damage and consequent cognitive impairments must nevertheless be considered when resettling these people, especially the children. The disaster zone in Figure 1 needs refining so that the locations of where people died or were affected by the gas can be more clearly demarcated. It may be possible to show more precisely which areas remained unaffected because of their altitude or for other reasons and these would obviously be recommended as locations for future settlements until a warning system for a future gas release from Lake Nyos is in place. Emergency disaster planning should also be organised as another gas release without warning from Lake Nyos or other Cameroon lakes cannot be ruled out on present knowledge. As in other natural disasters, medical teams offering emergency treatment have to be
P.J. BAXTER AND M. KAPILA
in the field within hours of the incident if they are to have an impact in terms of reducing loss of life and the severity of injuries, and such teams should be trained beforehand in the methods of monitoring for volcanic gases in the environment and for the treatment of gas casualties. The Lake Nyos disaster has demonstrated the need to form a team of medical scientists to join in the disaster response so that epidemiological, toxicological and pathological investigations are begun as soon as possible. Ideally, multi-disciplinary teams of volcanologists and medical scientists should be established on an international basis to provide the emergency skills needed if we are to advance our understanding of the mechanisms and effects of large scale gas emissions of volcanic origin.
Acknowledgements We thank the Cameroon Government and Cameroon relief workers for their collaboration. The assistance of medical colleagues in Cameroon in sharing their information was indispensible; in particular we are indebted to Professor L. Kaptud, Drs. O. Nana, G. Ngufor and Pisoh, and Dr. D. Mfonfu whose photographs and epidemiological data provide a unique record of this tragedy. Our visits were made possible by the support of the U.K. Overseas Development Administration Disaster Unit with the unstinting co-operation of the staff of the British Embassy in Yaounde, in particular Ms. K. Oliver and Mr. R. Osborne. We are also grateful for the assistance provided by Mr. D. Hughes and Mr. A. Ndonyi of the Mission de la Developpement de la Province du Nord-ouest, and Mr. Gamnge, regional geologist. We thank Father F. ten Horn at the Roman Catholic Mission, Wum, for assisting us in our visits to the refuge camps and for information on the local impact of the disaster. We are indebted to numerous colleagues and organisations for their advice, in particular Prof. A. Gresham and Prof. C. Douglas (University
ACUTEHEALTHIMPACTOFTHE GASRELEASEAT LAKENYOS,CAMEROON
of Cambridge); Drs. G. Park, R. Pye and I. Wilkinson (Addenbrooke's Hospital, Cambridge), Dr. A. Newman-Taylor (Brompton Hospital, London); Dr. T. Shallice (MRC Applied Psychology Unit, Cambridge); Mr. J. Groves (Health and Safety Executive, London); Dr. I. Hymes (SRD, U.K. Atomic Energy Authority); the Ministry of Agriculture, Fisheries and Food, Weybridge and Lowestoft; the Chemical Defence Establishment, Porton Down; Dr. J. Durand (Institut Pasteur, Yaounde); Dr. W. Winner (Virginia Polytechnic Institute and State University); and Mr. D. Zeitlyn who provided valuable anthropological advice. The British Red Cross Society, London, facilitated the visit of Dr. Kapila. Photographs and film were also kindly provided by Helimission, Cameroon Television and the BBC. The manuscript was typed by Mrs. M. Ratcliffe. Finally our thanks go to our two geologist colleagues, Drs. S. Freeth and L. Kay for their invaluable collaboration. References Baxter, P.J., Stoiber, R.E. and Williams, S.N., 1982. Volcanic gases and health: Masaya volcano, Nicaragua. Lancet, 2: 150-151. Beveridge, G.W. and Lawson, A.A.H., 1965. Occurrence of bullous lesions in acute barbiturate intoxication. Br. Med. J., 1: 835-837. Brown, E.W., 1930. The physiological effects of high concentrations of carbon dioxide. U.S. Navy Med. Bull., 28: 721-734. Clark, C.J., Campbell, D. and Reid, W.H., 1981. Blood car-
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