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The Meuse Valley fog of 1930: an air pollution disaster
DEPARTMENT OF MEDICAL HISTORY
Department of medical history
The Meuse Valley fog of 1930: an air pollution disaster Benoit Nemery, Peter H M Hoet, Abderrahim Nemmar Most courses, lectures, textbook chapters,1,2 and review articles3–6 on the health effects of air pollution begin by referring to the London fog of December, 1952, which led to an increase in deaths of about 4000.7 The London fog became a landmark in air pollution epidemiology because of the scale of the disaster and because it allowed researchers to do the first detailed analysis of the relation between levels of air pollutants and increased morbidity and mortality.8,9 However, an earlier landmark is the fog that affected the Meuse Valley, Belgium, in December, 1930. This episode led to the first scientific proof of the potential for atmospheric pollution to cause deaths and disease, and it clearly identified the most likely causes. Although many present-day investigators1,2,6,9 mention the Meuse Valley fog, few people have probably read the original report, which was presented to the Royal Academy of Medicine of Belgium on May 19, 1931.10 The report was also published, in 1933, as part of a book on air pollution11 and a short version appeared in English in 1936.12
The Meuse Valley fog of December, 1930 The area of Liège on the River Meuse, was once one of the most heavily industrialised areas of continental Europe, with steelworks, zinc smelters, glass manufacturers, and fertiliser and explosives plants established since the industrial revolution. Between Dec 1 and Dec 5, 1930, a thick fog covered a large part of Belgium. From Dec 3 onwards, hundreds of people in the villages situated in the narrow portion of the Meuse Valley between the towns of Huy and Liège (figure 1) started to have severe respiratory signs and symptoms. More than 60 people died in the next 3 days. People in the entire country and abroad were deeply shocked and the deadly fog received considerable media attention. Many dignitaries, including Queen Elisabeth of the Belgians, visited the affected area (figure 2). The event was reported in medical and scientific journals in many countries.13–23 On Dec 6, the Royal Prosecutor of Liège opened a judicial inquiry and a committee of experts was appointed that included Jean Firket (1890–1958), who became professor of pathological anatomy and forensic medicine at the University of Liège after having spent 2 years (1919–21) at Johns Hopkins Medical School, as one of the first fellows of the Belgian American Foundation.24 Other committee members were J Bovy, a forensic specialist; Prof M Schoofs for toxicological analyses; Prof M Dehalu for meteorological observations; and Prof J Mage and Prof G Batta for studies of industrial chemistry. We analysed the expert committee’s report10—the quotes shown below are our translations from the report. Lancet 2001; 357: 704–08 Katholieke Universiteit Leuven, Unit of Lung Toxicology, Laboratory of Pneumology, B-3000 Leuven, Belgium (Prof B Nemery MD, P H M Hoet PhD, A Nemmar DVM) Correspondence to: Prof B Nemery (e-mail: [email protected])
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The expert committee’s report Medical data were obtained by questioning of family physicians and patients in the days immediately after the fog. On the third day the fog reached its maximum opacity and the first symptoms arose simultaneously in people throughout the valley. Most people had laryngeal irritation, retrosternal pain, coughing fits, and “dyspnoeic breathing characterised by paroxysms and slowed expiration, like asthma,” which was rapidly relieved by adrenaline-based drugs. Some patients had “dyspnoea which did not have an asthmatic rhythm, but which was accompanied by signs of pulmonary oedema such as cyanosis, rapid breathing, and even frothy sputum.” Nausea and vomiting were common, but there were no clinical signs of systemic poisoning. Respiratory problems rapidly improved after the fog cleared on Dec 5. The most affected, even when they had remained indoors, were people who were elderly, asthmatic, debilitated, or those with cardiac disease. Even people who were previously healthy were wheezing. Children were described as being indisposed and a few were seriously affected, though none died. There were also respiratory problems in cattle. 60 deaths that were attributed to the fog occurred on Dec 4 and 5. Engis, a town of 3500 inhabitants, had the highest number of deaths.14 The report does not contain demographic or clinical details of the victims, but we calculated from the names and ages of 48 of those listed in newspaper reports (eg, Le Soir, Dec 7 and 8, 1930), that their average age was about 62 years and ranged from 20 to 89 years. The 27 male victims were younger than the 21 female victims, with average ages of about 56 and 70 years, respectively. Ten necropsies that were done showed respiratory tract alterations only. All toxicological analyses of blood or viscera were negative. In all necropsies, there was “congestion of tracheal mucosa and large bronchi— sometimes with an exudate of mucus and fibrin—and areas of epithelial loss, capillary dilatation of the dermis, and a slight leucocyte exudate” (figure 3a). In lung parenchyma, “there were foci of haemorrhage next to areas of moderate oedema and desquamations of alveolar epithelium” (figure 3b). Pure carbon dust particles of 0·5–1·35 m diameter were seen free within the alveoli or engulfed in polynuclear leucocytes. Investigators concluded that the signs and symptoms were entirely and solely due to a local irritant action towards the mucosae directly exposed to the outside air. They ruled out the low temperature and the density of the fog, since similar weather conditions had prevailed over large parts of Belgium. Respiratory infections were also excluded, mainly on clinical grounds. The weather from Dec 1 to 5, was characterised by anticyclonic conditions with high atmospheric pressures and a very feeble (1–3 km/h) easterly wind that blew from the city of Liège into the narrow valley, which had 90–120 m hills on each side. These conditions produced a persistent fog. In the fog the temperature was 1–2°C. However, a temperature inversion at about 70–80 m above ground—ie, just above the tallest chimneys in the valley— prevented the fumes from rising. This atmospheric ceiling forced emitted gases and impurities to accumulate in the
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Figure 1: Map of the Meuse Valley between Liège and Huy, indicating the fog-covered area and location of fatalities and factories Reproduced and modified from figure 1 of Firket and colleagues’ report.10
corridor formed by the valley between Liège and Huy. The report writers calculated that, in the water-saturated and virtually motionless atmosphere, soot particles of 1–4 m diameter would take 1·5–6 days to settle from a height of 60 m. Small and slowly settling solid or liquid particles are easily inhaled, not only in fog but also indoors. Fog that
lasted more than 3 days had only occurred five times in the area over the previous 40 years (in 1901, 1911, 1917, 1919, and 1930). In the fog of January, 1911, cattle had died in a small valley perpendicular to the Meuse valley.25,26 Concentrations of air pollutants in the fog were unknown and subsequent chemical analyses of soil, plants, water, or
Rights were not granted to include this image in electronic media. Please refer to the printed journal.
Figure 2: Funeral cortege of a 60-year-old fog victim, halted in front of Queen Elisabeth Reproduced from Le Soir Illustré Dec 13, 1930.
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Figure 3: Histology of airways and alveolar region in post-mortem specimens from fog victims A) bronchial mucosa with desquamation of epithelium and congestion of submucosal blood vessels; B) alveolar oedema and haemorrhage with small soot particles. Reproduced from figures 4 and 7 of Firket and colleagues’ report.10
other materials were not useful, because of background pollution. There was no evidence of an abnormal release of toxic chemicals by industry. Therefore, the only choice left to the investigators was to measure the fumes, gases, and dusts released by the plants of the area. They identified about 30 substances released by 27 factories. Most pollutants (including CO2, CO, H2, H2S, AsH3, NO2, NH3, HCl, acetylene and other hydrocarbons, sulphites, chlorides, and fluorides and nitrates of zinc or iron) were excluded on the basis of calculations of the worst case scenarios for the amounts released and the symptoms of those affected. Lack of oxygen was dismissed as the cause of the victims’ suffocation. However, “the diffuse superficial mucosal congestion that occurred throughout the respiratory tract down to the bronchioles and lung parenchyma . . . could be attributable to fine irritant particles”. The free or phagocytosed particles in alveoli suggested that they had been inhaled a short time before death. However, carbon particles should have been innocuous, unless they had adsorbed irritant acids. The report writers thus postulated that: “fine soot particles, onto which irritant gases had been adsorbed, had a major role in the noxiousness of the fog”. Investigators attempted to discover which of the irritant agents were most likely to have caused the adverse health effects and deaths. Hydrofluoric acid (HF) was investigated first because it was released from a fertiliser plant in Engis, and had previously affected plants and grazing animals, and damaged light bulbs and window panes. However, the estimated maximum concentration of HF (0·4 mg/m3 for the whole valley) and the simultaneous occurrence of the first symptoms downwind and upwind of Engis meant that a single central source of pollution was unlikely.27 Nevertheless, HF could not be completely ruled out as a contributory cause in the vicinity of the plant. Eventually, sulphur compounds proved the most abundant compounds emitted in the valley. On the basis of the amount of coal burned in industrial and domestic fires (on assumption of a daily consumption of 15 kg per household and a 1% sulphur content in the coal), investigators estimated that more than 60 000 kg of SO2 706
were produced per day, with a resultant SO2 concentration of up to 100 mg/m3 after 4 days of fog. This SO2 concentration exceeded its threshold of toxicity (20–30 mg/m3 for prolonged exposure) and could account for the victims’ symptoms. Moreover, if only one-tenth of the SO2 had been oxidised, a toxic concentration of H2SO4 (then assumed to be 4 mg/m3) would have been exceeded. The report writers pointed out that overpopulation and growing industrialisation had increased sulphur compound pollution, shown by a ten-fold increase in SO3 measured in fresh snow from 1899 to 1931. After a process of successive elimination, the commission concluded “that the sulphur produced by coal burning has had a deleterious effect, either as sulphurous anhydride or acid, or as sulphuric acid; the production of which was made possible by unusual weather conditions”. Various other fanciful explanations, such as the release of war gases by aircraft or abnormal releases of especially toxic chemicals by factories taking advantage of poor visibility during the fog, were dismissed. The narrow topography of the Meuse Valley explained why similar accidents had not occurred in other areas, most notably in London, UK, where much higher levels of SO2 occurred and where dense fogs also persisted for many days; however, in London polluted air probably escaped through lateral diffusion. The report writers warned that a disaster similar to the Meuse Valley one, with a 10·5-fold increase in mortality, if repeated in London would cause 3179 deaths.
Comments and conclusions The air pollution episode in the Meuse Valley 70 years ago revealed a problem that had hitherto received little attention, except in Great Britain.8 Fog episodes had previously been associated with increased mortality in London and Glasgow, but cold weather and viral epidemics could not be ruled out as contributory factors.28,29 The Meuse fog disaster provided incontrovertible evidence that air pollution could kill and therefore it attracted considerable attention from the scientific community. In an editorial in the British Medical Journal, Haldane14 stated that
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“the possibility of a similar disaster happening in this country is a matter of great public health interest”. He thought that disaster had been avoided so far in London because the city emitted a lot of heat, which produced convection currents. Nevertheless, he warned against plans to build big electricity generating stations. Storm van Leeuwen,15 from Leiden, who visited the Meuse Valley, wrote an account of this giant experiment of nature15 from his own observations and conversations with Firket and others. The account shows how new the notion of industrial air pollution was. Storm van Leeuwen evoked and quickly discounted various hypotheses for the catastrophe, such as emission of war gases or toxic sand blown from the Sahara desert. The toxic-sand theory had been aired in the popular and scientific press.20 Another unlikely explanation was that toxic gases had escaped from the polluted soil.18 The possibility that HF was the main culprit was favoured by some writers,19,30 but the commission was probably correct to rule HF and fluorides out for a major role.14,27 The expert commission was remarkable in its mix of disciplines, which included physicians, chemists, and a meteorologist. Their methods were sound. In the absence of air monitoring, comparing medical observations with the possible toxic agents released by industry made sense, as did use of worst-case estimates of exposure concentrations. Some of these simple box-model estimates can be criticised—eg, SO2 concentration was probably overestimated by a factor of ten, at least31 and the estimated concentrations were not always consistent in the report— but they were able to be used to eliminate some of the possible causes. Some detailed analyses—eg, the exclusion of lack of oxygen as a cause of the disaster—might now seem unduly elaborate. However, the experts had to work in a subject area that was still largely unexplored, particularly with respect to quantitative dose-effect relations of inhaled pollutants. Thus, the report contains less than ten references to published work and only two of these pertain to toxicology. A weak aspect of the study was its formal epidemiological methods. Descriptions of symptoms and signs, the temporal and spatial distribution of patients, estimation of the number of deaths and their relation to exposure, and identification of susceptible people are anecdotal. Many basic characteristics, such as the age and sex of those affected, were not recorded systematically. Clinical information was not obtained from written records or by standardised questionnaires, but was noted from conversations with local physicians and examination of an undisclosed number of people from unspecified locations. The committee noted that “several hundreds” of people were affected severely, but did not include the total number of people who lived in the area (around 9000). Excess mortality was calculated by comparison of the total number of deaths with the mean daily deaths over the preceding 5 years in the seven villages where deaths had occurred; investigators did not stratify for age or sex or take into account seasonal or other trends. No graphs were drawn or statistical tests done. Although the Meuse Valley investigation did not have the thoroughness of John Snow’s investigation of the cholera point source in the 1850s,32 it was done with similar logical methods. The increase in morbidity and the sudden ten-fold rise in mortality made detailed statistical analysis unnecessary—unlike the 1952 London fog, when the doubled mortality only became apparent after scrutiny of death certificates.29 The committee established, for the first time, the roles of temperature inversion and fog in air pollution. They concluded that the culprits were coal burning by industry
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Figure 4: Statue and plaque inaugurated in Engis on Dec 2, 2000, in commemoration of those who died in the fog of December, 1930 The text refers first to the youngest victim, a 22-year-old woman, then to the 60 victims in the villages of Amay, Engis, Flémalle, and Seraing. By permission of D Dizier
and by private households. They reasoned that emitted SO2 was a main factor, but that, in addition, fog increased oxidation reactions that led to H2SO4 production, which could be catalysed by iron or zinc. Further (less extensive) studies lent support to these conclusions.33 The possible contribution of very fine soot particles onto which irritants had adsorbed was also noted. The report writers stated that small particles remained in suspension for a long time, that they contaminated even indoor air, and that they penetrated deeply into the respiratory tract. After the Meuse disaster the government appointed another commission, headed by Viscount Berryer, to assess the legislation with respect to industrial air pollution, and to propose improvements. This commission concluded that a central office should grant industrial exploitation permits rather than local authorities. In a book about the Meuse disaster,11 the writers recommended adoption of the British approach of monitoring air pollution. However, little was done since air pollution was considered an unavoidable consequence of prosperity, and the responsibility of industry was carefully played down.11 Thus, although the report states that the Meuse Valley had almost permanent industrial air pollution, the possibility that this could lead to chronic disease was not considered. Diseases caused by air pollution would take many more years to be studied, even by Firket himself.34 Having excluded an exceptional chemical accident as a cause of the disaster, the report’s writers10 concluded that “if the same weather conditions were to take place for the same length of time and with continuation of the same industrial activity, the same accident would happen again”. No major incident has since occurred in the Meuse Valley,
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but the warnings did not prevent similar events taking place in 1948 in Donora, Pennsylvania, and then in London, 1952.7,9,29 Moreover, in Engis and neighbouring villages, a pollution incident on a foggy day in September, 1972, caused respiratory systems in people and, allegedly, deaths in domestic animals; more than 200 complaints were filed (unpublished). Other peaks of air pollution are likely to have increased morbidity and mortality in the area, as recorded in many other locations.35 On Dec 2, 2000, a bronze statue by local artist Paul Vandersleyen and plaque were inaugurated in Engis to commemorate the victims of the deadly fog (figure 4). The final sentence on the plaque reads: “all human endeavours, even industrial ones, are perfectable”. We thank L Mestdagh, H Vanhooren, the staff of the biomedical library of the K U Leuven, F Sartor (IPH-L Pasteur, Brussels), R Braham (Le Soir, Brussels), and GlaxoWellcome for their help with references and documents, E Kempeneers for his help with artwork, and D Dizier for the photograph of the statue.
References 1
Balmes JR. Outdoor air pollution. In: Harber P, Schenker MB, Balmes JR, eds. Occupational and environmental respiratory disease. St Louis: Mosby, 1996: 808–26. 2 Costa DL, Amdur MO. Air pollution. In: Klaassen CD, Amdur MO, Doull J, eds. Casarett & Doull’s toxicology. The basic science of poisons. New York: McGraw-Hill, 1996; 857–82. 3 Godlee F. Air pollution I: From pea souper to photochemical smog. BMJ 1991; 303: 1459–61. 4 Abramson M, Voigt T. Ambient air pollution and respiratory disease. Med J Aust 1991; 154: 543–53. 5 Gong H Jr. Health effects of air pollution: a review of clinical studies. Clin Chest Med 1992; 13: 201–14. 6 Schenker M. Air pollution and mortality. N Engl J Med 1993; 329: 1807–08. 7 Logan WPD. Mortality in the London fog incident, 1952. Lancet 1953; 1: 336–38. 8 Brimblecombe P. Air pollution and health history. In: Holgate S, Samet JM, Koren HS, Maynard RL, eds. Air pollution and health. San Diego, London, Boston, New York, Sydney, Tokyo, Toronto: Academic Press, 1999: 5–18. 9 Anderson HR. Health effects of air pollution episodes. In: Holgate S, Samet JM, Koren HS, Maynard RL, eds. Air pollution and health. San Diego, London, Boston, New York, Sydney, Tokyo, Toronto: Academic Press, 1999: 461–82. 10 Firket J. Sur les causes des accidents survenus dans la vallée de la Meuse, lors des brouillards de décembre 1930: résultats de l’expertise judiciaire faite par MM Dehalu, Schoofs, Mage, Batta, Bovy et Firket. Bull Acad R Méd Belg 1931; 11: 683–734.
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11 Batta G, Firket J, Leclerc E. Les problèmes de pollution de l’atmosphère. Liège: Georges Thone, 1933: 1–462. 12 Firket J. Fog along the Meuse valley. Trans Faraday Soc 1936; 32: 1192–97. 13 Anonymous. Atmospheric pollution and pulmonary diseases. BMJ 1931; 1: 277. 14 Haldane J. Atmospheric pollution and fogs. BMJ 1931; 1: 366–67. 15 Storm van Leeuwen W. Die Nebelkatastrophe im Industriegebiet südlich von Lüttich. Münch Med Wochenschr 1931; 78: 4–5. 16 Alke A. Nebelkatastrophen. Münch Med Wochenschr 1931; 78: 160. 17 Grimm G. Nebelkatastrophen. Münch Med Wochenschr 1931; 78: 283. 18 Wolter F. Die Nebelkatastrophe im Maastal südlich von Lüttich. Klin Wochenschr 1931; 10: 785–88. 19 Fenner G. Zur Nebelkatastrophe im Industriegebiet südlich von Lüttich. Chemiker-Zeitung 1931; 55: 69–70. 20 Lambrette A, Hoelper, Fenner G. Zur Nebelkatastrophe im Industriegebiet in der Nähe von Lüttich. Chemiker-Zeitung 1931; 55: 260. 21 Anonymous. Effect of air pollution on health: report of the Committee on Public Health Relations of the New York Academy of Medicine. Bull NY Acad Med 1931; 7: 751–75. 22 Bellelli F. La nebbia che uccide. Riforma Med 1931; 47: 386. 23 Gram HC. Taagekatastrofen i Meusedalen. Ugeskr Laeger 1931; 93: 109. 24 Moureau P. Eloge académique du Professeur Jean Firket (1890–1958). Mém Acad R Méd Belg 1965; 5: 5–26. 25 Bertyn F. Le brouillard et le bétail. Ann Gembloux 1913; 25: 153–73. 26 Bertyn F. Sur les brouillards de la vallée de la Meuse. Ann Gembloux 1931; 37: 20–35. 27 Mage J, Batta G. Le rôle de l’acide fluorhydrique dans la nocivité du brouillard de la Meuse en 1930. Chim Ind 1933; 30: 787–88. 28 Brimblecombe P. The big smoke: a history of air pollution in London since medieval times. London & New York: Routledge, 1988: 1–185. 29 Committee of Departmental Officers and Expert Advisers appointed by the Minister of Health. Mortality and morbidity during the London fog of December 1952: reports on public health and medical subjects, no 95. London: HM Stationery Office. 1954. 30 Roholm K. The fog disaster in the Meuse valley, 1930: a fluorine intoxication. J Indust Hyg Toxicol 1937; 19: 126–37. 31 Lipfert FW. The air pollution disasters. In: Lipfert FW, ed. Air pollution and community health: a critical review and data sourcebook. New York: Van Nostrand Reinhold, 1994: 111–41. 32 Brody H, Rip MR, Vinten-Johansen P, Paneth N, Rachman S. Map-making and myth-making in Broad Street: the London cholera epidemic, 1854. Lancet 2000; 356: 64–68. 33 Mage J, Batta G. Résultats de l’expertise judiciaire sur la cause des accidents survenus dans la vallée de la Meuse pendant les brouillards de décembre 1930. Chim Ind 1932; 27: 961–75. 34 Firket J. The problem of cancer of the lung in the industrial area of Liège during recent years. Proc R Soc Med 1958; 51: 347–52. 35 Schwartz J. Air pollution and daily mortality: a review and meta analysis. Environ Res 1994; 64: 36–52.
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Department of medical history
The Meuse Valley fog of 1930: an air pollution disaster Benoit Nemery, Peter H M Hoet, Abderrahim Nemmar Most courses, lectures, textbook chapters,1,2 and review articles3–6 on the health effects of air pollution begin by referring to the London fog of December, 1952, which led to an increase in deaths of about 4000.7 The London fog became a landmark in air pollution epidemiology because of the scale of the disaster and because it allowed researchers to do the first detailed analysis of the relation between levels of air pollutants and increased morbidity and mortality.8,9 However, an earlier landmark is the fog that affected the Meuse Valley, Belgium, in December, 1930. This episode led to the first scientific proof of the potential for atmospheric pollution to cause deaths and disease, and it clearly identified the most likely causes. Although many present-day investigators1,2,6,9 mention the Meuse Valley fog, few people have probably read the original report, which was presented to the Royal Academy of Medicine of Belgium on May 19, 1931.10 The report was also published, in 1933, as part of a book on air pollution11 and a short version appeared in English in 1936.12
The Meuse Valley fog of December, 1930 The area of Liège on the River Meuse, was once one of the most heavily industrialised areas of continental Europe, with steelworks, zinc smelters, glass manufacturers, and fertiliser and explosives plants established since the industrial revolution. Between Dec 1 and Dec 5, 1930, a thick fog covered a large part of Belgium. From Dec 3 onwards, hundreds of people in the villages situated in the narrow portion of the Meuse Valley between the towns of Huy and Liège (figure 1) started to have severe respiratory signs and symptoms. More than 60 people died in the next 3 days. People in the entire country and abroad were deeply shocked and the deadly fog received considerable media attention. Many dignitaries, including Queen Elisabeth of the Belgians, visited the affected area (figure 2). The event was reported in medical and scientific journals in many countries.13–23 On Dec 6, the Royal Prosecutor of Liège opened a judicial inquiry and a committee of experts was appointed that included Jean Firket (1890–1958), who became professor of pathological anatomy and forensic medicine at the University of Liège after having spent 2 years (1919–21) at Johns Hopkins Medical School, as one of the first fellows of the Belgian American Foundation.24 Other committee members were J Bovy, a forensic specialist; Prof M Schoofs for toxicological analyses; Prof M Dehalu for meteorological observations; and Prof J Mage and Prof G Batta for studies of industrial chemistry. We analysed the expert committee’s report10—the quotes shown below are our translations from the report. Lancet 2001; 357: 704–08 Katholieke Universiteit Leuven, Unit of Lung Toxicology, Laboratory of Pneumology, B-3000 Leuven, Belgium (Prof B Nemery MD, P H M Hoet PhD, A Nemmar DVM) Correspondence to: Prof B Nemery (e-mail: [email protected])
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The expert committee’s report Medical data were obtained by questioning of family physicians and patients in the days immediately after the fog. On the third day the fog reached its maximum opacity and the first symptoms arose simultaneously in people throughout the valley. Most people had laryngeal irritation, retrosternal pain, coughing fits, and “dyspnoeic breathing characterised by paroxysms and slowed expiration, like asthma,” which was rapidly relieved by adrenaline-based drugs. Some patients had “dyspnoea which did not have an asthmatic rhythm, but which was accompanied by signs of pulmonary oedema such as cyanosis, rapid breathing, and even frothy sputum.” Nausea and vomiting were common, but there were no clinical signs of systemic poisoning. Respiratory problems rapidly improved after the fog cleared on Dec 5. The most affected, even when they had remained indoors, were people who were elderly, asthmatic, debilitated, or those with cardiac disease. Even people who were previously healthy were wheezing. Children were described as being indisposed and a few were seriously affected, though none died. There were also respiratory problems in cattle. 60 deaths that were attributed to the fog occurred on Dec 4 and 5. Engis, a town of 3500 inhabitants, had the highest number of deaths.14 The report does not contain demographic or clinical details of the victims, but we calculated from the names and ages of 48 of those listed in newspaper reports (eg, Le Soir, Dec 7 and 8, 1930), that their average age was about 62 years and ranged from 20 to 89 years. The 27 male victims were younger than the 21 female victims, with average ages of about 56 and 70 years, respectively. Ten necropsies that were done showed respiratory tract alterations only. All toxicological analyses of blood or viscera were negative. In all necropsies, there was “congestion of tracheal mucosa and large bronchi— sometimes with an exudate of mucus and fibrin—and areas of epithelial loss, capillary dilatation of the dermis, and a slight leucocyte exudate” (figure 3a). In lung parenchyma, “there were foci of haemorrhage next to areas of moderate oedema and desquamations of alveolar epithelium” (figure 3b). Pure carbon dust particles of 0·5–1·35 m diameter were seen free within the alveoli or engulfed in polynuclear leucocytes. Investigators concluded that the signs and symptoms were entirely and solely due to a local irritant action towards the mucosae directly exposed to the outside air. They ruled out the low temperature and the density of the fog, since similar weather conditions had prevailed over large parts of Belgium. Respiratory infections were also excluded, mainly on clinical grounds. The weather from Dec 1 to 5, was characterised by anticyclonic conditions with high atmospheric pressures and a very feeble (1–3 km/h) easterly wind that blew from the city of Liège into the narrow valley, which had 90–120 m hills on each side. These conditions produced a persistent fog. In the fog the temperature was 1–2°C. However, a temperature inversion at about 70–80 m above ground—ie, just above the tallest chimneys in the valley— prevented the fumes from rising. This atmospheric ceiling forced emitted gases and impurities to accumulate in the
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Figure 1: Map of the Meuse Valley between Liège and Huy, indicating the fog-covered area and location of fatalities and factories Reproduced and modified from figure 1 of Firket and colleagues’ report.10
corridor formed by the valley between Liège and Huy. The report writers calculated that, in the water-saturated and virtually motionless atmosphere, soot particles of 1–4 m diameter would take 1·5–6 days to settle from a height of 60 m. Small and slowly settling solid or liquid particles are easily inhaled, not only in fog but also indoors. Fog that
lasted more than 3 days had only occurred five times in the area over the previous 40 years (in 1901, 1911, 1917, 1919, and 1930). In the fog of January, 1911, cattle had died in a small valley perpendicular to the Meuse valley.25,26 Concentrations of air pollutants in the fog were unknown and subsequent chemical analyses of soil, plants, water, or
Rights were not granted to include this image in electronic media. Please refer to the printed journal.
Figure 2: Funeral cortege of a 60-year-old fog victim, halted in front of Queen Elisabeth Reproduced from Le Soir Illustré Dec 13, 1930.
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Figure 3: Histology of airways and alveolar region in post-mortem specimens from fog victims A) bronchial mucosa with desquamation of epithelium and congestion of submucosal blood vessels; B) alveolar oedema and haemorrhage with small soot particles. Reproduced from figures 4 and 7 of Firket and colleagues’ report.10
other materials were not useful, because of background pollution. There was no evidence of an abnormal release of toxic chemicals by industry. Therefore, the only choice left to the investigators was to measure the fumes, gases, and dusts released by the plants of the area. They identified about 30 substances released by 27 factories. Most pollutants (including CO2, CO, H2, H2S, AsH3, NO2, NH3, HCl, acetylene and other hydrocarbons, sulphites, chlorides, and fluorides and nitrates of zinc or iron) were excluded on the basis of calculations of the worst case scenarios for the amounts released and the symptoms of those affected. Lack of oxygen was dismissed as the cause of the victims’ suffocation. However, “the diffuse superficial mucosal congestion that occurred throughout the respiratory tract down to the bronchioles and lung parenchyma . . . could be attributable to fine irritant particles”. The free or phagocytosed particles in alveoli suggested that they had been inhaled a short time before death. However, carbon particles should have been innocuous, unless they had adsorbed irritant acids. The report writers thus postulated that: “fine soot particles, onto which irritant gases had been adsorbed, had a major role in the noxiousness of the fog”. Investigators attempted to discover which of the irritant agents were most likely to have caused the adverse health effects and deaths. Hydrofluoric acid (HF) was investigated first because it was released from a fertiliser plant in Engis, and had previously affected plants and grazing animals, and damaged light bulbs and window panes. However, the estimated maximum concentration of HF (0·4 mg/m3 for the whole valley) and the simultaneous occurrence of the first symptoms downwind and upwind of Engis meant that a single central source of pollution was unlikely.27 Nevertheless, HF could not be completely ruled out as a contributory cause in the vicinity of the plant. Eventually, sulphur compounds proved the most abundant compounds emitted in the valley. On the basis of the amount of coal burned in industrial and domestic fires (on assumption of a daily consumption of 15 kg per household and a 1% sulphur content in the coal), investigators estimated that more than 60 000 kg of SO2 706
were produced per day, with a resultant SO2 concentration of up to 100 mg/m3 after 4 days of fog. This SO2 concentration exceeded its threshold of toxicity (20–30 mg/m3 for prolonged exposure) and could account for the victims’ symptoms. Moreover, if only one-tenth of the SO2 had been oxidised, a toxic concentration of H2SO4 (then assumed to be 4 mg/m3) would have been exceeded. The report writers pointed out that overpopulation and growing industrialisation had increased sulphur compound pollution, shown by a ten-fold increase in SO3 measured in fresh snow from 1899 to 1931. After a process of successive elimination, the commission concluded “that the sulphur produced by coal burning has had a deleterious effect, either as sulphurous anhydride or acid, or as sulphuric acid; the production of which was made possible by unusual weather conditions”. Various other fanciful explanations, such as the release of war gases by aircraft or abnormal releases of especially toxic chemicals by factories taking advantage of poor visibility during the fog, were dismissed. The narrow topography of the Meuse Valley explained why similar accidents had not occurred in other areas, most notably in London, UK, where much higher levels of SO2 occurred and where dense fogs also persisted for many days; however, in London polluted air probably escaped through lateral diffusion. The report writers warned that a disaster similar to the Meuse Valley one, with a 10·5-fold increase in mortality, if repeated in London would cause 3179 deaths.
Comments and conclusions The air pollution episode in the Meuse Valley 70 years ago revealed a problem that had hitherto received little attention, except in Great Britain.8 Fog episodes had previously been associated with increased mortality in London and Glasgow, but cold weather and viral epidemics could not be ruled out as contributory factors.28,29 The Meuse fog disaster provided incontrovertible evidence that air pollution could kill and therefore it attracted considerable attention from the scientific community. In an editorial in the British Medical Journal, Haldane14 stated that
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“the possibility of a similar disaster happening in this country is a matter of great public health interest”. He thought that disaster had been avoided so far in London because the city emitted a lot of heat, which produced convection currents. Nevertheless, he warned against plans to build big electricity generating stations. Storm van Leeuwen,15 from Leiden, who visited the Meuse Valley, wrote an account of this giant experiment of nature15 from his own observations and conversations with Firket and others. The account shows how new the notion of industrial air pollution was. Storm van Leeuwen evoked and quickly discounted various hypotheses for the catastrophe, such as emission of war gases or toxic sand blown from the Sahara desert. The toxic-sand theory had been aired in the popular and scientific press.20 Another unlikely explanation was that toxic gases had escaped from the polluted soil.18 The possibility that HF was the main culprit was favoured by some writers,19,30 but the commission was probably correct to rule HF and fluorides out for a major role.14,27 The expert commission was remarkable in its mix of disciplines, which included physicians, chemists, and a meteorologist. Their methods were sound. In the absence of air monitoring, comparing medical observations with the possible toxic agents released by industry made sense, as did use of worst-case estimates of exposure concentrations. Some of these simple box-model estimates can be criticised—eg, SO2 concentration was probably overestimated by a factor of ten, at least31 and the estimated concentrations were not always consistent in the report— but they were able to be used to eliminate some of the possible causes. Some detailed analyses—eg, the exclusion of lack of oxygen as a cause of the disaster—might now seem unduly elaborate. However, the experts had to work in a subject area that was still largely unexplored, particularly with respect to quantitative dose-effect relations of inhaled pollutants. Thus, the report contains less than ten references to published work and only two of these pertain to toxicology. A weak aspect of the study was its formal epidemiological methods. Descriptions of symptoms and signs, the temporal and spatial distribution of patients, estimation of the number of deaths and their relation to exposure, and identification of susceptible people are anecdotal. Many basic characteristics, such as the age and sex of those affected, were not recorded systematically. Clinical information was not obtained from written records or by standardised questionnaires, but was noted from conversations with local physicians and examination of an undisclosed number of people from unspecified locations. The committee noted that “several hundreds” of people were affected severely, but did not include the total number of people who lived in the area (around 9000). Excess mortality was calculated by comparison of the total number of deaths with the mean daily deaths over the preceding 5 years in the seven villages where deaths had occurred; investigators did not stratify for age or sex or take into account seasonal or other trends. No graphs were drawn or statistical tests done. Although the Meuse Valley investigation did not have the thoroughness of John Snow’s investigation of the cholera point source in the 1850s,32 it was done with similar logical methods. The increase in morbidity and the sudden ten-fold rise in mortality made detailed statistical analysis unnecessary—unlike the 1952 London fog, when the doubled mortality only became apparent after scrutiny of death certificates.29 The committee established, for the first time, the roles of temperature inversion and fog in air pollution. They concluded that the culprits were coal burning by industry
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Figure 4: Statue and plaque inaugurated in Engis on Dec 2, 2000, in commemoration of those who died in the fog of December, 1930 The text refers first to the youngest victim, a 22-year-old woman, then to the 60 victims in the villages of Amay, Engis, Flémalle, and Seraing. By permission of D Dizier
and by private households. They reasoned that emitted SO2 was a main factor, but that, in addition, fog increased oxidation reactions that led to H2SO4 production, which could be catalysed by iron or zinc. Further (less extensive) studies lent support to these conclusions.33 The possible contribution of very fine soot particles onto which irritants had adsorbed was also noted. The report writers stated that small particles remained in suspension for a long time, that they contaminated even indoor air, and that they penetrated deeply into the respiratory tract. After the Meuse disaster the government appointed another commission, headed by Viscount Berryer, to assess the legislation with respect to industrial air pollution, and to propose improvements. This commission concluded that a central office should grant industrial exploitation permits rather than local authorities. In a book about the Meuse disaster,11 the writers recommended adoption of the British approach of monitoring air pollution. However, little was done since air pollution was considered an unavoidable consequence of prosperity, and the responsibility of industry was carefully played down.11 Thus, although the report states that the Meuse Valley had almost permanent industrial air pollution, the possibility that this could lead to chronic disease was not considered. Diseases caused by air pollution would take many more years to be studied, even by Firket himself.34 Having excluded an exceptional chemical accident as a cause of the disaster, the report’s writers10 concluded that “if the same weather conditions were to take place for the same length of time and with continuation of the same industrial activity, the same accident would happen again”. No major incident has since occurred in the Meuse Valley,
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but the warnings did not prevent similar events taking place in 1948 in Donora, Pennsylvania, and then in London, 1952.7,9,29 Moreover, in Engis and neighbouring villages, a pollution incident on a foggy day in September, 1972, caused respiratory systems in people and, allegedly, deaths in domestic animals; more than 200 complaints were filed (unpublished). Other peaks of air pollution are likely to have increased morbidity and mortality in the area, as recorded in many other locations.35 On Dec 2, 2000, a bronze statue by local artist Paul Vandersleyen and plaque were inaugurated in Engis to commemorate the victims of the deadly fog (figure 4). The final sentence on the plaque reads: “all human endeavours, even industrial ones, are perfectable”. We thank L Mestdagh, H Vanhooren, the staff of the biomedical library of the K U Leuven, F Sartor (IPH-L Pasteur, Brussels), R Braham (Le Soir, Brussels), and GlaxoWellcome for their help with references and documents, E Kempeneers for his help with artwork, and D Dizier for the photograph of the statue.
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