recovered from the air samplers and those recovered from the cargo hold, together with the placement of the samplers close to the harbor and inside the urban district in which most cases of asthma were registered. Spheroidal particles identified as starch have already been described as a component of soybean dust.22
All the above findings led us to conclude that the unloading of soybeans gave rise to a sudden, massive release of soybean dust that reached the urban area under appropriate meteorologic conditions and caused the outbreaks. In addition, a preliminary analysis of the data on asthma emergencies in Barcelona each day during the 16-month period after the installation of appropriate bag filters at silo A (September 1987) indicates that outbreaks of asthma have disappeared completely.
These results are consistent with those obtained in a serologic case-control study that we carried out recently.35 In 64 of 86 cases occurring during asthma epidemics (74.4 percent), a reaction with commercial soybean-antigen extracts was shown, as compared with only 4 of the 86 matched controls (odds ratio, 61; lower limit of the 95 percent confidence interval, 8.07). No other serologic covariates (total serum IgE levels or specific IgE levels against the most common airborne allergens or legumes) confounded the association between serum antisoybean IgE antibodies and epidemics of asthma. In addition, preliminary characterization of the antigens involved in the outbreaks of asthma in Barcelona has shown that the patients with asthma reacted specifically to an acidic and low-molecular-weight protein band of the dust and hull of the soybean (Morell F, Rodrigo MJ: personal communication).
Asthma epidemics have been described in other cities, including New Orleans,2 New York,1 and Birmingham, England,5 but their specific causes have been controversial. Only castor-bean dust has been reported to be specifically causative of asthma epidemics.8–10 In New Orleans, the marked decline in asthma outbreaks has recently been attributed both to better socioeconomic conditions and the availability of better medical care for indigent patients with asthma, rather than to the disappearance of specific allergens or industrial chemical pollutants.11 In New York City, asthma-epidemic days were more likely to occur when susceptible persons spent more time indoors, suggesting an exposure to agents in the home.28 No relation was found, however, between outdoor air pollution and outbreaks of asthma,36 as in Barcelona.16 In Birmingham, a large asthma outbreak appeared to be caused by Didimella exitialis,5 but a more recent study could not confirm this hypothesis,37 and the question of the origin of the epidemic remains open.38
Soybeans have been identified as causing bronchial asthma, although infrequently so. Most of the cases reported were among mill workers,39–44 and soybean dust is included among the occupational causes of asthma.45–47 Both the frequency of the Barcelona epidemics and the large number of persons affected contrast sharply with the relatively few cases reported hitherto. This unusual epidemiologic presentation may be explained, at least in part, by several local factors: the harbor borders the most densely populated district of the city, soybean dust was released during unloading because of the lack of bag filters in a silo, and outbreaks occurred on days when weather conditions favored the transportation of dust to the city. These conditions may not be unique to Barcelona, and we recommend that whenever outbreaks of asthma occur, the release of soybean dust be considered as a possible cause.
We are indebted to the following members of the Barcelona Asthma Collaborative Group, who participated in various parts of this study: Area de Salut Pública, Ajuntament de Barcelona: José I. Cuervo, Salvador Rueda; Consell Superior d’Investigacions Científiques: Josep Rivera, Domènec Turuguet; Conselleria de Sanitat, Generalitat de Catalunya: Joan Puigdollers; Corporació Metropolitana de Barcelona: Mercè Aceves, Josep M.Serena; Hospital Clínic: Albert Agustí-Vidal, Antoni Ferrer, Francisco Muñoz-López, César Picado, Evaristo Tardío; Hospital de l’Esperança: Josep Lloreta, Carles Sanjuas; Hospital del Mar: Xavier Aran, Joan Broquetas, Eulàlia Tauler; Hospital de Sant Pau: Raimon Cornudella, Joan Nadal, Ignacio Vidal-Quadras; Hospital Sant Joan de Deu: Francesc Fibla, José L.Séculi; Hospital Vall d’Hebron: Jaume Botey, Javier Degracia, José L.Eseverri, Ramon Orriols, María J. Rodrigo; Institut Nacional de Seguretat i Higiene en el Treball: María J.Berenguer, Emili Castejón; and Institut Nacional de Toxicologia: Antonio Garfia, José L.Valverde. We are also indebted to Joan Clos for his constant encouragement and general support; to the medical and nursing staff of the medical wards for their support; to Edwin Kilbourne, Ruth Etzel, Alice Greife, and Henry Falk for scientific advice and technical help; to George Knox for constant scientific support; to Inge Goldstein for her critical review of the epidemic identification method; and to Marta Pulido and Penny Lock for their assistance in editing the manuscript.
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