Poliomyelitis resurfaced Virtual elimination of paralytic poliomyclitis from most countries of the Western world constitutes a marvel of modern preventive medicine. The first decline from the annual incidence of 20 to 200 paralytic cases per million Canadians, which prevailed between 1924 and 1954, was observed after the introduction of routine immunization with inactivated poliovirus (Salk) vaccine in 1955; one more epidemic occurred in 1959. After extensive use of live, trivalent, oral poliovirus (Sabin) vaccine, especially between 1962 and 1966, the rate of 5 paralytic cases per million Canadians in 1962 declined to 0.2 or less per million each year from 1967 to 1976.1 However, the risk of contracting paralytic poliomyelitis still exists for unvaccinated Canadians who visit countries of high poliovirus endemicity such as Mexico and Bolivia.2 Comparable declines in the rate of poliomyelitis have been noted in the United States since 1 964,. but disease contracted in foreign countries continues to occur (e.g., in June 1975, paralytic disease affecting an unvaccinated infant who had just returned from Mexico4). Clusters of cases of paralytic poliomyelitis have also involved groups of unvaccinated Americans within their own country (e.g., 11 students at a residential school in Greenwich, Connecticut, in whom paralytic disease developed during the fall of 1972.). In this issue (page 25) Sattar and Westwood report the isolation of five strains of poliovirus type 1, with laboratory characteristics different from those of vaccine strains, from sewage effluent from two primary treatment plants near Ottawa during March and April 1974; this demonstrates the continued prevalence of this serious human pathogen in an urban area of central Canada despite the absence of paralytic disease. Between January and April 1974, 140 samples of effluent from the two sewage treatment plants yielded in addition 10 vaccine strains

of poliovirus, 1 strain of coxsackievirus B4 and 56 isolates of reovirus. During an epidemic of paralytic poliomyelitis in greater Chicago during the summer of 1962 the monthly rate of isolation of enteric viruses, including poliovirus, from sewage was 92% in July, declin ing steadily to 60% during October and zero in November.6 Virus was recovered both from raw sewage and from sluggish river water that received effluent aeration treatment of sewage. In suburban San Diego, California, where the endemic prevalence of enteroviruses is high, enteric viruses were recovered from virtually 100% of samples of raw sewage and primary effluent from treatment plants between 1962 and 19657 Only after activated sludge treatment, retention in an oxidation pond for 30 days, percolation through a sand bed, and chlorination of the percolated fluid with 4 ppm, was virus infectivity of the sewage effluent removed completely. Thus primary treatment alone is ineffective for removal of enteric viruses including important human pathogens such as p0liovirus. Continued discharge of these effluents into natural waters that are used for domestic or recreational purposes may constitute an infectious hazard. Techniques for the reduction of this hazard have recently been augmented through the use of calcium hydroxide in a pilot investigation.8 Despite the low incidence of paralytic poliomyelitis in Canada during the past decade, recovery of potentially virulent poliovirus type 1 strains from sewage effluent must shatter complacency regarding the status of poliomyelitis immunization. Results of serologic surveys of Ottawa primary-school children during October 1972 revealed that 87% had antibodies to all three poliovirus types,9 while 86 to 95% of children and young adults throughout New Brunswick during 1973 had antibodies to the various poliovirus serotypes.10 In Ontario during 1969 and

1970, where Salk vaccine was used routinely, only 65% of children aged 4 to 6 years had antibodies to all three poliovirus types." The proportion of children with antibodies was considerably lower among those who had received Salk vaccine alone than among those who had received a booster of Sabin oral poliovirus vaccine. The proportion of older children with antibodies was higher, presumably because of inapparent natural infection while they were partially protected by Salk vaccine or because of the use of Sabin vaccine during a mass vaccination campaign in 1962. Declining rates of seroimmunity to poliovirus in recent years, combined with the isolation of virulent pol iovirus from environmental samples, provide an important stimulus for a new and vigorous drive towards 100% immunization of the Canadian population with Sabin vaccine. Poliovirus immunization rates among children throughout the US have declined notably from 73.9% in those aged 1 to 4 years and 92.1% in those aged 10 to 14 years during 1965, to 62.9% and 81.9%, respectively, in 1 972.. Sabin vaccine was virtually the sole immunizing agent in use by 1972, when 24.7 million doses were distributed. Equally disconcerting is the absence of antibody to the two important paralytogenic serotypes, poliovirus types 1 and 3, in 7 to 21% of residents under 30 years of age in Tecumseh, Michigan during 1971 ;12 in those aged 5 to 9 years the proportion who were devoid of antibodies to these two serotypes increased from 14 to 18% between 1966 and 1971. Full courses of oral or inactivated poliovirus vaccines had been received by only 42.7% of those under 30 years. In four private practices in Idaho during 197313 only 36% of 813 children aged 2 to 3 years had completed the US Public Health Service recommended immunization schedule, which included Sabin vaccine, in contrast to 49% of

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children who were immunized through a public health unit. Attempts to rectify this deficit in immunization against infectious diseases have been undertaken jointly by governmental, professional and private groups during each October since 1973, which has been designated "immunization action month". Advantages of immunization with Sabin vaccine far outweigh disadvantages. Immunization of infants is started at 4 to 12 weeks of age simultaneously with diphtheria-pertussis-tetanus (DPT) injections, with a second dose 6 to 8 weeks later and a third dose around the first birthday. Seroimmunity persists for many years, even in the absence of natural infection, and there is minimal virus replication in the intestine upon subsequent encounters with wild virus strains. The risk of contracting paralytic disease associated with ingestion of live, attenuated polioviruses in vaccine by index patients or their contacts is at least 30 times less than the risk of paralysis from wild virus infections in nonimmunized subjects. Live vaccine may be

administered rapidly to entire communities to contain the spread of epidemics.5 Although Salk vaccine has induced high levels of seroimmunity in communities initially, antibody levels wane unless boosted by inapparent natural infections,11 and intestinal carriage of wild poliovirus continues unabated.14 With continuing circulation of paralytogenic strains of poliovirus in Canadian urban communities, renewed efforts of professional groups and government agencies should be undertaken to close the nationwide gaps in the immunization program through the extensive use of Sabin vaccine. D.M. MCLEAN, MD, FRCP[C] Professor of medical microbiology University of British Columbia Vancouver, BC

References 1. VARUGHESE P, WHIm F: Poliomyelitis in Canada 1924-1974. Can Dis Wkly Rep 1: 113, 1975 2. VAs SI, CosoRova JBR, SALIT I, Ct al: Paralytic poliomyditis in a traveller - implications for hospital staff. Ibid, p 45 3. Reported morbidity and mortality in the United States 1975. Morb Mortal Wkly Rep annual supp? summary 1975

4. Poliomyclitis - Texas, Connecticut. Morb Mortal Wkly Rep 24: 303, 1975 5. US Public Health Service, Center for Disease Control: Poliomyelitis surveillance, annual summary 1972, Oct 1974 6. LAMa GA, CHIN TDY, SCARCE LE: Isolations of enteric virus from sewage and river water in a metropolitan area. Am J Trop Med Hyg 80: 320, 1964 7. ENGLAND B, LEACH RE, ADAMS B, et al: Virologic assessment of sewage treatment at Santee, California, in Transmission of Viruses by the Water Route, BERG G (ed), New York, Wiley, 1967, p 401 8. SATrAR SA, RAMIA S. WEsTwooo JCN: Calcium hydroxide (lime) and the elimination of human pathogenic viruses from sewage: studies with experimentally-contaminated (poliovirus type 1, Sabin) and pilot plant samples. Can I Public Health 67: 221, 1976 9. Fuansz J: An antibody survey of children in an Ottawa public school. Can I Public Health 64: 398, 1973 10. WYLIE HW, FRANcIs D, DEVADASON C: Immunity survey in New Brunswick 1971/72. Can I Public Health 65: 124, 1974 11. MACLEoo DRE, ING WK, BELCOURT RJP, et al: Antibody status to poliomyelitis, measles, - rubella, diphtheria and tetanus, Ontario, 19691970: deficiencies discovered and remedies required. Can Med Assoc 1 113: 619, 1975 12. OBERHOFER TR, BROWN GC, MONTO AS: Seroimmunity to poliomyelitis in an American community. Am I Epidemiol 101: 333, 1975 13. MCDANIEL DB, PAn-ON EW, MAThER JA: Immunization activities of private-practice physicians - record audit. Pediatrics 56: 504, 1975 14. GELFAND HM, LESLANC DR, POTASH L, et al: Studies on the development of natural immunity to poliomyelitis in Louisiana. IV. Natural infections with polioviruses following immunization with a formalin-inactivated vac-

cine. Am I Trop Med Hyg 70: 312, 1959

Urban stress Urban stress is discussed as if there were a consensus about its meaning, as if the stressors were identified and their pathogenicity known. In fact, the meaning of the term varies with the discipline and perspective of the ..aser. There has never been an inventory of urban stressors because of a lack of taxonomy of the interfaces between man and the environment in terms of *man's behaviour, much less his health. Hence, the stressors identified vary with the user. Moreover, the effects of urban stress are unknown. For one thing, these effects depend on the nature of the stressors and their pathogenic threshold, beyond which maladaptation would occur. For another, the sheer number of identifiable stressors determines the probability of interaction and of cybernetic, cumulative and latent effects, which in turn affect the total pathogenicity of urban stress. Consequently, there has not been any agreement even on the harmful effect or potentially beneficial stimulus of urban stress to mass urban adaptation. Most physicians in the wake of environmental stress repair the human damage and work at random against the shock wave of the etiology of disease. But if medicine is not to lose what is left of its leadership in preserv-

ing and fostering physical, mental and social health - not only in the attempt to heal disease, but also in its prevention and the positive promotion of health and fitness - then physicians must look to the source. Thus, physicians must join with those of their colleagues who are attempting to prevent illness and enhance the quality of life, at the man! environment interface, particularly in urban areas. This does not mean public health, environmental medicine, epidemiology, or even environmental health, for some of these disciplines have become rather narrow in perspective or restricted by tradition (e.g., environmental health should, but does not, deal with the health of the environment). In short, looking at the source of environmental hazards to health means joining transdisciplinary teams, ranging from architects and ecologists to philosophers and scientists, in order to conceptualize and research the physical environment (both natural and artifactual) and the human environment (both social and psychological). The purpose is to find the source of disease and promote health and fitness, which are vital components of the quality of life. Some have explored a taxonomy of the entire field of health and the environment1'2 and taken in the whole range of the en-

vironment, from its natural elemental forms and climatic hazards, to the man/machine interface and the hazards of public and private behaviour. This classification comprises the entire medical nomenclature and attempts to rationalize its idiosyncrasies by placing everything on an etiologic basis. The model for this taxonomy, which provides an inventory of urban stress, is epidemiologic, where a pathogen is identified, in its range of dimensions and threshold; a mode of transmission is described along with the target or population at risk. The dimensions of the stressors are estimated by means of six measurable variables - type of stress, amount, intensity, duration, onset and frequency. This omits the meaning of stress to the person, which cannot be measured in the same way as the other variables. Overcrowding is an example. For this the amount is determined by the population density; its intensity by the peaks it reaches, in public transportation, on streets and in living quarters; its duration by the possibility of avoidance; its onset by the time it began in the life of the individual and of the city; its frequency is self-evident. In addition, the meaning of overcrowding for an individual will depend not only on the location and type of the crowd but also on the pref-

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