[The short-term effects of air pollution on mortality. The results of the EMECAM project in the city of Vigo, 1991-94. Estudio Multicéntrico Español sobre la Relación entre la Contaminación Atmosférica y la Mortalidad]. / Efectos a corto plazo de la contaminación atmosférica sobre la mortalidad. Resultados del proyecto EMECAM en la ciudad de Vigo, 1991-94.

BACKGROUND: In the Autonomous Region of Galicia, no study has been made of the impacts of air pollution on human health, despite the fact that several of its major cities have moderate levels of pollution. Therefore, we have considered the need of making this study in the city of Vigo. The main objective of this analysis is that of analyzing the short-term impact of air pollution on the daily death rate for all reasons in the city of Vigo throughout the 1991-1994 period, by using the procedure for analysis set out as part of the EMECAM Project. METHOD: The daily fluctuations in the number of deaths for all causes with the exception of the external ones are listed with the daily fluctuations of sulfur dioxide and particles using Poisson regression models. A non-parametric model is also used in order to better control the confusion variables. RESULTS: Using the Poisson regression model, no significant relationships have been found to exist between the pollutants and the death rate. In the non-parametric model, a relationship was found between the concentration of particles on the day immediately prior to the date of death and the death rate, an effect which remains unchanged on including the autoregressive terms. CONCLUSIONS: Particle-based air pollution is a health risk despite the average levels of this pollutant falling within the air quality guideline levels in the city of Vigo.

Epidemiology of otorhinolaryngological squamous cell papillomas in a Spanish subpopulation during a 20 year period.

We present a study of the incidence of squamous cell papillomas on the otorhinolaryngological field, in a population of approximately 500,000 inhabitants between 1973 and 1992. We have reviewed 234 papillomas. The overall incidence of ENT papillomas was 2.4737 x 10(5) inhabitants per year. The most frequent location was the pharynx, followed by oral cavity, larynx and sinonasal tract. In the ear these lesions were very rare. No significant increase in incidence rates were found over the four year periods, except for pharyngeal papillomas. The median age at onset of ENT papillomas was 47.11 years (range = 4 to 83 years). Only 7,3% of papillomas were of juvenile type. The male to female ratio was 2,1. Male preponderance occurred in pharyngeal and laryngeal papillomas. Only lesions of the ear were most frequent in the female population. 54,9% of patients were smokers. The highest incidence of smoking habit was found in laryngeal papillomas. Only two patients in our series had HIV infection, and in both cases the papillomas were located in the oral cavity. This study shows that the incidence of ENT papillomas has remained constant and that adult preponderance is more marked in our population than in others reported previously. The pathogenesis of the ENT squamous papillomas in our population is related with an acquired HPV infection without clear relation to genital disease.

[ORL emergencies at a health center: a study of the incidence during 1990]. / Urgencias ORL en un centro de salud: estudio de la incidencia durante el año 1990.

We present a retrospective study of 942 ENT emergencies in a Health Center (primary care), during the year 1990, treated by family physicians. They are analysed under different parameters such as date, time, sex, age, diagnosis, drug prescription and dispatch of the patients to the hospital. We carried out an analysis of the quality of the attention given.

[The evolution of the incidence of tuberculosis in the La Coruña health area]. / Evolución de la incidencia de enfermedad tuberculosa en el área sanitaria de La Coruña.

BACKGROUND: Tuberculosis represents a major public health problem. In Spain, the incidence of tuberculosis is among the highest in the European Community, and shows an increasing trend. The aim of this study is to determine the incidence and temporal trends of tuberculosis in the catchment area of the "Hospital Juan Canalejo" (La Coruña, Spain), between 1982 and 1991. METHODS: Revision of all case records of tuberculosis with positive bacteriology and detected by the Epidemiological Vigilance System of the Preventive Medicine Unit of the "Hospital Juan Canalejo", diagnosed between January 1982 and December 1991. The incidence of tuberculosis as a function of age, sex, period, and county, was modeled with Poisson regression. RESULTS: 1120 cases were studied. The relative risk of tuberculosis in females with respect to males was 0.50 (95% confidence interval 0.44 to 0.56; p < 0.001) with a peak of increased risk between 15 and 35 years of age in both genders. With respect to temporal trends, the risk of tuberculosis increased from 1986 in females and from 1987 in males. CONCLUSIONS: Over the last decade, the incidence of tuberculosis has increased in the study area, with higher risk in males and young adults.

Immunoresponses to Neisseria meningitidis epitopes: suppression of secondary response to phosphorylcholine is carrier specific.

Results of our previous work have shown that Neisseria meningitidis serogroup B M986 can induce a phosphorylcholine (PC)-specific plaque-forming cell immunoresponse in mice. Also, a single injection of a relatively low dose of meningococci in NBF1 female mice induced a priming time-dependent suppression on subsequent meningococcus challenge. This suppression was not due to switching to another class of immunoglobulin nor to the presence of a capsule on N. meningitidis. In this study we show that suppression induced by meningococcus is carrier specific. Furthermore, we offer evidence suggesting that the structure(s) on meningococcus that trigger this suppression is heat labile and different from the antigenic structure(s) recognized by the suppressed B cells. In addition, we found that there is a gradual increase in antibody secretion rates of N. meningitidis-induced anti-PC plaque-forming cells that correlates with N. meningitidis priming time. Rather unexpected was the fact that pretreatment of mice with PC-keyhole limpet hemocyanin (thymus-dependent antigen) had a great influence on the subsequent PC-specific immunoresponses induced by N. meningitidis and PC-coupled heat-inactivated meningococcus [PC-(NMB)HI], as shown by (i) a striking decrease in T15 idiotype expression, (ii) concomitant direct anti-PC plaque-forming cells reduction, (iii) switching to immunoglobulin G (N. meningitidis-induced immunoresponse) or immunoglobulin G plus immunoglobulin A [PC-(NMB)HI-induced immunoresponse], and (iv) a significant increase in heterogeneity of plaque-forming cell secretion rates. The possibility that N. meningitidis, PC-(NMB)HI, and PC-KLH stimulate B lymphocytes pertaining to three different subpopulations embedded in distinct regulatory circuits is discussed, with emphasis on the interrelationships between T-dependent and T-independent lymphocyte compartments. We focus on the possibility of the existence of high-level regulatory circuits in which lymphocyte subpopulations or sets of lymphocyte subpopulations with different requirements of activation are connected.

Effects of antigen and internal environment on anti-phosphorylcholine immune responses of autoimmune aged NZB/W F1 mice.

The idiotypic profile of anti-phosphorylcholine plaque-forming cell responses and their evolution with ageing were studied in (NZB X NZW) F1 mice. Our results showed that the anti-phosphorylcholine plaque-forming cell response induced by phosphorylcholine coupled to keyhole limpet haemocyanin and, paralleling, the T15 idiotype clonal dominance declined with ageing. This loss of immune competence was also observed with another thymus-dependent (phosphorylcholine coupled to egg globulin) as well as thymus-independent (capsular polysaccharide of Streptococcus pneumoniae strain R36a) antigens. In contrast, old mice challenged with an antigenic preparation of Neisseria meningitidis showed an immune response not significantly different from that elicited by the same antigen in young mice. The hapten-augmentable plaque-forming cells were assayed to determine whether a putative auto-antiidiotypic regulation underlies this loss of immune competence. Only minimal numbers and non-significant differences between young and old mice immunized with any antigen could be detected. Further studies using an adoptive transfer system demonstrated that cells from aged mice were able to support a normal anti-phosphorylcholine response when transferred into lethally irradiated young recipients. Our results suggest that no permanent cellular defects, but rather internal environment or/and radioresistant suppressor cells, are involved in this loss of immune competence. The role played by these factors and their effect on distinct subpopulations of B cells are discussed.

Immunoresponses to Neisseria meningitidis epitopes: in vivo analysis of immunocompetent cells involved in suppression of secondary response to phosphorylcholine.

The immune response to phosphorylcholine (PC) antigens has been extensively studied in recent years. Neisseria meningitidis serogroup B M986 (NMB) was recently reported to induce a PC-specific plaque-forming cell (PFC) immuno-response in mice, a characteristic useful for the study of immunomodulating properties of N. meningitidis. With this technique, priming mice with low doses of NMB has been shown greatly to impair their ability, one month after priming, to mount an anti-PC response induced by NMB; this suppression is permanent, does not involve switching from IgM to another immunoglobulin class, transiently affects the T15 idiotype expression and is carrier specific. We report, based on an analysis of spleen cells from NMB-primed mice in an adoptive transfer model, that this suppression does not appear to be mediated by B lymphocytes nor does it seem to be under the direct control of T lymphocytes; rather, it involves radio-resistant cells. Additionally, our results show that NMB modulates the idiotype composition of the anti-phosphorylcholine response, probably by enhancing the expression of so called hapten-augmentable PFC. These results demonstrate that NMB can interfere effectively with the immune response in a variety of ways.

[Anti-phosphorylcholine response of autoimmune NZB/W mice: variations with age of serum titers and homogeneity]. / Respuesta antifosforilcolina de ratones autoinmunes NZB/W: variaciones con la edad del título y homogenidad de los sueros.

Antibody titers and avidity of sera of autoimmune NZB/W mice in responses induced by different antigens were determined. Results show an age-dependent decrease of the antibody titer in sera from female mice immunized with phosphorylcholine coupled to keyhole limpet haemocyanin. This decrease was not detected when using as immunogen an antigenic preparation of Neisseria meningitidis that naturally induces anti-phosphorylcholine antibodies, but was detected with a modification of this antigen (heat inactivation and further coupling with the hapten). Determinations of inhibition profiles of antisera suggest that this loss of immune competence is paralleled by a decrease in avidity and homogeneity of antisera. This finding may be related to the loss of idiotypic clonal dominance recently reported to occur in these mice.

Immunoresponses to Neisseria meningitidis epitopes: immunomodulation by meningococcus B acts on more than one meningococcal surface epitope.

Neisseria meningitidis group B strain M986 (serotypes 2a, 7) (NMB) elicits a specific primary antiphosphorylcholine immune response in mice but not a secondary response. The ability of other serotype and serogroup meningococci to induce similar primary responses in mice was studied, as was the immunogenicity of trinitrophenyl coupled NMB (TNP-NMB) in primary and secondary antitrinitrophenyl responses. Except for NMB, all other strains tested (three serogroup B and one serogroup A meningococcal strains) were found to be very poor phosphorylcholine immunogens. TNP-NMB, however, though proving to be a very good TNP antigen, was only a weak phosphorylcholine antigen. Priming NBF1 female mice with TNP-NMB one month or more before challenging them with the same antigen induced a strong depression of anti-TNP response in the subsequent challenge. However, this effect was not observed with Xid NBF1 male mice. Furthermore, priming mice with NMB weakly affected the anti-TNP response, but greatly depressed the antiphosphorylcholine response, after TNP-NMB challenge. In addition, whereas apparently only one TNP-specific B cell subpopulation was responding in unprimed mice challenged simultaneously with TNP-NMB and TNP-Ficoll (non-additive response), priming mice with NMB appeared to facilitate the independent activation of two different TNP-specific B cell subpopulations (additive response).