Vaccinations, infections and antibacterials in the first grass pollen season of life and risk of later hayfever.

BACKGROUND: It has been hypothesized that early-life exposure to vaccinations, infections or antibacterials influence allergic disease development. Concurrent exposure to grass pollens may alter any effect. OBJECTIVE: To test the hypothesis that exposure to antibacterials, vaccinations (DTP or MMR) or specific infections during the first grass pollen seasons of life influences the risk of hayfever more than at any other time of the year. METHODS: Nested case-control studies were based on birth cohorts within two large databases of computerized patient records from UK general practices: the General Practice Research Database (GPRD) and Doctors' Independent Network (DIN). Seven thousand ninety-eight hayfever cases, diagnosed after age 2, were matched to controls for practice, age, sex and follow-up of control to case ascertainment date. Conditional logistic regression was used to compare exposure by age 1 (age 2 for MMR) inside vs. outside the grass pollen season (May, June, July). Odds ratios (ORs) were pooled across databases. RESULTS: There were no associations in either database between MMR during vs. outside the grass pollen season and later hayfever. Of 23 infections studied, none were statistically significant; although analyses for the less common conditions were limited by low statistical power. The pooled OR for hayfever comparing exposure to antibacterials only in the grass pollen season with only outside it was 1.20 (95% CI 0.98-1.47) and for DTP was 0.84 (95% CI 0.72-0.98). CONCLUSION: Although an interaction between early exposure to microbial agents and concurrent grass pollen exposure on hayfever risk seemed plausible, there was little evidence to support it across a range of analyses. However, the effect of DTP though weak deserves further study.

The role of environmental factors in asthma.

Although the everyday experience of asthmatic patients provides ample anecdotal evidence that environmental exposures provoke bronchospasm, it has proved more difficult to assess the impact of air quality on the timing of asthma attacks and the prevalence of asthma in populations. Spectacular 'asthma epidemic days' are sometimes attributable to exceptional outdoor aero-allergen exposures. By comparison, effects of inorganic particles and gaseous pollutants in outdoor air on the incidence of asthma attacks are subtle and poorly quantified. Environmental tobacco smoke and mould growth are the indoor factors most consistently associated with respiratory morbidity, but their roles in initiating allergic asthma remain uncertain. Evidence relating asthma risk to fumes from gas cooking, and to allergens from dust mites and household pets remains confused and controversial. It is unlikely that trends in either outdoor or indoor air pollution have contributed substantially to the rise in prevalence of asthma and allergic disease in recent decades.

Air pollution, pollens, and daily admissions for asthma in London 1987-92.

BACKGROUND: A study was undertaken to investigate the relationship between daily hospital admissions for asthma and air pollution in London in 1987-92 and the possible confounding and modifying effects of airborne pollen. METHODS: For all ages together and the age groups 0-14, 15-64 and 65+ years, Poisson regression was used to estimate the relative risk of daily asthma admissions associated with changes in ozone, sulphur dioxide, nitrogen dioxide and particles (black smoke), controlling for time trends, seasonal factors, calendar effects, influenza epidemics, temperature, humidity, and autocorrelation. Independent effects of individual pollutants and interactions with aeroallergens were explored using two pollutant models and models including pollen counts (grass, oak and birch). RESULTS: In all-year analyses ozone was significantly associated with admissions in the 15-64 age group (10 ppb eight hour ozone, 3.93% increase), nitrogen dioxide in the 0-14 and 65+ age groups (10 ppb 24 hour nitrogen dioxide, 1.25% and 2.96%, respectively), sulphur dioxide in the 0-14 age group (10 micrograms/m3 24 hour sulphur dioxide, 1.64%), and black smoke in the 65% age group (10 micrograms/m3 black smoke, 5.60%). Significant seasonal differences were observed for ozone in the 0-14 and 15-64 age groups, and in the 0-14 age group there were negative associations with ozone in the cool season. In general, cumulative lags of up to three days tended to show stronger and more significant effects than single day lags. In two-pollutant models these associations were most robust for ozone and least for nitrogen dioxide. There was no evidence that the associations with air pollutants were due to confounding by any of the pollens, and little evidence of an interaction between pollens and pollution except for synergism of sulphur dioxide and grass pollen in children (p < 0.01). CONCLUSIONS: Ozone, sulphur dioxide, nitrogen dioxide, and particles were all found to have significant associations with daily hospital admissions for asthma, but there was a lack of consistency across the age groups in the specific pollutant. These associations were not explained by confounding by airborne pollens nor was there convincing evidence that the effects of air pollutants and airborne pollens interact in causing hospital admissions for asthma.

Family structure, neonatal infection, and hay fever in adolescence.

OBJECTIVE: To determine whether increased numbers of siblings and infection in early life protect against allergic sensitisation. DESIGN: Historical cohort study. SETTING: Sheffield, UK. SUBJECTS: 11,765 children aged 11-16 years for whom a history of neonatal infectious illness had been recorded systematically at 1 month of age. METHODS: A history of hay fever and family structure was obtained by postal questionnaire; neonatal illness history was ascertained from health visitor records; 723 children underwent skin prick testing with mixed grass pollen extract. RESULTS: The prevalence of hay fever was reduced (p < 0.0001) among children of younger mothers, and those from larger families. The number of older siblings exerted a stronger independent effect than the number of younger siblings (p < 0.001). Infants breast fed exclusively during the first month were at higher risk (p < 0.05) of subsequent hay fever, independent of demographic factors. Adolescents at high risk of hay fever by virtue of their family structure were more likely to be sensitised to grass pollen (p < 0.002). No significant relations emerged between hay fever and infection in the first month of life, even among children born in June. CONCLUSIONS: The association of hay fever with family structure is not due to reporting bias and reflects an environmental influence on allergic sensitisation. The effects of sibship size, birth order, and infant feeding are consistent with a protective influence of postnatal infection. The first month of life and the first postnatal exposure to allergen are not the critical periods during which this protective effect is determined.