Background and aims
Development of coeliac disease involves an interaction between environmental factors (especially dietary wheat, rye, and barley antigens) and genetic factors (there is strong inherited disease susceptibility). The known human leucocyte antigen (HLA)‐DQ2 and ‐DQ8 association explains only a minority of disease heritability. A recent study in the Dutch population suggested that genetic variation in the 3′ region of myosin IXB (MYO9B) predisposes to coeliac disease. MYO9B is a Rho family GTPase activating protein involved in epithelial cell cytoskeletal organisation. MYO9B is hypothesised to influence intestinal permeability and hence intestinal antigen presentation.
Four single nucleotide polymorphisms were chosen to tag all common haplotypes of the MYO9B 3′ haplotype block (exons 15–27). We genotyped 375 coeliac disease cases and 1366 controls (371 healthy and 995 population based). All individuals were of White UK Caucasian ethnicity.
UK healthy control and population control allele frequencies were similar for all MYO9B variants. Case control analysis showed no significant association of any variant or haplotype with coeliac disease.
Genetic variation in MYO9B does not have a major effect on coeliac disease susceptibility in the UK population. Differences between populations, a weaker effect size than originally described, or possibly a type I error in the Dutch study might explain these findings.
coeliac disease; myosin IXB; MYO9B
Allergic disorders are common in the UK. This study reviews recent UK time trends in the prevalence, morbidity and mortality for allergic disorders, excluding asthma.
A trend analysis was performed over recent decades of national, representative or repeat surveys, primary care consultations, prescriptions, hospital admissions, and mortality.
Serial surveys showed that the prevalence of diagnosed allergic rhinitis and eczema in children have both trebled over the last three decades. While these long term trends were paralleled by the prevalence of disease symptoms, more recent symptom prevalence data suggest a decline. Similarly, GP consultation rates rose by 260% for hay fever and by 150% for eczema overall during the period 1971–91, but rates have stabilised over the past decade. Hospital admissions for eczema have been stable since 1995, and hospital admissions for allergic rhinitis have fallen to about 40% of their 1990 levels. Since 1990, admissions for anaphylaxis have increased by 700%, for food allergy by 500%, for urticaria by 100%, and for angio‐oedema by 40%. Prescriptions issued for all types of allergy have increased since 1991.
The prevalence and healthcare usage for eczema and hay fever have increased substantially over recent decades, but may now be stabilising or even falling. In contrast, admissions for some systemic allergic diseases have risen sharply in the last decade which may indicate a rising incidence of these conditions. Although changes in treatment and other healthcare factors may have contributed to these trends, there may also be a change in the aetiology of allergic disease in the UK.
trend; allergic disease; epidemiology
Outdoor aeroallergens are one of a number of environmental factors thought to precipitate asthma exacerbations.
To investigate the short term associations between daily fungal spore concentrations and indicators of daily asthma exacerbations in a large urban population.
Daily counts of visits for asthma to family physicians and hospital accident and emergency (A&E) departments and emergency hospital admissions in London 1992–93 were compiled. Daily concentrations of fungal spores (30 species), daily average temperature, humidity, and concentrations of pollen and outdoor air pollution were also compiled. The analysis was restricted to the period when fungal spores were most prevalent (June to mid October). Non‐parametric regression time series methods were used to assess associations controlling for seasonality, day of week, and meteorological factors. The sensitivity of the findings to the inclusion of pollen and air pollution into the models was also assessed.
In children aged 0–14 years the relative risks for increases in the number of A&E visits and hospital admissions associated with changes in fungal spore concentrations from the lower to upper quartiles were 1.06 (95% CI 0.94 to 1.18) and 1.07 (0.97 to 1.19) respectively. The addition of pollen or air pollutants had little impact on the observed associations. A number of individual spore taxa, in particular Alternaria, Epicoccum, Agrocybe, Mildews, and both coloured and colourless Basidiospores and Ascospores, were associated with increases in the number of emergency visits and hospital admissions for asthma, although the precision of these estimates were low. No evidence was found for associations in adults.
Fungal spore concentrations may provoke or exacerbate asthma attacks in children resulting in visits to A&E departments and emergency hospital admissions. These findings were unlikely to be due to confounding by other environmental factors. The associations were comparable to those observed for ambient air pollution from similarly designed studies.
aeroallergens; asthma exacerbations; time series
Hospital admission rates for asthma in Britain rose during the 1980s and fell during the 1990s, but less is known about recent trends in the prevalence of asthma.
In 1991 and 2002 the same questionnaire was distributed to parents of all school pupils in year 3 (aged 7–8 years) in the London borough of Croydon. Parents of currently wheezy children were then invited for home interview (100% targeted in 1991, 66% in 2002).
The prevalence of wheeze during the previous year increased from 12.9% in 1991 to 17.8% in 2002 (prevalence ratio 1.39 (95% CI 1.23 to 1.56)). Increases were observed in frequent (1.54 (95% CI 1.16 to 2.03)) and infrequent attacks, severe speech limiting episodes (2.25 (95% CI 1.34 to 3.77)), and night waking (1.36 (95% CI 1.07 to 1.72)), and in the reported use of steroids (19.9% v 64.1% of currently wheezy children). Nevertheless, the proportions reporting a visit to the GP at his/her surgery for wheeze in the previous year (prevalence ratio 1.15 (95% CI 0.91 to 1.45)) or an outpatient visit (0.98 (95% CI 0.49 to 1.94)) changed little and an increase in reported casualty attendance (1.66 (95% CI 0.89 to 3.07)) was non‐significant.
There is evidence of an increase in the prevalence of asthma among British primary school children between 1991 and 2002. The absence of a corresponding increase in health service utilisation data may reflect more widespread prophylactic treatment and/or changes in the use and provision of medical services.
asthma; prevalence; children; medical services
Patterns of wheezing during early childhood may indicate differences in aetiology and prognosis of respiratory illnesses. Improved characterisation of wheezing phenotypes could lead to the identification of environmental influences on the development of asthma and airway diseases in predisposed individuals.
Data collected on wheezing at seven time points from birth to 7 years from 6265 children in a longitudinal birth cohort (the ALSPAC study) were analysed. Latent class analysis was used to assign phenotypes based on patterns of wheezing. Measures of atopy, airway function (forced expiratory volume in 1 s (FEV1), mid forced expiratory flow (FEF25-75)) and bronchial responsiveness were made at 7–9 years of age.
Six phenotypes were identified. The strongest associations with atopy and airway responsiveness were found for intermediate onset (18 months) wheezing (OR for atopy 8.36, 95% CI 5.2 to 13.4; mean difference in dose response to methacholine 1.76, 95% CI 1.41 to 2.12 %FEV1 per μmol, compared with infrequent/never wheeze phenotype). Late onset wheezing (after 42 months) was also associated with atopy (OR 6.6, 95% CI 4.7 to 9.4) and airway responsiveness (mean difference 1.61, 95% CI 1.37 to 1.85 %FEV1 per μmol). Transient and prolonged early wheeze were not associated with atopy but were weakly associated with increased airway responsiveness and persistent wheeze had intermediate associations with these outcomes.
The wheezing phenotypes most strongly associated with atopy and airway responsiveness were characterised by onset after age 18 months. This has potential implications for the timing of environmental influences on the initiation of atopic wheezing in early childhood.
OBJECTIVE--To investigate the current prevalence of Helicobacter pylori infection in childhood, the risk factors for infection, and the effect of infection on growth in preadolescent schoolchildren. DESIGN--Population based sample of 7 year old schoolchildren followed up at age 11; data on risk factors for infection collected at age 7; presence of infection at age 11 determined by measurement of salivary IgG against H pylori by a newly developed enzyme linked immunosorbent assay (ELISA). Height was measured at 7 and 11 years of age. SUBJECTS--554 schoolchildren from Edinburgh. RESULTS--62 (11%) children had H pylori infection. Independent risk factors for infection were single parent families (adjusted odds ratio = 2.5; 95% confidence interval 1.1 to 5.7), the 10% most crowded homes (3.1; 1.3 to 7.2), and schools serving predominantly rented housing estates (2.5; 1.0 to 6.5). School catchment area was more important than parental social class or housing tenure. Growth in height between 7 and 11 was diminished in infected children by a mean of 1.1 cm (0.3 to 2.0 cm) over four years. This growth reduction was largely confined to girls (1.6 cm over four years), among whom it correlated with salivary IgG (P = 0.015). CONCLUSION--Data from salivary assay to investigate the epidemiology of H pylori suggest that factors relating to the type of community in which the child lives may now be as important for acquisition of this infection as features of the family home. The greater reduction of growth among infected girls raises the possibility that H pylori infection may delay or diminish the pubertal growth spurt.
OBJECTIVE--To test the null hypothesis that there has been no change in the prevalence or severity of childhood asthma over recent years. DESIGN--Repeated population prevalence survey with questionnaires completed by parents followed by home interviews with parents. SETTING--London borough of Croydon, 1978 and 1991. SUBJECTS--All children in one year of state and private primary schools aged 7 1/2 to 8 1/2 years at screening survey. MAIN OUTCOME MEASURES--Trends in symptoms, acute severe attacks, and chronic disability. RESULTS--For 1978 and 1991 respectively, the response rates were 4147/4763 and 3070/3786, and home interviews were obtained from 273/288 and 319/395 parents of currently wheezy children. Between 1978 and 1991 there were significant relative increases in prevalence ratios in the 12 month prevalence of attacks of wheezing or asthma (1.16; 95% confidence interval 1.02 to 1.31), the one month prevalence of wheezing episodes (1.78; 1.15 to 2.74), and the one month prevalence of night waking (1.81; 1.01 to 3.23) but not in frequent (> or = 5) attacks over the past year (1.05; 0.79 to 1.40). There were substantial and significant decreases in the 12 month prevalence of absence from school of more than 10 days due to wheezing (0.52; 0.30 to 0.90), any days in bed (0.67; 0.44 to 1.01), and restriction of activities at home (0.51; 0.31 to 0.83) and an equivalent but not significant fall in speech limiting attacks (0.51; 0.24 to 1.11). CONCLUSION--The small increase in the prevalence of wheezy children and relatively greater increase in persistent wheezing suggests a change in the environmental determinants of asthma. In contrast and paradoxically the frequency of wheezing attacks remains unchanged and there are indications that severe attacks and chronic disability have fallen by about half; this may be due to an improvement in treatment received by wheezy children.
OBJECTIVES: A previous study of the short term effects of air pollution in London from April 1987 to March 1992 found associations between all cause mortality and black smoke and ozone, but no clear evidence of specificity for cardiorespiratory deaths. London data from 1992 to 1994 were analysed to examine the consistency of results over time and to include particles with a mean aerodynamic diameter of 10 microns (PM10) and carbon monoxide. METHODS: Poisson regression was used of daily mortality counts grouped by age and diagnosis, adjusting for trend, seasonality, calendar effects, deaths from influenza, meteorology, and serial correlation. The pollutants examined were particles (PM10 and black smoke), nitrogen dioxide, ozone, sulphur dioxide, and carbon monoxide with single and cumulative lags up to 3 days. RESULTS: No significant associations were found between any pollutant and all cause mortality, but, with the exception of ozone, all estimates were positive. Each pollutant apart from ozone was significantly associated with respiratory mortality; PM10 showed the largest effect (4% increase in deaths of all ages for a 10th-90th percentile increment). The pollutants significantly associated with cardiovascular deaths were nitrogen dioxide, ozone, and black smoke but there was no evidence of an association with PM10. In two pollutant models of respiratory deaths, the effect of black smoke, which in London indicates fine particles of diesel origin, was independent of that of PM10, but not vice versa. CONCLUSION: These results from a new data set confirm a previous report that there are associations between various air pollutants and daily mortality in London. This new study found greater specificity for associations with respiratory and cardiovascular deaths, and this increases the plausibility of a causal explanation. However, the effects of ozone found in the earlier study were not replicated. The fraction of PM10 which comprises black smoke accounted for much of the effect of PM10.
STUDY OBJECTIVE: To describe the epidemiology of Epstein-Barr virus (EBV) among primary school children by testing saliva with a new EBV capsid antigen "G" antibody capture radioimmunoassay (GACRIA). DESIGN: A population based sample of 7 year old schoolchildren were followed up at age 11. SETTING: 30 randomly chosen primary schools in Edinburgh, Scotland. PARTICIPANTS: 552 schoolchildren. MEASUREMENTS: Data on risk factors for infection were collected by questionnaire at ages 7 and 11. Saliva samples collected at age 11 were examined by GACRIA for evidence of previous infection with EBV. For 102 subjects, a second salivary specimen collected approximately one month after the first sample was available for testing as a measure of the repeatability of the method. MAIN RESULTS: Unequivocal results were found in 91% of samples and the repeatability of the test was good (kappa = 0.71). Fifty six per cent of children had antibodies to EBV. In a logistic regression analysis, independent risk factors for infection were sharing a room (odds ratio 1.78, 1.14, 2.79), head of household's social class IV/V compared with I (odds ratio 2.87, 1.08, 7.34), and schools serving predominantly rented housing estates (odds ratio 2.3, 1.09, 4.84). CONCLUSION: This study is the first application of EBV viral capsid GACRIA to salivary samples. The method was successfully used to describe the epidemiology of EBV. In this study, characteristics of the home seemed to be more important than those of the school in determining the likelihood of infection with EBV.
BACKGROUND: A systematic quantitative review of the evidence relating parental smoking to the prevalence of asthma and respiratory symptoms was conducted amongst school age children. METHODS: Sixty relevant studies were identified after consideration of 1593 articles selected by electronic search of the Embase and Medline databases using keywords relevant to passive smoking in children. The search was completed in April 1997 and identified 25 studies of asthma, 41 of wheeze, 34 of chronic cough, seven of chronic phlegm and six of breathlessness which were included in a quantitative overview. RESULTS: The pooled odds ratios for either parent smoking were 1.21 (95% CI 1.10 to 1.34) for asthma, 1.24 (95% CI 1.17 to 1.31) for wheeze, 1.40 (95% CI 1.27 to 1.53) for cough, 1.35 (95% CI 1.13 to 1.62) for phlegm, and 1.31 (95% CI 1.08 to 1.59) for breathlessness. Adjustment for confounding had little effect. Evidence of heterogeneity between studies appeared largely explicable by publication bias with a superfluity of small studies with large odds ratios. However, excluding these had little effect on the pooled odds ratios. The prevalence of all symptoms increased with the number of parents who smoked. While maternal smoking had a greater effect than paternal smoking, the effect of father only was clearly significant. CONCLUSIONS: The relationship between parental smoking and respiratory symptoms seems very likely to be causal given statistical significance, robustness to adjustment for confounding factors, consistency of the findings in different countries, and evidence of dose response. The raised risk in households where the father, but not the mother, smoked argues for a postnatal effect.
BACKGROUND: A systematic quantitative review was conducted of evidence relating parental smoking to acute lower respiratory illness in the first three years of life. METHODS: Fifty relevant publications were identified after consideration of 692 articles selected by electronic search of the Embase and Medline databases using keywords relevant to passive smoking in children. The search, completed in April 1997, identified 24 studies ascertaining illnesses in a community setting, including five surveys of schoolchildren with retrospective ascertainment of early chest illness, and 17 studies of admissions to hospital for lower respiratory illness in early life. Thirty eight studies were included in a quantitative overview using random effects modelling to derive pooled odds ratios. RESULTS: The results of community and hospital studies are broadly consistent, with only one publication reporting a reduced risk among children of smokers. The pooled odds ratios were 1.57 (95% CI 1.42 to 1.74) for smoking by either parent and 1.72 (95% CI 1.55 to 1.91) for maternal smoking. There is a significantly increased risk of early chest illness associated with smoking by other household members in families where the mother does not smoke (1.29, 95% CI 1.16 to 1.44). The associations with parental smoking are robust to adjustment for confounding factors, and show evidence of a dose-response relationship in most studies in which this has been investigated. CONCLUSIONS: The relationship between parental smoking and acute lower respiratory illness in infancy is very likely to be causal. Although it is impossible to distinguish the independent contributions of prenatal and postnatal maternal smoking, the increased risk associated with smoking by other household members suggests that exposure to environmental tobacco smoke after birth is a cause of acute chest illness in young children.
OBJECTIVE: To determine whether serum concentrations of the cytokines tumour necrosis factor alpha (TNF alpha) and interleukin 6 (IL-6), which regulate C reactive protein, are associated with cardiovascular risk factors and prevalent coronary heart disease. DESIGN: A population based cross sectional study. SUBJECTS AND METHODS: 198 men aged 50 to 69 years were part of a random population sample drawn from south London. Serum cytokine and C reactive protein concentrations were determined by enzyme linked immunosorbent assay. The presence of coronary heart disease was determined by Rose angina questionnaire and Minnesota coded electrocardiogram. RESULTS: Serum TNF alpha concentrations were positively related to body mass index and Helicobacter pylori infection, but inversely related to alcohol consumption. IL-6 concentrations were positively associated with smoking, symptoms of chronic bronchitis, age, and father having a manual occupation. TNF alpha was associated with increased IL-6 and triglycerides, and reduced high density lipoprotein cholesterol. IL-6 was associated with raised fibrinogen, sialic acid, and triglycerides. ECG abnormalities were independently associated with increases in IL-6 and TNF alpha, each by approximately 50% (P < 0.05 for TNF alpha, P < 0.1 for IL-6). The corresponding increases in men with an abnormal ECG or symptomatic coronary heart disease were 28% for TNF alpha and 36% for IL-6 (P = 0.14 for TNF alpha and P < 0.05 for IL-6). CONCLUSIONS: This study confirms that many of the phenomena with which C reactive protein is associated, are also associated with serum levels of cytokine, which may be the mechanism.
BACKGROUND: Prevalence surveys of asthma and/or wheezing among all children aged between 7 1/2 and 8 1/2 attending state and private schools in the London Borough of Croydon were conducted in February 1978 and February 1991. Two population based case-control studies drawn from the survey responders were used to investigate the association between childhood wheeze and characteristics of the home environment and to assess whether changes in these characteristics between 1978 and 1991 may have contributed to an increase in the population prevalence of wheeze among school children. METHODS: Information on exposure to potential indoor environmental risk factors was obtained from parents by home interview and compared between cases-that is, children with frequent (> or = 5) or in-frequent (1-4) attacks of asthma or wheezing in the past 12 months- and controls, with adjustment for study. Changes in exposure over time were assessed by comparing control groups. RESULTS: Between 1978 and 1991 the population prevalence odds of wheeze increased by 20% (OR 1.20; 95% CI 1.04 to 1.39). Change in parental smoking, gas cooking, pet ownership, and central heating did not appear to explain the rise. Use of non-feather pillows was positively associated with childhood wheeze even after adjusting for other risk factors and after re-coding from non-feather to feather cases thought to have changed pillow in response to symptoms (OR 1.54; 95% CI 1.13 to 2.10). The proportion of control children reportedly using non-feather pillows was 44% in 1978 and 67% in 1991. CONCLUSIONS: Increased use of non-feather pillows was the only domestic indoor exposure studied which appeared to explain a modest rise in prevalence of wheeze from 1978 to 1991. Our analysis attempts to address behavioural change in response to the child's symptoms but an artifact arising from lifelong avoidance of feather bedding in atopic families cannot be entirely discounted.
BACKGROUND: There is growing concern about health effects of air pollution in the UK. Studies in the USA have reported adverse effects on lung function among children but no comparable studies have been published in the UK. This study investigates the relationship between daily changes in ambient air pollution and short term variations in lung function in a panel of school children. METHODS: One hundred and fifty four children aged 7-11 attending a primary school adjacent to a major motorway in Surrey, south-east England, were studied. Bellows spirometry was performed daily on 31 schooldays between 6 June and 21 July 1994. Levels of ozone, nitrogen dioxide, and particulates of less than 10 microns in diameter (PM10) were measured continuously at the school and the pollen count was measured six miles away. Relationships between daily changes in forced expiratory volume in 0.75 seconds (FEV0.75), forced vital capacity (FVC), the FEV0.75/FVC ratio and pollutants were analysed using separate autoregressive models for each child. A weighted average of the resulting slopes was then calculated. RESULTS: There was a significant inverse relationship between daily mean PM10 levels lagged one day and FVC, with a reduction in lung function of 1% (95% CI 0.3% to 2%) across the whole range of PM10 levels (20-150 micrograms/m3). The effect on FEV0.75 was similar (-0.5%) but was not significant when weighted by 1/SE2 (95% CI -1.2% to 0.2%). There was no effect of PM10 levels on the FEV0.75/FVC ratio. No significant association was seen between FEV0.75, FVC, or the FEV0.75/FVC ratio and either ozone or nitrogen dioxide levels. There was no evidence that wheezy children were more affected than healthy children. Pollen levels on the previous day had no effect on lung function and did not change the air pollution results. CONCLUSIONS: There is a very small, but statistically significant, adverse effect of airborne respirable particulate matter, measured as PM10, on lung function in this study group. There is no evidence for an inverse association of lung function with levels of ozone or NO2 measured on the previous day.
BACKGROUND: In Western societies there is a winter peak in mortality, largely accounted for by respiratory and cardiovascular deaths. In view of the known seasonal variation in vitamin D, and of the postulated link between tuberculosis and vitamin D deficiency, a study was undertaken to examine whether the presentation of tuberculosis had the same seasonal rhythm as other pulmonary infections. METHODS: Using cosinor analysis the presence or absence of seasonality was determined for 57,313 tuberculosis notifications for England and Wales. OPCS data in four weekly notifications over a 10 year period (1983-92) were examined as two quinquential sets (1983-7 and 1988-92). These were compared with two groups of acute respiratory illness: 138,992 notifications to OPCS of pneumonia deaths for 1988-92 and all admissions to Scottish hospitals with respiratory disease (252,163 cases) during 1980-4. RESULTS: Analysis of notifications of tuberculosis revealed a summer peak with an amplitude of 10%. This pattern differs markedly from other respiratory disorders in which a winter peak and summer trough is observed. CONCLUSIONS: The unusual seasonality of tuberculosis is currently unexplained. One possibility is that low post-winter trough levels of vitamin D (which are known to affect macrophage function and cell mediated immunity) might result in impaired cellular immunity leading, after a latent period, to reactivation of dormant mycobacterial infection.
BACKGROUND--In a previous retrospective study of tuberculosis in south London among Asian immigrants from the Indian subcontinent Hindu Asians were found to have a significantly increased risk for tuberculosis compared with Muslims. This finding has been further investigated by examining the role of socioeconomic and lifestyle variables, including diet, as risk factors for tuberculosis in Asian immigrants from the Indian subcontinent resident in south London. METHODS--Using a case-control study technique Asian immigrants from the Indian subcontinent diagnosed with tuberculosis during the past 10 years and two Asian control groups (community and outpatient clinic controls) from the Indian subcontinent were investigated. Cases and community controls were approached by letter. A structured questionnaire concerning a range of demographic, migration, socioeconomic, dietary, and health topics was administered by a single trained interviewer to subjects (56 cases and 100 controls) who agreed to participate. RESULTS--The results confirmed earlier findings that Hindu Asians had an increased risk of tuberculosis compared with Muslims. However, further analysis revealed that religion had no independent influence after adjustment for vegetarianism (common among Hindu Asians). Unadjusted odds ratios for tuberculosis among vegetarians were 2.7 (95% CI 1.1 to 6.4) using community controls, and 4.3 (95% CI 1.8 to 10.4) using clinic controls. There was a trend of increasing risk of tuberculosis with decreasing frequency of meat or fish consumption. Lactovegetarians had an 8.5 fold risk (95% CI 1.6 to 45.4) compared with daily meat/fish eaters. Adjustment for a range of other socioeconomic, migration, and lifestyle variables made little difference to the relative risks derived using either community or clinic controls. CONCLUSIONS--These results indicate that a vegetarian diet is an independent risk factor for tuberculosis in immigrant Asians. The mechanism is unexplained. However, vitamin D deficiency, common among vegetarian Asians in south London, is known to affect immunological competence. Decreased immunocompetence associated with a vegetarian diet might result in increased mycobacterial reactivation among Asians from the Indian subcontinent.
OBJECTIVE: To investigate variations in the prevalence of self reported symptoms, diagnosis, and treatment of asthma in 12-14 year old children. DESIGN: Self completion questionnaire. SETTING: Great Britain. SUBJECTS: All pupils aged 12-14 years in a stratified cluster sample of 93 large mixed secondary schools in 1995. MAIN OUTCOME MEASURES: Self reported prevalence of symptoms, diagnosis, and treatment of asthma at four geographical levels. RESULTS: 27,507 questionnaires were completed (85.9% response rate). The national 12 month prevalence of any wheezing, speech limiting wheeze, four or more attacks of wheeze, and frequent night waking with wheeze was 33.3% (n = 9155), 8.8% (2427), 9.6% (2634), and 3.7% (1023) respectively. The prevalence of ever having had a diagnosis of asthma was 20.9% (5736). In total, 19.8% (5438/27,507) of pupils reported treatment with anti-asthma drugs in the past year, but, of pupils reporting frequent nocturnal wheeze in the past year, 33.8% (342/1012) had no diagnosis of asthma and 38.6% (395/1023) denied receiving inhaler therapy. The 12 month prevalence of wheeze was highest in Scotland (36.7%, 1633/4444), but in England and Wales there was no discernible north-south or east-west gradient. Wheeze prevalence was slightly higher in non-metropolitan areas (35.0%, 6155/17,605) than in metropolitan areas (30.3%, 3000/9902). The prevalence of self reported asthma diagnosis and inhaler use showed no discernible national, regional, north-south, or east-west geographical pattern but was higher in non-metropolitan areas. CONCLUSION: Prevalence of self reported symptoms, diagnosis, and treatment of asthma was high among 12-14 year olds throughout Great Britain with little geographical or urban-rural variation. Underdiagnosis and undertreatment were substantial.
OBJECTIVE: To investigate whether changes in certain perinatal and social factors explain the increased prevalence of hay fever and eczema among British adolescents between 1974 and 1986. DESIGN: Two prospective birth cohort studies. SETTING: England, Wales, and Scotland. SUBJECTS: 11,195 children born 3-9 March 1958 and 9387 born 5-11 April 1970. MAIN OUTCOME MEASURES: Parental reports of eczematous rashes and of hay fever or allergic rhinitis in the previous 12 months at age 16. RESULTS: The prevalence of the conditions over the 12 month period increased between 1974 and 1986 from 3.1% to 6.4% (prevalence ratio 2.04 (95% confidence interval 1.79 to 2.32)) for eczema and from 12.0% to 23.3% (prevalence ratio 1.93 (1.82 to 2.06)) for hay fever. Both conditions were more commonly reported among children of higher birth order and those who were breast fed for longer than 1 month. Eczema was more commonly reported among girls and hay fever among boys. The prevalence of hay fever decreased sharply between social classes I and V, increased with maternal age up to the early 30s, and was lower in children whose mothers smoked during pregnancy. Neither condition varied significantly with birth weight. When adjusted for these factors, the relative odds of hay fever (1986 v 1974) increased from 2.23 (2.05 to 2.43) to 2.40 (2.19 to 2.63). Similarly, the relative odds of eczema rose from 2.02 (1.73 to 2.36) to 2.14 (1.81 to 2.52). CONCLUSIONS: Taken together, changes between cohorts in sex, birth weight, birth order, maternal age, breast feeding, maternal smoking during pregnancy, and father's social class at birth did not seem to explain any of the observed rise in the prevalence of hay fever and eczema. However, correlates of these factors which have changed over time may still underlie recent increases in allergic disease.
OBJECTIVE: To describe risk factors for infantile colic. DESIGN: Questionnaire administered by health visitors. SETTING: Sheffield. SUBJECTS: Mothers of 76,747 infants born between 1 August 1975 and 31 May 1988, interviewed when the infant was 1 month old. MAIN OUTCOME MEASURES: Reporting of infantile colic and its duration; weight of infant leeding, state of the home, socioeconomic characteristics of the parents, parents' age, and mother's parity. RESULTS: The odds of reporting infantile colic were increased with breast feeding (odds ratio of breast v bottle feeding 1.35 (95% confidence interval 1.28 to 1.43)), increasing parental age, lower parity, increasing parental age at leaving full time education, and more affluent homes and districts of residence. In a logistic regression analysis, mother's age and parity and socioeconomic factors remained the most important risk factors for the reporting of infantile colic (each P < 0.005), and the effect of breast feeding was attenuated (odds ratio of breast v bottle feeding 1.09 (1.02 to 1.15)). CONCLUSION: At a population level, dietary factors contribute little to mothers' reporting of infantile colic, and dietary change should not be the primary intervention.
OBJECTIVE AND SETTING: To examine time trends in stroke mortality in Greater London compared with the surrounding South East Region of England. DESIGN: Age-cohort analysis based on routine mortality data. SUBJECTS: Resident population aged 45 years or more. MAIN OUTCOME MEASURE: Age specific stroke mortality rates, 1951-92. MAIN RESULTS: In 1951, stroke mortality was lower in Greater London than the surrounding South East Region in all age bands over 45. It has been declining in both areas but the rate of decline has been significantly slower in Greater London (p < 0.0001). The differences in rates of decline were such that stroke mortality is now higher in Greater London for people under 75. The crossover of age specific stroke mortality rates occurred at different periods in different age bands and is consistent with a cohort effect, with similar rates in Greater London and the surrounding south east for men and women born around 1916-21. This cohort effect does not appear to be consistent with past maternal and neonatal mortality rates in these areas, nor, within the limitations of the data, with the ethnic composition of cohorts. CONCLUSIONS: There seems to be a cohort effect on stroke mortality which is not explained by past maternal and neonatal mortality. If the decline in stroke mortality continues at its current rate, the Health of the Nation stroke target is unlikely to be achieved in Greater London.
BACKGROUND: Previous studies of the effects of passive exposure to smoke on spirometric indices in children have largely relied on questionnaire measures of exposure. This may have resulted in underestimation of the true effect of passive smoking. Biochemical measures offer the opportunity to estimate recent exposure directly. METHODS: The relation between spirometric indices and passive exposure to tobacco smoke was examined in a large population sample of 5-7 year old children from 10 towns in England and Wales. The effects of passive exposure to smoke on lung function were assessed by means of both salivary cotinine concentration and questionnaire measurements of exposure. Analyses of the relation between spirometric values and cotinine concentrations were based on 2511 children and of the relation between spirometric values and questionnaire measures on 2000 children. RESULTS: Cotinine concentration was negatively associated with all spirometric indices after adjustment for confounding variables, which included age, sex, body size, and social class. The strongest association was with mid expiratory flow rate (FEF50), the fall between the bottom and top fifths of the cotinine distribution being 6%, equivalent to a reduction of 14.3 (95% confidence limits (CL) 8.6, 20.0) ml/s per ng/ml cotinine. Salivary cotinine concentrations were strongly related to exposure to cigarette smoke at home but 88% of children who were from non-smoking households and not looked after by a smoker had detectable cotinine concentrations, 5% being in the top two fifths of the cotinine distribution. A composite questionnaire score based on the number of regular sources of exposure was as strongly related to mid and end expiratory flow rates as the single cotinine measure. The fall in FEF50 per smoker to whom the child was exposed was 51.0 (26.5, 75.5) ml/s. The relationships between the questionnaire score and forced vital capacity (FVC) or forced expiratory volume in one second (FEV1) were not statistically significant. CONCLUSIONS: These effects of passive smoking on respiratory function are consistent with the results of previous studies and, although small in absolute magnitude, may be important if the effects of exposure are cumulative. In children aged 5-7 years the use of a single salivary cotinine concentration as a marker of passive exposure to smoke resulted in clear relationships between exposure and FVC and FEV1, whereas the associations were much weaker and not significant when based on the questionnaire score. The associations between exposure and mid or end expiratory flow rates were of similar magnitude for cotinine concentration and the questionnaire score. The use of salivary cotinine concentration in longitudinal studies may help to determine the extent to which these effects are cumulative or reversible.
OBJECTIVE--To investigate the relation between seropositivity to chronic infections with Helicobacter pylori and Chlamydia pneumoniae and both coronary heart disease and cardiovascular risk factors. DESIGN--Cross sectional study of a population based random sample of men. Coronary heart disease was assessed by electrocardiography, Rose angina questionnaire, and a history of myocardial infarction; serum antibody levels to H pylori and C pneumoniae were measured, risk factor levels determined, and a questionnaire administered. SETTING--General practices in Merton, Sutton, and Wandsworth, south London. SUBJECTS--388 white south London men aged 50-69. MAIN OUTCOME MEASURES--Evidence of coronary risk factors and infection with H pylori or C pneumoniae. RESULTS--47 men (12.1%) had electrocardiographic evidence of ischaemia or infarction. 36 (76.6%) and 18 (38.3%) were seropositive for H pylori and C pneumoniae, respectively, compared with 155 (45.5%) and 62 (18.2%) men with normal electrocardiograms. Odds ratios for abnormal electrocardiograms were 3.82 (95% confidence interval 1.60 to 9.10) and 3.06 (1.33 to 7.01) in men seropositive for H pylori and C pneumoniae, respectively, after adjustment for a range of socioeconomic indicators and risk factors for coronary heart disease. Cardiovascular risk factors that were independently associated with seropositivity to H pylori included fibrinogen concentration and total leucocyte count. Seropositivity to C pneumoniae was independently associated with raised fibrinogen and malondialdehyde concentrations. CONCLUSIONS--Both H pylori and C pneumoniae infectins are associated with coronary heart disease. These relations are not explained by a wide range of confounding factors. Possible mechanisms include an increase in risk factor levels due to a low grade chronic inflammatory response.