Explore the vast range of titles available.

Background:Low birth weight is associated with lower values for spirometry in adults but it is not known if birth weight influences other measures of pulmonary function. It is also unclear whether postnatal growth affects adult lung function. The associations between birth weight, postnatal growth and adult lung function were assessed in an unselected birth cohort of 1037 children.Methods:Birth weight, weight gain between birth and age 3 years, and lung function at age 32 years were measured. Analyses were adjusted for adult height and sex and further adjusted for multiple other potential confounding factors.Results:Birth weight was positively correlated with spirometric (forced expiratory volume in 1 s and forced vital capacity) and plethysmographic (total lung capacity and functional residual capacity) lung function and with lung diffusing capacity. These associations persisted after adjustment for confounding factors including adult weight, exposure to cigarette smoke in utero and during childhood, personal smoking, socioeconomic status, asthma and gestational age. Weight gain between birth and age 3 years was also positively associated with lung diffusing capacity, and with higher values of lung volumes in men after adjustment for covariates. Neither birth weight nor postnatal weight gain was associated with airflow obstruction.Conclusions:Low birth weight and lower weight gain in early childhood are associated with modest reductions in adult lung function across a broad range of measures of lung volumes and with lower diffusing capacity. These findings are independent of a number of potential confounding factors and support the hypothesis that fetal and infant growth is a determinant of adult lung function.

Asthma exacerbations may be triggered by a number of atmospheric and domiciliary environmental factors as well as by those encountered in schools and workplaces. The majority of exacerbations, particularly in children, coincide with respiratory viral infections, most commonly rhinovirus. As most respiratory viruses and many aeroallergens appear in seasonal patterns, asthma exacerbations, particularly those requiring emergency treatment, show analogous seasonal cycles which differ in form in children and adults. While similar in form between the sexes, they differ in amplitude, with boys having higher risks of exacerbation in childhood and women in adult life. Simultaneous exposure of asthmatics with respiratory viral infections to allergens or air pollutants may significantly increase the risks of exacerbation. Access to and compliance with inhaled corticosteroid treatment is an important predictor of the likelihood of asthma exacerbations occurring, including those that occur during respiratory viral infections. Epidemiologically, the degree of asthma control achieved by asthmatics is an important predictor of the likelihood of disease exacerbation including respiratory failure, death, and health service consumption.

Although genetic predisposition is clearly evident, geneby- environment interaction probably explains much of the international variation in prevalence rates for allergy and asthma. Environmental factors such as infections and exposure to endotoxins may be protective or may act as risk factors, depending in part on the timing of exposure in infancy and childhood. Some prenatal risk factors, including maternal smoking, have been firmly established, but diet and nutrition, stress, use of antibiotics and mode of delivery may also affect the early development of allergy and asthma. Later in childhood, putative risk factors include exposure to allergens, breastfeeding (which may initially protect and then increase the risk of sensitization), family size and structure, and sex and gender. In adulthood, recurrence of childhood asthma may be just as common as new-onset asthma, which may have an occupational basis. A better understanding of these risk factors may eventually lead to opportunities for primary prevention of asthma. Viral infections of the lower respiratory tract affect early childhood wheezing. Whether lower respiratory tract infection promotes sensitization to aeroallergens causing persistent asthma is controversial: childhood viral infections might be pathogenic in some children but protective in others.102-106 Infants of mothers with allergy or asthma have a relatively persistent maturational defect in Th1 cytokine synthesis in the first year of life, which may play a role in the development of persistent or severe viral infections.107 Severe viral infection of the lower respiratory tract in genetically susceptible infants who are already sensitized to inhalant allergens may lead to deviation toward Th2 responses promoting asthma. It is unclear whether these effects of lower respiratory tract infection are virus-specific (e.g., respiratory syncytial virus, rhin ovirus) or whether synergistic exposures to allergens can induce asthma even in individuals who are not genetically susceptible. Interactions of genes with environmental exposures (including allergens, air pollution, environmental tobacco smoke and diet) modulate the host response to infections.108,109 It remains controversial whether the occurrence or timing of childhood infection is pathogenic or protective for the development and long-term outcome of asthma and allergy and of nonallergic wheeze phenotypes. This controversy relates in part to small sample size, cross-sectional analysis, lack of precise case definition and incomplete microbial assessment in studies of this phenomenon.110,111 The relation between exposure to substances in the workplace and new-onset adult asthma was explored among 6837 participants with no previously reported asthma symptoms in phase I of the European Community Respiratory Health Study.187 Exposure to substances known to cause occupational asthma was associated with a higher risk of asthma overall (relative risk [RR] 1.6, 95% confidence interval [CI] 1.1-2.3) and of asthma defined by airway hyperresponsiveness (RR 2.4, 95% CI 1.3-4.6). Of common occupations, nursing was associated with the highest risk of occupational asthma (RR 2.2, 95% CI 1.3-4.0, p = 0.007), whereas exposure to an acute inhalation event, such as fire, mixing of cleaning agents or a chemical spill, was associated with an even higher risk (RR 3.3, 95% CI 1.0-11.1, p = 0.05). The population attributable risk of occupational exposure for adult asthma in that study ranged from 10% to 25%.

Background: Previous guidelines recommend doubling the daily dose of maintenance inhaled corticosteroid to treat or prevent progression of exacerbations of asthma. Methods: Over a 6 month period a cohort of patients were evaluated prospectively and randomised in a double blind controlled trial to treatment with either a continued maintenance dose (MD) of inhaled corticosteroid or doubling the dose (DD) at the time of an exacerbation. Results: A total of 290 patients were randomised (33% male) and 98 (DD, n = 46) experienced evaluable asthma exacerbations during the study period. Mean (SD) baseline characteristics at randomisation (age 33.5 (14.0) years; forced expiratory volume in 1 second (FEV1) 2.8 (0.7) l; peak expiratory flow (PEF) 422.9 (110.5) l/min) were similar in both groups. In the DD group 41% of patients were considered treatment failures because they either required systemic steroids (n = 12), had an unscheduled visit to a physician (n = 1), or their asthma did not return to baseline (n = 6). This did not differ from the MD group in which 40% were treatment failures (n = 9, 0, and 12, respectively; p = 0.94). Conclusions: In patients who regularly take an inhaled corticosteroid, doubling the maintenance dose may not affect the pattern of the exacerbation.

There is increased interest in assessing the family history of psychiatric disorders for both genetic research and public health screening. It is unclear how best to combine family history reports into an overall score. We compare the predictive validity of different family history scores. Probands from the Dunedin Study (n=981, 51% male) had their family history assessed for nine different conditions. We computed four family history scores for each disorder: (1) a simple dichotomous categorization of whether or not probands had any disordered first-degree relatives; (2) the observed number of disordered first-degree relatives; (3) the proportion of first-degree relatives who are disordered; and (4) Reed's score, which expressed the observed number of disordered first-degree relatives in terms of the number expected given the age and sex of each relative. We compared the strength of association between each family history score and probands' disorder outcome. Each score produced significant family history associations for all disorders. The scores that took account of the number of disordered relatives within families (i.e. the observed, proportion, and Reed's scores) produced significantly stronger associations than the dichotomous score for conduct disorder, alcohol dependence and smoking. Taking account of family size (i.e. using the proportion or Reed's score) produced stronger family history associations depending on the prevalence of the disorder among family members. Dichotomous family history scores can be improved upon by considering the number of disordered relatives in a family and the population prevalence of the disorder.

Background/Objectives:Breastfeeding may protect against excessive weight gain during infancy. However, the breast milk components responsible for this effect are unknown. We examined the variation of three breast milk hormones (adiponectin, leptin and insulin) according to maternal characteristics and determined their association with infant body composition.Subjects/Methods:We studied a representative subset of 430 breastfed infants in the CHILD birth cohort. Breast milk was collected at 4 months postpartum and hormone concentrations were measured using the MesoScale Discovery System. Weight-for-length (WFL) and body mass index (BMI) z-scores were calculated according to the World Health Organization reference standard from infant anthropometrics measured at 4 months and 1 year. Maternal BMI and demographics were self-reported.Results:Breast milk hormone concentrations varied widely between mothers. The geometric mean (range) was 19.4 (3.7-74.4) ngml-1 for adiponectin; 361 (31-3968) pgml-1 for leptin; and 589 (53-5557) pgml-1 for insulin. Maternal BMI was positively correlated with breast milk insulin (r=+0.40, P<0.0001) and leptin (r=+0.71, P<0.0001), but not adiponectin (r=-0.02, P=0.68). Breast milk hormone concentrations were also associated with maternal ethnicity, parity and breastfeeding exclusivity at sample collection. Independent of these factors and maternal diabetes, smoking and breastfeeding duration, higher breast milk leptin was associated with lower infant WFL z-score at 4 months (β -0.67, 95% confidence interval (CI): -1.17, -0.17 for highest vs lowest quintile) and 1 year (β -0.58, 95% CI: -1.02, -0.14). Insulin showed a U-shaped association, with intermediate concentrations predicting the lowest infant WFL z-score at 4 months (β -0.51, 95% CI: -0.87, -0.15 for third vs lowest quintile) and 1 year (β -0.35, 95% CI: -0.66, -0.04). Similar results were seen with infant BMI. Breast milk adiponectin was not significantly associated with infant body composition.Conclusions:Breast milk hormone concentrations were associated with several fixed and modifiable maternal characteristics. Higher concentrations of leptin and intermediate concentrations of insulin were associated with lower infant WFL in the first year of life.

Sears discusses the epidemiology of childhood asthma. Asthma is a complex genetic disorder.

BACKGROUND A study was undertaken to investigate the relationship between birth anthropometric measures and the subsequent development of asthma, airway hyperresponsiveness, and atopy in later childhood. METHODS A longitudinal study was performed on 734 subjects (71%) from a cohort of children born in Dunedin, New Zealand in 1972–73. The birth anthropometric measures were available from hospital records and the main outcome measures of reported asthma, skin prick tests, and methacholine hyperresponsiveness were measured at the age of 13 years, while the serum total IgE was measured at 11 years. RESULTS After adjustment for other factors, infants with a larger head circumference at birth tended to have higher serum total IgE at 11 years of age (p = 0.02) but IgE was not associated significantly with birth length or birth weight. The adjusted odds ratio for raised serum IgE (>150 IU/ml) in infants with a head circumference of 37 cm or more was 3.4 (95% CI 1.4 to 7.9). In contrast, recent asthma symptoms were positively associated with birth length (p = 0.04) but not with head circumference. The adjusted odds ratio for asthma in the previous two years in infants with a birth length of 56 cm or more was 6.4 (95% CI 2.0 to 19.8). Infants with a birth weight of less than 3.0 kg had an odds ratio for reported asthma of 0.2 (95% CI 0.0–0.6). There were no significant associations of any of the birth parameters with skin prick positivity, reported hay fever, or eczema. CONCLUSIONS These results suggest that increased fetal growth is related to an increased risk of asthma and atopy in childhood. The precision of the findings is limited by the small numbers in the extreme categories of each birth parameter, but the results are consistent with intrauterine programming of the developing respiratory and immune systems.

ASTHMA is often associated, especially in childhood, with atopy manifested by positive skin tests, a clinical history of allergen-induced wheezing episodes, or concomitant eczema or allergic rhinitis. 1 However, some children and many adults with asthma are apparently not atopic and are considered to have intrinsic (nonallergic) disease. 2 The concept of nonallergic and allergic asthma as two distinct forms has recently been challenged. 3 In one study, the prevalence of asthma was closely related to serum IgE levels standardized according to age and sex. Those with low IgE levels reported no asthma, whereas 28 percent of those with the highest IgE levels . . .