This study examines the association between air pollution exposure and health using a representative survey sample from Siddharthanagar municipality of Nepal. Our data on household characteristics, spatial locations and individual lung function allow us to understand heterogeneity in exposure and respiratory health. We examine exposure differential through three potential mechanisms – occupation, residence and exposure avoidance. We employ a simultaneous equations model to account for the endogenous choice of avoidance and spatial error models to control for the spatial spillover of health outcomes. We find that outdoor workers and those residing near brick kilns have lower lung function. Exposure avoidance positively correlates with lung function. Exposure avoidance, however, is low among marginalized outdoor workers and individuals residing in polluted areas, further exacerbating the exposure gap among socioeconomic subgroups. The study advances the case of environmental inequity through the ‘triple jeopardy’ of low socioeconomic status, exposure differences and poor health.

Vitamin D deficiency has previously been linked to higher rates of exacerbation and reduced lung function in asthmatics. Previous randomised controlled trials investigating the effect of vitamin D supplementation have mainly focused on children with asthma. Trials involving adults have typically used bolus dosing regimens, and the main outcomes have been patient-focused without investigating underlying inflammation. The present study aimed to conduct a 12-week placebo-controlled randomised controlled trials administering a daily 125 µg vitamin D3 supplement to adults with mild to moderate asthma. A total of 32 participants were randomised to receive either the 125 μg vitamin D3 supplement or an identical matching placebo. The primary outcome of the study was lung function measured by the ratio of FEV1:FVC (effect size 2·5) with secondary outcomes including asthma symptoms and inflammatory biomarkers. There was a small but statistically significant higher increase in the mean (±sd) ratio of FEV1:FVC from baseline to post-intervention in the vitamin D group (+0·05 ± 0·06) compared with the placebo group (+0·006 ± 0·04, P = 0·04). There was no effect of the intervention on asthma control test scores, or the inflammatory biomarkers measured. There was a moderate, significant association between baseline plasma 25(OH)D concentration and baseline plasma IL-10 (r = 0·527, P = 0·005) and TNF-α (r = −0·498. P = 0·008) concentrations. A daily vitamin D3 supplement led to slightly improved lung function in adult asthmatics and may be a useful adjunct to existing asthma control strategies, particularly for individuals with suboptimal vitamin D status.

This study aimed to investigate the association between n-3 PUFA and lung function. First, a cross-sectional study was conducted based on the National Health and Nutrition Examination Survey (NHANES) 2007–2012 data. n-3 PUFA intake was obtained from 24-h dietary recalls. A multivariable linear regression model was used to assess the observational associations of n-3 PUFA intake with lung function. Subsequently, a two-sample Mendelian randomisation (MR) was performed to estimate the potential causal effect of n-3 PUFA on lung function. Genetic instrumental variables were extracted from published genome-wide association studies. Summary statistics about n-3 PUFA was from UK Biobank. Inverse variance weighted was the primary analysis approach. The observational study did not demonstrate a significant association between n-3 PUFA intake and most lung function measures; however, a notable exception was observed with significant findings in the highest quartile for forced vital capacity (FVC) and % predicted FVC. The MR results also showed no causal effect of circulating n-3 PUFA concentration on lung function (forced expiratory volume in one second (FEV1), β = 0·01301, se = 0·01932, P = 0·5006; FVC, β = −0·001894, se = 0·01704, P = 0·9115; FEV1:FVC, β = 0·03118, se = 0·01743, P = 0·07359). These findings indicate the need for further investigation into the impact of higher n-3 PUFA consumption on lung health.

Premature birth, bronchopulmonary dysplasia or restrictive nutrition in the first weeks of postnatal life may have repercussions on lung development and affect long-term lung function outcomes. This prospective observational study is based on a cohort of 313 very low birth weight (VLBW) neonates, born between 1 January 2008 and 1 December 2016. The daily intake of calories, protein, fat and carbohydrates during the first week of life and evidence of inadequate weight gain (Δwt) until week 36 of gestational age (GA) were recorded. FEV1, FEF25–75 %, forced vital capacity (FVC) and the FEV1/FVC ratio were determined. The relations between these parameters were determined by regression analysis. Spirometric parameters were obtained for 141 children with a mean age of 9 years (95 % CI 7, 11); 69 of them (48·9 %) had presented wheezing episodes on more than three occasions. In addition, 60 (42·5 %) had a history of bronchopulmonary dysplasia. Of these, n 40 (66·6 %) had a history of wheezing. Significant association between protein/energy intake in the first week of life and the lung function parameters analysed was observed. Poor Δwt to GA week 36 was significantly associated with decreased mean pulmonary flow. Inadequate protein/energy intake in the first week of life of VLBW newborns and poor Δwt to week 36 of GA is associated with a significant worsening of lung function parameters.

Adipocytokines, which are secreted during fetal development by both mothers and fetuses, may influence fetal lung development, but little human data are available. We used data from the HOME Study to investigate the associations of cord blood adipocytokine concentrations with children’s lung forced expiratory volume (FEV1; N = 160) and their risk of wheeze (N = 281). We measured umbilical cord serum adipocytokine concentrations using enzyme-linked immunosorbent assays and FEV1 using a portable spirometer at ages 4 and 5 to calculate the percent predicted FEV1 (%FEV1). Parents completed standardized questionnaires of their child’s wheeze symptoms every 6 months from birth to age 5, then again at ages 6 and 8. We used multivariable linear mixed models and modified Poisson regression with generalized estimating equations to estimate associations of adipocytokine concentrations (log2-transformed) with children’s %FEV1 and the risk of wheeze, respectively, adjusting for sociodemographic, perinatal, and child factors. Cord serum leptin was not associated with children’s %FEV1. Higher cord serum adiponectin concentrations were associated with higher %FEV1 in girls (β = 3.1, 95% confidence interval [CI]: 0.6, 5.6), but not in boys (β = −1.3, 95% CI: −5.9, 3.3) (sex × adiponectin p-value = 0.05). Higher leptin was associated with lower risk of wheeze in girls (RR = 0.74, 95% CI: 0.66, 0.84), but not boys (RR = 0.87, 95% CI: 0.69, 1.11) (sex × leptin p-value = 0.01). In contrast, higher adiponectin concentrations were associated with lower risk of wheeze (RR = 0.84, 95% CI: 0.73, 0.96) in both boys and girls. These data suggest that fetal adipocytokines may impact lung development and function in early childhood. Future studies are needed to confirm these findings and explore the mechanisms underlying these associations.

Asthma-obesity is a multifactorial disease with specific asthma phenotypes that aggravate due to overweight and an unbalanced diet. Furthermore, obese asthmatic patients are corticotherapy-resistant. Therefore, the aims of the present study were to evaluate the effects of an interdisciplinary intervention on food consumption, body composition, lung function and adipokines in asthmatic and non-asthmatic obese adolescents and to investigate the influence of nutrients on lung function. Obese non-asthmatic (n 42) and obese asthmatic (n 21) adolescents of both sexes were enrolled in the present study. Food intake, adipokine levels, body composition, asthma symptoms and lung function were assessed across the study. After the intervention of 1 year, there was a reduction (P ≤ 0·01) in BMI, body fat percentage, visceral and subcutaneous fat and an increase (P ≤ 0·01) in lean mass and all lung function variables in both groups, except the relation between forced expiratory volume in 1 s and forced vital capacity (FEV1:FVC) in non-asthmatic patients. Moreover, both groups decreased lipid and cholesterol consumption (P ≤ 0·01). The highest energy consumption (β = −0·021) was associated with lower values of FVC. Similarly, carbohydrate consumption (β = −0·06) and cholesterol were negative predictors (β = −0·05) in FEV1:FVC. However, the consumption of Ca (β = 0·01), fibres (β = 1·34) and vitamin A (β = 0·01) were positive predictors of FEV1:FVC. Asthma-obesity interdisciplinary treatment promoted an improvement on food consumption and lung function in adolescents and demonstrated that the consumption of nutrients influenced an increase in lung function.

Lutein, a fat-soluble carotenoid with antioxidant properties, may have an effect on respiratory health. However, the evidence is inconsistent. We aimed to cross-sectionally investigate the association between lutein intake and lung function by measuring forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC% in adults (aged 45–79 years). We included 4402 participants from the Rotterdam Study, a prospective cohort study in The Netherlands. Lutein intake was assessed using a validated FFQ. Lung function was assessed using spirometry around the same time point as the dietary assessment. No independent association was found between lutein intake and FEV1 (−12·17 (95 % CI −34·21, 9·87) ml per sd increase in lutein) after adjustment for age, sex, height, cohort effect, ethnicity, education, weight, total daily energy intake, smoking status, physical activity, and intakes of fatty acids, dietary fibre, alcohol, β-carotene, β-crypotoxanthin, lycopene and zeaxanthin. There was also no association between lutein and FVC or FEV1/FVC%. However, after stratification by smoking status, lutein intake was significantly associated with lower FEV1/FVC% in current smokers (−1·69 (95 % CI −2·93, −0·45) % per sd increase of lutein) independent of other carotenoids. The present study does not support an independent association between lutein intake and lung function in adults. However, future studies should focus on the potential inverse association between high lutein intake and lung function in specific risk groups such as smokers.

The aim of this study is to explore the effectiveness of microgravity simulated by head-down bed rest (HDBR) and artificial gravity (AG) with exercise on lung function. Twenty-four volunteers were randomly divided into control and exercise countermeasure (CM) groups for 96 h of 6° HDBR. Comparisons of pulse rate, pulse oxygen saturation (SpO2) and lung function were made between these two groups at 0, 24, 48, 72, 96 h. Compared with the sitting position, inspiratory capacity and respiratory reserve volume were significantly higher than before HDBR (0° position) (P < 0.05). Vital capacity, expiratory reserve volume, forced vital capacity, forced expiratory volume in 1 s, forced inspiratory vital capacity, forced inspiratory volume in 1 s, forced expiratory flow at 25, 50, and 75%, maximal mid-expiratory flow and peak expiratory flow were all significantly lower than those before HDBR (P < 0.05). Neither control nor CM groups showed significant differences in pulse rate, SpO2, pulmonary volume and pulmonary ventilation function over the HDBR observation time. Postural changes can lead to variation in lung volume and ventilation function, but a HDBR model induced no changes in pulmonary function and therefore should not be used to study AG countermeasures.

Asthma is a common childhood disease and several risk factors have been identified; however, the impact of genes and environment is not fully understood. The aim of the Swedish Twin study On Prediction and Prevention of Asthma (STOPPA) is to identify environmental (birth characteristics and early life) and genetic (including epigenetic) factors as determinants for asthmatic disease. Based on the Child and Adolescent Twin Study in Sweden (CATSS) (parental interview at 9 or 12 years, N ~23,900) and an asthma and/or wheezing algorithm, we identified a sample of monozygotic (MZ) and dizygotic (DZ) same-sexed twin pairs. The twin pairs were classified as asthma concordant (ACC), asthma discordant (ADC) and healthy concordant (HCC). A sample of 9- to 14-year-old twins and their parents were invited to participate in a clinical examination. Background characteristics were collected in questionnaires and obtained from the National Health Registers. A clinical examination was performed to test lung function and capacity (spirometry with reversibility test and exhaled nitric oxide) and collect blood (serology and DNA), urine (metabolites), feces (microbiota), and saliva (cortisol). In total, 376 twin pairs (752 individual twins) completed the study, response rate 52%. All participating twins answered the questionnaire and >90% participated in lung function testing, blood-, and saliva sampling. This article describes the design, recruitment, data collection, measures, and background characteristics, as well as ongoing and planned analyses in STOPPA. Potential gains of the study include the identification of biomarkers, the emergence of candidates for drug development, and new leads for prevention of asthma and allergic disease.

Maternal nutritional status during pregnancy has been reported to be associated with childhood asthma and atopic disease. The Avon Longitudinal Study of Parents and Children has reported associations between reduced umbilical cord Fe status and childhood wheeze and eczema; however, follow-up was short and lung function was not measured. In the present study, the associations between maternal Fe status during pregnancy and childhood outcomes in the first 10 years of life were investigated in a subgroup of 157 mother–child pairs from a birth cohort with complete maternal, fetal ultrasound, blood and child follow-up data. Maternal Fe intake was assessed using FFQ at 32 weeks of gestation and Hb concentrations and serum Fe status (ferritin, soluble transferrin receptor and TfR-F (transferrin receptor:ferritin) index) were measured at 11 weeks of gestation and at delivery. Maternal Fe intake, Hb concentrations and serum Fe status were found to be not associated with fetal or birth measurements. Unit increases in first-trimester maternal serum TfR concentrations (OR 1·44, 95 % CI 1·05, 1·99) and TfR-F index (OR 1·42, 95 % CI 1·10, 1·82) (i.e. decreasing Fe status) were found to be associated with an increased risk of wheeze, while unit increases in serum ferritin concentrations (i.e. increasing Fe status) were found to be associated with increases in standardised mean peak expiratory flow (PEF) (β 0·25, 95 % CI 0·09, 0·42) and forced expiratory volume in the first second (FEV1) (β 0·20, 95 % CI 0·08, 0·32) up to 10 years of age. Increasing maternal serum TfR-F index at delivery was found to be associated with an increased risk of atopic sensitisation (OR 1·35, 95 % CI 1·02, 1·79). The results of the present study suggest that reduced maternal Fe status during pregnancy is adversely associated with childhood wheeze, lung function and atopic sensitisation, justifying further studies on maternal Fe status and childhood asthma and atopic disease.

The first Hungarian Twin Registry was established in Budapest in 1970 through the mandatory reporting of multiple-births. In the 1980s a second, volunteer adult registry was also founded. Unfortunately, both registries ceased to exist in the 1990s. Efforts started in 2006 to revive a Hungarian twin registry. The team spearheading this effort reports here on this progress. Currently, the voluntary Hungarian Twin Registry consists of 310 adult twin pairs and multiplets. Current research focuses on cardiovascular and respiratory health and yielded multiple awards and publications. Efforts are on the way to expand into social, psychological, and obesity studies.

Most studies on lung function heritability have been conducted in smokers and non-smokers using cross-sectional study design. Smoking patterns may, however, confound the contribution of genetic factors. We investigated heritability of forced expiratory volume in one second (FEV1), forced vital capacity (FVC), and FEV1/FVC ratio longitudinally, excluding the effects of smoking. A sample of never smoking female twins (n = 374), aged 63–76 at baseline, answered health questionnaires and attended spirometry in years 2000 and 2003. Bivariate structural equation modeling, restricted to adequate spirometry performances (baseline n = 339, follow-up n = 252), was used to estimate genetic and environmental influences on consecutive measurements of FEV1, FVC, and FEV1/FVC. The best-fitting models included additive genetic and non-shared environmental effects. Heritability estimates of 32% and 36% for FEV1, 41% and 37% for FVC, while 46% and 16% for FEV1/FVC were found at baseline and at follow-up. Genetic correlation between FEV1 and FEV1/FVC heritability estimates approached unity, whereas correlation between FVC estimates was 0.80. Environmental correlations were 0.69 for FEV1, 0.62 for FVC, and 0.07 for FEV1/FVC. In never smokers, additive genetic and non-shared environmental effects explain the inter-individual variations in FEV1, FVC, and FEV1/FVC. One third of the variation in FEV1 and FVC is explained by genetic and two thirds by environmental effects. Between 2000 and 2003, environmental effects on FEV1/FVC changed, and the proportion of variance explained by environmental effects increased remarkably. Genetic effects on FEV1 and FEV1/FVC are common to consecutive measurements, whereas at follow-up, new genetic factors explained 14% of the observed variance in FVC.