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Background and Objective: The association between birth weight, particularly relative to gestational age, and adult lung function is uncertain. We investigated the associations between birth weight relative to gestational age and measures of lung function in middle age, and mediation of these associations by adult height. Methods: Participants in the Tasmanian Longitudinal Health Study who had both known birth weight and lung function assessment at age 45 years were included (n = 849). Linear regression models were fitted to investigate the association between small for gestational age and birth weight with post‐bronchodilator lung function measures (forced expiratory volume in 1 second [FEV1], forced vital capacity [FVC], FEV1/FVC, diffusing capacity for carbon monoxide [DLco], residual volume [RV] and total lung capacity [TLC]), adjusting for potential confounders. The contribution of adult height as a mediator of these associations was investigated. Results: Compared with infants born with normal weight for gestational age, those born small for gestational age had reduced FEV1 (coefficient: −191 ml [95%CI: −296, −87]), FVC (−205 ml [−330, −81]), TLC (−292 ml [−492, −92]), RV (−126 ml [−253, 0]) and DLco (−0.42 mmol/min/kPa [−0.79, −0.041]) at age 45 years. However, they had comparable FEV1/FVC. For every 1 kg increase in birth weight, lung function indices increased by an average of 117 ml (95%CI: 40, 196) for FEV1, 124 ml (30, 218) for FVC, 215 ml (66, 365) for TLC and 0.36 mmol/min/kPa (0.11, 0.62) for DLco, independent of gestational age, but again not for FEV1/FVC. These associations were significantly mediated by adult height (56%–90%). Conclusion: Small for gestational age was associated with reduced lung function that is likely due to smaller lungs with little evidence of any specific parenchymal impairment. [ABSTRACT FROM AUTHOR]

Background and objective: Early menarche is increasing in prevalence worldwide, prompting clinical and public health interest on its links with pulmonary function. We aimed to investigate the relationship between early menarche and lung function in middle age. Methods: The population‐based Tasmanian Longitudinal Health Study (born 1961; n = 8583), was initiated in 1968. The 5th Decade follow‐up data (mean age: 45 years) included age at menarche and complex lung function testing. The 6th Decade follow‐up (age: 53 years) repeated spirometry and gas transfer factor. Multiple linear regression and mediation analyses were performed to determine the association between age at menarche and adult lung function and investigate biological pathways, including the proportion mediated by adult‐attained height. Results: Girls reporting an early menarche (<12 years) were measured to be taller with greater lung function at age 7 years compared with those reporting menarche ≥12 years. By 45 years of age, they were shorter and had lower post‐bronchodilator (BD) forced expiratory volume in 1 s (adjusted mean difference: −133 mL; 95% CI: −233, −33), forced vital capacity (−183 mL; 95% CI: −300, −65) and functional residual capacity (−168 mL; 95% CI: −315, −21). Magnitudes of spirometric deficits were similar at age 53 years. Forty percent of these total effects were mediated through adult‐attained height. Conclusion: Early menarche was associated with reduced adult lung function. This is the first study to investigate post‐BD outcomes and quantify the partial role of adult height in this association. This is the first longitudinal study with data on key early life confounders to link early age at menarche to lung function deficits in middle age and provide novel evidence on potential biological pathways contributing to this link. [ABSTRACT FROM AUTHOR]

Abstract: Background and objective: Chronic obstructive pulmonary disease (COPD) has potential origins in childhood but an association between childhood measles and post‐bronchodilator (BD) airflow obstruction (AO) has not yet been shown. We investigated whether childhood measles contributed to post‐BD AO through interactions with asthma and/or smoking in a non‐immunized middle‐aged population. Methods: The population‐based Tasmanian Longitudinal Health Study (TAHS) cohort born in 1961 (n = 8583) underwent spirometry in 1968 before immunization was introduced. A history of childhood measles infection was obtained from school medical records. During the fifth decade follow‐up (n = 5729 responses), a subgroup underwent further lung function measurements (n = 1389). Relevant main associations and interactions by asthma and/or smoking on post‐BD forced expiratory volume in 1 s/forced vital capacity (FEV1/FVC; continuous variable) and AO (FEV1/FVC < lower limit of normal) were estimated by multiple regression. Results: Sixty‐nine percent (n = 950) had a history of childhood measles. Childhood measles augmented the combined adverse effect of current clinical asthma and smoking at least 10 pack‐years on post‐BD FEV1/FVC ratio in middle age (z‐score: −0.70 (95% CI: −1.1 to −0.3) vs −1.36 (−1.6 to −1.1), three‐way interaction: P = 0.009), especially for those with childhood‐onset asthma. For never‐ and ever‐smokers of <10 pack‐years who had current asthma symptoms, compared with those without childhood measles, paradoxically, the odds for post‐BD AO was not significant in the presence of childhood measles (OR: 12.0 (95% CI: 3.4–42) vs 2.17 (0.9–5.3)). Conclusion: Childhood measles infection appears to compound the associations between smoking, current asthma and post‐BD AO. Differences between asthma subgroups provide further insight into the complex aetiology of obstructive lung diseases for middle‐aged adults. [ABSTRACT FROM AUTHOR]

Exhaled nitric oxide continues to reflect airway hyperresponsiveness and disease activity in inhaled corticosteroid-treated adult asthmatic patients REID DW, JOHNS DP, FELTIS B, WARD C, WALTERS EH. Respirology 2003; 8: 479–486 Exhaled nitric oxide (eNO) has been used as a surrogate of airway inflammation in mild asthma. However, whether eNO levels reflect disease activity in symptomatic asthmatics receiving moderate doses of inhaled corticosteroid (ICS) is more uncertain. To examine the relationship between eNO levels, sputum and blood eosinophils (SpE and PbE), PD20 methacholine as a marker of airway hyperresponsiveness (AHR) and clinical status in 28 ICS-treated asthmatic subjects with persistent asthma compared to that in 25 symptomatic asthmatics managed with β2-agonists alone. As expected, eNO levels were normalized in ICS-treated subjects and significantly elevated in the β2-agonist only group ( P < 0.001). SpE, PbE and PD20M did not differ between asthmatic groups but FEV1 was significantly worse in ICS-treated subjects ( P < 0.01). Exhaled NO levels correlated with PbE within both asthmatic groups ( P < 0.005), but with SpE only in ICS-untreated subjects (r(s) = 0.6, P < 0.05). In contrast, PD20M was negatively correlated with eNO and PbE in ICS-treated subjects only (r(s) = − 0.4, r(s) = − 0.4, respectively, P < 0.05). SpE and PbE were strongly correlated in both asthmatic groups (r(s) = 0.8, r(s) = 0.7, respectively, P < 0.005). Exhaled NO levels, SpE and PbE were all positively associated with increased nocturnal awakenings ( P < 0.05) in ICS-treated subjects, but not in ICS-untreated subjects. In ICS-treated asthma, eNO reflects clinical activity, PbE and AHR but not eosinophilic airway inflammation. Exhaled NO levels are quantitatively and relationally different in asthmatic subjects treated with ICS and continue to have potential for use as a surrogate of asthma pathophysiology in this group. [ABSTRACT FROM AUTHOR]