Background: Lung function, expressed as forced expiratory volume in 1 second (FEV1), reaches its maximum at 20–30 years of age. A lower maximal lung function has been associated with a higher risk of chronic obstructive pulmonary disease in later adulthood, but the impact of smoking and indoor environmental exposures on this maximum remains unclear. Methods: Using data from 858 participants of the Dutch PIAMA birth cohort (mean age: 25.7 years), we investigated associations between smoking, second-hand smoke (SHS), dampness or mold, furry pets, and gas cooking exposure with maximal lung function. Exposure data were collected via questionnaires from pregnancy through early adulthood, and life-course exposure trajectories were derived using latent class growth modeling. We assessed associations with FEV1 and forced vital capacity (FVC) using linear regression, adjusting for potential confounders. Results: Pre- and post-bronchodilator spirometry was available for 846 and 806 participants, respectively. We found no associations between exposure to dampness or mold, furry pets, or gas cooking and lung function. Current and life-course active smoking was associated with higher post-bronchodilator FEV1, and pre- and post-bronchodilator FVC [regression coefficient β for pre-bronchodilator FVC (ml) (95% confidence interval): current (yes vs. no) 175 (68, 281), life-course (regular vs. occasional or none) 168 (55, 281)]. Current SHS was positively associated with post-bronchodilator FVC. Conclusion: No associations were found between indoor environmental exposures and maximal lung function in early adulthood. The observed positive associations with active smoking likely reflect bias arising from a selective uptake of smoking by individuals with higher pre-existing lung function, rather than a true physiological effect.
Diana M. Hendrickx, G. Koppelman, J. Vonk et al.· Environmental Epidemiology· 0 citations
BACKGROUND
Air pollution and diet both affect lung health and may interact. We investigated whether a healthy diet may modify associations between air pollution and lung function in adults.
METHODS
Modelled annual-average concentrations of nitrogen dioxide (NO2) and particulate matter with aerodynamic diameters ≤10 μm (PM10) and ≤2.5 μm (PM2.5) were linked to residential address points of 260,982 individuals in the UK Biobank cohort. Averaged air pollution concentrations in the year of spirometry and two years prior to spirometry measurements were used. The healthy diet score (HDS) was calculated based on dietary data collected at baseline. Effect modifications by HDS and individual food components (fruit and vegetables) on the associations of air pollution and lung function were investigated.
RESULTS
Participants in the highest HDS group had higher forced expiratory volume in 1-second(FEV1) and forced vital capacity(FVC) than those in the lowest group in both males and females. Interactions between HDS and air pollution were not seen. Suggestive evidence of total fruit intake effect modification on PM2.5-FEV1 was observed in females. Exposure to PM2.5 per 5 μg/m3 increment was associated with reduced FEV1 in the low of -14.4 mL(95%CI: -26.8, -2.2) but not in medium and high fruit intake groups (+2.9 mL(95%CI: -13.8,19.7) and +9.7 mL(95%CI: -4.1,23.6), respectively). A similar pattern was observed for FVC.
CONCLUSIONS
We found suggestive evidence that higher consumption of fruit may partially reduce the adverse effects of air pollution on lung function in females. These findings merit investigation to see if they replicate in other cohorts.
Pimpika Kaewsri, F. Dudbridge, J. Cade et al.· Environmental Research· 0 citations
Evidence on the link between air pollution and inflammatory responses is scarce, especially during early life. This study investigates the associations between air pollution exposure, respiratory outcomes, and cytokine responses during the first year of life, and whether these are modified by sex and temperature. The association of residential exposure to ambient PM2.5, PM10, and NO2 with the prevalence of bronchitis and wheezing in 1-year-old infants (n = 606) was examined using logistic regression. In the subcohort (n = 508) with cytokine data (TNF-α, MCP-1, IL-8, IL-6, and IL-10, pg/mL) after lipopolysaccharide stimulation, single pollutants were correlated with inflammatory biomarkers by linear regression, and mixture effects were estimated using Bayesian kernel machine regression (BKMR). All models were stratified by sex and adjusted for covariates and residential greenness. Estimates were calculated per IQR increase in PM2.5, PM10, and NO2 exposures: 2.0, 2.8, and 9.1 μg/m3, respectively. In boys, an IQR increase in PM2.5 was associated with higher odds of bronchitis (aOR = 1.50, 95% CI: 1.02 - 2.23) and IL-8 concentrations (23.8%, 95% CI: 11.2 - 37.9%). In girls, an IQR increase in PM2.5 was associated with elevated concentrations of IL-8 (31.9%, 95% CI: 18.6 - 46.7%) and TNF-α (12.8%, 95% CI: 3.9 - 22.6%). All air pollutants were consistently associated with increased IL-10 concentrations in girls, with PM2.5 having the strongest effect (35.7%, 95% CI: 14.4 - 61.1%) per IQR increment. BKMR mixture analyses revealed a positive non-linear association between the air pollutant mixture, IL-8, and TNF-α when all air pollutants exceeded their 60th percentile. Infants in the upper temperature tertile showed stronger associations with IL-8 in response to PM2.5 and NO2 exposures. Altogether, our findings suggest that PM2.5 is the primary predictor of respiratory outcomes and inflammatory responses during the first year of life.
S. Gómez-Olarte, S. Röder, K. de Hoogh et al.· Environmental Pollution· 0 citations
INTRODUCTION
Air pollution is a leading environmental risk factor for cardiovascular disease (CVD), yet its relationship with metabolic syndrome (MetS) and its components in sub-Saharan Africa are unclear. This study aimed to examine the association between long-term PM2.5 exposure and MetS (and its component conditions) in a Ghanaian adult cohort.
METHODS
We performed a cross-sectional analysis of 1,833 adults (40-60 years) from the Awi-Gen study. Long-term PM2.5 exposure (2007-2015) was estimated via a satellite-based model. MetS was defined using harmonized criteria. We used multivariable logistic regression with sequential adjustment for covariates.
RESULTS
A positive association was observed between PM2.5 and hypertension, while no association was found for MetS overall or its component conditions. Each 1 μg/m3 increase in PM2.5 was associated with 6% higher odds of hypertension (OR: 1.06, 95% CI: 1.02-1.11). PM2.5 quartiles also showed a dose-response relationship with hypertension (p-trend=0.003), with the highest exposure linked to a 50% greater likelihood of hypertension. The calculated population attributable fraction for PM2.5 and hypertension was 18.6%.
INTERPRETATION
In this rural Ghanaian population, long-term PM2.5 exposure was associated with hypertension but not with metabolic syndrome or its other components. These findings provide important evidence from an understudied sub-Saharan African population and support the integration of air quality management into cardiovascular disease prevention strategies.
Ali Moro, E. Nonterah, Godfred Agongo et al.· Environmental Research· 0 citations
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