Sex-specific associations between ambient air pollution exposure thresholds and lung function in middle-aged and older Canadians: an analysis of CLSA data.
Ambient air pollution is associated with reduced lung function, but whether sex modifies the association with threshold-based exposures remains unclear. This cross-sectional study examined sex-specific associations between threshold-based exposures to fine particulate matter (PM2.5), nitrogen dioxide (NO2), ozone (O3), and lung function.
Methods
Data from 21,339 adults aged 45-85 years in the Canadian Longitudinal Study on Aging were analyzed. Annual average air pollutant concentrations representing multi-year exposure estimates (2012-2015) were assigned to participants based on their residential postal codes. Decision tree regression was used to derive exposure cut points and classify participants into low, intermediate, and high exposure thresholds for each pollutant with respect to lung function (FEV1, FVC, and FEV1/FVC ratio). Survey-weighted multivariable linear regression models were used to estimate sex-specific associations with percent-predicted lung function, including interaction terms between sex and exposure thresholds.
Results
Significant sex interactions were observed for PM2.5 and NO2 with percent-predicted FEV1 and FVC, and for O3 with percent-predicted FVC and the FEV1/FVC ratio. Among males, high vs. low PM2.5 exposure was associated with lower FEV1 (-3.11%; 95% CI: -4.47, -1.74) and FVC (-2.72%; 95% CI: -3.76, -1.69). Among females, a significant but smaller FVC reduction was observed (-1.53%; 95% CI: -2.59, -0.47) but not for FEV1. High vs. low NO2 exposure was associated with greater reductions in FEV1 among males (-5.00%; 95% CI: -7.16, -2.84) than among females (-1.99%; 95% CI: -2.79, -1.19), and significantly reduced FVC among males(-3.58%; 95% CI: -5.15, -2.00) but not among females (-1.64%; 95% CI: -3.39, 0.11). High vs. low O3 exposure was associated with reduced FVC in both sexes, with a stronger association among males (-3.34%; 95% CI: -4.37, -2.31) than among females (-2.60%; 95% CI: -3.56, -1.65).
Conclusions
Sex significantly modified the inverse associations between ambient air pollution exposure thresholds and lung function, with greater reductions observed in males. These associations occurred at exposure thresholds at or below current regulatory standards, underscoring the need for continuous reassessment of air quality guidelines to better protect respiratory health.
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
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
BACKGROUND
Chronic lung diseases (CLD) pose a substantial public health burden. Although air pollution is a recognized risk factor, atmospheric humidity may influence respiratory health. Evidence evaluating multidimensional humidity indicators together with air pollution in relation to chronic lung disease in China remains limited.
METHODS
Data from 16,204 adults aged ≥45 years from the 2011, 2013, and 2015 waves of the China Health and Retirement Longitudinal Study (CHARLS) were analyzed. Annual exposures to six air pollutants (CO, NO2, O3, PM2.5, PM10, SO2) and six humidity indicators (RH, AVP, VPD, DPT, MR, SH) were estimated at 1-km resolution. Multivariable logistic regression and restricted cubic spline models were applied. Stratified and sensitivity analyses were conducted.
RESULTS
Higher concentrations of CO, NO2, O3, PM2.5, and SO2 were linearly associated with increased self-reported CLD risk, while PM10 showed an approximate U-shaped relationship. Each interquartile-range increase in air pollutant concentrations was associated with an 18-45% higher odds of self-reported CLD. AVP, VPD, DPT, MR, and SH were positively associated with self-reported CLD risk, whereas RH exhibited an inverted U-shaped pattern. Weighted quantile sum analyses showed significant positive associations for both air pollution and humidity mixtures. A significant interaction between RH and sex was observed. Sensitivity analyses across different lag structures confirmed that air pollutants and atmospheric humidity were consistently associated with self-reported CLD risk.
CONCLUSIONS
Long-term exposure to ambient air pollution and multidimensional humidity indicators was independently associated with higher self-reported CLD risk, highlighting the importance of considering meteorological factors in disease prevention.
Zong-Hui Yang, Xiao-Xia Li· Journal of Asthma· 0 citations
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
AIMS
Despite the high burden of air pollutants, the association between air pollutant exposures and thyroid function in the general population is inconclusive. This study aimed to investigate the association between annual exposure to air pollutants and thyroid function in Korean adults.
METHODS
This cross-sectional study included a total of 16,193 participants (8,812 males, 7,381 females; mean age: 53.8 ± 13.1 years) who underwent health examinations at Seoul National University and had thyroid-stimulating hormone (TSH) concentrations within the range of 0.1-10.0 mIU/L. The yearly average levels of five air pollutants, including particulate matter (PM2.5 and PM10), NO2, SO2, and CO, were estimated using the Community Multiscale Air Quality model. Multivariable linear and logistic regression models were used to examine the associations between annual ambient air pollutant exposures and thyroid function parameters, including TSH and free thyroxine (FT4).
RESULTS
Interquartile range (IQR) increases for PM2.5, PM10, NO2, SO2, and CO were positively associated with TSH and negatively associated with FT4 (all P < 0.001). Significant non-linear associations were observed for PM2.5 and NO₂ with log-transformed TSH, whereas all air pollutants showed non-linear associations with log-transformed FT4. The IQR increases of all air pollutants showed positive associations with the highest quartile of TSH (high TSH) and the lowest quartile of FT4 (low FT4), respectively. When thyroid function was categorized into four groups based on high/low TSH and/or high/low FT4, significantly positive associations were demonstrated with high TSH-low FT4 group, with the strongest association observed for PM10 (adjusted odds ratio [aOR], 1.55; 95% confidence interval [CI], 1.42-1.69), followed by SO2 (1.38, 1.28-1.49), NO2 (1.36,1.23-1.50), PM2.5 (1.25, 1.17-1.34), and CO (1.23, 1.15-1.31). The sex-stratified analyses demonstrated more prominent associations among females.
CONCLUSIONS
Yearly exposure levels of air pollutants were positively associated with TSH, negatively associated with FT4 levels, and significantly associated with high TSH-low FT4. These findings suggest that exposure to ambient air pollution may contribute to thyroid function alterations at the population level, highlighting the importance of air quality improvement. Further longitudinal studies were warranted to consolidate these findings.
Sinyoung Cho, Seo Eun Hwang, J. Yun et al.· Journal of Endocrinological...· 0 citations
Positive associations between long-term exposure to NO2 and CKD incidence were greater in never smokers than in ever-smokers, and stronger associations among never-smokers suggest that environmental exposures may independently influence kidney health.
Gonzalo Hevia-Ramos, Jiawei Zhang, Stephane Tuffier et al.· Journal of Exposure Science...· 0 citations
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