Long-term exposure to air pollutants is associated with an increased burden of anemia in children and adolescents, and attention should be focused on vulnerable groups such as girls and underweight children.
Abstract
Background
Air pollution is associated with anemia in children, however, longitudinal data supporting this association are insufficient.
Methods
From 2019 to 2023, we conducted a dynamic cohort study involving 33,900 participants from 119 primary and secondary schools across 16 districts in Shanghai. We obtained the daily average concentrations of five air pollutants (PM2.5, O₃, NO₂, SO₂, and CO) based on school addresses using the China High Air Pollutants (CHAP) dataset to assess the exposure levels of the study subjects. We used latent class mixed models to determine the longitudinal trajectories of hemoglobin (Hb) and multinomial logistic regression models to estimate odds ratios (ORs) and 95% confidence intervals (CIs) between trajectory categories. Linear and logistic regression models were used to evaluate the associations between air pollutant exposure level and Hb and anemia risk, respectively, and Cox regression models was used for longitudinal validation. Interaction terms for gender, age, and body mass index (BMI) were used to explore the modifying effects of these factors.
Results
At the baseline survey, 3,213 students (9.48%) were identified as anemic, with a higher proportion of girls (63.8%). During an average follow-up period of 3.16 years, 1,685 participants (4.9%) were observed to develop anemia. Children's hemoglobin levels showed three different trajectory patterns throughout the study period. Exposure to PM2.5 [OR (95% CI) = 2.124(1.853, 2.433)] was associated with adverse trajectory changes characterized by "low hemoglobin". Longitudinal analysis shows that exposure to PM2.5 [HR = 1.213, 95% CI: (1.068, 1.376)], NO2 [HR = 1.409, 95% CI: (1.254, 1.584)], and SO2 [HR = 1.268, 95% CI: (1.172, 1.372)] is associated with an increased risk of anemia. Stratified analysis showed that the adverse effects of PM2.5 exposure on anemia were more pronounced in younger or underweight children. The adverse effects of NO2 exposure on anemia were more significant in older or obese children. The association between SO2 exposure and the impact on anemia mainly appeared in male or younger children.
Conclusions
Long-term exposure to air pollutants is associated with an increased burden of anemia in children and adolescents, and attention should be focused on vulnerable groups such as girls and underweight children.
Long-term exposure to air pollutants, particularly NO2 and PM10, is associated with an increased risk of microvascular complications among individuals with diabetes, and the observed risk appears to be persistent and may begin at relatively low exposure levels, underscoring the need for preventive strategies targeting environmental risk factors.
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
Household air pollution (HAP) contributes to the global cardiovascular disease burden. Early life exposures may impact future disease risk; however, evidence of HAP’s impact on blood pressure (BP) among children in low-resource settings is limited. We assessed baseline cross-sectional associations between personal exposure to fine particulate matter (PM2.5) and black carbon (BC) and children’s (8–15 years) systolic and diastolic BP (SBP, DBP) from the Sustainable Household Energy Adoption in Rwanda study. We enrolled 626 households in rural Eastern Rwanda that used traditional biomass fuels for cooking. Children wore Ultrasonic Personal Aerosol Samplers for 48 h monitoring of personal exposure, followed by BP measurement using standard protocols. Multiple linear regression was used to characterize associations between PM2.5 and BC exposure and BP in separate models; effect modification by age and sex was evaluated. Among 622 children (mean age = 11.8 years, standard deviation [SD] = 2.1; males = 303, females = 319), the average SBP and DBP were 105.8 mmHg (SD = 10.0) and 68.3 mmHg (SD = 7.6), respectively. BP percentiles were higher than those in a US reference population (e.g. 59.0% and 85.5% had SBP and DBP percentiles >50th, respectively; 24% were classified as having elevated BP and/or were hypertensive, defined as ⩾90th percentile). The median 48 h PM2.5 and BC concentrations were 192.9 µg m−3 (25th percentile [Q1] = 119.7, 75th percentile [Q3] = 336.0) and 9.85 µg m−3 (Q1 = 6.56, Q3 = 13.23), respectively. We did not observe evidence of associations between HAP and BP levels (e.g. PM2.5–SBP = 0.51 mmHg per interquartile range [IQR, 211.7 μg m−3] increase, 95% confidence interval: −0.46, 1.49). We did not observe clear evidence of effect modification. Exposures well above international health-based guidelines may have limited our ability to observe associations if the true exposure–response is flat in that part of the global exposure continuum. Importantly, our BP data suggest an elevated cardiovascular disease burden among children in this low-resource setting compared to in the US, demonstrating a need for more research and the development of more appropriate reference data in these settings. ClinicalTrials.gov Identifier: NCT05668624.
C. Sewor, Kylie Tanner, Vincent Cleveland et al.· Environmental Research: Heal...· 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
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
BACKGROUND
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.
Ugochukwu Odimba, J. Farrell, M. Sadatsafavi et al.· Inhalation Toxicology· 0 citations
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