Introduction: Short-term associations between ambient air pollution and cardiovascular morbidity remain inconsistent across different settings. This study evaluated these associations using Generalized Additive Models (GAMs) and examined the robustness of the findings through lag and sensitivity analyses.

Materials and methods: An ecological time-series analysis was conducted using a publicly available environmental–health dataset comprising 5,811 daily observations of air pollutant concentrations, meteorological variables, and aggregated cardiovascular morbidity indicators. GAMs with penalized smoothing splines were fitted to assess potentially non-linear exposure–response relationships while adjusting for meteorological covariates. Lag structures (Lag 0–3 days), alternative spline dimensions, and multi-pollutant models were evaluated as sensitivity analyses.

Results: The final GAM demonstrated limited explanatory capacity (AIC=25,602.9; AICc=25,604.6; explained deviance=1.04%). Pollutant smooth terms showed shallow non-linear exposure–response patterns (effective degrees of freedom: 8.36-9.40), but none were statistically significant (PM₂.₅: p=0.357; PM₁₀: p=0.950; NO₂: p=0.594; SO₂: p=0.339; O₃: p=0.530). Sensitivity analyses produced consistent results across alternative lag structures and spline dimensions, and model diagnostics indicated satisfactory fit without evidence of substantial over dispersion.

Conclusion: Only shallow, statistically non-significant short-term associations were identified. These findings should be interpreted within the limitations of the ecological design, potential exposure misclassification, and residual confounding.

Introduction: Traffic-Related Air Pollution (TRAP) is a major source of urban air pollution, with vehicular emissions releasing Particulate Matter (PM₂.₅ and PM₁₀), Nitrogen dioxide (NO₂) and Carbon monoxide (CO) into the atmosphere . Short-term exposure to these pollutants has been linked to adverse cardiovascular effects, including increased blood pressure, reduced Heart Rate Variability (HRV) and arterial stiffness . However, evidence on the immediate cardiovascular responses of healthy young adults following roadside exposure remains limited. This study evaluated the acute cardiovascular effects of short-term exposure to TRAP.

Materials and methods: Sixty healthy volunteers aged 18-25 years participated in a 45-min  roadside exposure study at a busy urban location. Ambient PM₂.₅, PM₁₀, NO₂, and CO concentrations were continuously monitored using validated portable air quality sensors and integrated monitoring techniques . Cardiovascular parameters, including systolic and diastolic blood pressure, HRV (RMSSD and SDNN) and arterial stiffness, were measured before and after exposure using standardized non-invasive instruments . Pre- and post-exposure differences were analyzed using paired t-tests and correlation analysis was performed to examine associations between pollutant concentrations and cardiovascular responses.

Results: PM₂.₅ concentrations ranged from 92–118 µg/m³ and NO₂ concentrations from 58–72 ppb, exceeding the World Health Organization air quality guideline values. Following exposure, systolic blood pressure increased by 4–6 mmHg, HRV indices decreased by 10–20% and arterial stiffness increased. PM₂.₅ concentrations were significantly associated with increased blood pressure and reduced HRV, consistent with previous studies.

Conclusion: Short-term exposure to traffic-related air pollution produced measurable cardiovascular changes in healthy young adults, including elevated blood pressure, reduced HRV, and increased arterial stiffness. These findings highlight the importance of strengthening urban air quality management and reducing roadside pollution exposure to minimize cardiovascular health risks.

Introduction: Ambient air pollution poses significant public health challenges across urban and semi-urban India. Karnataka, encompassing coastal, plateau, highland, and semi-arid environments, provides an ideal setting for evaluating regional air quality variability and associated health risks. This study assessed the spatio-temporal characteristics of ten criteria and hazardous air pollutants measured at five Central Pollution Control Board (CPCB) Continuous Ambient Air Quality Monitoring Stations (CAAQMS) across Karnataka during 2024.

Materials and methods: Monthly mean concentrations of Particulate Matters (PM₂.₅, PM₁₀), Nitrogen dioxide (NO₂), Sulfur dioxide (SO₂), Carbon monoxide (CO), Ozone (O₃), Ammonia (NH3), and benzene were analysed across four India Meteorological Department (IMD) seasons. Serial autocorrelation was assessed using the lag-1 Kendall statistic prior to applying the Mann–Kendall test and Sen's slope estimator as an exploratory assessment of intra-annual monotonic tendencies. Spatial variability was evaluated using one-way ANOVA with Tukey's HSD post-hoc test and validated using the Kruskal–Wallis test. Inhalation health risks were assessed using the USEPA Risk Assessment Guidance for Superfund (RAGS) methodology by estimating Hazard Quotient (HQ), Hazard Index (HI), and Lifetime Cancer Risk (LCR).

Results: Bengaluru recorded the highest annual mean PM₂.₅ (40.2 µg/m³) and PM₁₀ (80.4 µg/m³) concentrations, with PM₂.₅ equal to the CPCB National Ambient Air Quality Standard (NAAQS) and PM₁₀ exceeding it by approximately 34%. Annual mean PM₂.₅ concentrations at all stations exceeded the WHO 2021 Air Quality Guideline (15 µg/m³). The southwest monsoon produced the greatest reduction in particulate concentrations. Exploratory Mann–Kendall analysis yielded negative Sen's slopes for PM₂.₅ at all stations, although none were statistically significant (p>0.05). One-way ANOVA confirmed significant spatial heterogeneity among monitoring stations (p < 0.001). Screening-level health risk assessment indicated HI values >1.0 at all stations (1.756–3.290). Estimated PM₂.₅ LCR ranged from 1.76 × 10⁻³ to 3.34 × 10⁻³ and represents hypothetical upper-bound screening estimates rather than regulatory cancer risk values.

Conclusion: Particulate matter remains the dominant air quality concern across Karnataka, particularly in Bengaluru. Strengthened emission control measures, continued multi-year monitoring, and agricultural ammonia management are recommended to support long-term improvements in air quality and public health.

Introduction: Stunting affects approximately one-quarter of children globally. This study aims to examine how exposure to Household Air Pollution (HAP) from solid fuel use contributes to growth faltering among children.

Materials and methods: The study utilized data from the National Family Health Survey (NFHS-5, 2019–21) and included 185,721 rural children aged 0–59 months. Bivariate and multivariable logistic regression analyses were performed to evaluate the association between household cooking fuel and childhood stunting, with findings reported as 95% Confidence Intervals (CIs). A mediation analysis was further undertaken to examine the potential mediating role of child morbidity.

Results: Using clean fuels was inversely associated with stunting; the odds of stunting were 62% and 54% lower among children in households using only clean fuels compared to those exposed to solid fuels. Based on the adjusted multivariable logistic regression, clean cooking fuel was significantly associated with a decreased prevalence of stunting (β = − 0.029, p = 0.050). Mediation analysis indicated significant effects of cooking fuel on stunting for the controlled direct effect (CDE = 0.972, p = 0.050) and natural direct effect (NDE = 0.973, p = 0.044) but not for the natural indirect effect via morbidity (NIE = 1.000, p = 0.893). The marginal total effect (MTE=0.973, p = 0.044) supported a small but significant protective association of child stunting with clean cooking fuel.

Conclusion: The findings suggest that reducing exposure to household air pollution through clean cooking fuels, alongside broader socio-economic interventions, may contribute to lowering childhood stunting in India.

Introduction: Exposure to ambient air pollution is a critical environmental health risk, with growing evidence linking it to adverse pregnancy outcomes. However, long-term data from Iran remain limited. This study aimed to investigate the association between maternal exposure to major air pollutants and the risk of preterm birth in Tehran.

 Materials and methods: This cohort study utilized 20 years of data (2000–2020) from the Tehran Lipid and Glucose Study (TLGS). We analyzed 697 pregnancies, assessing maternal exposure to Particulate Matter (PM₂.₅, PM₁₀), Ozone (O₃), Carbon monoxide (CO), Nitrogen dioxide (NO₂), and Sulfur dioxide (SO₂) from 10 validated monitoring stations. Historical PM₂.₅ concentrations (pre-2010) were reconstructed using archival data. The association between pollutant exposure and preterm birth was analyzed using Generalized Estimating Equation (GEE) models, adjusting for maternal age and Body Mass Index (BMI).

Results: The incidence of preterm birth was 3.7% (26 cases). The adjusted GEE analysis showed a positive and statistically significant association between maternal CO exposure and preterm birth (coefficient = 0.537; 95% CI: 0.158 to 0.917; P = 0.005).

Conclusion: No statistically significant associations were observed for PM₂.₅, PM₁₀, NO₂, SO₂, and O₃ in the adjusted models. Our findings provide evidence suggesting a potential association between maternal exposure to ambient carbon monoxide and preterm birth in this urban population. These findings highlight the potential public health relevance of traffic-related CO exposure for pregnant women in highly polluted urban settings.

Introduction: Indoor air pollution is a growing public health concern, particularly in communities near industrial operations. This study evaluated indoor concentrations of fine and coarse Particulate Matter (PM_2.5 and PM₁₀) and radon in residential buildings located near cement factories in a selected town in Ogun State, Nigeria. The primary aim of this study was to investigate the concurrent indoor exposure to PM_2.5 and PM₁₀ and radon gas in residences near cement manufacturing facilities, quantify the associated non-carcinogenic and carcinogenic health risks, and examine the correlation between these co-occurring pollutants.

Materials and methods: Air quality measurements were carried out in 20 residential buildings near cement plants. PM_2.5 and PM₁₀ levels were measured using the Elitech Temtop LKC-1000S+ air quality monitor, while indoor radon concentrations were assessed with CR-39 solid-state nuclear track detectors. Particulate matter sampling was conducted twice daily over 30 consecutive days, while CR-39 detectors were deployed for a 30-day exposure period. Health risk evaluations followed standard models for both non-carcinogenic and carcinogenic assessments. Correlation analysis was conducted to examine the relationship between particulate matter and radon.

Results: Mean indoor concentrations of PM2.5 and PM10 were 39.94 μg/m³ and 60.83 μg/m³, respectively, both above WHO limits. Radon concentrations averaged 92.48 Bq/m³, with 40% of sampled homes exceeding the WHO recommended level of 100 Bq/m³. Hazard quotients for PM2.5 ranged from 2.3 to 3.0 and for PM10 from 1.0 to 1.5, yielding an average hazard index of 3.89. Elevated annual effective doses and excess lifetime cancer risks were also associated with radon. A positive correlation was found between particulate matter and radon levels.

Conclusion: The study reveals a significant combined health risk from PM and radon exposure in homes near cement factories. Targeted mitigation, improved regulation, and public health awareness are urgently needed to reduce exposure and protect residents.

Prenatal exposure to fine Particulate Matter (PM_2.5) has been associated with adverse neurodevelopmental outcomes in offspring. However, the biological mechanisms underlying these effects remain incompletely understood. This study aimed to systematically review and synthesize current evidence regarding inflammatory and oxidative stress pathways involved in PM_2.5-induced fetal neurodevelopmental toxicity. A systematic review and meta-analysis were conducted following PRISMA 2020 guidelines and prospectively registered in PROSPERO (CRD420261386294). Six electronic databases (Scopus, PubMed, Web of Science, Embase, ScienceDirect, and PsycINFO) were searched up to April 2026. Human, animal, and in vitro studies evaluating prenatal PM2.5 exposure and neuroinflammatory or oxidative stress outcomes were included. Risk of bias was assessed using ROBINS-I, SYRCLE, and ToxRTool. A total of 43 primary studies (12 human, 22 animal, 9 in vitro) were included. Meta-analysis showed significant increases in inflammatory markers (IL-6: SMD = 1.47; 95% CI 1.02–1.92; I² = 64%) and oxidative stress markers (SMD = 1.21; 95% CI 0.78–1.64). Effects were stronger in male offspring and during late gestation. Most studies consistently reported PM_2.5-induced neuroinflammation and oxidative damage. Prenatal PM_2.5 exposure is associated with substantial neuroinflammatory and oxidative stress responses in fetal brain development, supporting a mechanistic role of the maternal–placental–fetal axis. These findings highlight the importance of environmental pollution control and preventive strategies to protect maternal and fetal health.

Introduction: The growing concern over the health risks associated with indoor air pollutants has led to extensive research on the relationship between indoor air pollution and public health (IAPPH).

Objective: This study critically examined the scientific progress and technological developments in IAPPH research.

Methods: Publication trends, bibliometric analysis, and literature review methods were employed to analyze publications indexed in the Scopus database between 2001 and 2024. The keywords “indoor air pollution,” “health,” and “public health” were used to identify relevant studies. Bibliometric networks and visualizations were generated using VOSviewer.

Result: Findings revealed 151 publications, consisting of 56.29% articles, 17.88% reviews, and 11.26% conference papers. Stakeholder analysis, which considered leading authors, affiliations, funding agencies, and countries, highlighted Majid Ezzati (United Kingdom) and the University of California, Berkeley (United States) as the most productive contributors. Their high output was linked to strong financial support and international collaborations. Funding analysis indicated that organizations in the United States and China were the primary sponsors of IAPPH research. The literature review identified particulate matter, volatile organic compounds, and carbon oxides (COx) as major indoor pollutants responsible for allergic, cardiovascular, and respiratory diseases, especially among women, children, and the elderly.

Conclusion: These findings underscore the urgent need for mitigation strategies such as cleaner fuels, improved stove efficiency, and better ventilation systems to minimize emissions and protect human health, safety, and the environment. Overall, the study demonstrates that IAPPH is a complex, interdisciplinary research field with significant social, economic, and scientific implications.

The purpose of this review was to examine the relationship between NO₂ exposure and the increase likelihood of Diabetes Mellitus (DM) or Type 2 Diabetes (T2D). We conducted the systematic review of cohort studies published between 2015-2025 by carrying out searches in several electronic databases. Nine cohort were included in this meta-analysis. The pooled HR was 1.09 (95% CI = 1.04-1.15) for the impact of NO₂ exposure towards the increasing likelihood of DM. In conclusion, the risk of T2D was increasing because the exposure of NO₂.