Indoor exposure to potentially toxic elements (PTEs) presents a global health concern, yet comprehensive seasonal assessments in Thailand remain limited, particularly during air pollution episodes. We assessed 15 PTEs in household dust collected across eight provinces of upper northern Thailand (UNT) during the haze and non-haze seasons to evaluate contamination levels, identify sources, and assess health risks. Five elements (Cr, Mo, Ni, Pb, and Zn) showed significantly higher concentrations during the haze season (p < 0.05), accompanied by corresponding increases in contamination indices and more diverse pollution sources being identified compared to the non-haze season, with Sb showing the highest enrichment degree (EF = 117.8). Source identification revealed potential enrichment from mixed anthropogenic sources, natural soil, industrial activities, agricultural inputs, and biomass burning. Health risk assessment showed that children faced unacceptable non-carcinogenic risks (HI = 2.51), increasing to 2.79 during the haze season, exceeding safe thresholds. Both adults and children experienced unacceptable carcinogenic risks from chromium exposure, particularly through inhalation during haze episodes. Total lifetime cancer risks increased from 1.20 × 10⁻⁴ to 1.74 × 10⁻⁴ for children and from 4.02 × 10⁻⁴ to 6.06 × 10⁻⁴ for adults during the haze season. These findings underscore the critical need for integrated pollution control strategies addressing biomass burning emissions to reduce indoor dust contamination and protect public health in biomass-burning-impacted regions.

Seasonal haze in northern Thailand raises concerns about the health impacts of PM_2.5-bound metals. This study assessed PM_2.5-bound metals and inhalation health risks across three contrasting land use environments during the haze season in Chiang Mai Province, Thailand: Chiang Mai University (CMU; an urban site), Mae Chaem (MC; an agricultural rural site), and Chom Thong (CT; a roadside rural site). In total, 101 24 h PM_2.5 samples were collected during the haze season from 15 January to 22 April 2020. CT showed the highest median PM_2.5 concentrations (64.9 µg m⁻³), metal enrichment, and overall estimated health risks. Notably, although MC (42.1 µg m⁻³) had lower PM_2.5 than CMU (50.3 µg m⁻³), its non-carcinogenic hazard index (HI = 2.10) and cancer risk (TCR = 2.37 × 10⁻⁴) exceeded those of CMU (HI = 1.34; TCR = 1.18 × 10⁻⁴), indicating that PM_2.5 mass alone may not adequately capture differences in estimated health risks. HI exceeded the reference level (HI > 1) at all sites, with the highest HI at CT (2.69), and TCR exceeded the benchmark (1 × 10⁻⁴) at all sites, with the highest TCR at CT (3.63 × 10⁻⁴) and chromium as the dominant contributor. Se, Cd, and As showed the strongest anthropogenic enrichment, and PCA identified potential source-related associations consistent with biomass burning, traffic emissions, agricultural activities, and crustal or road dust. These findings show that agricultural and roadside rural environments may present distinct health risk profiles that are not captured by PM_2.5 mass alone, underscoring the need for composition-specific mitigation and public health interventions across the urban–rural continuum in northern Thailand.

Ambient fine particulate matter (PM_2.5) exposure has been associated with oxidative stress, inflammation, and biological aging; however, evidence regarding its relationship with leukocyte telomere length (LTL) remains inconsistent, particularly in rural Southeast Asian populations. This study aimed to investigate the association between ambient PM_2.5 exposure and LTL across multiple exposure windows and examine whether oxidative stress and systemic inflammation were associated with PM_2.5 exposure and LTL. This cross-sectional study included 179 adults from rural communities in Northern Thailand affected by biomass-burning pollution. Cumulative average ambient PM_2.5 exposure was estimated for lag 0–7, 0–14, 0–30, 0–60, and 0–90 days, corresponding to 8, 15, 31, 61, and 91 days, respectively, including the blood-collection date (day 0). Relative LTL was quantified using quantitative polymerase chain reaction. Serum 8-hydroxy-2′-deoxyguanosine (8-OHdG), the Systemic Immune-Inflammation Index (SII), and the Systemic Inflammation Response Index (SIRI) were also assessed. Analyses included covariate-adjusted linear regression, exploratory wild cluster bootstrap inference, and sensitivity analyses. All p-values were unadjusted for multiple comparisons. Median relative LTL was 0.81 T/S units (Q1–Q3: 0.72–0.89). Adjusted models showed positive associations between PM_2.5 and LTL at 0–30-, 0–60-, and 0–90-day windows, but not at 0–7- and 0–14-day windows. Per window-specific IQR increase in PM_2.5 (8.13, 7.25, and 6.25 µg/m³, respectively), relative LTL was higher by 0.050 T/S units (95% CI: 0.012–0.089; nominal p = 0.011), 0.079 T/S units (95% CI: 0.035–0.123; nominal p < 0.001), and 0.094 T/S units (95% CI: 0.041–0.147; nominal p < 0.001). The reported confidence intervals and conventional p-values did not account for site–date clustering. In exploratory wild cluster bootstrap analyses using eight site-date groups, none of the five associations reached nominal significance (p = 0.247–0.787). The 0–30-day PM_2.5 model explained an additional 3.8% of the variance in LTL (ΔR² = 0.038; p = 0.011), while 8-OHdG contributed a further 2.4% (ΔR² = 0.024; p = 0.041); SII and SIRI did not significantly improve model fit (p = 0.499 and 0.603, respectively). Sensitivity analyses showed positive longer-window associations with substantially varying magnitudes, whereas inverse shorter-window associations emerged in the NTAQHI-only analysis. Higher estimated ambient PM_2.5 exposure was positively associated with higher measured LTL across the 0–30-, 0–60-, and 0–90-day windows in conventional adjusted models. However, sensitivity to sample composition and nonsignificant wild cluster bootstrap findings limit confidence in the robustness of these associations. Adding serum 8-OHdG, SII, or SIRI produced modest changes in model fit and did not establish mediation by oxidative stress or systemic inflammation. These exploratory findings should not be interpreted as evidence of within-person telomere change or a causal or protective effect of PM_2.5.