Indoor exposure to heavy metals poses human health risks worldwide, but study reports from Thailand are still limited, particularly in rural and urban areas. We measured the heavy metals in a hundred indoor household dust samples collected from urban and rural areas in Chiang Mai and Lamphun provinces and found a significantly higher concentration of As in rural areas and Cd in urban areas with industrial activities. The source identification of the heavy metals showed significant enrichment from traffic emissions, paint, smoking, and mixed sources with natural soil. From health risk assessment models, children were more vulnerable to noncarcinogenic risks (HI = 1.45), primarily via ingestion (HQ = 1.39). Lifetime cancer risks (LCRs) due to heavy metal exposure were found in adults (LCR = 5.31 × 10⁻⁴) and children (LCR = 9.05 × 10⁻⁴). The cancer risks from As were higher in rural areas via ingestion, while Cr and Ni were higher in urban areas via inhalation and ingestion, respectively. This study estimated that approximately 5 out of 10,000 adults and 9 out of 10,000 children among the population may develop cancer in their lifetime from exposure to indoor heavy metals in this region.

Epidemiologic studies have suggested an association between agrochemical exposure and risk of renal injury. Farmers face great risks to developing adverse effects. The most appropriate biomarker related to renal injury needs to be developed to encounter earlier detection. We aim to study the association between early renal biomarker and occupational herbicide exposure in maize farmers, Thailand. Sixty-four farmers were recruited and interviewed concerning demographic data, herbicide usage, and protective behavior. Two spot urines before (pre-work task) and after (post-work task) herbicide spraying were collected. To estimate the intensity of exposure, the cumulative herbicide exposure intensity index (cumulative EII) was also calculated from activities on the farm, type of personal protective equipment (PPE) use, as well as duration and frequency of exposure. Four candidate renal biomarkers including π-GST, sirtuin-1, mitochondrial DNA (mtDNA) were measured. Most subjects were male and mostly sprayed three herbicides including glyphosate-based herbicides (GBH), paraquat, and 2,4-dichlorophenoxyacetic acid (2,4-D). A type of activity in farm was mixing and spraying herbicide. Our finding demonstrated no statistical significance of all biomarker levels between pre- and post-work task urine. To compare between single and cocktail use of herbicide, there was no statistical difference in all biomarker levels between pre- and post-work task urine. However, the urinary mtDNA seems to be increased in post-work task urine. Moreover, the cumulative EII was strongly associated with change in mtDNA content in both ND-1 and COX-3 gene. The possibility of urinary mtDNA as a valuable biomarker was promising as a noninvasive benchmark for early detection of the risk of developing renal injury from herbicide exposure.

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.

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.