Ambient exposure to fine particulate matter (PM_2.5) remains a critical global public health concern; however, the speciation and bioaccessibility mechanisms of particle-bound heavy metals within the lung environment are still insufficiently understood. In particular, the role of soluble and insoluble metal species in simulated lung fluids requires further clarification. Road dust, a major contributor to PM_2.5, contains heavy metals that pose significant inhalation risks, leading to oxidative stress, DNA damage, and systemic toxicity. This study investigated the contamination characteristics, bioaccessibility, pollution level, and speciation of heavy metals in PM_2.5-fractionated road dust (PM_2.5RD) collected from Karachi (a megacity with >27 million inhabitants) and Shikarpur (a medium-sized city of ~0.3 million) in Pakistan. A grid-based sampling approach was applied across four functional zones (residential, school, hospital, and office), yielding 48 samples. Inhalation bioaccessibility was evaluated using artificial lysosomal fluid (ALF; pH 4.5, 37 °C, 24 h), revealing moderate bioaccessibility of Cr, As, and Pb. Pollution status was assessed using contamination factor (CF), integrated pollution index (IPI), pollution load index (PLI), and potential ecological risk index. Geochemical modeling with PHREEQC 3.0 and Visual MINTEQ 3.1 was employed to simulate metal speciation, release behavior, and mineral saturation states. Overall, this study provides mechanistic insights into speciation-driven toxicity of As, Pb, and Cr in simulated lung environments, offering a scientific basis for improved risk assessment and regulatory strategies for PM_2.5-associated metal exposure.

Although particulate matter has been associated with sleep problems, the effects of PM_2.5-bound organophosphate esters (OPEs) on children’s sleep remain unclear. OPEs have neurotoxic and endocrine-disrupting effects that may disrupt sleep–wake regulation during neurodevelopment, supporting biological plausibility for sleep impacts. In this study, we quantified the individual and mixture effects of PM_2.5-bound OPEs on the sleep disorder domain. This cross-sectional study included 110,169 children aged 6–18 years from primary and secondary schools in the Pearl River Delta (PRD), China. Sleep disorders were evaluated using the validated Sleep Disturbance Scale for Children (SDSC). Elastic net and mixed effect models identified specific OPE–sleep associations, while weighted quantile sum regression evaluated mixture effects. All odds ratios indicate a change in the likelihood of sleep disorders per interquartile range (IQR) increase in OPE concentrations. The strongest individual associations were observed for TDCIPP with short sleep duration (OR = 1.56–1.61; moderate association), TEHP with short sleep duration (OR = 1.59–1.64; moderate association), and TPHP with overall sleep disorder (OR = 1.32–1.42; modest association). Combined OPE exposure was positively associated with all sleep disorder domains (ORs = 2.02–2.85; moderate-to-large associations). These results indicate that inhaling PM_2.5-bound OPE mixtures could negatively impact children’s sleep health. This emphasizes a critical developmental period and highlights the importance of public health concerns related to emerging airborne contaminants.