The Household Air Pollution Intervention Network trial is a multi-country study on the effects of a liquefied petroleum gas (LPG) stove and fuel distribution intervention on women's and children's health. There is limited data on exposure reductions achieved by switching from solid to clean cooking fuels in rural settings across multiple countries. As formative research in 2017, we recruited pregnant women and characterized the impact of the intervention on personal exposures and kitchen levels of fine particulate matter (PM₂.₅) in Guatemala, India, and Rwanda. Forty pregnant women were enrolled in each site. We measured cooking area concentrations of and personal exposures to PM₂.₅ for 24 or 48 h using gravimetric-based PM₂.₅ samplers at baseline and two follow-ups over two months after delivery of an LPG cookstove and free fuel supply. Mixed models were used to estimate PM₂.₅ reductions. Median kitchen PM₂.₅ concentrations were 296 μg/m³ at baseline (interquartile range, IQR: 158–507), 24 μg/m³ at first follow-up (IQR: 18–37), and 23 μg/m³ at second follow-up (IQR: 14–37). Median personal exposures to PM₂.₅ were 134 μg/m³ at baseline (IQR: 71–224), 35 μg/m³ at first follow-up (IQR: 23–51), and 32 μg/m³ at second follow-up (IQR: 23–47). Overall, the LPG intervention was associated with a 92% (95% confidence interval (CI): 90–94%) reduction in kitchen PM₂.₅ concentrations and a 74% (95% CI: 70–79%) reduction in personal PM₂.₅ exposures. Results were similar for each site. The intervention was associated with substantial reductions in kitchen and personal PM₂.₅ overall and in all sites. Results suggest LPG interventions in these rural settings may lower exposures to the WHO annual interim target-1 of 35 μg/m³. The range of exposure contrasts falls on steep sections of estimated exposure-response curves for birthweight, blood pressure, and acute lower respiratory infections, implying potentially important health benefits when transitioning from solid fuels to LPG.

We investigated the spatio-temporal trends of polycyclic aromatic compounds (PACs) deposition in the Athabasca Oil Sands Region (AOSR) between 2008 and 2017, and applied source apportionment tools to assess sources using snowpacks. Estimated PAC mass deposition was significantly correlated with crude oil production (R² = 0.48, p = 0.03), and increased between 2008 and 2017. Loadings of alkylated PACs c1-, c2-fluorenes/pyrenes and c1-, c3-benzo[a]anthracenes/chrysenes/triphenylenes significantly increased at mid-field sites (25–50 km from central industrial reference site, AR6) (Mann-Kendall, p < 0.05) reflecting physical expansion of the AOSR. The distance from emission sources was important in the deposition of PACs, including the distance from AR6 (R² = 0.69–0.91), nearest petcoke storage (R² = 0.77–0.88), 0.89) and upgrader stack (R² = 0.56–0.61). Source apportionment PAC distribution profiles of the source materials (petcokes, oil sand ores, road dust) did not show unique matching profiles with the snowpacks. However, the minimal presence of retene in petcokes and an abundance of benzo[ghi]fluoranthene in road dust was observed, and suggests potential for these compounds as chemical markers in distinguishing sources. Furthermore, correlations between PACs and selected metal(loid)s in the AOSR snowpacks were assessed to infer potential common sources. Significant positive (p < 0.05) correlations between metal(loid)s enriched in bitumen (vanadium, molybdenum, nickel) and PACs, at near to mid-field (0–50 km from AR6) sites suggests common sources or similar transfer and fate processes. The results of our study convey data necessary for monitoring studies in the constantly developing AOSR, advance our knowledge of PACs profiles in source materials (including the much less studied alkylated PACs and dibenzothiophenes), which will be valuable for other studies related to oil pollution, urban run-off and forest fires.PACs mass deposition increasing between 2008 and 2017 coincident with crude oil production, and retene and benzo[ghi]fluoranthene show potential in distinguishing AOSR sources.

To enable and/or facilitate analysis of microplastics from environmental samples, a purification process is required to reduce the organic matter content. The development of such process has as one main concern, besides achieving efficient organic matter reduction, the preservation of the microplastics. In this study, a three-step method for sewage sludge purification was proposed employing sodium dodecyl sulfate and hydrogen peroxide. The effects of the purification method on seven polymers (LLDPE, HDPE, PP, PS, PET, PA66 and SBR) were evaluated in terms of mass change, surface characteristics, mechanical properties, thermal properties and functional groups change. It was also assessed how the polymers were affected by the purification chemicals without the presence of sewage sludge. The purification process led to changes in all tested plastics, but in different intensities. LLDPE, HDPE, PP, PS and PET did not suffer considerable degradation. PET was more affected by hydrolysis than oxidation. On the other hand, the integrities of PA66 and SBR were noticeably affected. The effects of the purification process were considered to be due to the plasticizer behavior of water and oxidation on PA66 and loss of filler and oxidation on SBR. For both polymers there was a reduction on the tensile strength of around 50–60% after the purification, indicating they could be prone to fragmentate into smaller pieces along the process. After purification, PA66 also started to decompose at a temperature around 10 °C lower comparing to virgin samples. Except for SBR, the presence of sewage sludge and its oxidation was more harmful to the polymers than the purification chemicals without the presence of sewage sludge. This study serves as an evaluation of the effects of the purification process on the degradation of microplastics and a methodology for such assessment when designing a purification process.

Children’s respiratory health are particularly vulnerable to outdoor air pollution, but evidence is lacking on the very acute effects of air pollution on the risk of acute upper respiratory infections (AURI) and acute lower respiratory infections (ALRI) in children. This study aimed to evaluate the risk of cause-specific AURI and ALRI, in children within 24 h of exposure to air pollution. We obtained data on emergency cases, including 11,091 AURI cases (acute pharyngitis, acute tonsillitis, acute obstructive laryngitis and epiglottitis, and unspecified acute upper respiratory infections) and 11,401 ALRI cases (pneumonia, acute bronchitis, acute bronchiolitis, unspecified acute lower respiratory infection) in Brisbane, Australia, 2013–2015. A time-stratified case-crossover analysis was used to examine the hourly association of AURI and ALRI with high concentration (95th percentile) of four air pollutants (particulate matters with aerodynamic diameter <10 μm (PM₁₀) and <2.5 μm (PM₂.₅), ozone (O₃), nitrogen dioxide (NO₂)). We observed increased risk of acute tonsillitis associated with PM₂.₅ within 13–24 h (odds ratio (OR), 1.45; 95% confidence interval [CI], 1.02–2.06) and increased risk of unspecified acute upper respiratory infections related to O₃ within 2–6 h (OR, 1.38, 95%CI, 1.12–1.70), NO₂ within 1 h (OR, 1.19; 95%CI, 1.01–1.40), and PM₂.₅ within 7–12 h (OR, 1.21; 95%CI, 1.02–1.43). Cold season and nigh-time air pollution has greater effects on AURI, whereas greater risk of ALRI was seen in warm season and daytime. Our findings suggest exposures to particulate and gaseous air pollution may transiently increase risk of AURI and ALRI in children within 24 h. Prevention measures aimed at protecting children’s respiratory health should consider the very acute effects of air pollution.

As a novel brominated flame retardant (NBFR), decabromodiphenyl ethane (DBDPE) has been poorly understood for the environmental fate and toxicity in terrestrial invertebrates. For the first time, the bioaccumulation, elimination, metabolism and detoxification of DBDPE in earthworms as well as its potential impacts on soil microbes were investigated. The results showed much higher DBDPE concentrations in casts than in earthworms. The bioaccumulation factor (BAF) and elimination rate constant (kₑ) values were 0.028–0.213 (gdw, worm/gdw, soil) and 0.323–0.452 (day⁻¹), respectively. The detoxifying enzymes (CYP450 and GST) could be induced by DBDPE within the range of exposure dosage, and the activities were significantly increased at 21 d (p < 0.05). The results were identified by GC-ECNI-MS, and it showed that at least eleven unknown peaks were separately observed in the earthworms, which were the biotransformation products of DBDPE in earthworms. Additionally, the damages, including skin shrinkage, setae impairment, and intercellular vacuolization, were clearly observed by SEM/TEM. Based on these data, DBDPE could accumulate in earthworms, yet, with low bioaccumulation ability. Moreover, DBDPE exposure resulted in minimal harmful impacts on microbial activities including microbial biomass C (MBC), Microbial basal respiration (MBR), Urease (US) activity and fluorescein diacetate hydrolase (FDA) activity (p < 0.05). Our findings would provide some essential information for interpreting the ecological risks of DBDPE in soil.

The historical air pollution with halogenated flame retardants (HFRs) in Germany was assessed by investigating tree leaf and shoot samples which have been archived in the German environmental specimen bank. Samples covered the period from 1985 to 2016. 43 HFRs comprising polybrominated diphenyl ethers as well as emerging brominated and chlorinated compounds such as Dechlorane Plus, DBDPE, or DPTE, were analysed in 115 samples from ten sub sites originating from six areas characterised by different land uses, including urban as well as a background site. HFRs were observed in each sample showing the widespread distribution of HFRs in Germany in tree leaves and shoots as bioindicators of past and present atmospheric pollution. Analytes observed at elevated concentrations were BDE 209, DBDPE and DPTE. Observed HFR-levels differed between analytes as well as sampling locations, particularly prior to the year 2000. They were typically highest at conurbation areas. Concentrations at the background site often belonged to the lowest ones observed, however, lowest values were not exclusively found there. The quantification frequencies appeared to decrease from the past to most recent samples. With few exceptions, atmospheric pollution of both, legacy and emerging HFRs, decreased significantly.

Iron-bearing nanoparticles (IBNPs) were abundant in particulate matter (PM). Due to their high reactivity, IBNPs were considered hazardous to human health, however, their toxic mode-of-action(s) are highly unclear. Ferroptosis is a novel programmed cell death (PCD) that highly associated with intracellular iron. However, the pro-ferroptotic effect of IBNPs has not been characterized. To this end, we ought to investigate whether and how IBNPs (synthetic γ-Fe₂O₃ and Fe₃O₄ NPs were selected as the model compounds) are involved in ferroptosis. We found that human umbilical vein endothelial cells (HUVECs) phagocytized large qualities of γ-Fe₂O₃ and Fe₃O₄ NPs, resulting in increased intracellular iron level. We further observed the disrupted cystine/glutamate reverse transporter (System Xc⁻) and glutathione peroxidase 4 (GPX4) signaling in γ-Fe₂O₃ and Fe₃O₄ NPs-challenged HUVECs. γ-Fe₂O₃ and Fe₃O₄ NPs could also cause mitochondrial fusion and fission dysregulation, activate lipid peroxidation and iron metabolism-related genes in a P53-dependent manner. Together, the ferroptotic activity of IBNPs should be acknowledged for the risk assessment of PM associated health effects.

Nitrate (NO₃⁻) is one of the common inorganic nitrogen compound pollutants in natural ecosystems, which may have serious risks for aquatic organisms. However, its toxicological mechanism remains unclear. In the current study, juvenile turbot (Scophthalmus maximus) were exposed to different concentrations of NO₃⁻ (CK− 3.57 ± 0.16, LN − 60.80 ± 1.21, MN − 203.13 ± 10.97 and HN − 414.16 ± 15.22 mg/L NO₃–N) for 60 d. The blood biochemical assays results revealed that elevated NO₃⁻ exposure significantly increased the concentrations of plasma NO₃⁻, NO₂⁻, MetHb, K⁺, cortisol, glucose, triglyceride, lactate, while significantly decreased the concentrations of plasma Hb, Na⁺ and Cl⁻, which meant that NO₃⁻ caused hypoxic stress and further affected the osmoregulation and metabolism in fish. Besides, exposure to MN and HN induced a significant decrease in the level of antioxidants, including SOD (Point: 60th day, MN, HN v.s. CK: 258.36, 203.73 v.s. 326.95 U/mL), CAT (1.97, 1.17 v.s. 2.37 U/mL), GSH (25.38, 20.74 v.s. 37.00 μmol/L), and GPx (85.32, 71.46 v.s. 129.36 U/mL), and a significant increase of MDA (7.54, 9.73 v.s. 5.27 nmol/L), suggesting that NO₃⁻ exposure leading to a disruption of the redox status in fish. Also, further research revealed that NO₃⁻ exposure altered the mRNA levels of p53 (HN: up to 4.28 folds) and p53-regulated downstream genes such as Bcl-2 (inferior to 0.44 folds), caspase-3 (up to 2.90 folds) and caspase-7 (up to 3.49 folds), indicating that NO₃⁻ exposure induced abnormal apoptosis in the fish gills. Moreover, IBRv2 analysis showed that the toxicity of NO₃⁻ exposure to turbot was dose-dependent, and the toxicity peaked on the 15th day. In short, NO₃⁻ is an environmental toxicological factor that cannot be ignored, because its toxic effects are long-term and could cause irreversible damage to fish. These results would be beneficial to improve our understanding of the toxicity mechanism of NO₃⁻ to fish, which provides baseline evidence for the risk assessment of environmental NO₃⁻ in aquatic ecosystems.

Chemosensory perception is crucial for fish reproduction and survival. Direct contact of olfactory neuroepithelium to the surrounding environment makes it vulnerable to contaminants in aquatic ecosystems. Copper nanoparticles (CuNPs), which are increasingly used in commercial and domestic applications due their exceptional properties, can impair fish olfactory function. However, the molecular events underlying olfactory toxicity of CuNPs are largely unexplored. Our results suggested that CuNPs were bioavailable to olfactory mucosal cells. Using RNA-seq, we compared the effect of CuNPs and copper ions (Cu²⁺) on gene transcript profiles of rainbow trout (Oncorhynchus mykiss) olfactory mucosa. The narrow overlap in differential gene expression between the CuNP- and Cu²⁺-exposed fish revealed that these two contaminants exert their effects through distinct mechanisms. We propose a transcript-based conceptual model that shows that olfactory signal transduction, calcium homeostasis, and synaptic vesicular signaling were affected by CuNPs in the olfactory sensory neurons (OSNs). Neuroregenerative pathways were also impaired by CuNPs. In contrast, Cu²⁺ did not induce toxicity pathways and rather upregulated regeneration pathways. Both Cu treatments reduced immune system pathway transcripts. However, suppression of transcripts that were associated with inflammatory signaling was only observed with CuNPs. Neither oxidative stress nor apoptosis were triggered by Cu²⁺ or CuNPs in mucosal cells. Dysregulation of transcripts that regulate function, maintenance, and reestablishment of damaged olfactory mucosa represents critical mechanisms of toxicity of CuNPs. The loss of olfaction by CuNPs may impact survival of rainbow trout and impose an ecological risk to fish populations in contaminated environments.