River sediments contain environmental fingerprints that provide useful ecological information. However, the geochemistry of River Atuwara sediments has received less attention over the years. One hundred and twenty-six sediments from 21 locations were collected over a two-season period from River Atuwara, and a detailed investigation of the land use and land cover (LULC) change between 1990 and 2019, analysis of selected toxic and potentially toxic metal(oid)s (TPTM) (Cu, As, Cd, Pb, Ni, Cr, Zn, Fe, Co and Al) using ICP-OES, pollution index assessment, potential source identification (using center log-transformation approach), potential ecological, and human health risk assessment were conducted. The results of the LULC change revealed that the built-up area increased by 95.58 km², at an average rate of 3.186 km²/year over the past 30 years. The mean concentration of metal(oid)s increased in the order of Cd < As < Cr < Pb < Co < Ni < Cu < Zn < Fe < Al, and Cd < As < Cr < Co < Pb < Ni < Cu < Zn < Fe < Al during the dry and wet seasons, respectively. Meanwhile, the statistical analysis of the data spectrum inferred possible contamination from lithological and anthropogenic sources. According to the pollution load index, 90.48% of the sediment samples are polluted by the metal(oid)s. Potential ecological risk assessment identified Ni, As, and Cd as problematic to the ecological community of River Atuwara. Regarding the metal-specific hazard quotient via ingestion route, the risks are in order of Co ≫ As ≫ Pb > Cr > Cd > Al > Ni > Cu > Zn > Fe for both seasons and the carcinogenic risk for children via ingestion route presented a value higher than the safe limits for As, Cd, Cr, and Ni during both seasons. This outcome highlights the need for prompt action towards the restoration of environmental quality for communities surrounding River Atuwara.

Pyrolysis bio-oil was used to partially substitute for phenol in reacting with formaldehyde for the production of bio-oil phenol formaldehyde plywood (BPFP) panels, with the phenol substitution ratio being 20%, 40%, or 60%. Emissions of formaldehyde and volatile organic compounds (VOCs) from the BPFP panels were studied using solid-phase micro-extraction (SPME) followed by headspace gas chromatography/mass spectrometry (GC/MS), and were compared to those from the phenol formaldehyde plywood (PFP) panels. The sources for VOCs were analyzed, and the health risks associated with the BPFP were examined. Results showed that at 80 °C: (1) Formaldehyde emissions from the BPFP panels were increased to about 4 times that of PFP; (2) VOCs emissions were significantly reduced by up to 84.9% mainly due to the greatly reduced phenol emissions, although the total number of VOCs was increased from 20 to 35; (3) BPFP presents greatly increased carcinogenic and non-carcinogenic health risks because of its much stronger emissions of formaldehyde, N,N-dimethylformamide, benzofuran, furfural, and many chemicals from the bio-oil. It is highly advisable that the health risks are properly taken care of before the wide application of BPFP, or similar bio-oil based engineered wood products.

Glyphosate is one of the most used herbicides in the world. The fate of glyphosate in tropical soils may be different from that in soils from temperate regions. In particular, the amounts and types of non-extractable residues (NER) may differ considerably, resulting in different relative contributions of xenoNER (sorbed and sequestered parent compound) and bioNER (biomass residues of degraders). In addition, environmental conditions and agricultural practices leading to total organic carbon (TOC) or pH variation can alter the degradation of glyphosate. The aim of this study is thus to investigate how the glyphosate degradation and turnover are influenced by varying temperature, pH and TOC of sandy loam soil from Colombia. The pH or TOC of a Colombian soil was modified to yield five treatments: control (pH 7.0, TOC 3%), 4% TOC, 5% TOC, pH 6.5, and pH 5.5. Each treatment received 50 mg kg⁻¹ of ¹³C₃¹⁵N-glyphosate and was incubated at 10 °C, 20 °C and 30 °C for 40 days. Rising temperature increased the mineralization of ¹³C₃¹⁵N-glyphosate from 13 to 20% (10 °C) to 32–39% (20 °C) and 41–51% (30 °C) and decreased the amounts of extractable ¹³C₃¹⁵N-glyphosate after 40 days of incubation from 13 to 26% (10 °C) to 4.6–12% (20 °C) and 1.2–3.2% (30 °C). Extractable ¹³C₃¹⁵N-glyphosate increased with higher TOC and higher pH. Total ¹³C-NER were similar in all treatments and at all temperatures (47%–60%), indicating that none of the factors studied affected the amount of total ¹³C-NER. However, ¹³C-bioNER dominated within the ¹³C-NER pool in the control and the 4% TOC treatment (76–88% of total ¹³C-NER at 20 °C and 30 °C), whereas in soil with 5% TOC and pH 6.5 or 5.5 ¹³C-bioNER were lower (47–61% at 20 °C and 30 °C). In contrast, the ¹⁵N-bioNER pool was small (between 14 and 39% of the ¹⁵N-NER). Thus, more than 60% of ¹⁵N-NER is potentially hazardous xenobiotic NER which need careful attention in the future.

The goal of this study was to assess biomarkers of exposure to glyphosate and assess potential associations with renal function in children. Glyphosate is used ubiquitously in agriculture worldwide. While previous studies have indicated that glyphosate may have nephrotoxic effects, few have examined potential effects on kidney function in children. We leveraged three cohorts across different phases of child development and measured urinary levels of glyphosate. We evaluated associations of glyphosate with three biomarkers of kidney injury: albuminuria (ACR), neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury marker 1 (KIM-1). Multivariable regression analyses examined associations of glyphosate with kidney injury biomarkers controlling for covariates. We identified glyphosate in 11.1% of the total participants. The herbicide was detected more frequently in the neonate population (30%). Multivariable regression models failed to identify significant associations of log-transformed glyphosate with any of the kidney injury biomarkers, controlling for covariates age, sex, and maternal education. While we confirm detectability of glyphosate in children’s urine at various ages and stages of life, there is no evidence in this study for renal injury in children exposed to low levels of glyphosate. Further studies of larger sample size are indicated to better understand putative deleterious effects of the herbicide after different levels of exposure.

The presence of Eschericia coli O157:H7 in the natural environment is a serious threat to human health. The native microbial community in soil plays an important role in resisting E. coli O157:H7 invasion. This study examined the responses of soil microbial community to E. coli O157:H7 invasion during a 32-day incubation. The E. coli O157:H7 persisted longer in γ-irradiated soil than non-irradiated soil while glucose addition decreased its persistence in the irradiated soil which was associated with an increasing recovery of the native community. The invasion of E. coli O157:H7 increased soil organic carbon mineralization, an indicator of microbial activity, in both non-irradiated and irradiated soils, while glucose addition significantly promoted the carbon mineralization process. The 16S rRNA sequencing data showed the gradual recovery of the native bacterial population including specific taxa such as proteobacteria and actinobacteria following irradiation. It is concluded that soil microbial function and structure can affect persistence of E. coli O157:H7 and that lower biodiversity of the native community favors its persistence.

Fine particulate matter is one of the leading threats to cardiovascular health worldwide. The exploration of novel and sensitive biomarkers to detect damaging effect of fine particulate matter on cardiac tissues is of great importance in the better understanding of haze-caused myocardial injury. A link between heart failure and PPARα-regulated energy metabolism has been confirmed previously. Herein, the study intends to reveal the critical biomarkers of fine particulate matter induced myocardial damage from the PPARα-regulated energy metabolism. Ambient fine particulate matter induced severe pathological alterations in cultured cells, accompanied by the decrease in ATP content. Additionally, the expressions of CPT1/CPT2 and levels of CS and MDH, crucial members in β-oxidation and the TCA cycle, were significantly decreased. In direct contrast, fine particulate matter increased the biomarkers of glycolysis, as measured by the accumulation of pyruvate and lactate contents, and the enhanced activities of HK and PKM1/2. Importantly, fine particulate matter-exposed cardiomyocytes exhibited the reduced PPARα level, that increased when cardiomyocytes were co-incubation with WY-14643 and fine particulate matter. Simultaneously, the adverse impact of fine particulate matter on critical biomarkers were observed in β-oxidation, TCA cycle and glycolysis, associated with WY-14643 additional complement. Fine particulate matter caused the myocardial energy metabolism transformation through the regulation of PPARα expression and translation, which provided novel and critical biomarkers for haze particles-caused myocardial damage.

Household air pollution is the dominant contributor to population air pollutant exposure, but it is often of less concern compared with ambient air pollution. One of the major knowledge gaps in this field are detailed quantitative source contributions of indoor pollutants, especially for gaseous compounds. In this study, temporally, spatially, and vertically resolved monitoring for typical indoor gases including CO₂, CO, formaldehyde, methane, and the total volatile organic compounds (VOCs) was conducted to address pollution dynamics and major sources in an urban apartment. The indoor concentrations were significantly higher than the simultaneously measured outdoor concentrations. A new statistic approach was proposed to quantitatively estimate contributions of different sources. It was estimated that outdoor CO₂ contributed largely to the indoor CO₂, while main indoor sources were human metabolism and cooking. Outdoor infiltration and cooking contributed almost equally to the indoor CO. The contribution of outdoor infiltration to methane was much higher than that to formaldehyde. Cooking contributed to 24%, 19%, and 25% of indoor formaldehyde, methane, and VOCs, whereas the other unresolved indoor sources contributed 61%, 19%, and 35% of these pollutants, respectively. Vertical measurements showed that the uplifting of hot air masses led to relatively high concentrations of the pollutants in the upper layer of the kitchen and in the other rooms to a lesser extent.