Urban parks are an important part of the urban ecological environment. The environmental quality of parks is related to human health. To evaluate sources of polycyclic aromatic hydrocarbons (PAHs) in soils of urban parks and their possible health risks, soil samples from 122 parks in Beijing, China, were collected and analyzed. The total content of 16 PAHs between 0.066 and 6.867 mg/kg. Four-ring PAHs were predominant, followed by 5-ring PAHs, while the fraction of 2-ring PAHs was the lowest. The dominant PAHs sources were found to be coal combustion and oil fuels such as gasoline and diesel. A conditional inference tree (CIT) was used to identify the key influencing factors for PAHs. Traffic emissions was the most important factor, followed by coal consumption, as well as the history and location of the park. Incremental lifetime cancer risk (ILCR) for urban park soil in Beijing were low under normal conditions. The soil PAHs exposure pathway risk for both children and adults decreased in the following order: ingestion > dermal contact > inhalation. The risk from soil in parks to children’s health is slightly higher than that of adults, although the health risk due to exposure to PAHs was not extraordinary. Ecosystem risk was negligible.

The understanding for the impact of petrochemical pollutants exposure on renal functions is limited.Our study examined the associations between renal functions and pollutants exposure in adult residents living in the vicinity of a petrochemical industry.We recruited 2069 adult residents near a big petrochemical complex in Taiwan in 2009–2012, and they were categorized into high exposure (HE) and low exposure (LE) groups based on their address to source by 10 km radius. Study subjects were measured the urinary levels of arsenic, cadmium, mercury, thallium, and 1-hydroxypyrene (1-OHP). The estimated glomerular filtration rate (eGFR) was calculated using the Taiwanese Chronic Kidney Disease Epidemiology Collaboration equation, and the chronic kidney disease (CKD) prevalence and risks were defined according to KDIGO 2012 guidelines. Adjusted generalized linear and logistic regression models were applied to evaluate the associations between petrochemical exposure and renal functions.Subjects in the HE areas had significantly lower eGFR, higher CKD prevalence, and higher levels of urinary arsenic, cadmium, mercury, thallium and 1-OHP. The closer to complex and high exposure group of study subjects were significantly associated with the decrease in eGFR, higher ORs for CKD and high-intermediate risk of CKD. In addition, the study subjects who had two-fold urinary arsenic and 1-OHP levels were significantly with decreased 0.68 and 0.49 ml/min/1.73 m2 of eGFR, respectively.Residing closer and higher arsenic and polycyclic aromatic hydrocarbon exposure were associated with the renal impairment and risks of CKD among the residential population near the petrochemical industry.

Although association between polycyclic aromatic hydrocarbons (PAHs) exposure and mitochondrial DNA copy number (mtDNAcn) was researched by traditional linear model extensively, most of these studies analyzed independent effect of each PAHs metabolite and adjust for the confounding other metabolites concomitantly, without considering others interactions. As a complex organic pollutant, a reasonable statistical method is needed to study toxic effects of PAHs.Therefore, we aimed to conduct a novel statistical approach, Bayesian Kernel Machine Regression (BKMR), to explore the effect of PAHs exposure on mtDNAcn among coke oven workers. In this cross-sectional study, the concentrations urinary of PAHs metabolites were measured using high performance liquid chromatography mass spectrometry (HPLC-MS). The mtDNAcn was measured using real-time quantitative polymerase chain reaction (RT-PCR) in peripheral blood of 696 Chinese coke oven workers. The relationship of urinary of PAHs metabolites and mtDNAcn were evaluated by BKMR model. And the results showed a significant negative effect of PAHs metabolites on mtDNAcn when PAHs metabolites concentrations were all above 35th percentile compared to the median and the statistically significant negative single-exposure effect of 2-OHNAP and 2-OHPHE on mtDNAcn when all of the other PAHs are fixed at a particular threshold (25th, 50th, 75th percentile). The changes in log 2-OHNAP and 2-OHPHE from the 25th to the 75th percentile when other PAHs metabolites were at the 50th percentile were associated with change in mtDNAcn of −0.082 (−0.021, −0.124) and −0.048 (−0.021, −0.090) respectively. And evidence of a linear effect of urinary 2-OHNAP and 2-OHPHE were found. Finally, our findings suggested that PAHs cumulative exposures and particularly single-exposure of 2-OHNAP and 2-OHPHE might compromise mitochondrial function by decreasing mtDNAcn in Chinese coke oven workers.

Approximately 3 billion people world-wide are exposed to air pollution from biomass burning. Herein, particulate matter (PM) emitted from artisanal cashew nut roasting, an important economic activity worldwide, was investigated. This study focused on: i) chemical characterization of polycyclic aromatic hydrocarbons (PAHs) and oxygenated (oxy-) PAHs; ii) intracellular levels of reactive oxygen species (ROS); iii) genotoxic effects and time- and dose-dependent activation of DNA damage signaling, and iv) differential expression of genes involved in xenobiotic metabolism, inflammation, cell cycle arrest and DNA repair, using A549 lung cells. Among the PAHs, chrysene, benzo[a]pyrene (B[a]P), benzo[b]fluoranthene, and benz[a]anthracene showed the highest concentrations (7.8–10 ng/m³), while benzanthrone and 9,10-anthraquinone were the most abundant oxy-PAHs. Testing of PM extracts was based on B[a]P equivalent doses (B[a]Pₑq). IC₅₀ values for viability were 5.7 and 3.0 nM B[a]Pₑq at 24 h and 48 h, respectively. At these low doses, we observed a time- and dose-dependent increase in intracellular levels of ROS, genotoxicity (DNA strand breaks) and DNA damage signaling (phosphorylation of the protein checkpoint kinase 1 – Chk1). In comparison, effects of B[a]P alone was observed at micromolar range. To our knowledge, no previous study has demonstrated an activation of pChk1, a biomarker used to estimate the carcinogenic potency of PAHs in vitro, in lung cells exposed to cashew nut roasting extracts. Sustained induction of expression of several important stress response mediators of xenobiotic metabolism (CYP1A1, CYP1B1), ROS and pro-inflammatory response (IL-8, TNF-α, IL-2, COX2), and DNA damage response (CDKN1A and DDB2) was also identified. In conclusion, our data show high potency of cashew nut roasting PM to induce cellular stress including genotoxicity, and more potently when compared to B[a]P alone. Our study provides new data that will help elucidate the toxic effects of low-levels of PAH mixtures from air PM generated by cashew nut roasting.

Whereas non-extractable residue (NER) formation is recognized as an important process affecting the ecological risk of organic contaminants in soils, it is commonly neglected in regional-scale multi-media models assessing chemical environmental fate and risk. We used a combined field and modeling study to elucidate the relative importance of NER formation to the reduction in available organic contaminants compared with fate processes commonly considered in risk assessment models (volatilization, leaching, and biodegradation). Specifically, four polycyclic aromatic hydrocarbons (PAHs), i.e., phenanthrene (Phe), pyrene (Pyr), benzo[a]pyrene (BaP), and benzo[ghi]perylene (BghiP), were spiked and measured in a one-year field pot experiment at four sites with diverse environmental conditions on the eastern Tibetan Plateau. The rate of NER formation was derived as the difference between the overall rate of decline in total-extractable PAH concentrations, obtained by fitting a biphasic first-order model to the measured concentrations, and the sum of the calculated rates of volatilization, leaching, and biodegradation. Our work shows that the total-extractable PAH concentration undergoes a rapid decline and a slow decline, with shorter overall half-lives (especially for BaP and BghiP) than those observed in earlier studies. Generally, NER formation was assessed to be the dominant contributor (64 ± 33%) to the overall decline of PAHs, followed by biodegradation (35 ± 32%); volatilization and leaching were the smallest contributors. In particular, heavier PAHs (i.e. BaP and BghiP) tend to have shorter half-lives in the rapid and the overall decline phase, indicating that the erroneous estimation of environmental fate and risks might be more pronounced for organic contaminants with a large molecular size. The trend of overall decline rates of PAHs displayed a combined effect of NER formation and biodegradation. This work indicates the need to consider NER formation as a process in multi-media models of chemical fate and risk.

Addressing the presence of rutile nanoparticles (NPs) in the air is a work in progress, and the development of methodologies for the identification of NPs in atmospheric dust is essential for the assessment of its toxicological effects. To address this issue, we selected the fast growing desertic city of Hermosillo in northern Mexico. Road dust (n = 266) and soils (n = 10) were sampled and bulk Ti-contents were tested by portable X-ray fluorescence. NPs were extracted from atmospheric dust by PM₁.₀-PTFE filters and further characterized by Confocal Raman Microscopy, Energy-dispersive X-ray spectroscopy (EDS) coupled to Transmission Electron Microscopy (TEM) and Scanning Electron Microscopy (SEM). Results showed (i) the average concentration of Ti in road dust (3447 mg kg⁻¹) was similar to natural values and worldwide urban dusts; (ii) the bulk geochemistry was not satisfactory for Ti-NPs identification; (iii) 76% of the total extracted PM₁.₀ sample corresponded to NPs; (iv) mono-microaggregates of rutile NPs were identified; (v) ubiquitous polycyclic aromatic hydrocarbons (PAHs) were linked to NPs. The genotoxicity of rutile and PAHs, in connection with NPs content, make us aware of a crucial emerging environmental issue of significant health concern, justifying further research in this field.

Following the 16TAN Husky oil spill along the North Saskatchewan River (NSR), the occurrence and natural attenuation of the petroleum hydrocarbons were assessed by analyzing the littoral zone sediments/oil debris collected from July 2016 to October 2017. Husky oil-free, mixed sediment-Husky oil, and Husky oil debris samples were identified for all the collected samples. Shoreline sediments were contaminated by mixed biogenic, pyrogenic and petrogenic inputs prior to the spill. Oil stranded on the shoreline of NSR was moved or buried due to the very dynamic conditions of the shoreline, or cleaned through a series of cleanup activities after the spill. Most normal alkanes were naturally weathered, whereas most of the branched alkanes and all of the saturated petroleum biomarkers remained. Some lighter molecular weight (e.g., 2 to 3-ring) polycyclic aromatic hydrocarbons (PAHs) were lost rapidly after the spill, whereas sulfur containing components, e.g., dibenzothiophenes and benzonaphthothiiophenes, and those having a heavier molecular weight did not change markedly even 15 months post-spill. Similarly, some light hydrocarbons (e.g., <C₁₀) were lost over the first kilometers from the point of entry (POE), while heavier hydrocarbons did not show any major differences away from the POE. Very large inter-site and inter-survey discrepancies were found for samples. Evaporation into the air and dissolution into water, combined with biodegradation, were together or independently the main contributors to the loss of the light molecular hydrocarbons.

The Deepwater Horizon (DWH) oil spill caused an estimated 100,000 bird mortalities. However, mortality estimates are often based on the number of visibly oiled birds and likely underestimate the true damage to avian populations as they do not include toxic effects from crude oil ingestion. Elevated susceptibility to disease has been postulated to be a significant barrier to recovery for birds that have ingested crude oil. Effective defense against pathogens involves integration of physiological and behavioral traits, which are regulated in-part by cytokine signaling pathways. In this study, we tested whether crude oil ingestion altered behavioral and physiological aspects of disease defense in birds. To do so, we used artificially weathered Mississippi Canyon 242 crude oil to orally dose zebra finches (Taeniopygia guttata) with 3.3 mL/kg or 10 mL/kg of crude oil or a control (peanut oil) for 14 days. We measured expression of cytokines (interleukin [IL]-1β, IL-6, IL-10) and proinflammatory pathways (NF-κB, COX-2) in the intestine, liver, and spleen (tissues that exhibit pathology in oil-exposed birds). We also measured heterophil:lymphocyte (H:L) ratio and complement system activity, and video-recorded birds to analyze sickness behavior. Finches that ingested crude oil exhibited tissue-specific changes in cytokine mRNA expression. Proinflammatory cytokine expression decreased in the intestine but increased in the liver and spleen. Birds exposed to crude oil had lower H:L ratios compared to the control on day 14, but there were no differences in complement activity among treatments. Additionally, birds exposed to 10 mL/kg crude oil had reduced activity, indicative of sickness behavior. Our results suggest cytokines play a role in mediating physiological and behavioral responses to crude oil ingestion. Although most avian population damage assessments focus on mortality caused by external oiling, crude oil ingestion may also indirectly affect survival by altering physiological and behavioral traits important for disease defense.

Telomeres are located at the end of eukaryotic chromosomes and vulnerable to exogenous chemical compounds. Exposure to coke oven emissions (COEs) leads to a dose-related telomere damage, and such chromosomal damage might trigger the cGAS/STING signaling pathway which plays an important role in immune surveillance. However, the relationship between the genetic variations in the cGAS/STING signaling pathway and telomere damage in the COEs-exposure workers has not been investigated. Therefore, we recruited 544 coke oven workers and 238 healthy control participants, and determined the level of COEs exposure, concentration of urinary 1-hydroxypyrene (1-OHPYR), genetic polymorphisms and telomere length. The results showed that the telomere length significantly decreased from the control-to high-exposure groups as defined by the external exposure level (P < 0.05). The results also indicated that STING rs7447927 CC, cGAS rs34413328 AA, and cGAS rs610913 AA could inhibit telomere shortening in the exposure group (P < 0.05), and cGAS rs34413328, urine 1-OHPYR and cumulative exposure dose (CED) had a significant association with telomere length by generalized linear model. In conclusion, telomere shortening was a combined consequence of short-term exposure, long-term exposure, and genetic variations among the COEs-exposure workers.

In order to investigate the impacts of dam-related water impoundment on the spatial-temporal variations and transport of anthropogenic organic pollutants, 15 priority polycyclic aromatic hydrocarbons (PAHs) were analyzed in water samples from the Shuikou Reservoir (SKR) of the Minjiang River. The SKR was formed after the construction of the Shuikou Dam, which is the largest hydropower station in Southeast China. The water samples were collected from the backwater zone of the SKR, in both the wet and dry seasons, corresponding to the drainage and impoundment periods of water flow, respectively. The concentrations of the dissolved PAHs in surface water from the wet season (average of 161 ± 97 ng L⁻¹) were significantly higher (ANOVA, p < 0.01) than those from the dry season (average of 43 ± 21 ng L⁻¹). PAH concentrations in the SKR decreased from upstream (industrialized cities) to downstream (rural towns or counties), indicating high PAH loads caused by intensive urbanization effects. The high proportions of 3-ring PAHs in the wet season were from local sources via surface runoff; while the elevated proportions of 4- to 6- ring PAHs in the dry season reflected atmospheric deposition emerged of these PAHs and/or volatilization of 3-ring PAHs enhanced. Molecular diagnostic ratios of PAH isomers in multimedium and principal component analysis indicated that PAH presence in the SKR was mainly attributed to pyrogenic origin. The isomeric ratios of fluoranthene to fluoranthene plus pyrene in the wet season were homogeneous, implying that there were continuous new inputs along the riverine runoff. However, these ratios showed spatial downward trend in the dry season, indicating continued degradation of PAHs occurred along the transport path during the impoundment period. The input and output fluxes of PAHs in the SKR were 5330 kg yr⁻¹ and 2991 kg yr⁻¹, revealing that the reservoir retained contaminants after impoundment of the hydropower dam.