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 molecular mechanism of evaluating 17β-estradiol (E₂)-induced toxicity in female Daphnia magna has not been determined. In this study, the transcriptome of D. magna was analyzed after exposure to three different concentrations (0, 10, and 100 ng L⁻¹) of E₂ at 3, 6, and 12 h. The results showed 351–17,221 significantly up-regulated and 505–10,282 significantly down-regulated genes (P < 0.05). Overall, the selected largest 10,282 (10 ng L⁻¹vs control at 12 h) down-regulated and 17,221 (100 vs 10 ng L⁻¹) up-regulated genes were identified; following annotation, pathways in cancer and RNA transport were found to be enriched according to the interaction network. Among all completed comparisons, KEGG pathways related to the immune system, cancer, disease infection, and active compound metabolism were identified by short time series expression miner analysis. A different set of genes fluctuated in a “U”-shaped pattern over time and at different concentrations of E₂, whereas some genes associated with disintoxication showed a reverse “U”-shaped response as E₂ administration was increased. These results suggest that E₂ exposure caused transcriptional changes in the immune system, disintoxication, disease prevention, and the protein degradation pathway.

Atmospheric particulate matter (PM) pollution levels and human health risks resulting from exposure to non-anthropogenic pollution sources, such as coal mine-fires, are serious global issues. The toxicity of PM₁₀-bound metals and polycyclic aromatic hydrocarbons (PAHs) was assessed according to their non-cancer and cancer risks (CRs) at the mine-fire and in an adjacent city area. Health risks were estimated for inhalation, ingestion, and dermal absorption pathways. The non-cancer risks, presented in terms of the hazard index (HI) and hazard quotient (HQ), were found to be significant (>1) at all locations, except in the mining (for HQ-dermal) and city background area (for HQ-ingestion and HQ-dermal) in children and adults, respectively. The total CR was estimated to be highest at the city nearby the mine-fire area (3.31E-02 and 1.93E-02) followed by the mine-fire area (2.66E-02 and 1.71E-02) for children and adults, respectively. The total CR and CR via individual exposure routes were estimated to be in the high risk (10⁻³ ≤ CR < 10⁻¹) category at the mine-fire site and adjacent city area. For all exposures, CR levels were calculated to be higher than the acceptable range (from 1.00E-06 to 1.00E-04), except for the CR-inhalation level at the A5 location. Among all elements, Cd and BaPₑqᵤ were more significant for the CR at the coal mine-fire and the adjacent city area. Hence, this study concluded that non-anthropogenic sources, such as coal mine-fires, could be part for the significant health risk (carcinogenic and non-carcinogenic) levels in the study area.

Inspired by methods used for life cycle impact assessment (LCIA), we constructed a series of indicators to appreciate the noxiousness of radioactive materials and wastes for human and ecosystem health. According to known potential human health and ecological effects of such materials, six main impact categories were considered to initiate the development of the method: human cancer and non-cancer effects vs. ecotoxicity, considering both chemotoxicity and radiotoxicity. For ecosystems, the noxiousness indicator is based on the concept of Potentially Affected Fraction (PAF), used as a damage indicator at the ecosystem level. The PAF express the toxic pressure on the environment due to one substance. It has been enlarged to mixtures of substances as multi-substances PAF (ms-PAF), and applied to a mix of stable and radioactive substances. Combining ecotoxicity data and a simplified model of exposure of fauna and flora, we proposed a chemotoxicity indicator and a radiotoxicity indicator, ultimately aggregated into a single indicator simply by addition.According to acknowledged practices in LCIA and corresponding available data, we suggested implementing to human health an approach similar to that applied to ecosystems. We produced eigth basic indicators combining effects categories (cancer and non cancer), exposure pathways (ingestion and inhlation) and substances (chemicals and radionuclides). The principle of additivity supporting the whole proposed approach allows their complete aggregation into a single indicator also for human health. Different source terms may be then easily directly compared in terms of human and ecological noxiousness.Applied to the time evolution of a High Level radioactive Waste (HLW), the method confirmed over 1 million years the dominance of the radiotoxicity in the noxiousness of the material for both humans and environment. However there is a change with time in the ranking of the most noxious substances, with stable metals contribution going progressively up. Finally, the HLW global noxiousness, integrating human health and ecological aspects, was assessed through time at three stages and showed a temporal decrease as expected from the dominance of the radiotoxicity.

This study aimed to assess the carcinogenic and non-carcinogenic risks of in-vehicle exposure in Tehran, Iran to formaldehyde and acetaldehyde for different models of taxis, and to explore the effects of city zone, taxi vehicle type, the taxi's age (<1, 1–5, 5–10), fuel type (gasoline, CNG, and LPG), and refueling activities on the estimated health risks based on previously measured concentrations. The overall and age-specific carcinogenic and non-carcinogenic risks of these compounds for taxi drivers and passengers were estimated separately using Monte Carlo simulations. Three scenarios of exposure frequency were defined for taxis commuting in different zones of city: Restricted Traffic Zone (RTZ) and Odd-Even Zone (OEZ) as two plans to reduce air pollution, and no-restriction zone (NRZ). The carcinogenic risks for drivers and passengers, the average risks of formaldehyde and acetaldehyde for most cases were above the 1 × 10⁻⁴. The health risks were greater in Restricted Traffic Zone (RTZ) and Odd-Even Zone (OEZ) in comparison to no-restriction zone (NRZ). The carcinogenic risk from formaldehyde exposures were higher than those for acetaldehyde in all cases. Taxis fueled with LPG showed lower cancer risks for both acetaldehyde and formaldehyde. Refueling increased the carcinogenic risk from both compounds. For non-carcinogenic risks from acetaldehyde, the average hazard ratios for both drivers and passengers were >1, indicating a non-negligible risk. Cancer and non-cancer risks for the taxi drivers were greater than the passengers given the higher time of occupancy. The present study showed that transportation in taxis can impose significant long-term health risks to both passengers and drivers. Development and investment in cleaner choices for public transportations are required.

Environmental contaminants, to which humans are widely exposed, cause or worsen several diseases, like cardiovascular diseases and cancers. Among these molecules, polycyclic aromatic hydrocarbons (PAHs) stand out since they are ubiquitous pollutants found in ambient air and diet. Because of their toxic effects, public Health agencies promote development of research studies aiming at increasing the knowledge about PAHs and the discovery of biomarkers of exposure and/or effects.Extracellular vesicles (EVs), including small extracellular vesicles (S-EVs or exosomes) and large extracellular vesicles (L-EVs or microvesicles), are delivery systems for multimolecular messages related to the nature and status of the originating cells. Because they are produced by all cells and detected within body fluids, EV releases could act as cell responses and thereby serve as biomarkers.To test whether EVs can serve as biomarkers of PAHs exposure, we evaluate the effects of these pollutants on EV production using an in vitro approach (human endothelial cell line, HMEC-1) and an in vivo approach (urine samples from PAHs-exposed rats). Our study indicates that, i) PAH exposure increases in vitro the EV production by endothelial cells and in vivo the release of EVs in urine, and that the stimulating effects of PAHs concern both S-EVs and L-EVs; ii) PAH exposure and more particularly exposure to B[a]P, can influence the composition of exosomes produced by endothelial cells; iii) the aryl hydrocarbon receptor, a cytosolic receptor associated to most deleterious effects of PAHs, would be involved in the PAH effects on the release of S-EVs, but not L-EVs.These results suggest that EVs may have utility for monitoring exposure to PAHs, and more particularly to B[a]P, considered as reference PAH, and to detect the related early cellular response prior to end-organ damages.

This study characterized spatio-temporal variations in the concentration of benzene, toluene, ethylbenzene, and xylene (BTEX) compounds in the vicinity of gas and compressed natural gas (CNG) stations in Tehran, Iran. Health risk assessment (HRA) was computed using Monte Carlo simulations (MCS) for evaluating inhalation lifetime cancer risk (LTCR), the hazard quotient (HQ), and sensitivity analysis (SA) for BTEX exposure in different age groups (birth to <81) and as a function of distance (0–250 m) from the center of the stations. For all monitoring stations, the average values of benzene, toluene, ethylbenzene, and xylene in winter were 466.09 ± 132.25, 873.13 ± 233.51, 493.05 ± 141.22, and 910.57 ± 145.40 μg m⁻³, respectively. The mean wintertime ratios of T/B for the 12 stations ranged from 1.69 to 2.04. Furthermore, there was no significant relationship between the concentration of BTEX with either the specific month or distance from the center of stations (p > 0.05). Factors promoting BTEX formation in the study region were fuel evaporation and gas/CNG station emissions. The LTCRs for the target compounds in the winter for different age groups and distances from the center of stations was limited to 2.11 × 10⁻⁴ to 1.82 × 10⁻³ and 2.30 × 10⁻⁴ to 2.01 × 10⁻³, respectively, which exceeded proposed values by U.S. EPA. Moreover, the HQs for BTEX for three age groups and distances were limited to between 2.89 × 10⁻⁵ and 9.33 × 10⁻², which were lower than the acceptable limit (HQs < 1). The results of this work are applicable to similar areas that are heavily populated with vehicular traffic. This study motivates a closer look at mitigation strategies to limit the health effects of carcinogenic emissions such as benzene and ethylbenzene from gas/CNG stations.

Inhalation exposure to flame retardants used as additives to minimize fire risk and plasticizers is ubiquitous in human daily activities, but has not been adequately assessed. To address this research gap, the present study conducted an assessment of human health risk for four age groups through inhalation exposure to size fractionated particle-bound and gaseous halogenated flame retardants (polybrominated diphenyl ethers (PBDEs) and alternative halogenated flame retardants (AHFRs)) and organophosphate esters (OPEs) at indoor and outdoor environments (school, office, and residence) in three districts of a megacity (Guangzhou, China). Results demonstrated that OPEs were the dominant components among all targets. Indoor daily intakes of PBDEs and OPEs were 13–16 times greater than outdoor levels for all age groups. Gaseous OPEs contributed significantly greater than particle-bound compounds to daily intakes of all target compounds. Based on the different life scenarios, hazard quotient (HQ) and incremental life cancer risk (ILCR) from adults exposure to PBDEs and OPEs in indoor and outdoor settings were the greatest, followed by adolescents, children, and seniors. The estimated HQ and ILCR for all age groups both indoors and outdoors were lower than the safe level (HQ = 1 and ILCR = 10−6), indicating that the potential health risk for local residents in Guangzhou via inhalation exposure to atmospheric halogenated flame retardants and OPEs was low.

Perfluoroalkyl substances (PFAS) are a diverse class of manufactured compounds used in a wide range of industrial processes and consumer products and have been detected in human serum worldwide. Previous cross-sectional and cohort studies in humans have suggested exposure to PFAS is associated with a wide array of chronic diseases, including endocrine disruption, developmental health effects, cancer and metabolic changes. We examined the associations between a panel of eight PFAS and indicators of thyroid disruption, kidney function, and body mass index (BMI), all of which were measured at repeated time points (1990–2008) over the course of the study. Participants (N = 210) were selected from the Fernald Community Cohort based on household water supply from a PFAS-contaminated aquifer. In adjusted repeated measures models, we observed several notable associations between serum PFAS and thyroid hormones as well as kidney function as measured by estimated glomerular filtration rate (eGFR). An interquartile (IQR) increase in serum PFOS was associated with a 9.75% (95% CI = 1.72, 18.4) increase in thyroid stimulating hormone. An IQR increase in serum PFNA, PFHxS, and PFDeA was associated with a −1.61% (95% CI = −3.53, −0.59), −2.06% (95% CI = −3.53, −0.59), and −2.20% (95% CI = −4.25, −0.14) change in eGFR, respectively. On the other hand, an IQR increase in serum Me-PFOSA was associated with a 1.53% (95% CI = 0.34, 2.73) increase in eGFR. No significant associations with BMI and serum PFAS were noted. Our findings are in agreement with previous reports that serum PFAS are associated with altered kidney and thyroid function.

The mechanisms contributing to toxic effects of airborne lower-chlorinated PCB congeners (LC-PCBs) remain poorly characterized. We evaluated in vitro toxicities of environmental LC-PCBs found in both indoor and outdoor air (PCB 4, 8, 11, 18, 28 and 31), and selected hydroxylated metabolites of PCB 8, 11 and 18, using reporter gene assays, as well as other functional cellular bioassays. We focused on processes linked with endocrine disruption, tumor promotion and/or regulation of transcription factors controlling metabolism of both endogenous compounds and xenobiotics. The tested LC-PCBs were found to be mostly efficient anti-androgenic (within nanomolar – micromolar range) and estrogenic (at micromolar concentrations) compounds, as well as inhibitors of gap junctional intercellular communication (GJIC) at micromolar concentrations. PCB 8, 28 and 31 were found to partially inhibit the aryl hydrocarbon receptor (AhR)-mediated activity. The tested LC-PCBs were also partial constitutive androstane receptor (CAR) and pregnane X receptor (PXR) agonists, with PCB 4, 8 and 18 being the most active compounds. They were inactive towards other nuclear receptors, such as vitamin D receptor, thyroid receptor α, glucocorticoid receptor or peroxisome proliferator-activated receptor γ. We found that only PCB 8 contributed to generation of oxidative stress, while all tested LC-PCBs induced arachidonic acid release (albeit without further modulations of arachidonic acid metabolism) in human lung epithelial cells. Importantly, estrogenic effects of hydroxylated (OH-PCB) metabolites of LC-PCBs (4-OH-PCB 8, 4-OH-PCB 11 and 4′-OH-PCB 18) were higher than those of the parent PCBs, while their other toxic effects were only slightly altered or suppressed. This suggested that metabolism may alter toxicity profiles of LC-PCBs in a receptor-specific manner. In summary, anti-androgenic and estrogenic activities, acute inhibition of GJIC and suppression of the AhR-mediated activity were found to be the most relevant modes of action of airborne LC-PCBs, although they partially affected also additional cellular targets.