Tin is a naturally occurring heavy metal that occurs in the environment in both inorganic and organic forms. Human exposure to tin is almost ubiquitous; however, surprisingly little is known about factors affecting environmental tin exposure in humans. This study analyzed demographic, socioeconomic and lifestyle factors associated with total urinary tin levels in adults (N = 3522) and children (N = 1641) participating in the National Health and Nutrition Examination Survey (NHANES) 2011–2014, a nationally representative health survey in the United States. Urinary tin levels, a commonly used biomarker of environmental tin exposure, were determined by inductively coupled plasma mass spectrometry (ICP-MS). Detection frequencies of tin were 87.05% in adults and 91.29% in children. Median and geometric mean levels of urinary tin in the adult population were 0.42 μg/L and 0.49 μg/L, respectively. For children, median and geometric mean levels of urinary tin were 0.60 μg/L and 0.66 μg/L, respectively. Age was identified as an important factor associated with urinary tin levels. Median tin levels in the ≥60 year age group were almost 2-fold higher than the 20–39 year age group. Tin levels in children were 2-fold higher than in adolescents. Race/ethnicity and household income were associated with tin levels in both adults and children. In addition, physical activity was inversely associated with urinary tin levels in adults. These results demonstrate that total tin exposures vary across different segments of the general U.S. population. Because the present study does not distinguish between organic and inorganic forms of tin, further studies are needed to better characterize modifiable factors associated with exposures to specific tin compounds, with the goal of reducing the overall exposure of the U.S. population.

This paper summarizes the historical and scientific foundations of the Linear No-Threshold (LNT) cancer risk assessment model. The story of cancer risk assessment is an extraordinary one as it was based on an initial incorrect gene mutation interpretation of Muller, the application of this incorrect assumption in the derivation of the LNT single-hit model, and a series of actions by leading radiation geneticists during the 1946–1956 period, including a National Academy of Sciences (NAS) Biological Effects of Atomic Radiation (BEAR) I Genetics Panel (Anonymous, 1956), to sustain the LNT belief via a series of deliberate obfuscations, deceptions and misrepresentations that provided the basis of modern cancer risk assessment policy and practices. The reaffirming of the LNT model by a subsequent and highly influential NAS Biological Effects of Ionizing Radiation (BEIR) I Committee (NAS/NRC, 1972) using mouse data has now been found to be inappropriate based on the discovery of a significant documented error in the historical control group that led to incorrect estimations of risk in the low dose zone. Correction of this error by the original scientists and the application of the adjusted/corrected data back to the BEIR I (NAS/NRC, 1972) report indicates that the data would have supported a threshold rather than the LNT model. Thus, cancer risk assessment has a poorly appreciated, complex and seriously flawed history that has undermined policies and practices of regulatory agencies in the U.S. and worldwide to the present time.

Traffic emissions are a complex and variable cocktail of toxic chemicals. They are the major source of atmospheric pollution in the parts of cities where people live, commute and work. Reducing exposure requires information about the distribution and nature of emissions. Spatially and temporally detailed data are required, because both the rate of production and the composition of emissions vary significantly with time of day and with local changes in wind, traffic composition and flow. Increasing computer processing power means that models can accept highly detailed inputs of fleet, fuels and road networks. The state of the science models can simulate the behaviour and emissions of all the individual vehicles on a road network, with resolution of a second and tens of metres. The chemistry of the simulated emissions is also highly resolved, due to consideration of multiple engine processes, fuel evaporation and tyre wear. Good results can be achieved with both commercially available and open source models. The extent of a simulation is usually limited by processing capacity; the accuracy by the quality of traffic data. Recent studies have generated real time, detailed emissions data by using inputs from novel traffic sensing technologies and data from intelligent traffic systems (ITS). Increasingly, detailed pollution data is being combined with spatially resolved demographic or epidemiological data for targeted risk analyses.

Urban water pollution poses risks of waterborne infectious diseases. Therefore, in order to improve urban liveability, effective pollution mitigation strategies are required underpinned by predictions generated using water quality models. However, the lack of reliability in current modelling practices detrimentally impacts planning and management decision making. This research study adopted a novel approach in the form of Bayesian Networks to model urban water quality to better investigate the factors that influence risks to human health. The application of Bayesian Networks was found to enhance the integration of quantitative and qualitative spatially distributed data for analysing the influence of environmental and anthropogenic factors using three surrogate indicators of human health risk, namely, turbidity, total nitrogen and fats/oils. Expert knowledge was found to be of critical importance in assessing the interdependent relationships between health risk indicators and influential factors. The spatial variability maps of health risk indicators developed enabled the initial identification of high risk areas in which flooding was found to be the most significant influential factor in relation to human health risk. Surprisingly, population density was found to be less significant in influencing health risk indicators. These high risk areas in turn can be subjected to more in-depth investigations instead of the entire region, saving time and resources. It was evident that decision making in relation to the design of pollution mitigation strategies needs to account for the impact of landscape characteristics on water quality, which can be related to risk to human health.

The temporal and spatial trends in sediment of 22 poly- and perfluorinated (PFAS) compounds were investigated in the southern Great Lakes Erie and Ontario as well as Lake St. Clair. Surface concentrations measured by Ponar grab samples indicated a trend for greater concentrations near to urban sites. Mean concentrations ∑22PFAS were 15.6, 18.2 and 19 ng g−1 dm for Lakes St. Clair, Erie and Ontario, respectively. Perfluoro-n-butanoic acid (PFBA) and Perfluoro-n-hexanoic acid (PFHxA) were frequently determined in surface sediment and upper core samples indicating a shift in use patterns. Where PFBA was identified it was at relatively great concentrations typically >10 ng g−1 dm. However as PFBA and PFHxA are less likely to bind to sediment they may be indicative of pore water concentrations Sedimentation rates between Lake Erie and Lake Ontario differ greatly with greater rates observed in Lake Erie. In Lake Ontario, in general concentrations of PFAS observed in core samples closely follow the increase in use along with an observable change due to regulation implementation in the 1970s for water protection. However some of the more water soluble PFAS were observed in deeper core layers than the time of production could account for, indicating potential diffusion within the sediment. Given the greater sedimentation rates in Lake Erie, it was hoped to observe in greater resolution changes since the mid-1990s. However, though some decrease was observed at some locations the results are not clear. Many cores in Lake Erie had clearly observable gas voids, indicative of gas ebullition activity due to biogenic production, there were also observable mussel beds that could indicate mixing by bioturbation of core layers.

Tetrabromobisphenol A (TBBPA) and tetrachlorobisphenol A (TCBPA) are persistent toxic environmental pollutants that cause severe reproductive toxicity in animals. The goal of this study was to compare the reproductive toxic effects of TBBPA and TCBPA on male Rana nigromaculata and to expound on the mechanisms leading to these effects. Healthy adult frogs were exposed to 0, 0.001, 0.01, 0.1, and 1 mg/L of TBBPA and TCBPA for 14 days. Sperm numbers were counted by erythrometry. Sperm mobility and deformities were observed under a light microscope (400 ×). We used commercial ELISA kits to determine the serum content of testosterone (T), estradiol (E2), luteinizing hormone (LH) and follicle stimulating hormone (FSH). Expression of androgen receptor (AR) mRNA was detected using real-time qPCR. Sperm numbers and sperm mobility were significantly decreased and sperm deformity was significantly increased in a concentration dependent manner following exposure to TBBPA and TCBPA. Sperm deformity was significantly greater in the 1 mg/L TCBPA (0.549) treatment group than in the 1 mg/L TBBPA (0.397) treatment group. Serum T content was significantly greater in the 0.01, 0.1 and 1 mg/L TBBPA and TCBPA experimental groups compared with controls, while E2 content was significantly greater in only the 1 mg/L TBBPA and TCBPA experimental groups. Expression levels of LH and FSH significantly decreased in the 1 mg/L TBBPA and TCBPA treatment groups. AR mRNA expression decreased markedly in all the treated groups. Our results indicated that TBBPA and TCBPA induced reproductive toxicity in a dose-dependent manner, with TCBPA having greater toxicity than TBBPA. Furthermore, changes in T, E2, LH, and FSH levels induced by TBBPA and TCBPA exposure, which led to endocrine disorders, also caused disturbance of spermatogenesis through abnormal gene expressions of AR in the testes.

In recent years, air pollution events have occurred frequently in China during the winter. Most studies have focused on the physical and chemical composition of polluted air. Some studies have examined the bacterial bioaerosols both indoors and outdoors. But few studies have focused on the relationship between air pollution and bacteria, especially pathogenic bacteria. Airborne PM samples with different diameters and different air quality index values were collected in Hangzhou, China from December 2014 to January 2015. High-throughput sequencing of 16S rRNA was used to categorize the airborne bacteria. Based on the NCBI database, the “Human Pathogen Database” was established, which is related to human health. Among all the PM samples, the diversity and concentration of total bacteria were lowest in the moderately or heavily polluted air. However, in the PM2.5 and PM10 samples, the relative abundances of pathogenic bacteria were highest in the heavily and moderately polluted air respectively. Considering the PM samples with different particle sizes, the diversities of total bacteria and the proportion of pathogenic bacteria in the PM10 samples were different from those in the PM2.5 and TSP samples. The composition of PM samples with different sizes range may be responsible for the variances. The relative humidity, carbon monoxide and ozone concentrations were the main factors, which affected the diversity of total bacteria and the proportion of pathogenic bacteria. Among the different environmental samples, the compositions of the total bacteria were very similar in all the airborne PM samples, but different from those in the water, surface soil, and ground dust samples. Which may be attributed to that the long-distance transport of the airflow may influence the composition of the airborne bacteria. This study of the pathogenic bacteria in airborne PM samples can provide a reference for environmental and public health researchers.

Laccases are capable of rapidly oxidizing benzo[a]pyrene. It is thought that the metabolites with an increase in water solubility caused by the oxidation of benzo[a]pyrene may stimulate the subsequent mineralization. However, to date, there has been no experimental evidence to support this. In this study, the fate of benzo[a]pyrene in soil affected by laccase amendment and the resulting soil bacterial responses were investigated. Laccase amendment promoted benzo[a]pyrene dissipation (15.6%) from soil, accompanied by trace mineralization (<0.58 ± 0.02%) and substantial bound residue formation (∼80%). An increase of ∼15% in the bound residue fraction was observed by laccase amendment, which mainly resulted from covalent binding of the residues to humin fraction. During the incubation, the abundance of bacterial 16S rRNA and polycyclic aromatic hydrocarbon ring-hydroxylating dioxygenase genes did not change markedly. In contrast, benzo[a]pyrene treated with laccase resulted in a smaller shift in the bacterial community composition, indicating a reduced disturbance to the soil microbial communities. These results here suggest that benzo[a]pyrene contaminated soil can be detoxified by laccase amendment mainly due to the enhanced bound residue formation to soil organic matter via covalent binding.

Avoidance behaviour offers a highly relevant information as it reveals the ability to avoid (or not) possible toxic compounds in the field, hence it provides information on reasons for the presence/absence in the field. The earthworm Eisenia fetida was used to study avoidance behaviour to four silver forms (three nanomaterials (NMs) and one salt) over four time points (24, 48, 72 and 96 h), using OECD standard soil. Avoidance behaviour depended on both exposure material and concentration, but in general changed little with exposure duration. Avoidance was highest for the salt (AgNO₃) for all exposure durations and showed a continuous higher avoidance with time (based on EC₅₀ values). The AgNMs avoidance was in the order NM300K<AgNM-non coated = AgNM- PVP coated. It was not possible to identify one soil solution fraction that correlated with EC₅₀ across materials.

Hypermethylation of СpG islands in the promoter regions of several genes with basic protective function in blood leukocytes of individuals exposed to ionizing radiation long time ago (2–46 years), and differential effects of age and radiation exposure on hypermethylation was reported in our previous work. To validate these results, epigenetic modifications were assessed in an independent series of 49 nuclear industry workers from the “Mayak” facility (67–84 years old at sampling) with documented individual accumulated doses from the prolonged external γ-radiation exposure (95.9–409.5 cGy, end of work with radiation:0.3–39 years ago), and in 50 non-exposed persons matched by age. In addition to the genes analyzed before (RASSF1A, p16/INK4A, p14/ARF, GSTP1), four additional loci were analyzed: TP53, ATM, SOD3, ESR1. The frequency of individuals displaying promoter methylation of at least one of the 8 genes (71.4%) was significantly higher in exposed group as compared to the control group (40%), p = .002, OR = 3.75. A significantly elevated frequency of individuals with hypermethylated СpG islands in GSTP1, TP53, SOD3 promoters was revealed among exposed subjects as compared to the control group (p = .012, OR = 8.41; p = .041, OR = 4.02 and p = .009, OR = 3.42, respectively). A similar trend (p = .12, OR = 3.06) was observed for the p16/INK4A gene. As a whole, p16/INK4A and GSTP1 promoter hypermethylation in irradiated subjects from both previously and currently analyzed groups was pronounced. Thus, the direction of the effects was fully confirmed, suggesting the result reproducibility. No statistically significant correlation between promoter methylation and individual radiation dose was found. Further studies are required to create an array of blood epigenetic markers of radiation exposure associating with premature aging and age-related diseases and to accurately evaluate radiation-added effect across the range of doses.The results of studies of epigenetic changes in two independent samples of irradiated subjects indicated the significance of radiation factor in the induction of hypermethylation of CpG islands in gene promoters that is revealed in blood cells years and decades after exposure.