Trace elements can be toxic when they cannot be easily removed after entering an ecosystem, so a long-term assessment is fundamental to guide ecosystem restoration after catastrophic pollution. In 1998, a pyrite mining accident in Aznalcóllar (south-western Spain) spilled toxic waste over a large area of the Guadiamar river basin, where, after restoration tasks, the Guadiamar Green Corridor was established. Eight years after the mine accident (2005–2006), the ground-dwelling insectivorous lizard Psammodromus algirus registered high trace-element levels within the study area compared to specimens from a nearby unpolluted control site. In 2017, 20 years after the accident, we repeated the sampling for this lizard species and also quantified trace elements in vegetation as well as in arthropod samples in order to identify remnant trace-element accumulation with the aim of assessing the transfer of these elements through the trophic web. We found remnant trace-element contamination in organisms of the polluted site compared to those from the unpolluted site. All trace-element concentrations were higher in arthropods than in plants, suggesting these compounds bioaccumulate through the trophic web. Lizards from the polluted areas had higher As, Cd, and Hg concentrations than did individuals from the unpolluted area. Lizard abundance between sampling periods (2005–06 and 2017) did not vary in unpolluted transects but strongly declined at polluted ones. By contrast, the Normalized Difference Vegetation Index indicated that in the study period, the vegetation was similar at the two sampling sites. These results suggest that, 20 years after the accident, the trace-element pollution could be the cause of a severe demographic decline of the lizard in the polluted area.

Organochlorine pesticides (OCPs) had been widely used in agriculture and disease prevention from the 1940s–1960s. Currently, OCPs are raising global concerns due to their associated prevalent contamination and adverse health effects, such as endocrine disruption. Several epidemiological studies have explored the underlying association of OCPs on thyroid hormone (TH) status in adults and newborns, but the results of studies performed on newborns are often inconclusive. This exploratory study was conducted with the purpose of assessing the potential association of the prenatal exposure to OCPs with the concentrations of TH in the cord blood of newborns from China. Cord blood and information on demographic characteristics were collected from 115 newborns between November 2013 and June 2014. The exposure levels of 17 OCPs were measured with a gas chromatography/mass spectrometry, and TH levels including free triiodothyronine (FT3), free thyroxine (FT4), and thyroid-stimulating hormone (TSH) were detected using electrochemiluminescence immunoassay methods. After adjusting for confounding factors (the age of pregnant mothers, education level, monthly household income, parity, and sex of the newborns), we found marginally significant inverse associations of cord plasma measurements of ∑hexachlorcyclohexanes (∑HCHs), 1,1-dichloro-2,2-di(4-chlorophenyl)ethylene (ρ,ρ′-DDE) and methoxychlor with FT4 levels, but not with FT3 and TSH levels. Moreover, higher cord plasma levels of aldrin, dieldrin, ∑dichlorodiphenyltrichloroethanes (∑DDTs), ∑Drins, and ∑OCPs were found to be related to the increase in cord plasma TSH levels after the adjustment for confounders. The results of this exploratory study indicate that in utero exposure to certain OCPs may affect TH status in newborns, and therefore, pose potential effects on early human development. Further research, with larger sample sizes, should be conducted to confirm these findings.

Mercury (Hg) is a globally ubiquitous pollutant that has received much attention due to its toxicity to humans and wildlife. The development of non-destructive sampling techniques is a critical step for sustainable monitoring of Hg accumulation. We evaluated the efficacy of non-destructive sampling techniques and assessed spatial, temporal, and demographic factors that influence Hg bioaccumulation in turtles. We collected muscle, blood, nail, and eggs from snapping turtles (Chelydra serpentina) inhabiting an Hg contaminated river. As predicted, all Hg tissue concentrations strongly and positively correlated with each other. Additionally, we validated our mathematical models against two additional Hg contaminated locations and found that tissue relationships developed from the validation sites did not significantly differ from those generated from the original sampling site. The models provided herein will be useful for a wide array of systems where biomonitoring of Hg in turtles needs to be accomplished in a conservation-minded fashion.

Inflammation may play an important role in the association between exposure to polycyclic aromatic hydrocarbons (PAHs) and atherosclerotic cardiovascular disease (ASCVD) risk. However, the underlying mechanisms remain unclear.To investigate the association of PAHs exposure with ASCVD risk and effects of mean platelet volume (MPV) or Club cell secretory protein (CC16) on the association.A total of 2022 subjects (689 men and 1333 women) were drawn from the baseline Wuhan residents of the Wuhan-Zhuhai Cohort study. Data on demography and the physical examination were obtained from each participant. Urinary monohydroxy PAH metabolites (OH-PAHs) levels were measured by a gas chromatography-mass spectrometry. We estimated the association between each OH-PAHs and the 10-year ASCVD risk or coronary heart disease (CHD) risk using logistic regression models, and further analyze the mediating effect of MPV or plasma CC16 on the association by using structural equation modeling.The results of multiple logistic regression models showed that some OH-PAHs were positively associated with ASCVD risk but not CHD risk, including 2-hydroxyfluoren (β = 1.761; 95% CI: 1.194–2.597), 9-hydroxyfluoren (β = 1.470; 95% CI: 1.139–1.898), 1-hydroxyphenanthrene (β = 1.480; 95% CI: 1.008–2.175) and ΣOH-PAHs levels (β = 1.699; 95% CI: 1.151–2.507). The analysis of structural equation modeling shows that increased MPV and increased plasma CC16 levels contributed 13.6% and 15.1%, respectively, to the association between PAHs exposure and the 10-year ASCVD risk (p < 0.05).Exposure to PAHs may increase the risk of atherosclerosis, which was partially mediated by MPV or CC16.

Studies have showed the increasing environmental and public health risks of toxic emissions from natural gas and oil mining, which have become even worse as fracking is becoming a dominant approach in current natural gas extraction. However, governments and communities often overlook the serious air pollutants from oil and gas mining, which are often quantified lower than the significant levels of adverse health effects. Therefore, we are facing a challenging dilemma: how could we clearly understand the potential risks of air toxics from natural gas and oil mining.This short study aims at the design and application of simple and robust methods to enhance and improve current understanding of the becoming worse toxic air emissions from natural gas and oil mining as fracking is becoming the major approach. Two simple ratios, the min-to-national-average and the max-to-national-average, are designed and applied to each type of air pollutants in a natural gas and oil mining region. The two ratios directly indicate how significantly high a type of air pollutant could be due to natural gas and oil mining by comparing it to the national average records, although it may not reach the significant risks of adverse health effects according to current risk screening methods. The min-to-national-average and the max-to-national-average ratios can be used as a direct and powerful method to describe the significance of air pollution by comparing it to the national average. The two ratios are easy to use for governments, stakeholders, and the public to pay enough attention on the air pollutants from natural gas and oil mining. The two ratios can also be thematically mapped at sampled sites for spatial monitoring, but spatial mitigation and analysis of environmental and health risks need other measurements of environmental and demographic characteristics across a natural gas and oil mining area.

High levels of phthalates in name-brand cosmetics products have raised concerns about phthalate exposure and the associated risk for cosmetics sales clerks. We assessed the exposure and risk of phthalates in 23 cosmetics, 4 perfume, and 9 clothing department store sales clerks. We collected 108 urine samples pre- and post-shift and analyzed for phthalate monoesters through liquid chromatography–electrospray ionization–tandem mass spectrometry. Phthalates in 32 air samples were collected and analyzed through gas chromatography–mass spectrometry. Demographic characteristics and information on the exposure scenarios were obtained through questionnaires. Principal component analysis, cluster and risk analysis were applied to identify the exposure profile and risk of phthalate.Median post-shift levels of urinary mono-2-ethylhexyl phthalate (MEHP) and monomethyl phthalate (MMP) were significantly higher than the corresponding pre-shift levels in cosmetics group (53.3 vs. 30.9 μg/g-c for MEHP; 34.4 vs. 22.5 μg/g-c for MMP; both P < 0.05) and the post-shift levels of urinary MMP was significantly higher than the corresponding pre-shift levels in perfume group (26.6 vs. 14.9 μg/g-c, P < 0.05). Median levels of air diethyl phthalate (DEP) in cosmetics (1.77 μg/m³) and perfume (1.75 μg/m³) groups and di-(2-ethylhexyl) phthalate (DEHP) in perfume group (6.98 μg/m³) were higher than those in clothing group (DEP: 0.89; DEHP: 2.16 μg/m³). Over half of cosmetic (70%) and perfume sale clerks had exceeded cumulative risk of phthalate exposure for anti-androgenic effect. We concluded that cosmetic and perfume workers had increased risks of reproductive or hepatic effects for DBP and DEHP exposure. We suggest that not only inhalation but dermal exposure is important route of phthalate exposure for cosmetics and perfume workers.

This study evaluated whether short term exposures to NO2, O3, particulate matter <10 mm in diameter (PM10) were associated with higher risk of mortality. A total of 223,287 hypertensive patients attended public health-care services and newly prescribed at least 1 antihypertensive agent were followed-up for up to 5 years. A time-stratified, bi-directional case-crossover design was adopted. For all-cause mortality, significant positive associations were observed for NO2 and PM10 at lag 0–3 days per 10 μg/m3 increase in concentration (excess risks 1.187%–2.501%). Significant positive associations were found for O3 at lag 1 and 2 days and the excess risks were 1.654% and 1.207%, respectively. We found similarly positive associations between these pollutants and respiratory disease mortality. These results were significant among those aged ≥65 years and in cold seasons only. Older hypertensive patients are susceptible to all-cause and respiratory disease-specific deaths from these air pollutants in cold weather.

Contraceptive drugs are nowadays found in aquatic environments around the globe. Particularly, 17α-ethinylestradiol (EE2) may act even at low concentrations, such as those recorded in natural ecosystems. We evaluated the physiological effects of EE2 on cyclopoids and calanoids, common copepods in both marine and freshwater communities. We used three EE2 concentrations and assessed its impact on activity of different physiological endpoints: Acetylcholinesterase (neurotransmission), Glutathione S-transferase (detoxifying system), and Caspase-3 (apoptosis). While EE2 exerts, distinctive effect on detoxifying and apoptotic systems, no effect on AChE was observed at environmental doses. Our results show that EE2 exposure affects differently copepod physiology endpoints, altering moulting process, adult recruitment in calanoids and calanoid to cyclopoid ratio. The ecological consequences of this underlying physiological process may affect since life history to population and community structures, and this represent a new aspects of this xenobiotic in natural systems.