The present study is a literature-based analysis investigating occurrence and the possible consequences of polycyclic aromatic hydrocarbons (PAH) in marine protected areas (MPAs) of Latin America and Caribbean. The approach using overlapping of georeferenced MPA polygons with data compiled from peer-reviewed literature, published during the last 15 years, showed 341 records of PAH in 9 countries. PAH was reported to occur within the boundaries of 36 MPAs located in Argentina, Brazil, Colombia, Mexico, Nicaragua and Uruguay. According to quality guidelines, low to moderate impacts are expected in MPAs categorized in different management classes. Considering sediment samples, 13% of the records presented concentrations enough to cause occasional toxicity. Such level of risk was also seen in Ramsar sites and in Amazonian MPAs. In addition, based on concentrations reported in biota, occasional deleterious effects on organisms from Biosphere Reserves might occur. Diagnostic ratios pointed out petrogenic and pyrolytic processes as PAH predominant sources, and were mainly attributed to the proximity to ports, industries and urban areas. MPAs located in the vicinity of impact-generating areas may be under threat and require government attention and action, mainly through implementation of contamination monitoring programs.

The feasibility and effectiveness of iron turning waste as low cost and sustainable permeable reactive barrier (PRB) media for remediating dieldrin, endrin, dichlorodiphenyltrichloroethane (DDT), and lindane individually (batch system) and combined (continuous flow column) in water were investigated. After 10 min of reaction in a batch system, removal of endrin, dieldrin, and DDT was higher (86–91 %) than lindane (41 %) using 1 g of iron turning waste in 200 mL of pesticide solution (20 μg/L for each pesticide). Among the studied pesticides, only lindane removal decreased substantially in the presence of nitrate (37 %) and magnesium (18 %). Acidic water environment (pH = 4) favored the pesticide removal than neutral and basic environments. For the column experiments, sand alone as PRB media was ineffective for remediating the pesticides in water. When only iron turning was used, the removal efficiencies of lindane, endrin, and dieldrin were 83–88 % and remained stable during 60 min of the experiments. DDT removal was less than other pesticides (58 %). Sandwiching the iron turning waste media between two sand layers improved DDT removal (79 %) as well as limited the iron content below a permissible level in product water. In a long-term PRB column performance evaluation, iron turning waste (150 g) removed all pesticides in water (initial concentration of each pesticide = 2 μg/L) effectively (≥94 %) at a hydraulic retention time of 1.6 h. Iron turning waste, which was mainly in the form of zerovalent iron (Fe⁰), was oxidized to ferrous (Fe²⁺) and ferric (Fe³⁺) iron during its reaction with pesticides, and electrons donated by Fe⁰ and Fe²⁺ were responsible for complete dechlorination of all the pesticides. Therefore, it can be used as inexpensive and sustainable PRB media for groundwater remediation especially in developing countries where groundwater contamination with pesticides is more prevalent.

Arsenic is a well-recognized environmental contaminant that occurs naturally through geogenic processes in the aquifer. More than 200 million people around the world are potentially exposed to the elevated level of arsenic mostly from Asia and Latin America. Many adverse health effects including skin diseases (i.e., arsenicosis, hyperkeratosis, pigmentation changes), carcinogenesis, and neurological diseases have been reported due to arsenic exposure. In addition, arsenic has recently been shown to contribute to the onset of non-communicable diseases, such as diabetes mellitus and cardiovascular diseases. The mechanisms involved in arsenic-induced diabetes are pancreatic β-cell dysfunction and death, impaired insulin secretion, insulin resistance and reduced cellular glucose transport. Whereas, the most proposed mechanisms of arsenic-induced hypertension are oxidative stress, disruption of nitric oxide signaling, altered vascular response to neurotransmitters and impaired vascular muscle calcium (Ca²⁺) signaling, damage of renal, and interference with the renin-angiotensin system (RAS). However, the contributions of arsenic exposure to non-communicable diseases are complex and multifaceted, and little information is available about the molecular mechanisms involved in arsenic-induced non-communicable diseases and also no suitable therapeutic target identified yet. Therefore, in the future, more basic research is necessary to identify the appropriate therapeutic target for the treatment and management of arsenic-induced non-communicable diseases. Several reports demonstrated that a daily balanced diet with proper nutrient supplements (vitamins, micronutrients, natural antioxidants) has shown effective to reduce the damages caused by arsenic exposure. Arsenic detoxication through natural compounds or nutraceuticals is considered a cost-effective treatment/management and researchers should focus on these alternative options. This review paper explores the scenarios of arsenic contamination in groundwater with an emphasis on public health concerns. It also demonstrated arsenic sources, biogeochemistry, toxicity mechanisms with therapeutic targets, arsenic exposure-related human diseases, and onsets of cardiovascular diseases as well as feasible management options for arsenic toxicity.

Piscivorous avian species may be affected by mercury (Hg) which tends to accumulate in aquatic environments and biomagnifies across the food webs. One of such species is the black stork, whose population increase recently slowed down due to unknown reasons. At the same time Hg contamination and its effects were almost unaudited for this species, so it may have exerted deleterious effects on the population and an evaluation is necessary. This is the first study of this species concerning Hg contamination. Thus, Hg concentrations were investigated in the down of black stork chicks (N = 90) from breeding locations in central and southern Poland (Europe) between 2015 and 2017. As well as Hg levels, morphometric parameters and age were evaluated. Mean Hg concentrations reached 0.7 μg/g d.w. and differed significantly between years, from the lowest value noted in 2017 (mean 0.5 μg/g), through 2016 (0.7 μg/g), to the highest one in 2015 (0.9 μg/g), and between nest locations where higher Hg levels were generally found in northern parts of the study area. Hg concentrations were also unrelated to morphometric parameters. Contrarily, morphometric parameters revealed high correlations between themselves, which was confirmed by the cluster analysis (revealing only two clusters) and principal component analysis (the first PC explained 96.8% of the variance). Hg levels in the down of black storks were rather low with the fluctuation between years and nest locations probably caused by parental exposure during wintering, migration, pre-breeding season and recent exposure through food provided by parents. Such low Hg concentrations seemed not to affect the population from the region studied.

Pharmaceuticals and personal care products (PPCPs) have been widely distributed and posed ecotoxicological risks in the aquatic environment. This study aims to evaluate the toxic effects after chronic exposure to PPCPs mixture at the environment relevant concentrations (ERCs). Our results indicated that PPCPs induced serious metabolic effects by disturbing the carbohydrate and lipid metabolism pathways. Chronic exposure caused a significant reduction in the hepatosomatic index (HSI), the gut weight ratios, and histological alterations in liver and gut tissues. Further, exposure to the combined PPCPs disrupted the carbohydrate metabolism via significant upregulation of hk1, gk, pck1, and insr genes. The lipid metabolism was affected with higher ppars expression levels that increased the fatty acid β-oxidation and ultimately decreased the lipidogenesis. Moreover, the altered responses of the insulin growth factor (IGF) pathway more in male gut tissue than that of female revealed sex-dependent disturbance in the gut homeostasis induced by PPCPs mixture. In conclusion, chronic exposure to PPCPs mixtures at ERCs can induce developmental effects and metabolic dysfunction in both male and female fish. The consumption and environmental disposal of these PPCPs should be regulated to ensure ecological health and environmental safety.

(S,S)-ethylenediaminedisuccinic acid (EDDS) has a strong capacity to mobilize potentially toxic elements (PTEs) in phytoextraction. It can release NH₄⁺-N via biodegradation, which can enhance N supply to soil thereafter promote plant growth and plant resistance to PTEs. However, the advanced feature of released N in the EDDS-enhanced phytoextraction remains unclear. In the current study, the effects of N supply released from EDDS on ryegrass phytoextraction and plant resistance to PTEs were investigated in detail by a comparison with urea. Our results supported that the addition of both EDDS and urea increased N concentration in soil solution, yet EDDS needed more time to release available N for plant uptake and transported more N from root to shoot. Additionally, EDDS significantly increased the concentration of all targeted PTEs, i.e. Cu, Zn, Cd, and Pb, in the soil solution, which results in higher levels of their occurrence in plant biomass compared with urea. By contrast, the supply of N slightly enhanced the ryegrass uptake of micro-nutrients, i.e. Cu and Zn, yet it caused negligible effects on nonessential elements, i.e. Cd and Pb. The mobilized PTEs by EDDS lead to elevated oxidative stress because higher levels of malondialdehyde and O₂•⁻ were observed. The supply of N attenuated oxidative stress caused by O₂•⁻ and H₂O₂, which was associated with enhanced activities of superoxide dismutase and peroxidase. Our results advanced the understanding of the exogenous N supply and metal resistance mechanisms in the EDDS-enhanced phytoextraction. This study also highlighted that EDDS can serve as a N source to ease N-deficient problems in PTEs-contaminated soils.

DNA methylation (DNAm) plays a significant role in deleterious health effects inflicted by fine particulate matter (PM₂.₅) on the human body. Recent studies have reported that DNAm of imprinted control regions (ICRs) in imprinted genes may be a sensitive biomarker of environmental exposure. Less is known about specific biomarkers of imprinted genes after PM₂.₅ exposure. The relationship between PM₂.₅ and its chemical constituents and DNAm of ICRs in imprinted genes after short-term exposure was investigated to determine specific human biomarkers of its adverse health effects. A panel study was carried out in healthy young people in Guangzhou, China. Mixed-effects models were used to evaluate the influence of PM₂.₅ and its constituent exposure on DNAm while controlling for potential confounders. There was no significant correlation between DNAm and personal PM₂.₅ exposure mass. DNAm changes in eight ICRs (L3MBTL1, NNAT, PEG10, GNAS Ex1A, MCTS2, SNURF/SNRPN, IGF2R, and RB1) and a non-imprinted gene (CYP1B1) were significantly associated with PM₂.₅ constituents. Compared to non-imprinted genes, imprinted gene methylation was more susceptible to interference with PM₂.₅ constituent exposure. Among those genes, L3MBTL1 was the most sensitive to personal PM₂.₅ constituent exposure. Moreover, transition metals derived from traffic sources (Cd, Fe, Mn, and Ni) significantly influenced DNAm of the imprinted genes, suggesting the importance of more targeted measures to reduce toxic constituents. Bioinformatics analysis indicated that imprinted genes (RB1) may be correlated with pathways and diseases (non-small cell lung cancer, glioma, and bladder cancer). The present study suggests that screening the imprinted gene for DNAm can be used as a sensitive biomarker of PM₂.₅ exposure. The results will provide data for prevention of PM₂.₅ exposure and a novel perspective on potential mechanisms on an epigenetic level.

People use a particulate respirator in order to reduce exposure to ambient fine particulate matter (PM₂.₅). Acute exposure to PM₂.₅ is known to increase blood pressure. However, systematic reviews or meta-analyses on blood pressure-related benefits of using a particulate respirator is lacking. Therefore, we reviewed randomized crossover intervention studies on blood pressure-related effects of particulate matter respirator use. We conducted a literature review of articles found on Embase, Medline, and Cochrane library on August 31, 2020. The study outcomes were systolic and diastolic blood pressure and mean arterial pressure. A random-effect model was used in the meta-analysis. Subgroup analyses, based on age (adult < 60 years, elderly ≥ 60 years), personal PM₂.₅ exposure levels (High: ≥ 25 μg/m³, Low: < 25 μg/m³), and types of monitoring methods (ambulatory and resting blood pressure) were conducted. We identified 297 references, and seven studies were included in our systematic review. None of the studies used a sham respirator as control and complete allocation concealment and blinding were impossible. The use of a particulate respirator was associated with a −1.23 mmHg (95% confidence interval (CI): −2.53, 0.07) change in systolic blood pressure and a −1.57 mmHg (95% CI: −3.85, 0.71) change in mean arterial pressure. There were significant heterogeneities and possibilities for publication bias. The subgroup analyses revealed that studies involving elderly individuals, those conducted in high PM₂.₅ personal exposure, and those in which resting blood pressure was monitored demonstrated a larger decrease in blood pressure resulting from respirator use. Further intervention studies with a large sample size and subjects with diverse characteristics and different personal PM₂.₅ levels may add the evidence to current literature.

Exposure to endocrine disrupting chemicals (EDCs) is ubiquitous. EDC exposure, especially during critical periods of development like the prenatal window, may interfere with the body’s endocrine system, which can affect growth and developmental outcomes such as puberty. Most studies have examined one EDC at a time in relation to disease; however, humans are exposed to many EDCs. By studying mixtures, the human experience can be more closely replicated. We investigated the association of prenatal exposure to persistent EDCs (poly- and perfluoroalkyl substances (PFAS), polychlorinated biphenyls (PCBs), and organochlorine pesticides (OCPs)) as mixtures with early menarche among female offspring in a nested case-control study within the Avon Longitudinal Study of Parents and Children (ALSPAC) recruited in the United Kingdom in 1991–1992. Concentrations of 52 EDCs were quantified in maternal serum samples collected during pregnancy. Daughter’s age at menarche was ascertained through mailed questionnaires sent annually. We used repeated holdout weighted quantile sum (WQS) regression and Bayesian kernel machine regression (BKMR) to examine the association between prenatal exposure to multiple EDCs and early menarche (<11.5 (n = 218) vs. ≥11.5 years (n = 230)) for each chemical class separately (PFAS, PCBs, and OCPs) and for all three classes combined. Models adjusted for maternal age at menarche, maternal education, parity, pre-pregnancy body mass index, maternal age, prenatal smoking, and gestational week at sample collection. Mixture models showed null associations between prenatal exposure to EDC mixtures and early menarche. Using WQS regression, the odds ratio for early menarche for a one-decile increase in chemical concentrations for all three classes combined was 0.89 (95% CI: 0.76, 1.05); using BKMR, the odds ratio when all exposures were at the 60th percentile compared to the median was 0.98 (95% CI: 0.91, 1.05). Results suggest the overall effect of prenatal exposure to persistent EDC mixtures is not associated with early menarche.

Carbon disulfide (CS₂) has been reported to induce disorder of glucose metabolism. However, the associations of CS₂ exposure with plasma glucose levels and risk of diabetes have not been explored in general population, and the underlying mechanisms remain unclear. We aim to examine the relationships between CS₂ exposure and fasting plasma glucose (FPG) levels, as well as diabetes, and assess the potential role of oxidative stress among the abovementioned relationships in Chinese general adults. The concentrations of urinary biomarkers of CS₂ exposure (2-thiothiazolidin-4-carboxylic acid, TTCA), and biomarkers for lipid peroxidation (8-isoprostane, 8-iso-PGF₂α) and DNA oxidative damage (8-oxo-7,8-dihydro-20-deoxyguanosine, 8-OHdG) were measured among 3338 urban adults from the Wuhan-Zhuhai cohort. Additionally, FPG levels were tested promptly. Generalized linear models and logistic regression models were used to quantify the associations among urinary TTCA, oxidative damage markers, FPG levels and diabetes risk. Mediation analysis was employed to estimate the role of oxidative damage markers in the association between urinary TTCA and FPG levels. We discovered a significant relationship between urinary TTCA and FPG levels with regression coefficient of 0.080 (95% CI: 0.002,0.157). Besides, the risk of diabetes was positively related to urinary TTCA (OR:1.282, 95% CI: 1.055,1.558), particularly among those who did not exercise regularly. Each 1% increase of urinary TTCA concentration was associated with a 0.096% and 0.037% increase in urinary 8-iso-PGF₂α and 8-OHdG, respectively. Moreover, we found an upward trend of FPG level as urinary 8-iso-PGF₂α gradually increased (Pₜᵣₑₙd<0.05), and urinary 8-iso-PGF₂α mediated 21.12% of the urinary TTCA-associated FPG increment. Our findings indicated that urinary CS₂ metabolite was associated with increased FPG levels and diabetes risk in general population. Lipid peroxidation partly mediated the association of urinary CS₂ metabolite with FPG levels.