Particulate-filtering respirators (PFRs) have been recommended as a practical personal-level intervention to protect individuals from the health effects of particulate matter exposure. However, the cardiovascular benefits of PFRs including improvements in key surrogate endpoints remain unclear. We performed a systematic review and meta-analysis of randomized studies (wearing versus not wearing PFRs) reporting the effects on blood pressure (BP) and heart rate variability (HRV). The search was performed on January 3, 2022 to identify published papers until this date. We queried three English databases, including PubMed, Web of Science Core Collection and Scopus. Of 527 articles identified, eight trials enrolling 312 participants (mean age ± standard deviation: 36 ± 19.8; 132 female) met our inclusion criteria for analyses. Study participants wore PFRs from 2 to 48 h during intervention periods. Wearing PFRs was associated with a non-significant pooled mean difference of −0.78 mmHg (95% confidence interval [CI]: −2.06, 0.50) and −0.49 mmHg (95%CI: −1.37, 0.38) in systolic and diastolic BP (SBP and DBP). There was a marginally significant reduction of mean arterial pressure (MAP) by nearly 1.1 mmHg (95%CI: −2.13, 0.01). The use of PFRs was associated with a significant increase of 38.92 ms² (95%CI: 1.07, 76.77) in pooled mean high frequency (power in the high frequency band (0.15–0.4 Hz)) and a reduction in the low (power in the low frequency band (0.04–0.15Hz))-to-high frequency ratio [−0.14 (95%CI: −0.27, 0.00)]. Other HRV indices were not significantly changed. Our meta-analysis demonstrates modest or non-significant improvements in BP and many HRV parameters from wearing PFRs over brief periods. However, these findings are limited by the small number of trials as well as variations in experimental designs and durations. Given the mounting global public health threat posed by air pollution, larger-scale trials are warranted to elucidate more conclusively the potential health benefits of PFRs.

Microplastics are sometimes considered not harmful at environmentally relevant concentrations. Yet, such studies were conducted under standard thermal conditions and thereby ignored the impacts of higher mean temperatures (MT), and especially daily temperature fluctuations (DTF) under global warming. Moreover, an evolutionary perspective may further benefit the future risk assessment of microplastics under global warming. Here, we investigated the effects of two generations of exposure to an environmentally relevant concentration of polystyrene microplastics (5 μg L⁻¹) under six thermal conditions (2 MT × 3 DTF) on the life history, physiology, and behaviour of Daphnia magna. To assess the impact of thermal evolution we thereby compared Daphnia populations from high and low latitudes. At the standard ecotoxic thermal conditions (constant 20 °C) microplastics almost had no effect except for a slight reduction of the heartbeat rate. Yet, at the challenging thermal conditions (higher MT and/or DTF), microplastics affected each tested variable and caused an earlier maturation, a higher fecundity and intrinsic growth rate, a decreased heartbeat rate, and an increased swimming speed. These effects may be partly explained by hormesis and/or an adaptive response to stress in Daphnia. Moreover, exposure to microplastics at the higher mean temperature increased the fecundity and intrinsic growth rate of cold-adapted high-latitude Daphnia, but not of the warm-adapted low-latitude Daphnia, suggesting that thermal evolution in high-latitude Daphnia may buffer the effects of microplastics under future warming. Our results highlight the critical importance of DTF and thermal evolution for a more realistic risk assessment of microplastics under global warming.

A large number of toxicity studies report abnormalities in early life-stage (ELS) fish that are described here as a sublethal toxicity syndrome (TxSnFELS) and generally include a reduced heart rate, edemas (yolk sac and cardiac), and a variety of morphological abnormalities. The TxSnFELS is very common and not diagnostic for any chemical or class of chemicals. This sublethal toxicity syndrome is mostly observed at high exposure concentrations and appears to be a baseline, non-specific toxicity response; however, it can also occur at low doses by specific action. Toxicity metrics for this syndrome generally occur at concentrations just below those causing mortality and have been reported for a large number of diverse chemicals. Predictions based on tissue concentrations or quantitative-structure activity relationship (QSAR) models support the designation of baseline toxicity for many of the tested chemicals, which is confirmed by observed values. Given the sheer number of disparate chemicals causing the TxSnFELS and correlation with QSAR derived partitioning; the only logical conclusion for these high-dose responses is baseline toxicity by nonspecific action and not a lock and key type receptor response. It is important to recognize that many chemicals can act both as baseline toxicants and specific acting toxicants likely via receptor interaction and it is not possible to predict those threshold doses from baseline toxicity. We should search out these specific low-dose responses for ecological risk assessment and not rely on high-concentration toxicity responses to guide environmental protection. The goal for toxicity assessment should not be to characterize toxic responses at baseline toxicity concentrations, but to evaluate chemicals for their most toxic potential. Additional aspects of this review evaluated the fish ELS teratogenic responses in relation to mammalian oral LD50s and explored potential key events responsible for baseline toxicity.

Several studies highlighted the ubiquitous presence of ibuprofen and aluminum in the aquatic environment around the world and demonstrated their potential to induce embryotoxic and teratogenic defects on aquatic species individually. Although studies that evaluate developmental alterations induced by mixtures of these pollutants are scarce; and, since environmental contamination presented in the form of a mixture of toxicants with different chemical properties and toxicity mechanisms capable of generating interactions; the objective of this study was to evaluate the developmental defects, teratogenic alterations, and oxidative stress induced by individual forms and the mixture of ibuprofen (IBU) and aluminum (Al) on zebrafish embryos. Oocytes exposed to environmentally relevant concentrations of IBU (0.1–20 μg L-1) and Al (0.01–8 mg L-1) and one binary mixture. The LC50 and EC50 were obtained to calculate the teratogenic index (TI). The IBU LC50, EC50, and TI were 8.06 μg L-1, 2.85 μg L-1 and 2.82. In contrast, Al LC50 was 5.0 mg L-1with an EC50 of 3.58 mg L-1 and TI of 1.39. The main alterations observed for individual compounds were hatching alterations, head malformation, skeletal deformities, hypopigmentation, pericardial edema, and heart rate impairment. The mixture also showed significant delays to embryonic development. Moreover, oxidative stress biomarkers of cellular oxidation and antioxidant defenses at 72 and 96 hpf significantly increased. Results show that environmentally relevant concentrations of ibuprofen (IBU), aluminum (Al), and their mixture promote a series of developmental defects, teratogenic effects, and oxidative disruption on D. rerio embryos, and the interaction of both substances altered the response. In conclusion, morphological and biochemical tests are suitable tools for assessing the health risk of aquatic wildlife by exposure to individual and mixed pollutants in freshwater bodies.

Diclofop-methyl (DM) is one of the most widely used herbicides in agriculture production and has been frequently detected in both freshwater and environments, even agricultural products. However, the potential toxic effects of DM on organisms and the underlying mechanisms are still poorly understood. In this study, we utilized zebrafish to evaluate the toxicity of DM during the cardiovascular developmental process. Exposure of zebrafish embryos to 0.75, 1.0 and 1.25 mg/L DM induced cardiac defects, such as pericardial edema, slow heart rate and long SV-BA distance but the vascular development in zebrafish larvae was not influenced by DM treatment. The expression of cardiac-related genes were disordered and DM exposure initiated disordering cardiogenesis from the period of precardiac mesoderm formation. Moreover, the apoptosis and proliferation of cardiomyocytes were not influenced but the levels of oxidative stress were upregulated by DM exposure. Fullerenes and astaxanthin was able to rescue cardiac defects caused by DM via downregulating oxidative stress. Wnt signaling was downregulated after DM treatment and activation of Wnt signaling could rescue cardiac defects. Therefore, our results suggest that DM has the potential to induce cardiac developmental toxicity through upregulation of Wnt-Mediated (reactive oxygen species) ROS generation in zebrafish larvae.

Because of its analgesic properties, acetaminophen (AAP) is widely used to relieve headache. AAP is generally considered safe for humans, but its effects on aquatic organisms are not well known. Here, we have hypothesis that effects of AAP on aquatic organisms would be environmental temperature dependent, because their physiological function depend on the temperature. To test this hypothesis, we used medaka (Oryzias latipes) as a model, because they can live at a wide range of temperatures (0–40 °C). We exposed medaka larvae to 0 (control), 50, or 150 mg/L of AAP at 15, 25 (optimal temperature), or 30 °C for 4 days. Egg yolk absorption was accelerated with raising temperature at any AAP dose. AAP exposure did not have biologically significant effects on survival ratio and body length of larvae at any tested temperature or dose, but heart rate decreased as the dose of AAP and environmental temperature increased. In addition, as the temperature increased, amount of ATP in individual larvae increased in control group, but decreased in AAP exposed group. Subsequently, exposure to 150 mg/L of AAP at 30 °C decreased the number of red blood cells in the gills; we used 150 mg/L of AAP in subsequent hematological and histological analyses. Hematological analysis showed that rising temperature increased the proportion of morphologically abnormal red blood cells in AAP-exposed larvae, suggesting that AAP induced anemia-like signs in larvae. Histological observation of the kidney, which is a hematopoietic organ in fish, revealed no abnormalities. However, in the liver, which is responsible for drug metabolism, the proportion of vacuoles increased with increasing temperature. Although the exposure concentration we tested was higher than environmentally relevant concentrations, our data indicated that rising temperature enhances the toxicity of AAP to medaka larvae, suggesting an ecological risk of AAP due to global warming.

As a new type of pollutant, fluoroquinolones (FQs) antibiotics are ubiquitous in environment and have some threat to human health and ecological environment. Their ecological toxicity to the environment urgently need to be assessed. Therefore, we firstly explored the toxic effects and possible mechanism of cardiovascular toxicity induced by gatifloxacin (GTFX) and ciprofloxacin (CPFX) using zebrafish model. After 24 h exposure, the zebrafish treated with GTFX showed pericardial edema which was further investigated by histopathological examination, while CPFX exposure did not induce morphological abnormalities. However, both of them induced cardiac dysfunction, such as decreased heart rate and cardiac output which was showed a positive correlation with the concentration. To better understand the possible molecular mechanisms underlying cardiovascular toxicity in zebrafish, we investigated the transcriptional level of genes related to calcium signaling pathway and cardiac muscle contraction. The results indicated that the expression of ATPase (atp2a1l) and cardiac troponin C (tnnc1a) genes were significantly inhibited, the expression of calcium channel (cacna1ab) gene showed slight promoted trend after CPFX exposure. For zebrafish treated with GTFX, the expression of atp2a1l genes was also significantly inhibited, while the expression of tnnc1a genes was slightly inhibited and cacna1ab genes expression had no obvious effect. The present study firstly revealed that GTFX exposure can induce morphological and functional abnormalities on the cardiovascular system of zebrafish. Though CPFX exposure did not induce morphological abnormalities, the function of cardiovascular system was still damaged. Mechanistically, this toxicity might result from the pressure of down-regulation of genes associated with calcium signaling pathway and cardiac muscle contraction. The results of this study can provide a valuable theoretical basis for the establishment of FQs environmental quality standards in water environment, environmental drug regulation and risk management.

Dichlorvos (2,2-dichlorovinyl-dimethylphosphate), an organophosphorus pesticide used for indoor insect and livestock parasite control, is among the most common commercially available pesticides. However, there are significant concerns over its toxicity, especially due to its relative stability in water, soil, and air. Zebrafish, an important developmental model, has been used for studying the effects of toxic compounds. The aim of this study was to evaluate the exposure to dichlorvos at early life stages (1 h postfertilization - 7 days postfertilization) in the zebrafish and its toxicological effects during the development, through morphological (7 days postfertilization), locomotor and social behavior analysis (7, 14, 30, 70, and 120 days postfertilization). Dichlorvos (1, 5, and 10 mg/L) exposure reduced the body length and heartbeat rate at 7 days postfertilization (dpf), as well as the surface area of the eyes (5 and 10 mg/L). The avoidance behavior test showed a significant decrease in escape responses at 7 (1, 5, and 10 mg/L) and 14 (5 and 10 mg/L) dpf zebrafish. The evaluation of larval exploratory behavior showed a reduction in distance traveled, mean speed (1, 5, and 10 mg/L) and time mobile (10 mg/L) between control and dichlorvos groups. In addition, the analysis performed on adult animals showed that the changes in distance traveled and mean speed remained reduced in 30 (1, 5, and 10 mg/L) and 70 dpf (5 and 10 mg/L), recovering values similar to the control at 120 dpf. The social behavior of zebrafish was not altered by exposure to dichlorvos in the early stages of development. Thus, the exposure to organophosphorus compounds at early stages of development induces an increased susceptibility to behavioral and neuronal changes that could be associated with several neurodegenerative diseases.

Indoor air pollution is associated with numerous adverse health outcomes. Air purifiers are widely used to reduce indoor air pollutants. Ionization air purifiers are becoming increasingly popular for their low power consumption and noise, yet its health effects remain unclear. This randomized, double-blind crossover study is conducted to explore the cardiorespiratory effects of ionization air purification among 44 children in Beijing. Real or sham purification was performed in classrooms for 5 weekdays. Size-fractionated particulate matter (PM), black carbon (BC), ozone (O₃), and negative air ions (NAI) were monitored, and cardiorespiratory functions were measured. Mixed-effect models were used to establish associations between exposures and health parameters. Real purification significantly decreased PM and BC, e.g. PM₀.₅, PM₂.₅, PM₁₀ and BC were decreased by 48%, 44%, 34% and 50%, respectively. O₃ levels were unchanged, while NAI was increased from 12 cm⁻³ to 12,997 cm⁻³. Real purification was associated with a 4.4% increase in forced exhaled volume in 1 s (FEV₁) and a 14.7% decrease in fractional exhaled nitrogen oxide (FeNO). However, heart rate variability (HRV) was altered negatively. Interaction effects of NAI and PM were observed only on HRV, and alterations in HRV were greater with high NAI. Ionization air purifier could bring substantial respiratory benefits, however, the potential negative effects on HRV need further investigation.

Epidemiological studies and animal experiments have suggested that exposure to Di-(2-ethylhexyl) phthalate (DEHP) is strongly associated with an increase in blood pressure. However, the mechanisms that result in the detrimental effects of DEHP exposure on blood pressure are unclear. In our study, mice were orally exposed to DEHP dosages of 0.1, 1, 10 mg/kg/day for 6 weeks. The results showed that DEHP could induce a significant increase in systolic blood pressure (SBP) and heart rate, and a significant thickening of the ventricular wall. To explore the underlying mechanism, we measured the level of: angiotensin converting enzyme (ACE); bradykinin B2 receptor (BK2R); endothelial nitric oxide synthase (eNOS); bradykinin and Ca²⁺ in cardiac cytoplasm as well as in serum nitric oxide (NO). The results suggested that DEHP could induce an increase in ACE levels, and a decrease in bradykinin levels. Moreover, BK2R, Ca²⁺, eNOS and NO decreased when mice were exposed to 10 mg/kg/day DEHP. Interestingly, 5 mg/kg/day angiotensin converting enzyme inhibitor (ACEI) treatment inhibited the increase in blood pressure, and inhibited the decrease in the levels of BK2R, Ca²⁺, eNOS, and NO, that were induced by DEHP exposure. Our results suggest that DEHP might increase blood pressure by activating ACE expression, and inhibiting the bradykinin-NO pathway.