Massive additional quantities of disinfectants have been applied during the COVID-19 pandemic as infection preventive and control measures. While the application of disinfectants plays a key role in preventing the spread of SARS-CoV-2 infection, the effects of disinfectants applied during the ongoing pandemic on non-target organisms remain unknown. Here we collated evidence from multiple studies showing that chemicals used for major disinfectant products can induce hormesis in various organisms, such as plants, animal cells, and microorganisms, when applied singly or in mixtures, suggesting potential ecological risks at sub-threshold doses that are normally considered safe. Among other effects, sub-threshold doses of disinfectant chemicals can enhance the proliferation and pathogenicity of pathogenic microbes, enhancing the development and spread of drug resistance. We opine that hormesis should be considered when evaluating the effects and risks of such disinfectants, especially since the linear-no-threshold (LNT) and threshold dose-response models cannot identify or predict their effects.

COVID-19 pandemic has led to concerns on the circulation of SARS-CoV-2 in the environment, its infectivity from the environment and, the relevance of transmission via environmental compartments. During 31 weeks, water samples were collected from a heavily contaminated stream going through an urban, underprivileged community without sewage collection. Our results showed a statistically significant correlation between cases of COVID-19 and SARS in the community, and SARS-CoV-2 concentrations in the water. Based on the model, if the concentrations of SARS-CoV-RNA (N1 and N2 target regions) increase 10 times, there is an expected increase of 104% [95%CI: (62–157%)] and 92% [95%CI: (51–143%)], respectively, in the number of cases of COVID-19 and SARS. We believe that differences in concentration of the virus in the environment reflect the epidemiological status in the community, which may be important information for surveillance and controlling dissemination in areas with vulnerable populations and poor sanitation. None of the samples were found infectious based cultures. Our results may be applicable globally as similar communities exist worldwide.

Pollen allergens, widely present in the atmosphere, are the main cause of seasonal respiratory diseases that affect millions of people worldwide. Although previous studies have reported that nitrogen dioxide (NO₂) and ozone (O₃) promote pollen allergy, the specific biological processes and underlying mechanisms remain less understood. In this study, Platanus pollen grains were exposed to gaseous pollutants (NO₂ and O₃). We employed environmental electron microscopy, flow cytometry, western blot assay, enzyme-linked immunoassay, ultraviolet absorption spectrometry, circular dichroism, and protein mass spectrometry to characterise the subpollen particles (SPPs) released from pollen grains. Furthermore, we determined the immunogenicity and pathogenicity induced by Platanus pollen allergen a 3 (Pla a 3). Our results demonstrated that NO₂ and O₃ could damage the pollen cell membranes in SPPs and increase the amount of Pla a 3 allergen released into the atmosphere. Additionally, NO₂ and O₃ altered the structure of Pla a3 protein through nitrification and oxidation, which not only enhanced the immunogenicity of allergens but also increased the stability of the protein. In vivo analysis using an animal model indicated that NO₂ and O₃ greatly aggravated pollen-induced pneumonia. Thus, our study provides guidance for the prevention of pollen allergic diseases.

In December 2019, a novel disease, coronavirus disease 19 (COVID-19), emerged in Wuhan, People’s Republic of China. COVID-19 is caused by a novel coronavirus (SARS-CoV-2) presumed to have jumped species from another mammal to humans. This virus has caused a rapidly spreading global pandemic. To date, over 300,000 cases of COVID-19 have been reported in England and over 40,000 patients have died. While progress has been achieved in managing this disease, the factors in addition to age that affect the severity and mortality of COVID-19 have not been clearly identified. Recent studies of COVID-19 in several countries identified links between air pollution and death rates. Here, we explored potential links between major fossil fuel-related air pollutants and SARS-CoV-2 mortality in England. We compared current SARS-CoV-2 cases and deaths from public databases to both regional and subregional air pollution data monitored at multiple sites across England. After controlling for population density, age and median income, we show positive relationships between air pollutant concentrations, particularly nitrogen oxides, and COVID-19 mortality and infectivity. Using detailed UK Biobank data, we further show that PM₂.₅ was a major contributor to COVID-19 cases in England, as an increase of 1 m³ in the long-term average of PM₂.₅ was associated with a 12% increase in COVID-19 cases. The relationship between air pollution and COVID-19 withstands variations in the temporal scale of assessments (single-year vs 5-year average) and remains significant after adjusting for socioeconomic, demographic and health-related variables. We conclude that a small increase in air pollution leads to a large increase in the COVID-19 infectivity and mortality rate in England. This study provides a framework to guide both health and emissions policies in countries affected by this pandemic.

Air pollution can increase the risk of respiratory diseases, enhancing the susceptibility to viral and bacterial infections. Some studies suggest that small air particles facilitate the spread of viruses and also of the new coronavirus, besides the direct person-to-person contagion. However, the effects of the exposure to particulate matter and other contaminants on SARS-CoV-2 has been poorly explored. Here we examined the possible reasons why the new coronavirus differently impacted on Italian regional and provincial populations. With the help of artificial intelligence, we studied the importance of air pollution for mortality and positivity rates of the SARS-CoV-2 outbreak in Italy. We discovered that among several environmental, health, and socio-economic factors, air pollution and fine particulate matter (PM2.5), as its main component, resulted as the most important predictors of SARS-CoV-2 effects. We also found that the emissions from industries, farms, and road traffic - in order of importance - might be responsible for more than 70% of the deaths associated with SARS-CoV-2 nationwide. Given the major contribution played by air pollution (much more important than other health and socio-economic factors, as we discovered), we projected that, with an increase of 5–10% in air pollution, similar future pathogens may inflate the epidemic toll of Italy by 21–32% additional cases, whose 19–28% more positives and 4–14% more deaths. Our findings, demonstrating that fine-particulate (PM2.5) pollutant level is the most important factor to predict SARS-CoV-2 effects that would worsen even with a slight decrease of air quality, highlight that the imperative of productivity before health and environmental protection is, indeed, a short-term/small-minded resolution.

Sensing of pathogens by specialized receptors is the hallmark of the innate immunity. Innate immune response also mounts a defense response against various allergens and pollutants including particulate matter present in the atmosphere. Air pollution has been included as the top threat to global health declared by WHO which aims to cover more than three billion people against health emergencies from 2019 to 2023. Particulate matter (PM), one of the major components of air pollution, is a significant risk factor for many human diseases and its adverse effects include morbidity and premature deaths throughout the world. Several clinical and epidemiological studies have identified a key link between the PM existence and the prevalence of respiratory and inflammatory disorders. However, the underlying molecular mechanism is not well understood. Here, we investigated the influence of air pollutant, PM₁₀ (particles with aerodynamic diameter less than 10 μm) during RNA virus infections using Highly Pathogenic Avian Influenza (HPAI) – H5N1 virus. We thus characterized the transcriptomic profile of lung epithelial cell line, A549 treated with PM₁₀ prior to H5N1infection, which is known to cause severe lung damage and respiratory disease. We found that PM₁₀ enhances vulnerability (by cellular damage) and regulates virus infectivity to enhance overall pathogenic burden in the lung cells. Additionally, the transcriptomic profile highlights the connection of host factors related to various metabolic pathways and immune responses which were dysregulated during virus infection. Collectively, our findings suggest a strong link between the prevalence of respiratory illness and its association with the air quality.

With increased industrial development, cadmium is an increasingly important environmental pollutant. Studies have identified various adverse effects of cadmium on human beings. However, the relationships between cadmium pollution and the pathogenesis of preeclampsia remain elusive. The objective of this study is to explore the effects of cadmium on immune system among preeclamptic patients and rats. The results showed that the cadmium levels in the peripheral blood of preeclamptic patients were significantly higher than those observed in normal pregnancy. Based on it, a novel rat model of preeclampsia was established by the intraperitoneal administration of cadmium chloride (CdCl2) (0.125 mg of Cd/kg body weight) on gestational days 9–14. Key features of preeclampsia, including hypertension, proteinuria, placental abnormalities and small foetal size, appeared in pregnant rats after the administration of low-dose of CdCl2. Cadmium increased immunoglobulin production, mainly angiotensin II type 1-receptor-agonistic autoantibodies (AT1-AA), by increasing the expression of activation-induced cytosine deaminase (AID) in B cells. AID is critical for the maturation of antibody and autoantibody responses. In addition, angiotensin II type 1-receptor-agonistic autoantibody, which emerged recently as a potential pathogenic contributor to PE, was responsible for the deposition of complement component 5 (C5) in kidneys of pregnant rats via angiotensin II type 1 receptor (AT1R) activation. C5a is a fragment of C5 that is released during C5 activation. Selectively interfering with C5a signalling by a complement C5a receptor-specific antagonist significantly attenuated hypertension and proteinuria in Cd-injected pregnant rats. Our results suggest that cadmium induces immune abnormalities that may be a key pathogenic contributor to preeclampsia and provide new insights into treatment strategies of preeclampsia.

Many contaminants were carried by dust, a common environment media that is easy to contact with human beings, and antibiotic resistance genes (ARGs) as an emergency pollutant also harbor in dust and pose serious threats to human health especially those carried by opportunistic pathogens because inactivation of antibiotics caused by ARGs may enhance pathogenicity. Considering there is a gap of investigation of dust ARGs, 16 S rRNA gene sequences and high-throughput quantitative PCR were employed to obtain information of microbial communities and accumulated ARGs in dust from different urban places, including the malls, hospitals, schools and parks, to investigate the distribution and influencing factors of ARGs and discover the potential hosts of ARGs in dust. Here, 9 types of ARGs such as sulfonamide, tetracycline, and beta-lactamase and 71 subtypes of ARGs like sul1, tetM-01, and drfA1 were detected in dust. ARGs had varying distribution in different public places and seasons in dust. The abundances of total ARGs, MLSB and tetracycline genes were higher in spring than summer. The diversity of ARGs was highest in malls, follow by hospitals, schools, and parks. Additionally, multi-drug resistance genes in dust were more abundant in hospitals than in schools and parks. The microbes were distinguished as the most important driving factors for ARGs in dust, followed by the mobile genetic elements (MGEs) and different places, while dust physicochemical parameters only exert a negligible impact. Notably, several opportunistic pathogens like the Streptococcus, Vibrio, and Pseudomonas were inferred as potential hosts of high-risk ARGs such as mecA, tetM-02, and tetO-01 in dust because of strongly positive co-occurrence. These results imply that dust is likely an important reservoir of ARGs. We should realize that ARGs may be harbored in some opportunistic pathogens occur in dust and endanger human health because of dust contacting to human easily.

Microplastics (MPs) are found to be ubiquitous and serve as vectors for other contaminants, and the inevitable aging process changes MP properties and fates. However, whether the MPs in aging process affects the fates of antibiotic resistance gene (ARGs) in aquatic environments is poorly understood. Herein, the physicochemical property alteration of MPs being aged in landfill leachate, an important reservoir of MPs and ARGs, was investigated, and microbial community evolution and ARGs occurrence of MP surface during the aging process were analyzed. Aging process remarkably altered surface properties, including increasing specific surface areas, causing the formation of oxygen-containing groups, and changing surface morphology, which further increased the probability of microbial colonization. The bacterial assemblage on MPs showed higher biofilm-forming and pathogenic potential compared to leachate. ARGs quantification results suggested that MPs exhibited selective enrichment for ARGs in a ratio of 5.7–10³ folds, and the aging process enhanced the enrichment potential. Further co-occurrence networks suggested that the existence of non-random, closer and more stable ARGs-bacterial taxa relations on MP surface affected the ARG transmission. The study of ARG partitioning on MPs indicated that extracellular DNA was a nonnegligible reservoir of ARGs attached on MP surface, and that biofilm bacterial community influenced ARGs partitioning pattern during the aging process. This study confirmed that the aging process could enhance the potential of MPs as vectors for ARGs, which would promote the holistic understanding of MP behavior and risk in natural environments.

The increased use of pesticides during recent years necessitates a reevaluation of the effect of those compounds by extending the range of nontarget species commonly used in risk assessment. In the present work, we thus determined the impact of the pesticides glyphosate, carbendazim, and malathion on the parasite Chordodes nobilii in both natural and reconstituted freshwater as the assay medium and tested the sensitivity of three of this species's ecologically relevant parameters—e. g., embryo nonviablity and the infective capability of larvae exposed for 48 or 96 h either in ovo or after hatching via the infection index mean abundance—to compare those parameters to data from previous trials with reconstituted freshwater. In natural-freshwater assays, at environmentally relevant concentrations, all three pesticides inhibited the preparasitic-stage endpoints; with carbendazim being the most toxic pesticide and the subsequent infectivity of larvae exposed in ovo the most sensitive endpoint. In general, the 50%-inhibitory concentrations assayed in reconstituted freshwater were higher than those obtained in natural freshwater, indicating a certain protective effect; whereas the maximal toxicity of the three pesticides in both aqueous environments was essentially similar. The sensitivity of C. nobilii to these agents demonstrated that this species is one of the most susceptible to toxicity by all three pesticides. These findings with the assay methodology provide relevant information for a future assessment of the risk of toxicity to aquatic ecosystems and furthermore underscore the need to include parasitic organisms among the nontarget species canvassed. We also recommend that in the bioassays in which the risk assessment is carried out, water from a nontarget species's natural environment be used in parallel in order to obtain more conclusive results.