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Microplastics are ubiquitous in estuarine, coastal, and deep sea sediments. The impacts of microplastics on sedimentary microbial ecosystems and biogeochemical carbon and nitrogen cycles, however, have not been well reported. To evaluate if microplastics influence the composition and function of sedimentary microbial communities, we conducted a microcosm experiment using salt marsh sediment amended with polyethylene (PE), polyvinyl chloride (PVC), polyurethane foam (PUF) or polylactic acid (PLA) microplastics. We report that the presence of microplastics alters sediment microbial community composition and nitrogen cycling processes. Compared to control sediments without microplastic, PUF- and PLA-amended sediments promote nitrification and denitrification, while PVC amendment inhibits both processes. These results indicate that nitrogen cycling processes in sediments can be significantly affected by different microplastics, which may serve as organic carbon substrates for microbial communities. Considering this evidence and increasing microplastic pollution, the impact of plastics on global ecosystems and biogeochemical cycling merits critical investigation. Plastic pollution has infiltrated every ecosystem, but few studies have quantified the biogeochemical or ecological effects of plastic. Here the authors show that microplastics in ocean sediment can significantly alter microbial community structure and nitrogen cycling.

On the road to understand the toxicity of nanoplastics, it is important to determine their capacity to interact with other molecules, as this is the first condition that must be met. In particular, polyvinyl chloride (PVC) is a versatile plastic widely used in construction. It can be degraded producing micro and nanoplastics, which can be formed when PVC pipes are cut during the manufacturing of products. PVC is considered to be one of the most toxic plastics, so it is important to analyze potential detrimental effects. This is the main aim of this research. On the basis of Density Functional Theory calculations, we investigated different vinyl chloride oligomers (as models of PVC nanoplastics). Degradation energies, electron donor acceptor capacities to analyze possible oxidation reactions, and interaction energies with different molecules were calculated. The vinyl chloride oligomers used in this investigation are saturated and monounsaturated. This is important since monounsaturated variant is dominant in experimental conditions. We found that none of the oligomers are good electron donors or acceptors. We also investigated different oligomers interacting with ciprofloxacin and •OOH. The interaction energies with ciprofloxacin and •OOH are negative or less than 13 kcal/mol, indicating weak interactions. This theoretical investigation indicates that vinyl chloride oligomers are not expected to be reactive or toxic, considering the electron transfer and the interaction energies with other molecules.

Globally, plastics are used in various products. Concerns regarding the human body’s exposure to plastics and environmental pollution have increased with increased plastic use. Microplastics can be detected in the atmosphere, leading to potential human health risks through inhalation; however, the toxic effects of microplastic inhalation are poorly understood. In this study, we examined the pulmonary toxicity of polystyrene (PS), polypropylene (PP), and polyvinyl chloride (PVC) in C57BL/6, BALB/c, and ICR mice strains. Mice were intratracheally instilled with 5 mg/kg of PS, PP, or PVC daily for two weeks. PS stimulation increased inflammatory cells in the bronchoalveolar lavage fluid (BALF) of C57BL/6 and ICR mice. Histopathological analysis of PS-instilled C57BL/6 and PP-instilled ICR mice showed inflammatory cell infiltration. PS increased the NLR family pyrin domain containing 3 (NLRP3) inflammasome components in the lung tissue of C57BL/6 and ICR mice, while PS-instilled BALB/c mice remained unchanged. PS stimulation increased inflammatory cytokines, including IL-1β and IL-6, in BALF of C57BL/6 mice. PP-instilled ICR mice showed increased NLRP3, ASC, and Caspase-1 in the lung tissue compared to the control groups and increased IL-1β levels in BALF. These results could provide baseline data for understanding the pulmonary toxicity of microplastic inhalation.

Plastic pollution and global warming are widespread issues that lead to several impacts on aquatic organisms. Despite harmful studies on both subjects, there are few studies on how temperature increases plastics’ adverse effects on aquatic animals, mainly freshwater species. So, this study aims to clarify the potential impact of temperature increases on the toxicological properties of polyvinyl chloride nano-plastics (PVC-NPs) in Nile tilapia ( Oreochromis niloticus ) by measuring biochemical and oxidative biomarkers. The fish groups were subjected to three distinct temperatures (30, 32, and 34 °C) and subsequently separated into two groups: 0 and 10 mg/L of PVC-NPs, as it is expected that these temperatures may modify their chemical properties, which can influence their absorption and toxicity in fish. After 4 days, the biochemical response of fish exposed to PVC-NPs and elevated temperatures showed a significant increase in the levels of plasma total proteins, albumin, globulin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), creatinine, and uric acid. Additionally, the level of oxidative stress biomarkers in the liver, gills, and brain was found to have a significant increase in malondialdehyde (MDA) concentration and a decrease in glutathione reduced (GSH) concentration and catalase (CAT) activity in all studied groups. Finally, the current findings revealed a synergistic cytotoxic effect of PVC-NPs and temperatures on the metabolic and oxidative stress indices of O. niloticus .

Plastic pollution is a global threat to marine ecosystems. Plastic litter can leach a variety of substances into marine environments; however, virtually nothing is known regarding how this affects photosynthetic bacteria at the base of the marine food web. To address this, we investigated the effect of plastic leachate exposure on marine Prochlorococcus , widely considered the most abundant photosynthetic organism on Earth and vital contributors to global primary production and carbon cycling. Two strains of Prochlorococcus representing distinct ecotypes were exposed to leachate from common plastic items: high-density polyethylene bags and polyvinyl chloride matting. We show leachate exposure strongly impairs Prochlorococcus in vitro growth and photosynthetic capacity and results in genome-wide transcriptional changes. The strains showed distinct differences in the extent and timing of their response to each leachate. Consequently, plastic leachate exposure could influence marine Prochlorococcus community composition and potentially the broader composition and productivity of ocean phytoplankton communities. Sasha Tetu et al. have examined the effects of plastic leachate exposure on the marine bacteria Prochlorococcus , the most abundant photosynthetic organism on Earth. They find plastic leachates impair growth, photosynthetic capacity and cause global changes in transcription.

This study delved into the impact of aging on the properties of five common microplastic types, including polymethylmethacrylate (PMMA), polystyrene (PS), polyvinyl chloride (PVC), polyethylene (PE), and polypropylene (PP). The aging process significantly altered the particle size distribution: PS, PP, and PMMA underwent a contraction, with average sizes decreasing by 6.8%, 3.2%, and 1.7%, respectively, whereas PE and PVC experienced an expansion, with increases of 3.1% and 1.7%. Notably, aging generally increased the specific surface area of all microplastics by more than 20%, a change that could influence their environmental interactions. Scanning electron microscopy revealed marked surface cracks and depressions in aged PE and PVC, in contrast to minor surface alterations in PS and PMMA. Fourier transform infrared spectroscopy further indicated modifications in the characteristic peaks of aged PMMA, PP, and PE microplastics. Exposure experiments demonstrates that increasing microplastic concentrations from 100 mg/L to 5000 mg/L accelerated mortality rates in clams, with juveniles exhibiting slower mortality onset compared to adults. Prolonged exposure led to rising mortality rates across all groups, suggesting a cumulative toxic effect from long-term microplastic exposure. These findings underscore the environmental ecological risks associated with the altered physicochemical properties of aged microplastics, particularly for the Philippine clam. This study provides an essential insight for advancing our understanding of microplastic behavior and their ecological impacts, highlighting the need for further research to mitigate these environmental threats.

Asthma is a chronic inflammatory respiratory disease influenced by genetic and environmental factors. Emerging evidence suggests that microplastics and nanoplastics (NPs) pose significant health risks. When inhaled, these tiny particles can accumulate in the lungs, triggering inflammation, oxidative stress, and other disruptions in pulmonary function. This study investigates the role of polyvinyl chloride (PVC) NPs, which are extensively used in products such as packaging, medical devices, and construction materials, in asthma pathogenesis. Using an ovalbumin (OVA)‐induced murine asthma model, it is demonstrated that PVC NPs exposure exacerbates airway hyperresponsiveness, increases inflammatory cell infiltration, and elevates inflammatory cytokine levels in the lungs. Further mechanistic studies reveal that PVC NPs suppress Ribonuclease H1 (RNASEH1), leading to RNA–DNA hybrid loop (R‐loop) accumulation and activation of the Cyclic GMP‐AMP Synthase (cGAS)‐Stimulator of Interferon Genes (STING) inflammatory pathway. The critical involvement of this pathway is confirmed using STING‐deficient mice, where pathway inhibition alleviates the inflammation exacerbated by PVC NPs exposure. These findings provide new insights into the potential role of NPs pollutants in modulating immune responses through R‐loop formation, linking PVC NPs to asthma pathogenesis. This study highlights the importance of addressing environmental exposure to NPs in asthma prevention and management and identifies potential molecular targets for therapeutic intervention. Polyvinyl chloride (PVC) nanoplastics (NPs) are shown to aggravate allergic airway inflammation in asthma by triggering R‐loop accumulation and activating the cGAS‐STING pathway in macrophages. This study reveals a novel immunotoxic mechanism linking environmental plastic exposure to asthma pathogenesis and highlights potential molecular targets for mitigating nanoplastic‐induced respiratory inflammation.

ObjectivesTo investigate types of cancer caused by occupational exposure to vinyl chloride monomer (VCM) and the temporal mortality trends of these cancers in workers from polyvinyl chloride (PVC) manufacturing factories in Taiwan, with follow-up of the cohort extended by 15 years, from 1980 to 2007.MethodsA retrospective cohort study of workers from six PVC factories in Taiwan was conducted. 3336 male PVC workers were enrolled and further linked with the National Mortality Registry and National Household Registry databases. Standardised mortality ratios (SMR) with 95% CIs were calculated and compared to the general Taiwanese male population. Cause-specific mortality between two study periods, 1980–1997 and 1998–2007, was compared. Six-year moving averages of the SMRs were calculated to examine mortality trends.ResultsLiver cancer mortality increased during 1989–1994 (SMR 1.90, 95% CI 1.01 to 3.25), reached a peak during 1991–1996 (SMR 2.31, 95% CI 1.39 to 3.61) and became non-significant during 1994–1999 (SMR 1.42, 95% CI 0.80 to 2.34). Leukaemia mortality significantly increased during 1984–1989 (SMR 6.06, 95% CI 1.24 to 17.53), reached a peak during 1985–1990 (SMR 7.56, 95% CI 2.06 to 19.35) and became non-significant during 1991–1996 (SMR 3.24, 95% CI 0.39 to 11.69). The mortality trend for haemolymphopoietic cancer showed a similar pattern to that of leukaemia.ConclusionsVCM may increase the risk of liver cancer and leukaemia. When VCM exposure was controlled at worksites, mortality from these cancers returned to background levels.

Background: Polyvinyl chloride (PVC) materials have been linked to asthma in several epidemiologic studies, but the possible causal factors remain unknown. Participants: We challenged 10 subjects experimentally to degraded PVC products under controlled conditions. All of the subjects had previously experienced respiratory symptoms suspected to be caused by this kind of exposure in their work place. Five subjects had doctor-diagnosed asthma. Methods: The subjects were exposed to degraded PVC material in an exposure chamber; a challenge with ceramic tile was used as the control test. We followed exhaled nitric oxide, nasal NO, lung functions, cytokines [tumor necrosis factor-α (TNF-α), interleukin-4 (IL-4), IL-6, and IL-12] and NO in nasal lavage fluid (NAL) during and after the exposures. We also measured 2-ethylhexanol in exhaled breath samples and NAL. Results: On the morning after the PVC exposure, subjects reported respiratory tract symptoms significantly more often than they did after the control test (50% vs. 0%, respectively; p = 0.029; n = 10). We did not detect any changes in lung functions or levels of exhaled NO, nasal NO, or NO in NAL after PVC challenge compared with the control test. Cytokine levels increased after both exposures, with no statistically significant difference between situations. All of the exhaled breath samples collected during the PVC exposure contained 2-ethylhexanol. Conclusions: PVC flooring challenge can evoke respiratory tract symptoms in exposed subjects. Our results do not support the hypothesis that PVC materials themselves evoke immediate asthmatic reactions. The chamber test used is well suited to this type of exposure study.

PVC is now ubiquitous. Th e second most widely used plastic, it is found in everything from house plumbing to biomedical equipment, clothing and vinyl gramophone records. But the plastic has been under threat ever since it was found in 1972 that its constituent monomer, vinyl chloride, might cause liver cancer.