RESUMO
The growing environmental consequences caused by plastic pollution highlight the need for a better understanding of plastic polymer cycles and their associated additives. We present a novel, comprehensive top-down method using inflow-driven dynamic probabilistic material flow analysis (DPMFA) to map the plastic cycle in coastal countries. For the first time, we covered the progressive leaching of microplastics to the environment during the use phase of products and modeled the presence of 232 plastic additives. We applied this methodology to Norway and proposed initial release pathways to different environmental compartments. 758 kt of plastics distributed among 13 different polymers was introduced to the Norwegian economy in 2020, 4.4 Mt was present in in-use stocks, and 632 kt was wasted, of which 15.2 kt (2.4%) was released to the environment with a similar share of macro- and microplastics and 4.8 kt ended up in the ocean. Our study shows tire wear rubber as a highly pollutive microplastic source, while most macroplastics originated from consumer packaging with LDPE, PP, and PET as dominant polymers. Additionally, 75 kt of plastic additives was potentially released to the environment alongside these polymers. We emphasize that upstream measures, such as consumption reduction and changes in product design, would result in the most positive impact for limiting plastic pollution.
Assuntos
Plásticos , Noruega , Monitoramento Ambiental , Microplásticos , Poluentes Químicos da ÁguaRESUMO
Low-carbon technologies are essential for the aluminum industry to meet its climate targets despite increasing demand. However, the penetration of these technologies is often delayed due to the long lifetimes of the industrial assets currently in use. Existing models and scenarios for the aluminum sector omit this inertia and therefore potentially overestimate the realistic mitigation potential. Here, we introduce a technology-explicit dynamic material flow model for the global primary (smelters) and secondary (melting furnaces) aluminum production capacities. In business-as-usual scenarios, we project emissions from smelters and melting furnaces to rise from 710 Mt CO2-eq./a in 2020 to 920-1400 Mt CO2-eq./a in 2050. Rapid implementation of inert anodes in smelters can reduce emissions by 14% by 2050. However, a limitation of emissions compatible with a 2 °C scenario requires combined action: (1) an improvement of collection and recycling systems to absorb all the available postconsumer scrap, (2) a fast and wide deployment of low-carbon technologies, and (3) a rapid transition to low-carbon electricity sources. These measures need to be implemented even faster in scenarios with a stronger increase in aluminum demand. Lock-in effects are likely: building new capacity using conventional technologies will compromise climate mitigation efforts and would require premature retirement of industrial assets.
Assuntos
Alumínio , Modelos Teóricos , Carbono , Tecnologia , ReciclagemRESUMO
Probiotics and lactoferrin are currently being used in neonatal intensive care units in the hopes of reducing rates of sepsis and necrotizing enterocolitis (NEC). While studies have shown that these measures can be clinically beneficial to premature babies, and there are ongoing trials to measure their impact on NEC and sepsis rates, little is known about how they may impact microbiota development. We thus employed a newborn piglet model to assess the impact of feeding probiotics or a combination of probiotics and lactoferrin on development of the gastrointestinal microbiota. Healthy full-term piglets were fed either probiotics alone or probiotics and a bovine lactoferrin supplement over the first weeks of life, and their microbiota profiles were compared with unsupplemented controls. We found that both probiotic and probiotic plus lactoferrin treatments impacted the microbial composition within the gastrointestinal tract, with differing impacts on various regions within the gut. In addition, the impact of probiotics was often reversed by the presence of lactoferrin and both feeding interventions altered the microbiota's genetic propensity to use ferric versus ferrous ions. These results suggest that iron availability may be a key factor to consider when designing feeding interventions that target the microbiome.
Assuntos
Anti-Infecciosos/farmacologia , Microbioma Gastrointestinal/efeitos dos fármacos , Lactoferrina/farmacologia , Probióticos/farmacologia , Animais , Anti-Infecciosos/administração & dosagem , Lactoferrina/administração & dosagem , Probióticos/administração & dosagem , SuínosRESUMO
Background: Very-low-birth-weight (VLBW; born weighing <1500 g) infant feeding with mother's own milk (mother's milk) is associated with numerous beneficial health outcomes. Several interventions, including the prophylactic use of probiotics, are being adopted to promote a gastrointestinal microbiota favorable to the gut health of VLBW infants. An improved understanding of the microbiota that results from mother's milk feeding would therefore facilitate progress in this field. Objective: A preplanned primary objective of this research was to characterize the development of the gut microbiota in exclusively mother's milk-fed VLBW infants and describe the reference taxonomic profile that results from mother's milk feeding. Methods: In this prospective longitudinal cohort study, we collected weekly stool samples from exclusively mother's milk-fed VLBW infants admitted to Mount Sinai Hospital and profiled their gastrointestinal microbiota development from birth (primary outcome of stool collection). In total, we profiled 231 stools from 54 exclusively mother's milk-fed VLBW infants with the use of V6-16S ribosomal RNA gene sequencing. Results: Bacterial evenness, but not bacterial richness, increased over time in VLBW infants (P < 0.001). Bifidobacterium relative abundances were consistently low in all microbiotas at all time points (<0.5% in 97% of samples). VLBW infant microbiotas did not cluster by birth mode, gestational age, or weeks after birth and instead clustered as a function of patient identity (R2 = 0.51, P < 0.001). Conclusions: Exclusively mother's milk-fed VLBW infants rapidly develop personalized gut microbiotas that show increasing evenness and are seemingly unaffected by birth mode or gestational age at birth. The benefits from mother's milk feeding are likely modulated through microbes or pathways that are not dependent on Bifidobacterium because these microbes are present at low levels in VLBW infants. These results help define a reference VLBW infant microbiota profile derived from mother's milk, the optimal source of nutrition for these infants. This trial was registered at ISRCTN (http://www.isrctn.com/) as ISRCTN35317141.
Assuntos
Bifidobacterium/crescimento & desenvolvimento , Peso ao Nascer , Aleitamento Materno , Microbioma Gastrointestinal , Recém-Nascido Prematuro , Recém-Nascido de muito Baixo Peso , Leite Humano , Técnicas de Tipagem Bacteriana/métodos , Bifidobacterium/genética , Colo/microbiologia , Feminino , Idade Gestacional , Humanos , Lactente , Fórmulas Infantis , Recém-Nascido , Lactação , Estudos Longitudinais , Masculino , Mães , Nascimento Prematuro , Probióticos , Estudos Prospectivos , RNA Ribossômico 16S/genéticaRESUMO
In addition to their chemical antimicrobial nature, bile acids are thought to have other functions in the homeostatic control of gastrointestinal immunity. However, those functions have remained largely undefined. In this work, we used ileal explants and mouse models of bile acid administration to investigate the role of bile acids in the regulation of the intestinal antimicrobial response. Mice fed on a diet supplemented with 0.1% chenodeoxycholic acid (CDCA) showed an upregulated expression of Paneth cell α-defensins as well as an increased synthesis of the type-C lectins Reg3b and Reg3g by the ileal epithelium. CDCA acted on several epithelial cell types, by a mechanism independent from farnesoid X receptor (FXR) and not involving STAT3 or ß-catenin activation. CDCA feeding did not change the relative abundance of major commensal bacterial groups of the ileum, as shown by 16S analyses. However, administration of CDCA increased the expression of ileal Muc2 and induced a change in the composition of the mucosal immune cell repertoire, decreasing the proportion of Ly6G+ and CD68+ cells, while increasing the relative amount of IgGκ+ B cells. Oral administration of CDCA to mice attenuated infections with the bile-resistant pathogens Salmonella enterica serovar Typhimurium and Citrobacter rodentium, promoting lower systemic colonization and faster bacteria clearance, respectively. Our results demonstrate that bile acid signaling in the ileum triggers an antimicrobial program that can be potentially used as a therapeutic option against intestinal bacterial infections.
Assuntos
Ácido Quenodesoxicólico/administração & dosagem , Infecções por Enterobacteriaceae/imunologia , Íleo/microbiologia , Imunidade nas Mucosas , Infecções por Salmonella/imunologia , alfa-Defensinas/imunologia , Animais , Carga Bacteriana , Citrobacter rodentium/efeitos dos fármacos , Íleo/imunologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Celulas de Paneth/imunologia , Celulas de Paneth/microbiologia , Salmonella typhimurium/efeitos dos fármacosRESUMO
BACKGROUND: Enterohepatic bacterial infections have the potential to affect multiple physiological processes of the body. Fibroblast growth factor 15/19 (FGF15 in mice, FGF19 in humans) is a hormone that functions as a central regulator of glucose, lipid and bile acid metabolism. FGF15/19 is produced in the intestine and exert its actions on the liver by signaling through the FGFR4-ßKlotho receptor complex. Here, we examined the in vivo effects of enterohepatic bacterial infection over the FGF15 endocrine axis. RESULTS: Infection triggered significant reductions in the intestinal expression of Fgf15 and its hepatic receptor components (Fgfr4 and Klb (ßKlotho)). Infection also resulted in alterations of the expression pattern of genes involved in hepatobiliary function, marked reduction in gallbladder bile volumes and accumulation of hepatic cholesterol and triglycerides. The decrease in ileal Fgf15 expression was associated with liver bacterial colonization and hepatobiliary pathophysiology rather than with direct intestinal bacterial pathogenesis. CONCLUSIONS: Bacterial pathogens of the enterohepatic system can disturb the homeostasis of the FGF15/19-FGFR4 endocrine axis. These results open up a possible link between FGF15/19-FGFR4 disruptions and the metabolic and nutritional disorders observed in infectious diseases.