The urgency of measuring fluorinated greenhouse gas emission factors from the treatment of textile and other substrates

The fashion industry is responsible for up to 10% of global CO2 emissions (Niinimäki et al., 2020), and according to the United Nations Framework Convention on Climate Change the sector's emissions are expected to rise by more than 60% by 2030 (UNFCCC 2018). While the vast majority of the sector's carbon footprint results from CO2 emissions, an additional source – still unaccounted for and growing – likely results from emissions of fluorinated greenhouse gasses (F-GHGs) during the treatment of textile and leather. Indeed, fluorine-based treatment of fibers and other substrates (paper, metals, plastics, etc.) is increasingly performed using wet- or plasma-based methods to functionalize surfaces for water and oil repellence, soil and stain release, improved textile breathability, softening, dyeing ability, increased mechanical strength, reduced adherence, antibacterial and anti-odor properties, and to fabricate wrinkle-free materials. For more information see Chapter 8 of (IPCC 2019). Although F-GHG emissions only represent 2.6% of global greenhouse gas emissions, F-GHGs have long atmospheric life (up to 50,000 years for CF4) and high global warming potential (GWP, up to 23,500 for SF6). Thus, it is concerning that the atmospheric concentration of some of these gasses is higher than what is predicted through bottom-up analyses i.e., when estimating emissions using the 2006 IPCC Guidelines for National GHG Inventories for all processes and industrial sectors known to emit F-GHGs. During the 2015–2016 Technical Assessment of the 2006 IPCC Guidelines, potential emissions from the textile industry were accounted, among others, as a possible reason for the gap between top-down and bottom-up estimates of F-GHG emissions (IPCC 2016). Surprisingly, although several international and national reports refer to possible atmospheric emissions of F-GHGs during finishing of textile, carpet, leather, and paper, no corresponding emission factors (EFs) were found to have been measured and published in the open literature. For more information see Chapter 8 of (IPCC 2019). While the existing literature on the environmental impacts of textile finishing processes typically focuses on formaldehyde emissions, total volatile organic compounds (VOCs) release, and the impacts of a limited number of long chains perfluoroalkane sulfonic acids (PFASs) such as perfluorooctanesulfonate (PFOS), perfluorooctanoic acid (PFOA), and their precursors, the literature is silent on the potential climate impacts of these compounds and other fluorinated surface treatment chemicals. Fluorinated wet treatment processes include several application techniques but about 80% of the processes use the pad-dry-cure method, where the dry fabric is immersed in a F-based finishing liquor and then squeezed between rollers before being dried and finally cured, usually at temperatures up to 180 °C. Chemicals used for wet treatment processes include fluorotelomer alcohols, and perfluoroalkyl carboxylic acids. Although such chemicals may not be GHGs by themselves, it is unclear whether fluorinated ethers, unreacted monomers or by-products formed during the deposition processes, and in the atmosphere, can produce relevant F-GHGs. For more information see Appendix 1 of (IPCC 2019). Notwithstanding, it has been proved that during the drying and curing phases, F-based off-gas emissions can be produced by the volatility of the active substances themselves as well as by their constituents through evaporative losses and cracking. For more information see Appendix 1 of (IPCC 2019). Moreover, high-GWP perfluoropolyethers were identified as being used in a number of commercial applications, including for textile treatment, increasing the concerns about the atmospheric release of these compounds. For more information see Chapter 6 of (IPCC 2019). Recently, due to the persistent and bio-accumulative nature of the chemicals used in wet-based treatment processes, several manufacturers have developed alternate plasma-based treatments for specialized fibers and substrates (Tudoran et al., 2020). Plasma technology can be tailored to achieve many desirable properties and may provide equal or even better performance than wet methods. Plasma processes can be divided into three process types: (1) plasma treatment, (2) plasma polymerization and (3) plasma etching. Plasma treatment and polymerization are the main processes of concern because they can use large quantities of F-GHG feedstocks such as CF4, C2F6, C3F6, C3F8, C4F8, C5F10, CHF3, SF6, and other larger molecules such as perfluoroalkyl acrylates to deposit thin films on a substrate. Because the application of high plasma power densities could damage fragile substrates, it is highly probable that feedstock molecules are not fully disassociated by the plasma. Further, the plasma disassociation of F-GHGs is well known to result in the formation of other F-GHG byproducts (e.g., of CF4 from C2F6). For more information see Appendix 1 of (IPCC 2019). Therefore, plasma-based fluorinated treatment of textile, carpet, leather, paper, and other substrates is expected to lead to higher F-GHG emissions than wet chemistry methods. The authors of the 2019 Refinement to the 2006 IPCC Guidelines for National Greenhouse Gas Inventories have proposed four distinct tiered methods (Tier 1, Tier 2a, Tier 2b, and Tier 3) to account for emissions from wet- and plasma-based fluorinated treatment of textile, leather, carpet, and paper. For more information see Appendix 1 of (IPCC 2019). However, because no Tier 1 or Tier 2 default (industry average) factors are available, only the Tier 3 method is currently practicable, using equipment-specific, process-specific, or site-specific measured emission factors. Measurements should preferentially be performed by Fourier transform infrared spectroscopy (FTIR) due to part per billion (ppb) sensitivity and portability or by gas chromatography followed by mass spectrometry (GC/MS), allowing near real time measurements. Without experimentally measured emission factors, it is not possible to estimate the potential global climate impact of the above-mentioned processes. Thus, there is a critical need of consistent research on the fate and atmospheric chemistry of volatile PFASs, fluorinated ethers, perfluoropolyethers and unreacted precursors and greenhouse gas by-products formed during the wet, plasma, and other thermal coating processes used for the fluorinated treatment of textiles and other substrates. Research should particularly focus on establishing a database of experimental emission factors that can be used to estimate GHG emissions per mass of input chemicals consumed, or per surface area or mass of substrates treated. Once a representative set of emission factors will have been measured, it will then be possible to derive default (industry-average) EFs that could be used to estimate industry-wide emissions. In parallel with the measurement of emission factors to establish the industry's baseline emissions, a coordinated research effort should be undertaken to mitigate climate impacts. Emissions reduction strategies could include – in decreasing order of priority from an ecological standpoint: (1) replacement (not using fluorinated precursors that may emit F-GHGs), (2) optimization (reducing emissions through process improvements), (3) capture and recycle, and (4) abatement. While replacement may prove difficult – especially for the most demanding applications –, optimization of processes to increase the utilization efficiency of fluorinated precursors certainly appears as a viable option, especially for plasma-based processes. Indeed, previous experience in optimizing F-based plasma processes in the electronics industry have proved that it is possible to increase the utilization efficiency of the precursors, thereby reducing their consumption and overall emissions, while lowering costs and improving productivity (e.g., through shorter processing times). For more information see Chapter 6 (IPCC 2019). Also, even if complete replacement of fluorinated chemistries may not always be possible, using alternate fluorinated precursors that are easier to disassociate (e.g., NF3 instead of CF4) or have lower GWPs (e.g., c-C5F8 instead of c-C3F6) can be viable options. While capture and recycling may be costly, abatement of F-GHGs is an established technology that offers low mitigation costs for high-GWP fluorinated gasses. Indeed, combustion-, catalytic-, absorption-, hot-wet-, and plasma-based abatement solutions have been developed to provide up to 99% destruction removal efficiencies (DREs), notably in the electronics industry. For more information see Chapter 6 of (IPCC 2019). Emissions of F-GHGs from wet- and plasma-based fluorinated treatment of textile, leather, paper fibers, and other substrates may be substantial due to the large volume of materials treated and the sheer size and global nature of these industrial sectors. It is therefore urgent to measure the corresponding emissions factors and to create a comprehensive international database of such factors in order to estimate and mitigate emissions from these yet-unaccounted-for sources.Centro de Ciência e Tecnologia Têxtil (2C2T) of the Universidade do Minho for the travel expenses reimbursement through the project UID/CTM/00264/2019 of the Portuguese Fundação para a Ciência e Tecnologia (FCT

Fluorinated greenhouse gas and net-zero emissions from the electronics industry: the proof is in the pudding

The electronics industry has made remarkable progress over the past 25 years in reducing the emission intensity of long-lived volatile fluorinated compounds (FCs) that typically represent 80 to 90% of uncontrolled direct (scope 1) greenhouse gas (GHG) emissions during the manufacturing of semiconductor, display, and photovoltaic devices. However, while Normalized Emission Rates (NERs) have decreased in terms of CO2-equivalent emissions per surface area of electronic devices produced, absolute FC emissions from the sector have continued to grow at a compound annual rate of 3.4% between 1995 and 2020. Despite these trends, industry has not, to date, renewed their sectoral commitments to strengthen global FC emission reduction goals for the 2020–2030 decade, and it is unlikely that recently announced net-zero emission objectives from a few leading companies can reverse upwards industry emission trends in the near-term. Meanwhile, the persisting gap between “top-down” atmospheric measurements-based FC emission estimates and “bottom-up” emissions estimates is increasingly concerning as recent studies suggest that the gap is likely due, in part, to an underestimation of FC emissions from the electronics sector. Thus, the accuracy of industry-average (Tier 2) emission factors is increasingly questionable. Considering that most FCs essentially permanently persist in the atmosphere on a human time scale, the electronics industry needs to reassert its collective leadership on climate action, increase its ambition to reduce absolute emissions, and ground net-zero commitments in science by embarking on a concerted effort to monitor, report, and verify their process and abatement emission factors. To this effect, this article provides practicable solutions to cross-check bottom-up and top-down emission factors at the facility level and suggests that further implementing cost-effective FC abatement technologies, possibly in conjunction with a sectoral cap-and-trade mechanism, can help achieve residual FC emission levels compatible with net-zero neutralization principles and the 1.5 °C objective of the Paris Agreement

A High‐Affinity Calmodulin‐Binding Site in the CyaA Toxin Translocation Domain is Essential for Invasion of Eukaryotic Cells

This article also appears in:Hot Topic: MembranesInternational audienceThe molecular mechanisms and forces involved in the translocation of bacterial toxins into host cells are still a matter of intense research. The adenylate cyclase (CyaA) toxin from Bordetella pertussis displays a unique intoxication pathway in which its catalytic domain is directly translocated across target cell membranes. The CyaA translocation region contains a segment, P454 (residues 454-484), which exhibits membrane-active properties related to antimicrobial peptides. Herein, the results show that this peptide is able to translocate across membranes and to interact with calmodulin (CaM). Structural and biophysical analyses reveal the key residues of P454 involved in membrane destabilization and calmodulin binding. Mutational analysis demonstrates that these residues play a crucial role in CyaA translocation into target cells. In addition, calmidazolium, a calmodulin inhibitor, efficiently blocks CyaA internalization. It is proposed that after CyaA binding to target cells, the P454 segment destabilizes the plasma membrane, translocates across the lipid bilayer and binds calmodulin. Trapping of CyaA by the CaM:P454 interaction in the cytosol may assist the entry of the N-terminal catalytic domain by converting the stochastic motion of the polypeptide chain through the membrane into an efficient vectorial chain translocation into host cells

Dynamics and structural changes of calmodulin upon interaction with the antagonist calmidazolium

International audienceBackground Calmodulin (CaM) is an evolutionarily conserved eukaryotic multifunctional protein that functions as the major sensor of intracellular calcium signaling. Its calcium-modulated function regulates the activity of numerous effector proteins involved in a variety of physiological processes in diverse organs, from proliferation and apoptosis, to memory and immune responses. Due to the pleiotropic roles of CaM in normal and pathological cell functions, CaM antagonists are needed for fundamental studies as well as for potential therapeutic applications. Calmidazolium (CDZ) is a potent small molecule antagonist of CaM and one the most widely used inhibitors of CaM in cell biology. Yet, CDZ, as all other CaM antagonists described thus far, also affects additional cellular targets and its lack of selectivity hinders its application for dissecting calcium/CaM signaling. A better understanding of CaM:CDZ interaction is key to design analogs with improved selectivity. Here, we report a molecular characterization of CaM:CDZ complexes using an integrative structural biology approach combining SEC-SAXS, X-ray crystallography, HDX-MS, and NMR. Results We provide evidence that binding of a single molecule of CDZ induces an open-to-closed conformational reorientation of the two domains of CaM and results in a strong stabilization of its structural elements associated with a reduction of protein dynamics over a large time range. These CDZ-triggered CaM changes mimic those induced by CaM-binding peptides derived from physiological protein targets, despite their distinct chemical natures. CaM residues in close contact with CDZ and involved in the stabilization of the CaM:CDZ complex have been identified. Conclusion Our results provide molecular insights into CDZ-induced dynamics and structural changes of CaM leading to its inhibition and open the way to the rational design of more selective CaM antagonists. Graphical abstract Calmidazolium is a potent and widely used inhibitor of calmodulin, a major mediator of calcium-signaling in eukaryotic cells. Structural characterization of calmidazolium-binding to calmodulin reveals that it triggers open-to-closed conformational changes similar to those induced by calmodulin-binding peptides derived from enzyme targets. These results provide molecular insights into CDZ-induced dynamics and structural changes of CaM leading to its inhibition and open the way to the rational design of more selective CaM antagonists

Calcium-dependent disorder-to-order transitions are central to the secretion and folding of the CyaA toxin of Bordetella pertussis, the causative agent of whooping cough

International audienceThe adenylate cyclase toxin (CyaA) plays an essential role in the early stages of respiratory tract colonization by Bordetella pertussis, the causative agent of whooping cough. Once secreted, CyaA invades eukaryotic cells, leading to cell death. The cell intoxication process involves a unique mechanism of translocation of the CyaA catalytic domain directly across the plasma membrane of the target cell. Herein, we review our recent results describing how calcium is involved in several steps of this intoxication process. In conditions mimicking the low calcium environment of the crowded bacterial cytosol, we show that the C-terminal, calcium-binding Repeat-in-ToXin (RTX) domain of CyaA, RD, is an extended, intrinsically disordered polypeptide chain with a significant level of local, secondary structure elements, appropriately sized for transport through the narrow channel of the secretion system. Upon secretion, the high calcium concentration in the extracellular milieu induces the refolding of RD, which likely acts as a scaffold to favor the refolding of the upstream domains of the full-length protein. Due to the presence of hydrophobic regions, CyaA is prone to aggregate into multimeric forms in vitro, in the absence of a chaotropic agent. We have recently defined the experimental conditions required for CyaA folding, comprising both calcium binding and molecular confinement. These parameters are critical for CyaA folding into a stable, monomeric and functional form. The monomeric, calcium-loaded (holo) toxin exhibits efficient liposome permeabilization and hemolytic activities in vitro, even in a fully calcium-free environment. By contrast, the toxin requires sub-millimolar calcium concentrations in solution to translocate its catalytic domain across the plasma membrane, indicating that free calcium in solution is actively involved in the CyaA toxin translocation process. Overall, this data demonstrates the remarkable adaptation of bacterial RTX toxins to the diversity of calcium concentrations it is exposed to in the successive environments encountered in the course of the intoxication process

High Risk of Anal and Rectal Cancer in Patients With Anal and/or Perianal Crohn’s Disease

International audienceBackground & AimsLittle is known about the magnitude of the risk of anal and rectal cancer in patients with anal and/or perineal Crohn’s disease. We aimed to assess the risk of anal and rectal cancer in patients with Crohn’s perianal disease followed up in the Cancers Et Surrisque Associé aux Maladies Inflammatoires Intestinales En France (CESAME) cohort.MethodsWe collected data from 19,486 patients with inflammatory bowel disease (IBD) enrolled in the observational CESAME study in France, from May 2004 through June 2005; 14.9% of participants had past or current anal and/or perianal Crohn’s disease. Subjects were followed up for a median time of 35 months (interquartile range, 29–40 mo). To identify risk factors for anal cancer in the total CESAME population, we performed a case-control study in which participants were matched for age and sex.ResultsAmong the total IBD population, 8 patients developed anal cancer and 14 patients developed rectal cancer. In the subgroup of 2911 patients with past or current anal and/or perianal Crohn’s lesions at cohort entry, 2 developed anal squamous-cell carcinoma, 3 developed perianal fistula–related adenocarcinoma, and 6 developed rectal cancer. The corresponding incidence rates were 0.26 per 1000 patient-years for anal squamous-cell carcinoma, 0.38 per 1000 patient-years for perianal fistula–related adenocarcinoma, and 0.77 per 1000 patient-years for rectal cancer. Among the 16,575 patients with ulcerative colitis or Crohn’s disease without anal or perianal lesions, the incidence rate of anal cancer was 0.08 per 1000 patient-years and of rectal cancer was 0.21 per 1000 patient-years. Among factors tested by univariate conditional regression (IBD subtype, disease duration, exposure to immune-suppressive therapy, presence of past or current anal and/or perianal lesions), the presence of past or current anal and/or perianal lesions at cohort entry was the only factor significantly associated with development of anal cancer (odds ratio, 11.2; 95% CI, 1.18-551.51; P = .03).ConclusionsIn an analysis of data from the CESAME cohort in France, patients with anal and/or perianal Crohn’s disease have a high risk of anal cancer, including perianal fistula–related cancer, and a high risk of rectal cancer