Many researches mention the need to identify the land-based sources of riverine macrolitter but few field data on litter amount, composition and sources are available in the scientific literature. Describing macrolitter hotspot dynamics would actually allow a better estimation of fluxes in the receiving environments and a better identification of the more appropriate mitigation strategies. This study provides new insights in roadway macrolitter production rates, typologies and input sources (i.e. deliberate or accidental). The macrolitter from an 800 m portion of a highly frequented roadway (around 90,000 vehicles per day) was collected during almost one year. Typologies were defined using the OSPAR/TGML classification. Results show high annual loads of macrolitter (42.8 kg/yr/ha), suggesting significant contributions of the road runoff to the litter fluxes in urban stormwater. Over the course of a year, 88.5 kg of debris were collected, including 53.2 kg (60%) of plastic debris. In total, 36,439 items were characterized, of which 84% were plastics. The macrodebris collected present a low diversity of components with Top 10 items accounting for 92% by count and a majority of small and lightweight items like plastic fragments (31%) or cigarette butts (18%). Input sources were estimated for 43% of the mass collected in which 37.2% were deliberately littered and 62.8% were accidental leaks, illustrating a major contribution of uncovered trucks and unsecured loads. The accumulation rates show a linear correlation with the road traffic. Such data are of prime interest since they enable to determine the potential contribution of road traffic to plastic fluxes to the environment.

Cigarette smoke extract (CSE), a complex mixture of compounds, contributes to a range of eye diseases; however, the underlying pathophysiological responses to tobacco smoke remain ambiguous. The purpose of the present study was to evaluate the cigarette smoke-induced phenotypic and transcriptomic changes in the corneal epithelium with a view to elucidating the likely underlying mechanism. Accordingly, for the first time, we characterized the genome-wide effects of CSE on the corneal epithelium. The ocular surface of the mice in the experimental groups was exposed to CSE for 1 h per day for a period of one week, while mice in the control group were exposed to preservative-free artificial tears. Corneal fluorescein staining, in vivo confocal microscopy and scanning electron microscopy were performed to examine the corneal ultrastructure. Transcriptome sequencing and bioinformatics analysis were performed followed by RT-qPCR to validate gene expression changes. The results indicate that CSE exposure disrupted the structural integrity of the superficial epithelium, decreased the density of microvilli, and compromised the corneal epithelial barrier intactness. RNA-seq revealed 667 differentially expressed genes, and functional analysis highlighted the enhancement of several biological processes such as antioxidant activity and the response to oxidative stress. Moreover, the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis showed that glutathione metabolism and drug metabolism cytochrome P450 were the most relevant pathways contributing to the effects of CSE on the corneal epithelium. Protein–protein interaction (PPI) network analysis illustrated that GCLC, NQO1, and HMOX1 were the most relevant nodes. In conclusion, the present study indicates that CSE exposure induces changes in the phenotype and genotype of the corneal epithelium. The antioxidant response element is essential for counteracting the effects of cigarette smoke on this tissue layer. These results shed novel insights into how cigarette smoke damages this ocular surface.

Cigarette smoke (CS) affects immune functions, leading to severe outcomes in smokers. Robust evidence addresses the immunotoxic effects of combustible tobacco products. As heat-not-burn tobacco products (HNBT) vaporize lower levels of combustible products, we here compared the effects of cigarette smoke (CS) and HNBT vapor on Jurkat T cells. Cells were exposed to air, conventional cigarettes or heatsticks of HNBT for 30 min and were stimulated or not with phorbol myristate acetate (PMA). Cell viability, proliferation, reactive oxygen species (ROS) production, 8-OHdG, MAP-kinases and nuclear factor κB (NFκB) activation and metallothionein expression (MTs) were assessed by flow cytometry; nitric oxide (NO) and cytokine levels were measured by Griess reaction and ELISA, respectively. Levels of metals in the exposure chambers were quantified by inductively coupled plasma mass spectrometry. MT expressions were quantified by immunohistochemistry in the lungs and liver of C57Bl/6 mice exposed to CS, HNBT or air (1 h, twice a day for five days: via inhalation). While both CS and HBNT exposures increased cell death, CS led to a higher number of necrotic cells, increased the production of ROS, NO, inflammatory cytokines and MTs when compared to HNBT-exposed cells, and led to a higher expression of MTs in mice. CS released higher amounts of metals. CS and HNBT exposures decreased PMA-induced interleukin-2 (IL-2) secretion and impaired Jurkat proliferation, effects also seen in cells exposed to nicotine. Although HNBT vapor does not activate T cells as CS does, exposure to both HNBT and CS suppressed proliferation and IL-2 release, a pivotal cytokine involved with T cell proliferation and tolerance, and this effect may be related to nicotine content in both products.

Environmental exposures are one of the greatest threats to human health, yet we lack tools to answer simple questions about our exposures: what are our personal exposure profiles and how do they change overtime (external exposome), how toxic are these chemicals, and what are the sources of these exposures? To capture variation in personal exposures to airborne chemicals in the gas and particulate phases and identify exposures which pose the greatest health risk, wearable exposure monitors can be deployed. In this study, we deployed passive air sampler wristbands with 84 healthy participants (aged 60–69 years) as part of the Biomarkers for Air Pollutants Exposure (China BAPE) study. Participants wore the wristband samplers for 3 days each month for five consecutive months. Passive samplers were analyzed using a novel gas chromatography high resolution mass spectrometry data-processing workflow to overcome the bottleneck of processing large datasets and improve confidence in the resulting identified features. The toxicity of chemicals observed frequently in personal exposures were predicted to identify exposures of potential concern via inhalation route or other routes of airborne contaminant exposure. Three exposures were highlighted based on elevated toxicity: dichlorvos from insecticides (mosquito/malaria control), naphthalene partly from mothballs, and 183 polyaromatic hydrocarbons from multiple sources. Other exposures explored in this study are linked to diet and personal care products, cigarette smoke, sunscreen, and antimicrobial soaps. We highlight the potential for this workflow employing wearable passive samplers for prioritizing chemicals of concern at both the community and individual level, and characterizing sources of exposures for follow up interventions.

Cadmium (Cd) is a heavy metal toxicant as a common pollutant derived from many agricultural and industrial sources. The absorption of Cd takes place primarily through Cd-contaminated food and water and, to a significant extent, via inhalation of Cd-contaminated air and cigarette smoking. Epidemiological data suggest that occupational or environmental exposure to Cd increases the health risk for osteoporosis and spontaneous fracture such as itai-itai disease. However, the direct effects and underlying mechanism(s) of Cd exposure on bone damage are largely unknown. We used primary bone marrow-derived mesenchymal stromal cells (BMMSCs) and found that Cd significantly induced BMMSC cellular senescence through over-activation of NF-κB signaling pathway. Increased cell senescence was determined by production of senescence-associated secretory phenotype (SASP), cell cycle arrest and upregulation of p21/p53/p16ᴵᴺᴷ⁴ᵃ protein expression. Additionally, Cd impaired osteogenic differentiation and increased adipogenesis of BMMSCs, and significantly induced cellular senescence-associated defects such as mitochondrial dysfunction and DNA damage. Sprague-Dawley (SD) rats were chronically exposed to Cd to verify that Cd significantly increased adipocyte number, and decreased mineralization tissues of bone marrow in vivo. Interestingly, we observed that Cd exposure remarkably retarded bone repair and regeneration after operation of skull defect. Notably, pretreatment of melatonin is able to partially prevent Cd-induced some senescence-associated defects of BMMSCs including mitochondrial dysfunction and DNA damage. Although Cd activated mammalian target of rapamycin (mTOR) pathway, rapamycin only partially ameliorated Cd-induced cell apoptosis rather than cellular senescence phenotypes of BMMSCs. In addition, a selective NF-κB inhibitor moderately alleviated Cd-caused the senescence-related defects of the BMMSCs. The study shed light on the action and mechanism of Cd on osteoporosis and bone ageing, and may provide a novel option to ameliorate the harmful effects of Cd exposure.

Smoked cigarette filters a. k.a. “butts”, composed of plastic (e.g. cellulose acetate) are one of the world’s most common litter items. In response to concerns about plastic pollution, biodegradable cellulose filters are being promoted as an environmentally safe alternative, however, once smoked, both contain toxins which can leach once discarded. The impacts of biodegradable butts as littered items on the receiving environment, in comparison with conventional butts has not yet been assessed. A freshwater mesocosm experiment was used to test the effects of leachate from smoked cellulose acetate versus smoked cellulose filters at a range of concentrations (0, 0.2, 1 and 5 butts L⁻¹) on the mortality and behaviour of four freshwater invertebrates (Dreissena polymorpha, Polycelis nigra, Planorbis planorbis and Bithynia tentaculata). Leachate derived from 5 butts L⁻¹ of either type of filter caused 60–100% mortality to all species within 5 days. Leachate derived from 1 butt L⁻¹ of either type resulted in adults being less active than those exposed to no or 0.2 butts L⁻¹ leachate. Cigarette butts, therefore, regardless of their perceived degradability can cause mortality and decreased activity of key freshwater invertebrates and should always be disposed of responsibly.

Although human exposure to polycyclic aromatic hydrocarbons (PAH) has been associated with in vivo oxidative damage, and hydroxyPAH metabolites have been used as biomarkers to assess PAH-induced oxidative stress, few studies have looked at the likely causative compounds for oxidative stress in humans - PAH quinones. We developed a method using pre-column derivatization - liquid chromatography-heated electrospray ionization-tandem mass spectrometry (LC-HESI-MS/MS) to analyze ortho-phenanthrene quinones (PheQs) in human urine. 1,2-PheQ and 3,4-PheQ were identified and quantified in 3 mL of human urine; their total concentrations were higher in cigarette smokers (0.79 ± 0.98 nmol/6h urine) than in nonsmokers (0.20 ± 0.98 nmol/6h urine) (p < 0.01). The total of 1,2-PheQ and 3,4-PheQ were more strongly correlated with urinary (Z)-7-[1R,2R,3R,5S)-3,5-dihydroxy-2-[(E,3S)-3-hydroxyoct-1-enyl]cyclopentyl]hept-5-enoic acid (8-iso-PGF₂α), a biomarker of lipid peroxidation (R² = 0.53, p < 0.001), than the other phenanthrene metabolites including phenanthrene tetraol (PheT), phenanthrene-1,2-dihydrodiol (1,2-PheD), and total phenanthrene phenols (OHPhe), consistent with the concept that PheQs and likely other PAH quinones play a causal role in the generation of reactive oxygen species (ROS) in humans. Thus, PheQs may be suitable as biomarkers to assess human exposure to oxygenated PAH and the subsequent oxidative damage. This study provides unique support, by analysis of human urinary metabolites, for the PAH quinone mediated oxidative damage hypothesis of PAH carcinogenesis.

Rivers are an important source of marine anthropogenic litter, but the particular origins of riverine litter itself have not been well established. Here we used a citizen science approach where schoolchildren examined litter at riversides and identified possible sources at over 250 sampling spots along large and small rivers in Germany, during autumn 2016 and spring 2017. Litter densities have an overall median of 0.14, interquartile range 0–0.57 items m−2 and an overall average (±standard deviation) of 0.54 ± 1.20 litter items m−2. Litter quantities differed only little by sampling year. The principal litter types found were plastics and cigarette butts (31% and 20%, respectively), followed by glass, paper, and metal items, indicating recreational visitors as the principal litter source. At many sites (85%), accumulations of litter, consisting principally of cigarettes and food packaging, have been found. At almost all sampling sites (89%), litter potentially hazardous to human health has been observed, including broken glass, sharp metal objects, used personal hygiene articles and items containing chemicals. In the search for litter sources, the schoolchildren identified mainly people who use the rivers as recreational areas (in contrast to residents living in the vicinity, illegal dumping, or the river itself depositing litter from upstream sources). These results indicate the urgent need for better education and policy measures in order to protect riparian environments and reduce input of riverine litter to the marine environment.

This study aimed to elucidate the origin of the widespread nicotine contamination of plant-derived commodities, by conducting field experiments with various herbs and spice plants. By scattering tobacco and cigarette butts on the field and subsequent nicotine analyses of the acceptor plants, we verified that the alkaloid is leached out into the soil and is taken up by the crop plants. This path of contamination pertains even when there is only one cigarette butt per square meter. Even such minor pollution results - at least in the case of basil and peppermint - in considerable high nicotine contaminations, which exceed the maximum residue level by more than 20-fold.The data reported here clearly outline the large practical relevance of this soil-borne contamination path and imply that unthoughtful disposal of cigarette butts in the field by farm workers may be the reason for the widespread occurrence of nicotine contamination in plant-derived commodities. Therefore, such misbehavior needs to be prevented using education and sensitization, and by including this issue into the guidelines of good agricultural practice.

Aerosols from eight e-cigarettes at different nicotine levels and flavoring were characterized as particle number size distributions in the range 5.6–560 nm by FMPS and CPC. Results were used to provide dosimetry estimates applying the MMPD model.Particle number concentrations varied between 3.26 × 109 and 4.09 × 109 part cm−3 for e-liquids without nicotine and between 5.08 × 109 and 5.29 × 109 part cm−3 for e-liquids with nicotine. No flavor effects were detected on particle concentration data. Particle size distributions were unimodal with modes between 107–165 nm and 165–255 nm, for number and volume metrics, respectively.Averagely, 6.25 × 1010 particles were deposited in respiratory tree after a single puff. Highest deposition densities and mean layer thickness of e-cigarette liquid on the lung epithelium were estimated at lobar bronchi.Our study shows that e-cigarette aerosol is source of high particle dose in respiratory system, from 23% to 35% of the daily dose of a no-smoking individual.