Graphene-based nanomaterials (GBNs) consist of a single or few layers of graphene sheets or modified graphene including pristine graphene, graphene nanosheets (GNS), graphene oxide (GO), reduced graphene oxide (rGO), as well as graphene modified with various functional groups or chemicals (e.g., hydroxyl, carboxyl, and polyethylene glycol), which are frequently used in industrial and biomedical applications owing to their exceptional physicochemical properties. Given the widespread production and extensive application of GBNs, they can be disseminated in a wide range of environmental mediums, such as air, water, food, and soil. GBNs can enter the human body through various routes such as inhalation, ingestion, dermal penetration, injection, and implantation in biomedical applications, and the majority of GBNs tend to accumulate in the respiratory system. GBNs inhaled and substantially deposited in the human respiratory tract may impair lung defenses and clearance, resulting in the formation of granulomas and pulmonary fibrosis. However, the specific toxicity of the respiratory system caused by different GBNs, their influencing factors, and the underlying mechanisms remain relatively scarce. This review summarizes recent advances in the exposure, metabolism, toxicity and potential mechanisms, current limitations, and future perspectives of various GBNs in the respiratory system.

Background The prevalence of tuberculosis (TB) in low and middle-income countries is a significant public health and social concern. TB is a common infectious disease caused by the Mycobacterium tuberculosis infection, which has a widespread infection rate. Health care-seeking delay maybe one of the most important neglected risk factors for the spread of TB. Objectives The aim of this study was to understand the situation of health care-seeking delay among rural tuberculosis patients in Hubei Province, and explore its risk factors. Methods A total of 1408 rural tuberculosis patients were surveyed using a standard structured questionnaire in three cities of Hubei Province during the past two years. Results For the 1408cases of pulmonary tuberculosis, 39.70% of them were health care-seeking delayed. Logistic regressions indicate that the Han nationality, farming careers, the over 45 min walk to the township’s hospital, and awareness of the national TB free treatment policy, were significantly associated with higher odds of a delay in care seeking. Conclusions The prevalence of health care-seeking delay among tuberculosis patients was high in rural areas. It is essential to take comprehensive targeted interventions to reduce care-seeking delay.

Di(2-ethylhexyl)phthalate (DEHP) is a typical endocrine-disrupting chemical and reproductive toxicant. Although previous studies have attempted to describe the mechanism by which DEHP exposure results in reproductive dysfunction, few studies focused on puberty, a critical period of reproductive development, and the increased susceptibility to injury in adolescents. To elucidate the mechanism underpinning the testicular effects of DEHP in puberty, we sought to investigate the JAZF1/TR4 pathway in the testes of pubertal rats. Specifically, we focused on the role of the JAZF1/TR4 pathway in male reproduction, including the genes JAZF1, TR4, Sperm 1, and Cyclin A1. In the present study, rats were exposed to increasing concentrations of DEHP (0, 250, 500, and 1000 mg/kg/day) by oral gavages for 30 days. Then we assayed testicular zinc and oxidative stress levels. Our results indicated that DEHP exposure could lead to oxidative stress and decrease the contents of testicular zinc. Additionally, significant morphological changes and cell apoptosis were observed in testes exposed to DEHP, as identified by hematoxylin and eosin staining and the terminal deoxynucleotidyl transferase-mediated nick and labeling assay. By measuring the expression levels of the above relevant genes by qPCR, we found the DEHP-induced increased expression of JAZF1 and decreased expression of TR4, Sperm 1, and Cyclin A1. Therefore, we have demonstrated that in vivo exposure to DEHP might induce reproductive toxicity in pubertal male rats through the JAZF1/TR4 pathway and oxidative stress.