Although some toxicological studies have reported that exposure to titanium dioxide nanoparticles (nano-TiO) may elicit adverse cardiopulmonary effects, related data collected from human are currently limited. The purpose of this study is to explore cardiopulmonary effects among workers who were exposed to nano-TiO and to identify biomarkers associated with exposure. A cross-sectional study was conducted in a nano-TiO manufacturing plant in eastern China. Exposure assessment and characterization of TiO particles were performed in a packaging workshop. Physical examination and possible biomarkers for cardiopulmonary effects were examined among 83 exposed workers and 85 controls. In packaging workshop, the total mass concentration of particles was 3.17 mg/m. The mass concentration of nanoparticles was 1.22 mg/m accounting for 39% of the total mass. Lung damage markers (SP-D and pulmonary function), cardiovascular disease markers (VCAM-1, ICAM-1, LDL, and TC), oxidative stress markers (SOD and MDA), and inflammation markers (IL-8, IL-6, IL-1β, TNF-α, and IL-10) were associated with occupational exposure to nano-TiO. Among those markers, SP-D showed a time (dose)-response pattern within exposed workers. The data strongly suggest that nano-TiO could contribute, at least in part, to the cardiopulmonary effects observed in workers. The studied markers and pulmonary function tests may be useful in health surveillance for workers exposed to nanomaterials.

Long-term exposure to fine particulate matter (PM 2.5 ) is associated with kidney dysfunction. However, few studies have investigated acute effects of PM 2.5 elemental constituents on renal function. We evaluated associations between personal PM 2.5 and its elemental constituents and kidney function, assessed by an estimated glomerular filtration rate (eGFR) in Biomarkers of Air Pollutants Exposure in the Chinese aged 60−69 study. Seventy one older individuals were visited monthly between September 2018 and January 2019. Each participant wore a PM 2.5 monitor for 72 h, responded to a questionnaire, and underwent a physical examination with blood sampling. Linear mixed-effect models were used to estimate associations between personal PM 2.5 elemental constituents and eGFR. We found that significant changes in eGFR from −1.69% [95% confidence interval (CI): −3.34%, −0.01%] to −3.27% (95% CI: −5.04%, −1.47%) were associated with interquartile range (IQR) increases in individual PM 2.5 exposures at various lag periods (7−12, 13−24, 0−24, 25−48, and 49−72 h). An IQR increase in 72 h moving averages of copper, manganese, and titanium in personal PM 2.5 corresponded to −2.34% (95% CI: −3.67%, −0.99%) to −4.56% (95% CI: −7.04%, −2.00%) changes in eGFR. Personal PM 2.5 and some of its elemental constituents are inversely associated with eGFR in older individuals.

Background: Insulin resistance (IR) affects the development of type 2 diabetes mellitus (T2DM), which is also influenced by accumulated fine particle air pollution [particulate matter (PM) with aerodynamic diameter of ( )] exposure. Previous experimental and epidemiological studies have proposed several potential mechanisms by which contributes to IR/T2DM, including inflammation imbalance, oxidative stress, and endothelial dysfunction. Recent evidence suggests that the imbalance of the gut microbiota affects the metabolic process and may precede IR. However, the underlying mechanisms of , gut microbiota, and metabolic diseases are unclear. Objectives: We investigated the associations between personal exposure to and fasting blood glucose and insulin levels, the IR index, and other related biomarkers. We also explored the potential underlying mechanisms (systemic inflammation and sphingolipid metabolism) between and insulin resistance and the mediating effects between and sphingolipid metabolism. Methods: We recruited 76 healthy seniors to participate in a repeated-measures panel study and conducted clinical examinations every month from September 2018 to January 2019. Linear mixed-effects (LME) models were used to analyze the associations between and health data (e.g., functional factors, the IR index, inflammation and other IR-related biomarkers, metabolites, and gut microbiota). We also performed mediation analyses to evaluate the effects of mediators (gut microbiota) on the associations between exposures ( ) and featured metabolism outcomes. Results: Our prospective panel study illustrated that exposure to was associated with an increased risk of higher IR index and functional biomarkers, and our study provided mechanistic evidence suggesting that exposure may contribute to systemic inflammation and altered sphingolipid metabolism. Discussion: Our findings demonstrated that was associated with the genera of the gut microbiota, which partially mediated the association between and sphingolipid metabolism. These findings may extend our current understanding of the pathways of and IR. https://doi.org/10.1289/EHP9688

No abstract

No abstract