Particulate matter with an aerodynamic diameter of ≤ 2.5 µm (PM2.5) has been linked to adverse health outcomes in welding workers. The objective of this study was to investigate associations of chronic exposure to metal fume PM2.5 in shipyard workers with health outcomes. A longitudinal study was conducted to determine the effects of metal fume PM2.5 on FeNO, urinary metals, urinary oxidative stress, inflammation, and stress hormones in workers. There were 20 office workers and 49 welding workers enrolled in this study who were followed-up for a second year. We observed that Fe, Zn, and Mn were abundant in PM2.5 to which welding workers were personally exposed, whereas PM2.5 to which office workers were personally exposed was dominated by Pb, Cu, and Zn. We observed in the first and/or second visits that urinary 8-iso-prostaglandin F2-α (PGF2α) and 8-hydroxy-2'-deoxy guanosine (8-OHdG) were significantly increased by exposure. An increase in urinary interleukin (IL)-6 and decreases in urinary serotonin and cortisol were observed in the first and/or second visits after exposure. PM2.5 was associated with decreases in urinary 8-OHdG and cortisol among workers. Next, we observed that urinary Ni, Co, and Fe had significantly increased among workers after a year of exposure. Urinary metals were associated with decreases in urinary 8-iso-PGF2α and cortisol among workers. Urinary Ni, Cu, and Fe levels were associated with an increase in urinary IL-6 and a decrease in urinary cortisol among workers. In conclusion, chronic exposure to metal fume PM2.5 was associated with inflammation and a cortisol deficiency in shipyard workers, which could associate with adrenal glands dysfunction.

Background: Breast cancer is the leading cause of cancer incidence worldwide and in Taiwan. The relationship between breast cancer and occupational types remains unclear. This study aimed to investigate lifetime breast cancer incidence by different occupational industries among female workers in Taiwan. Methods: A population-based retrospective case–control study was conducted using three nationwide population-based databases. Matched case and control groups were identified with 1-to-4 exact matching among 103,047 female workers with breast cancer diagnosed in 2008–2017 and those without breast cancer. Their lifetime labor enrollment records were tracked using the National Labor Insurance Database, 1950–2017. Conditional logistic regression was used to analyze the association between types of occupational industries and risk of incident breast cancer. Results: Our study found slightly significant breast cancer risk among the following major occupational classifications: manufacturing (OR: 1.027, 95% CI: 1.011–1.043); wholesale and retail trade (OR: 1.068, 95% CI: 1.052–1.084); information and communication (OR: 1.074, 95% CI: 1.043–1.105); financial and insurance activities (OR: 1.109, 95% CI: 1.086–1.133); real estate activities (OR: 1.050, 95% CI: 1.016–1.085); professional, scientific, and technical activities (OR: 1.118, 95% CI: 1.091–1.145); public administration, defense, and social security (OR: 1.054, 95% CI: 1.023–1.087), education (OR: 1.199, 95% CI: 1.168–1.230); and human health and social work activities (OR: 1.125, 95% CI: 1.096–1.156). Conclusions: Greater percentages of industrial occupations (i.e., manufacturing, wholesale and retail, or health professionals) were associated with slightly increased breast cancer risk. Further studies should investigate the possible risk factors among female workers in those industries with slightly higher incidence of breast cancer.

We investigated roles of Hippo signaling pathway components in alveolar type II cells (AECII) after zinc oxide nanoparticle (ZnONP) exposure. ZnONPs physicochemistry was characterized using field emission-scanning electron microscopy (FE-SEM) and energy-dispersive X-ray (EDX) microanalysis. ZnONP deposition in human respiratory tract was estimated using multiple-path particle dosimetry (MPPD) model. MLE-12 AECII were cultured and exposed to 0, 1, and 5 μg/mL of ZnONPs for 24 h. Western blots were used to investigate signaling pathways associated with Yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ), cell adherens junctions, differentiation, and senescence. ZnONPs morphology was irregular, with Zn and O identified. Approximately 72% of inhaled ZnONPs were deposited in lungs, with 26% being deposited in alveolar regions. ZnONP exposure increased nuclear YAP expression and decreased cytoplasmic YAP expression by AECII. Adherens junction proteins, E-cadherin, α-catenin, and β-catenin, on AECII decreased after ZnONP exposure. ZnONP exposure of AECII increased alveolar type I (AECI) transition protein, LGALS3, and the AECI protein, T1α, while decreasing AECII SPC expression. ZnONP exposure induced Sirt1 and p53 senescence proteins by AECII. Our findings showed that inhalable ZnONPs can deposit in alveoli, which promotes YAP nuclear localization in AECII, resulting in decrease tight junctions, cell differentiation, and cell senescence.