Acute arsenic exposure exacerbates lipopolysaccharide-induced lung injury possibly by compromising the integrity of the lung epithelial barrier in rats.

Inhalation of large amounts of arsenic can damage the respiratory tract and may exacerbate the development of bacterial pneumonia, but the exact mechanism remains unclear. In this study, male Wistar rats were randomly divided into control, arsenic trioxide (16.0 µg/kg ATO), lipopolysaccharide (0.5 mg/kg LPS), and ATO combined with LPS (16.0 µg/kg ATO + 0.5 mg/kg LPS) groups. Blood and lung tissue samples were collected from each group 12 h after exposure. The results showed that exposure to ATO or LPS alone produced different effects on leukocytes and inflammatory factors, while combined exposure significantly increased serum interleukin-6, interleukin-10, lung water content, lung lavage fluid protein, and p38 protein phosphorylation levels. Alveolar interstitial thickening, alveolar membrane edema, alveolar type I and II cell matrix vacuolization, and nuclear pyknosis were observed in rats exposed to either ATO or LPS. More severe ultrastructural changes were found in the combined exposure group, and chromatin splitting was observed in alveolar type I cells. Lanthanum nitrate particles leaked from the alveolar vascular lumen in the ATO-exposed group, whereas in the combined exposure group, Evans Blue levels were increased and lanthanum nitrate particles were present in the lung parenchyma. Claudin-3 protein expression increased and claudin-4 expression decreased after ATO or LPS exposure, while claudin-18 expression was unchanged. The changes in claudin-3 and claudin-4 protein expression were further exacerbated by combined exposure. In conclusion, these results suggest that inhalation of ATO may exacerbate the development of bacterial pneumonia and that common mechanisms may exist to synergistically disrupt epithelial barrier integrity.

Hypertonic saline resuscitation protects against kidney injury induced by severe burns in rats.

BACKGROUND: Proper fluid resuscitation can relieve visceral damage and improve survival in severely burned patients. This study compared the effectiveness of resuscitation with 400mEq/L hypertonic saline (HS) and sodium lactate Ringer's solution (LR) in rats with kidney injury caused by burn trauma. METHODS: Rats (Sprague-Dawley) underwent burn injury and were randomized into sham, LR, and HS groups. Samples from the kidney were assayed for water content ratio, histopathology, and oxidative stress (superoxide dismutase (SOD) and malondialdehyde (MDA)). Serum sodium, renal function (creatinine and cystatin (Cys)-C), and inflammatory response (tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and high mobility group protein box (HMGB)-1) were also examined as serum markers. RESULTS: Hypertonic saline resuscitation reduced the renal water content ratio and improved renal histopathology caused by severe burns. This effect was accompanied by reductions in serum creatinine and Cys-C as well as TNF-α, IL-1ß, and HMGB1. Serum sodium concentration and SOD activity were increased, whereas MDA content was decreased in the kidney tissue of the HS group. CONCLUSIONS: The data indicate that 400mEq/L HS solution reduces hyponatremia and renal edema, inhibits the release of inflammatory mediators, and alleviates oxidative stress injury, thus protecting against kidney injury induced by severe burns.

Assessment of the inhalation risks associated with working in printing rooms: a study on the staff of eight printing rooms in Beijing, China.

The concentration of pollution directly determines the occupational health risk, and the exposure time is an important influencing factor. We evaluated the inhalation risks of working in a printing room. Eight units with centralized printing rooms were randomly selected. Formaldehyde, ozone, benzene, toluene, xylene, and fine particulate matter were detected by spectrophotometry, gas chromatography, and direct reading instruments, respectively. The U.S. EPA inhalation risk assessment model was used to assess cancer and non-cancer risks. The formaldehyde inhalation cancer risk value was 1.35-3.45 × 10-6, which is greater than the limit of 1 × 10-6, suggesting a risk of squamous cell carcinoma. The benzene inhalation cancer risk in five of the rooms was 1.09-4.65 × 10-6, which is greater than the limit of 1 × 10-6, suggesting a risk of leukemia. In terms of non-cancer risk, in five of the rooms, the hazard quotient (HQ) was > 1 (range 1.99-4.69) due to benzene pollution, suggesting a risk of reduced lymphocyte count. In one room, due to benzene and xylene pollution, the HQ was > 1, suggesting a risk of lymphocyte count drop and motor coordination impairment. Collectively, the study concludes that staff members of printing rooms are exposed to both cancer and non-cancer occupational health risks.