MATERIAL AND METHODS: Urine samples were collected from plastic factory workers and from control subjects after their shift. Air samples were collected using gas analyzers from 5 sampling positions in the injection molding unit work area and from ambient air. The level of BPA in airborne and urine samples was quantified by the gas chromatography mass spectrometry - selected ion monitoring (GCMS-SIM) analysis.
RESULTS: Bisphenol A was detected in the median range of 8-28.3 ng/m³ and 2.4-3.59 ng/m³ for the 5 sampling points in the plastic molding factory and in the ambient air respectively. The median urinary BPA concentration was significantly higher in the workers (3.81 ng/ml) than in control subjects (0.73 ng/ml). The urinary BPA concentration was significantly associated with airborne BPA levels (ρ = 0.55, p < 0.01).
CONCLUSIONS: Our findings provide the first evidence that workers in a molding factory in Malaysia are occupationally exposed to BPA. Int J Occup Med Environ Health 2017;30(5):743-750.
METHODS: Rats were fed with illicit (a concoction of street ketamine) ketamine in doses of 100 (N=12), or 300 mg/kg (N=12) for four weeks. Half of the rats were sacrificed after the 4-week feeding for necropsy. The remaining rats were taken off ketamine for 8 weeks to allow for any potential recovery of pathological changes before being sacrificed for necropsy. Histopathological examination was performed on the kidney and urinary bladder.
RESULTS: Submucosal bladder inflammation was seen in 67% of the rats fed with 300 mg/kg illicit ketamine. No bladder inflammation was observed in the control and 100 mg/kg illicit ketamine groups. Renal changes, such as interstitial nephritis and papillary necrosis, were observed in rats given illicit ketamine. After ketamine cessation, no inflammation was observed in the bladder of all rats. However, renal inflammation remained in 60% of the rats given illicit ketamine. No dose-effect relationship was established between oral ketamine and changes in the kidneys.
CONCLUSION: Oral ketamine caused pathological changes in the urinary tract, similar to that described in exposure to parenteral ketamine. The changes in the urinary bladder were reversible after short-term exposure.