Bleaching of bagasse-pulp using short TCF and ECF sequence

More than 70 % bleached chemical pulp is produced in India through elemental chlorine-free bleaching in which chlorine-based compounds like chlorine dioxide is a dominant chemical which generates chlorinated organic toxins harmful to the environment. Present studies demonstrate short sequence of bleaching combined with acid treatment, followed by pressurized oxygen delignification. It was found that efficiency of oxygen improved by adding hydrogen peroxide as an additive in oxygen delignification with subsequent treatment with ozone or chlorine dioxide as bleaching agents. It was observed that by using additive in ODL process, pulp can achieve 70±1 (%ISO) brightness. Reduction attains in kappa number 65–70 % as compared to 45–50 % in control oxygen delignification stage. Through AOpZ and AOpD bleaching sequences, full brightness achieved 84–85 (%ISO) without considerable loss in mechanical strength properties compared to DEpD sequence. A potential reduction in COD, color, and AOX was 28, 53.3, and 88 % respectively were observed in AOpZ short bleaching sequence compared to DEpD bleaching.

Role of Macrophages in Cytotoxicity, Reactive Oxygen Species Production and DNA Damage in 1,2-Dichloropropane-Exposed Human Cholangiocytes In Vitro

1,2-Dichloropropane (1,2-DCP), a synthetic chlorinated organic compound, was extensively used in the past in offset color proof-printing. In 2014, the International Agency for Research on Cancer (IARC) reclassified 1,2-DCP from its initial Group 3 to Group 1. Prior to the reclassification, cholangiocarcinoma was diagnosed in a group of workers exposed to 1,2 -DCP in an offset color proof-printing company in Japan. In comparison with other forms of cholangiocarcinoma, 1,2-DCP-induced cholangiocarcinoma was of early onset and accompanied by extensive pre-cancerous lesions in large bile ducts. However, the mechanism of 1,2-DCP-induced cholangiocarcinoma is poorly understood. Inflammatory cell proliferation was observed in various sites of the bile duct in the noncancerous hepatic tissues of the 1,2-DCP-induced cholangiocarcinoma. The aim of this study was to enhance our understanding of the mechanism of 1,2-DCP-related cholangiocarcinogenesis. We applied an in vitro system to investigate the effects of 1,2-DCP, using MMNK-1 cholangiocytes cultured alone or with THP-1 macrophages. The cultured cells were exposed to 1,2-DCP at 0, 0.1, 0.2, 0.4, and 0.8 mM for 24 h, and then assessed for cell proliferation, cell cytotoxicity, DNA damage, and ROS production. Exposure to 1,2-DCP increased proliferation of MMNK-1 cholangiocytes cultured alone, but not those cultured with macrophages. 1,2-DCP also increased LDH cytotoxicity, DNA damage, and ROS production in MMNK-1 cholangiocytes co-cultured with macrophages but not those cultured alone. 1,2-DCP increased TNFα and IL-1β protein expression in macrophages. The results highlight the role of macrophages in enhancing the effects of 1,2-DCP on cytotoxicity, ROS production, and DNA damage in cholangiocytes.