Mutation Research - Genetic Toxicology and Environmental Mutagenesis 866 (2021) 503349 Available online 16 March 2021 1383-5718/© 2021 Elsevier B.V. All rights reserved. Consumption pattern and genotoxic potential of various smokeless tobacco products in Assam, India: A public health concern Sarbani Giri a, *, Dharmeswar Barhoi a , Sweety Nath Barbhuiya a , Anirudha Giri b , Samrat Das a , Aparajita Das a , Salam Himika Devi a , Doli Talukdar a , Puja Upadhaya a , Pimily Langthasa a , Neelam Pandey a , Supriya Singh a a Molecular and Cell Biology Laboratory, Department of Life Science and Bioinformatics, Assam University, Silchar, 788011, India b Laboratory of Environmental and Human Toxicology, Department of Life Science and Bioinformatics, Assam University, Silchar, 788011, India A R T I C L E INFO Keywords: Smokeless tobacco DNA damage Genome instability Nuclear division index Buccal micronucleus cytome assay Cytokinesis-block micronucleus assay ABSTRACT Smokeless tobacco (SLT) consumption is presumed to be one of the major causes of high incidence of oral cancer in India. The present study aimed to document various types of SLT products consumed and their potential impact on the genome instability on the population from Assam state in Northeast India. A cross-sectional study (n = 5000) showed that 60.56 % of the study population consumed at least one of the three forms (sadagura, zarda and khaini) of SLT of which 52.0 % were only sadagura users. Genotoxicity assessment using buccal cytome assay in 240 age and sex matched volunteers revealed that except for zarda, other forms of SLT induced signifcantly higher incidence micronuclei in the buccal epithelial cells compared to the control individuals. Similar effects were also observed in other cytome parameters related to cell proliferation, cytokinesis defects and cell death. Signifcantly higher incidence of micronucleus was observed among sadagura and khaini users in lymphocyte cytokinesis-blocked micronucleus assay. The addition of lime in sadagura increased the pH and anion levels which possibly result in higher absorption and may lead to the development of cellular anomalies. 1. Introduction Tobacco consumption, either in the form of smoking and/or smokeless tobacco (SLT) has the potential to cause various adverse health effects including cancer. In addition to different lifestyle factors, usage of tobacco has been accounted for as one the major causes for the development of cancer of lungs, esophagus, and the lip and oral cavity [1]. According to the report of the Population-Based Cancer Registry of India (2012–2014), the proportion of tobacco-related cancers in India is quite high in case of males [2]. The magnitude of the situation in the northeastern part of the country is more critical as 57 % of all cancers in males and 28.3 % of all cancers in females are caused due to indis- criminate consumption of tobacco [3]. In India, usage of both commercial SLT products like khaini, zarda, gutka and other local forms with or without additives like lime are prevalent [4,5]. The population used for survey and data collection in this study belongs to the northeastern part of India, where in addition to commercially available SLT products like zarda and khaini, a unique homemade product commonly known as sadagura is consumed arbi- trarily [6]. Recently, we have reported that long-term co-exposure of SLT and arsenic with poor nutritional status has immense potential to cause genotoxicity and oxidative stress in murine test system [7,8]. Previously Kausar and co-workers (2014) have found that consumption of SLT and pesticide exposure can cause changes in the buccal cell population and hematological parameters [9]. The alkaloids present in tobacco and related products have been found to cause genotoxicity and play a crucial role in tobacco-related carcinogenesis [10]. Nicotine is one of such major alkaloids detected in tobacco and related products. Chronic exposure to nicotine may lead to activation of growth-promoting path- ways and provide a suitable environment for the development of cancer and also hamper the activity of anticancer agents by activating survival * Corresponding author. E-mail addresses: girisarbani@gmail.com (S. Giri), barhoidharamesh@gmail.com (D. Barhoi), sweetynath91@gmail.com (S. Nath Barbhuiya), rudha124@yahoo. com (A. Giri), das.samrat1985@gmail.com (S. Das), aparajita.das46@gmail.com (A. Das), himikasalam6@gmail.com (S.H. Devi), dolitalukdar@yahoo.com (D. Talukdar), poojaupadhaya97@yahoo.com (P. Upadhaya), langthasapimili@gmail.com (P. Langthasa), neelampandey05@gmail.com (N. Pandey), sup_riya6@ rediffmail.com (S. Singh). Contents lists available at ScienceDirect Mutation Research - Genetic Toxicology and Environmental Mutagenesis journal homepage: www.elsevier.com/locate/gentox https://doi.org/10.1016/j.mrgentox.2021.503349 Received 8 September 2020; Received in revised form 2 March 2021; Accepted 12 March 2021