Arsenic is a key environmental toxicant having significant impacts on human health. Millions of people in developing countries such as Bangladesh, Mexico, Taiwan, and India are affected by arsenic contamination through groundwater. Environmental contamination of arsenic leads to leads to various types of cancers, coronary and neurological ailments in human. There are several sources of arsenic exposure such as drinking water, diet, wood preservatives, smoking, air and cosmetics, while, drinking water is the most explored route. Inorganic arsenic exhibits higher levels of toxicity compared its organic forms. Exposure to inorganic arsenic is known to cause major neurological effects such as cytotoxicity, chromosomal aberration, damage to cellular DNA and genotoxicity. On the other hand, long-term exposure to arsenic may cause neurobehavioral effects in the juvenile stage, which may have detrimental effects in the later stages of life. Thus, it is important to understand the toxicology and underlying molecular mechanism of arsenic which will help to mitigate its detrimental effects. The present review focuses on the epidemiology, and the toxic mechanisms responsible for arsenic induced neurobehavioral diseases, including strategies for its management from water, community and household premises. The review also provides a critical analysis of epigenetic and transgenerational modifications, mitochondrial oxidative stress, molecular mechanisms of arsenic-induced oxidative stress, and neuronal dysfunction.

Air pollution is an immense problem due to its detrimental health effects on human populations. This study investigates the distribution of particle-bound heavy metals and associated health risks in three diverse areas (Durgapur as an industrial complex, Kolkata as an urban area, and Bolpur as a semi-urban region) in West Bengal, India. Twenty-one (84 samples) sampling sites were chosen, covering industrial, traffic, residential, and sensitive zones. The respirable suspended particulate matter (RSPM) samples were collected using a portable Mini-Vol Tactical Air Sampler, and heavy metal concentrations (Cd, Cr, Mn, Ni, Pb, and As) were analyzed using ICP-OES. The non-carcinogenic and carcinogenic health risks were assessed using exposure concentration (EC), hazard quotient (HQ), hazard index (HI), and additional lifetime cancer cases. The results highlight variations in heavy metal concentrations across the regions, with industrial areas exhibiting higher levels. Principal component analysis (PCA) unveiled distinct metal co-variation patterns, reflecting sources such as industrial emissions, traffic, and natural contributors. The sum of non-carcinogenic risks (HI) of all heavy metals exceeded the US EPA’s risk limit (HI<1) in both Kolkata and Durgapur, except for Bolpur. Similarly, the sum of cancer risk in three distinct areas exceeded the USEPA limits (1.00E-06). The Monte Carlo simulation revealed the 5th and 95th percentile range of cancer risk was 9.12E-06 to 1.12E-05 in Bolpur, 3.72E-05 to 4.49E-05 in Durgapur and 2.13E-05 to 2.57E-05 in Kolkata. Kolkata had the highest additional lifetime cancer cases compared to Bolpur and Durgapur. This study provides information on the complex connections between heavy metal pollution and possible health risks in industrial, urban, and semi-urban regions.

Selenium (Se) is an essential element, but causes toxic effects in fish at a slightly elevated level beyond the threshold. However, the degree of Se t