Lead is a nonessential metal which enters the body through various means and is considered as one of the most common health toxins. Several cases of lead poisoning are reported as a result of inhalation or ingestion of lead in employees working as painters, smelters, electric accumulator manufacturers, compositors, auto mechanics, and miners. In addition to occupational lead exposure, several cases of lead poisoning are reported in the general population through various sources and pathways. Innumerable signs and symptoms of lead poisoning observed are subtle and depend on the extent and duration of exposure. The objective of this review article is to discuss occupationally and nonoccupationally exposed lead poisoning cases reported in India and the associated symptoms, mode of therapy, and environmental intervention used in managing these cases. Lead poisoning cases cannot be identified at an early stage as the symptoms are very general and mimic that of other disorders, and patients might receive only symptomatic treatment. Knowledge about the various symptoms and potential sources is of utmost importance. Medical practitioners when confronted with patients experiencing signs and symptoms as discussed in this article can speculate the possibility of lead poisoning, which could lead to early diagnosis and its management.

Bisphenol A (BPA) is an industrial chemical used extensively to manufacture polycarbonate plastics and epoxy resins. Because of its estrogen-mimicking properties, BPA acts as an endocrine-disrupting chemical. It has gained attention due to its high chances of daily and constant human exposure, bioaccumulation, and the ability to cause cellular toxicities and diseases at extremely low doses. Several elegant studies have shown that BPA can exert cellular toxicities by interfering with the structure and function of mitochondria, leading to mitochondrial dysfunction. Exposure to BPA results in oxidative stress and alterations in mitochondrial DNA (mtDNA), mitochondrial biogenesis, bioenergetics, mitochondrial membrane potential (MMP) decline, mitophagy, and apoptosis. Accumulation of reactive oxygen species (ROS) in conjunction with oxidative damage may be responsible for causing BPA-mediated cellular toxicity. Thus, several reports have suggested using antioxidant treatment to mitigate the toxicological effects of BPA. The present literature review emphasizes the adverse effects of BPA on mitochondria, with a comprehensive note on the molecular aspects of the structural and functional alterations in mitochondria in response to BPA exposure. The review also confers the possible approaches to alleviate BPA-mediated oxidative damage and the existing knowledge gaps in this emerging area of research.