Speaker Biography

Chanda Siddoo-Atwal

Canada

Title: A role for heavy metal toxicity and air pollution in respiratory tract cancers

Biography:

Chanda Siddoo-Atwal,  completed her B.Sc. in Biochemistry from the University of London. Her Ph.D. was taken in Applied Sciences from Simon Fraser University in Burnaby (her research conducted at the BC Cancer Research Centre) and she did a Post-doctoral fellowship in the Biochemistry Department at the Medical College of Wisconsin. Cancer is her subject of specialization and started with research on Ataxia-telangiectasia (AT) patients, who are genetically prone to lymphomas. Since then, she has focussed mainly on mechanisms of carcinogenesis in various models including the AT disease state and ionizing radiation-induced cancer, mycotoxin-induced and chemically-induced cancers, microwave-induced cancers, and ultraviolet radiation-induced skin cancer. She is the President and Primary Biochemist of Moondust Cosmetics Ltd and her current research activity includes the formulation of a novel sunscreen to combat apoptotic sunburn that has been associated with skin cancer and other suncare products for the repair of skin damage related to sun exposure. She has been invited to present her research papers at conferences around the world and is the author of a recent book called, “A New Approach to Cancer Risk Assessment: An Overview” published by Lambert Academic Publishing. In addition, she has been asked to contribute chapters to textbooks by various international publishers including Springer and INTECH. Recently, she received a Drishti Award in recognition of her scientific contribution and commitment to education in the sunscreen industry.

Abstract:

Cigarette smoke and air pollution have been associated with lung cancer and nasopharyngeal and laryngeal cancer, respectively. Significant concentrations of select heavy metals including lead and cadmium have been isolated in popular cigarette brands and these heavy metals can be inhaled via smoking. Lead is able to mimic the activity of calcium in the human body thereby leading to toxic effects in a variety of target organs. These biochemical effects include the calcium-dependent inhibition of release of several neurotransmitters and augmentation of calcium-dependent events involving protein kinase C and calmodulin. Lead perturbs and alters the release of intracellular calcium stores from organelles like the endoplasmic reticulum (ER) and mitochondria. Mitochondrial calcium accumulation and resultant membrane depolarization due to its release have been linked to the initiation of a cell death pathway in mitochondria. A rise in mitochondrial calcium also stimulates the generation of reactive oxygen species (ROS) and free fatty acids which can further promote calcium release and, ultimately, result in cell death. In the case of cadmium, the renal proximal tubule of the kidney accumulates freely filtered and metallothionein bound metal, which is degraded in endosomes and lysosomes. This results in the release of free cadmium into the cytosol where it can generate reactive oxygen species and activate cell death pathways. In developing countries, indoor air pollution due to the domestic use of unprocessed biomass fuels such as wood, dung, and coal is another cause of respiratory tract cancers in humans. In some developed countries such as Australia and Canada, the alarming increase in forest fire frequency due to climate-change and the associated smoke released into the environment is also likely to pose a future human health risk. Polycyclic organic particles in biomass and forest fire smoke can include carcinogens such as benzo[a]pyrene, which is also found in cigarette smoke. Benzo[a]pyrene can induce apoptosis in mammalian cells by initiating mitochondrial dysfunction; activating the intrinsic caspase pathway (caspase-3 and caspase-9); and, via p53 activation. The constitutive activation of apoptotic pathways has been linked to carcinogenesis in a number of cancer models.