Cancer is characterized by cell proliferation, prevention or bypass of
programmed cell death, genomic instability, angiogenesis, invasion and metastasis
which are influenced by environmental pollutants. It is the major cause of death in
world wide. Lifestyle factors such as diet, smoking and use of alcohol are responsible
for the development of cancer in a large part of the population of developed countries.
Existence of carcinogens or co-carcinogens in polluted air and drinking water, as well
as in food, played a significant contribution in our country. Endocrine disrupters
modify the risk of breast, endometrial and prostate cancer. Laryngeal, oropharyngeal,
hypopharyngeal, sinonasal, nasopharyngeal, oral and lung cancer are positively
associated with smoking and air pollutants. Tobacco smoking induces DNA adducts
formation which is responsible for mutations at K-RAS and TP53 gene in the lung and
pancreatic adenocarcinomas. Tobacco smoking induces promoter hypermethylation of
p16 and DAPK genes in Non-Small Cell Lung Cancer (NSCLCs). Aflatoxin B1
(AFB1) causes promoter hypermethylation of tumour-suppressor genes RASSF1,
MGMT, and p16 in human hepatocellular carcinoma (HCC) patients. Down-regulation
of p15, p16, PRKG1, PARD3, and EPHA8 genes at mRNA level due to
hypermethylation and increased expression of STAT3, IFNGR1 at mRNA level due to
hypomethylation were reported in patients having benzene exposure. Methylationinduced
transcriptional inactivation of tumor suppressor genes, including p53,
CDKN2A (p16INK4A), Ras association domain family member 1 (RASSF1A), and
death-associated protein kinase (DAPK) were reported in arsenic exposed individuals.
The genetic and epigenetic alterations respond to environmental carcinogens have
significant contribution for biomarker development in assessment of health risk.
Keywords: Arsenic Contamination, Asbestos, Benezene, Biomarkers, Bisphenol
A, Cadmium, Cancer, DNA Methylation, Dioxins, Endocrine Disruptors, Gene
Mutations, Inflammation, miRNA Alterations, Pesticides, PAHs, Tobacco, Tumor
Microenvironment, Tumorigenesis.
