Cobaltous 2-ethylhexanoate (cobalt octoate) is an accelerator in the polyester resins. There have been several reports of allergic contact dermatitis resulting from cobaltous 2-ethylhexanoate. It was demonstrated, that cobalt octoate induced DNA strand breakage in vitro (in human cells), but the damage appeared to be explained by oxidative damage resulting from reactive oxygen species, probably caused by the cobalt cation.

AFLATOXIN M1 is a 4-hydroxylated metabolite of AFLATOXIN B1, one of the MYCOTOXINS from ASPERGILLUS tainted food. It is associated with liver damage and cancer resulting from its P450 activation to the epoxide which alkylates DNA. Toxicity depends on the balance of liver enzymes that activate it (CYTOCHROME P-450) and others that detoxify it (GLUTATHIONE S TRANSFERASE). Primates and rat are sensitive while mouse and hamster are tolerant. Aflatoxin M1 (AFM1) is associated with carcinogenicity, genotoxicity, mutagenicity, and teratogenicity and as a result, represents a human health problem worldwide.

Aflatoxin G1 ((7aR,10aS)-3,4,7a,10a-tetrahydro-5-methoxy-1H,12H-furo[3',2':4,5]furo[2,3-h]pyrano[3,4-c][1]benzopyran-1,12-dione) is a food contaminant produced by various species of the common soil fungus, Aspergillus and is associated with toxicity and hepatocarcinogenicity in human and animal populations. Epidemiological studies have shown that Aflatoxin G1 is one of the most frequently detected contaminating mycotoxins in grains and foodstuffs in areas with high-incidence of lung and esophageal cancer

Aflatoxins consist of a group of approximately 20 related fungal metabolites, although only aflatoxins B1, B2, G1 and G2 are normally found in foods. Aflatoxin G2 was established as the dihydroxy derivative of Aflatoxin G1. Aflatoxin G2 is a minor mycotoxin produced by Aspergillus flavus Aflatoxin G2 belongs to the family of Difurocoumarolactone Series. The main target organ in mammals is the liver so aflatoxicosis is primarily a hepatic disease. Protracted exposure to aflatoxins may cause liver damage and necrosis, cholestasis, and hepatomas. Moreover, protracted exposure to aflatoxins has been associated with hepatocellular carcinoma, acute hepatitis, Reye's syndrome, bile duct cell proliferation, periportal fibrosis, hemorrhages, mucous membrane jaundice, fatty liver changes, cirrhosis in malnourished children, and kwashiorkor. However, aflatoxins accumulate in the presence of liver disease, and the association with hepatic cancer is confounded by the occurrence of hepatitis-B. Thus, it is not clear in these various instances whether aflatoxin is a primary cause of the disease, is an innocent bystander which accumulates secondary to the disease process, or is a contributing cause in conjunction with other factors. It is also mutagenic and teratogenic. Inhaled aflatoxins may produce pulmonary adenomatosis. Aflatoxins modify the immune system by affecting antibody formation, complement, cell-mediated immunity, and phagocytosis.

N‑Nitrosonornicotine (NNN) is a nitrosamine compound. It is produced by nitrosation of nicotine during the curing, aging, processing, and smoking of tobacco. About half of the NNN originates in the unburnt tobacco, whereas the remainder is formed during burning. NNN is reasonably anticipated to be a human carcinogen based on sufficient evidence of carcinogenicity from studies in experimental animals. NNN induces deleterious mutations in oncogenes and tumor suppression genes by forming DNA adducts, which could be considered as tumor initiation. Meanwhile, the binding of NNN to the nicotinic acetylcholine receptor promotes tumor growth by enhancing and deregulating cell proliferation, survival, migration, and invasion, thereby creating a microenvironment for tumor growth.

Lucidin-3-O-primeveroside (LuP) is an anthraquinone derivative present in Rubia tinctorum L. (madder root), which has been used as a coloring agent and food additive. LuP can be metabolically converted to genotoxic compound lucidin, which subsequently forms lucidin-specific N2-2'-deoxyguanosine (N2-dG) and N6-2'-deoxyadenosine (N6-dA) DNA adducts. Lucidin is mutagenic and carcinogenic in rodents but has low carcinogenic risks in humans. Lucidin adduct destabilizes DNA structure and reduces fidelity and processivity of DNA synthesis.