carcinogen” because even a very small dose can induce cancers. The main target
organ for this compound is studied to be liver, whereas other tissues such as thyroid,
lung and oral cavity were also found to be affected by cancer. The onset of cancer
because of dioxins and furans is almost 50% dependent on the sex of the organism.
In a standard hepatic carcinogenic study with mice and rats, male mice were most
affected by cancer, and on the other hand, female rats were most affected by cancer.
There are also several epidemiological case studies which reported the development
of cancer because of dioxins and furans contamination. One such study was done
with the population of Seveso, Italy, where the people were accidentally exposed to
remarkable doses of dioxins and furans in the year 1976. These people were exposed
to dioxins and furans nearly 100–1000 times compared with the general population.
Several types of cancers such as myeloma, lymphoma, sarcoma and liver cancer
were seen to be predominant among the groups of tested people of Seveso. In general
population, zero or no cases were seen attributing to dioxins and furans exposure.
There are several biochemical receptors in the human body that are majorly affected
by dioxins and furans. These include glucose transporter proteins, vitamin C uptake,
lipoprotein lipases, low-density lipoprotein receptor and insulin secretion receptor.
The mechanism of action of both dioxins and furans is that they directly change or
modify the key protein kinase activity by activating the mitotic signals. This
eventually modifies the nuclear transcription factors, thereby altering the primary
response genes through receptor-mediated mechanisms. The main role of such
nuclear transcription factors includes regulation of nutritional indexes and protection
of the hormone-sensitive genes. Besides this, dioxins and furans act on several
enzymes in the body such as cytochromes, estrogen receptors, interleukins and
cytokines. This leads to cellular oxidative stress and blockage in growth factors.
This ultimately leads to apoptosis which thereby results in the death of healthy cells.
Estrogen receptor-positive cases of breast cancer were directly associated with the
long-term airborne exposure of dioxins/furans (Danjou et al. 2019). Another mechanism by which dioxins and furans cause cancer effects in humans is by inducing both
cell proliferation and cell differentiation which leads to hypoplasia, hyperplasia,
metaplasia and neoplasia. All these forms of abnormalities are directly linked to
several types of cancers including Hodgkin disease, non-Hodgkin disease and
sarcoma. Effects of one of the most toxic forms of dioxin, TCDD, were studied on
rodents, which showed the development of several forms of tumours in thyroid, skin,
liver, lung, oral cavity and other tissues. It directly suppresses the immunity,
indirectly causing the carcinogenic effects. Tests conducted on animals are more
evident than that of humans that TCDD has the most carcinogenic effect among all
congeners of dioxin and furan families.
Xu et al. (2016) provided detailed epidemiological evidence about the carcinogenic effects of TCDD on the human hematopoietic system through several types of
cancers. The aryl hydrocarbon receptor mechanism of action by dioxins and furans is
the most accepted mechanism by which dioxins and furans cause carcinogenic
effects. Similarly, dioxins are known to upregulate the enzymes which regulate the
metabolic activity of several drugs which leads to an imbalance in hormone secretion. Wimmerová et al. (2016) assessed the human risk associated with dioxin
14 Biological Implications of Dioxins/Furans Bioaccumulation in Ecosystems
409
organ for this compound is studied to be liver, whereas other tissues such as thyroid,
lung and oral cavity were also found to be affected by cancer. The onset of cancer
because of dioxins and furans is almost 50% dependent on the sex of the organism.
In a standard hepatic carcinogenic study with mice and rats, male mice were most
affected by cancer, and on the other hand, female rats were most affected by cancer.
There are also several epidemiological case studies which reported the development
of cancer because of dioxins and furans contamination. One such study was done
with the population of Seveso, Italy, where the people were accidentally exposed to
remarkable doses of dioxins and furans in the year 1976. These people were exposed
to dioxins and furans nearly 100–1000 times compared with the general population.
Several types of cancers such as myeloma, lymphoma, sarcoma and liver cancer
were seen to be predominant among the groups of tested people of Seveso. In general
population, zero or no cases were seen attributing to dioxins and furans exposure.
There are several biochemical receptors in the human body that are majorly affected
by dioxins and furans. These include glucose transporter proteins, vitamin C uptake,
lipoprotein lipases, low-density lipoprotein receptor and insulin secretion receptor.
The mechanism of action of both dioxins and furans is that they directly change or
modify the key protein kinase activity by activating the mitotic signals. This
eventually modifies the nuclear transcription factors, thereby altering the primary
response genes through receptor-mediated mechanisms. The main role of such
nuclear transcription factors includes regulation of nutritional indexes and protection
of the hormone-sensitive genes. Besides this, dioxins and furans act on several
enzymes in the body such as cytochromes, estrogen receptors, interleukins and
cytokines. This leads to cellular oxidative stress and blockage in growth factors.
This ultimately leads to apoptosis which thereby results in the death of healthy cells.
Estrogen receptor-positive cases of breast cancer were directly associated with the
long-term airborne exposure of dioxins/furans (Danjou et al. 2019). Another mechanism by which dioxins and furans cause cancer effects in humans is by inducing both
cell proliferation and cell differentiation which leads to hypoplasia, hyperplasia,
metaplasia and neoplasia. All these forms of abnormalities are directly linked to
several types of cancers including Hodgkin disease, non-Hodgkin disease and
sarcoma. Effects of one of the most toxic forms of dioxin, TCDD, were studied on
rodents, which showed the development of several forms of tumours in thyroid, skin,
liver, lung, oral cavity and other tissues. It directly suppresses the immunity,
indirectly causing the carcinogenic effects. Tests conducted on animals are more
evident than that of humans that TCDD has the most carcinogenic effect among all
congeners of dioxin and furan families.
Xu et al. (2016) provided detailed epidemiological evidence about the carcinogenic effects of TCDD on the human hematopoietic system through several types of
cancers. The aryl hydrocarbon receptor mechanism of action by dioxins and furans is
the most accepted mechanism by which dioxins and furans cause carcinogenic
effects. Similarly, dioxins are known to upregulate the enzymes which regulate the
metabolic activity of several drugs which leads to an imbalance in hormone secretion. Wimmerová et al. (2016) assessed the human risk associated with dioxin
14 Biological Implications of Dioxins/Furans Bioaccumulation in Ecosystems
409