14.7.3 Cardiovascular Disorders
Heart and its related organs are some among the main targets of toxic pollutants such
as dioxins and furans. Several studies have been performed to estimate the damage it
does to the cardiovascular system. Henríquez-Hernández et al. (2017) associated the
persistence of cardiovascular diseases to the levels of dioxins/furans through contamination from various dietary sources of food. Kopf and Walker (2009) reported
the reduced heart size, reduced blood flow to the heart and reduced contraction rate
in the heart in fish model studies. Thinner ventricle walls, extensive cardiac dilation
and reduced responsiveness to chronotropic stimuli were observed in the chicken
embryo. Cardiocyte proliferation and cardiovascular apoptosis was commonly seen
in all animal models exposed to higher levels of dioxins/furans.
Upregulation of several genes such as atrial natriuretic peptide (ANP), myosin
heavy chain beta (MHC-β), and endothelin 1 (ET-1) resulted in heart failure as well
as cardiac hypertrophy in mice models exposed to high doses of dioxins/furans
(Fujisawa et al. 2019). Exposure to dioxins and furans in humans has also resulted in
hypertension and cardiovascular diseases. Thackaberry et al. (2005) elaborated
about the heart-related ailments in mammals using mice models. The disruption of
aryl hydrocarbon receptors (AhR receptors) is the mechanism by which the toxicants
cause human congenital heart disorder. The direct correlation between the amounts
of exposure to body weight also plays an important role in the onset of several
cardiovascular diseases. Studies have also shown that the human embryo is less
sensitive to cardiovascular diseases which are induced by both dioxins and furans,
but the developmental exposure will result in serious cardiovascular diseases.
14.7.4 Neurological Disorders
Several forms of dioxins and furans have known to cause multiple neurodegenerative disorders in humans as well as wildlife and such diseases, which have been
studied over the past two decades. The direct target of dioxin compounds such as
2,3,7,8-TCDD decreases the effect of reactive oxygen species, thereby inhibiting the
proliferation of nervous system cells. Because of its extensive usage as pesticides,
hydraulic fluids, flame retardants, etc., dioxins and furans become easily
accumulated in the food chain and biomagnified easily. During the early 1970s,
the first study was carried out to understand the effects of dioxins and furans as a
neurotoxic agent since there was acute and chronic exposure of chlorinated
pesticides in the environment. After several studies, it is now established that dioxins
and furans have adverse effects on attacking the central nervous system and to have
neurobehavioral changes.
Fonnum and Mariussen (2009) reported the neurotoxic mechanisms (oxidative
stress, calcium homeostasis disturbance and neurotransmitter transport) associated
with environmental exposure of dioxins and furans. These chemicals directly target
and induce the phospholipase A2 mobilization and induce protein kinase C, thereby
creating oxidative stress to the nervous system (Fonnum and Mariussen 2009). They
14 Biological Implications of Dioxins/Furans Bioaccumulation in Ecosystems
411
Heart and its related organs are some among the main targets of toxic pollutants such
as dioxins and furans. Several studies have been performed to estimate the damage it
does to the cardiovascular system. Henríquez-Hernández et al. (2017) associated the
persistence of cardiovascular diseases to the levels of dioxins/furans through contamination from various dietary sources of food. Kopf and Walker (2009) reported
the reduced heart size, reduced blood flow to the heart and reduced contraction rate
in the heart in fish model studies. Thinner ventricle walls, extensive cardiac dilation
and reduced responsiveness to chronotropic stimuli were observed in the chicken
embryo. Cardiocyte proliferation and cardiovascular apoptosis was commonly seen
in all animal models exposed to higher levels of dioxins/furans.
Upregulation of several genes such as atrial natriuretic peptide (ANP), myosin
heavy chain beta (MHC-β), and endothelin 1 (ET-1) resulted in heart failure as well
as cardiac hypertrophy in mice models exposed to high doses of dioxins/furans
(Fujisawa et al. 2019). Exposure to dioxins and furans in humans has also resulted in
hypertension and cardiovascular diseases. Thackaberry et al. (2005) elaborated
about the heart-related ailments in mammals using mice models. The disruption of
aryl hydrocarbon receptors (AhR receptors) is the mechanism by which the toxicants
cause human congenital heart disorder. The direct correlation between the amounts
of exposure to body weight also plays an important role in the onset of several
cardiovascular diseases. Studies have also shown that the human embryo is less
sensitive to cardiovascular diseases which are induced by both dioxins and furans,
but the developmental exposure will result in serious cardiovascular diseases.
14.7.4 Neurological Disorders
Several forms of dioxins and furans have known to cause multiple neurodegenerative disorders in humans as well as wildlife and such diseases, which have been
studied over the past two decades. The direct target of dioxin compounds such as
2,3,7,8-TCDD decreases the effect of reactive oxygen species, thereby inhibiting the
proliferation of nervous system cells. Because of its extensive usage as pesticides,
hydraulic fluids, flame retardants, etc., dioxins and furans become easily
accumulated in the food chain and biomagnified easily. During the early 1970s,
the first study was carried out to understand the effects of dioxins and furans as a
neurotoxic agent since there was acute and chronic exposure of chlorinated
pesticides in the environment. After several studies, it is now established that dioxins
and furans have adverse effects on attacking the central nervous system and to have
neurobehavioral changes.
Fonnum and Mariussen (2009) reported the neurotoxic mechanisms (oxidative
stress, calcium homeostasis disturbance and neurotransmitter transport) associated
with environmental exposure of dioxins and furans. These chemicals directly target
and induce the phospholipase A2 mobilization and induce protein kinase C, thereby
creating oxidative stress to the nervous system (Fonnum and Mariussen 2009). They
14 Biological Implications of Dioxins/Furans Bioaccumulation in Ecosystems
411