adipose tissue without manifestation of toxicity. For this reason, obesity in
humans is considered protective against chronic toxicity of these chemicals.
Similarly, the body fat in a well-fed animal is known to store organochlorine
pesticides. Fat mammals, fish, and birds are thus more resistant to DDT
poisoning than their thinner counterparts. In times of food deprivation,
however, organic chemicals, such as DDT and PCB, may be mobilized from
their fat deposits and reach concentrations potentially toxic to the animal.
A recent report by the U.S. Institute of Medicine (IOM), stating the need to
reduce saturated fat intake among the population as a means of reducing
human exposure to dioxins, raises another concern about the toxicants. The
report points out that saturated fats are a key source of human exposure to
dioxins. Dioxins are a collection of more than 200 related compounds that may
be linked to hormonal changes, neurodevelopmental problems in children, and
cancer, in addition to other effects. They are ubiquitous agents that
contaminate food as they cycle through the biosphere. Because dioxins are
lipid soluble, they accumulate in many varieties of foods. According to the
IOM, saturated fats in meat, dairy products, and certain species of fish are the
biggest sources of human exposure to these chemicals.
20
The role of dietary lipids in affecting pollutant toxicity has been fairly well
defined for a few specific chemicals, including lead (Pb), fluoride, and
hydrocarbon carcinogens. For example, high-fat diets are known to increase
Pb absorption and retention. Moreover, competitive absorption of Pb and
calcium (Ca) also occurs, which is probably due to competition for the Cabinding protein (CaBP) whose synthesis is mediated by vitamin D, a fat-soluble
vitamin. Studies have shown that a high-fat diet causes increased body burden
of fluoride, resulting in higher toxicity. This is attributed to the delay of gastric
emptying caused by high fat levels. Consequently, enhanced fluoride absorption may occur, leading to increased body burden of fluoride. Dietary fat does
not increase metabolic toxicity of fluoride itself, however. As is well-known,
AFB 1 is a potent liver cancer-causing agent. A high-fat diet offers protection
from lethal effects of the toxin, presumably through dissolution of the
carcinogen.
5.8.6 VITAMIN A
Many reports describe vitamin A and its synthetic analogues as a potential
factor in the prevention and treatment of some cancers. There is growing
evidence that vitamin A may also alleviate pollutant toxicity. Epidemiological
studies using a cohort of 8000 men showed a low incidence of lung cancer in
those with a high level of vitamin A in their diet, while incidence was higher in
individuals with a diet with low levels of vitamin A . In experimental studies,
rats exposed to PCB, DDT, and dieldrin showed a 50% reduction in the liver
vitamin A store. In other studies, rats deficient in vitamin A exhibited lowered
cytochrome P450 activity in the liver. The effect of vitamin A deficiency on
MFO enzymes, however, depends on several factors, such as substrate, tissue,
and animal species. Recent studies have demonstrated that rats exposed to
76
Environmental Toxicology
[16:54 26/8/04 P:/CRC PRESS/4365 MING-HO.751 (1670)/4365-005.3d]
Ref: 4365 MING-HO YU Chap-005 Page: 76 65-84
humans is considered protective against chronic toxicity of these chemicals.
Similarly, the body fat in a well-fed animal is known to store organochlorine
pesticides. Fat mammals, fish, and birds are thus more resistant to DDT
poisoning than their thinner counterparts. In times of food deprivation,
however, organic chemicals, such as DDT and PCB, may be mobilized from
their fat deposits and reach concentrations potentially toxic to the animal.
A recent report by the U.S. Institute of Medicine (IOM), stating the need to
reduce saturated fat intake among the population as a means of reducing
human exposure to dioxins, raises another concern about the toxicants. The
report points out that saturated fats are a key source of human exposure to
dioxins. Dioxins are a collection of more than 200 related compounds that may
be linked to hormonal changes, neurodevelopmental problems in children, and
cancer, in addition to other effects. They are ubiquitous agents that
contaminate food as they cycle through the biosphere. Because dioxins are
lipid soluble, they accumulate in many varieties of foods. According to the
IOM, saturated fats in meat, dairy products, and certain species of fish are the
biggest sources of human exposure to these chemicals.
20
The role of dietary lipids in affecting pollutant toxicity has been fairly well
defined for a few specific chemicals, including lead (Pb), fluoride, and
hydrocarbon carcinogens. For example, high-fat diets are known to increase
Pb absorption and retention. Moreover, competitive absorption of Pb and
calcium (Ca) also occurs, which is probably due to competition for the Cabinding protein (CaBP) whose synthesis is mediated by vitamin D, a fat-soluble
vitamin. Studies have shown that a high-fat diet causes increased body burden
of fluoride, resulting in higher toxicity. This is attributed to the delay of gastric
emptying caused by high fat levels. Consequently, enhanced fluoride absorption may occur, leading to increased body burden of fluoride. Dietary fat does
not increase metabolic toxicity of fluoride itself, however. As is well-known,
AFB 1 is a potent liver cancer-causing agent. A high-fat diet offers protection
from lethal effects of the toxin, presumably through dissolution of the
carcinogen.
5.8.6 VITAMIN A
Many reports describe vitamin A and its synthetic analogues as a potential
factor in the prevention and treatment of some cancers. There is growing
evidence that vitamin A may also alleviate pollutant toxicity. Epidemiological
studies using a cohort of 8000 men showed a low incidence of lung cancer in
those with a high level of vitamin A in their diet, while incidence was higher in
individuals with a diet with low levels of vitamin A . In experimental studies,
rats exposed to PCB, DDT, and dieldrin showed a 50% reduction in the liver
vitamin A store. In other studies, rats deficient in vitamin A exhibited lowered
cytochrome P450 activity in the liver. The effect of vitamin A deficiency on
MFO enzymes, however, depends on several factors, such as substrate, tissue,
and animal species. Recent studies have demonstrated that rats exposed to
76
Environmental Toxicology
[16:54 26/8/04 P:/CRC PRESS/4365 MING-HO.751 (1670)/4365-005.3d]
Ref: 4365 MING-HO YU Chap-005 Page: 76 65-84