companies are producing DDT. The primary supporting evidence for adverse health
effects in humans comes from an epidemiological study performed by Rogan in
North Carolina [10] in which blood levels of DDE (a metabolite of DDT) were
determined in pregnant women. Once the blood levels were determined for each
woman, neurologic testing was then performed on the infants that were born from
these pregnancies. A very strong correlation was found linking increased blood
levels of DDE with poor performance of the neurologic tests by these infants
[10, 11]. Strong correlation of maternal serum levels of DDE, a metabolite of
DDT, with defects in muscular tone and hyporeflexia was observed in their children.
More convincing evidence of endocrine effects has been observed in an ecological
setting [12–14]. The initial reports were of egg shell thinning in bald eagles as well
as vitellogenin (a protein that is normally only produced in the livers of female
amphibians and fish) production in male African clawed frogs [12]. Primary exposure routes for humans are inhalation, ingestion, and dermal contact.
In spite of the 1972 ban of DDT in the USA, human exposure to DDT is
potentially high due to its prior extensive use and the persistence of DDT and its
metabolites in the environment. DDT has been detected in air, rain, soil, water,
animal and plant tissues, food, and work environment [9]. Breakdown products in
the soil environment are DDE and DDD, which are also highly persistent. Due to its
extremely low solubility in water, DDT is mainly retained by soils and soil fractions
with higher proportions of soil organic matter. While it is generally immobile or only
very slightly mobile, DDT may leach into groundwater over long periods of time.
DDT may reach surface waters primarily by runoff, atmospheric transport, drift, or
direct application. DDT has been widely detected in ambient surface water sampling
in the USA at a median level of one ng/L (nanogram per liter equal part per trillion).
DDT is regulated by EPA under the Clean Water Act (CWA). Effluent discharge
guidelines and water quality criteria have been set under the CWA [9].
3.1.2 Endosulfan
Endosulfan is a chlorinated hydrocarbon insecticide which acts as a poison for a
wide variety of insects and mites on contact. Although it may be used as a wood
preservative, it is used primarily on a wide variety of food crops, including tea,
coffee, fruits, and vegetables, as well as on rice, cereals, maize, sorghum, or other
grains. Human exposure to endosulfan is primarily through breathing air, drinking
water, eating food, or working where endosulfan is used. Exposure to endosulfan
mainly affects the central nervous system [15]. The effects of long-term/low-dose
exposure are unknown. The most convincing evidence of endocrine effects in
mammals is taken from laboratory animal studies in which doses of 5 mg/kg/d
resulted in reduced sperm counts and altered testicular enzyme levels in male
rats [9].
4 Endocrine Disruptors
177
effects in humans comes from an epidemiological study performed by Rogan in
North Carolina [10] in which blood levels of DDE (a metabolite of DDT) were
determined in pregnant women. Once the blood levels were determined for each
woman, neurologic testing was then performed on the infants that were born from
these pregnancies. A very strong correlation was found linking increased blood
levels of DDE with poor performance of the neurologic tests by these infants
[10, 11]. Strong correlation of maternal serum levels of DDE, a metabolite of
DDT, with defects in muscular tone and hyporeflexia was observed in their children.
More convincing evidence of endocrine effects has been observed in an ecological
setting [12–14]. The initial reports were of egg shell thinning in bald eagles as well
as vitellogenin (a protein that is normally only produced in the livers of female
amphibians and fish) production in male African clawed frogs [12]. Primary exposure routes for humans are inhalation, ingestion, and dermal contact.
In spite of the 1972 ban of DDT in the USA, human exposure to DDT is
potentially high due to its prior extensive use and the persistence of DDT and its
metabolites in the environment. DDT has been detected in air, rain, soil, water,
animal and plant tissues, food, and work environment [9]. Breakdown products in
the soil environment are DDE and DDD, which are also highly persistent. Due to its
extremely low solubility in water, DDT is mainly retained by soils and soil fractions
with higher proportions of soil organic matter. While it is generally immobile or only
very slightly mobile, DDT may leach into groundwater over long periods of time.
DDT may reach surface waters primarily by runoff, atmospheric transport, drift, or
direct application. DDT has been widely detected in ambient surface water sampling
in the USA at a median level of one ng/L (nanogram per liter equal part per trillion).
DDT is regulated by EPA under the Clean Water Act (CWA). Effluent discharge
guidelines and water quality criteria have been set under the CWA [9].
3.1.2 Endosulfan
Endosulfan is a chlorinated hydrocarbon insecticide which acts as a poison for a
wide variety of insects and mites on contact. Although it may be used as a wood
preservative, it is used primarily on a wide variety of food crops, including tea,
coffee, fruits, and vegetables, as well as on rice, cereals, maize, sorghum, or other
grains. Human exposure to endosulfan is primarily through breathing air, drinking
water, eating food, or working where endosulfan is used. Exposure to endosulfan
mainly affects the central nervous system [15]. The effects of long-term/low-dose
exposure are unknown. The most convincing evidence of endocrine effects in
mammals is taken from laboratory animal studies in which doses of 5 mg/kg/d
resulted in reduced sperm counts and altered testicular enzyme levels in male
rats [9].
4 Endocrine Disruptors
177