Environmental Engineering Reference
In-Depth Information
in mammals (Ecobichon et al. 1990). Specifically, OP insecticides are potent
neurotoxicants.
iv. Reproductive effects : A number of pesticides clearly have the potential to cause
reproductive toxicity in animals, and several compounds (e.g., DBCP, EDB, chlor-
decone, carbaryl) are known to affect human reproduction (Mattison et al. 1990).
Kelce et al. (1995) demonstrated that the primary DDT metabolite, p,p′-DDE, inter-
feres with the action of male sex hormones, or androgens, suggesting that the
feminizing action of DDT resulted from the antiandrogenic action of the DDT
metabolite.
v. Infertility of men : It is well known that exposure to pesticides at occupational levels
can adversely affect the semen quality. In the late 1970s, the nematocide DBCP
affected more than 26,000 plantation workers in 12 countries; 64% had low sperm
concentrations and 28% were involuntarily childless (Slutsky et al. 1999). Ethylene
dibromide was an active component of approximately 100 pesticides. Its use was
severely restricted in 1984 because of reduced sperm counts and semen volume
in exposed workers (Schrader et al. 1988). More recently, a small study of herbi-
cide sprayers in Argentina showed decreased sperm concentration and morphol-
ogy related to high urinary levels of 2,4-D metabolites (Lerda and Rizzi 1991).
Pesticides may affect male fertility by several mechanisms, including induction
of developmental abnormalities of the male reproductive tract and by directly or
indirectly affecting the function of normally developed gonads. It can be of signif-
icance in this context to note that albeit endocrine disruption is currently regarded
as the prominent mechanism, whereby pesticides possibly mediate disruption of
male fertility, and also other mechanisms, including excessive radical oxygen spe-
cies (ROS) generation, may be involved (Meeker et al. 2004). It is noteworthy in
this respect that the sperm cells appear to be particularly vulnerable to ROS, being
deprived of the cytoplasmic defense enzyme with scavenging properties (Meeker
et al. 2004).
vii. Developmental effects : Mammalian developmental toxicity does not refer only to the
effects during in utero development, but also includes adverse effects on the devel-
oping organism that may have resulted from exposure of either parent before con-
ception, of the mother during prenatal development, or postnatal to the time of
sexual maturation. The embryo is most vulnerable to the initiation of major birth
defects between 3 weeks and 2 months of gestation, the critical period of organo-
genesis. Exposure to toxic chemicals during the first 2 weeks typically leads to
fetal death, while exposure after organogenesis is more likely to cause growth
retardation and functional deficits (Hodgson and Levi 1996). In humans and
rodents, exposure to hormonally active chemicals, such as methoxychlor (Gray
1992), DDT (Kelce et al. 1995), and vinclozolin (Gray et al. 1994), during the period
of sex differentiation can produce a wide range of abnormal sexual phenotypes,
including masculinized and defeminized females and feminized and demascu-
linized males.
vii. Endocrine disrupting effects : An endocrine disrupting chemical (EDC) is defined as
an exogenous substance that causes adverse health effects in an intact organism,
or its progeny, secondary to the changes in the endocrine function. Their effects
on humans, wildlife, and the environment have been the subject of much attention
by the international scientific community, since concerns about them were first
raised by Colborn et al. (1993). Recently, the potential of certain pesticides to act as
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