Endocrine-Disrupting Pesticides - Pesticides: Evaluation of Environmental Pollution - page 620

term risks of early exposure to organohalogens. Several of the mechanisms involved are
similar to those of polychlorinated biphenyls (PCBs), each group also works via own spe-
cific pathways. The fact that persistent organohalogens can amplify the neurotoxic effects
of other environmental pollutants such as heavy metals further increases their risk for
human and animal neurodevelopment.
Benotti et al. (2009) have described results of a comprehensive survey of 20 pharmaceu-
ticals, 25 known or potential EDCs and 6 other water contaminants including atrazine in
source water, finished drinking water, and distribution system (tap) water from 19 US drink-
ing water treatment plants sampled during 2006-2007. The results provide an assessment
of the actual concentrations to which people are exposed from drinking water. Occurrence
data were used to propose a set of indication compounds that can predict the presence of
pharmaceuticals and EDCs as well as monitor the efficacy of treatment processes.
Ejaz et al. (2004) have developed a possible correlation between pesticides exposure and
growing incidences of cancer disrupting in Pakistan. They have claimed that majority of
endocrine-disrupting pesticides are carcinogenic. Farmers may therefore be at higher risk
for acute and chronic health effects associated with pesticides. Cancer of breast, ovary,
prostate, testis, and thyroid are hormone-dependent, which fostered research on the
potential risk associated with occupational and environmental exposure to the so-called
endocrine-disrupting pesticides. Professional as well as public exposure to pesticides
raises cancer risk. Interaction with adjuvant and with other toxicants increases the actual
risk. Furthermore, organochlorine pesticides and triazine herbicides require further inves-
tigation for possible etiologic role in some hormone-dependent cancers.
Prins (2008) has published commentary on increasing evidence both from epidemiology
studies and animal models that specific endocrine-disrupting compounds may influence
the development or progression of prostate cancer. In large part, these effects appear to be
linked to interference with estrogen signaling, either through interacting with estrogen
receptors (ERs) or by influencing steroid metabolism and altering estrogen levels within
the body. In humans, epidemiologic evidence links specific pesticides, PCBs, and inorganic
arsenic exposures to elevated prostate cancer risk. In animal models, there was also aug-
mentation of prostate carcinogenesis with several other environmental estrogenic com-
pounds including cadmium, UV filters, and bisphenol A. He has concluded that infants
and children may be considered a highly susceptible population for endocrine-disruptor
exposure and increased possible risk of prostate cancer with aging.
McKinlay et al. (2008) have reviewed the known routes of human pesticide exposure with
particular reference to endocrine-disrupting pesticides (EDPs). Many EDPs are harmful at
very low doses, especially if exposure occurs during sensitive stages of developments via
epigenetic changes. They also reviewed the available deterministic and probabilistic models
commonly used to calculate human exposure and the creation of more holistic models of
human pesticide exposure including a requirement for new quantitative data sets.
Eskenazi et al. (2007) have reported an adverse association of prenatal organophosphate
pesticide exposure as measured by dialkylphosphates (DAPs) with mental development
problems at 24 months of age.
20.9 Endocrine Action of DDT
As already discussed in paragraph 6, endocrine disruptors affect in many ways (Hester
and Harrison 1999).