Introduction to Endocrine Disrupting Chemicals

are at least partially caused through cholinesterase- and endocannabinoid- signaling
(111). The neurotransmitter acetylcholine is involved in signaling of nerve cells
in the brain, and it is metabolized by the enzyme cholinesterase. The endocannabinoid
pathways of the brain are also important for neural functions. This is why
chlorpyrifos’s most potent effects are on the brain. Developmental exposures to
chlorpyrifos at levels typically observed in people caused hyperactivity and reduced
learning in rodents, the latter associated with changes in thyroid hormone (112,
113). Additional endocrine disruption by chlorpyrifos is suggested by changes in
the endocrine adrenal gland weight and structure in rodent experiments.
Cholinergic symptoms, e.g. salivation, urination, defecation, gastrointestinal
distress, and vomiting that are caused by nervous system damage, are present in
acute chlorpyrifos poisonings of adult people, and nerve damage was observed
weeks later. Adult agricultural workers use OP pesticides as mixtures, and workers
with moderate OP exposure, inclusive of chlorpyrifos, also have signs of neurotoxicity,
such as impaired peripheral nervous system function (114). Two studies of US
residents exposed to mixtures of pesticides found that chlorpyrifos was associated
with Parkinson’s disease (115, 116). Although it is difficult to find human studies
that have examined the neurotoxicity effects of chlorpyrifos in isolation from other
pesticides, a study of chlorpyrifos applicators found they did not perform as well
on neurological tests compared to people with much lower chlorpyrifos exposure
(117). They also reported memory problems, fatigue, and loss of muscle strength
(117).
Developmental susceptibility appears to be an important risk factor for human
neurotoxicity associated with exposure to chlorpyrifos. Indeed the majority of scientific
experts on a scientific panel on chlorpyrifos toxicity agreed that chlorpyrifos
should be banned from home use due to resulting neurodevelopment defects (92).
For example, prenatal and childhood chlorpyrifos exposures are linked to attention
deficit hyperactivity disorder, and impaired mental- and motor- skill development
in young children (92, 110). Extensive animal studies also support a strong
role of chlorpyrifos in causing neurotoxicity during development * (118).
Emerging experimental evidence indicates that developmental exposure to chlorpyrifos
also alters the regulation of lipid and glucose metabolism. Developing rats
exposed to doses comparable to levels typical in people had elevated cholesterol,
triglycerides, and insulin in adulthood (119). These findings raise the possibility
that people exposed to chlorpyrifos would have increased risk of type 2 diabetes
and cardiovascular disease. To date, this prediction has not yet been evaluated in
well-designed human studies.
* http://www.panap.net/sites/default/files/monograph-chlorpyrifos.pdf
Introduction to EDCs (December 2014) 43