Effects of Pesticides on the Endocrine System

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Transcript Effects of Pesticides on the Endocrine System

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Effects of Pesticides on the
Endocrine System
Pesticide Health Effects Medical Education Database (PHEMED)
Definition
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Synthetic chemicals that mimic hormones
Disruption by:
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Receptors over-respond to the mimic
Receptors respond at inappropriate times
Block a receptor by competing with other hormones
Stimulate or inhibit the endocrine system causing
over or under production of natural hormones
(thyroid)
Chemicals with established links to
endocrine disruption
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DES – diethylstibesterol
Dioxins – CDD’s polychlorinated dioxins
PCB’s – polychlorinated biphenyls
DDT
mimics estrogen
 DDE (major byproduct) interferes with
testosterone function
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DES
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Vaginal CA in offspring of women taking DES as
morning after pill or during pregnancy to avert
SAB’s
DES daughters increased risk for infertility,
miscarriages, ectopic pregnancies.
DES sons: evidence of increased risk:
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undescended testicles
smaller penis size
poorer sperm quality
Dioxins
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Formed during:
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chlorine bleaching process at pulp and paper mills
chlorination of waster and water treatment
contaminant of chlorinated phenols (2,4,5-TCP, PCP)
chlorinated pesticides or herbicides (such as 2,4,5-T,
older 2,4-D, hexachlorophene, Silvex® ) none
currently in use
Agent Orange (combination of 2,4,5-T+ 2,4-D)
Interferes with sex hormones
PCB’s
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Persists in the environment + body (lipophylic)
Banned uses that would disperse PCB’s:
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Continued use in ‘closed systems’
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capacitors and insulating fluids in transformers
vacuum pump fluids and hydraulic fluids
Human exposure
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plasticizers in paints and cements
fire retardant fabric treatments
heat stabilizing additives for PVC electrical insulation
Adhesives/ paints and water-proofing
railway ties
appliances, fluorescent light fixtures, electrical equipment > 30 years
old
Contaminated food (contaminated fish, dairy, meat)
Air from hazardous waste sites
Workplaces where closed systems are repaired
Minics estrogen + interferes with thyroid hormones
Pesticides Suspected to be
Endocrine Disruptors
Herbicides:
2,4-D
Alachlor
Amitrole
Atrazine
Metribuzin
Nitrofen*
Trifluralin
http://www.nrdc.org/health/kids/ocar/chap5e.asp
Pesticides Suspected to be
Endocrine Disruptors
Fungicides:
Benomyl
Fenarimol
Mancozeb
Maneb
Vinclozolin
Metiram Zineb
Tributyltin Ziram
Fumigants:
DBCP*
http://www.nrdc.org/health/kids/ocar/chap5e.asp
Pesticides Suspected to be
Endocrine Disruptors
Insecticides:
Aldicarb
Aldrin*
Carbaryl
Chlordane*
Dicofol
Dieldrin*
Endosulfan
Endrin*
Fenvalerate
Heptachlor*
Kepone*
Lindane
Malathion
Methomyl
Methoxychlor
Mirex*
Parathion*
Pentachlorophenol
Permethrin
Toxaphene*
http://www.nrdc.org/health/kids/ocar/chap5e.asp
Health Effects of Endocrine Disruptors (ED’s)
in Humans
No firm causal evidence w/low exposure
 Suggestive relationship with :
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Reproduction
Endometriosis
Precocious puberty
Nural function
Immune function
Cancers: breast, endometrial, testicular, prostate,
thyroid
Source: WHO/IPCS. Global assessment of the state-of-the-science of
endocrine disruptors. WHO/PCS/EDC/02.2
Reproductive
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Decline in human sperm quality
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Impaired fertility and increased SAB’s
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Relationship to ED’s speculative
Declining sex ratios
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Meta analysis studies reached different conclusions
Not necessarily due to endocrine disrupters (ED’s)
Evidence of unidentified external causes but mechanism
unknown
Developmental male reproductive tract
abnormalities
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ED exposure evidence unclear
Experimental data with a number of chemicals
demonstrate they can disrupt male reproductive tracts.
Gynecological
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Endometriosis
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Association with ED reported but studies
equivocal
Precocious Puberty
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Concern regarding influence of ED’s on early
onset of puberty
Role of other factors such as nutrition needs
clarification
Neural Function
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Prenatal exposure to ED’s (PCB’s) result
in neurodevelopmental, behavioral and
neuro-endocrine function problems.
Human and animal data
Effects more likely a result of altered
thyroid or neuro-transmitters.
In most instances ED mechanism not
demonstrated
Immune Function
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Some ED’s alter human and animal
immunity
Unknown if these alterations due to an
endocrine mediated mechanism
Cancers of Hormonally Sensitive Organs
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Temporal association between rise in
hormone sensitive organ cancers and
wide spread use of industrial chemicals
Increase incidence not explained by
improved diagnostic techniques.
Hypothesis – is it from ED’s?
Breast Cancer
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Studies measuring DDE (DDT metabolite
stored in fat tissue) in adult women do not
support a causative relationship.
New study measuring the more active
p,p´-DDT metabolite in frozen blood from
women at delivery from the 1950’s show a
5 fold relationship. *
*Cohen et al. (2007) DDT and Breast Cancer in Young Women: New Data on the Significance of
Age at Exposure. EHP. 115(10) 1406-1414.
Other Cancers
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Endometrial - limited data – no causal
relationship established.
Prostate – some associations positive and
some negative. Mechanism unknown.
Testicular – temporal rise without link to
same time frame as use of ED’s
Thyroid – no direct link to ED exposure
has been demonstrated.
Future
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Adverse health outcomes appear biologically
plausible given:
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Known effects of endogenous and exogenous
hormones sensitive organs
Demonstrated effects on wildlife and laboratory
animals
They are a high priority research area is
required –
EPA required to screen products for potential
effects on the endocrine system
Other non-ED mechanisms must also be
explored