Health Effects of Pyrethrin Pesticides on People,
Animals, Fish, and Beneficial Insects: Review
B. Windham (Ed.) 2020
Pyrethroid Pesticides are documented to be Endocrine
Disrupting Chemicals and to Commonly Cause Harm to People, Bees,
Fish, Cats, and other animals. Chronic exposure can result in
serious chronic neurological effects in addition to acute allergic reactions
and immune effects. Those most commonly and significantly affects are the
elderly, people with chronic health conditions such as
multiple chemical sensitivity
or chronic
neurological conditions, children, pregnant women, and especially the
developing fetus during organ development (12). Pyrethrin pesticides are
documented to be genotoxic (19b).
Pyrethroid pesticides are synthetic compounds developed to be
similar to the pyrethrin pesticides that are developed from
chrysanthemum flowers. Other ingredients such
as piperonyl butoxide are usually added to increase the
lethality of the pesticide to insects. Piperonyl butoxide(PBO) is a
potent
cytochrome P450
and non-specific esterase
inhibitor. This families of these
enzymes
act as the
principal detoxification pathways for many pesticides. Inhibiting the
detoxification pathway allows higher unmetabolized systemic
concentrations of the active insecticide to remain within the target animal for
a longer period. Cytochrome P450 enzymes are present in most
tissues of the body, and play important roles in
hormone
synthesis and
breakdown (including
estrogen
and
testosterone
synthesis and
metabolism),
cholesterol
synthesis, and
vitamin D
metabolism. Cytochrome P450
enzymes also function to metabolize potentially toxic compounds,
including
drugs
and products
of endogenous metabolism such as
bilirubin
, principally in
the
liver
. Health
effects of PBO are primarily through its effects on
the Cytochrome P450 function and its synergistic effect with
pesticides, having much more effect synergistically than alone. In
2004 the EPA Agency reviewed Poison Control Center data covering the years 1993
through 1998, andconcluded that there was a greater risk of moderate or
major symptoms among those exposed to products
containing pyrethrins and piperonyl butoxide (PBO)
than those exposed to pyrethrins alone. PBO is a pesticide synergist,
which is often co-formulated with the pyrethrins active ingredient to
increase the insecticidal potency of the active ingredient. The data also
indicated that respiratory symptoms (bronchospasm, coughing or choking,
or dyspnea) and selected dermal symptoms (dermal irritation, pain,
itching, or rash) were more likely if the exposure included PBO (Blondell,
2004) (1)
An EPA review (1) of pyrethrin pesticide
effects on animals includes dose-response data that have been recently
generated demonstrating consistent findings for low-dose, acute, oral exposure
to pyrethroids in small rodents.
All pyrethroidstested
(i.e.,
about twenty compounds), regardless of structure,
produce a decrease in
motor activity in a variety of test protocols
. The range of relative potencies
varies more than two orders of magnitude, and
thresholds for motor
activity were found well below doses that produce overt signs of poisoning.
Six
compounds
(allethrin, permethrin, cis-permethrin, deltamethrin, cypermethrin,
and fenvalerate)
impair schedule-controlled operant responding
,
seven compounds (pyrethrum, bifenthrin, S-bioallethrin, permethrin,
beta-cyfluthrin, cypermethrin, and deltamethrin)
decrease
grip strength,
and two compounds (deltamethrin and
alpha-cypermethrin) produce
incoordinationusing the rotarod
.
In addition, while compounds lacking an alpha-cyano group
(e.g., cismethrin, permethrin, bifenthrin)
induce an
increase in acoustic-evoked startle response amplitude
, cyano compounds
(e.g., deltamethrin,cypermethrin, cyfluthrin) produce the
opposite
outcome.
Other endpoints (e.g., tremor intensity, sensory response)
have been only occasionally explored. A synthesis of the neurobehavioral
evidence relating to the action of pyrethroidsindicates that some
differences in the experimental findings across compounds are also present in
the low-effective dose range. For risk assessment purposes, a strategy that
takes into account data from an array of neurobehavioral endpoints is needed to
capture the heterogeneity of pyrethroid-induced adverse effects and
accurately inform policy decisions.
Only the insecticide category of
organophosphates has more reported poisonings, as reported to the EPA by poison
control centers. (2) Reported health effects have been increasing in
recent years, and approximately 10% of reported medical incidents were
classified as major symptoms(3). Effects can be acute or
chronic (from long term accumulation). The most common
symptoms of acute pyrethrum poisoning are headaches, burning and itching eyes,
dizziness, asthma attacks, and difficulty breathing. Other symptoms include
skin rashes, hives, respiratory distress and heart failure. (1) These
side effects are sometimes classified as allergic reactions but can have
systemic and/or chronic effects. Pyrethrins are classified as
potential carcinogens. Studies in lab animals show increased occurrence of
cancer from pyrethrum exposure. Agricultural workers exposed
to pyrethrins also have a higher incidence of cancer development
(2)
A major study for assessment
of pyrethrin pesticide effects found characteristics of the
intoxication do not consist in singular symptoms but in combinations and
correlations of symptoms, i.e. of
central-neurological with peripheral-
and autonomic-neurological as well as with characteristic immunological disturbances(4).
Neurological
symptoms consist
in cerebro-organic disfunctions, locomotory disorders
reminiscent of multiple sclerosis or M. Parkinson
, and
sensory, motoric and
vegetative polyneuropathy, leading, for instance, to cardiovascular
regulatory disorder like sympathicotoniaor, orthostatic hypotonia.
Non-neurological
symptoms include immunosuppression with consecutive opportunistic
infections, like candida albicans, most frequently of the alimentary
tract, but also dermal and mucosal swellings,
lichen-ruber-like efflorescences, loss of hair, conjunctivitis. Other
symptoms are: hypoglycaemic crises inhibition of fertility,
disturbances of blood clotting, and most frequently in children,
suspected hematopoetic disorders.
Type I pyrethroids do not include
a cyano group, and their effects in rodents typically include rapid
onset of aggressive behavior and increased sensitivity to external stimuli,
followed by fine tremor, prostration with coarse whole body tremor, elevated
body temperature, coma, and death. (1b)
Type II pyrethroids include a cyano group in
the alpha position, and their effects in rodents are usually characterized by
pawing and burrowing behavior, followed by profuse salivation, increased
startle response, abnormal hindlimb movements, and coarse whole
body tremor that progresses to sinuous writhing (choreoathetosis). Almost
all systemic effects of exposure to pyrethrins and their derivatives
are targeted to the nervous system.
The American Association of Poison
Control Centers database includes reports of over
200,000 pyrethrins and pyrethroid total incidents recorded
from 1993-2005. It�s unlikely that most incidents are reported to
this data base, but over 20,000 incidents were reported each year in recent
years, with an increasing trend, with over 20 cases per year of significant
harm and 1 to 2 deaths per year. Of eight deaths that may be
attributable to exposure
to pyrethrins and/or pyrethroidproducts in recent years,
four victims showed respiratory symptoms, two showed other symptoms such as
feeling ill and headaches, and burning hands, and no particular symptoms were
reported for the remaining two victims. The eight deaths involved exposures to
one or a combination of the following pyrethrins and pyrethroid active
ingredients: pyrethrins, permethrin, cyfluthrin, cyhalothrin, bifenthrin,
and esfenvalerate.
The Washington State Department of
Health and the Oregon Public Health Division collected pesticide poisoning
surveillance data from 2001 through 2005. Cases were included if they involved
exposure to at least one pyrethrin or pyrethroidinsecticide.
Descriptive statistics were calculated. A total of 407
cases fit our definition. Overall, the rate of poisoning in Oregon
was significantly higher than in Washington (incidence rate ratio 1.70, 95%
confidence interval 1.40, 2.07), and rates for both states generally increased
during the time period. For both states, most exposures resulted in low
severity illnesses (92%). Only about one-fourth of cases were related
to a person�s work. The most common category of clinical signs and symptoms of
illness was respiratory (52% of cases), followed by neurological (40% of
cases). Exposure route was predominantly inhalation; there was no association
between route and case severity. There was a significant association between
illness severity and losing time from work or regular
activities. A woman in Oregon died of �sudden cardiac
arrhythmia following exposure to pyrethroidinsecticide in an elderly
woman with significant heart disease.�
(16)
The principal
effects of pyrethroids as a class are various signs of
excitatory neurotoxicity(6). Historically, pyrethroids were
grouped into two subclasses (
Types I and II
) based on chemical structure
and the production of either the T (
tremor
) or CS (
choreoathetosis with
salivation
) intoxication syndrome following intravenous
or intracerebral administration to rodents. Although this
classification system is widely employed, it has several shortcomings for the
identification of common toxic effects. In particular, it does not reflect the
diversity of intoxication signs found following oral administration of
various pyrethroids. Pyrethroids act in vitro on a variety of
putative biochemical and physiological target sites, four of which merit consideration
as sites of toxic action. Voltage-sensitive sodium channels, the sites of
insecticidal action, are also important target sites in mammals. Unlike
insects, mammals have multiple sodium channel isoforms that vary in
their biophysical and pharmacological properties, including their differential
sensitivity to pyrethroids. Pyrethroids also
act on
some isoforms of voltage-sensitive calcium and chloride channels
,
and these effects may contribute to the toxicity of some compounds. Effects on
peripheral-type benzodiazepine receptors are unlikely to be a principal cause
of pyrethroidintoxication but may contribute to or
enhance
convulsions
caused by actions at other target sites. In contrast,
other putative target sites that have been identified in vitro do not appear to
play a major role in pyrethroid intoxication. The diverse toxic
actions and pharmacological effects of pyrethroids suggest that
simple additivity models based on combined actions at a single target
are not appropriate to assess the risks of cumulative exposure to
multiple pyrethroids(6).
Pyrethrin pesticide reports
have, shown that pharmacotherapy is difficult and that the
duration of
poisoning can be unexpectedly long.
Pyrethroids are
ion
channel toxins prolonging neuronal excitation
. Two basic poisoning
syndromes are seen.
Type I pyrethroids produce
reflex hyperexcitabilityand fine tremor
.
Type
II pyrethroids produce
salivation, hyperexcitability,choreoathetosis, and seizures.
Both
produce potent sympathetic activation. Local effects are also seen:
skin
contamination producing paresthesia and ingestion producing
gastrointestinal irritation.
Carboxyesterase inhibitors can
enhance pyrethroid toxicity in high-dose experimental studies. Hence,
the unauthorized pyrethroid/organophosphate mixtures marketed in some
developing countries may precipitate human
poisoning. Pyrethroid paresthesia can be treated by
decontamination of the skin, but systemic poisoning is difficult to control
with anticonvulsants.
Pentobarbitone
, however, is surprisingly
effective as therapy against systemic type II pyrethroid poisoning in
rats, probably due to its dual action as a chloride channel agonist and a
membrane stabilizer.
Occupational and experimental studies
indicate that pyrethroids can cause clinical, biochemical and
neurological changes, and that
exposure
to pyrethroidsduring organogenesis and early developmental period is
especially harmful
. The neurotoxicity caused by mosquito repellant has
aroused concern among public regarding their use. In one study, the effect of
exposure of rat pups during early developmental stages to
a pyrethroid-based MR (allethrin, 3.6% w/v, 8h per day through
inhalation) on blood-brain barrier (BBB) permeability was investigated.
Sodium fluororescein (SF) and Evan's blue (EB) were used
as micromolecular and macromolecular tracers, respectively. Exposure
during prenatal (gestation days 1-20), postnatal (PND1-30)
and perinatal (gestation days 1-20 + PND1-30) periods showed significant
increase in the brain uptake index (BUI) of SF by 54% (P < 0.01), 70% (P
< 0.01), 79% (P < 0.01), respectively. This increase persisted (68%, P
< 0.01) even 1 week after withdrawal of exposure (as assessed on PND37). EB
did not exhibit significant change in BBB permeability in any of the group. The
results suggest that mosquito repellant
inhalation during early
prenatal/postnatal/perinatal life may have adverse effects on infants
leading to central nervous system (CNS) abnormalities,
if a mechanism
operates in humans similar to that in rat pups(12).
Pyrethroids are
insecticides extensively used to control pests around houses as well as in
agriculture. It has been suggested that type II pyrethroids may act
on GABA receptors as benzodiazepine antagonists. Because benzodiazepines are
used in anxiety, the present study(8) was undertaken to investigate the
possible anxiogenic effects of fenvalerate, a type
II pyrethroid, in rats. Behavior in the open-field, social interaction,
plus-maze behavior, and one-way passive avoidance were studied in rats orally
treated with 1, 10, or 30 mg/kg fenvalerate.
This pyrethroid reduced locomotion and rearing frequencies and
increased immobility duration. Ten and 30 mg/kg
of fenvalerate reduced social interaction, whereas the 1 mg/kg dose
had no effect on this behavior. The behavioral alterations observed in this
study suggest that fenvalerate has an anxiolytic effect on
rats.
For evidence of differential
susceptibility and drug interaction effects, a study cytochrome P450
indicated that
a reactive metabolite of deltamethrin is
formed by the body�s Cytochrome P450 enzyme
system catalysedreactions which is involved in the neurobehavioral
toxicity of deltamethrin
. The administration of Phenobarbital (PB)
or MC(3-methylcholanthrene) alone did not produced any symptoms of
neurobehavioral toxicity. While a
single oral administration
of deltamethrin produced tremors in two out of 10 rats and decreased
the spontaneous locomotoractivity
,
pretreatment with MC or PB
potentiated the deltamethrininduced neurobehavioral toxicity with 50%
of the treated rats exhibiting tremors
.
Half of the animals
pretreated with MC prior to exposure to deltamethrin also
exhibited choreoathetosis
. The
decrease in the
spontaneous locomotor activity was found to be much more significant
in PB- or MC-pretreated animals exposed to deltamethrin.
To assess the effects of pyrethrin pesticides on large
mammals a study was conducted on sheep at a
veterinary hospital(10). The findings clearly suggest
that supermethrin administration at lower doses has
harmful
effects primarily on the digestive tract causing failure to gain weight and
diarrhea
, but at higher doses these effects are more intensive accompanied
by the
effects on the CNS
.
Spraying with Pesticides has adverse effects
on anyone in the area of spray, as well as on all animal and insect life in the
area, especially
bees.
Children and the fetus
of
pregnant women are especially
susceptible. It doesn�t just affect a few
people with chronic immune weakness due to past chemical exposures(approx. 5%
of general population suffer from
MCS
and up to 30
% to lesser degree). Among people with chronic health
conditions, a higher percentage are affected.
Pyrethroid pesticides
are documented to be a significant factor in ALS (5,18) or to
cause ALS like symptoms and other chronic neurological problems or
autoimmune problems such as Parkinson�s(13) and Lupus(14). Repeated
exposure to pesticides has also been found to increase Alzheimer�s
Disease risk (11) & increase mortality rate (19).
Pyrethroids are a
class of insecticides involved in different
neurological disorders(13a,b,c,d). They cross the blood-brain barrier and
exert their effect on dopaminergic system, contributing to the burden
of oxidative stress in Parkinson's disease through several pathways. Our
studies suggest that neonatal exposition
to permethrin or cypermethrin induces long-lasting effects
after developmental exposure giving changes in open-field behaviors, striatal monoamine
level, and increased oxidative stress. (13b) Low doses
of permethrin can reduce the amount of dopamine
transporter immunoreactive protein in the caudate-putamen of the
dorsal striatum of the brain(13a)
. The study also suggests that previously reported reductions in
dopamine uptake of striatalsynaptosomes of high-dose mice may be due
to nondegenerative tissue damage within this region as opposed to
reductions of dopamine transporter protein or death of nigrostriatal terminals. Another
study found an increase in DNA fragmentation, an index of apoptosis, in cells
exhibiting reduced uptake at 30 min and 24 hours of exposure
to pyrethrin pesticides(13c). These data suggest that
up-regulation of DAT by in vivo pyrethroid exposure is an indirect effect
and that longer-term exposure of cells results in apoptosis. Since DAT can
greatly affect the vulnerability of dopamine neurons to neurotoxicants,
up-regulation of DAT by deltamethrin and permethrin may
increase the susceptibility of dopamine neurons to toxic insult, which may
provide insight into the association between pesticide exposure and PD.
Treatment
with deltamethrin caused nerve cell loss and the appearance of signs
of neuronal sufferance primarily in layer III of frontal cortex as well as in
the dentate gyrus
and to a lesser extent in the CA1 and CA3
subfields of hippocampus(13d). Deltamethrin induced also astrogliosis.
Dopamine and the dopamine plasma membrane transporter
decreased
significantly in hippocampus and striatum
. These findings indicate that
dermal exposure to
the pyrethroid insecticide deltamethrinusing an
administration module mimicking a possible long-lasting occupational skin
contact is
accompanied by cerebrocortical injury and loss
of hippocampal and striatal dopamine and dopamine
transporter
. The sensitivity of dopaminergic system in our
experimental model suggests that
dermal exposure
to deltamethrin could represent a risk factor for Parkinson's
disease. Exposure to some insecticides may cause a cascade of chemical
events in the brain that could lead to Parkinson's Disease, researchers
have found(13e).
A team from Virginia Polytechnic Institute
studied levels of key chemicals in the brain of mice exposed to various levels
of the insecticide permethrin. They found that the insecticide stimulated
a reduction in levels of an important transmitter chemical called dopamine.
Parkinson's symptoms such as the muscle rigidity, shuffling gait, and a
rhythmic tremor have been linked to the loss of dopamine production in the
brain. The researchers also found that exposure
to permethrin was linked to increased production of a protein
called alpha-synuclein. This protein is a major component of fibrous tangles
called Lewy bodies, which are found in the brain of patients with
Parkinson's. Exposure to low levels of the insecticide seemed to
have a more immediate effect than exposure to higher doses. But the researchers
believe this could be because high levels simply overwhelm the delicate systems
within the brain, which takes time to come to terms with and react accordingly.
Researcher Dr Jeffrey Bloomquist said a tiny dose - less
than one thousandth of that needed to kill a mouse - was enough to produce
effects on the brain.
Collectively These studies
provide further evidence that insecticides can affect the primary
neurodegenerative substrate of Parkinson's disease.
Organophosphate pesticides are
documented to cause
ADHD and
developmental deficits
. Pyrethroid pesticides are becoming more
commonly used as documentation of major effects by the organophosphate
pesticides has accumulated. But pyrethroid pesticides have similar
mechanisms of activity and effects as organophosphates, and studies suggest
that low dose prenatal exposure to pyrethroids has the potential to
produce long lasting developmental and behavioral effects through effects on
the expression of xenobioticmetabolizing cytochrome P450s in
brain and liver of the offspring as well as DNA damage and other
neurological effects(1g).
Short-term effects of pyrethroids on human health are
better and well identified, whereas long-term risk's estimation remains
difficult, especially those affecting the
reproductive function
.
Macroscopic studies showed an influence of PRMT on the testes,
the epididymides and body weight (15).
The pyrethroid induces a testis disturbance traduced by a
deregulation of spermatogenesis and an epididymis dysfunction by the
appearance of strong deformations into the microstructure of
the epididymides. A hormonal disruption was evidenced by the measurement
of the plasma testosterone concentrations. The findings of the present
investigation mentioned a significant increase (p</=0.05) in lipoperoxidation,
after 45 or 60 days, when we measured the
plasma malondialdehyde (MDA) concentrations. In conclusion the study
shows that subcutaneous PRMT treatment causes an arrest of spermatogenesis, and
a significant disharmony in testosterone concentration and MDA levels. These
effects are related to dose, length of treatment and to the
lipid peroxidation, which may be one of the molecular mechanisms involved
in PRMT-induced gonads and epididymides toxicity. Other studies
demonstrated that cypermethrin induces systemic genotoxicity in
mammals as it causes DNA damage in vital organs like brain, liver, kidney,
apart from that in the hematopoietic system (13c, f).
The
synthetic pyrethroid insecticide cis-bifenthrin
induced chronic toxicity in both aquatic invertebrate animals and
mammalian cells(15b).
There are
documented links in the medical
literature
between pyrethroids and
1.
breast Cancer
2.
testosterone decreases
3.
childhood brain cancers
4.
weakens and damages
Blood-Brain-Barrier
5.
neurological
and cardiological damage, esp. to infants and children
6.
thyroid damage and reduced
intellectual performance
7.
the ATP Energy Cycle and sensomotor-polyneuropathy
8.
Lou Gehrig�s Disease (ALS),
Parkinson�s, Multiple Sclerosis. Alzheimer�s
9.
Synergistic effects
with Malathion, Deet, etc.
Pyrethrin pesticides
have a major negative effect on bee and beneficial insect
populations:
http://www.myflcv.com/PyretBee.html
Pyrethrin pesticides harm cats
and other animals:
http://www.myflcv.com/PyretCat.html
&
Pyrethrin pesticides harm fish
and aquatic populations.
http://www.myflcv.com/PyreFish.html
Both
natural pyrethrins and synthetic pyrethroids are extremely toxic
to aquatic life and should not be used near waterways(1b).
The pesticide used in the Leon County
mosquito control program is anvil. Though there have been few studies on this
specific pyrethroid pesticide,
adverse effects
have been
documented and there is more information on the class of pyrethroid
pesticides that it belongs to.
The current Leon County
program has low emphasis and activity on
prevention and education
. These
should be the biggest priorities. They are where the largest potential
benefits lie at the least cost, and with the least harm to the
public.
Additional documentation of common
adverse health effects due to pesticides can be found at:
http://www.myflcv.com/pesticid.html
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