Health
Effects of Pyrethrin Pesticides on People, Animals,
Fish, and Beneficial Insects: Review
B. Windham (Ed.) 2010
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).
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 unmetabolised
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, and concluded 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 pyrethroids tested (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 incoordination using 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 pyrethroids indicates 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 sympathicotonia
or, 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 pyrethroid
products 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 pyrethroid insecticide. 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 pyrethroid insecticide 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 pyrethroid intoxication 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 hyperexcitability
and 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 pyrethroids
during 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 catalysed reactions 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 locomotor activity, pretreatment with MC or PB potentiated the deltamethrin induced 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)
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)
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 striatal synaptosomes 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 deltamethrin using 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 researches 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 xenobiotic
metabolizing 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: www.flcv.com/PyretBee.html
Pyrethrin
pesticides harm cats and other animals: www.flcv.com/PyretCat.html &
Pyrethrin
pesticides harm fish and aquatic populations. www.flcv.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: www.flcv.com/pesticid.html
References:
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(Fern Fischer covers topics of organic gardening, health, rural lifestyle, home and family.)
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