Priority Issues


Pesticides are a pervasive and insidious threat to human health, undermining the very safety of our food, water, and environment. These toxic chemicals, aggressively marketed by agrochemical giants, permeate our daily lives, exposing us to a host of serious health risks. From immediate symptoms like nausea and dizziness to long-term consequences including cancer, reproductive issues, and developmental disorders, the dangers of pesticide exposure are both extensive and alarming. It’s imperative to confront the harsh realities of pesticide use and advocate for sustainable, non-toxic alternatives that protect our health and the planet. This page delves into the myriad ways pesticides endanger human well-being and calls for a collective effort to eliminate their harmful presence.

State agencies always fall back on “EPA approval” and “use according to the label” as a rationalization for claiming that their use of pesticides have no health consequences. We strongly disagree, as does independent medical research. As we told KSL, here’s an analogy:  The FDA has “approved” the sale of cigarettes, that does not mean that cigarettes are safe to smoke if smoked “according to the label.”  Likewise the EPA has “approved”  the sale of thousands of pesticides. That does not mean that there is no health consequences to being exposed to pesticides. As we state on our report on glyphosate (Roundup):

“Strategies to achieve otherwise worthy environmental goals, should not include large-scale use of herbicides. Manufacturers of glyphosate and glyphosate-based herbicides (GBH, like Roundup) [and other pesticides] have carefully crafted a reputation for these products that is far different from the conclusions that should be drawn by public health experts. Independent research now thoroughly challenges, and in many cases outright contradicts claims of glyphosate’s ecological, wildlife, and human safety.  The medical research is very strong that, at real life environmental exposures, GBHs are hazardous to human health, including as carcinogens, reproductive toxins, and neurotoxins.”

Most pesticides are “endocrine disruptors,” meaning they are toxic to humans at extremely small concentrations. Even worse, we know that many pesticides are laced with PFAS (“forever chemicals”) and even the EPA has stated that essentially there is no safe level of exposure to PFAS chemicals.  Yet Utah state agencies are not testing the pesticides for the presence of these even more toxic contaminants.  That is the very least the state should be doing, but they are not.t

UPHE will continue to publicly call for more sensible and safe policy regarding the use of pesticides.

UPHE Reports on Pesticides:

Mosquito Pesticide Spraying

Send a message to the Salt Lake City Mosquito Abatement District (SLCMAD) Board of Directors and Salt Lake City Council Members to oppose mosquito spraying in Salt Lake City.  

Sign Our Petition Here. 
Spanish Translation of Petition

Read the documents UPHE was able to obtain from SLCMAD with GRAMA (Government Records Access and Management ACT).

“Say No to Mosquito Pesticide Spraying” Flyer, English and Spanish

Another “Downwinder” Threat to Utahns – 2023

PDF of Report

Much has changed in the last 100 years.

“New research suggests that the use of airplanes to spray anti-mosquito pesticides may increase the risk of autism spectrum disorder and developmental delays among children.”

American Academy of Pediatrics, conference presentation 20161

The Salt Lake City Mosquito Abatement District (SLCMAD)’s Environmental Assessment (EA) states, “[SLCMAD] was created in 1923 to protect Salt Lake City residents from the large numbers of these pestiferous mosquitoes.” The EA seems to be using a mandate that is nearly 100 years old as part of their justification for their spraying strategy. Obviously much has changed in the last 100 years. This mandate, and the mere continued presence of mosquitoes in their natural habitat in the Northwest Quadrant is not enough to justify pesticide spraying.

For just about every human on earth pesticides now contaminate our air, drinking water, food and soil. They are detected on Mt Everest,in the deepest parts of the ocean,and in rainfall from the sky. While contamination is global, for Salt Lake Valley residents, the most important place to reduce chemical usage in the Valley itself.

Utah Physicians for a Healthy Environment (UPHE) have had serious concerns about what might be done to control the mosquito population in the area of the inland port ever since the port first emerged from the legislature in 2018. Our concerns have grown significantly after learning that SLCMAD has been conducting massive aerial spraying of pesticides for many years over approximately 160,000 acres in the Northwest Quadrant of Salt Lake City  within a few miles of population centers on the West side, North Salt Lake, and West Bountiful. SLCMAD proposes to use known neurotoxins: permethrin, the synergist piperonyl butoxide (PBO), and the organophosphate pesticide (OP), naled.

In recent years numerous medical experts and entire medical societies have made strong position statements regarding the danger to humans of even small doses of chemicals, and their link to obesity, cancer, heart disease, birth defects, reproductive pathology, and neurologic and brain disorders such as Parkinson’s, impaired intellect, autism and attention deficit disorder. The American Academy of Pediatrics, American College of Obstetricians and Gynecologists, American Society for Reproductive Medicine, International Federation of Gynecology and Obstetrics (FIGO), World Health Organization, and the Endocrine Society are all mainstream medical organizations that have, in one form or another, called for a sharp reduction in human exposure to chemicals broadly, and pesticides in particular.

A recent review by 12 of the most knowledgeable researchers on endocrine disrupting chemicals (EDCs), (chemicals that mimic or inhibit key human hormones at very small doses which includes most pesticides) concluded that, “Whether low doses of EDCs influence certain human disorders is no longer conjecture, because epidemiological studies show that environmental exposures to EDCs are associated with human diseases and disabilities,” and that, “For every chemical that we looked at that we could find a low-dose cutoff, if it had been studied at low doses it had an effect at low doses”5

Toxicologist Linda Birnbaum, the director of the U.S. National Institute of Environmental Health Sciences (NIEHS), stated that “existing US regulations have not kept pace with scientific advances showing that widely used chemicals cause serious health problems at levels previously assumed to be safe.”6 This speaks to SLCMAD repeatedly invoking EPA approval of the pesticides it is using for spraying.

At the top of the list of chemicals of concern are pesticides (insecticides and herbicides) because they function as biological poisons to all living cells, from pest insects to humans and everything in between. Prominent researchers and medical societies have for years advocated a complete re-evaluation of the rationale for, and justification of, their use. It is increasingly clear that much of society’s use of pesticides is cavalier, poorly reasoned, often counterproductive to the intended goal, and represents poor priorities by causing unacceptable public health risk for dubious benefit. That is particularly true of using pesticide spraying for mosquito control. 

Executive Summary

1. Pesticides in general, including those used by SLCMAD, are a widespread risk to human health even at low doses, especially for fetuses and infants.

2. Decisions on the risks vs. benefits of exposing the public to dangerous chemicals  should not be made by people with no expertise in public health, toxicology, or environmental toxins.

3. The VOCs from pesticide spraying is a significant contributor to local air pollution.

4. Pesticide spraying has created a chemical arms race, is not effective in reducing mosquito populations long term, is losing its effectiveness even in the short term, and can even be counterproductive. 

5. We must not allow a cure worse than the disease. The incidence of severe outcomes from West Nile Virus is so low that preventing those outcomes should not be allowed to eclipse the long list of other health and environmental concerns from pesticide use.

6. Spraying does not re  duce the incidence of WNV.

7. Claims of safety for pesticide spraying use faulty logic and outdated, faulty science. It makes no sense to expose hundreds of thousands of people to neurotoxic chemicals in an attempt to prevent a neurotoxic disease in a few dozen people.

8. Pesticide spraying has adverse impacts on beneficial insects, bird populations, wildlife, the ecosystem of the Great Salt Lake and beyond.

9. There are better ways to control mosquitoes.

10.  SLCMAD does not need or deserve to raise your taxes to increase the spreading of neurotoxic chemicals.


The scientific and empirical evidence is overwhelming that spraying adulticides to kill mosquitoes, especially aerial spraying, is ineffective, and can be even counterproductive, over the long term, and even the short term, to both goals of controlling mosquito populations and preventing West Nile Virus. Furthermore, the medical literature strongly indicates that routine aerial spraying over Salt Lake City’s airshed represents a broad-based danger to public health. Utah Physicians for a Healthy Environment (UPHE) implore SLCMAD to end all of their insecticide spraying for mosquitoes, whether from back packs, trucks, drones, or airplanes. This practice is an institutionalized relic of the 1950s and should be stopped immediately.

1.  Pesticides Represent a Widespread Risk to Human Health

Almost regardless of where they are applied, through drift and volatilization, pesticides end up causing ubiquitous, global, environmental contamination. The logical extension is now well documented; pesticides are universally found in the blood and urine7 of almost all human beings everywhere, in amniotic fluid, new-born babies, in mother’s breast milk, 8 and in domestic drinking water worldwide. In studies dating back ten years, glyphosate, and 2,4-D, two of the most widely used herbicides globally, have been found in rain water and in air samples from the Midwest. “It is out there in significant levels. It is out there consistently,” said Paul Capel, environmental chemist and head of the agricultural chemicals team at the U.S. Geological Survey Office, part of the U.S. Department of Interior.Glyphosate was found in every stream sample examined in Mississippi in a two-year period and in most air samples taken.” This speaks to the pervasive spread of pesticides throughout our environment. That the SLCMAD would contribute to this global problem would be difficult to justify unless there was a clear benefit. We believe there is no benefit to offset this concern.

In the early 1990s growing awareness of the toxicity of pesticides led to a National Academy of Sciences Report, Pesticides in the Diets of Infants and Children (NAS, 1993).10 The report emphasized that children’s pesticide burdens differ from adults quantitatively and qualitatively and questioned the validity of risk tolerances used by the EPA to declare “safety.” (More about that in later sections). The report estimated that 50% of lifetime pesticide exposure occurs during the first 5 years of life.  By the age of 6 the brain reaches 90% of its eventual adult volume and that corresponds to about 90% of its overall, permanent organizational and architectural structure,11 obviously the most critical developmental window for organogenesis, especially for the brain.

The NAS report raised the profile of concerns about children being a uniquely susceptible subgroup to organophosphate pesticides (OP). The new concerns highlighted the vast physiologic differences between children and adults that go far beyond differences in size. Children at the pre-natal and early infant stages of development are much more chemically sensitive for multiple reasons, one of which is that they have a decreased ability to metabolize chemical toxins.12,13,14 For example, children do not have the necessary enzymes to detoxify pesticides like OPs or  permethrins.15 In eight day old rats permethrin is nearly five times more acutely toxic than in adults because they lack permethrin-specific esterases.16 In humans the blood brain barrier (BBB) doesn’t mature for at least six months after birth.17 That allows more of any toxic chemical to reach brain tissue.

Children consume far more food, calories, and water, inhale far more air, and have a greater surface area per unit of weight than do adults, significantly increasing their exposure. The same amount of exposure yields higher blood and brain levels in an infant for numerous reasons. It is no surprise that children 6-11 yrs. of age had levels of organophosphate metabolites twice as high in their urine as adults 20-59 yrs of age.18 At the same time, organ growth is obviously rapid during the early stages of fetal and infant development, especially for the brain, yet the BBB is not completely formed allowing higher concentrations of toxic, exogenous chemicals to accumulate in the brain at the worst possible time, with permanent consequences.19 Pesticides can cross the placenta,20 contaminate the intrauterine environment, including the embryonic and fetal brain, and impair development. This is far more than a theoretical concern. The most widely used insecticides work by attacking the nerve cells of insects. A nerve cell in a mosquito is almost identical to a nerve cell in a fetus. Furthermore, a nerve cell in a fetus can be just as critical to the fetus as it is to a mosquito and just as vulnerable to chemical attack. They can both be damaged by the same insecticide. Prominent researchers put it this way. “The molecular targets of pesticides are often shared between pest and non-target species, including humans. This is particularly true for the neurotoxic organochlorine, organophosphate, and pyrethroid pesticides.”21

Last year researchers at NYU concluded that 81% of the cognitive loss in children from environmental neurotoxins came from exposures to polybrominated diphenyl ethers (PDBEs) and organophosphate pesticides, far eclipsing that caused by heavy metals like lead and mercury.40

Maternal exposure continues the threat to an infant in the postnatal period. Characteristics such as lack of ionization, small molecular weight, low volume of distribution, low maternal serum protein binding, and high lipid solubility all contribute to the transport of these chemicals into human breast milk. Human breast milk in the Salt Lake Valley no doubt already has contaminants, but aerial spraying by SLCMAD will add to that burden. A study of contaminants in human breast milk from multiple countries found every milk sample from every country was contaminated with pyrethroid pesticides,22 and at levels high enough to cause neurologic and endocrine effects.23 Other studies show contamination even in households where no pesticide is used.24 Organophosphate pesticides have also been found routinely in breast milk.25

On the other end of the spectrum of health consequences, children have more future potential years of life. This allows more time in which to develop chronic diseases like cancer and heart disease known to be triggered by early exposure to environmental toxicants.

Researchers looking for reasons behind disturbing epidemiologic studies, have found evidence of auxiliary mechanisms of toxicity beyond the standard route recognized for lethality in insects.26, 27, 28

New research shows a link between OP exposure among children growing up in an agricultural area and loss of lung function.301

SLCMAD’s environmental assessment (EA) of its pesticide use lists only six studies to support their statement that “several studies on this procedure have not found any negative impact on human health.” 29,30,31,32,33,34 We assume this means these studies are the strongest evidence SLCMAD has to defend the practice. Three of the studies only looked at temporally related cases of hospital and outpatient visits for acute asthma and skin rashes. One study only sought to estimate dermal absorption of permethrin, and two studies used modeled exposure estimates combined with EPA toxicology risk assessments to declare no health impact. As a group these few studies simply do not address the real health consequences of pesticide spraying and are almost irrelevant to the issue. Asthma attacks is not one of the most important disease outcomes from pesticide exposure and cannot be considered a surrogate or marker for other more serious outcomes. SLCMAD’s director keeps using these studies to claim there is no health effects from the pesticides they use. But these studies do not claim that, in fact, have virtually nothing to do with the issue. 

The first draft of this document was completed before SLCMAD abandoned the proposal to involve the US Air Force. SLCMAD’s director replied to that draft with a rebuttal document listing a total of 12 references, but even those do not address the health consequences in any meaningful way either. The failure of traditional risk assessments  (TRAs) to reflect human health hazards will be address later and in the Appendix.

Below we address the medical research on specific components of the spraying mix.


The primary and most consistent human effect of insecticide exposure is neurotoxicity. That is hardly a surprise given their origin as nerve agent chemical weapons. For over 40 years pyrethroid compounds have been the most commonly used insecticides for controlling adult mosquitos. “The main metabolites of pyrethroids have frequently been detected in urine samples from the general population, confirming widespread exposure of children and adults to one or more pyrethroids.”35,36

For SLCMAD to repeatedly claim that exposure levels are so low as to avoid clinical consequence is contrary to robust research, overlooking multiple, important lines of evidence. Humans lack a critical enzyme, serum carboxylesterases, a primary avenue of pyrethroid detoxication through hydrolysis.37 To that point, physiological differences and diffusion modeling shows that exposure to the pyrethroid deltamethrin was predicted to result in a two-fold greater peak brain concentration in humans compared to rats.38

The research showing the toxicity of pyrethroids to human health is direct and extensive. Pesticides in general, and pyrethroids in particular, are toxic to the brain, associated with a wide range of neurologic and brain diseases, especially impaired brain development, and loss of intellect and behavioral disorders in children. The damage to the nervous system from pyrethroids is comparable to that from the banned legacy pesticide, DDT.39 Recently the mode of action of pyrethroids has been found to be similar to chlorinated pesticides which were banned in the 1980s because of their harm to human health and the environment. Implicating the risk of pyrethroids to fetuses at extremely low concentrations are studies showing toxicity to small invertebrates at concentrations of as little as two parts per trillion.41 In 1999, after a heavy pyrethroid spraying campaign on Long Island in the wake of Hurricane Floyd, 10 million lobsters, 90% of the population, died off. The lobstermen sued the pesticide manufacturers for $125 million. This kind of devastation of marine life is a chilling warning about the destructive potential to humans, especially at the fetal stage.

Adverse outcomes are found among individuals whose exposure is comparable to what the general population experiences, and not limited to only highly or occupationally exposed individuals. Experimentally, pyrethroid exposure in lab animals during development has a broad range of toxic effects on neurotransmitter systems, the BBB, and neurobehavior.42  Experimental studies showed pyrethroids cause dopaminergic related neurodegeneration and alter mitochondrial function in vitro and in vivo.43 Other studies showed pyrethroids cause neuroinflammation and damage to glial cell function, critical to the immune system that protects the brain.

The neurotransmitter acetylcholine, central to memory, learning, and attention span, is lower in parts of the brain in children with autism.273 Interfering with acetylcholine is the primary mechanism of these insecticides. An in vitro study of cortical neurons found that pesticide exposure caused specific transcriptional changes similar to changes characteristic of the autistic human brain.274 Low level pyrethroid exposure affects learning, motor activity and sexual behavior in lab animals.47

Consistent with this research, several epidemiologic studies have found an increased risk of autism with more pyrethroid exposure.86,275,276 The clinical findings of specific studies are worth highlighting. Children with autism and developmental delay were more likely than a control cohort to have had agricultural–pyrethroids, OPs, or other pesticides–applied near their mothers’ place of residence, especially during the third trimester.86 In a swampy region in central New York, an observational study showed that children living in ZIP codes in which aerial pesticide spraying was conducted every summer since 2003, were 37% more likely to be diagnosed with autism or a developmental delay compared to those in ZIP codes where pesticides were used with other methods of distribution, such as manually spreading granules or using hoses or controlled droplet applicators.44 This is particularly alarming because of the similarities with the circumstances in the Northwest Quadrant of SLC. More about this study later.

Pyrethroid pesticide exposure is inversely associated with performance on intelligence tests in six year olds.45 Levels of pyrethroid breakdown products in the urine were proportionally associated with a higher level of behavioral problems in children.46 Attention deficit disorder in children is also associated with pyrethroid exposure.48,49 A study that found higher rates of autism with intellectual disability among children who lived within 2,000 meters of agricultural field that used pesticides, and the risk increased further if the children were also exposed as infants.50 Among 11 pesticides examined in this study, the one with the highest risk was permethrin, which was even greater than chlorpyrifos, the one organophosphate that the EPA recently banned for almost uses and is widely banned in other countries. Pyrethroids are associated with increased risk of brain cancer.51

Exposure to common pyrethroids speeds the onset of puberty in boys.52 A critically important study was just published in Jan. 2020 that showed a 56% increased rate of overall mortality among adults exposed to higher levels of pyrethroids over a period of 14 years.53

Most pyrethroid compounds are endocrine disruptor chemicals (EDCs) and as such can interfere with human reproduction and act as carcinogens.54,55 One of the defining characteristics of EDCs is that they can interfere with normal organ development at very low doses, particularly at vulnerable stages, i.e. pre-and perinatal development. In 2009 The Endocrine Society, the medical organization with expertise most relevant to developmental chemical toxicity, publicly stated with regard to EDCs, “Even infinitesimally low levels of exposure indeed, any level of exposure at all, may cause endocrine or reproductive abnormalities, particularly if exposure occurs during a critical developmental window. Surprisingly, low doses may even exert more potent effects than higher doses.”56

Another characteristic of EDCs is that the adverse human health effects may not be apparent for many years after exposure and therefore cannot be assessed using traditional dose response models that are the key to toxicology risk assessments used for determining safe thresholds. Making matters worse, pyrethroid metabolites have greater endocrine disrupting activity than their parent compounds. Indeed, it is through endocrine disruption that many of the now documented adverse health outcomes occur from low dose exposure typical of what much of the human population is now exposed to. To quote the authors of one review paper, “their [pyrethrins’] structural resemblance to TH [thyroid hormone]s, with the fact that in vitro and in vivo animal studies demonstrate clear interference with TH homeostasis and action argues for more caution in their use and more intense scrutiny of their long-term effects.”57

Organophosphates (OPs)

Given that SLCMAD is using naled, an organophosphate (OP), repeatedly via airplanes, it is important to examine the medical literature on the toxicity of this group of pesticides. OPs are progeny of nerve gas agents originally used in WWI that were debilitating or lethal by causing restlessness, seizures and respiratory arrest. OP are acetylcholinesterase (AChE) inhibitors, killing insects by the same biochemical process that sarin gas kills humans, provoking a marked acceleration of nerve impulses causes a buildup of acetylcholine, resulting in paralysis of the insect. AChE is essential in all mammals, including humans. OPs were adapted from chemical weapons to be lethal to insects at low doses via the same mechanism. Naled has the same method of action common to other OPs, including the recently banned chlorpyrifos. Acute toxicity in humans follows the same pattern as it does in insects, but the human effects of greatest concern are more related to chronic exposure to adults, and acute, low dose exposure to fetuses and infants.

Over 30 years ago, the Office of Technology Assessment (OTA) of the US Congress released an extensive report entitled “Neurotoxicity: Identifying and Controlling Poisons of the Nervous System.” One of the two primary targets of the report was chemical pesticides. They stated, “Of particular concern are the delayed effects of some of the organophosphate pesticides.”58

Naled leaves a breakdown product, dichlorvos, which is also an insecticide with similar acute and chronic effects as the parent compound which serves to prolong the toxicity. In fact, dichlorvos, is classified by the EPA as a group C (possible) human carcinogen, while naled itself is not. Dichlorvos exposure during pregnancy or childhood has been linked to an elevated incidence of brain tumors and leukemia.59,60

Naled is far more toxic by inhalation exposure than by ingestion, maybe as much as 20 times more toxic,278 and the EPA has outlined numerous restrictions for potentially exposed applicators. However, the EPA has not calculated the potential for “bystander” exposure despite stating that there are no risks to bystanders, an inexplicable, critical omission. Another study found that small droplets of naled (the size produced by the ultra-low volume sprayers that SLCMAD boasts about using) were about four times more acutely toxic than larger droplets.279

There are numerous studies in animals showing that naled at low dose exposures causes a wide variety of adverse health outcomes, including diseases of the nervous, circulatory, reproductive, and immune systems. 

OPs as a group, like pyrethroids, are endocrine disruptors. And like with pyrethroids, one of the mechanisms of endocrine disruption and therefore impact on brain development by OPs is inhibition of thyroid hormone production.61 Other clinical outcomes associated with pre-natal OP pesticide exposure include abnormal primitive reflexes in newborns; mental and motor delays among preschoolers; and decreases in working and visual memory, processing speed, verbal comprehension, perceptual reasoning, and IQ among elementary school–age children. Prenatal exposures are also associated with elevated risks for symptoms or diagnoses of attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD).62  

Other systematic reviews and multiple epidemiologic studies have linked OP exposures during fetal development with poorer cognitive, behavioral, and social development in children.63,64,65,66,67 In one review, adverse effects of OP pesticide exposure on neurodevelopment were seen in all but one of the 27 studies evaluated; the strongest associations occurred following prenatal exposures,68 but it has also been found with post-natal exposure as well.68 Another study showed that young mammals, including humans, may be at risk of impaired neurological development from organophosphate pesticides, even at low, commonly encountered environmental levels.69

More specific studies are worth mentioning. A meta-analysis by researchers at University College London found chronic, low-level exposure to organophosphate pesticides causes permanent damage to cognition, including information processing and working memory.70 Urinary levels of organophosphate metabolites in pregnant mothers were measured, then the children they gave birth to were tested at age 7. Children from those mothers who were in the highest 20% of exposure, showed an average IQ deficit of a stunning 7 points.71 The relationship between biomarkers of organophosphate exposure in pregnant mothers and neurologic tests at one year, two years, and 6-9 years, showed that more prenatal exposure caused a loss of perceptual reasoning as early as one year of age, and continued through childhood.72 Prenatal exposure to organophosphates was associated with delayed mental milestones in 2 year olds.73 In another study prenatal exposure to organophosphates was associated with decreased non-verbal IQ measured at age 6.74 The US Congress produced a report back in 1990 that showed an organophosphate pesticide, in this case malathion, can damage the nervous system after just one exposure.75

A higher likelihood of an ASD diagnosis was observed for children born to women residing within 1.5 km of OP pesticide applications on agricultural fields.76 Living in a residence close to an agricultural site with OP use during fetal development was associated with a reduction in children’s IQs measured at age 7.77 Risks for impaired neurodevelopment increased in children of farmworkers who experience higher exposures to OP.78 Higher OP pesticide metabolite levels in the urine of pregnant mothers were associated with ASD traits in adolescence in those children.79 

Some children are genetically more susceptible to organophosphates.80 Children with genetic disadvantages that reduce capacity to detoxify OP pesticides have higher rates of neurodevelopmental disorders.63 Prenatal exposure to one of the most potent OPs, chlorpyrifos, has also been shown to have an association with decreases in brain volume in the areas responsible for attention, receptive language processing, social cognition, and regulation of inhibition.81

OP pesticides can interfere with brain development at levels previously thought to be safe or inconsequential, and through mechanisms other than the lethal mode of action for insects.76,82,83,84 This is an indication of an additional, as yet undetermined mechanism of toxicity.85,86 Consistent with human studies, experimental animal studies also confirm the toxicity of early-life OP pesticides on neurodevelopment, resulting in impaired motor activity, behavior, and cognition, even at doses below the known mechanism by which they kill insects. 

Within a population of 25.5 million children 0 to 5 years of age, researchers calculate a total loss of 16.9 million IQ points due to common background exposure to just organophosphates. This estimation does not take into account all the other known environmental neurotoxins like heavy metals, PCB, flame retardants, many other neurotoxic chemicals, including pesticides, which only add to that total.87

In Japan, between 1957 and 1971, school children saw a huge increase in impaired vision eventually tied to the use of an OP in agriculture. One town near an agricultural area now has an eye disease named after them, “Saku disease.” In that town 98% of the children had visual acuity problems linked to the regular application of an OP on near-by agricultural fields.88 In California a boy became blind after being outside while a helicopter was spraying an OP.89 An ingredient in naled, trichlorfon, was found in a study to cause severely reduced brain weight in test animals exposed.90

In keeping with their potential to mimic or interfere with human hormones, exposure to OPs is a risk factor for acquiring hormone-related cancers, i.e. including breast, thyroid, ovary and lymphoma.91 Recall that dichlorvos is classified as a group C carcinogen by the EPA. Exposure during pregnancy or childhood is linked to an increased incidence of brain tumors and leukemia.60,92 Researchers found an association between exposure to dichlorvos saturated “no-pest” strips during pregnancy and childhood and the incidence of three types of childhood cancer: leukemias, brain tumors, and lymphoma.282 A Missouri Department of Health study found similar results for childhood brain cancer.283

Pesticides attack the immune system. Both pyrethroids and organophosphates have been found to specifically inhibit a critical enzyme in white blood cells, and impair the growth and survival of those cells.93,94 A World Resources Institute’s report entitled “Pesticides and the Immune System: The Public Health Risks,”95 concludes that immunosuppression by pesticides can provoke allergies, autoimmune disorders such as lupus, and cancer. It may also lead to increased susceptibility to viral infections (like COVID and WNV) and bacterial infections. The immunosuppressive effects of pesticides will be raised again in discussing whether pesticide spraying decreases the public health risk of WNV.

Animals studies have found that naled causes anemia, and birth defects in laboratory animals.281Labels on naled acknowledge it is a “severe” eye irritant, and “causes eye damage” and is “corrosive” to skin.280

The commercial preparation of naled, Dibrom, contains other ingredients that according to US pesticide law can be classified as “inert,” but are hardly benign. They include the aromatic hydrocarbons naphthalene and 1,2,4- trimethylbenzene. Naphthalene is a toxin classified by the EPA as a possible human carcinogen, and causes neurologic disorders and anemia in newborns. 1,2,4- trimethylbenzene is a tissue irritant and depresses brain function. 

Naled has been banned in the European Union.  The director of SLCMAD, Ary Faraji, has recently claimed that the EU didn’t ban naled as we have publicly stated, rather that the manufacturer didn’t apply for re-licensure for economic reasons. That claim is easily disproved. Official EU states in no uncertain terms that naled represented an “unacceptable risk” to human health and the environment, and that naled was to be removed from all European markets, Nov. 1 2012. 284, 285, 286, 287, 288, 289

Naled can persist in the atmosphere for several days. Researchers at UC Davis measured both naled and its breakdown product dichlorvos in the air around a treated orange grove for three days after application.299

Low concentrations of naled celebrated by SLCMAD as “safe” also need to be viewed in this context: chlorpyrifos, a pesticide in the same category as naled, causes brain damage in humans at the lowest possible detectable dose. That’s why the EPA recently banned 90% of uses for chlorpyrifos. A recent study found that naled, more than being just another organophosphate in the same category as chlorpyrifos, it joined chlorpyrifos in being the most neurotoxic of 30 organophophates.300

Naled is one of the most neurotoxic organophosphate pesticides in use 

Piperonyl Butoxide (PBO)

Exposure to more than one pesticide at a time can cause synergistic toxicity.96 But the SLCMAD’s use of naled by airplanes and pyrethroids from the ground virtually guarantees it. The intentional role of PBO is to act as a synergist to pyrethroids, and it can magnify their toxicity by a factor of ten. There is every reason to believe that synergistic toxicity to mosquitos is matched by synergistic toxicity to humans. PBO’s mode of action is the slowing down of metabolism of these compounds in the liver of the mosquitoes by interfering with cytochrome P450 monooxygenase enzyme. This enzyme is also the most important enzyme to humans’ ability to metabolize toxic xenobiotics and endogenous compounds.

Not surprisingly, PBO also delays the metabolism of other toxins, which can obviously magnify their effect, including that of endogenous hormones. This further increases the risk to humans, especially with fetal exposure,97,98 in precipitating impaired development and function of hormonal organs such the thyroid, pituitary, and adrenal glands. PBO is also classified by the EPA as a group C carcinogen. PBO is an immunosuppressant through its action of inhibiting lymphocytes.99 Some studies in animals have shown PBO to have reproductive toxicity,100,101,102 and it has been shown to cause liver tumors in rats and mice.103

There are several studies to suggest that PBO is, itself, also a neurotoxin,104,105,106 which contradicts the official statement by the EPA that it is not. One of the most alarming studies on neurotoxicty from pesticides, published in the flag ship journal of the American Academy of Pediatrics, showed that children in the highest PBO exposed group, compared to the lowest exposed group, showed delayed neurodevelopment at 36 months, and loss of intelligence of about 4 points, comparable to that from lead toxicity.107 This clearly identifies this “non-pesticide” ingredient as yet another potent neurotoxin in SLCMAD’s pesticide inventory. The toxicity impact of PBO is likely enhanced by the fact that humans lack serum carboxylesterases, a primary mechanism of pyrethroid detoxication through hydrolysis.37

Other studies show that the toxic synergism of PBO when mixed with pyrethrins perpetuates its ecological impact.108

Other Pesticides

SLCMAD’s EA also says that “other EPA approved adulticides with the same class of active ingredients may be used as well.” Given the broad latitude that SLCMAD is allowing itself to use virtually whatever type and amount of pesticides it chooses, and without any meaningful medical scrutiny, and given that most pesticides have similar modes of action, it is also important to look at the medical literature on other pesticides used for mosquito control and pesticides in general.

Studies of pregnant women exposed to more pesticides, including organophosphates, gave birth to infants with smaller head size, thinner cerebral cortex, and other brain architectural abnormalities. 69,109,110,111  Prenatal and first year of life exposure to organochlorides, DDT, organophosphates, and other common agricultural pesticides increases the risk of intellectual disability, developmental delays, and autism.112,113,114,115,116 A meta-analysis showed impairment of cognitive functions such as psychomotor speed, executive function, visuospatial ability, working and visual memory with low dose exposure to pesticides.118 Neurodevelopmental scores at age 7 are lower with prenatal exposure to chlorpyrifos. Children in the top 25 percent of exposure levels scored 5.5 percent lower in working memory tests and 2.7 points lower in IQ.71,72,119 One study even showed more behavioral problems in children during the peak of pesticide spraying season.120  Numerous other studies show children growing up near agricultural pesticide use have higher rates of autism.117,121

Risks of Parkinson’s Disease, Alzheimer’s and adult cognitive decline are increased with pesticide exposure.118,122,123,124,125 Individual’s with a particular genetic make-up may be particularly sensitive to the neurodegenerative effects of certain pesticides. 123,125,126,127,128 

Maternal exposure to pesticides, including OPs, during pregnancy correlated with shorter gestational age, smaller length and lower birth weight.129,130 Women exposed to higher levels of pesticides have higher rates of infertility,131 and men have lower sperm counts. Pesticide exposure in women is associated with higher rates of endometriosis probably through their action as endocrine disruptors.132

Normal brain, frontal plane           Alzheimer’s brain, frontal plane

 In addition to contributing to neurologic diseases, impaired intellect, and endocrine disruption, repeated spraying of neighborhoods in mosquito abatement programs creates problems for chemically sensitive individuals. Multiple chemical sensitivity syndrome can afflict as much as 15-20% of the adult population.133,134 For them, chemical exposures can be a debilitating nightmare that includes profound fatigue, nausea, coughing, bronchospasm, rashes, severe headaches and impaired mentation. Insecticides are the most common triggers for the syndrome which can be precipitated by as little as one exposure event. “In a survey of 6,800 persons claiming to be chemically sensitive, 80 percent asserted they knew when, where, with what, and how they were made ill. Of the 80 percent, 60 percent blamed pesticides.” Even a single spraying can provoke clinical symptoms in [genetically] predisposed individuals.135 In 2008, the Center for Public Integrity analyzed 90,000 reports of adverse reactions to pyrethroids and found they had increased 300 times over ten years.136 If the intent of pesticide spraying is to protect public health, the impact on chemically sensitive individuals is by itself enough of a reason to stop pesticide spraying.

Pesticide exposure can cause genetic damage.137 Numerous studies have found that pesticides, including pyrethroids and OPs, can precipitate oxidative stress by increasing free radicals inside in the cell, damaging such critical macromolecules as RNA, DNA, DNA repair proteins and other proteins, causing genetic mutations, compromising antioxidant defense mechanisms and detoxification and scavenger enzymes.138,139,140,141,142 This is not only a mechanism for causing a diseases like cancer, but is also a pathway for causing harm to subsequent generations.

Given the genotoxicity it is not surprising that numerous studies have found significant associations between pesticide exposure in general and several types of cancer, such as non-Hodgkin’s lymphoma, multiple myeloma, soft tissue and lung sarcoma, pancreatic, stomach, liver, bladder, and gall bladder cancer.143

Genotoxicity and endocrine disruption are the likely mechanisms for reproductive pathology associated with pesticides. “Every class of pesticides has at least one agent capable of affecting a reproductive or developmental endpoint in laboratory animals or people,”144according to the author of a review article on the subject.

Disruption can occur in all stages of hormonal activity: hormone synthesis; hormone release and storage; hormone transport and clearance; hormone receptor recognition and binding; hormone post receptor activation; thyroid function; and the central nervous system.145 In epidemiological studies, pesticides are linked with menstrual cycle disturbances, endometriosis, reduced fertility, prolonged time-to-pregnancy, spontaneous abortion, stillbirths, and birth defects.146,147,148,149,150,302

One of the researchers that helped discover the effect of pesticides on epigenetics and transgenerational harm, Dr. Paul Winchester, a pediatrician, said this, “Every one of the chemicals [pesticides] tested so far produces infertility, and the industrial world has reached the lowest level of fertility on record.”151

Other research has found subsequent, multi-generational harm after exposure to just the first generation. Even more alarming, the pathologies were more extensive and more severe in subsequent generations.152 Those diseases included prostate disease, obesity, kidney disease, ovarian disease, and birth abnormalities. Other studies showed not only does pesticide exposure significantly increase the risk of type II diabetes and obesity in humans and obesity in animals, but the effect can last through three generations.153,154,155

The insecticide pyriproxyfen used against mosquito larvae, causes reproductive abnormalities in keystone organisms persisting for multiple generations. Even 71 parts per trillion produced abnormalities.156

PFAS Contamination

Recent news reports have revealed that mosquito abatement pesticides are widely contaminated with one of the most toxic group of chemicals known, the C8 group, or PFAS. This family of compounds has been linked to a long list of disorders and disease, including: liver toxicity, immune disruption, developmental disorders, birth defects, thyroid disease, ulcerative colitis, and cancer of the kidneys, testicles, and pancreas. 

The principal characteristic of the environmental and human toxicity of these compounds is that they do not break down either endogenously or exogenously, accumulating over time. Because of that their common nickname is “forever chemicals.” They have been used to extend shelf life and increase dispersion of pesticides, and may also exist as a contaminant from the containers used to store pesticides. Manufacturers may get away with using the chemical because they claim it is inert, and therefore not required to be listed as an ingredient.

PFAS compounds are among the most toxic compounds ever produced by industry, yet they are completely unregulated by the EPA. This despite the EPA having concluded that anything above 70 parts per trillion (ppt) is not safe. Seventy parts per trillion is the equivalent of a few grains of sand in an Olympic size swimming pool. Even that level is widely considered far too high.157 For example, the Agency for Toxic Substances and Disease Registry has recommended a limit of 12 ppt. Michigan considers one of these compounds unsafe at concentrations greater than 6 parts per trillion.158  PFAS compounds bioaccumulate in the food chain. Recently the fish in southeastern Michigan were declared unsafe to eat because they were contaminated with concentrations of PFAS thousands of times greater, i.e. in parts per billion. 

Massachusetts recently discovered significant PFAS contamination of pesticides that were widely used in that state. Afterwards, elevated levels of PFAS were found in municipal drinking water in Massachusetts. PFAS contamination of the environment and public drinking water is already a nationwide, serious concern. 

Adding more toxic compounds to the pesticide mix raises the possibility of further synergism. SLCMAD is merely relying on assurances from the pesticide manufacturers that the pesticides it is spreading all over the city do not contain PFAS. This is wholly adequate to address the concern. They should be doing their own testing to make sure. If contamination is found it would add yet another reason to reject the spraying program. 

Health Risk for SLCMAD’s Pesticide Workers

When weighing the risks and benefits of spraying, SLCMAD should also consider the extensive medical literature on the health consequences to those who are occupationally exposed. The health consequences just to their pesticide workers would likely more than offset any benefit to the community in theoretically reduced cases of WNV.

Certainly the many studies on the increased risk of neurologic disorders and neurodegenerative diseases like Parkinson’s, Alzheimer’s and cognition decline should be of serious concern to pesticide exposed employees.70,122,159,160 Just one significant pesticide exposure “event” is enough to precipitate significant cognitive decline among pesticide applicators.161,162 Research cited earlier in this report about a significant increase in all-cause mortality with pesticide exposure53 is particularly relevant to the employees, as are the studies linking exposure to type II diabetes,153 rates of depression and suicide.163

Pesticide applicators, including those that used permethrin, have shortened telomeres, chromosomal markers of shortened life expectancy.164 Pesticides are toxic to the bone marrow, increasing susceptibility to aplastic anemia, a frequently fatal blood disorder.165,166,167 Widespread media attention has been generated over the lawsuits regarding frequent use of glyphosate and cancer, especially lymphoma.168 Women exposed to DDT before puberty, especially during infancy, had much higher rates of breast cancer.169

Men exposed to more pesticide residues from eating fruits and vegetables have lower sperm counts,170 and women have more problems with endometriosis,96,302 and reproductive toxicity, including birth defects and miscarriages.171

Looking for genetic toxicity and mutagenic damage in those occupationally exposed among agricultural and public health care workers, researchers from several studies found “a high rate of oxidative and DNA damage,” compared to non-occupationally exposed controls.143,172,173 Some studies actually showed that the disease burden increased among subsequent, unexposed generations.17

2. Decisions on the risks vs. benefits of exposing the public to dangerous chemicals  should not be made by people with no expertise in public health, toxicology, or environmental toxins.

Decisions that affect public health should only be made by public health experts. Decisions about whether to expose hundreds of thousands of people to repeated applications of chemicals proven to harmful to public health, wildlife, and the environment in general should only be made by a panel with expertise in those disciplines. SLCMAD does not have that expertise. The director who seems to be the primary decision maker, has a PhD in entomology. That is not synonymous with expertise in the relevant disciplines. While there is a physician on SLCMAD’s board, she does not demonstrate any real expertise on these issues.

3. Spraying Pesticides Increases Air Pollution

SLCMAD acknowledges that the spraying will release VOCs, but then dismisses the significance stating, “this activity would not exceed local standards for air emissions and would not result in nonconformance with the Clean Air Act” (CAA). This is irrelevant and is misleading regarding public health consequences. It reveals that the SLCMAD does not understand the significance of VOCs or how air pollution affects public health. It is another manifestation of their lack of public health/environment expertise. 

Given the time of year of spraying(summer and early fall), warm temperatures enhance VOC volatilization. VOCs are a precursor of ozone in the summer and of particulate pollution (PM2.5) in the winter, both of which have been recognized as serious health hazards for over 50 years and regulated as such by the Clean Air Act (CAA). Utah is already struggling with high summer time ozone levels statewide, and the Wasatch Front has perennially been in violation of EPA’s 24 hr. PM2.5 standard since 2006. Rural parts of Utah are experiencing higher summer time levels of ozone than the Los Angeles Basin. Almost undoubtedly the VOCs from spraying pesticides increase ozone levels locally, as well as at sites remote from the sprayed area, as ozone can form thousands of miles away from where its precursors are released.     

Most pesticide mixtures that contain solvents release high rates of VOCs.175 In the San Joaquin Valley (SJV) of California, 65% of VOC emissions are from non-fumigant pesticides.175 In the SJV, VOCs in the air and soil spike after pesticide spraying, and ozone spikes up to 15 ppb occur downwind immediately afterward, and don’t return to pre-spray baseline levels for 1-2 days.176 The study also detected predominantly high molecular weight aromatic hydrocarbons, the most toxic type of VOCs. With multiple rounds of spraying these ozone spikes will occur repeatedly throughout the season creating a significant source of summer time ozone.

Any presumption that short-term spikes in VOCs and ozone from pesticide spraying will not impact public health reflects a misunderstanding about the pathophysiology of air pollution. Virtually all of the components of air pollution–particulates, ozone, VOCs, toxic chemicals, NOx, and SOx-–precipitate an immediate inflammatory response that takes days or weeks to fully subside. The clinical consequences, including heart attacks, strokes, and increased mortality, are apparent within hours, and don’t return to baseline for weeks or longer.177,178  

Repeated episodes of elevated VOCs and ozone during a several month-period represent a risk to fetal development and viability for any exposed pregnant mothers during that time period.179,180

Increases in ozone just in the few days prior to delivery are associated with increases in still birth.181 Furthermore, the zone of exposure to spikes of ozone and VOCs will almost certainly be larger than that for pesticide drift.

Reducing VOCs has been a prominent part of the Utah Division of Air Quality’s strategy to improve Utah’s air quality.182 Yet because the release of VOCs is from a mobile source, not a stationary source, the DAQ does not require a permit for the spraying. That is not because these VOCs don’t matter, it is only because of a regulatory loophole that should be closed.

SLCMAD’s statement in the EA, “this activity would not exceed local standards for air emissions and would not result in nonconformance with the Clean Air Act,” needs to be addressed. There is no local standard for VOCs. Neither is there a state or federal standard for VOCs and the SLCMAD statement is not acute or informative on the issue of health consequences. In addition to their contribution to PM2.5 and ozone, there is a wealth of research showing that VOCs are also, themselves, one of the most hazardous components of urban and industrial air pollution. They are potent carcinogens, reproductive toxins, and neurotoxins. Unfortunately, this is unaddressed by the CAA and certainly not by SLCMAD’s EA. Multiple events of aerial pesticide spraying would add to the already disproportionate toxic air pollution burden borne by the nearby residents of the West side, North Salt Lake and Bountiful.

Furthermore, VOC emissions from the spraying and the ozone spikes will occur during wildfire season, when we are now consistently experiencing some of the worst air quality of the year. The addition of VOCs to an already unhealthy backdrop of wildfire pollution (from both PM2.5 and ozone), is not a trivial matter, cannot be brushed off by SLCMAD.

4. Spraying pesticides has created a chemical arms race, is not effective in reducing mosquito populations long term, is losing its effectiveness even in the short term, and can even be counterproductive. 

SLCMAD acknowledges that spraying is not effective. Their EA states, “In many instances, the numbers of mosquitoes collected in some of the traps do not decrease after aerial ULV adulticide operations are conducted.” The obvious questions are: “Then why continue spraying?” 

For effective mosquito control 90% of adults must be killed.183 Only a few studies of the efficacy of spraying have been reported. Most of those studies do not suggest that kill threshold is achieved or that the strategy works. After ground spraying only a 34% reduction was achieved in Greenwich, CT, and in Houston only a 30% reduction. Little is accomplished unless spraying is done at least every 7 days. Zero mosquitoes will be killed upwind by an insecticide spray, and the spray will not eliminate larval mosquitoes.184 The average upwind and downwind kill is only 21% to 45%. 

Using ULV aerial equipment results in only 10% to 25% of the insecticide reaching the general target area, and up to 90% drifting away from the target into the environment at large, i.e. over the near-by communities and the Great Salt Lake.185,186

Depending on the study, the amount of pesticide that actually makes contact with a mosquito target can be less than 0.0000001% of the insecticide applied, but the average is probably around 0.0001% for flying insects (obviously more difficult than crawling insects).187  Sprays must be composed of tiny particles so they will float in the air rather than fall to the ground, which is the purpose of the ULV technique. To ensure insects fly into the insecticide spray droplets, they must have a size in the range of  2-16 microns.188 Even low winds easily blow mists of those size particles away from target areas.

Pesticide Resistance

Ecologist Garret Hardin has stated that “every biocide selects for its own failure.” Continued use of pesticides creates resistant “super-mosquitoes” that require ever increasingly toxic chemicals to kill them.189

The resistance of insects like mosquitoes to pesticides is well established evolutionary science and has been observed in just about every country over several decades. Mosquitoes that survive pesticide exposure pass on genetic adaptations to their progeny that allow them to start developing resistance. Because of the short life cycle of mosquitoes that resistance can emerge very quickly. While it is common for mosquito numbers to drop for a few days after a spraying, the success is short lived because a new generation of more resistant mosquitoes quickly replace the deceased. A catch 22 is created. If spraying is done frequently enough to reduce the number of mosquitoes, it simultaneously accelerates the evolution of genetic resistance, and the resistance is passed onto to subsequent generations via epigenetic modifications such as DNA methylation, histone modifications, and small RNAs, triggered by insecticide-induced stress.190 Pesticide “priming” may even enable insects to be more tolerant of other types of induced stress, offering further survival advantages.190 In fact it is worse than a catch 22. There is evidence that human disturbance of an area, including pesticides spraying not only increases the number of mosquitoes, it increases the number of disease-carrying insects.191

In hundreds of insect species, repeated application of pesticides on broad populations results in large numbers of resistant insects thriving in the sprayed areas. For example, the number of Anopheles albimanus mosquitoes in Guatemala that were responsive to DDT dropped from nearly 100 percent in 1959 to approximately 5 percent 20 years later.192

The headline of an article in Science Magazine from 2016 reads, “After 40 years, the most important weapon against mosquitoes may be failing.”193 It goes on to say that mosquitoes are developing resistance to pyrethroids “at alarming rates.” The article quotes Maureen Coetzee, director of the Wits Research Institute for Malaria at the University of the Witwatersrand in Johannesburg, South Africa. “Nobody dreamt that insecticide resistance would spread the way it has spread throughout Africa.” In Africa resistance to five mainstream insecticides increased dramatically between 2005 and 2017.194 In Puerto Rico, which has been battling Zika cases since 2016, pyrethroids have become ineffective.195

Applying pyrethroids as surface sprays leads to a significant increase in the resistance of mosquitoes.196 Mosquitoes from sprayed areas tolerated ten times the amount of chemical as did mosquitoes from non-sprayed areas.197 Within a two-week lifespan, mosquitoes can develop resistance within a single season. A 2003 study found that WNV and malaria infected mosquitoes developed resistance to organophosphate insecticides as a result of a single genetic mutation.198

Damage to Mosquito Predator Populations

Of the numerous predators to mosquito larvae–dragonflies, ladybugs, lacewings, goldfish, guppies, fish, bats, and several types of birds—almost all have a longer life cycle than the mosquitoes. If a pesticide harms both mosquitoes and their predators, the later will take longer to restore their numbers giving the mosquitoes an advantage with each spraying.

A headline in National Geographic reads, “How pesticides can actually increase mosquito numbers.”199 The article cites a study that shows mosquitoes evolve resistance to common pesticides but their predators, in this case damselfly larvae, have not developed that resistance. The end result is that pesticide spraying is actually counterproductive, doubling the number of mosquitoes in sprayed areas compared to unsprayed areas. The lead author of the study is Edd Hammill from Utah State University.200 

Attempts to control medfly infestations in Florida and another in California, both using OPs backfired because beneficial insects and the pests’ natural predators suffered greater damage. It took more than ten years for California agencies to acknowledge the pesticide spraying failure and replaced it with before preventative, nonchemical control program.

Damage to sympatric species

Spraying can adversely alter the balance with sympatric species (species that occupy the same ecological niche).

Over eleven years, Cicero Swamp in New York State was sprayed fifteen times with naled. During that time the mosquito population grew fifteen-fold.201 When the populations of non-EEE [Eastern Equine Encephalitis] carrying mosquitoes were killed off, the EEE-carrying mosquitoes took their place. “In their research summary the authors of the study noted that the increase in disease- spreading mosquitoes ‘discredits the rationale that preventive applications of naled reduce the risk of EEE.”202 The authors also concluded that “Ecological balance between the 2 species [of mosquitoes] may be restored by reducing naled applications to these swamps.” 

Data and graph courtesy of Vásquez Analytics Consulting

5. We Must Not Allow a Cure Worse Than the Disease.

The CDC states that adulticides should only be used as a last resort. “The underlying philosophy of mosquito control is based on the fact that the greatest control impact on mosquito populations will occur when they are concentrated, immobile and accessible. This emphasis focuses on habitat management and controlling the immature stages before the mosquitoes emerge as adults. This policy reduces the need for widespread pesticide application in urban areas.”203 We are hardly in a state where a “last resort” is needed or even helpful.

It is no small irony that the ostensible public health goal of spraying is to avoid significant neurologic disease and disability (and very rarely death) from WNV in a small number of people. But in doing so, the most common public consequence of spraying is to accept a risk for a small amount of neurologic disease in a large number of people. 

While all the factors in the epidemic of autism and brain developmental disorders in children have not been completely determined, key insights have been established that are relevant to this issue. About two thirds of the risk for autism comes from exposure to environmental toxins at an early stage in brain development. The other third is from genetic vulnerability, much of which is sex specific.204 That etiologic combination is undoubtedly also highly applicable to other brain developmental disorders.

Numerous studies show that typical urban air pollution is also a major risk for all brain developmental disorders. This combination means that those Salt Lake communities that are on the West side, near the airport, near the oil refineries and other industrial pollution, near the major freeways, and soon to be neighbors of the inland port, are already at significantly increased risk and are already victims of “environmental injustice.” Pesticide spraying from SLCMAD in the Northwest Quadrant will make that even worse as pesticides are at the top of the list of environmental neurotoxins.

Attempting to quantify just one adverse public health end point, rates of autism, paints a very disturbing picture. Extrapolating from the observational New York study of aerial spraying and autism,  for spraying in the Northwest Quadrant, this calculation can be made: 

According to the Kem Gardner Policy Institute, the prevalence of autism is 1.7% of the Utah population.205 Vasquez Analytics estimates that 12,200 people live within 2.5 kilometers of the proposed spray area, an area comparable in geographic positioning to that in the New York study. That suggests there are 207 cases of autism within the closest influence zone. If aerial pesticide spraying increased the rate of autism as much in Utah as it did in New York that means 77 cases could be attributed to pesticide aerial spraying. Even that is likely an underestimation of what may be happening in Utah for several reasons. 

The New York exposure only involved one neurotoxic pesticide and the SLCMAD proposal involves two, plus a synergistic agent capable of greatly magnifying the toxicity. Furthermore, the control group in the New York study was not truly unexposed, they were still exposed to mosquito abatement pesticides (hydraulic spraying, manual dispensing of granules, or controlled droplet application) just not aerial spraying. The control groups also included zip codes as close as 2.5 km from the aerial spraying, so they were also likely exposed from chemical drift, just at lesser concentrations. The rate of autism is likely higher in influence area #1 than the Utah statewide average of 1.7%. The area is already exposed to numerous neurotoxic hazards, especially air pollution and lead that are known risk factors for autism, so the assumed 207 cases of autism is likely an underestimation. Finally, SLCMAD has acknowledged that they have been aerial spraying for decades, and routinely over an entire acreage of about four times the 43,000 acres proposed for Air Force spraying, and about which this calculation was made.

Even despite a rise in rates of West Nile Virus in 2021, cases have been dropping precipitously over the last 16 years and cannot be considered a health crisis severe enough to warrant exposing everyone to toxic chemicals

Even people bitten by an infected female mosquito, the carrier of WNV virus, run very little risk of serious illness.

SLCMAD offers a rationale for spraying stating that since 2003, there have been 422 documented cases of WNV in the state, with most of those in the Salt Lake Valley. If so, that is an average of only 23 cases a year, and 2021 had less than the average, and certainly not all those cases originated from mosquitoes from the Northwest Quadrant. That is hardly a serious public health threat. But looking deeper into the case history of WNV nationally and in Utah is even more revealing.

In Africa, where WNV was first found sixty years ago, very few human epidemics have been identified. WNV first appeared in the US in 1999. Northeastern communities like Boston and NYC that first responded to WNV with massive spraying have since scaled back their use of adulticides after demonstrating a lack of efficacy, and after three times more people became symptomatically ill from the spraying than from WNV. 

Within a few years after 1999 there was every reason to believe that infection rates would subside as West Nile Virus becomes “endemic” to the United States, and will be characterized by low baseline infection rates interrupted by sporadic outbreaks. In fact that pattern appears to be the case. The number of cases in the US peaked in 2003 at around 10,000 and has declined significantly and steadily since. In 2020 there were only 557 total cases. Nationally, in 2002 there were 199 deaths, in 2020 there were only 38, and 40% of those were in Texas where the population increased 50% in those 20 years.206 So far this year, nationwide, there have only been 725 WNV cases, and 35 deaths.

The case rate in Utah is following a similar step decline. The annual number of WNV cases peaked in Utah in 2006 at 158. Since 2008, the average annual number of cases in Utah has been 12, and in most years the number of cases is in the single digits. From 2008 to 2016 the average annual number of WNV case fatalities in Utah has been 0.2 cases. Adding in the two years of spikes in 2007 and 2017, that number increases only to 1.1 fatal cases per year.207

The Utah Department of Health (UDOH) stated that in 2018 11 residents contracted the virus and one person died.207 In 2020 Utah recorded one case of “neuroinvasive WNV,” and one case of non-neuroinvasive WNV, and no deaths.208 As of October, the Utah Dept. of Health is reporting 21 human WNV cases in the state for 2021, and two deaths.  Nationally, as of Oct. 5 the CDC has reported 725 WNV cases and 35 deaths. 

While Salt Lake County often has the most cases of all the counties in Utah, the majority of Utah cases do not occur in Salt Lake County contrary to SLCMAD’s claim. Nationally and in Utah, the number of cases of WNV is low, and for nearly 15 years has been  trending lower despite occasional spikes. This is hardly a public health crisis in Salt Lake County warranting aggressive, repeated, wide spread spraying of biologic poison over large areas of the county. 

The same trend has been observed in the United States with related infections, such as St. Louis encephalitis and Eastern equine encephalitis, where 30 or more years may pass between human outbreaks. The last outbreak of WEE (Western Equine Encephalitis) in Utah occurred in 1958. There has never been an outbreak of SLE (St. Louis Encephalitis) in Utah. It is disingenuous for the SLCMAD to list these two diseases as justification for spraying.

Chart of WNV cases in Utah 2003-2018.

Note the pattern on this chart that is consistent with a downward trend and low level in the number of WNV cases, despite a peak in 2017. Note also that after tracking closely with the mosquito counts in the mid 2000s, cases of WNV have not kept pace with the mosquito population. Indeed as hotter temperatures and extremes of precipitation (both floods and drought ), signatures of the climate crisis, have led to increased mosquito populations, the number of WNV cases continues its steep decline. As of the w riting of this draft in October, the Utah Dept. of Health reports that the number of mosquito pools that are positive for WNV are at recording breaking numbers, about 8% of the total. The most recent year with that high of a percentage was 2017, and during that year there were 62 WNV cases. So the trend in human WNV cases is still downward despite a growing mosquito population.  Further, although there are numerous reasons for an increasing mosquito population, the aggressive spraying campaign cannot be said to be suppressing that growth.

New York City, the epicenter of the 1999 WNV outbreak, found that out of more than 7 million, 62 people — or less than .0009% — became ill with the virus, and 7 died (one in one million).

Putting this is context, that same year in New York City, 2,474 people died from influenza or pneumonia in 1999, 400 times the number of WNV mortalities.209

About 80% of people who are infected with WNV develop no symptoms, about 20% of people will develop mild symptoms. Less than 1% of individuals infected will develop a serious neurologic illness, such as meningitis.210 

Dr. Gochfeld, Prof. of Environmental and Community Medicine at the Robert Wood Johnson Medical School and School of Public Health reported that, based upon his experience and other West Nile Virus epidemics, typically less than one tenth of one percent of people bitten by infected mosquitoes develop any clinical signs of disease; in other words less than one in 1000 persons bitten by infected mosquitoes will develop some health problem.  Gochfeld said:

In weighing the risks and benefits of mosquito control, we should consider the disease itself and the risk to the human population. The media always paired the words “lethal” or “deadly” with “West Nile” or “encephalitis,” reinforcing in the public’s mind the danger from the disease. But it would be equally appropriate to characterize West Nile virus infection as “unapparent,” “usually asymptomatic,” or “occasionally serious.” Seven deaths in a population of over 10 million people over a one month period is certainly tragic, but pales beside the number of deaths from many other diseases that are addressed less aggressively.”211

The U.S. Fish and Wildlife Services states, “Contrary to media descriptions of ‘the deadly West Nile virus,’ [it] is rarely fatal in humans. Less than one percent of people who acquire the disease will experience severe illness like encephalitis or meningitis. 214 Within this small proportion, the fatality rate is about 3-15%.212 In other words the fatality rate is about one in 1,500 of those that become infected. Someone infected with WNV may have life-long immunity even if they show no symptoms. Most pregnant women infected with WNV give birth to normal, uninfected babies.

Pesticide exposure causes immunosuppression,215 specifically inhibiting the survival and growth of leukocytes (white blood cells) by inducing apoptosis or cell cycle arrest and interfering with the function of each type of immune cells.216  Those most at risk for a neurologic case or death from WNV are the immunosuppressed and the elderly, especially elderly males.217 Pesticide exposure will only increase their risk. Those over 80 years old are at 43 times the risk for either one.218 With such a low rate of death or serious disease for the population at large means that this is almost exclusively a disease of the elderly, especially elderly males, and everyone else must be at an almost imperceptibly low risk. A more complete public messaging strategy from health departments including this differentiation would itself go a long way to helping to protect the at-risk population while not creating unnecessary alarm and pressure for poor public policy.

6. Spraying Does Not Reduce the Incidence of WNV, WEE, or SLE

An analysis of rates of WNV showed that in 7 cities that used spraying programs for mosquito control, there were no lower rates of WNV compared to 7 comparable cities that did not use pesticide spraying. The communities that sprayed adulticides had an average of 1.37 people with West Nile virus per 100,000. The communities that didn’t spray had 1.19 people with West Nile virus per 100,000.219 Communities that did not spray put a strong emphasis on public education, selective larviciding and some employ seasonal help to locate breeding sites of mosquitoes.

The EA states that “90% of the mosquitoes” that are the intended target of the spraying are Ae. dorsalis and Cx. Tarsalis. But Ae. dorsalis do not carry pathogens, and therefore this species is only a nuisance mosquito, as are male mosquitoes of both species, because it is only female mosquitoes that bite. High bite rates to humans are an indication that the relevant breeding areas are nearby, and very unlikely to come from an uninhabited area miles away.

The primary mosquito target relevant to public health is the female Culex tarsalis, the principal vector for WNV, and the EA does not give us any data on that specific species population. Adult Culex females live between 2-4 weeks, depending on multiple factors. Mosquitoes have a maximum flight range of between 50 m and 50 km, depending on the species. Few specimens survive long-distance flights “and do not relate to nuisance situations.”220 Female Culex mosquitoes are usually poor fliers and do not move far from their larval habitat. At the most they are capable of flying up to two miles away from their breeding grounds in uncommon circumstances. Even then they would have to find a new favorable breeding ground to present a meaningful risk for disease. So the key to preventing mosquitoes from infiltrating population centers is still eliminating standing water where people are. 

 In that case, SLCMAD’s spraying 170,000 sparsely inhabited acres in the Northwest Quadrant would have little impact on the number of WNV infected mosquitoes in populated areas.

Pesticides can act as immunosuppressants not only to humans but to wildlife as well. Immunosuppression in wildlife makes them more susceptible to encephalitis if bitten by an infected mosquito, creating a feed-back loop due to more mosquitoes carrying the encephalitis pathogen and spreading the disease. Moreover, pesticide spraying can increase the biting aggressiveness of mosquitoes for up to two hours after a spraying.221

From an open letter written nearly 20 years ago, entitled, “Stop the Indiscriminate Spraying of ‘Friendly Fire’ Pesticides,”222 the group Concerned Physicians and Scientists make these points.  “There is a widely accepted erroneous belief that mass spraying of pesticides protects the population against mosquitoes. In fact, the opposite is true: the mass spraying will result in a deterioration of public health by exposing millions of people to “friendly fire” pesticides. Ironically, such spraying is especially dangerous to those with impaired immunity for whose “protection” such spraying is mainly being done.”

7. Claims of Pesticide Safety Use Faulty Logic and Faulty Science

Because of the limited range of the female Culex tarsalis, SLCMAD cannot simultaneously claim their spraying is safe because it occurs only over unpopulated areas, but at the same time claim it is effective when it only occurs over unpopulated areas. 

SLCMAD leans almost exclusively on EPA approval of the pesticides for their position that the program of spraying is safe for the public. American citizens, especially those in Utah, have a long and painful history of being victimized by the mistakes and the regulatory failures of government agencies. Public exposure to atmospheric radiation, nerve gas storage, lead, mercury, cigarette smoke, asbestos, Agent Orange, military burn pits, perchlorate, PCBs and countless other toxic chemicals, continued, in many cases, for decades after the science was clear that these were causing death and disease. And in many cases those exposures continue today, especially with pesticides. It seems we have learned nothing sixty years after Rachael Carson’s Silent Spring should have transformed how we use chemicals that spread throughout our environment. Spraying against weeds and insects continues in Utah almost as a ritual conducted by every layer of government with little to no thought about the cumulative impact or the evidence for efficacy of the practice. 

Several books written by EPA whistle blowers and extensive investigative reporting have exposed the disconcerting reality that the EPA has established protocols that protect chemical manufacturers at the expense of public health223,224,225,226,227,228,229,230,231The agency functions as much as a political agency as it does a scientific agency.

In the history of the EPA they have only completely banned eight substances and chemicals. The EPA still hasn’t even completely banned lead in all gasoline, or all uses of asbestos. Under administrations of both political parties, the EPA has a long history of regulatory inertia lagging far behind the advancement of scientific evidence, as they are right now in not updating the national air quality standards. In most cases not only was the government far too slow in taking action, the pressure to act at all usually came from the public listening to the scientists. 

We are in a similar situation now with the outdated and dangerous practice of pesticide spraying to control mosquitoes. Approval by the EPA of these chemicals for use on mosquitoes is no exoneration of the SLCMAD’s strategy. Illustrating the point, the EPA has approved 85 pesticides that have been banned or are being phased out in other countries,232 including some banned in countries like China and Brazil which are hardly known for robust environmental protection. In fact, recent documents reveal that the US EPA has been directly involved with chemical industry lobbyists in pressuring countries like Mexico to reverse their ban on certain pesticides.233 The EPA has recently deliberately downplayed the extent of PFAS contamination in public drinking water.234 The overwhelming number of pesticides ever withdrawn from the US market are done so by industry, not because of bans from the EPA. 

It makes no sense to expose hundreds of thousands of people toneurotoxic chemicals in a vain attempt to prevent a neurotoxicdisease in a few dozen people

Regarding the EPA approval process for chemicals, Dr. Winchester said, “…in the current paradigm…the only thing companies have to prove is that it doesn’t kill you if you drink it or take a big dose of it.”151

Furthermore, the EPA does little to evaluate mixes of multiple pesticides with synergistic agents, like the one SLCMAD uses, nor do they make any attempt to evaluate harmful epigenetic and genetic changes that are passed down to subsequent generations as mentioned earlier in this report, something toxicology risk assessments are not designed to detect. 

Against this disconcerting backdrop it is all the more revealing that, nonetheless, the EPA did prohibit use of naled indoors or around the exterior of homes by anyone other than professional applicators, and it has been banned completely in the European Union.235 

Many people who are likely to be exposed to the pesticides are also using mosquito repellants like DEET. A study from Duke University researchers has found that combination of DEET and permethrin exposure in lab animals causes the death of neurons and gross brain malformations.236

Claims of rapid breakdown of pyrethroids outdoors do not account for the pesticide seeping indoors within any residences near where spraying is conducted. Indoors they accumulate in dust and on household surfaces because they don’t break down indoors like they do in direct sunlight outdoors. Children end up with 50% higher blood concentrations of these chemicals than adults do because they spend more time near the floor and have much more hand to mouth activity.41 Human exposure also occurs because these chemicals linger on vegetation, vegetables and fruit. 

At any one moment in time, between 40,000 and 50,000 women are pregnant in the state of Utah, many thousands of them will be exposed to some degree to known neurologic poisons from this aerial spraying proposal during the most critical stages of embryologic and fetal development. It has been universal advice from obstetricians for many years that their patients avoid any unnecessary pharmaceuticals, chemical exposures, and other contaminants to protect the integrity of fetal development, and that axiom certainly applies to pesticides. 

Safety claims regarding pyrethroids do not adequately take into account cumulative exposures. It is one thing for SLCMAD to claim that one spraying event is benign. It is quite another to claim that multiple rounds of spraying, week after week, month after month, year after year are benign. Some residents will be exposed to repeated aerial spraying, and then any additional spraying that SLCMAD does in their neighborhood as a “service call.” A pregnant mother living in one of the neighborhoods near the Northwest Quadrant could be exposed to repeated, and perhaps frequent doses of the insecticide by SLCMAD for weeks or months. Those same children could be further exposed after birth during each season of spraying, and again from the breast milk of its mother after birth. This cumulative and repeated exposure during the most critical stages of brain development in a person’s life, represents a much greater level of risk than just one spraying event. 

The aphorism “death by a thousand cuts” shouldn’t mean no one is responsible, it should mean everyone is. 

Because no one is exposed to just one toxic chemical, or even just one pesticide, the toxicologic studies on chemical exposures never adequately assess the clinical consequences of our total toxic exposures. Again, this is particularly relevant to fetuses and infants. An attitude on the part of decision-makers that justifies a specific source of toxins as being only a small part of the total problem is indefensible. The aphorism “death by a thousand cuts” shouldn’t mean no one is responsible, it should mean everyone is responsible, and that everyone must stop contributing to the ultimate adverse outcome including the SLCMAD. And the most important “cuts” to eliminate are those closest to home.

According to the Stockholm Convention,237 an international treaty intended to minimize the environmental and global health consequences of persistent organic pollutants (POPs), organic compounds with an atmospheric half-life of over two days are considered POPs. By that definition these mosquito pesticides are considered POPs. The EPA states, “Because they can be transported by wind and water, most POPs generated in one country can and do affect people and wildlife far from where they are used and released. They persist for long periods of time in the environment and can accumulate and pass from one species to the next through the food chain.”238 Ten of the 12 chemicals banned in that treaty are pesticides.

Between 15 and 40% of applied chemicals are dispersed in the atmosphere by volatilization or droplet drift processes.239,240 Pesticide off-gasing can continue for many hours or even days. When this occurs, the pesticide vapors may be subject to multiple, consecutive inversion cycles (more about that below), increasing the fugitive spread, and decreasing the dispersion predictability. Through either or both mechanisms, the pesticides can travel far from the site of release, and given that the breakdown times for OPs can range from several days to a few months, there is every reason to be concerned for the potential for spread of the actively toxic chemicals far off site.

In the EA, SLCMD cites difficult circumstances for effective spraying in the target area stating, “Some of the challenges to aerial adult mosquito control in the Salt Lake City area include extreme temperature inversions that occur at sunset and remain until sunrise.” Indeed, Salt Lake City is ground zero for temperature inversions. North Dakota State University (NDSU) states, “… some of the seemingly best weather conditions for pesticide application are often the worst. That is because those conditions are caused by air temperature inversions. Air temperature inversions provide near-perfect conditions for tiny, aerosol-size droplets to drift away from their targets… Spraying during an inversion may cause increased lateral movement of fine drops and pesticide vapor.” 241

SLCMAD states that spraying only will happen when wind speeds are between 1 and 10 mph. But the NDSU advisory is, “Wind speeds 4-6 mph do not disrupt the inversion, and under these circumstances the smallest size droplets can drift laterally. “Smaller droplets (200 microns in 

The more effective the spray, the more likely it is to drift away from the target area and into nearby neighborhoods. 

diameter and less) fall as little as a few inches per second and may float along with the air for long distances.”241 “Even if the wind speed is only 1 or 2 mph, a small droplet can move a significant distance.” Indeed, while the smaller the droplet size the more effective the spray will be against flying insects, but the more likely that spray will drift off target. 

SLCMAD’s airplane spraying is conducted from a height of between 100 and 300 ft. The Biomist label says that with aerial spraying below 200 ft. “the spray equipment must be adjusted so that the volume median diameter (VMD i.e. half of the total volume of spray droplets are larger than the specific size and the remaining half of the volume of spray droplets are smaller than that size),  produced is less than 60 microns, and that 90% of the spray is contained in droplets smaller than 100 microns.” For aerial applications above 200 ft. those stipulations change to 70 microns and 145 microns. In turn, the label for Dibrom states that for aerial application (it does not specify height from the ground), the VMD must be less than 60 microns, and that “90% of the spray [must be] contained in droplets smaller than 115 microns.”

However, the State of California’s Department of Pesticide Regulation, Pest Control Aircraft Pilot Study Guide242 goes to great length in discussing the inverse relationship between droplet size and the potential for drift (and from which both of the above diagrams were taken). For example, it states that “it takes approximately 4 minutes for a 20-micron droplet to travel a vertical distance of 10 feet, it takes only 2 seconds for a 400-micron droplet to travel the same distance.”  Further, “research also has proven those droplets smaller than 200 microns are very prone to drift. Those that are 100 microns or smaller are defined as driftable fines…The droplet size at which spray drift becomes a concern is 200 microns and below…Droplets smaller than 50 microns in diameter remain suspended in the air indefinitely or until they evaporate. Droplets of this size have no benefit to a pest control program because they are never likely to reach target surfaces.”  This suggests that aerial spraying cannot be simultaneously safely limited to a specific site and still be effective. The more effective the spray, the more likely it is to drift away from the target area and into nearby neighborhoods. We emphasize that this discussion assumes a height of 10 ft. from the ground, yet all these conflicting considerations would be far more applicable to a height of 100 to 300 ft., the height from which spraying airplanes typically fly.

Moreover, evaporation of the spray begins as soon as a droplet is released into the atmosphere. The longer it is exposed, the smaller the droplet becomes, and the more it will drift. Hot summer air temperatures and low humidity will accelerate evaporation and therefore drift.  

Vapor drift can travel even further than particle drift.243 A 2001 study by Texas A&M University found that pesticides can volatilize into the gaseous state and be transported over long distances rapidly through wind and rain.244 A U.S. Geological Survey report reached similar conclusions.272 A report from California in 2003, Secondhand Pesticides,245 found that airbourne pesticides routinely exceed even far too lax health standards measured in the air, miles from where they are released. Concentrations of two different organophosphate pesticides were found near spray areas in concentrations that exceeded acceptable health levels by 184 and 39 times, respectively. The report also found that for almost half of the of pesticides applied in California, the concentrations in the atmosphere peak between eight and 24 hours after an application starts allowing plenty of time for further fugitive drift.

Drifting off target is not only an issue for pesticides leaving the targeted 170,000 acres, but also creating uneven distribution within that area, undoubtedly making some acreage receiving double doses and others receiving less or none. 

NDSU emphasizes that, “…spray applicators need to use extreme caution in mountainous areas, protected valleys, basins, and the lower areas and shaded hillsides of some steeply rolling topography because cold air drainage can cause very intense inversions in these areas.” And that, “Late afternoon spraying (two to three hours before sunset) has been found to be one of the worst times to spray. This is the time when inversions are beginning to form and often will intensify after sunset and continue all night…Based on these data and other observations, evening inversions pose a greater risk for spray drift…An inversion, plus low wind speed, is the best possible situation for long distance damaging drift of spray droplets.”

Given these multiple conditions common to summer an early fall in the Salt Lake Valley, identified above as contrary to “safe” spraying, it is appropriate to ask if “safe” conditions actually ever exist. SLCMAD uses ULV nozzles, the purpose of which is to create extremely small droplets to prolong the suspension of the product in the air in order to intercept flying insects. But that also increases the drift of the product to non-target species and locations.

Several studies confirm that pesticides can become adsorbed to fine particulate matter, and as such can stay in the atmosphere between 3 and 10 days. Semivolatile pesticides, including permethrin, are mostly adsorbed to atmospheric particles, and “are very persistent with respect to the highly reactive hydroxyl radicals (OH) that is the self-cleaning agent of the atmosphere.”246 The authors of this study stated that the half-lives of this particulate phase for these chemicals can be several days to over a month, increasing the opportunity for these chemicals to travel long distances.247,248 During that time the pesticide can travel thousands of miles, especially if released from aircraft up to 300 ft above the ground as indicated by the SLCMAD’s EA.

Radioactively tagged pesticides have been shown to travel thousands of miles across oceans and to other hemispheres. For example, pesticides spread in the UK were found in the Southern United States 5-7 days later. Pesticides sprayed in the tropics have been traced to the Arctic. Naled is detectable in the atmosphere even in the absence of local naled use.249

As mentioned previously, pesticides are the chemical progeny of chemical weapons used in WWI. Few people are aware that the main reason why chemical weapons were banned after WWI is that it was widely recognized that it was impossible to control their atmospheric and geographic spread.250,137 In fact in recent years chemical drift of the herbicide dicamba, with its high vapor pressure, has led to the chemical being banned in some states because of millions of acres of damage to non-target soybeans fields. Naled and its breakdown product DDVP also have relatively high vapor pressure which adds to its potential for fugitive drift.251  

A pillar of the argument used to defend spraying is the contention that human exposure to the pesticides is low enough to be inconsequential. The validity of that assumption depends on whether traditional toxicology risk assessments (TRA)s by the EPA are valid expressions of human health harm. We join many other medical groups in the contention that they are not in and of themselves stand-alone determinants of disease potential and are often contradictory to research from the medical community. Please see Appendix A for a more detailed discussion of the scientific shortfalls of TRAs.

In 2011, the EPA made a statement supporting the supposed safety of pyrethroids based almost exclusively on experiments with adult rats. This type of narrow investigation is all too common a part of the EPA’s reliance on toxicology risk assessments. For SLCMAD to de-emphasize or ignore all the other experimental research and the human epidemiologic research, is cherry picking the science, and guarantees a poor conclusion. Presumptions of safety of low dose exposure are no longer valid using this methodology, including for permethrin.253 

Beyond poorly designed risk assessments, focusing on “extremely low” concentrations, is by no means the entire issue of human health risk. For the most vulnerable subset of the population, i.e fetuses and infants, what is most important is not the concentration of exposure as much as the timing of exposure in relationship to critical developmental windows. Conceptually it is fair to say if the chemical concentration is enough to be effective against mosquitoes after a single spraying, it is enough to be effective in harming fetal brain development after repeated spraying.

If that seems difficult to comprehend, consider this. A single drop of water, contaminated with just 1 part per billion of a toxic chemical, can contain 2.65 trillion molecules of that chemical, almost 30 molecules for every cell in a newborn baby’s brain. In their action as endocrine disruptors, the health consequences may not be linearly related to the dose. More specifically, some harm can occur at barely measurable doses, putting at risk hundreds of thousands of residents of the Salt Lake Valley from this spraying.

There is an inherent contradiction in the contention that neighborhoods are far enough away to avoid clinically relevant exposure to the pesticides, but at the same time they are close enough to the breeding areas to be victimized by the targeted mosquitoes. Although a few mosquito species can become “tourists” traveling hundreds of miles, most prefer to stay within 50 to 100 meters laterally, or 10 meters vertically from their nest, as long as their food supply is adequate.254 This is true of female Culex tarsalis mosquitoes, the species of greatest public health concern. They will not survive unless they are able to re-establish new breeding sites in human neighborhoods with food and water. The idea that the almost completely uninhabited (until the arrival of the inland port) Northwest Quadrant is a significant source of mosquitoes for humans miles away is not consistent with the evidence. If SLCMAD has evidence to the contrary they should offer that to the public. The real problem leading to human exposure lies in the neighborhoods themselves. In fact, most biting mosquito complaints from residents actually come from mosquitoes breeding on the residences’ own property rather than from miles away.

The assumption that surrounding neighborhoods are far enough away to avoid clinically relevant pesticide exposure is further contradicted by studies that show significantly higher levels of pesticides in the indoor dust of homes near agricultural fields and in the concentrations of pesticide metabolites in children who lived in those homes.252

In a recent SL Tribune article the SLCMAD Director tried to make the case that the amount of pesticide used in this project would be much lower than is used in agricultural and implied that epidemiologic studies finding adverse health outcomes for communities near agricultural pesticide use were therefore not applicable. If that comparison is being used to dispute epidemiological studies from agricultural exposed populations, the Director is misinformed or being disenguous.

The EA says SLCMAD plans to use 0.5 to 1 fluid oz. of Dibrom (naled) per acre, but can use up to 2 fl. oz. every seven days, and further they can use 104 fl. oz. (10.73 pounds) per acre per year. It also opens the door to even more spraying. “More frequent treatments may be made to prevent or control a threat to public and/or animal health determined by a state, tribal or local health or vector control agency” (which we assume is the SLCMAD).

By comparison, the instructions on naled specify various limitations for agricultural use, including 0.9 to 1.9 lbs per acre per year for almonds: for beans and peas–4.2 lbs per season: for broccoli, cabbage, cauliflower, brussels sprouts, kale, and collards—9.4 lbs. per acre per season: for cantaloupes and muskmelons—1.9 lbs per acre per season.  There was not a single crop listed for which the instructions on the use of naled, allowed as much pesticide to be used per acre as the SLCMAD has allowed for themselves in their EA.255

7. There are multiple oversights, inadequacies, omissions, inconsistencies, and errors in SLCMAD’s 

Environmental Assessment of their pesticide use.

SLCMAD’s EA states:“Surveillance results by the Salt Lake City Mosquito Abatement District indicate that mosquito species present in the northwest quadrant of Salt Lake City are extremely numerous during summer months and capable of transmitting serious human diseases. The mosquito populations are large enough to cause human pain, discomfort, and stress. The nuisance caused by mosquitoes during the summer can decrease the overall morale and quality of life within Salt Lake City if the mosquito number are not controlled.”

The EA goes on to justify the spraying program with a two-fold “purpose and need.” One, the mosquitoes are a nuisance. Two, to reduce “pathogen transmission.” To use “nuisance” as a justification for exposing thousands of people to toxic chemicals is inappropriate and represents priorities that we believe much of the community would dispute. Likewise, “service requests,” from the public cannot be considered justification for spraying environmental toxins. We contend that the community has a greater “ purpose and need” to not be exposed repeatedly to neurotoxins.

The EA states, “In the many years of its use, there have been no reports of toxic effects of Biomist 30+30 to people, pregnant women, pets, or other mammals.” The same could be said of just about any known toxins, radiation, lead, mercury, PCBs, etc. The toxicity to the population at large is primarily from chronic low-level exposure. The EA statement reflects a dangerous misunderstanding of the toxic effects of the product, as the previous part of our report provides in detail. We can only assume that the SLCMAD is alluding to acute, severe, life-threating reactions to the pesticide among those directly handling the product. Nonetheless, it reflects a completely inadequate appreciation of the public health consequences of the spraying program. 

According to a letter from the EPA, the label on naled says “Do not apply over bodies of water (lakes, rivers, permanent streams, natural ponds, commercial fish ponds, swamps, marshes or estuaries),” and “This product is toxic to fish, aquatic invertebrates, and wildlife.”255 As close as the designated area is to the Great Salt Lake, this seems like it’s use would be contradictory to what is allowed by even by the manufacturer.

That same letter says, “Applications must not occur during local, low-level temperature inversions. Temperature inversions restrict vertical air mixing, which causes small, suspended droplets to remain in a concentrated cloud. This cloud can move in unpredictable directions due to the light variable winds common during inversions.” However, the label for Biomist (permethrin) says that best results are obtained with, “weather conditions conducive to keeping the spray cloud close to the ground. And inversion of air temperatures and a light breeze is preferable.” It seems that the appropriate weather conditions are different and contradictory for each of the two pesticides.

The Biomist label also says,“This product is highly toxic to bees exposed to direct treatment on blooming crops or weeds,” and the EA admits the same. However, the naled label says “Do not apply this product as an Ultra Low Volume (ULV) spray (>1/2 gallon per acre), or in any carrier other than water,” and… “Aerial applications must not be made at a height greater than 10 feet above the top of the target plants unless a greater height is required for aircraft safety. Making applications at the lowest height that is safe reduces exposure of droplets to evaporation and wind.”255 All of these stipulations are contradicted by the plans detailed in SLCMAD’s EA.

The naled label says, “Do not apply this product in a way that will contact workers or other persons, either directly or through drift. Only protected handlers may be in the area during application.” SLCMAD does virtually nothing to notify the public prior to their spraying. The Director believes that it is ok to spray directly on anyone in the area because it is not forbidden by the EPA, stating, “If people prefer to stay inside when spraying takes place they can, but it is not necessary.” 

In Section 6 of the EA, Cumulative Impacts, there is no mention at all of cumulative impacts on human health which is a clear indication that the SLCMAD has no understanding of the issue, as detailed previously. In section 2.3 of the EA, various thresholds are listed to trigger aerial spraying on mosquito counts, but not on the number of mosquitoes infected with WNV. This again reflects an inappropriate priority by the SLCMAD. Public nuisance alone is not justification for spraying. 

In section 2.5 after listing the products intended to be used, the EA then leaves the door wide open to use virtually any insecticide, “Because of operational, biological, ecological, or economic needs, other EPA-approved adulticides with the same class of active ingredients may be used as well.” Given that the EPA has “approved” insecticides even more toxic than naled and permethrin, this phase must be stricken from the EA.

8. Pesticide spraying has adverse impacts on beneficial insects, 

bird populations, wildlife, the ecosystem of the 

Great Salt Lake and beyond

“Plants and insects are the fabric of this planet, and we’re ripping it to shreds.”—Scott Black, director Xerces Society273  

A recent headline in Smithsonian Magazine reads, “Insects Are Dying Off at an Alarming Rate”256Another from National Geographic reads, “You’ll Miss Them When They’re Gone.”257

The increase in mosquito populations obscures the fact that globally the overall mass of insects and the number of insect species is in steep decline.258 That this trend has been documented not just in agricultural areas, but also in the wild where insect populations have plummeted as much as 76%259 over the last 27 years, speaks to the sensitivity of this part of the animal world, if not the entire animal world, to the damage being done by ubiquitous, low levels of pesticides found throughout the entire globe, including areas far removed from where spraying occurs.

Insects are irreplaceable in keeping the world’s ecosystems and food chains viable, yet 40% of insects species are threatened with extinction.260 Species higher in the food chain suffer population losses (like birds on the Great Salt Lake), waste is not broken down as efficiently, slowing the transition to nutrients, pest insects gain advantage over their predators, pollinator populations decline (some bumble bees are now endangered species 260), and nutrition and water retention in soil declines which kills plant life and expands deserts. 

While there are multiple causes, pervasive use of pesticides is a major contributor to this loss of biodiversity and insect life. Unfortunately, insects like mosquitoes, flies, cockroaches, and agricultural pests with faster breeding cycles appear to be thriving for multiple reasons, including pesticides killing their predators, and global warming increasing their geographic domain. Pressure for more and more pesticide use will likely be brought to bear, so it becomes increasingly important that SLCMAD not succumb to poor, counterproductive, unscientific policy. Poor local policy playing out in tens of thousands of locations has brought us to this global ecological precipice. Tunnel vision from the SLCMAD contributes to this much broader problem with its pesticide spraying program.

It seems we have learned nothing 60 years after Rachael Carson’s Silent Spring. 

We defer to other groups like the Audubon Society for comments on the impact of pesticide spraying on birds in the Great Salt Lake ecosystem. But from a larger perspective, a recent headline in the Scientific American is chilling; “Silent Skies: Billions of North American Birds Have Vanished.” Bird populations have declined by 3 billion since the 1970s, a decline of about 30%.261 The cause of this alarming drop is multi-factorial, but there is no doubt that the loss of insects and the pesticides themselves have contributed significantly to this precipitous decline.

For more information and research on the impact on the Great Salt Lake ecosystem we refer you to the comments submitted by David Richards, Ph.D, OreoHelix Ecological.

9. There are Better Ways to Control Mosquitoes

Numerous cities and counties have adopted mosquito control strategies that do not include spraying adulticides. This group includes Lyndhurst, Ohio, Washington, DC, York County, Virginia, Dallas, Texas, Ft. Worth, Texas, Nassau County, New York, Marblehead, MA, Boulder, Colorado, Lane County, OR, and Seattle, WA.

Below are links to strategies in three communities that have been effective and avoided spraying adulticides: Boulder County, CO, Washington, DC, Madison, Wi., and an excellent control strategy from the Xerces Society.


The scientific and empirical evidence is overwhelming that spraying adulticides to kill mosquitoes, especially aerial spraying, is ineffective, and can be even counterproductive, over the long term, and even the short term, to both goals of controlling mosquito populations and preventing West Nile Virus. Furthermore, the medical literature strongly indicates that routine aerial spraying over Salt Lake City’s airshed represents a broad-based danger to public health. Utah Physicians for a Healthy Environment (UPHE) implore SLCMAD to end all of their insecticide spraying for mosquitoes, whether from back packs, trucks, or airplanes. This practice is an institutionalized relic of the 1950s and should be stopped immediately.

Brian Moench, MD
President, Utah Physicians for a Healthy Environment (UPHE)
Salt Lake City, UT

Kirtly Parker Jones MD
Professor Emerita
Department of Obstetrics and Gynecology
University of Utah
Board member, UPHE
Salt Lake City, UT

John R Macfarlane, MD
Board member, UPHE
Salt Lake City, UT

Park Willis, MD MD, FACP
Emeritus Professor of Medicine
University of North Carolina at Chapel Hill
Board member, UPHE

Richard E. Kanner, MD
Professor of Internal Medicine
University of Utah Health Sciences Center
Department of Internal Medicine
Division of Respiratory, Critical Care & Occupational Medicine
Board member, UPHE
Salt Lake City, UT

E. Thomas Nelson, MD
Emergency Medicine Physician
Board member, UPHE
Salt Lake City, UT

Courtney Henley, MD
Board member, UPHE
Salt Lake City, UT

Sarah Johnson, MD, MPH
Board member, UPHE
Salt Lake City, UT

Lou Borgenicht, MD
Retired Pediatrician
Salt Lake City, UT

Phyllis Leppert, MD, PhD
Emerita Professor of Obstetrics and Gynecology.
Duke University School of Medicine
President, The Campion Fund

Michael A. Kalm, M.D., D.L.F.A.P.A,
Past president Utah Psychiatric Association, Clinical Assistant Professor, University of Utah Medical School Department of Psychiatry.
(Distinguished Life Fellow of the American Psychiatric Association)
Salt Lake City, UT

Tom Metcalf, MD
Murray, UT

Megan Link MD
Reproductive Endocrinology and Infertility
University of Utah

Meredith Humphreys MD
Reproductive Endocrinology and Infertility
University of Utah

Laruen Elizabeth Verrilli MD
Reproductive Endocrinology and Infertility
University of Utah

Appendix A—Problems with Toxicology Risk Assessments

“The ultimate effect of these institutional defects is that chemical risk assessments in the US and the EU have a safety bar for approval that is so low that regulators virtually never decline to approve a chemical. In contrast, the exact same institutions use standards for taking any chemical off the market that are so high that such an event nearly never happens. Yet if both standards were based purely on science, as they claim to be, both bars would be the same height…

Chemical risk assessments themselves are the problem”

—Jonathan Latham, PhD, 
the Cornucopia Institute

Virtually all toxicity data used by the EPA comes from a testing program called “toxicology risk assessments (TRAs),” the same approach that polluting industries, chemical manufacturers, and unfortunately regulatory bodies use to assess whether a certain project such as citing of a pollution source, like a refinery or incinerator, or a chemical spraying program will create a public health risk. It is an antiquated, inadequate and scientifically deeply flawed process.

The science of toxicology is still tethered to a principle first advocated by the father of toxicology, Paracelsus (Theophrastus von Hohenheim), a 15th-16th Century Swiss physician, alchemist, and astrologer. His contribution to the Renaissance was the fundamental classic toxicology theory that “the dose makes the poison.” In other words, there is a threshold at which low concentrations of toxic substances no longer present a threat to human health and above that threshold, the harm is proportional to the dose. That is still the basis of modern-day toxicology and government environmental regulations. But that assumption and the methodology based upon that assumption was flawed when it was adopted in the 1970s and it is all the more so now. 

Regulatory toxicology testing primarily has consisted of high dose testing on adult animals, usually mice or rats, and subsequent testing at progressively lower doses in an attempt to establish a dose response model from which a threshold can be derived below which effects, usually death or cancer, could no longer be identified.

This methodology is deeply flawed for numerous reasons, and has contributed greatly to a barrage of unsafe and inadequately tested chemicals being unleashed upon the public and the environment.

How TRAs originated is instructive. They were first used by the EPA in 1975 under pressure from industry to dismiss health risks of one of the earliest known toxins, vinyl chloride. The EPA felt like they could respond authoritatively if they could calculate the number of cancers that would be caused by exposing the population to vinyl chloride. Federal regulators then started adopting that technique with many other environmental controversies and disputes with industry, and that methodology continues today. The makers of toxic chemicals and industrial polluters are content to see it continue because with supposedly hard, mathematical data, the risks of chemicals and contaminants are easily obscured. Below are eleven reasons why TRAs fail to identify many health risks, and usually underestimate the toxicity of chemicals.

1. Most of the research used in risk assessments is supplied by the chemical manufacturers themselves or from contract labs hired by the companies. The potential for corruption of that system is obvious, but starkly illustrated by the history of Industrial Bio-Test Labs (IBT). For three decades IBT performed one third of all the toxicology testing in the United States. Several of its executives were convicted in 1983 of extensive scientific misconduct for fraudulent research favoring industry.262,263 IBT had performed over 2,000 key product safety tests resulting in the release of 212 pesticides. After an extensive review in 1983, EPA determined that only 16% of IBT’s testing results were valid.264 Only a tiny number of the invalid studies have been replaced, the agency admits, and most of those pesticides continue to be marketed, sold, and used.262

As disturbing as this scandal is, the EPA process created in the wake of that scandal is even more so. EPA has established a research protocol called  Mutual Acceptance of Data (MAD), whose effect is to exclude truly independent, peer-reviewed scientific research, like from academia, in favor of industry produced research. 

Jonathan Latham, PhD, writes for the Cornucopia Institute,…“no EPA employee ever sets eyes on the original experiments or the primary data, and only a handful can access even the summarised results. This system has the consequence of excluding any formal possibility that whistleblowing on the part of Federal employees or FOIA requests (from outsiders) might reveal fraudulent or otherwise problematic tests. EPA calculatedly turned a blind eye to any potential future wrongdoing in the full knowledge that the chemical regulatory system it oversaw was systemically corrupt.” 

2. TRAs overlook the presence of non-monotonic dose-response curves, i.e. the relationship between dose and outcome is not linear. There are hundreds of studies that show non-linearity is also true for other thoroughly researched toxins like air pollution and lead. Non-linear dose response curves open the possibility that adverse health outcomes occur at concentrations below the classic toxicological no-observed-adverse-effect level (NOAEL). Indeed, numerous studies have shown that some toxins are actually more dangerous at lower concentrations than higher ones. Furthermore, these magical thresholds of safety don’t really exist even in those cases where the relationship is linear.

3. There are obviously numerous health outcomes beyond death and cancer that are more difficult or impossible to identify in animals, like infertility, immunosuppression, endocrine disruption, neurodegenerative diseases, altered behavior and subtle, reduced intellectual capacity, which are exactly the health outcomes of greatest concern with pesticides in general, and the specific chemicals that SLCMAD intends to use.

4. The impact of toxins on genetic and epigenetic integrity may show up in subsequent generations, even if they are not exposed. But examining subsequent generations are seldom part of the research.

5. There is increasing evidence that neurotoxicity can be very sex specific, something that is increasingly apparent in human studies, but seldom part of the animal studies done for risk assessments.

6. This strategy ignores critical differences in physiology, metabolism, microanatomy, hormones, liver function, and enzyme production between fetuses, infants, children and adults. Chemicals crossing the placenta and affecting fetal development has been an after-thought at best. 

7. Toxicology risk assessments are basically mathematical calculations. These calculations dramatically oversimplify very complex biologic, physiologic and molecular processes that don’t lend themselves to mathematical equations.

8. The assessments do not pass the acid test of scientific reproducibility. Two different “assessors” can come up with widely disparate results given the same input data, especially if they have different motivations___subjectivity rather than objectivity.  William Ruckelshaus the former EPA director wrote in 1984, “We should remember that risk assessment can be like the captured spy: If you torture it long enough, it will tell you anything you want to know.”265 In 1991, the National Academy of Sciences wrote, “Risk assessment techniques are highly speculative, and almost all rely on multiple assumptions of fact — some of which are entirely untestable.”266 

9. Through biological processes many toxic substances accumulate in organisms, concentrate in certain tissues of those organisms, and increase in concentration as they move up the food chain. Humans are at the top of the food chain and because our capacity to break down toxic chemicals is very limited, concentrations in our bodies usually increase over time. Lipophilic (fat-like) toxins will concentrate especially in human breast milk increasing the risk to progeny but that kind of exposure consequence is not addressed by the EPA’s methodology. 

10. Classical toxicology assessments almost never attempt to evaluate more than one toxin at a time, and the regulations derived from those risk assessments are similarly singularly focused. The default assumption is that the hazard posed by each individual compound, tested out of context and in isolation, can predict the hazard of the entire complex mixtures of chemicals. Obviously no one on earth is exposed to merely one chemical. No children on the West side, in North Salt Lake or West Bountiful are exposed to just one neurotoxin. Furthermore, the potential for toxicity may be much greater than just the additive sum of all these chemicals individually. Specifically, synergistic effects from chemical interactions are quite possible, if not likely, which would significantly increase the potential for health hazards.267 In fact SLCMAD intends to use a synergistic agent that may increase the lethality of the chemical mix to insects, and the toxicity to humans by a factor of ten.

Under the absurd methodology of only considering one toxin at a time, a safe dose of aspirin, combined with safe doses of ibuprofen, Oxycontin, Toradol, Celebrex, acetaminophen, three glasses of wine, and a pint of Jack Daniels would all be considered individually “safe,” but in reality might very well add up to be lethal. When a supposedly tolerable exposure to diesel exhaust is combined with a tolerable exposure to cadmium, fluoride, lead, arsenic, permethrin and naled, the end result can be an intolerable health consequence. But the source of each of these toxins can claim to the community that their toxin is safe.

Furthermore, it is routine for toxicology experiments to only use exposure to the “active ingredient” in a product, when the “inactive” compounds, like adjuvants and surfactants, are often toxic as well, and sometimes more so.

11. Traditional toxicology assessments wrongly assume that we have a comprehensive understanding of the complexity of biological processes and chemical toxicity when in reality there are vast information gaps. Lack of knowledge cannot be equated with safety; it can only be equated with lack of knowledge. Much of that lack of knowledge is deliberately orchestrated by the manufacturers. The most basic information is not available on over 90 percent of the industry inventory of chemical products.  The Government Accountability Office says that 95 percent of the information given to the EPA by companies on their new chemicals are wrapped up in confidentiality claims, which makes them unavailable to regulators. Almost all the data that is available is supplied by the manufacturer whose obvious self-interest obscures objectivity. And the cumulative health impact of exposure to all these chemicals is ignored.

Manufacturers don’t even have to reveal enough of the chemical mix of their products to allow government agencies to track their spread in the environment or to independently test for toxicity.  The TSCA requires manufacturers to submit safety data only if they have it. Most don’t, so the EPA is left with computer models to predict whether chemicals will pose health problems, and no one believes that is adequate. In those rare instances where evidence stacks up implicating a chemical as a serious hazard, industry response follows a well-worn path. “By the time the scientific community catches up to one chemical, industry moves on to another and they go back to their playbook of delay and denial,” said Deborah Rice, a former EPA toxicologist who now works for the Maine Center for Disease Control and Prevention.268 

Despite all this, the anachronistic premise that the “dose makes the poison,” established almost exclusively in lab animals, is still the basis of toxicology risk assessments. This testing frame work is now increasingly recognized within the medical community as a pillar of misunderstanding and misinformation routinely used by industry, especially chemicals corporations to claim their products are safe and which leads to regulatory agencies approving their use. It is this regulatory framework that the SLCMAD relies upon to exonerate their pesticide spraying program as a “safe,” or “acceptable” risk to public health. 

Because of the obvious short comings of risk assessments, countries in Europe began embracing a more protective approach to toxic chemical exposures guided by the “precautionary principle.” The principle can be expressed this way. When there is reasonable evidence of harm, society is compelled to act to protect the public, rather than wait for scientific proof. This adoption of the precautionary principle was even written into the Maastricht Treaty that formed the European Union. Journalist Peter Montague describes this difference between European and American regulation of chemicals this way. The European model asks, “How much is avoidable?”  The American model asks, “How much harm is acceptable?”269 The United States’ approach prioritizes protection of corporations and chemicals rather than public health. The precautionary principle has not been allowed to enter the arena of government regulation under either Democratic or Republican Administrations because of corporate pressure.  

The result has been frank regulatory failures, and the failures started with original chemical safety law, the Toxic Substances Control Act (TSCA), passed in 1976, virtually written by the chemical industry. It allowed all 62,000 chemicals that were on the market at the time to remain so, unless the EPA found at some later time that they represented unacceptable risk. 

Only undeniable health consequences and apparent toxicity after consumer use and wide spread environmental contamination of the products needed to be reported to the EPA. If this seems like closing the barn door after the horses have already escaped, bear in mind that before 1976, there was no barn door at all preventing or regulating chemicals that were unleashed upon the public. 

Furthermore, the law only allowed testing if information from the chemical makers themselves suggested it was likely to be dangerous. Moreover, the law allowed chemical corporations to claim just about everything was a trade secret allowing them to hide critical information from the public, regulators and even health care providers. As a result, the EPA has only tested about 200 of all 140,000 industrial chemicals produced since WWII. For chemicals entering the market since 1976 they are also allowed unless the EPA again determines they constitute unreasonable risk.270 But they only have 90 days to make that determination and hardly ever do they have all the data they need. The end result is virtually all the chemicals made by corporations will make it into the bodies of consumers. For example, despite it being an undeniable killer of tens of thousands of people, it is still legal to manufacture and sell asbestos.  

When the EPA tried to ban asbestos in 1991, the asbestos industry went to court, and a judge overruled the ban because they hadn’t considered the costs of the ban as required by the deeply flawed TSCA. While asbestos use has plummeted, it is still allowed in brake pads and to manufacture chlorine. The EPA in its entire history has only succeeded in completely banning eight chemicals–PCBs, dioxins, fully halogenated chlorofluoroalkanes (ozone depleters), hexavalent chromium (the Erin Brockovich chemical), and four metal working chemicals.  The last time the EPA banned anything completely was in 1984.271 However it should be noted that the EPA did ban indoor use of one of the chemical groups that SLCMAD intends to use (organophosphates) which, given the EPA’s history, speaks volumes about their toxicity.

Regulatory impotence flows from the default assumption that industrial chemicals are safe, unless or until, unequivocally proven unsafe. Essentially human consumers are today’s guinea pigs of the chemical industry, just like the previous generation was for DDT, PCBs, asbestos, radiation and lead.  Once a dangerous product is put on the market, it is only withdrawn after it has already caused large scale, undeniable damage and/or death.

Appendix B

A close examination of the literature cited by SLCMAD in their 

defense of pesticide spraying

Carney RM, Husted S, Jean C, Glaser C, Kramer V. 2005. Efficacy of aerial spraying of mosquito adulticide in reducing incidence of West Nile Virus, California. Emerging Infectious Diseases. 14:747-54.

Data from 2005–spraying works.

Currier M, McNeill, M, Campbell D, Newton N, Marr JS Perry E, Berg SW, Barr DB, Luber GE, Kieszak MA, Rogers HS, Backer LC Belson MG Bubin C Azziz-Baumgartner E, Duprey ZH. 2005. Human exposure to mosquito-control pesticides- Mississippi, North Carolina, and Virginia, 2002 and 2003. MMWR. 54: 529-532.

Not a study

Davis RS, Peterson RK. 2008. Effects of single and multiple applications of mosquito insecticides on nontarget arthropods. Journal of the American Mosquito Control Association. 24: 270-280.

Data from 2005—on “benign effect” non-target arthropods.

Duprey Z, Rivers S, Luber G, Becker A, Blackmore C, Barr D, Weerasekera G, Kieszak S, Flanders WD, Rubin C. 2008. Community aerial mosquito control and naled exposure. Journal of the American Mosquito Control Association. 24: 42-46.

2004 Study that showed less naled metabolites in urine after spraying than before, although metabolites till present 40 hours after.

Elnaiem DEA, Kelley K, Wright S, Laffey R, Yoshimura G, Reed M, Goodman G, Thiemann T,Reimer L, Reisen WK, and Brown D. 2008. Impact of aerial spraying of pyrethrin insecticideon Culex pipiens and Culex tarsalis (Diptera: Culicidae) abundance and West Nile virus infectionrates in an urban/suburban area of Sacramento County, California. Journal of MedicalEntomology. 45: 751–757.

2008 published date. An area aerially sprayed three consecutive night showed a 50% reduction in two species of mosquito that carry WNV 2 weeks later, but was not statistically significant for the species that is the primary vector for WNV in Utah, Culex tarsalis.  No information on long term mosquito populations and no correlation with human WNV cases. Note that it required three consecutive nights of spraying to achieve even that temporary reduction.

Holcomb KM, Reiner RC, Barker CM. 2021. Spatio-temporal impacts of aerial adulticideapplications on populations of West Nile virus vector mosquitoes. Parasites and Vectors. 14:

While this modeling study is the most recent of the ones cited by the Director, citing data up to 2017, aerial spraying only reduced Culex tarsalis by 30.7%

Karpati AM, Perrin MC, Matte T, Leighton J, Schwartz J, Barr RG. 2004. Pesticide spraying for West Nile virus control and emergency department asthma visits in New York City, 2000. Environmental Health Perspectives. 112: 1183-1187.

SLCMAD’s director keeps citing this study as evidence for no effect on human health. In addition to the comments made earlier in this report, please note this physician written editorial below that was published in the same journal in response to this study, mentioning many of the same critiques that we have. Also note that this critique was written in 2005 when the incidence of WNV was much greater than it is now.

Ziem G. Pesticide spraying and health effects. Environ Health Perspect. 2005;113(3):A150-A151. Doi:10.1289/ehp.113-a150a

“I noticed with interest the article “Pesticide Spraying for West Nile Virus Control and Emergency Department Asthma Visits in New York City, 2000” by Karpati et al. (2004). I am a physician who treats hundreds of patients with chronic illness from chemical overexposure. Many of these patients have toxic encephalopathy, reactive airway disease, and other chemically induced organ system damage. When my patients become ill from pesticide spraying, they usually do not head for an emergency room, where they typically experience long waits in an environment containing germicidal residue, scented products, carbonless copy paper, hospital linens with heavy fabric softener, and other exposures. In addition, they have learned from experience that emergency department personnel often do not understand their condition and do not know how to treat it. Thus your survey, while with admirable intent, greatly underestimates the problem of respiratory exacerbation from West Nile virus pesticide use. Many of my patients have experienced severe neurologic and respiratory exacerbations as well as other organ system damage, such as significant increase in liver enzymes, from exposure to residue from pesticide spraying for West Nile virus. In addition, it is my understanding that these pesticides are not effective for controlling adult mosquitoes and that the Centers for Disease Control and Prevention and other authorities recommend larvae control. The extent of exacerbation of illness caused by pesticide use for West Nile virus control is likely greater than the number of cases of West Nile virus.

Persons who are at increased risk for symptom exacerbation from pesticide spraying such as that used for West Nile virus control include individuals with migraines, chronic sinus problems, asthma, reactive airway disease, autoimmune diseases (many of which are exacerbated by pesticide exposure), and conventional allergies (Kipen et al. 1994). There is increased respiratory inflammation with conventional allergies, and pesticides more readily enter the body because the barrier function of the respiratory tract is further compromised. In addition, Karpati et al. (2004) failed to take note of the U.S. Environmental Protection Agency (EPA) final report “Principles of Neurotoxicity Risk Assessment” (U.S. EPA 1994). This document confirmed the lack of a blood–brain barrier between the nose and the brain, so that pesticides readily enter the body through the nose and pass directly to the brain. This report further confirmed the unusual vulnerability of the brain to neurotoxicants: pesticides are lipophilic and therefore seek out lipid tissue such as the brain, and because the brain has unusually long neurons, repair of damage in the neurons occurs much less readily than in other body cells.”

Other groups at increased risk of pesticides are those with chronic obstructive lung disease, toxic encephalopathy, and neural degenerative diseases. Pyrethroid pesticides are significant neurotoxins (Eells et al. 1992; McDaniel and Moser 1993; Tippe 1993; Vijverberg and van den Bercken 1990), and because they are increasingly replacing organophosphates, they now account for a large proportion of the pesticide-induced chronic illness among my patients. Emergency room visits are merely the tip of the iceberg, and patients with many of these disorders usually avoid the emergency room. Thus, the use of emergency rooms is not a sensitive indicator of body damage from pesticides.

Lothrop HD, Lothrop BB, Gomsi DE and Reisen WK. 2008. Intensive early season adulticide applications decrease arbovirus transmission throughout the Coachella Valley, Riverside County, California. Vector Borne and Zoonotic Diseases. 8: 475-490.

This study describes a spraying strategy from 2006 in California. Mosquitoes worldwide have demonstrated increased resistance since then. This study reported the results of extreme strategy of intense aerial spraying, 26 “treatments” over 40 nights. Still, the overall mosquito kill rate was still only 61%. We cited previously researchers that found in order to achieve effective mosquito control, kill rates needed to be above 90% (reference #183). Furthermore, the authors state that, “Too few dead birds or human cases were detected for meaningful statistical analysis.” This study provides weak if any support for SLCMAD’s current spraying strategy.

Macedo, PA, Schleier, III JJ, Reed M, Kelley K, Goodman GW, Brown DA and Peterson RKD. 2010. Evaluation of efficacy and human health risk of aerial ultra-low volume applications of pyrethrins and piperonyl butoxide for adult mosquito management in response to West Nile virus activity in Sacramento County, California. Journal of the American Mosquito Control Association. 26: 57-66.

SLCMAD cites this study as an indication that no human health risk occurs from spraying. This study does not provide any evidence to make such a claim. The study’s conclusions are based on modeled, estimated concentrations of exposure, not actual measured external exposures, or internal tissue or blood concentrations. And it uses EPA risk assessments (TRAs), the deficiency of which are thoroughly explained in Appendix A. Furthermore, the model used multiple assumptions that were not correct, such as exposure was limited to 24 hours. 

This study too estimated kill rates at 57% and 41% for pathogen carrying mosquitoes, well below the 90% threshold required for effective mosquito control. Furthermore, this study only included kill rates up to 12 hours after spraying, hardly a meaningful time frame in community mosquito control.

In defending pesticide spraying SLCMAD’s director has stated that strategies from other cities that successfully do not use pesticides, cannot be extrapolated to SLC because of different topography, weather, wind patterns, surface water, etc.  But at the same time SLC uses studies in done in other areas with where are these features are different to provide support that spraying pesticides work. SLCMAD is obviously starkly inconsistent, and cherry picking when they are willing to invoke evidence from other areas.

Peterson RKD, Macedo PA, Davis RS. 2006. A human-health risk assessment for West Nile virus and insecticides used in mosquito management. Environmental Health Perspectives. 114: 366- 372.

This 15 year-old study purports to evaluate the health consequences of mosquito pesticide spraying modeled, not actual exposures, and plugging those into traditional TRA methodology, compared to the risks of poor health outcomes from WNV. Again, TRAs do not come close to evaluating the actual consequences of pesticide exposure, nor does it address how or if pesticides may actually decrease the risk of WNV infections.

Reisen, W, Brault AC. 2007. West Nile virus in North America: perspectives on epidemiology and intervention. Pest Management Science. 63: 641-646.

This article has nothing to do with pesticide risk, in fact, if anything supports a no-spray strategy, the authors state, “because of the low prevalence of human infection during epidemics (<3%) and the relatively low rate of clinical illness in infected individuals, vaccination of the US population has not been considered a viable intervention option, even in high-risk areas.”

Staples JE, Shankar MB, Sejvar JJ, Meltzer MI, Fischer M. 2014. Initial and long-term costs of patients hospitalized with West Nile virus disease. American Journal of Tropical Medicine and

This review article does not provide any useful information on the issue.


1.  Aerial Pesticide Exposure Increases the Risk of Developmental Delay and Autism Spectrum Disorder. Steven D. Hicks, Vignesh Doraiswamy, Katherine Fry, Eric Wohlford. Pediatrics, Penn State Milton S. Hershey Medical Center, Hershey, PA; Pediatrics, SUNY Upstate Medical University, Syracuse, NY. Saturday, April 30, 2016

2.  Li J, et al. Ecotoxicology and Environmental Safety Observation of organochlorine pesticides in the air of the Mt. Everest region. Ecotoxicology and Environmental Safety. Volume 63, Issue 1, January 2006, Pages 33-41

3.  Jamieson, A., Malkocs, T., Piertney, S. et al. Bioaccumulation of persistent organic pollutants in the deepest ocean fauna. Nat Ecol Evol 1, 0051 (2017).


5.  Vandenberg L, et al. Hormones and Endocrine-Disrupting Chemicals: Low-Dose Effects and Nonmonotonic Dose Responses. Endocr Rev. 2012 Jun; 33(3): 378–455. Published online 2012 Mar 14. doi: 10.1210/er.2011-1050 PMCID: PMC3365860


7.  Li AJ, and Kannana K. Urinary concentrations and profiles of organophosphate and pyrethroid pesticide metabolites and phenoxyacid herbicides in populations in eight countries

Environ Int. 2018 Dec; 121(Pt 2): 1148–1154. Published online 2018 Oct 26. doi: 10.1016/j.envint.2018.10.033

8.  Witczak A, Pohoryło A, Abdel-Gawad H. Endocrine-Disrupting Organochlorine Pesticides in Human Breast Milk: Changes during Lactation. Nutrients 2021, 13, 229.


10.  National Research Council. Pesticides in the Diets of Infants and Children. Washington, DC: National Academy Press; 1993

11. Bretveld RW, Thomas CM, Scheepers PT, Zielhuis GA, Roeleveld N. Pesticide exposure: the hormonal function of the female reproductive system disrupted?. Reprod Biol Endocrinol. 2006;4:30. Published 2006 May 31. doi:10.1186/1477-7827-4-30

12.  Sheets LP (2000) A consideration of age-dependent differences in susceptibility to organophosphorus and pyrethroid insecticides. Neurotoxicology 21: 57–63 [PubMed: 10794385] 

13.  Anand SS, Kim KB, Padilla S, Muralidhara S, Kim HJ, Fisher JW, Bruckner JV (2006) Ontogeny of hepatic and plasma metabolism of deltamethrin in vitro: role in age-dependent acute neurotoxicity. Drug Metab Dispos 34: 389–397 Doi 10.1124/dmd.105.007807 [PubMed: 16326812]

14.  Fortin MC, Aleksunes LM, Richardson JR (2013) Alteration of the expression of pesticide- metabolizing enzymes in pregnant mice: potential role in the increased vulnerability of the developing brain. Drug Metab Dispos 41: 326–331 Doi 10.1124/dmd.112.049395 [PubMed: 23223497]

15.  Faustman EM, Silbernagel SM, Fenske RA, Burbacher TM, Ponce RA (2000) Mechanisms underlying Children’s susceptibility to environmental toxicants. Environ Health Perspect 108 Suppl 1: 13–21

16.  Cantalamessa F. Acute toxicity of two pyrethroids, permethrin and cypermethrin, in neo-natal and adult rats. Arch Toxicol.1993;67 :510– 513

17. Amaraneni M, Pang J, Mortuza TB, Muralidhara S, Cummings BS, White CA, Vorhees CV, Zastre J, Bruckner JV (2017) Brain uptake of deltamethrin in rats as a function of plasma protein binding and blood-brain barrier maturation. Neurotoxicology 62: 24–29 Doi 10.1016/j.neuro.2017.04.009 [PubMed: 28495520]

18.  Centers for Disease Control and Prevention. Second National Report on Human Exposure to Environmental Chemicals. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention; 2003. Available at:

19.  Zheng W. Neurotoxicology of the brain barrier: new implications. Clin Toxicol.2001;30 :711– 719

20.  Bradman A, Barr DB, Claus Henn BG, Drumheller T, Curry C, Eskenazi B. 2003. Measurement of pesticides and other toxicants in amniotic fluid as a potential biomarker of pre-natal exposure: a validation study. Environ Health Perspect. 111:1779-178214594631.

21.  Acta Neuropathol. 2019 September ; 138(3): 343–362. doi:10.1007/s00401-019-02033-9. 

22.  Corcellas C, Feo ML, Torres JP, Malm O, Ocampo-Duque W, Eljarrat E, Barceló D. Pyrethroids in human breast milk: occurrence and nursing daily intake estimation. Environ Int. 2012 Oct 15;47:17-22. doi: 10.1016/j.envint.2012.05.007. Epub 2012 Jun 19. PMID: 22717642.

23.  Bouwman H, Kylin H. Malaria control insecticide residues in breast milk: the need to consider infant health risks. Environ Health Perspect. 2009 Oct;117(10):1477-80. doi: 10.1289/ehp.0900605. Epub 2009 May 1. PMID: 20019894; PMCID: PMC2790498.

24.  Zehringer M , Herrmann A. Analysis of polychlorinated biphenyls, pyrethroid insecticides and fragrances in human milk using a laminar cup liner in the GC injector. Eur Food Res Technol. 2001;212:247-51.

25.  Salama A. Toxicology: Open Access. Salama, Toxicol Open Access 2017, 3:1

26.  Burke RD, Todd SW, Lumsden E, Mullins RJ, Mamczarz J, Fawcett WP, Gullapalli RP, Randall WR, Pereira EFR, Albuquerque EX (2017) Developmental neurotoxicity of the organophosphorus insecticide chlorpyrifos: from clinical findings to preclinical models and potential mechanisms. J Neurochem 142 Suppl 2: 162–177 Doi 10.1111/jnc.14077 [PubMed: 28791702]

27.  Terry AV Jr. (2012) Functional consequences of repeated organophosphate exposure: potential non-cholinergic mechanisms. Pharmacol Ther 134: 355–365 Doi 10.1016/j.pharmthera. 2012.03.001 [PubMed: 22465060]

28.  Singh N, Lawana V, Luo J, Phong P, Abdalla A, Palanisamy B, Rokad D, Sarkar S, Jin H, Anantharam V et al. (2018) Organophosphate pesticide chlorpyrifos impairs STAT1 signaling to induce dopaminergic neurotoxicity: Implications for mitochondria mediated oxidative stress

29.  Chung WM, Buseman CM, Joyner SN, Hughes SM, Fomby TB, Luby JP, Haley RW. 2013. The 2012 West Nile encephalitis epidemic in Dallas, Texas. J Am Med Assoc. 310: 297-307.

30.  Karpati AM, Perrin MC, Matte T, Leighton J, Schwartz J, Barr RG. 2004. Pesticide spraying for West Nile virus control and emergency department asthma visits in New York City, 2000. Environ Health Perspect. 112: 1183-1187

31.  Macedo PA, Peterson RK, Davis RS. 2007. Risk assessments for exposure of deployed military personnel to insecticides and personal protective measures used for disease-vector management.  J Toxicol Environ Health A. 70: 1758-1771. O’Sullivan BC, Lafleur J, Fridal K, Hormozdi S, Schwartz S, Belt M, Finkel M. 2005. The effect of pesticide spraying on the rate and severity of ED asthma. Am J Emerg Med. 23: 463-467.

32.  Preftakes CJ, Schleier JJ III, Peterson RK. 2011. Bystander exposure to ultra-low-volume insecticide applications used for adult mosquito management.  Int J Environ Res Public Health. 8: 2142-2152.

33.  O’Sullivan BC, Lafleur J, Fridal K, Hormozdi S, Schwartz S, Belt M, Finkel M. 2005. The effect of pesticide spraying on the rate and severity of ED asthma. Am J Emerg Med. 23: 463-467.

34.  Peterson RK, Macedo PA, Davis RS. 2006. A human-health risk assessment for West Nile virus and insecticides used in mosquito management.  Environ Health Perspect. 114: 366-372.

35. Trunnelle K, et al.  Urinary Pyrethroid and Chlorpyrifos Metabolite Concentrations in Northern California Families and Their Relationship to Indoor Residential Insecticide Levels, Part of the Study of Use of Products and Exposure Related Behavior (SUPERB)

Environmental Science & Technology 2014 48 (3), 1931-19

DOI: 10.1021/es403661a

36.  Saillenfait AM, Ndiaye D, Sabaté JP. Pyrethroids: exposure and health effects–an update. Int J Hyg Environ Health. 2015 May;218(3):281-92. doi: 10.1016/j.ijheh.2015.01.002. Epub 2015 Jan 15. PMID: 25648288.

37.  Crow JA, Borazjani A, Potter PM, Ross MK (2007) Hydrolysis of pyrethroids by human and rat tissues: examination of intestinal, liver and serum carboxylesterases. Toxicol Appl Pharmacol 221: 1–12 Doi 10.1016/j.taap.2007.03.002 [PubMed: 17442360]

38.  Godin SJ, DeVito MJ, Hughes MF, Ross DG, Scollon EJ, Starr JM, Setzer RW, Conolly RB, Tornero-Velez R (2010) Physiologically based pharmacokinetic modeling of deltamethrin: development of a rat and human diffusion-limited model. Toxicol Sci 115: 330–343 Doi 10.1093/ toxsci/kfq051 [PubMed: 20200215]

39.  Narahashi, T. Nerve membrane ion channels as the target site of environmental toxicants, Environmental Health Perspectives,71:25-9, April 1987.

40.  Gaylord A, et al. Trends in neurodevelopmental disability burden due to early life chemical exposure in the USA from 2001 to 2016: A population-based disease burden and cost analysis. Molecular and Cellular Endocrinology, 2020; 110666


42.  Shafer TJ, Meyer DA, Crofton KM (2005) Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Environ Health Perspect 113: 123–136 [PubMed: 15687048]

43.  Agrawal S, Singh A, Tripathi P, Mishra M, Singh PK, Singh MP (2015) Cypermethrin-induced nigrostriatal dopaminergic neurodegeneration alters the mitochondrial function: a proteomics study. Mol Neurobiol 51: 448–465 Doi 10.1007/s12035-014-8696-7 [PubMed: 24760363]

44. Hicks SD, Wang M, Fry K, Doraiswamy V and Wohlford EM (2017) Neurodevelopmental Delay Diagnosis Rates Are Increased in a Region with Aerial Pesticide Application. Front. Pediatr. 5:116. doi: 10.3389/fped.2017.00116. Aerial Pesticide Exposure Increases the Risk of Developmental Delay and Autism Spectrum Disorder.

45.  Viel J-F, et al. Pyrethroid insecticide exposure and cognitive developmental disabilities in children: The PELAGIE mother–child cohort. Environment International, 2015; 82: 69 DOI: 10.1016/j.envint.2015.05.009

46.  Oulhote Y, Bouchard MF. Urinary metabolites of organophosphate and pyrethroid pesticides and behavioral problems in Canadian children. Environ Health Perspect 121:1378–1384;

47.  Lazarini C, Florio J, Lemonica I, Bernardi M. 2001. Effects of prenatal exposure to deltamethrin on forced swimming behavior, motor activity, and striatal dopamine levels in male and female rats.Neurotoxicol Teratol 23:665-67311792535.

48.  Richardson JR, Taylor MM, Shalat SL, Guillot TS 3rd, Caudle WM, Hossain MM, Mathews TA, Jones SR, Cory-Slechta DA, Miller GW (2015) Developmental pesticide exposure reproduces features of attention deficit hyperactivity disorder. FASEB J 29: 1960–1972 Doi 10.1096/fj. 14-260901 [PubMed: 25630971] 

49.  Wagner-Schuman M, Richardson JR, Auinger P, Braun JM, Lanphear BP, Epstein JN, Yolton K, Froehlich TE (2015) Association of pyrethroid pesticide exposure with attention-deficit/ hyperactivity disorder in a nationally representative sample of U.S. children. Environ Health 14: 44 Doi 10.1186/s12940-015-0030-y [PubMed: 26017680]

50. von Ehrenstein OS, et al. Prenatal and infant exposure to ambient pesticides and autism spectrum disorder in children: population based case-control study. BMJ, 2019; l962 DOI: 10.1136/bmj.l962

51.  Pogoda, Janice M. and Susan Preston- Martin, “Household Pesticides and Risk of Pediatric Brain Tumors,” Environmental Health Perspectives,105:11, 1214-1220, November 1997.

52.  The Endocrine Society. “Pyrethroid pesticide exposure appears to speed puberty in boys.” ScienceDaily. ScienceDaily, 2 April 2017. < releases/2017/04/170402111320.htm>.

53.  Bao W, et al. Association Between Exposure to Pyrethroid Insecticides and Risk of All-Cause and Cause-Specific Mortality in the General US Adult Population. JAMA Intern Med. December 30, 2019. doi: jamainternmed.2019.6019

54. Brander S, et al. Pyrethroid Pesticides as Endocrine Disruptors: Molecular Mechanisms in Vertebrates with a Focus on Fishes.  viron Sci Technol. 2016 Sep 6;50(17):8977-92.  doi: 10.1021/acs.est.6b02253. Epub 2016 Aug 19.

55.  Garey, Joan and Wolff, Mary S., Estrogenic and Antiprogestagenic Activities of Pyrethroid Insecticides, Biochemical and Biophysical Research Communications 251, 855-859, 1998.


57.  Leemans M, et al. Pesticides With Potential Thyroid Hormone-Disrupting Effects: A Review of Recent Data. Front. Endocrinol., 09 December 2019.

58.  Office of Technology Assessment (OTA) of the US Congress, Neurotoxicity: identifying and Controlling Poisons of the Nervous System, 1990.

59.  Leiss, J. K., & Savitz, D. A. 1995. Home pesticide use and childhood cancer: a case-control study. American Journal of Public Health, 85(2), 249-252

60.  Davis, J. R., Brownson, R. C., Garcia, R., Bentz, B. J., & Turner, A. 1993. Family pesticide use and childhood brain cancer. Archives of Envi- ronmental Contamination and Toxicology, 24(1), 87-92.

61.  Suhartono S, Kartini A, Subagio HW, Budiyono B, Utari A, Suratman S, et al. Pesticide exposure and thyroid function in elementary school children living in an agricultural area, Brebes District, Indonesia. Int J Occup Environ Med. (2018) 9:137–44. doi: 10.15171/ijoem.2018.1207

62. Hertz-Picciotto I, Sass JB, Engel S, Bennett DH, Bradman A, Eskenazi B, Lanphear B, Whyatt R (2018) Organophosphate exposures during pregnancy and child neurodevelopment: Recommendations for essential policy reforms. PLoS Med 15: e1002671 Doi 10.1371/ journal.pmed.1002671

63.  Gonzalez-Alzaga B, Lacasana M, Aguilar-Garduno C, Rodriguez-Barranco M, Ballester F, Rebagliato M, et al. A systematic review of neurodevelopmental effects of prenatal and postnatal organophosphate pesticide exposure. Toxicol Lett. 2014;230(2):104–21. pmid:24291036.

64.  Koureas M, Tsakalof A, Tsatsakis A, Hadjichristodoulou C. Systematic review of biomonitoring studies to determine the association between exposure to organophosphorus and pyrethroid insecticides and human health outcomes. Toxicol Lett. 2012;210(2):155–68. pmid:22020228.

65. Munoz-Quezada MT, Lucero BA, Barr DB, Steenland K, Levy K, Ryan PB, et al. Neurodevelopmental effects in children associated with exposure to organophosphate pesticides: a systematic review. Neurotoxicology. 2013;39:158–68. pmid:24121005; PubMed Central PMCID: PMC3899350.

66.  U.S. EPA. EPA Revised Human Health Risk Assessment on Chlorpyrifos. December 2014. Docket ID EPA-HQ-OPP-2008-0850. Available from:

67.  U.S. EPA. Chlorpyrifos: Revised Human Health Risk Assessment for Registration Review. US Environmental Protection Agency Washington, DC; 2016. Document ID: EPA-HQ-2015-0653-0454. Available from:

68.  Liu P, et al. Adverse Associations of both Prenatal and Postnatal Exposure to Organophosphorous Pesticides with Infant Neurodevelopment in an Agricultural Area of Jiangsu Province, China. Environ Health Perspect, doi: 10.1289/EHP196 (2016).

69.  Carr R, Alugubelly N and Mohammed A (2018) Possible Mechanisms of Developmental Neurotoxicity of Organophosphate Insecticides Linking Environmental Exposure to Neurodevelopmental Disorders, 10.1016/bs.ant.2018.03.004, (145-188)

70.  Ross, S. M., McManus, I. C., Harrison, V., & Mason, O. 2013. Neurobehavioral problems following low-level exposure to organophosphate pesticides: a systematic and meta-analytic review. Critical reviews in toxicology, 43(1), 21-44.

71. Bouchard M, Chevrier J, Harley K, Kogut K, Vedar M, Calderon N, Trujillo C, Johnson C, Bradman A, Barr D, Eskenazi B. Prenatal Exposure to Organophosphate Pesticides and IQ in 7-Year Old Children. Environmental Health Perspectives, 2011; DOI: 10.1289/ehp.1003185

72.  Engel S, et al. Prenatal Exposure to Organophosphates, Paraoxonase 1, and Cognitive Development in Childhood. Environmental Health Perspectives, 2011; DOI: 10.1289/ehp.1003183

73. Eskenazi B, Marks AR, Bradman A, Harley K, Barr DB, Johnson Cet al.. 2007. Organophosphate pesticide exposure and neurodevelopment in young Mexican- American children.Environ Health Perspect 115:792-798; doi:10.1289/ehp. 982817520070. Google Scholar

74. Jusko T, van den Dries M, Pronk A, Shaw P, Guxens M, Spaan S, Jaddoe V, Tiemeier H and Longnecker M (2019) Organophosphate Pesticide Metabolite Concentrations in Urine during Pregnancy and Offspring Nonverbal IQ at Age 6 Years, Environmental Health Perspectives, 127:1, Online publication date: 1- Jan-2019.

75.  Office of Technology Assessment (OTA) of the US Congress, Neurotoxicity: identifying and Controlling Poisons of the Nervous System, 1990.

76. Abreu-Villaca Y, Levin ED. Developmental neurotoxicity of succeeding generations of insecticides. Environ Int. 2017;99:55–77. Epub 2016/12/03. pmid:27908457; PubMed Central PMCID: PMC5285268.

77.  Gunier RB, Bradman A, Harley KG, Kogut K, Eskenazi B. Prenatal Residential Proximity to Agricultural Pesticide Use and IQ in 7-Year-Old Children. Environ Health Perspect. 2017;125(5):057002. pmid:28557711.

78.  Engel SM, Bradman A, Wolff MS, Rauh VA, Harley KG, Yang JH, et al. Prenatal Organophosphorus Pesticide Exposure and Child Neurodevelopment at 24 Months: An Analysis of Four Birth Cohorts. Environ Health Perspect. 2016;124(6):822–30. pmid:26418669; PubMed Central PMCID: PMC4892910.

79. Sagiv SK, Harris MH, Gunier RB, Kogut KR, Harley KG, Deardorff J, et al. Prenatal Organophosphate Pesticide Exposure and Traits Related to Autism Spectrum Disorders in a Population Living in Proximity to Agriculture. Environ Health Perspect. 2018;126(4):047012. Epub 2018/04/28. pmid:29701446.

80.  Harley KG, Huen K, Aguilar Schall R, Holland NT, Bradman A, et al. (2011) Association of Organophosphate Pesticide Exposure and Paraoxonase with Birth Outcome in Mexican-American Women. PLoS ONE 6(8): e23923. doi:10.1371/journal.pone. 0023923

81. Shelton JF, Geraghty EM, Tancredi DJ, Delwiche LD, Schmidt RJ, Ritz B, et al. Neurodevelopmental disorders and prenatal residential proximity to agricultural pesticides: the CHARGE study. Environ Health Perspect. 2014;122(10):1103–9. pmid:24954055; PubMed Central PMCID: PMC4181917.

82. Banks CN, Lein PJ. A review of experimental evidence linking neurotoxic organophosphorus compounds and inflammation. Neurotoxicology. 2012;33(3):575–84. pmid:22342984; PubMed Central PMCID: PMC3358519.

83.  Bjorling-Poulsen M, Andersen HR, Grandjean P. Potential developmental neurotoxicity of pesticides used in Europe. Environ Health. 2008;7:50. pmid:18945337; PubMed Central PMCID: PMC2577708.

84. Lasram MM, Dhouib IB, Annabi A, El Fazaa S, Gharbi N. A review on the molecular mechanisms involved in insulin resistance induced by organophosphorus pesticides. Toxicology. 2014;322:1–13. pmid:24801903.

85. Rauh V. Polluting Developing Brains — EPA Failure on Chlorpyrifos. N Engl J Med 2018; 378:1171-1174. March 29, 2018. DOI: 10.1056/NEJMp1716809

86. Slotkin TA, Seidler FJ. Comparative developmental neurotoxicity of organophosphates in vivo: transcriptional responses of pathways for brain cell development, cell signaling, cytotoxicity and neurotransmitter systems. Brain Res Bull 2007;72:232-274.

87.  Bellinger DC. A strategy for comparing the contributions of environmental chemicals and other risk factors to neurodevelopment of children. Environ Health Perspect 2012;120:501-507.

88. Ishikawa S, and M. Miyata., “Development of myopia following chronic organophosphate pesticide intoxication: An epidemiological and experimental study,” in Merigan, W.H. and B. Weiss (eds.) Neurotoxicity of the visual system, NY: Raven Press, 1980.

89.  Lindsay A.E. “ Memo to Douglas D. Campt, director, U.S. EPA Office of Pesticide Programs: Section 18-USDA quarantine exemptions for use of malathion and diazinon to eradicate exotic fruit fly species in Florida,” 16 October 1991.

90.  Mehl A, et al. “The effect of trichlorfon and other organiphosphates on prenatal brain development in the guinea pig,” Neurochemical Research, 19(5),569-574, 1994.

91.  Lerro CC, Koutros S, Andreotti G, Friesen MC, Alavanja MC, Blair A, et al. Organophosphate insecticide use and cancer incidence among spouses of pesticide applicators in the Agricultural Health Study. Occup Environ Med. (2015) 72:736–44. doi: 10.1136/oemed-2014-102798

92.  Leiss J. K., Savitz D. A. 1995. Home pesticide use and childhood cancer: a case-control study. American Journal of Public Health, 85(2), 249-252

93.  Lee GH, Choi KC. Adverse effects of pesticides on the functions of immune system. Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology Volume 235, September 2020, 108789

94.  Lee, M. J. 1977. Inhibition of monocyte esterase activity by organophosphate insecticides. Blood, 50(5), 947-951.

95. World Resources Institute, Pesticide and the Immune System: The Public Health Risk, 1998.

96.  Takakura N, et al. In vitro combined cytotoxic effects of pesticide cocktails simultaneously found in the French diet. Food and Chemical Toxicology. Volume 52, February 2013, Pages 153–162

97. Scott JG, et al. 2000. Inhibition of cytocrome P450 6D1 by alkynylarenes, methylenedioxyarenes, and other substituted aromatics.” Pesticide Biochemistry

& Physiology. 67: 63-71.

98. Keseru, GM. 1999. Piperonyl butoxide-mediated inhibition of cytochrome P450-

catalyzed insecticide metabolism: a rational approach.” Pesticide Science. 55:


99.  Diel F, et al. 1999. Pyrethroids and piperonyl butoxide affect human T-lympho- cytes in vitro. Toxicol. Lett. 107: 65-74.

100.  Tanaka T, et al. 1994. Developmental toxicity evaluation of piperonyl butoxide in CD-1 mice. Toxicol Lett. 71: 123-129.

101.  Tanaka T. 2003. Reproductive & neurobehavioral effects of piperonyl butoxide administered to mice in the diet. Food Addit Contam 20: 207-14.

102.  US EPA. 2005. Human Health Risk Assessment. Sec. 1.3-6 Docket ID EPA-HQ- OPP-2005-0042 (accessed Jan 2006)

103.  City to Look Beyond Spraying for West Nile,” New York Times, 4 May 2001.

104.  Kakko I, Toimela T, Tahti H. 2000. Piperonyl butoxide potentiates the synapto-

some ATPase inhibiting effect of pyrethrin. Chemosphere 40: 301-5.

105.  Grosman, N, F Diel. 2005. Influence of pyrethroids & piperonyl butoxide on the Ca2+ – ATPase activity of rat brain synaptosomes and leukocyte membranes. Int.

Immunopharmacol. 5: 263-70.

106.  Friedman, M.A. and L. R. Eaton. 1978. Potentiation of methyl mercury toxicity

by piperonyl butoxide. Bull. Environ. Contam. Toxicol. 20: 9- 10.

107. Horton M, et al. Impact of Prenatal Exposure to Piperonyl Butoxide and Permethrin on 36-Month Neurodevelopment. Pediatrics 2011; 127:3 e699-e706; doi:10.1542/peds.2010-0133

108.  Weston DP, Amweg EL, Mekebri A, Ogle RS, Lydy MJ. Aquatic effects of aerial spraying for mosquito control over an urban area. Environ Sci Technol. 2006 Sep 15;40(18):5817-22. doi: 10.1021/es0601540. PMID: 17007146.

109.  Soesanti F, Idris NS, Klipstein-Grobusch K, Hendarto A, Grobbee DE, Uiterwaal CSPM. The effect of non-organophosphate household pesticides exposure during pregnancy on infants birth sizes and growth rate: a cohort study. BMC Pregnancy Childbirth. 2020 Aug 20;20(1):476. doi: 10.1186/s12884-020-03162-w. PMID: 32819320; PMCID: PMC7441723.

110.  Petit C, Chevrier C, Durand G, Monfort C, Rouget F, Garlantezec R, Cordier S. Impact on fetal growth of prenatal exposure to pesticides due to agricultural activities: a prospective cohort study in Brittany, France. Environ Health. 2010 Nov 15;9:71. doi: 10.1186/1476-069X-9-71. PMID: 21078166; PMCID: PMC2999589.

111.  Rauh V, et al. Brain anomalies in children exposed prenatally to a common organophosphate pesticide. PNAS 2012 109 (20) 7871-7876; published ahead of print April 30, 2012, doi:10.1073/pnas.1203396109

112. von Ehrenstein OS, et al. Prenatal and infant exposure to ambient pesticides and autism spectrum disorder in children: population based case-control study. BMJ, 2019; l962 DOI: 10.1136/bmj.l962

113.  Windham GC, et al. Polychlorinated Biphenyl and Organochlorine Pesticide Concentrations in Maternal Mid-Pregnancy Serum Samples: Association with Autism Spectrum Disorder and Intellectual Disability. Environmental Health Perspectives, 2016; DOI: 10.1289/EHP277

114.  Brown AS, et al. Association of Maternal Insecticide Levels With Autism in Offspring From a National Birth Cohort. American Journal of Psychiatry, 2018 DOI: 10.1176/ appi.ajp.2018.17101129

115.  Rauh VA, Garfinkel R, Perera FP, Andrews HF, Hoepner L, Barr DBet al.. 2006. Impact of prenatal chlorpyrifos exposure on neurodevelopment in the first 3 years of life among inner-city children. Pediatrics 118(6):1845-1859.

116.  Schmidt RJ, et al. Combined Prenatal Pesticide Exposure and Folic Acid Intake in Relation to Autism Spectrum Disorder. Environ Health Perspect. 2017 Sep 8;125(9): 097007. doi: 10.1289/EHP604.

117.  Shelton J, Geraghty E, Tancredi D, et al. Neurodevelopmental Disorders and Prenatal Residential Proximity to Agricultural Pesticides: The CHARGE Study. Environ Health Perspect; DOI:10.1289/ehp.1307044

118.  Ross S, McManus IC, Harrison V, Mason O. Neurobehavioral problems following low- level exposure to organophosphate pesticides: a systematic and meta-analytic review. Critical Reviews in Toxicology, Ahead of Print : Pages 1-24 (doi: 10.3109/10408444.2012.738645)

119.  Rauh V, Arunajadai S, Horton M, Perera F, Hoepner L, Barr DB, et al. 2011. Seven-Year Neurodevelopmental Scores and Prenatal Exposure to Chlorpyrifos, a Common Agricultural Pesticide. Environ Health Perspect 119:1196-1201. 10.1289/ehp.1003160

120.  Suarez-Lopez JR, et al. Potential short-term neurobehavioral alterations in children associated with a peak pesticide spray season: The Mother’s Day flower harvest in Ecuador. NeuroToxicology, 2017; DOI: 10.1016/j.neuro.2017.02.002

121.  von Ehrenstein O, et al. Prenatal and infant exposure to ambient pesticides and autism spectrum disorder in children: population-based case-control study. BMJ 2019;364:l962

122.  Pezzoli G, Cereda E. “Exposure to pesticides or solvents and risk of Parkinson disease” Neurology 2013; 80: 2035-2041.

123.  Richardson, J. et al. Elevated Serum Pesticide Levels and Risk for Alzheimer Disease JAMA Neurol. Published online January 27, 2014. doi:10.1001/jamaneurol.2013.6030

124.  Moisan F, et al. Association of Parkinson’s Disease and Its Subtypes with Agricultural Pesticide Exposures in Men: A Case–Control Study in France. Environ Health Perspect; DOI:10.1289/ehp.1307970

125.  Costello S, et al. 2009. Parkinson’s disease and residential exposure to maneb and paraquat from agricultural applications in the Central Valley of California. American Journal of Epidemiology 169: 919-926.

126.  Kelada SN, et al. 2006. 5′ and 3′ region variability in the dopamine transporter gene (SLC6A3), pesticide exposure and Parkinson’s disease risk: a hypothesis generating study. Human Molecular Genetics 15(20):3055-3062.

127.  Thiruchelvam M, et al. 2002. Developmental exposure to the pesticides paraquat and maneb and the Parkinson’s disease phenotype. NeuroToxicology 23:621-633.

128.  Barlow BK, Richfield EK, Cory-Slechtab DA, Thiruchelvam M. 2004. A fetal risk factor for Parkinson’s disease. Developmental Neuroscience 26:11-23.

129.  Harley KG, Engel SM, Vedar MG, Eskenazi B, Whyatt RM, Lanphear BP, Bradman A, Rauh VA, Yolton K, Hornung RW, Wetmur JG, Chen J, Holland NT, Barr DB, Perera FP, Wolff MS. Prenatal Exposure to Organophosphorous Pesticides and Fetal Growth: Pooled Results from Four Longitudinal Birth Cohort Studies. Environ Health Perspect. 2016 Jul;124(7):1084-92. doi: 10.1289/ehp.1409362. Epub 2015 Dec 18. PMID: 26685281; PMCID: PMC4937849.

130. Wohlfahrt-Veje C, Main KM, Schmidt IM, Boas M, Jensen TK, Grandjean P, Skakkebæk NE, Andersen HR. Lower birth weight and increased body fat at school age in children prenatally exposed to modern pesticides: a prospective study. Environ Health. 2011 Sep 20;10:79. doi: 10.1186/1476-069X-10-79. PMID: 21933378; PMCID: PMC3196902.

131.  Chiu YH, Williams PL, Gillman MW, Gaskins AJ, Mínguez-Alarcón L, Souter I, Toth TL, Ford JB, Hauser R, Chavarro JE; EARTH Study Team. Association Between Pesticide Residue Intake From Consumption of Fruits and Vegetables and Pregnancy Outcomes Among Women Undergoing Infertility Treatment With Assisted Reproductive Technology. JAMA Intern Med. 2018 Jan 1;178(1):17-26. doi: 10.1001/jamainternmed.2017.5038. PMID: 29084307; PMCID: 

132.  Upson K, AJ De Roos, ML Thompson, S Sathyanarayana, D Scholes, DB Barr, VL Holt. 2013. Organochlorine pesticides and risk of endometriosis: Findings from a population- based case-control study. Environmental Health Perspectives. ehp.1306648.

133.  Steinemann A. National Prevalence and Effects of Multiple Chemical Sensitivities. J Occup Environ Med. 2018 Mar; 60(3): e152–e156. Published online 2018 Jan 12

134.  Ross PM, Whysner J, Covello VT, Kuschner M, Rifkind AB, Sedler MJ, Trichopoulos D, Williams GM. Olfaction and symptoms in the multiple chemical sensitivities syndrome. Prev Med. 1999 May;28(5):467-80. doi: 10.1006/pmed.1998.0469. PMID: 10329337.

135. Ashford, N.A. and Miller, Claudia, “Chemical Exposures Low Levels and High Stakes”, Published by Van Nostrant Reinhold, New York 1991


137.  The Cumulative Multigenerational Degenerative Impacts of Pesticides on Health Especially the Physical, Emotional and Mental Development of Children and Future Generations: Canadian Government Responsibilities and Opportunities, A Submission to the House of Commons Standing Committee on Environment and Sustainable Development by Physicians and Scientists for a Healthy World, February, 2000.

138.  Tsitsimpikou C, Tzatzarakis M, Fragkiadaki P, Kovatsi L, Stivaktakis P, Kalogeraki A, Kouretas D, Tsatsakis AM. Histopathological lesions, oxidative stress and genotoxic effects in liver and kidneys following long term exposure of rabbits to diazinon and propoxur. Toxicology. 2013;307:109–14.

139.  Zepeda-Arce R, Rojas-García AE, Benitez-Trinidad A, Herrera-Moreno JF, Medina-Díaz IM, Barrón-Vivanco BS, Villegas GP, Hernández-Ochoa I, Sólis Heredia MDJ, Bernal-Hernández YY. Oxidative stress and genetic damage among workers exposed primarily to organophosphate and pyrethroid pesticides. Environ Toxicol. 2017;32(6):1754–64.

140. Mostafalou S, Abdollahi M. Pesticides and human chronic diseases: evidences, mechanisms, and perspectives. Toxicol Appl Pharmacol. 2013;268(2):157–77.

141. Ojha A, Yaduvanshi SK, Srivastava N. Effect of combined exposure of commonly used organophosphate pesticides on lipid peroxidation and antioxidant enzymes in rat tissues. Pestic Biochem Physiol. 2011;99(2):148–56.

142.  Kapeleka J, et al. (2019) Pesticide exposure and genotoxic effects as measured by DNA damage and human monitoring biomarkers, International Journal of Environmental Health Research, DOI: 10.1080/09603123.2019.1690132


144.  Frazier LM. Reproductive disorders associated with pesticide exposure. J Agromedicine. 2007;12(1):27-37. doi: 10.1300/J096v12n01_04. PMID: 18032334.

145.  Konkel L.  The Brain before Birth: Using fMRI to Explore the Secrets of Fetal Neurodevelopment.  Environmental Health Perspectives, Vol. 126, No. 11, 20 November 2018.

146. Abell A, Juul S, Bonde JP. Time to pregnancy among female greenhouse workers. Scand J Work Environ Health. 2000;26:131–136. [PubMed] [Google Scholar]

147. Idrovo AJ, Sanin LH, Cole D, Chavarro J, Caceres H, Narvaez J, Restrepo M. Time to first pregnancy among women working in agricultural production. Int Arch Occup Environ Health. 2005;78:493–500. doi: 10.1007/s00420-005-0615-9. [PubMed] [CrossRef] [Google Scholar

148. Fuortes L, Clark MK, Kirchner HL, Smith EM. Association between female infertility and agricultural work history. Am J Ind Med. 1997;31:445–451. doi: 10.1002/(SICI)1097-0274(199704)31:4<445::AID-AJIM11>3.0.CO;2-#. [PubMed] [CrossRef] [Google Scholar]

149. Smith EM, Hammonds-Ehlers M, Clark MK, Kirchner HL, Fuortes L. Occupational exposures and risk of female infertility. J Occup Environ Med. 1997;39:138–147. doi: 10.1097/00043764-199702000-00011. [PubMed] [CrossRef] [Google Scholar]

150. Frazier LM. Reproductive disorders associated with pesticide exposure. J Agromedicine. 2007;12(1):27-37. doi: 10.1300/J096v12n01_04. PMID: 18032334.


152.  Kubsad D, Nilsson, E.E., King, S.E. et al. Assessment of Glyphosate Induced Epigenetic Transgenerational Inheritance of Pathologies and Sperm Epimutations: Generational Toxicology. Sci Rep 9, 6372 (2019).

153.  Wu H, Bertrand KA, Choi AL, Hu FB, Laden F, Grandjean P, Sun Q. Persistent Organic Pollutants and Type 2 Diabetes: A Prospective Analysis in the Nurses’ Health Study and Meta-analysis. Environ Health Perspect (): .doi:10.1289/ehp.1205248

154.  La Merrill M, Karey E, Moshier E, Lindtner C, La Frano MR, et al. (2014) Perinatal Exposure of Mice to the Pesticide DDT Impairs Energy Expenditure and Metabolism in Adult Female Offspring. PLoS ONE 9(7): e103337. doi:10.1371/journal.pone.0103337

155.  Skinner M, Manikkam M, Tracey R, Guerrero-Bosagna C, Haque M and Nilsson E. Ancestral dichlorodiphenyltrichloroethane (DDT) exposure promotes epigenetic transgenerational inheritance of obesity. BMC Medicine 2013, 11:228 doi: 10.1186/1741-7015-11-228

156.  LeBlanc G, Wang Y, Holmes C, Kwon G, Medlock E. A Transgenerational Endocrine Signaling Pathway in Crustacea. PLoS ONE, 2013; 8 (4): e61715 DOI: 10.1371/ journal.pone.0061715


158.  Geological Society of America. “PFAS: These ‘forever chemicals’ are highly toxic, under-studied, and largely unregulated.” ScienceDaily. ScienceDaily, 29 October 2020. <>.

159. Richardson J, et al. Elevated Serum Pesticide Levels and Risk for Alzheimer Disease

JAMA Neurol. Published online January 27, 2014. doi:10.1001/jamaneurol.2013.6030

160. Kamel F, Engel LS, Gladen BC, Hoppin JA, Alavanja MC, Sandler DP (2005) Neurologic symptoms in licensed private pesticide applicators in the agricultural health study. Environ Health Perspect 113: 877–882 [PubMed: 16002376]

161.  Starks SE, Gerr F, Kamel F, Lynch CF, Alavanja MC, Sandler DP, Hoppin JA. High pesticide exposure events and central nervous system function among pesticide applicators in the Agricultural Health Study. Int Arch Occup Environ Health; doi: 10.1007/s00420-011-0694-8 [Online 7 September 2011].

162. Muller-Mohnssen H (1999) Chronic sequelae and irreversible injuries following acute pyrethroid intoxication. Toxicol Lett 107: 161–176 [PubMed: 10414793]

163.  Beard J, et al. Pesticide Exposure and Depression among Male Private Pesticide Applicators in the Agricultural Health Study. Environ Health Perspect; DOI:10.1289/ehp. 1307450.

164. Hou L, et al. Lifetime Pesticide Use and Telomere Shortening among Male Pesticide Applicators in the Agricultural Health Study. Environ Health Perspect; DOI:10.1289/ehp. 1206432

165.  Chatterjee S, Basak P, Chaklader M, Das P, Pereira JA, Chaudhuri S, Law S. Pesticide induced alterations in marrow physiology and depletion of stem and stromal progenitor population: an experimental model to study the toxic effects of pesticide. Environ Toxicol. 2014 Jan;29(1):84-97. doi: 10.1002/tox.20775. Epub 2011 Oct 11.

166.  Fleming LE, Timmeny W. Aplastic anemia and pesticides. An etiologic association? J Occup Med. 1993 Nov;35(11):1106-16.

167.  Prihartono N; Kriebel D; Woskie S; Thetkhathuek A; Sripaung N; Padungtod C; Kaufman D. Risk of aplastic anemia and pesticide and other chemical exposures. Asia Pac J Public Health. 2011; 23(3):369-77 (ISSN: 1941-2479)

168.  Bräuner EV,  Sørensen M,  Gaudreau E,  LeBlanc A,  Eriksen KT,  Tjønneland A, Overvad K,  Raaschou-Nielsen O.  A prospective study of organochlorines in adipose tissue and risk of non-Hodgkin’s Lymphoma. Environmental Health Perspectives

169.  Cohn B, et al. DDT and Breast Cancer: Prospective Study of Induction Time and Susceptibility Windows. JNCI: Journal of the National Cancer Institute, djy198, djy198. Published: 13 February 2019

170.  Chiu YH, et al. Fruit and vegetable intake and their pesticide residues in relation to semen quality among men from a fertility clinic. Hum. Reprod. (2015) doi: 10.1093/ humrep/dev064. First published online: March 30, 2015


172.  Benedetti, D; Nunes, E; Sarmento, M. S; Porto, C; Santos, C. E. I; Dias, J. F; Da Silva, J. (2013). Genetic damage in soybean workers exposed to pesticides: Evaluation with the comet and buccal micronucleus cytome assays. Mutation research. Genetic Toxicology and Environmental Mutagenesis. 752; 28-33.

173.  Alves, J. (2008). Avaliação da genotoxicidade e estresse oxidativo em em agricultores que trabalham na fumicultura. Canoas: ULBRA/PPGGTA. Dissertação de Mestrado. 60 pp.

174.  Manikkam M, Haque MM, Guerrero-Bosagna C, Nilsson EE, Skinner MK (2014) Pesticide Methoxychlor Promotes the Epigenetic Transgenerational Inheritance of Adult-Onset Disease through the Female Germline. PLoS ONE 9(7): e102091.


176. Kumar A, Howard CJ, Derrick D, Malkina IL, Mitloehner FM, Kleeman MJ, Alaimo CP, Flocchini RG, Green PG. Determination of volatile organic compound emissions and ozone formation from spraying solvent-based pesticides. J Environ Qual. 2011 Sep-Oct;40(5):1423-31. doi: 10.2134/jeq2009.0495. PMID: 21869504.

177.  Cai Y, et al. Associations of Short-Term and Long-Term Exposure to Ambient Air Pollutants With Hypertension: A Systematic Review and Meta-Analysis. Originally published 31 May 2016 Hypertension. 2016;68:62–70

178. Meng X, et al. Short-term associations of ambient nitrogen dioxide with daily total, cardiovascular, and respiratory mortality: multilocation analysis in 398 cities. BMJ 2021; 372 doi: (Published 24 March 2021)

179. Chang, M., Park, H., Ha, M. et al. The effect of prenatal TVOC exposure on birth and infantile weight: the Mothers and Children’s Environmental Health study. Pediatr Res 82, 423–428 (2017).

180. Salam MT, Millstein J, Li YF, Lurmann FW, Margolis HG, Gilliland FD. Birth outcomes and prenatal exposure to ozone, carbon monoxide, and particulate matter: results from the Children’s Health Study. Environ Health Perspect. 2005;113(11):1638-1644. doi:10.1289/ehp.8111

181. Mendola P, Ha S, Pollack AZ, et al. Chronic and Acute Ozone Exposure in the Week Prior to Delivery Is Associated with the Risk of Stillbirth. Int J Environ Res Public Health. 2017;14(7):731. Published 2017 Jul 6. doi:10.3390/ijerph14070731 


183. Pimentel, David. 2004. Encyclopedia of Pest Management.

184.  Jensen T, Lawler SP, Dritz DA. 1999. Effects of ultra-low volume pyrethrin, malathion, and permethrin on nontarget invertebrates, sentinel mosquitoes, and mosquitofish in seasonally impounded wetlands. J Am Mosq Control Assoc. 15(3):330-8.

185.  Bird, S.L.; Esterly, D.M.; Perry, S.G. Atmospheric pollutants and trace gases. J. Environ. Qual. 1996, 25, 1095– 1104.


186.  Pimentel, D.; McLaughlin, L.; Zepp, A.; Lakitan, B.; Kraus, T.; Kleinman, P.; Vancini, F.; Roach, W.J.; Graap, E.; Keeton, W.S.; Selig, G. Environmental and Economic Impacts of Reducing Agricultural Pesticide Use. In Pesticide Question: Environment, Economics and Ethics; Pimentel, D., Ed.; Chapman and Hall: New York, 1993; 223 – 278.

187.  Pimentel, D. 1995. Amounts of pesticides reaching target pests: Environmental impacts and ethics. Journal of Agricultural and Environmental Ethics 8 (1), 17-29.

188.  Lofgren, C.S., Anthony, D.W., & Mount, G.A. 1973. Size of aerosol droplets impinging on mosquitoes as determined with a scanning electron microscope. J. Econ. Ent. 66: 1085-1088.

189.  Environmental Advocates, ”Toward Safer Mosquito Control in New York State,” January 2000. On the web at profit/nycap/mosquitopaper.htm

190.  Brevik, K, et al. Transgenerational effects of insecticides—implications for rapid pest evolution in agroecosystems, Current Opinion in Insect Science. Volume 26, 2018,Pages 34-40,

191.  Schrama, M., Hunting, E.R., Beechler, B.R. et al. Human practices promote presence and abundance of disease-transmitting mosquito species. Sci Rep 10, 13543 (2020).



194.  Penelope A. Hancock, Chantal J. M. Hendriks, Julie-Anne Tangena, Harry Gibson, Janet Hemingway, Michael Coleman, Peter W. Gething, Ewan Cameron, Samir Bhatt, Catherine L. Moyes. Mapping trends in insecticide resistance phenotypes in African malaria vectors. PLOS Biology, 2020; 18 (6): e3000633 DOI: 10.1371/journal.pbio.3000633

195.  The New York Times. 2016. Zika Cases in Puerto Rico Are Skyrocketing. Available at zika-virus-puerto-rico.html?_r=0

196.  Gray, L., Florez, S.D., Barreiro, A.M. et al. Experimental evaluation of the impact of household aerosolized insecticides on pyrethroid resistant Aedes aegypti. Sci Rep 8, 12535 (2018).


198.  Weill, M., et al. 2003. “Insecticide Resistance in Mosquito Vectors.” Nature 423(6936): 136-137.


200.  Weathered, J., Hammill, E. Adaptation to agricultural pesticides may allow mosquitoes to avoid predators and colonize novel ecosystems. Oecologia 190, 219–227 (2019).

201.  Oliver Howard, “Impact of naled (Dibrom 14) on the mosquito vectors of eastern equine encephalitis virus,” Journal of the Am Mosquito Control Assoc, Dec; 13(4):315-25, 1997.

202. Howard, J. & Oliver, J. December, 1997. Impact of Naled (Dibrom 14) on the mosquito vectors of Eastern Equine Encephalitis virus. Journal of the American Mosquito Control Association 13 (4): 315-325.

203.  CDC. Website accessed September, 2001.

204.  Hallmayer J, Cleveland S, Torres A, et al. “Genetic Heritability and Shared Environmental Factors Among Twin Pairs With Autism,” Arch Gen Psychiatry. 2011; 68(11):1095-1102. doi:10.1001/archgenpsychiatry.2011.76





209. New York City Department of Health, “Summary of Vital Statistics,” 1999.

210. Bai F, Thompson EA, Vig PJS, Leis AA. Current Understanding of West Nile Virus Clinical Manifestations, Immune Responses, Neuroinvasion, and Immunotherapeutic Implications. Pathogens. 2019;8(4):193. Published 2019 Oct 16. doi:10.3390/pathogens8040193

211.  Gochfeld, Michael. Professor of Environ- mental and Community Medicine, Robert Wood Johnson Medical School and School of Public Health. Public Panic over West Nile Virus. American Butterflies. Summer, 2000.

212.  US Fish and Wildlife Service. 2003. Division of Environmental Quality. Pesticide Issues: Fighting the west nile virus- Prevention works best. (July 2, 2004)

213.  West Nile Virus Questions and Answers on Survey. New York City Department of Health. March 21, 2000. (July 1, 2004)

214.  Kymberly A. Gyure, MD, West Nile Virus Infections, Journal of Neuropathology & Experimental Neurology, Volume 68, Issue 10, October 2009, Pages 1053–1060,

215.  Gangemi S, et al. Occupational and environmental exposure to pesticides and cytokine pathways in chronic diseases (Review).  Int J Mol Med. 2016 Oct; 38(4): 1012–1020. Published online 2016 Sep 2. doi: 10.3892/ijmm.2016.2728

216.  Lee GH, Choi KC. Adverse effects of pesticides on the functions of immune system.  Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology

Volume 235, September 2020, 108789

217. Bai F, Thompson EA, Vig PJS, Leis AA. Current Understanding of West Nile Virus Clinical Manifestations, Immune Responses, Neuroinvasion, and Immunotherapeutic Implications. Pathogens. 2019;8(4):193. Published 2019 Oct 16. doi:10.3390/pathogens8040193

218.  Sampathkumar P. 2003. West Nile virus: epidemiology, clinical presentation, diagnosis, and prevention. Mayo Clin Proc 78:1137–1144.


220. Verdonschot PFM,  Besse-Lototskaya AA. Flight distance of mosquitoes (Culicidae): A metadata analysis to support the management of barrier zones around rewetted and newly constructed wetlands.  Limnologica. Volume 45, March 2014, Pages 69-79

221.  New York Public Interest Research Group, Interview with Dr. Ray Parsons. Harris County (Texas) Mosquito Control Division. September 11, 1999.











232.  Donley, N. The USA lags behind other agricultural nations in banning harmful pesticides. Environ Health 18, 44 (2019).



235.  European Union. 2012. EU: Non-inclusion of Naled in Annexes I, IA or IB of Biocides Directive 98/8/EC, Decision 2012/257/EU. http://

236.  Abdel-Rahman, Ali, Ashok K. Shetty, and Mohamed B. Abou-Donia (2001). “Subchronic Dermal Application of N,N-Diethyl m-Toluamide (DEET) and Permethrin to Adult Rats, Alone or in Combination, Causes Diffuse Neuronal Cell Death and Cytoskeletal Abnormalities in the Cerebral Cortex and the Hippocampus, and Purkinje Neuron Loss in the Cerebellum.” Experimental Neurology, Volume 172.

237. United Nations Environment Programme (UNEP) Stockholm Convention on Persistent Organic Pollutants. (2001) Available at: (Accessed : February 11, 2016).


239.  Sinfort C. et al. Influence des conditions et matériels de pulvérisation sur les pertes de pesticides au sol et dans l’air en viticulture Languedocienne. XXXIX congrès du Groupe Français des Pesticides (2009).

240.  Yates, S. R. et al. Emissions of 1,3-Dichloropropene and Chloropicrin after Soil Fumigation under Field Conditions. J. Agric. Food Chem. 63, 5354–5363 (2015).



243. Klein, B. 2002. “Reducing Pesticide Drift.” Crop Watch News Service. University of Nebraska Cooperative Extension.

244. Wade, T., et al. 2001. Atmospheric Deposition of PAH, PCB and Organochlorine Pesticides to Corpus Christi Bay. Texas A&M Geochemical and Environmental

Research Group. Presented at the National Atmospheric Deposition Program Committee Meeting.

245.  KegleyS, etal.2003. Secondhand Pesticides: Airborne Pesticide Drift in California. Pesticide Action Network North America, California Rural Legal Assistance Foundation, Pesticide Education Center, and Californians for Pesticide Reform. San Francisco, CA.

246.  Socorro, J., Durand, A., Temime-Roussel, B. et al. The persistence of pesticides in atmospheric particulate phase: An emerging air quality issue. Sci Rep 6, 33456 (2016).

247.  Jakobi, G. et al. Atmospheric bulk deposition measurements of organochlorine pesticides at three alpine summits. Atmos. Environ. 101, 158–165 (2015).

248.  Ma, Y. et al. The spatial distribution of organochlorine pesticides and halogenated flame retardants in the surface sediments of an Arctic fjord: The influence of ocean currents vs. glacial runoff. Chemosphere 119, 953–960 (2015).


250.  Steingraber, S., Living Downstream: An Ecologist Looks at Cancer and the Environment, Publishers, Addision Wesley, 1997.

251.  Hall, GL, et al. Development and Validation of an Analytical Method for Naled and Dichlorvos in Air. Journal of Agricultural and Food Chemistry 1997 45 (1), 145-148

DOI: 10.1021/jf9601224

252.  CS L, et al. Pesticide Exposure of Children in an Agricultural Community: Evidence of Household Proximity to Farmland and Take Home Exposure Pathways. December 2000Environmental Research 84(3):290-302

253.  Hill C, Myers JP, Vandenberg L. Nonmonotonic Dose–Response Curves Occur in Dose Ranges That Are Relevant to Regulatory Decision-Making. Dose Response. 2018 Jul-Sep; 16(3): 1559325818798282. Published online 2018 Sep 13. doi: 10.1177/1559325818798282





258. Sánchez-Bayo F, Wyckhuys K. Worldwide decline of the entomofauna: A review of its drivers, Biological Conservation,Volume 232, 2019, Pages 8-27, ISSN 0006-3207,

259.  Hallmann CA, Sorg M, Jongejans E, Siepel H, Hofland N, Schwan H, et al. (2017) More than 75 percent decline over 27 years in total flying insect biomass in protected areas. PLoS ONE 12(10): e0185809.


261. Rosenberg K, et al. Decline of the North American avifauna. Science  04 Oct 2019:Vol. 366, Issue 6461, pp. 120-124, DOI: 10.1126/science.aaw1313

262. Schneider, Keith (Winter 1983). “IBT – Guilty”. Amicus Journal. Archived from the original on 2012-07-19. Retrieved 2012-07-19.

263. Foster, Doug (1983-12-07). “Industrial Bio-Test Lab’s Dirty Research”. Oakland Tribune. Center for Investigative Reporting. Archived from the original on 2013-04-14. Retrieved 2012-07-11.

264. Shabecoff, Philip (1983-07-12). “E.P.A. Threatens to Suspend Approval of Pesticides over Test Flaws”. The New York Times. Retrieved 2012-07-16.



267. Curtis L, et al. Potentiation of the hepatotoxicity of carbon tetrachloride following preexposure to chlordecone (Kepone) in the male rat, Toxicology and Applied Pharmacology, Volume 51, Issue 2, 1979, Pages 283-293





272.  Majewski , M., et al. 2001. “Diazinon and Chlorpyrifos Loads in Precipitation and Urban and Agricultural Storm Runoff during January and February 2001 in the San Joaquin River Basin, California.” U.S. Geological Survey.

273.  Deutsch SI, Urbano MR, Neumann SA, Burket JA, Katz E. Cholinergic abnormalities in autism: is there a rationale for selective nicotinic agonist interventions? Clin Neuropharmacol (2010) 33(3):114–20. doi:10.1097/ WNF.0b013e3181d6f7ad

274. Pearson BL, Simon JM, McCoy ES, Salazar G, Fragola G, Zylka MJ. Identification of chemicals that mimic transcriptional changes associated with autism, brain aging and neurodegeneration. Nat Commun (2016) 7:11173. doi:10.1038/ ncomms11173

275.  Shelton JF, Hertz-Picciotto I, Pessah IN. Tipping the balance of autism risk: potential mechanisms linking pesticides and autism. Environ Health Perspect (2012) 120(7):944. doi:10.1289/ehp.1104553

276. Roberts EM, English PB, Grether JK, Windham GC, Somberg L, Wolff C. Maternal residence near agricultural pesticide applications and autism spectrum disorders among children in the California Central Valley. Environ Health Perspect (2007) 115:1482–9. doi:10.1289/ehp.10168

278.  Berteau, P.A. and W.A. Dean. 1978. A comparison of oral and inhalation toxicities of four in- secticides to mice and rats. Bull. Environ. Contam. Toxicol. 19: 113-120.

279.  Berteau, P.E., W.A. Deen, and R.L. Dimmick. 1977. Effect of particle size on the inhalation toxicity of naled aerosols. (Abstract.) Toxicol. Appl. Pharmacol. 41: 183.

280.  Platte Chemical Co. 1995. Dibrom 8 Miscible. Label.

281.  Beaudoin, A.R. and D.L. Fisher. 1981. An in vivo/in vitro evaluation of teratogenic action. T eratol. 23:57-61.

282. Leiss, J.K. and D.A. Savitz. 1995. Home pesticide use and childhood cancer: A case-control study. Amer. J. Publ. Health 85: 249-252. Davis, J.R. et al. 1993. Family pesticide use and childhood brain cancer. Arch. Environ. Contam. T oxicol. 24: 87-92.

283. Davis, J.R. et al. 1993. Family pesticide use and childhood brain cancer. Arch. Environ. Contam. T oxicol. 24: 87-92.







299. Hall, G.L. et al. 1997. Development and validation of an analytical method for naled and dichlorvos in air. J. Agric. Food Chem. 45:145-148.

300.  Silver MK, Shao J, Zhu B, Chen M, Xia Y, Kaciroti N, Lozoff B, Meeker JD. Prenatal naled and chlorpyrifos exposure is associated with deficits in infant motor function in a cohort of Chinese infants. Environ Int. 2017 Sep;106:248-256. doi: 10.1016/j.envint.2017.05.015. Epub 2017 Jun 8. PMID: 28602489; PMCID: PMC5533622.

301.  Rachel Raanan et al. Decreased lung function in 7-year-old children with early-life organophosphate exposure. Thorax, December 2015 DOI: 10.1136/thoraxjnl-2014-206622

302. Upson K, et al. Organochlorine Pesticides and Risk of Endometriosis: Findings from a Population-Based Case–Control Study. Environmental Health Perspectives, 2013; DOI: 10.1289/ehp.1306648