The URL can be used to link to this page

Home My WebLink About2016-0621 Documents Submitted at Mtg r~ T es . Lune 21, 2016 Dear Mayor and Council: Pollinator Project Rogue i./alley (P A') advocates, educates, and acts to create a better world for our pollinators, and therefore us. PRV is very concerned about the iT se of elta and as one of the control measures is treating certain areas for mos Uitos. This is very toxic to pollinators and aquatic organisms! x* Sii ice the Bear Creek Greenway is one of he areas t~-eated, w are very concerned about the impacts these chemicals have on the insect and aquatic creatures. not to mention humans, that live along the Creek. WO RV submits that,ja kson County Vector Control (jC VCD) shout take the following actions: Recognize that CVCD is a taxpayer funded entity and that it is time to establish a citizens advisory board to help JCVCD ramp up its Cory MUnity education % outreach about prevention strategies for mosquitos, JCVCD staff is already doing this, but there reeds to be more emphasis and edUcation about the responsibility that each of us has to reduce the number of adult mosquito populations. Effective with j VCEYs - budget, reallocate ouir tax payer money from paying for pesticides for 'nuisance mosquitos' to public education touireach and additional i CV staff' to do educational and preventative work in the community, Creating a volunteer advisor, board aind workforce will o a long way to providing the support that is needed without i eowirin additional funding, Learn from ether cities and towns that do NOT spray, because they realize it is the least effective and most harmful method for dealing with mosquitos. Biological controls are the way t go, One local example is the Bandon FrYlarsh Wildlife Refuge, which is currently using N biological rneans for rnOSCIuito redUCton ~ai~doi'~ arshalert.htrnl r Parrr,~., with 3 ~itn other organizations SUCh as NFRCT e;~ ;,Av~. /D3 ROga i~iv ~ ei ee~yer local ~ local governments, and others to get the word out and the woir done regarding MOSqUitO prevention strategies. Monitor the mosquito population regularly to determine if there is even a disease being carried, and consider not only the risk to the human population from mosquitos, but as affect these pesticides have on our ecosystem and our bodies- Monitor the mosquito population regula y to determine the resistance level of the Mo s uitos to the chemical, Pesticides should be used ONLY as last resort, when there is at,'f uadl y a critical need, n even then wilt' not be very effective. Less than ? ``%1 :x the mosquitos are actually kilied by the spray, and the ones that aren't killed can develop resistance in a very snort fir Fe. A great resource for understanding the dangers of thE. pesticides being applied to our air, water, and soil, and the creatures (inClUdin us) that live there, and the alternative solutions are provided here: [ o giuito Mana etrien and insect-~ orr;e Diseases- aRrf r"ovei"`!# IV OU11 pollinators and other insects - ; R v bees, honeybees, hUn!Min irds, butterflies, moths, bats. beetles, dragonflies are already in dire straight die to habitat loss and exposure to pesticides. The spraying of pesticides such as Deltagard for nuisance mosquitos is one more reason for their decline. and ii -I fact e. aver aces the problem, as the natural predators of mosquitos are either filled or weakened. Hummingbirds, dragonflies. Ears bats r all b gg mosquito consumers. Educating people on hog to attract and protect these creatures, along w'th effective prevention techniques and breeding habitat, wil go along way in reducing our mosquito population, Sincerely Pollinator Project Rogue /alley , rissina, Lefever Os lan , Ja# ie ick er (Talent), Cara Cruickshank (Ashland), Sharon, Schmidt (PP-hoeni Dolly Warden (Tal n Laura Huntington (Rogue River), °en a Swartz ( acksonville , Lee Finney l-Gold Hill),. Meal owsweel Levi (Talent) l=rom the label for eltagard: AC'TIVE INGREDIENT: Deltarnethrin ~.0re OTHER INGREDIENTS 98.0r'c TOTAL : 100.0E% ENVIRONMENTAL HAZARDS This product is extremely toxic to fresh water and estuarine fish and invertebrates. Runoff: Ir of treated areas into a body of water may be hazardous to fish and aquatic invertebrates. Do not apply over bodies of water "lakes, rivers; permanent streams, natural ponds, commercial ash ponds, swamps, marshes. or estuaries;, except when necessary to target areas where adult mosquitoes are present, and weather conditions = 1il facilitate movement of applied material away from the eater in order to minimize incidental disposing of equipment rinsate deposition into the ;Mater bogy. ~o not contaminate water when or wash waters. VvIhen used for nnosquito adulticiding, This pesticide is highly toxic to bees -exposed to direct treatment on blooming caps o weeds. Do not apply this product or allow daft when bees are foraging the treatment rea, except when applications are made to prevent or "OrItrol a threat to public and or animal health determined by a state, tribal or local health or vector control agency on the basis of documented evidence of disease caLlsing agents in vecto r n ;osquil es, or the occurrence of mosquito-borne disease in animal or human populations, or if specifically approved by the slate or t1;be during a natural, disaster recover v effort. When applied outdoors for fly control-, This pesticide is highly toxic to bees exposed to direct treatment on blooming crops or weeds. Do not apply this product or allow drift when bees are foraging the treatment area. Opening pargagraph in 'Alikipedia about deltamithrin; Usage .edit, DelLrri,5„'i.?t' i p"~ n t-n[ n ~ The ti Popular ?'-7 t l {'fiti widely used ~ ~ C § f insti id~+~s r n the -.FF 4.✓ t S~ r h €r: 1~ Products 9 t...~ s ~ r 3 5,,.~ r h~-`? Tn i ~Yt a.~S#st i in ~ i $ - 'r`fld~°§ "~-3 t~~;.-+]i{t-m y S"3 nee$..3e j an i "'L3` ~'S #"'sS~ ~f`"* i" bigqt".g~;i~kr.,.i F'~ '4' ''-O S !a# with rp#_. .°T Y` ~``'t E.~,3-. #"~C'e~it'y Op E"f = '...r ragoj and 7 €i a:.A inditk~idlas 41..r ..a c:.; s ~ `~'ttt # 3 _ ...^La'- .i.^r 7 1,..'~ k`~✓= ~.r#~ t `-..~i - a ivy f it I 'fy ) S,r+TZ° g.,~ ev. f 3'•ib i .Sf `gyp safes i,' ^v4: 3Jtiin: in ' h Lr€ ?iced at s,fi . € Ii , nnalC ri Al i a a ' 6 s. e. o . o,r e ' ? f S b 'C2s~~ k.~ k.}d IL ( •a`<< , a . ,^s, ' Y•r i vr- r y' .3 L. s -)I L 'y " 'L : f "`i x !t'in !'''.r=.~ -r' #°sh3 s *~"and e ' f _ ntF c rot hi ~.~estic koki _ :€g y= i it a a i, ar'i i = " , r r I.J Y safe i r°'. ry 1 -firE } P r"t wL% f nit 'N fig ' 'S ± ..R ^.e YrY € 1 considered i# r i used S r c fi a~C~on a y t 4 1 _ i ~d SC 4 8 0.v .l_ around', humans, it is stii€ i eu otaxic to hu al-Is, Delta e hrin i able to pass from a woman's skin through her blood and into her breast mil a12 ~a • ~--1 - V ~.c.~Ur Crhn1-I'al (~r-c5 • May, 2016 Guest Opinion for Mail Tribune More chemicals released for mosquito control in the Rogue Valley Endocrine (i.e., hormone) disruptors (EDs) cause or are associated with some $175 billion in annual medical costs in Europe. Figures aren't available for the U.S. but surely are similar in magnitude. (http://www.medscape.com/viewarticle/841025). Thirteen chronic medical conditions have strong scientific evidence for causation by endocrine- disrupting chemicals including autism, obesity, diabetes, I.Q. depression and intellectual disabilities in children, cancers, and male reproductive disorders. Greatest dollar costs come from neurological problems, including ADHD, and I.Q. depression associated with exposures to ED pesticides. Half of the known ED pesticides are used to kill fleas, ticks, mosquitoes, and other insect pests. Humans and beneficial creatures alike are continuously exposed to these pesticides from conventional agricultural pesticide practices, railroad and roadside maintenance, and from vector control sprays of insecticides that can appear in our environments (irrigation water, ponds, backyards, roadside ditches, Bear Creek, etc), wherever pests like mosquitoes have been treated. These chemicals often appear within our bodies. The public assumes that such chemicals are highly specific for target pests, and these pesticides have federal safety approvals. Sadly, such safety approvals are an erroneous assumption. No less than 6 of the Jackson County Vector Control mosquito insecticides (littp• `jcvcd orb%us/1roducts-uses/) are EDs. I make reference to the chemicals in Anvil, Deltamethrin, and four larvicides containing the chemical methoprene (Altosid). All of these chemicals are also extremely toxic to honey bees and other pollinators at the ppb levels, much like other neurologically based insecticides called neonicotinoids. For example, pyrethroids like Phenothrin used in Anvil are typically more toxic than the natural chemicals from flowers. When used improperly, pyrethroids can increase the risk of liver cancer in rats and mice; be poisonous to cats and dogs, bee toxic to pollinators, and is an ED. As an ED it stimulates multiplication of estrogen sensitive cancer cells (like glyphosate the active ingredient in Roundup) and it is also an antagonist of progesterone action (alters the body's preparation for pregnancy). Deltamethrin is one of the newer generation pyrethroids that is chemically altered to be 1,000 times more potent than the chemicals in Anvil. Talent, Phoenix, and Ashland are all nationally recognized "Bee Cities". As such this declaration means the local citizens and elected officials have assumed an obligation to raise awareness to the beneficial roles that pollinators play in sustaining three-quarters of the planet's plant species, including 1/3 of our food crops, and to agree to provide pollinators with healthy habitats in which to survive and proliferate. It does not mean expose pollinators to lethal concentrations of airborne insecticides that have a poor success rate - less than 1% - for reaching the target mosquito population. Mosquitos everywhere are growing resistant to the repeated treatments by the pyrethroid products associated with Anvil. This strongly argues for their judicial and intermittent use only when required, perhaps to strike down a declared public health emergency and to also use with proper concentrations of the active ingredient. These are practices that Rachel Carson warned us to do with selected chemicals like DDT and other pesticides some 55 years ago in her book Silent Spring. The Centers for Disease Control and Prevention (CDC) agrees that spraying adult mosquitoes with the ultra low volume (ULV) procedure used by Vector Control is a highly inefficient control method and does not always reduce the incidence of West Nile Virus disease in humans. It suggests that treatments concentrate on larval stages of mosquitoes where more specific, effective, and less toxic chemicals can be used http://www.beyondp esticides.org/programs/mosquitos-and-insect-borne- diseases/documents/the-truth-about-mosquitoes,-pesticides-and-west-nile- virus. I would like to learn more about JCVCD justifications for the use of these endocrine disrupting adulticide mosquito control chemicals and Altosid that kills developing mosquitoes. I would also encourage the VC Budget Board reallocate some existing monies for the use of more specific biological mosquito larvicides such as Bti, provide more funding for public education on the importance of mosquito habitat abatement measures that are much more efficient means to eliminate mosquitoes, and ask that they adopt a policy to use more toxic mosquito adulticides only during a declared public health emergency. These are the kinds of management practices that have led to a successful Bti-based and habitat abatement of mosquito problems at the Oregon Bandon Marsh National Wildlife Refuge (https://www.fws.gov/upIoadedFiles/Mosquito%20news%20update%20usf ws%202_11_15.pdf. Parenthetically, CDC's best estimate of the potential future range of the Zika carrying mosquito, Aedes aegyptl, ends around Sacramento CA. Ray-Seidler, US EPA research scientist, retired Guest Opinion: Vector Control committed to protecting public health Mosquito-borne pathogens kill people! Roughly 750,000 people, mostly children in impoverished countries, died last year because they were infected with a disease transmitted by the bite of a mosquito. Closer to home, West Nile virus has been identified in Jackson County in eight of the past 11 years. Besides making people sick, annoyance from mosquitoes decreases tourism and lowers productivity in livestock; they can even make some areas unlivable. But lots of things are dangerous and cause physical and economic harm. We don't have county-wide programs to control them, so why do mosquitoes get all this special attention? Simple: They fly. Because they fly, often long distances, individuals can't effectively control them on their own. Individuals can play a part, and no program can be effective without the help of the public, but mosquitoes cannot be effectively controlled by any means other than an organized, area-wide program. Recognizing this, the citizens of Jackson County voted to form the Jackson County Vector Control District (JCVCD) in 1968. For the 47 years since control measures began in 1969, the employees of JCVCD have been committed to protecting the citizens of the district by urging the public to take an active role in the reduction of mosquito populations, eliminating mosquito breeding sources, and applying safe, effective, Environmental Protection Agency-registered insecticides judiciously. Recently there have been statements made that mislead the public into thinking the EPA-registered products used by the district are far more dangerous than they are. We encourage the public to visit, ~.c.U~ '~_~~:r Tnc-~'.• iii:. •da to see for themselves that none of the public health pesticides used by the district has been shown to be an endocrine disruptor. The National Pesticide Information Center, ~ ~ . , - - ~Z . ti,is also a great resource for risk information on the products we use. In addition to the products we use being registered by EPA, the district itself falls under the regulation of the U.S. Fish and Wildlife Service, National Marine Fisheries Service, Occupational Safety and Health Administration, Oregon Fire Marshal, Oregon Secretary of State Audits Division, Oregon Department of Environmental Quality, Oregon Department of Agriculture, Oregon Department of Fish and Wildlife (ODFW) and the Oregon Health Authority (OHA). These multiple layers of regulation were put in place to ensure that public health pesticides are applied in a safe and effective manner without undue risk to the public or the environment. Integrated pest management (IPM) is fully supported by the World Health Organization, the U.S. Centers for Disease Control, ODFW, and OHA. IPM is a system where education, source reduction, biological control, surveillance, larval control and adult control measures are all used in concert to effectively control mosquito populations. Not only is this the most effective, economical and environmentally responsible method to control mosquito populations, it is also how we are legally required to perform mosquito control. The JCVCD will continue to perform our primary goal of protecting public health from the diseases transmitted by mosquitoes. VVe encourage the public to help us in this effort by removing containers that hold water from around their homes, stocking water troughs and ornamental ponds with fish, managing irrigation water to minimize standing water, wearing loose-fitting, light-colored clothing and EPA-registered insect repellent when outdoors, especially at dusk and dawn, and reporting mosquito problems or dead birds to the office. Please visit our website at > .•C ~-j.a for more information, and thank you for helping us keep our community safe from mosquito borne disease. James J. Lunders is manager and biologist for the Jackson County Vector Control District. .''ems ,'LtF'V!'lfl'. ~','s~F.., a."i. tF.:.'".. ~J •9 t?G't ?F: 4i?~~v' :L~~~s~Y:f`v~~\i t I : C5 /2 . BEYOND PESTICIDES 701 E Street, SE ■ Washington DC 20003 202-543-5450 phone ■ 202-543-4791 fax infoOa beyondpest:cides.org n w,.vw.beyondpesticides.org The Truth About Mosquitoes, Pesticides and Vest Nile virus A Beyond Pesticides Factsheet While communities have good intentions, many existing policies and programs may be dangerous to children, adults and wildlife and inadequate by relying too heavily on spraying pesticides to kill adult mosquitoes. NOT ALL MOSQUITOES CARRY WEST NILE VIRUS There are 175 different species of mosquitoes in the U.S. and only a handful of those are vectors for disease. Only adult female mosquitoes bite and require blood meals, males feed on flower nectar. Mosquitoes go through four stages in their life cycles - egg, larva, pupa, and adult. The complete cycle can take as little as four days or as long as one month, depending on the temperature. West Nile virus (WNv) and St. Louis encephalitis are primarily associated with the Culex mosquitoes.' Adult Culex females live between 2-4 weeks, depending on climate, species, predation, and a host of other factors. Culea mosquitoes are generally weak fliers and do not move far from their larval habitat, although they have been known to fly up to two miles.2 High bite rates usually indicate breeding areas are nearby. Mosquitoes are most active at 80°F, become lethargic at 60°F, and cannot function below 50°F.3 THE REAL THREAT OF WEST NILE vIRUS C' Less than one percent of those infected with WNv will develop severe illness, according to the Centers for Disease Control. The vast majority of people (about 80%) who become infected with WNv will show no symptoms and never become sick. Some 20% may experience mild flu-like symptoms within 3 - 15 days. ❑ Brian Rogers, D.O., MPH, City of Fort Worth Health Authority states, "The risk of becoming seriously ill and dying from West Nile is extremely minimal. Fewer than 1 percent of mosquitoes in areas where the virus has been found actually carry the virus_ "5 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. Within this small proportion, the fatality rate is about 3-15%."6 Risk for severe illness is most closely correlated with increasing age and a weakened immune system. From 2001 to 2003 there was a drop in the average age of WNv cases (which include flu-like symptoms), however the median age of fatal cases has not dropped. The rise in cases in younger people is probably due to the heightened detection of milder WNv cases. 7'$ A person who has been infected with WNv may have life-long immunity even if they show no symptoms.9 PESTICIDE SPRAY PROGRAMS ARE INEFFECTIVE According to the Centers of Disease Control and Prevention (CDC), spraying adulticides, pesticides intended to kill adult mosquitoes, is usually the least efficient mosquito control technique.10 Adulticiding programs spray pesticides indiscriminately and do not get at the mosquitoes until they have matured. They also do not restrict, control, or prevent mosquitoes from carrying WNv or continuing to breed. Close to 99.9 % of sprayed chemicals go off into the environment where they can have detrimental effects on public health and ecosystems, leaving 0.10% to actually hit the target pest. ' i Mosquitoes develop resistance to pesticides over time, rendering the chemicals ineffective. A 2003 study finds that mosquitoes carrying West Nile virus and malaria developed resistance to organophosphate and carbamate insecticides as a result of a single genetic mutation. 12 After Hurricane Floyd caused a surge in mosquito populations in Florida, state officials took bite counts before and after widespread aerial spraying and found that mosquito populations surged back to pre-spray levels within three days of the treatment." Programs usually measure post-spray mosquito populations within 3-5 days. Most do not retest the area to detect the resurge in populations to pre-spray levels after 7 or more days. Residences experiencing high mosquito bite rates typically find mosquitoes breeding on their property. ADULTICIDING IS NOT SHOWN TO REDUCE WNV INCIDENCE In 2003 the city of Boulder, CO practiced integrated mosquito management and adulticided only once in an isolated non-residential area. The program resulted in an 80% average reduction in mosquito populations and lower rates of serious illness per population than surrounding cities where abundant adulticiding took place." Despite high mosquito counts and large percentages of infected birds, Shaker Heights, Ohio refused to adult' like its neighboring cities in Cuyahoga County. 2002j5results reported only 2 WNV cases in Shaker Heights with the other 217 cases occurring throughout the county. The counties of Goshen and Platte, WY rely heavily on adulticides and in 2003 counted 80 WNv cases. 8 fatalities and 77 cases, 3 fatalities, respectively. Their neighbor Cheyenne, with 2 times the population and 3 times the landmass, used only larvicides and had 20 cases of WNv and 1 fatality. 16 PESTICIDE SPRAY PROGR AIS AFFECT PUBLIC HEALTH A.ND THE ENVIRONMENT The U.S. EPA warns, "no pesticide is 100 percent safe."`' National Research Council found that pregnant women and Synthetic pyrethroids, which include resmethrin children have a greater risk of getting sick from pesticides.`` (Scourge) and sumithrin (Anvil), are adulticides In NYC in 2000 more people were reported to have gotten sick patterned after pyrethrum, yet have been from pesticide exposure from spraying than from WNv.2' chemically engineered to have greater toxicity and Adulticides kill beneficial insects and natural mosquito longer breakdown times." Almost all synthetic predators, such as dragonflies, damselflies, and beetles, pyrethroid mosquito products use synergists like potentially increasing local populations of mosquitoes. 24 piperonyl butoxide (PBO), a petroleum distillate, Brian Rogers, Ft. Worth Health Authority states that, "Spraying which increases potency and compromises the 5 b for mosquitoes would harm more people than it would help." distillates ability to detoxify the pesticide. Petroleum distillates are carcinogenic and linked to birth New York State Department of Health states that adverse defects and other illnesses. Animal studies have outcomes during or after an aerial or ground spraying of shown children to be more sensitive than adults adulticides might include acute asthma attacks, other respiratory and that exposure may inhibit neonatal brain problems, and/or dermatological problems.25 development.lg Pyrethroids are highly toxic to fish Synthetic pyrethroids are neurotoxic and have been linked to and honey bees, even in low doses. cancer. People (particularly children) with respiratory problems, such as asthma, are especially vulnerable to these pesticides and Symptoms of exposure include: dermatitis and will suffer disproportionately from exposure. asthma-like reactiolns, eye and skin irritation and Washington, DC cites both lack of efficacy and asthma concerns flu-1~ice symptoms. Synthetic pyrethmids are 16 endocrine disruptors and have been linked to among reasons for its no-spray policy.- breast and prostate cancer. 20 People with asthma In 1999, malathion spraying was found responsible for the death and pollen allergies should be especially cautious. of over 2,000 fish on Staten Island .21 Exposure has resulted in deaths from respiratory On June 26, 2001, The Post Star reported that 37 young ball failure. Breakdown times range from a few hours players and spectators at a softball game in upstate New York to several months. were hospitalized after being poisoned. According to Moreau Emergency Squad Captain Andre Delvaux, a pesticide containing the organophosphate malathion, was being sprayed to control potential WNV carrying mosquitoes near the baseball field while a game was in progress. Studies published in 2001 by Duke University researchers found that combined exposure to DEFT (N,N-diethyl- m-toluamide) and permethrin could lead to motor deficits and learning and memory dysfunction. `s G In 1998, EPA rejected "child safety" claims for DEET products and required all such claims to be removed from existing products. 19 On June 3, 2001 the Associated Press reported that in New York more than 50% of dead crows collected in response to West Nile virus died from exposure to pesticides and lead, rather than from West Nile Virus.30 In 2000, five spray operators filed a complaint against New York City claiming they became sick due to improper training and prolonged exposure while spraying adulticides.'I A 1999 Mount Sinai School of Medicine study examined four pyrethroid pesticides, including sumithrm, and concluded, "[E]ach pyrethroid compound is unique in its ability to influence several cellular pathways. These findings suggest that pyrethroids should be considered to be hormone disruptors, and their potential to affect endocrine function in humans and wildlife should be 'investigated Commercial fishermen in Maine filed a $125 million lawsuit claiming that the dramatic decrease in the lobster harvest was due to the spraying of an adulticide containing malathion.33 Reports of inappropriate and/or illegal spraying practices are common. Children are known to follow spray trucks for entertainment. Other practices include fogging during daylight hours, during wind speeds higher than 10 mph, and in no-spray zones. Proper integrated pest management is often ignored. 34 Organophosphates, which include malathion (Fyfanon), naled (Dibrom) and chlorpyrifos (Mosquitomist), are a highly toxic class of pesticides that affect the central nervous, cardiovascular and respiratory systems. Symptoms of exposure include: numbness, tingling sensations, headache, dizziness, tremors, nausea, abdominal cramps, sweating, incoordination, blurred vision, 35 difficulty breathing, slow heartbeat, unconsciousness, incontinence, convulsions and fatality 36 Some organophosphates have been linked to birth defects and cancer. Breakdown times range from a few days to several months, depending on conditions. Revised 9.'8.%04 2 SAFE & EFFECTIVE MOSQUITO MANAGEMENT STRATEGIES The first step in managing mosquitoes is personal protection and source reduction. Use natural-based repellents and wear long-sleeves and pants if outside during dawn and dusk to avoid getting bitten. Remove all potential breeding areas - any place with standing or slow-moving water. Remove, puncture or regularly dram all water-retaining objects such as tin cans, buckets, holes in trees, clogged gutters and down spouts, old tires, birdbaths, trash can lids and shallow fishless ponds. Fix dripping outside water faucets and sprinklers. Monitor ponds and sources of water regularly for signs of mosquito larvae. Maintain window and door screens, and keep closed around dawn and dusk when mosquitoes are most active. Stock permanent water pools or ponds with fish that eat mosquito larvae and pupae, like Gambusia holbrooki. Least-toxic larvacides (killing mosquitoes in the larval stage) allow control measures to be targeted and kill mosquitoes before they become active, biting adults. Bacillus thuringiensis var. israelensis (Bti) is one of most effective and least hazardous biological larval controls. It is a bacterial strain that, when sprayed or dropped into larval pools, is ingested by feeding larvae and kills them. (Mosquito Dunks can be bought at local garden stores or on-line. They are safer for birdbaths, ditches, tree holes, roof gutters, etc. - anywhere water collects.) Vegetable based horticultural oils are effective in killing larvae in water and sinking egg rafts on the surface. but can also kill non-target organisms including some mosquito predators that breathe from the surface. Use natural-based repellents instead ofDEET and reapply often. Bile Blocker has a soy-base, others such as Beat It Bug Buster and Avon's Skin-so-Soft use an herbal-base. Herbal repellents can contain cedarwood, garlic, lemongrass, frankincense, cinnamon, geranium, eucalyptus, basil, rosemary, cloves, peppermint, lemon balm (citronella), onions, feverfew, thyme, neem oil, and/or merigold. Mosquito traps and attractants are effective, though different levels of success have been reported. These machines send out plumes of carbon dioxide to attract mosquitoes that are then sucked in and killed." The CDC recommends the formation of local WNv community task force with representatives from government, civic, business, health, and environmental sectors to achieve buy-in within the society.38 CONLML?NTrms TgAT )LAVE ADOPTED SAFER MOSQUITO AND WNV MA_N7AGEMF_vT PROGRAMS Lyndhurst, Ohio, passed a landmark ordinance in 2003 prohibiting the spraying of pesticides for WNv. During a Task Force sponsored forum, a panel of experts discussed the hazards and low efficacy of adulticides. The Council stated, "[T]here is substantial belief that the more effective way of controlling the mosquito populations is by larvacide treatment and thorough education..." Concluding that, "[T]he dangers of WNV are minimal and affect a very small segment of the population and that the long-term health and environmental risks of spraying with synthetic pesticides poses a much greater risk."39 Washington, DC health officials continue their no-spray policy stating that pesticide spraying is inappropriate in a heavily populated area with asthmatics. Instead, officials focus on larval control and pubic education, with education materials distributed in four languages. The Department of Health is also implementing a Tire Round- Up program for residents to discard old tires, a major breeding site for mosquitoes.`' In York County, Virginia, officials distribute the mosquito eating fish, Gambusia holbrooki, to residents in order to decrease pesticide use for mosquito control. Several thousand of the fish have been bred by the county's fishery as part of its mosquito prevention program. 40 In Dallas, Texas, the City Council's Health, Environment and Human Services Committee adopted a mosquito control plan in 2003 that calls for more public education and allows the use of pesticide sprays only as a last resort and upon approval of the pertinent council member.41 Ft. Worth, Texas has not sprayed for mosquitoes since 1991. In 2003, Ft. Worth had 3 WNV cases and no deaths. Brian Boerner, Director of Environmental Management, states, "the spraying of chemicals also has the potential of contaminating our waterways, killing the beneficial fish and organisms that feed on mosquito larva, adding harmful volatile organic chemicals to the atmosphere-a precursor chemical to ozone formation-and providing a potential inhalation or ingestion hazard to residents. C Nassau County, New York joins others in using predacious fish in hard to reach salt-water marshes 43 Marblehead, MA has a WNV Response Plan that requires a town hall meeting before any adulticides are used (and only if there's been a locally-acquired human death) 44 In 2003, Boulder, Colorado focused on larviciding, surveillance and public education without the use of adulticides and offered free WNv information workshops for neighborhood groups and distributes free samples of Mosquito Dunks, a least-toxic larvacide product, for use in stagnant water. 14 In preparation for WNv, Lane county, OR have an easy to read public educational flyer that is put in local newspapers and distributed with utility bills early in the season.4' In 2003, Seattle, Washington adopted an Integrated Pest Management Plan for Mosquito Control, which identifies public education, personal protection, and breeding source reduction on public property as, "...the most effective and appropriate techniques for the City to use.'"46 Revised 91'81%04 3 ' Centers for Disease Control and Prevention, Division of Vector-Borne Infectious Diseases. West Nile Virus: Entomology. 2004. 1--.- v, (July 1, 2004) and CDC Answers Your Questions About St. Louis Encephalitis. 2003. (July 1, 2004) Floore, T. 2004. Mosquito Information. The American Mosquito Control Association(July 1, 2004) ' Rutgers Entomology. 2001. FAQ's on Mosquitoes. (July 1, 2004) ° Center for Disease Control. 2004. WNV Factsheet. What you need to know. :(July 2, 2004) s Lunsford. Jessica. 2003. The truth about west nile virus. Pesticides and You 23 (1): 9-10. ° US Fish and Wildlife Service. 2003. Division of Environmental Quality. Pesticide Issues: Fighting the west nice virus- Prevention works best. _ ~ _ (July 2, 200 - - (July 2. 2004) CNN.com/HEALTH. August 16, 2002. CDC predicts West Nile upswing.:' _ s Haves. Ned. 2004. CDC Division of Vector-Borne Infectious Diseases. "Summary of West Nile Virus Activity in the United States, 2003." t: Jul , 2004) s West Nile Virus Questions and Answers on Surrey. New York City Department of Health. March 21. 2000. (July 1, 2004) 10 Centers for Disease Control and Prevention. 2001. Epidemic/Epizootic West Nile Virus in the United States: Revised Guidelines for Surveillance, Prevention, and Control. Atlanta- GA.:. (July 1, 2004) " Pimentel, D. 1995. "Amounts of Pesticides Reaching Target Pests: Em-ironmental Impacts and Ethics."J. ofAgEnyiron. Ethics 8(1):17-29. Weill, M,, et al. 2003. "Insecticide Resistance in Mosquito Vectors." Nature 423{6936): 136-137 "Nevus and Observer. 1996. State alters mosquito plans. 9/21/96 City of Boulder WNV Surveillance and Control Plan, 2003 Season a. r. 's Lynch, J. June/July 2004. Cuyahoga County Board of Health and Ryan Sullivan, Shaker Heights WNV Task Force. Personal Communication. s Lee. R. Apri12004. Director Environmental Management, City of Cheyenne and Latimer County. Personal Communication. 17 Gooselin, R. 1984. Clinical Toxicology of Commercial Products. Williams and Wilkins. Baltimore, MD. is Cantalamessa. F. 1993. Acute toxicity of two pyrethroids, permethrin and cypermethrin in neo-natal and adult rats. Archives of Toxicologv 67: 510-513. and Imamura L, et al. 2002. Neonatal exposure of newborn mice to pyrethroid (permethrin) represses activity-dependent c-fos mRNA expression in cerebellum. Archives of Toxicology 76(7): 392-39`. Extension Toxicology Network. 1994. "Pyrethroids." Pesticide Information Profiles. U.S. EPA and Oregon State University. r_ . (July 2, 2004) Vera Go, J., et al. 1999. "Estrogenic Potential of Certain Pyrethroid Compounds in the MCF-7 Human Breast Carcinoma Cell Line." Environmental Health Perspectives I07(3) and Alavanja, M.C.R., et al. 2003. Use of agricultural pesticides and prostate cancer risk in the agricultural health study cohort. American Journal of Epidemiology 157: 800-814. U.S. EPA. 2002. Questions and Answers: Pesticides and Mosquito Control. Department of Prevention, Pesticides and Toxic Substances. (July 2, 2004) National Research Council. 1993. Pesticides in the Diets of Infants and Children. National Academy Press. Washington, DC. " New York City Health Information. 2001. West Nile Virus Surveillance and Control: An Update for Health Care Providers in New York City. New York City Department of Health 20(2) (July 2, 2004) 24 Howard, J. et al. 1997. "Impact ofNaled (Dibrom 14) on the Mosquito Vectors of Eastern Equine Encephalitis Virus."Journal of the American Mosquito Control Association 13(4): 315-325. New York State Department of Health. West Nile Virus Response Plan, Appendix B Surveillance of Possible Health Effects from Pesticide Exposure. May 2000. •.i _ (July 2, 2004) 26 District Of Columbia, Department Of Health. 2003. Arbovirus Surveillance and Response Plan. Beyond Pesticides. 2000. Chemical Watch Factsheet: Malathion. July 2000. ,b Abou-Donia, M., et al. 2001. "Subchronic Dermal Application ofN,N-Diethyl m-Toluamide (DEET) and Permethrin to Adult Rats, Alone or in Combination, Causes Diffuse Neuronal Cell Death and Cytosketletal Abnormailieis in the Cerebral cortex and the Hippocampus, and Purkinje Neuron Loss in the Cerebellum." Fxperimental Neurologt, 172:153-171. U.S. EPA. 1998. Reregistration Eligibility Document Facts: DEFT. Office of Prevention, Pesticides and Toxic Substances- EPA-738-F95-010. 30 Beyond Pesticides. 2001. 'More Birds Dying from Pesticides and Other Toxies than West Nile Virus." Daily Nevus. Washington, DC. June 4. 31 Saulny, Susan. 2001."Workers Say Chemicals Used in Mosquito Spraying Made Them Ill." Alex, York Times. January 25. 32 Environmental Health Perspectives, March 1999. Vol. 107, no. 3, pages 173-177. 3' Southampton Press. 2000. '`Lobstermen Suing Pesticide Makers," September 7. 34 Beyond Pesticides. 2002. 'New York Times Photo Shows Children Drenched with Pesticides Sprayed for Mosquitoes." Daily News Photostorv. Washington, DC. September 20. _ Extension Toxicology Network. 1996. "Malathion." Pesticide Information Profiles. U.S. EPA and Oregon State University. - - (July 2, 2004) U.S. EPA. 1999. Recognition and Management of Pesticide Poisonings. 5°' edition. Office of Prevention. Pesticides, and Toxic Substances. " Quarles, William. 2003. Mosquito Attractants and Traps. Common Sense Pest Control Quarterly, Volume XIX, No. 2. 's Centers for Disease Control and Prevention. 2003. Epidemic/Epizootic West Nile Virus in the United States: Revised Guidelines for Surveillance, Prevention and Control. Atlanta GA. (Jul)' 1, 2004) 3s Beyond Pesticides. 2003. "Ohio City Adopts Landmark Law to Stop Pesticide Spraying for West Nile Virus." Daily Neu-s. Washington, DC. July 14. 40 York County Environment and Development Services. Div. Drainage and Mosquito Control (July 2, 2004) 41 Beyond Pesticides. 2003. "Virginia and Texas Towns Find Alternatives for West Nile Virus Control." Daily Nex•s. June 12, 2003. 42 Ft. Worth Public Health Department, Mosquito Prevention and Control-<<< _A_ (viewed July 6, 2004) Turrillion, G. 2002. Director of Mosquito Control Program in Nassau County, NY. Personal Communication. March. ' Town of Marblehead, MA West Nile Virus Protocol and Response Plan. 200' _ (July 6, 2004) 45 Northwest Coalition for Alternatives to Pesticides. Julv 2004. Personal Communication. 4e City of Seattle. Office ofSustainability and Environment. February 20, 2002. Integrated Pest Management Plan for Mosquito Control. - v:'(Jul , 2004) Revised 91'8104 4 Why Other Cities Haven Chosen Not to Spray aH-0 ti€F: Adams County and City of Natchez, Mississippi The "'Hw To: Natchez Democrat 8/24/03 "The best way to curb the OPT OUT. mosquito population - and thus, the spread of West Nile C«rjtact virus - is to kill the insects while they're still young, say Officals ~ many mosquito control experts." County employees will j)ettFil[?2'T I c.rtts a use Angique MMF spreading a thin film in breeding areas which drowns the mosquito larvae and pupae. UN SPPI- Y Fort Worth and Tarrant County, Texas Health _-NS Department Release 8/20/02 Fort Worth discontinued its spraying program in 1991. Several reason discussed, LISIGN criticizing the adulticide spraying. Summarizing: PETITION- i.) Spraying adulticides is ineffective as many mosquitoes What t`:ko are not hit, hiding in bushes, trees, etc. and larvae will continue to thrive, soon producing more adults. SPRAYING EMERGENCY ii) Adding harmful chemicals to the environment can have unwanted effects to both air and water. U-I Anvil 2+2 ~PcDs iii) Thousands of Fort Worth residents with respiratory problems such as asthma would be in danger. Asthma UlRead Ait and allergies are two of the top five health problems for About It (What Fort Worth residents. The potential inhalation hazard to Scientists Sa`) the general population does not seem worth the risk of LIF:xa killing a few mosquitoes. ~~:t~Ics (if `saferMosquito Control Murfreesboro, Rutherford County, Tennessee City's Pro;-Zranis website Headlines 9/9/02 The city does not spray adulticides. University of Tennessee advised such a U.Action.n;if program is ineffective and more cost prohibitive than other, more effective, options such as public education and providing larvacides for areas where standing water is a problem Spraying adulticides can adversely affect the health of those with breathing problems, and small children. Spraying also does not kill the larvae from which mosquitoes develop. Moreau, Northumberland and Wilton, NY (Saratoga County) Times-Union 4/24/02 The three towns have switched to Mosquito Dunks and stopped their adulticide spraying programs. Moreau dropped adulticide spraying after a softball field was accidentally sprayed in June 2100, sending 37 people to the hospital for treatment of dizziness and nausea. "Spraying is really a short-term type of thing," said Wilton Councilman Larry Gordon. "It doesn't diminish the overall populations as dunks do." Washington D. C. First Case of West Nile Diagnosed Here, Washington Post, 8/8/02 D. C. officials will not be spraying adulticides, saying such pesticide spraying is inappropriate because of the area's many asthma patients. The announcement was made the same day that a human case of West Nile was confirmed, and the mosquito pools tested positive for West Nile from 40 locations throughout Washington. The city will accelerate its program of larvaciding, placing tablets in more that 4200 catch basins and pools of standing water. Also, residents are encouraged to get rid of standing water, and to buy tablets (mosquito dunks) and put them in breeding areas such as garden ponds and birdbaths. Source: Canadian Coalition for Health and Environment, see the link "Great links for more information." HOT Lrws 111o is ai R?sli fio1' . ~y ers- E fec,s Ii m A-1j ji ; h1I~C iii ~r to ~`et mosquitoes to quit bugajrg `ou l ! ii L a C.ia'S ali ti 'Io :o L `~i> -.tact to L oil_p! .n i'~ 111E' 1 Zr-PORT { if you hav lna-d anv adN erse effects. click ~ I Ai T I OR-l (ifi1'Li-ks so ay peo- le outside o;' other Liz HO-ME Email: nospravi-Mshvilieu.iarthlink.net You Are Visitor 1%ti''t 7 _ P. 0. Box 128555, Nashville, TAI37?1?, (61.) 32 7-8. 15, JOURNAL OF PESTICIDE REFORM/SUMMER 2003 • VOL. 23, NO. 2 • I N S E C T I C I D E F A C T S H E E T SUMITHRIN (D-P-H-1ENOTHRIN) The synthetic pyrethroid insecticide sumithrin is commonly used to kill household insects and mosquitoes. The U.S. Environmental Protection Agency (EPA) estimates that about 100 million applications of sumithrin are made annually in U.S. homes, yards, and gardens. Sumithrin is a neuropoison. Symptoms of exposure include dizziness, headache, fatigue and diarrhea. In laboratory tests, sumithrin has damaged the liver and the kidneys. It has also caused anemia and increased the incidence of liver cancer. In breast cancer cells, sumithrin increases the expression of a gene that is involved with proliferation of cells in the mammary gland. Sumithrin can also mimic certain activities of the sex hormone estrogen and keep another sex hormone from binding to its normal receptors. Thousands of cat poisonings and some dog poisonings have been reported following the use of some sumithrin- containing flea control products. Low concentrations of sumithrin (as low as one part per billion) kill fish and other aquatic animals. Sumithrin is also highly toxic to bees. BY CAROLINE COX Environmental Protection Agency Figure 1 (EPA) surrey estimated in 1992 that Sumithrin almost 100 million applications of Surnithrin (see Figure 1) is an / sumithrin were made annuallN in L.S. insecticide in the synthetic pyrethroid homes, yards, and gardens. About 2%3 pesticide family. It is also called d- of these applications occurred indoors.6 COO-CH2 phenothrin. Marketed as an insecticide since 1977,1 it is sold by many pesti- 3-phenoxybenzyl (lP)- trans-chrysanthemate How Does Sumithrin cide companies using a variety of Kill Insects? brand names including Raid, Enforcer, Sumithrin kills insects by disrupting Ortho, and Anvil.'- There are about ` the transmission of nerve impulses 250 sumithrin-containing pesticide COO-CH2 / O / along axons, the elongated parts of products registered for sale in the U.S.' nerve cells. Synthetic pyrethroids al- 3-phenoxybenzy! (1 R)- cis-chrysanthemate Pyrethroid insecticides are related low excessive amounts of sodium at- chernicallti- to the insecticidally active oms to enter nerve cells, stimulating compounds called pyrethrins extracted including sumithrin, "are widely per- the nerve cells and eventually causing from chrysanthemum f1mvers. Chem- ceived as being safe according to paralysis. This mode of action is sirmi- ists have desined the structure of sN-n- one neurotoxicologist. However, su- lar to that of the organochlorine thetic pyrethroids to make them both mithrin poses a variety- of hazards for secticide DDT.3 potent and stable in sunlight.3 human and environmental health, and Pyrethroids' effects on human nerves Like most synthetic pyrethroid in- those are the focus of this article. are similar to their effects on insect secticides. sumithrin exists as a mix- nerves.' Hmvever, human nerves are ture of stereoisomers,l molecules that Use generally less susceptible to pyrethroid have the same atoms linked in the Sumithrin is priimarily used to kill poisoning. This is because human same order, but differ in their spatial household insects, insects 'which pose nerves are intrinsically less sensitive, arrangement.' Sumithrin is a mixture public health problems (mosquitoes, pyrethroids are less potent at the of 2 stereoisomers which are both in- for example), insects in stored grains, higher body temperatures in humans. secticidally active.' (See Figure 1.) and lice.' The International Programme and human nerves recover more Synthetic pyrethroid insecticides, on Chemical Safety- estimated in 1989 quickly from poisoning. that worldv\-ide use was about 70 to ■ 80 tons per year;' more recent esti- Synergists Caroline Cox is NCAP's staff scientist. mates are not publicly available. A U.S. About a dozen surithrin products. NORTHWEST COALITION FOR ALTERNATIVES TO PESTICIDES/NCAP 10 P.O. BOX 1393, EUGENE, OREGON 97440 / (541)344-5044 JOURNAL OF PESTICIDE REFORM/ SUMMER 2003 • VOL. 23, NO.2 including the Anvil products used to effects on the nen-ous systern.11 Ac- tion, concentrations of enzymes that kill mosquitoes, contain piperonyl bu- cording to Medical Univ-ersit}- of South are indicators of liver damage increased toxide.s This chemical is used to Carolina physicians, acute (short-tern) in exposed animals. These effects oc- svnergize (to make more toxic) su- symptoms of exposure to sumithrin curred at the middle and high dose mithrin and other insecticides. Pipero- and other s-y-nthetic pyrethroids in- levels tested in this experiment.` nyl butoxide is classified as a carcino- elude "dizziness, salivation, headache, Similar increases in liver -eight gen by EPA, causes atrophied testes, fatigue, diarrhea, and irritability to -~vere found in studies of dogs fed and reduces the activity of important sound and touch. 1712 sutnithrin and rats breathing sumithrin- immune svstem components. For de- contaminated air. Both studies -ere tailed infornation about the hazards Effects On the Liver conducted as part of the registration of piperontTl butoxide see TPR 22(2):12- According to a laboratory study sub- process. 14.15 20 or v wvv.pesticide.org. ratted to EPA by a manufacturer as Effects on the Kidneys part of the registration process, Inert Ingredients sumithrin damages the liver. In a loner T-,\-o laboratory studies submitted as Like most pesticides, sumithrin in- tern (two-Near) study in v.-hich rats part of the registration process sug- secticides contain ingredients in addi- -ere fed sumithrin, the HN,ers of ex- gest that male kidneys may be par- tion to sumitlirin. Mane of these in- posed animals weighed more than ticularly susceptible to sutnithrin.' i' gredients, according to U.S. pesticide those of unexposed animals. In addi- (See Figure 2.) At all dose levels tested. lam-. are called `inert. "9 In general, they have not been publicly identified, and are not included in most of the testing "INERT" required in order to register these pes- INGREDIENTS ticides.10 "Inert Ingredients" (right) summarizes the hazards of some inert Almost 100 surnithrin products contain petroleum distillates as inert ingredients used in sumithrin products. ingredients.' One of these distillates is hydrotreated kerosene (Chemical Abstracts Serv-ices (CAS) number 64742-47-8).=' According to the Intema- Symptoms of Exposure tional Agency- for Research on Cancer (IARC), exposure to hydrotreated Sumithrin and other synthetic pyre- kerosene caused skin tumors in a laboratory study .3-4 Three other petro- throids are "neuropo'sons" and s-\-mp- leum distillates (,v~-ith CAS numbers 64742-75-8, 6=17=12-56-9, and 6=17=12-94- toms of exposure are related to their 5) are used in Anvil mosquito control products.5-0 One of these petroleum distillates causes tremors and difficulty- breathing,' the second caused skin tumors, according to IARC,1•9 and the third contains mo hazardous Figure 2 chemicals, naphthalene and trimethyl benzene.10 Naphthalene exposure Sumithrin Damages Kidneys has caused lung tumors, cataracts, and anemiall while tri-methyl benzene 1.0 can depress the central nervous system and cause asthmatic bronchitis.'' Many household surnithrin products are sold in aerosol spray cans, and these products often contain "inert" propellants that pose a variety- of hazards. These propellants include propane and isobutane.- Both of these propellants can cause dizziness -hen inhaled and are "extremely flanunable."13.14 is 0) 0.8- 1. Based on a survey of labels of Sumithrin insecticide products conducted during May, 2003. .5 Labels were retrieved from: U.S. EPA and Calif. Dept. of Pesticide Regulation. 2003. USEPA/ 3: OPP chemical ingredients database. www.cdpr.ca.gov/docsiepa/epachem.htm. Q) 2_ U.S. EPA. 2002. Response to Freedom of Information Act request 01245-03. 3. National Institute for Occupational Safety and Health (NIOSH). 1997. Registry of Toxic Effects of .a Y Chemical Substances: Kerosene (petroleum), hydrotreated. ww.cdc.gov/niosh/rtecs/oa53fcOO.htmi. 4. International Agency for Research on Cancer (IARC). 1989. Occupational exposures in petro- leum refining. IARC Monographs 45:39. wwvv-cie.iarc.fr/htdocs,/monographs/vol45i45-Ol.htm. 0.6 5. Clarke Mosquito Control Products, Inc. 1999. Material safety data sheet: Anvil 2+2 ULV. Rosedale, IL. 0 1 2 3 4 5 6. Clarke Mosquito Control Products, Inc. 1999. Material safety data sheet: Anvil 10+10 ULV. Rosedale, IL. 7. NIOSH. 2000. Registry of Toxic Effects of Chemical Substances: Mineral oil, petroleum distil- Sumithrin dose lates. solvent - dewaxed light paraffinic (mild or no solvent - refining or hydrotreatment). (100 mg per kg of body weight per day) ww.cdc.gov/niosh,/rtecs/py7aaO95.htmi. 8. NIOSH. 2000. Registry of Toxic Effects of Chemical Substances: Mineral oil, petroleum distil- Source: U.S. EPA. Office of Pesticides and lates, hydrotreated (severe) light paraffinic. ww.cdc.gov/niosh.!rtecs!py7aac4c.html. Toxic Substances. 1989. Memo from E.R. 9. IARC. 1987. Mineral oils: Untreated and mildly-treated oils; Highly treated oils. IARC Mono- Budd, Health Effects Div. to J.M. Tavano, graphs (Suppl. 7):252. www-cie.iarc.fr/htdocs!monographsisuppl7,'mineraloils.htmi. Registration Div. Washington, D.C., Mar. 10. Shell Chemical Co. 2003. Material safety data sheet: Shellsora A150. ww.euapps.shell.com/ 16. See attached Data Evaluation Report MSDS/GotoMsds. for MRID No. 402764-02. 11. IARC. 2002. Naphthalene. [ARC Monographs 82:367. www-cie.iarc.fr/htdocs%monographs/vol8Z'82-06.htm1. 12. Hazardous Substance Data Bank (HSDB). 2002. 1,2.4-trimethylbenzene. http://toxnet.nim.nih.gov. 13. HSDB. 2002. Propane. http:/,'Ioxnet.nim.nih.gov. In male mice, surnithrin reduced kidney weight 14. HSDB. 2002. Isobutane. http:('toxnet.nlm.nih_gov. at all dose levels tested. NORTHWEST COALITION FOR ALTERNATIVES TO PESTICIDES/NCAP P.O. BOX 1393, EUGENE, OREGON 97440 / (541)344-5044 1~ JOURNAL OF PESTICIDE REFORMISUMMER 2003 • VOL. 23, NO. 2 Figure 3 Figure 4 Sumithrin Mimics the Activity of a Sex Sumithrin Displaces a Sex Hormone from its Hormone Receptors (D 6 W Note: Lines Bioallethrin above bars cu) 5 are standard ° deviations ru Fenvalerate 4 a~ a Sumithrin (1) 3 0 2 Permethrin i5 W a~ W 1 Resmethrin ) 0 0 0.2 0.4 0.6 0.8 1.0 Unexposed Exposed to Exposed to an Relative ability to displace an androgen sumithrin (30 EtM) estrogen (10 nM) (Bioallethrin = 1) Source: Go, V. et al. 1999. Estrogenic potential of certain pyrethroid Source: Eil, C. and B.C. Nisula. 1990. The binding properties of compounds in the MCF-7 human breast carcinoma cell line. Environ. pyrethroids to human skin fibroblast androgen receptors and to sex Health Persp. 107:173-177. hormone binding globulin. J. Steroid Biochem. 35:409-414. In laboratory tests, sumithrin disrupts the normal functioning of hormone systems. (t5- -50 milligrams per kilogram of caused by extremely small amounts" on reproduction in laboratory- studies. body- ,~\-eight (mg/"kg) per day), male of hormones or other chemicals that In the mo-generation study of rats mice exposed to surnithrin in a two- disrupt this syTstem.19 mentioned in the "Effects on Kidneys" year study developed smaller kidneys Sumithrin has these kinds of effects section, the uterus was smaller in fe- than unexposed males.16 A study in on hormones. Researchers at the Mt. male rats exposed to the middle and ,v~-hich rats -ere fed sumithrin for MTO Sinai School of Medicine shored that high doses of sumithrin than in unex- generations also found small kidneys surnithrin can mimic estrogens, sex posed rats.l in the first generation males. l hormones, in one of their biological in a second study of surnithrin's ef- activities. The researchers looked at fects on reproduction subnutted dur- Effeets on Blood the activity of a gene called pS2 be- ing the registration process, pregnant in the study of dogs mentioned on cause the expression of pS2 is acti- rabbits exposed to surnithrin (at a dose p. 11, sumithrin exposure also caused vated by estrogens. They found that of 500 mg%kg) had more miscarriages anemia. In dogs fed sunuthrin for one in human cells surnithrin (as well as than unexposed rabbits. In addition, year, both the number of red blood another synthetic pyrethroid insecti- the sex ratio of the offspring of ex- cells and the amount of hemoglobin cide, fenvalerate) activates the expres- posed mothers --as different from that the ox-y carry-cam,molecule in the sion in cells of pS2 like estrogens do.'° of unexposed mothers: more males blood') ',~Vere decreased." Anemia oc- (See Figure 3.) '-ere born to exposed animals. Also. curred at dose levels of 80 mg/kg per Sumithrin also keeps androgens. a brain-related defect occurred in the day. This --as the highest dose tested other sex hormones, from binding to offspring of rabbits exposed at the dose in this studv.` their normal receptors in human tis- level of 500 mg/'kg. This defect. hy- sue. Scientists from Bro« n University- drocephaly, results in an abnormally Effects on Hormones and the National Institutes of Health large amount of fluid around the brain, The impact of environmental con- shored that in genital skin cells leading to an enlarged skull and atro- taminants on the functions of human sumithrin could displace an androgen phy of the brain." and animal hormone systems has been from its normal receptors. When con- 1-Carcinogenicity a significant concern in the last de- pared to other synthetic pyrethroids. Ability to Cause Cancer) cade." Hormones are biologically ac- surnithrin is intermediate in its displace- tive molecules that control all re- ment potency. 21 (See Figure -i.) Sumithrin's ability- to cause cancer sponses and functions of the body. has not yet been evaluated by EPA Dramatic changes in the activist- of cells Effects on Reproduction (as of '\~1ay 2002).23 in humans and other animals -are Surnithrin has a variety of effects Ho--ever, in M70 of the laboratory NORTHWEST COALITION FOR ALTERNATIVES TO PESTICIDESINCAP 12 P.O. BOX 1393. EUGENE, OREGON 97440 / (541)344-5044 JOURNAL OF PESTICIDE REFORM/ SUMMER 2003 • VOL. 23. NO.2 carcinogenicity- studies submitted in detoxify- pyrethroids in marr pals. The Programme on Chemical Safety-, support of sumithrin's registration, activity- of these enzymes is inhibited sumithrin is "verb- toxic to aquatic or- long-term (t,~\-o-rear) exposure to by a conunon family of insecticides. ganisms.-29 In tests submitted as part sumithrin increased the incidence of the organophosphates; this means that of sumithrin's registration. the most liver cancer. The studies include one "simultaneous exposure to these in- sensitive fish species ~\-as the rainbo~\- done on mice and another done on secticides vvill increase the toxicity- of trout. The LC,O (median lethal concen- rats. In the study N~-ith mice, litrer can- pyrethrins and pyrethroids." tration; the dose that kills half of a cer R-as relatii,ely common (it occurred test population) for rainbow- trout ,A-as in 18 percent of the unexposed ani- Effects On Pets 1.4 parts per billion (ppb). All LC~Os teals tested) and sumithrin exposure Cats, especially young cats, are par- for fish ,~vere less than 100 ppb.30 caused cancer incidence to increase ticularly susceptible to pyrethroid in- The labels of about 80 sumithrin- to almost 25 percent.16 In the study secticides, possibly because cats' liN-- containing insecticides contain -,ivarn- ,~\-ith rats, liver cancer R-as relatively ers are relatively slov,- in detoxifying ing statements about toxicity to fish.s rare (no liver cancer xN-as found in pyrethroids.20 Two suntitiuin flea con- sumithrin also bioconcentrates in unexposed animals) but increased to trol products manufactured by Hartz fish. This means that the concentra- an incidence of almost 15 percent in Mountain Corporation have recently- tion of sumithrin in fish tissues is exposed aniinals.13 (See Figure 5.) caused a large number of cat poison- greater than the concentration in the In addition, a study from the ings. EPA estimates that there -ere Rater in v~-hich the fish lives. Accord- Sinai School of Medicine links thousands of incidents, including some ing to a study conducted by, Suinitomo sumithrin -with breast cancer. In this deaths, between May 2000 and No- Chemical Company. bioconcentration study, physicians used a culture of vember 2002. At that time Hartz agreed factors in carp range from 210 to 730.31 breast cancer cells. They looked at the to relabel the M o products to reduce (The bioconcentration factor is the ra- expression of a gene that is invohred cat exposure.' do bem7een the concentration of a in the proliferation of mammary- tis- Seizures and death have also oc- chemical in fish tissues and the con- sue, and therefore in the deNTelopment curred after use of sumithrin on dogs, centration in ~vater.32) When fish ,~\Tere of breast cancer. Exposure to sumithrin but not in as large numbers as the cat simultaneously exposed to sumithrin increased the expression of this gene.' incidents.28 and the synergist piperonyl butoxide (as in Anvil insecticide products), the Synergy Effects On Fish bioconcentration factor of one form of Enzymes called plasma esterases According to the international sumithrin increased dramatically. Bioconcentration factors in this experi- ment varied from 2400 to 3800.31 Figure 5 Ability of Sumithrin to Cause Cancer Effects On Other Aquatic Animals 15 Sumithrin is highly- toxic to rater fleas, a species that is used in pesti- cide testing to represent aquatic ani- `CZ' 12 vials. In a test submitted to EPA for sumithrin's registration, concentrations of less than 1 ppb reduced successful 3 9 egg hatch in N\-ater fleas. A slightly higher concentration (2 ppb') reduced the survival of larval rater fleas. 6 Sumithrin is even more toxic to shrimp; Q°, concentrations of 0.03 ppb killed mysid shrimp.30 c 3 a~ CD Effects on Bees CL 0 Since sunmithrin is a broad spectrum 0 200 400 600 800 1000 insecticide, it is perhaps not surpris- Dose of sumithrin ing that tiny amounts of sumithrin kill (milligrams per kilogram of body weight per day) bees. In a test submitted to EPA as part of sumithrin's registration. 0.07 Source: Calif. Environmental Protection Agency. Dept. of Pesticide Regulation. Medical imicrogranls killed honey bees.30 This Toxicology Branch. 1996. Summary of toxicology data: Phenothrin, June 20. www.cdpr.ca.gov/ docs/toxsums/toxsumlist.htm puts sumithrin into EPA's highest tox- icity group for bee toxicity. This toxic- In a laboratory study of rats, sumithrin increased the incidence of liver cancer. ity- group includes any pesticides that NORTHWEST COALITION FOR ALTERNATIVES TO PESTICIDES/NCAP P.O. BOX 1393, EUGENE, OREGON 97440 / (541)344-5044 13 JOURNAL OF PESTICIDE REFORM/ SUMMER 2003 • VOL. 23, NO. 2 kiLl bees in amounts of 2 micrograms search Triangle Park NC: Research Triangle In- ence Information Management Branch. Health stitute. Effects Division. 2002. List of chemicals evalu- per bee or less.33 7. Narahashi, T. et al. 1998. ion channels as tar- ated for carcinogenic potential. Unpublished gets for insecticides. NeuroToxicology 19:581- document dated May 22. Resistance 590. 24. Kasai. K.. V. Go, V., and B.G. Pogo. 2002. Ef- 8. Based on a survey of labels of sumithrin insecti- fects of pyrethroid insecticides and estrogen on Insecticide resistance occurs R'hen cide products conducted during May, 2003. La- WNT10B proto-oncogene expression. Environ. repeated exposure o,,-er generations bels were retrieved from: U.S. EPA and Calif. Int. 28:429-432. kills the most susceptible indiN71duals Dept. of Pesticide Regulation. 2003. USEPA/ 25. Campbell, A. and M. Chapman. 2000. Hand- OPP chemical ingredients database. book of poisoning in dogs and cats. Malden MA: in in insect population. The sun,ix'ors www.cdpr.ca.gov/does/epa/epachem.htm. Blackwell Science. Pp. 44. lia-'e genetically determined character- 9. Federal Insecticide. Fungicide and Rodenticide 26. Ref. # 25, pp. 42-45. Act § 2(a) and 2(m). 27. U.S. EPA. Undated. Questions and answers: istics that allo,' them to sun-,ive expo- 10. 40 Code of Federal Regulations § 158.340. Label instructions tightened on flea & tick con- sures to the insecticide that -,~vould usu- 11. United Nations Environment Programme, Inter- trol products for pets. www.epa.gov/pesticides/ all-,' be lethal.3, national Labour Organization, and World Health factsheets/hartzq_a.htm. Organization (WHO). 1990. d-Phenothrin. Envi- 28. U.S. EPA. Office of Prevention, Pesticides and Sumithrin resistance has been re- ronmental Health Criteria 96. Geneva, Switzer- Toxic Substances. Undated. Review of incident ported in cockroaches, aphids. mos- land: WHO. Pp. 9-10. data for four Hartz Mountain flea and tick con- 3- " 12. Reigart, J.R. and J.R. Roberts. 1999. Recogni- trot products (2596-146, -147, -148, -150). Memo qu itoes and lice. The resistance tion and management of pesticide poisonings. from V.A. Dobozy, Health Effects Div. to A. ratio, the ratio bemeen the amount of Fifth edition. Washington, D.C.: U.S. EPA. Pp. Layne, Registration Div. and others. surilithrin needed to kill a resistant in- 87-88• www.epa.gov/pesticides/safety; 29. International Programme on Chemical Safety and sect and the amount needed to kill a healthcare. the Commission of European Communities. 13. Calif. Environmental Protection Agency. Dept. 2001. d-Phenothrin. ICSC:0313. susceptible one, can be ONrer 50 in of Pesticide Regulation. Medical Toxicology www.inchem.org/documents/icsc/icsc/ both cockroaches and lice.36,39.40 Branch. 1996. Summary of toxicology data: eics0313.htm. Phenothrin, June 20. www.cdpr.ca.gov/does/ 30. U.S. EPA. Office of Pesticide Programs. 2003. The syriergist piperori~"1 butO ide is toxs u ms/toxsu m list. him Pesticide ecotoxicity database. Unpublished. sotlletimes used to "negate" resistance, 14. U.S. EPA. Office of Pesticides and Toxic Sub- Received from EPA on May 13. to liitl resistant individuals, but is not stances. 1989. Sumithrin (d-phenothrin) - review 31. Miyamoto. M. et al. 1992. Effect of metabolism of toxicity studies submitted by Sumitomo Chemi- on bioconcentration of geometric isomers of d- al ays SuCCessful.3 cal Company in support of EAP#1H45283 and phenothrin in fish. Chemosphere 24:2001-2007. Sumithrin resistance can be quite EPA Registration No. 10308-6. Memo from E.R. 32. BioTech Resources and Indiana Univ. 1995-98. Budd, Health Effects Div. to J.M. Tavano, Reg- BioTech life science dictionary. http:// conlnlOn. French physicians found that istration Div. Washington, D.C., Mar. 16. See biotech.icmb.utexas.edu/search/diet-search.him1. 60 percent of the lice populations in attached Data Evaluation Report for MRID No. 33. U.S. EPA. Office of Pesticide Programs. Un- the Paris elementan- school students 402764-01. dated- Label review manual. Chap. 9. Environ- 15. U.S. EPA. Office of Prevention, Pesticides, and mental hazards. www.epa.gov/oppteadl/labeling! they studied were resistant to su- Toxic Substances. 1995. D-phenothirin irm/chap-09.htm. mithrin.38 Widespread resistance has (sumithrin) -submission of a 90-day inhalation 34. Cochran, D.G. 1995. Insect resistance to pyre- also been found in lice in the tinted toxicity study in rats. (EPA ID 06905). Washing- thrins and pyrethroids. In J.E. Casida and G.B. ton, DC, June 13. Quistad, eds. Pyrethrum flowers: Production. Kingdom.' 16. U.S. EPA. Office of Pesticides and Toxic Sub- chemistry, toxicology, and uses. New York NY: Insects resistant to one pyrethroid stances. 1989. Sumithrin (d-phenothrin) - review Oxford Univ. Press. p. 234-248. insecticide are often resistant to man-,' of toxicity studies submitted by Sumitomo Chemi- 35. Michigan State Univ. Center for Integrated Plant cal Company in support of EAP#1 H45283 and Systems. Undated. The database of arthropods pyrethroids. This means that insects EPA Registration No_ 10308-6. Memo from E.R. resistant to pesticides. www.cips.msu.edu/resis- Can develop resistance to surnithrin Budd, Health Effects Div. to J.M. Tavano, Reg- lance. (See entries for both sumithrin and istration Div. Washington, D.C., Mar. 16. See phenothrin.) Without actually hai-ing been exposed attached Data Evaluation Report for MRID No. 36. Picoilo, M.I. et al. 1998. Laboratory studies of to the insecticide. 42 402764-02. susceptibility and resistance to insecticides in 17. U.S. EPA. Office of Pesticides and Toxic Sub- Pediculus capitis (Anoplura; Pediculidae). J. References stances. 1989. Sumithirin (d-phenothrin - review Med. Entomol. 35:814-817. of rat reproduction study. Memo from W. Dykstra, 37. Picolio, M.I. et al. 2000. Resistance to insecti- 1. United Nations Environment Programme, Inter- Health Effects Div. to J. Tavano, Registration cides and effect of synergists on permethrin tox- national Labour Organization, and World Health Div. Washington, D.C., Jul. 27. icity in Pediculus capitis (Anoplura: Pediculidae) Organization. 1989. d-Phenothrin health and 18. National Research Council- Commission on the from Buenos Aires. J. Med. Entomol. 37:721- safety guide. IPCS International Programme on Life Sciences. Board on Environmental Studies 725. Chemical Safety. Health and Safety Guide No. and Toxicology. Committee on Hormonally Ac- 38. Chosidow. O. et al. 1994. Controlled study of 32. www.inchem.org. tive Agents in the Environment. 1999. Hormon- malathion and d-phenothrin lotions for Pedicu- 2. U.S. EPA and Calif. Dept. of Pesticide Regula- ally active agents in the environment. Washing- lus humanus var capitis-infested schoolchildren. tion. 2003. USEPA/OPP chemical ingredients ton, D.C.: National Academy Press, p. 10. The Lancet 344:1724-1727. database. www.cdpr.ca.gov/docs,epal 19. Eubanks, M.W. 1997. Hormones and health. 39. Cochran, D.G. 1989. Monitoring for insecticide epachem.htm. Environ. Health. Persp. 105:482-487. resistance in field-collected strains of the Ger- 3. Ware, G.W. 2000. The pesticide book. 5th edi- 20. Go. V. et al. 1999. Estrogenic potential of cer- man cockroach (Dictyoptera:Blatellidae). J. Econ. tion. Fresno CA: Thomson Publications. Pp. 65- tain pyrethroid compounds in the MCF-7 human Entomol. 82:336-341. 67,177-178. breast carcinoma cell line. Environ. Health Persp. 40. Lee, C.Y. et al. 1996. Insecticide resistance and 4. National Library of Medicine. Undated. Medline 107:173-177. synergism in field collected German cockroaches Pius health information; Medical dictionary. 21. Eil, C. and B.C. Nisula. 1990. The binding prop- (Dictyoptera:Blateliidae) in peninsular Malaysia. www.nlm.nih.gov/medlineplus/mplusdictionary.html. erties of pyrethroids to human skin fibroblast Bull. Entomol. Res. 86:675-682. 5. Soderlund. D.M. 2002. Agents affecting sodium androgen receptors and to sex hormone binding 41. Downs, A.M.R. et al. 2002. Widespread insecti- channeis. In Handbook of neurotoxicology, vol. globulin. J. Steroid Biochem. 35:409-414. cide resistance in head lice to the over-the- 1, ed. E.J. Massaro. Totowa NJ: Humana Press 22. U.S. EPA. Office of Pesticides and Toxic Sub- counter pediculocides in England, and the emer- Inc. Pp. 47-68. stances. 1991. Sumithrin. Review of develop- gence of carbaryl resistance. Br. J. Dermatol. 6. Whitmore, R.W., J.E. Kelly, and P.L. Reading. mental toxicity in rabbits. Memo from P.M. 146:88-93. 1992. National home and garden pesticide use Hurley, Health Effects Div., to R. King, 42. Cochran, D.G. 1987. Selection for pyrethroid re- survey. Final report, vol. 1: Executive summary. Reregistration Div. Washington, D.C., Nov. 7. sistance in the German cockroach results, and recommendations. Table G.1. Re- 23. U.S. EPA. Office of Pesticide Programs. Sci- (Dictyoptera:Blatteliidae). J. Econ. Entomol. 80:1117-1121. NORTHWEST COALITION FOR ALTERNATIVES TO PESTICIDES/NCAP 14 P.O. BOX 1393, EUGENE, OREGON 97440 / (541)344-5044 hemicalWATCH Factsheet 00& A B E Y O N D P E S T I C I D E S / N C A M P F A C T S H E E T Piperonyl Butoxide (PBO) iperonyl Butoxide (PBO), a highly toxic substance that Acute Toxicity causes a range of short- and lonb term effects, includ- Studies suggest that by interfering with the metabolism of hor- ing cancer and adverse impacts on liver function and the moves, PBO may damage humeral organs such as the thyroid, nervous system, is one of the most commonly used synergists in adrenal, and pituitary glands." PBO has a low to moderate pesticide products. S}Tnergists are chemicals added to pesticide toxicity based on short-term laboratory animal studies. The formulations to enhance the toxicity of the active ingredients. PBO acute oral LD50, or dose that kills half the test population, was is frequently used, especially in aerosol products and mosquito determined to be 6.15 g/kg for rats.' The LD 50 for inhalation sprays, to increase the potency of pyrethrin and synthetic pyre- of PBO by rats is greater than 5.9 g/kg.14 It is predicted that the throids, as well as other types of insecticides.' Products generally oral lethal dose for a human is 5.15 g/kg, or between 1 pint contain between five to ten times as much PBO as pesticide.' and 1 quart for a 150 lb person.'' Many different formulations of insecticide products contain Symptoms caused by ingestion of PBO in large doses include PBO. These include dusts, sprays, foggers, repellents and pe- nausea, cramps, vomiting, and diarrhea." Inhalation of large diculicides (lice killers); garden lawn, ornamental plant, and, amounts of PBO may cause tearing, salivation, labored breath- agricultural pesticides; mosquito abatement products, termite ing,17 accumulation of fluids in the lungs," and may be linked treatments, veterinary pesticides; and insecticides for human to respiratory problems, including asthma. Acute and repeated clothing, bedding, and mattresses.' According to surveys by dermal (skin) and eye contact has been shown to be slightly the Environmental Protection Agency (EPA), PBO is one of the irritating, but is not linked to long-term damage.19 most commonly used ingredients in insecticides. It is currently Overdoses of PBO have been shown to cause hyperexcitibil- found in approximately 1600 to 1700 registered pest control ity; unsteadiness, coma, seizures, and brain damage in ani- products.4 On labels, PBO is sometimes listed as an active in- mals.20 Most rat deaths in studies are attributed to hemorrhages gredient, but may also be considered an inert ingredient and in the digestive tract, particularly the large intestine. Acute not listed. PBO may also be listed as Butacide, Pybuthrin, ENT exposure in animals has also triggered hepatic (liver) changes - 14250, and CAS Reg. No. 51-03-6.5 and injury, anemia and loss of appetite, as well as changes in Because of its widespread use, PBO is prevalent in the resi- the kidneys, nasal bleeding, loss of muscle coordination, and dential environment. A recent study of pregnant women from abdominal swelling.'-' northern Manhattan and the Bronx found PBO in air samples from over 80% of the women's residences.' The pesticides that Long-Term Toxicity are most commonly mixed with PBO, synthetic pyrethroids, are among the most frequently found in the human toxic body The primary effect of long-term exposure to PBO in animals burden by the Centers for Disease Control (CDC).' Residues is an increase in liver and thyroid weight, liver and kidney are also regularly found on food, especially lettuce, lemons, damage, and a decrease in body weight. These s~nnptoms were spinach and tomatoes,' as well as basil, chive, cilantro, herbs, observed in a diet of 52.8 mg/kg or more a day in a chronic mint, pears, bell peppers, oranges, squash, and other fruits and study with dogs.- vegetables.9 While EPA claims that acute dietary food risk is very low, and that chronic dietary exposure is below the accept- Cancer able intake limit, others site deficiencies in EPA reviews.10 PBO is labeled as a group C carcinogen, a possible human PBO functions as a synergist by slowing the breakdown of carcinogen. Currently there is no data from accidental ex- toxic chemicals in insects. The first step in the breakdown of posure available regarding its carcinogenicity in humans; the many types of chemicals in insects is oxidization by a group of only information is from animal studies. Several studies have microsomal enzymes called P450 mono-oxygenases, located in shown that PBO treatment in rats causes an increase in liver the liver. PBO inhibits the activity of these enzymes, and thus cancer at high doses.24 Some studies have shown that PBO prevents the metabolism of many types of molecules, includ- treatment in rats corresponds with a very slight increase in ing insecticides. This keeps the pesticide in its toxic form for thyroid cancer.' longer periods of time, increasing the amount of damage it can do to the insect. A heavy dose of PBO makes an organism Mutagenic Effects temporarily vulnerable to a variety of toxic chemicals that It is generally accepted that PBO does not demonstrate any would be easily tolerated otherwise.'','' significant potential for mutagenicity (genetic damage). 26,27 Vol. 26, No_ 1, 2006 Pesticides and You Page 17 Beyond Pesticides/National Coalition Against the Misuse of Pesticides However, this conclusion is not accepted by everyone, and some studies have shown evidence of genetic damage, 8 in are synergists? What eluding a study that demonstrated gene mutation in mouse lymphoma cells.29 Immune System Effects PBO weakens the immune system by inhibiting lymphocyte response.30 Lymphocytes are a class of white blood cells that consume potentially dangerous pathogens and release antibod- ies. Inhibiting lymphocyte response weakens the body's ability to defend against foreign invaders. Furthermore, by preventing the breakdown of toxic chemicals, PBO increases the damage of toxic insults that %could c,thcr\\J.,c he tolcratcd. they can do to the body. Reproductive Effects Tect PBO has been shown to adversely affect a variety of reproduc- tive functions. Two-generational laboratory studies on rats show that litter weight and size are less for mothers exposed to high concentrations of PBO, and there is an increase in birth defects and fetal death.31 In one study the difference in the EPA docket and most of' the referciicc-, iiscd in this average weight of PBO-exposed offspring immediately after birth is negligible, but 7-14 days post-natal is significantly PBO combinations. greater for those mothers that are exposed to PBO than for those that are not.32 EPA maintains that results for teratogenic- ity (the ability to produce birth defects) in animals have been mixed,33 and while some studies suggest some teratogenicity, damage has been found as well .4' Long-term ingestion of PBO most do not. PBO may also interfere with sexual development causes anemia, a decrease in the amount of hemoglobin (oxy- because the enzymes it inhibits are responsible not only for gen-transporting molecules) in blood,` and increases the blood the breakdown of toxic chemicals but also for the metabolism cholesterol level in rats."' PBO can also damage the larynx, and of other compounds such as steroids, which include the sex there have been reports that it can cause labored breathing, an hormones. Rats exposed to PBO over the course of two years accumulation of fluid in the lungs,48 nasal bleeding, abdominal experience an atrophy of the testes a decrease in weight of swelling, and loss of the ability to coordinate muscle move- the seminal vesicles (sperm producing structures), and an ment.49 There has been a fair amount of investigation into the increase in ovarian weights. 34 There is no evidence that PBO effects of dermal contact with PBO since it is used as a topical affects fertility.37 agent for lice, but there has been no evidence of it causing any local or systemic toxicity, and the amount of PBO absorbed from Neurotoxicity skin contact is characterized by some researchers as low." Data has shown that PBO alone interferes with enzymes that maintain homeostasis of sodium and calcium in the brain and Environmental Effects nervous system, possibly affecting neural response.36-3' Addi- PBO is considered moderately toxic to fish, moderately to tionally, it increases the neurotoxicity of other compounds.38 highly toxic to invertebrates (including crustaceans and Despite this data, EPA believes that these neurotoxic effects are insects), and highly toxic to amphibians.71 In one study, slight and maintains that PBO poses no neurological risk.39 concentrations of less than one part per million (ppm) killed Behavioral changes have been noted with PBO as well. In a water fleas, shrimp, and oysters.''- It is also very toxic to a laboratory experiment, exposed rats experience more trouble common type of earthworm." Ingested PBO has a low to very navigating a maze than unexposed rats. The exposed rats travel low toxicity in birds." longer distances and turned more frequently in the maze.40 PBO Not only does PBO kill organisms, it is known to interfere also induces changes in olfactory behavior of the offspring of with the reproduction of many types of wildlife at much lower exposed mothers. Offspring of exposed mothers are less likely concentrations than those required for mortality The bio-con- to enter a compartment that smells like home than unexposed centration potential for PBO is low,'' but can be moderate in mothers.4' Exploratory behavior in mice increases as the dose some aquatic organisms.'' PBO also inhibits the breakdown of of PBO they were treated with increased."- This data shows that toxic chemicals in wildlife and the soil, increasing the concen- PBO has the ability to affect behaviors in mammals. trations of other, more acutely potent, pesticides. Other Chronic Effects Environmental Fate Research on rats has found that PBO can cause intestinal ulcers PBO is relatively short-lived in the environment and has a low and bleeding.43 Liver damage is common in studies,"' and kidney to moderate potential to contaminate groundwater. One study Page 18 Pesticides and You Vol. 26, No. 1, 2006 Beyond Pesticides/National Coalition Against the Misuse of Pesticides Not only does PBO kill organisms, Common Products it is known to interfere with the Containing PBO reproduction of many types of wildlife dietary and xvaier eXPOSLII-e to 11110 is N-cl-N. lo-,N-.1 it is III dozens of products xvidely Lised III the lioine and coin- at much lower concentrations than those required for mortality.... PBO exposure to MY) is of concern because oftlieIr sPecial also inhibits the breakdown of toxic nionly used products on the inarkel containin,-, 11110. As an inuredient. P130 adds to flie overill toxicity of' oilier-,visc liazzirdous pesticide products. chemicals in wildlife and the soil, increasing the concentrations of other, Bayer - Advanced Garden Nlo,Liuito killer Plus more acutely potent, pesticides. found PBO in river water at a concentration of 9.7lig/L .57 It and Lice Killer is rapidly degraded when exposed to sunlight, with a degra- dation half life of about one day in soil exposed to sunlight, Deep 6 Wasp and 11ornct killcr and 14 days in soil without sunlight. The rate of degradation is also affected by how much oxygen is in the environment (particularly in aquatic systems), moisture levels, and applica-Garden Safe Brand Flying & Craxvlin- In--,cct Killer tion methods .s' There is less information available about PBO's Mir, persistence indoors, but one study found that PBO persisted Ortho Plant (-'are for at least two weeks after a cockroach treatment on toys and in dust in a kindergarten.59 Read\- to L --,c Regulatory Status and History In the late 1930's U.S. manufacturers of pesticides began Raid Flea Killer Plus Raid -~nt & Roach Killer looking for a way to increase the potency of pyrethrum, Raid Commercial Insect killcr which was being imported from Japan, out of concern that its import could be disrupted. PBO was first synthesized in 1947 Raid Hou-;c & Garden Bu,, killer by Herman Wachs, who worked for Dodge & Olcutt, Inc. It was made from the naturally occurring raw material safrole. From 1952 onwards the U.S. has been manufacturing large amounts of PBO.bo In April 2005, EPA released human health and environmen- tal fate and effects risk assessments and related documents for PBO. This docket is available at wA wregulations.gov, docket ID EPA-HQ-OPP-2005-0042. A public comment period was open through June 27, 2005, and the EPA review is projected to be completed by August 3; 2006. The main concern expressed by the public commentary re-Spectracide Bug Stop Insect killer. 'kcros-ol garding this docket is that EPA should not evaluate PBO alone, Tcorin-LT Lice Ti-catnicni. kit but also should evaluate its synergistic effects, as this is the Tcrro -Ant Killer context in which it is used, and the evaluations of pyrethrins do not take this increased toxicity= into account. Furthermore, Flea and Tick ~1~pray the review lacks urban environmental data, despite the fact that this is the primary use of PBO. Vol. 26, No. 1, 2006 Pesticides and You Page 19 Beyond Pesticides/National Coalition Against the Misuse of Pesticides Endnotes 3O Diet F. et al. 1999_ Pyrethroids and piperonyl butoxide affect human T-Iympho- I Cox, Caroline- 2002_ Insecticide Synergist Factsheet: Piperonyl Butoxide. Journal cytes in vitro. Toxicol. Lett 107: 65-74. ofPesticide Reform. 22:12-20. (accessed Jan 2006) wvwpesticide.org/Piperonyl- " Tanaka, T. et al. 1994. Developmental toxicity evaluation of piperonyl butoxide Butoxide.pdf. in CD-1 mice. Toxicol Lett. 71: 123-129. US Dept. of Health & Human Services: Agency for Toxic Substances & Diseases " Tanaka T. 2003. Reproductive & neurobehavioral effects of piperonyl butoxide Registry: Sept. 2003. Toxicological Profile for Pyrethrins and I"wethroids. (accessed administered to mice in the diet. Food Addit Contain 20: 207-14. Jan 2006) «Rvw.atsdr.cdc.gov/tox-profiles/tpl55pdf. " US EPA. 2005. Human Health Risk Assessment. Sec. 1.3-6 Docket ID EPA-HQ- 3 National Pesticide Telecommunications Network (NPTN). 2000. "Piperonyl OPP-2005-0042 (accessed Jan 2006) httpJ/www.regutations.gov. Butoxide: Technical Fact Sheet." (accessed Jan 2006) httpJ/npic.orst.edu/fact- " Breathnach, R 1998. (See Ref. #14). sheets/pbotech.pdf. 35 Breathnach, R. 1998. (See Ref. #14). 3 US EPA. 2005. "Overview of the Piperonyl Butoxide Risk Assessments." Docket ID Kakko I, Toimela T, Tahti H. 2000. Piperonyl butoxide potentiates the synapto- EPA-HQ-OPP-2005-0042 p.2 (accessed Jan 2006) http://vrww.regulations.gov. some ATPase inhibiting effect of pyrethrin. Chemosphere 40: 301-5. 5 US EPA/OPP Chemical Ingredients Database. Piperonyl Butoxide. (accessed Jan Grosman, N, F Diel. 2005. Influence of pyrethroids & piperonyl butoxide on the 2006). httpJ/ppis.cerisfperdue/edufhtbin/epachem.com. Ca" - ATPase activity of rat brain synaptosomes and leukocyte membranes. Int. 6 Whyatt, R.M. 2002. Residential pesticide use during pregnancy among a cohort Immunopharmacol. 5: 263-70. of urban minority women. Environ. Health Persp. 110: 507- 514. se Friedman, M.A. and L. R. Eaton. 1978. Potentiation of methyl mercury toxicity Centers for Disease Control (CDC). 2005. Third National Report on Human Expo- by piperony 1 butoxide. Bull. Environ. Contain Toxicol. 20: 9-10. sure to Environmental Chemicals. [http://a-w,;A~cdc.gov/ex-posurereport/I (.Accessed 39 US EPA. 2005. Human Health Risk Assessment. Sec. 1.2 Docket ID EPA-HQ- February 24, 2006). OPP-2005-0042 (accessed Jan 2006) http://vvww.regulations.gov. e PAN Pesticides Database. CAS#51-03-6: Piperonyl Butoxide. (accessed jan 2006) 40 Tanaka, T. 1993. Behavioral effects of piperonyl butoxide in male mice. Toxicol. www.pesticideinfo.org. Lett. 69: 155- 161. 9 California Department of Pesticide Regulation. 2002. Summary of Pesticde Use al Tanaka, T. 1992. Effects of piperonyl butoxide on Fl generation mice. Toxicol. Report Data. Indexed by Chemical. (accessed Jan 2006) wwwv.cdpr.ca.gov. Lett. 60: 83-90. 10 US EPA. 2005. "Human Health Risk Assessment." Sec. 4.2.2.2-4.2.2.3. Docket ID 42 Tauaka 2003 (Ref. # 32). EPA-HQ-OPP-2005-0042 p.2 (accessed Jan 2006) httpY/mw,v.regulations.gov. 41 Maekaw*a, A. et al_ 1985. Lack of evidence of carcinogenicity of technical-grade 11 Scott, JG et al. 2000. Inhibition of cytocrome P450 6D1 by alkynylarenes, piperonyl butoxide in F344 rats: Selective induction of ileocaecal ulcers. Fd. methylenedioxyarenes, and other substituted aromatics." Pesticide Biochemistry Chem Toxic. 23: 675-682. & Physiology 67: 63-71. " Fujitani, T., T. Tanaka, Y. Hashimoto, and M. Yoneyama. 1993. Subacute toxicity 12 Keseru, GM. 1999. Piperonyl butoxide-mediated inhibition of cytochrome P450- of piperom 1 butoxide in ICR mice. Toxicol. 83: 93-100. catalyzed insecticide metabolism: a rational approach." Pesticide Science. 55: 45 Fujitani, T., Y. Tada, and M. Yoneyama. 1993. Hepatotoxicity of piperonyl butoxide 10041006. in male F344 rats. Toxicol. 84: 171-183. is Graham, C. 1987.24-Month dietary toxicity and carcinogenicity study of piperonyl 46 butoxzde in the albino rat. Unpublished report No. 81690 from Bio-Research Ltd Takahashi, O. et al. 1994_ Chronic toxicity studies of piperonyl butoxide in Laboratory, Seneville, Quebec, Canada. Submitted to NATIO by Piperonyl Butoxide 2344 rats: Induction of hepatocellular carcinoma. Fund. Appl. Pharmacol. 22: 291-303. Task Force. In Caroldi, S. Piperonyl Butoxide. First Draft. IPCS INCHEM. (Accessed Jan 2006) bttpY/%-Aw.inchem.org/documents4mprjjmpmono/v92prl5.htm. i` Fujitam, T. et al. 1992. Sub-acute toxicity of piperonyl butoxide in F344 rats. 14 Breathnach, R. 1998. The safety- of piperonyl butoxide. In D.G_ Jones, ed_ Piperonyl Toxicol. 72: 291- 298. butoxide: The insecticide synergist. San Diego: Academic Press. p. 20. 46 Hayes, WJ., Jr., E.R. Laws Jr., (eds.). Handbook of Pesticide Toxicology Volume Gosselin, R.E., R.P Smith, H.C. Hodge. Clinical Toxicology ofCommercial Products. 1. General Principles. New York, NY: Academic Press, Inc., 199 1., p. 341 In Pi- 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-310. In Piperonyl Butoxide. peronyl Butoxide. National Library of Medicine: Hazardous Substance Database. http://toxnet.nlm.nih.gov. National Library of Medicine: Hazardous Substance Database. (accessedJan 2006) httpJ/tox-net.nlm.nih.goN 49 Breathnach, R. 1998 (See Ref. #14). 16 Prentiss, Inc. 1998. Material safety data sheet: 655-113 Prentox% piperonyl butoxide Breathnach, R. 1998 (See Ref. #14). technical. (accessed jan 2006). w,ww:prentiss.com/msds/pdf/655_113.pdf. 51 US EPA. 2005. Environmental Fate and Ecological Risk Assessment. Docket ID 17 World Health Organization and Food and Agricultural Organization. 1996. EPA-HQ-OPP-2005-0042 p. 5 (accessed Jan 2006) httpJfwww:regulations.gov, Pesticide residues in food - Evaluations 1995. [Part III Toxicological and en- PAN Pesticides Database. CAS#51-03-6: (Ref. #8). vironmental. Geneva. Switzerland: World Health Organization. Pp. 282. In Cox, 5' Osimitz, TG and JF Hobson. 1998. An ecological risk assessment of piperonyl Caroline. 2002. Insecticide Synergist Factsheet: Piperonyl Butoxide. Journal of butoxide. In D.G. Jones, ed. Piperonyl butoxide: The Insecticide synergist. San Deigo: Pesticide Reform. 22: 12-20. w~vw.pesticide.org/PiperonylButoxide.pdf. Academic Press. p. 122-135. le Bateman, D.N. 2000. Management of pyrethroid exposure. Clin. Toxicol. 38: 53 Roberts, B.L. and H.W. Dorough. 1984. Relative toxicities of chemicals to the 107-109. In Cox, Caroline. 2002. Insecticide Syncrgist Factsheet: Piperonyl earthworm Eisenia foetida. Environ. Toxicol. Chem. 3: 67- 78. In Cox, Caroline. Butoxide. Journal of Pesticide Reform 22: 12-20. a-w-w.pesticide.org/Piperonyl- 2002. Insecticide Synergist Factsheet: Piperonyl Butoxide. Journal of Pesticide Butoxide.pdf. Reform. 22: 12-20. wwww:pesticide.org/PiperonylButoxide.pdf. 19 Breathnach, R. 1998. (Ref. 914). 54 Osimitz, Hobson. 1998. (Ref. #52). 20 World Health Organization and Food and Agricultural Organization. 1996. (Ref. 55 Osimitz, Hobson. 1998. (Ref. #52). #17). 51, Meylan WM et al; 1999 Environ Toxicol Chem 18: 66472. In Piperonyl Butoxide. 21 Breathnach, R. 1998. (Ref. # 14). National Library of Medicine: Hazardous Substance Database. (accessedJan 2006) US EPA. 2005. Human Health Risk Assessment. Sec. 4.2.2.3. Docket fD EPA-HQ- http:/Itoxnet.nhn.nih.gov. OPP-2005-0042 (accessed Jan 2006) http://ww~wregulations.gov. 57 LeBlank, LA, JL. Orlando, KM Kuivila. 2004. Pesticide Concentrations in Water " Ibid. and in Suspended and Bottom Sediments in the New and Alamo Rivers, Salton Nat'l Cancer Inst. Carcinog. Tech. Rep. Ser. 1979. Bioassay of PBO for possible Sea Watershed, California, April 2003. U.S. Geological Survey. Data Series 104. carcinogenicity. 120: 1-131. Sacramento, California. (Accessed Jan 2006). httpJ/pennanent.access.gpo.gov/ 15 US EPA. 2005. Human Health Risk Assessment. Sec. 6.1.3 Docket ID EPA-HQ- w'aterusgsgov/%vater.usgs.gov/pubs/ds/ds104/inde-x.htm. OPP-2005-0042 (accessed Jan 2006) httpJ/vm-mregulations.gov. I Arnold, D.J. The Fate and Behavior of Piperonyl Butoxide in the Environment. 26 Butler, WH, KL Gabriel, FJ Preiss, TG Osimitz. 1996. Lack of genotoxiciy of In Piperonyl Butoxide: The Insecticide Synergist; Jones, D.G. ; Ed ; Academic: San piperonyl butoxide. Mutat Res 371: 249-58. Diego, CA, 1998. pp.105-119. Beamand, JA, et al. 1996. Lack of effect of piperonyl butoxide on unscheduled 59 Fischer, A, and T. Eikmann. 1996. Improper use of an insecticide at a kindergarten. DNA synthesis in presision-cut human liver slices. Mutat Resis. 371: 273-82_ Toxicol. Lett. 88: 359-364. 28 Cox, Caroline. 2002. (Ref. #1); US Dept. of Health & Human Services: Agency 60 Tozzi. A. 1998. A Short History of the Development of Piperonyl Butoxide as an for Toxic Substances & Diseases Registry, 2003. (Ref. #1). Insecticide Synergist. In D.G. Jones, ed. Piperonyl butoxide: The insecticide syner- McGregor, PB, et al. 1988. Responses of the L5178Y tk+/tk- mouse lymphoma gist. San Diego: Academic Press- Pp. 122-135. cell forward mutation assay: III. 72 coded chemicals. Environmental and Molecular 61 US EPA. 2005. Overview of the Piperonyl Butoxide Risk Assessments. Docket ID Ntatagenesis. 12: p.85-154. EPA-HQ-OPP-2005-0042 (accessed Jan 2006) h£tpJ/www:regulations.gov. Page 20 Pesticides and You Vol. 26, No. 1, 2006 Beyond Pesticides/National Coalition Against the Misuse of Pesticides ARTICLE Received 11 Jun 2015 Accepted 14 Apr 2016 Published 31 May 2016 Non-cultivated plants present a season-long route of pesticide exposure for honey bees Elizabeth Y. Long' & Christian H. Krupke2 Recent efforts to evaluate the contribution of neonicotinoid insecticides to worldwide pollinator declines have focused on honey bees and the chronic levels of exposure experienced when foraging on crops grown from neonicotinoid-treated seeds. However, few studies address non-crop plants as a potential route of pollinator exposure to neonicotinoid and other insecticides. Here we show that pollen collected by honey bee foragers in maize- and soybean-dominated landscapes is contaminated throughout the growing season with multiple agricultural pesticides, including the neonicotinoids used as seed treatments. Notably, however, the highest levels of contamination in pollen are pyrethroid insecticides targeting mosquitoes and other nuisance pests. Furthermore, pollen from crop plants represents only a tiny fraction of the total diversity of pollen resources used by honey bees in these landscapes, with the principle sources of pollen originating from non-cultivated plants. These findings provide fundamental information about the foraging habits of honey bees in these landscapes. Department of Entomology, The Ohio State University, OARDC, 1680 Madison Ave, Wooster, Ohio 44691, USA. 2 Department of Entomology, Purdue University, 901 West State Street, West Lafayette, Indiana 47907, USA. Correspondence and requests for materials should be addressed to C.H.K. (email: ckrupke@purdue.edu). 17:11629 1 DOL. 10.1038/ncomms11629 I www.nature.com/naturecommunications 1 ARTICLE he declines of honey bees and other pollinators have been with pesticides throughout the 16-week period and the at the forefront of recent scientific publications and overwhelming majority of pollen was collected from non- popular press. Accumulating evidence suggests that no cultivated plants. Pesticide residue analyses of bee-collected pol- single stressor alone is responsible for declines. Rather, it is len revealed contamination by up to 32 different pesticides probably a combination of abiotic and biotic factors acting in spanning 9 chemical classes (Table 1). The most common pes- synchrony, to have a negative impact on pollinator populations)-6 . ticide types detected in pollen samples across all sites were fun- Pesticides are stressors that have received considerable attention, gicides and herbicides. Honey bees visited a diverse assemblage of and among these no single class has received more recent attention flowering plants, collecting pollen from up to 30 plant families than the neonicotinoids7-14. These insecticides are acutely toxic to during the 16-week sampling period (Table 2). Regardless of the honey bees, environmentally persistent and mobile in the location of honey bee colonies, pollen loads were dominated by environment' 5-19. They are also among the most widely used the Fabaceae; a plant family that includes both wild and cultivated insecticide classes in grain and oilseed crops: in the United States, species such as clovers, alfalfa and soybeans. 36.6 million hectares of maize and 33.8 million hectares of soybeans were planted in 2014 (ref. 20), with 79-100% and Pesticides in pollen collected in non-agricultural areas. Analysis 34-44% of these seeds, respectively, treated before planting with a of the pollen collected by honey bees in the non-agricultural area formulation of neonicotinoid insecticides (typically thiamethoxam revealed contamination with 29 pesticides, the most common of or its metabolite clothianidin)2i. Although it is known that which were the fungicides azoxystrobin and trifloxystrobin neorucotinoids can and do move from crop fields during (93.3 and 63.3% of samples), the herbicide metolachlor (83.3%) planting, as dust, and afterwards in ground and surface water, and the pyrethroid insecticides prallethrin and phenothrin the extent of this contamination in the environment throughout (467 and 30% of samples) (Table 1). Carbamate, neonicotinoid the foraginE season of honey bees has only recently begun to be and or ano hos horus insecticides were also detected, although quantified' 39,22-26; therefore, this presents a relatively unexplored g P P route for pollinator exposure to this pesticide class. Moreover, the less frequently in 3-16.7% of pollen samples. Mean pesticide presence of other, potentially synergistic, pesticides encountered in concentrations in pollen over the sampling period varied from honey bee food resources has seldom been examined27 and most 6-317p.p.b., with no clear seasonal pattern (Fig. la). The highest published work in this area tends to focus exclusively on the mean concentrations of pesticides in pollen occurred during occurrence of neonicotinoid insecticides in pollen or nectar August and September, and were driven largely by the pyrethroid resources 7,28-33; however, exposures of mobile insects such as insecticide phenothrin. During these sampling periods, pollen pollinators to a single pesticide rarely occur in field situations 34. loads were dominated by the family Brassicaceae (mustards or Given the vast acreages devoted to these crops and concerns about crucifers). Pollen from plants in the Fabaceae (legumes, peas worldwide pollinator decline, we initiated this work to describe and beans) were present in highest quantity over the course of both how (that is, plant species) and when (that is, time in season), the season at the non-agricultural site; however, the greatest pollen-foraging honey bees are exposed to a range of pesticides in proportion of pollen collected by bees during any one sampling agricultural landscapes, with an eye towards clarifying potential period was from the Brassicaceae and likely from wild mustard, high-risk compounds and identifying common combinations of Sinapsis arvensis, an insect-pollinated annual species that was pesticides encountered in field environments. particularly common at that site. Although pollen from Pollen collected by honey bees was collected, identified and non-cultivated plants dominated honey bee loads over the course screened for agricultural pesticides over a period of 16 weeks in of our experiment, foragers did occasionally visit soybean 2011. We initiated this study after all planting of treated seeds in (Glyane max) and less frequently maize (Zea mays) to collect our study was completed, to minimize dust from pneumatic pollen, despite the distance from the meadow to surrounding planters as a direct source of pesticide residues. Two Langstroth crop fields (Table 2). Honey bees at this site collected 0.4% of their pollen from maize plants and this was restricted to the week hives were placed at each of three sites: (1) an open meadow with of 19 July, while up to 7.9% of their pollen was collected from wildflowers, woody shrubs and trees present (non-agricultural soybean plants over the course of 5 weeks (2-30 August). site), (2) the border of a maize field planted with seeds treated with the neonicotinoid clothianidin and three fungicides, and (3) the border of a maize field planted with seeds that received no Pesticides in pollen collected adjacent to untreated maize. We pesticide treatment. To characterize the landscape surrounding detected 31 different pesticide residues in pollen from honey bee honey bee hives, proportions of different land covers within a colonies placed at the maize field grown from untreated seed. As 2-km radius around each of the three sites were extracted from was the case at the non-agricultural site, the most common the 2012 Cropland Data Layer produced by the US National pesticides detected were the fungicides azoxystrobin and Agricultural Statistics Service using QGIS (QGIS Development trifloxystrobin (87.5 and 62.5% of samples), as well as the Team 2015). Honey bee colonies remained at each site for the herbicides metolachlor and atrazine (75 and 54°x6 of samples, length of the growing season and foraging bees had free access to respectively) (Table 1). Of the neonicotinoid insecticides detected, pollen from all crop and non-crop species in the vicinity. Analysis thiamethoxam was present most frequently in 33% of pollen of forager-collected pollen revealed that in all cases honey bees samples. Once again the carbamates, neonicotinoids and foraged primarily on non-cultivated plants and residues of organophosphates were generally less prevalent in pollen than multiple pesticides were found throughout the season. Although the fungicides and herbicides at this site, with 4-33% of a variety of agricultural pesticides were found at all sites, the pollen samples containing these residues. Mean levels of pesticide contaminants likely to provide the greatest hazard to honey bees contamination varied over the sampling period from 3-736 p.p.b., in our study were non-agricultural pyrethroid insecticides with no clear seasonal pattern, except that concentrations were targeting nuisance pests such as mosquitoes. higher later in the season than at any other period (Fig. 1b). The highest concentrations occurred mid-August and mid-September, and were again driven by spikes of the pyrethroid phenothrin. Results These periods corresponded with large proportions of common Foraging on pesticide-contaminated non-cultivated plants. ragweed pollen Ambrosia artemisiifolia and two other pollen Pollen collected by honey bees was consistently contaminated species, one unknown and another unidentified member of the 2 17:116291 DOI: 10.1038/ncomms11629 I www.nature.com/naturecommunications ARTICLE Table 1 The mean, median and range of concentrations for 32 pesticide active ingredients detected in pollen samples collected from honey bee colonies over a 16-week period, Chemical Pesticide type Site 1: Site 2: Site 3: LOD non-agricultural area untreated maize treated maize (p.p.b.) % of samples Mean, median % of samples Mean, median % of samples Mean, median detected conc. (p.p.10 detected conc. (p.p.b.) detected conc. (p.p.b.) (n = 30) (n = 24) (n = 32) Carbaryl Carbamate 6.67% <LOD, 0.0 8.33% 0.07, 0.0 25% 0.52, 0.0 0.02 (0.12-0.30) (0.20-1.45) (0.09-10.55) Methomyl 6.67% <LOD, 0.0 4.17% 0.09, 0.0 9.38% <LOD, 0.0 0.09 (012-0.15) (2.07-2.07) (0.17-0.63) Azoxystrobin Fungicide 9333% 1.63, 0.868 87.5% 1.90, 0.92 87.5% 2.39, 0.66 0.08 (0.1-10.39) (0.10-8.32) (0.09-28.31) Difenoconazole 6.67% 0.39, 0.0 12.5% 0.21, 0.0 6.25% <LOD, 0.0 0.14 (4.65-6.93) (0.54-2.73) (0.35-0.68) Dimoxystrobin 20% 0.01, 0.0 8.33% 0.003, 0.0 ND 0.002 (0.02-0.10) (0.01-0.05) Metalaxyl 26.67% 0.09, 0.0 33.33% 0.09, 0.0 31.25% 0.05, 0.0 0.004 (0.03-1.45) (0.03-0.68) (0.03-0.42) Propiconazole 23.33% 0.25, 0.0 37.5% 0.57, 0.0 21.88% 0.52, 0.0 0.05 (0.47-2.26) (0.12-4.34) (0.34-6.57) Pyraclostrobin 36.67% 1.74, 0.0 3333% 1.73, 0.0 28.13% 2.32, 0.0 0.04 (0.05-12.0) (0.62-11.67) (0.61-31.46) Trifloxystrobin 63.33% 0.97, 0.156 62.5% 0.52, 0.16 65.63% 0.35, 0.11 0.02 (0.03-15.16) (0.02-6.83) (0.03-3.32) 2,4-D Herbicide ND 12.5% <LOD, 0.0 ND 1.44 (4.08-1239) Acetochlor 10% 0.14, 0.0 25% 0.36, 0.0 34.38% 2.12, 0.0 0.12 (0.36-2.99) (0.13-3.33) (0.28-25.38) Atrazine 20% 0.82, 0.0 54.17% 1.63, 0.43 43.75% 4.66, 0.0 0.02 (0.42-7.29) (0.33-14.88) (0.21-45.26) Chlorimuron- 6.67% 0.30, 0.0 20.83% 0.25, 0.0 15.63% 0.11, 0.0 0.04 ethyl (3.51-5.35) (0.46-1.97) (0.20-1.38) Metolachlor 83.33% 0.33, 0.13 75% 0.36, 0.20 71.88% 0.58, 0.11 0.003 (0.01-2.45) (0.20-1.45) (0.01-713) DEET Repellent 100% 3.82, 1.37 100% 2.48, 0.82 100% 2.91, 0.55 0.004 (0.10-21.12) (0.08-2033) (0.07-26.20) Methoxyfenozide Insect growth 3.33% <LOD, 0.0 8.33% 0.06, 0.0 9.38% 0.35, 0.0 0.06 regulator (0.16-0.16) (0.48-0.91) (0.42-10.25) Spinetoram Fermentation 10% <LOD, 0.0 16.67% <LOD, 0.0 15.63% <LOD, 0.0 0.08 product (0.10-1.03) (0.13-0.46) (0.10-0.75) insecticide Spinosad 6.67% 0.06, 0.0 8.33% 0.05, 0.0 9.38% 0.03, 0.0 0.03 (0.87 -1.01) (0.57-0.64) (0.16-0.44) Acetamiprid Neonicotinoid ND 12.5% 0.04, 0.0 28.13% 0.32, 0.07 0.03 (0.07-0.65) (0.04-4.69) Clothianidin 3.33% 0.16, 0.0 16.67% 0.20, 0.0 21.88% 0.66, 0.0 0.09 (4.66-4.66) (0.70-1.79) (0.64-9.37) Dinotefuran 10% <LOD, 0.0 4.17% <LOD, 0.0 3.13% <LOD, 0.0 0.97 (4.85-6.31) (4.08-4.08) (4.52-4.52) Imidacloprid 6.67% <LOD, 0.0 ND ND 0.69 (0.94-1.05) Thiacloprid ND 4.17% <LOD, 0.0 3.13% <LOD, 0.0 0.12 (039-039) (0.25-0.25) Thiamethoxam 10% 0.12, 0.0 33.33% 0.23, 0.0 21.88% 0.08, 0.0 0.04 (0.52-1.69) (0.18-1.82) (0.07-0.95) Coumaphos Organophosphate 16.67% 032, 0.0 20.83% 0.25, 0.0 9.38% <LOD, 0.0 0.24 (0.70-4.21) (0.25-4.05) (0.26-1.44) Diazinon 10% 0.13, 0.0 16.67% 0.08, 0.0 15.63% 0.04, 0.0 0.007 (0.15-2.22) (0.20-0.74) (0.08-0.43) Dimethoate 3.33% 0.01, 0.0 20.83% 0.08, 0.0 15.63% <LOD, 0.0 0.01 (0.34-0.34) (0.03-1.43) (0.12-0.14) T-Fluvalinate Pyrethroid 10% <LOD, 0.0 4.17% <LOD, 0.0 ND 1.13 (2.31-14.48) (5.88-5.88) Phenothrin 30% 47.6, 0.0 16.67% 84.5, 0.0 28.13% 195.4, 0.0 1.28 (34.92-343.76) (250.39-728.85) (274.13-1,955) Prallethrin 46.67% 29.0, 0.0 25% 5.53, 0.0 15.63% 5.88, 0.0 0.68 (6.49-236.78) (5.59-55.06) (7.24-144.46) Tetramethrin 6.67% 0.15, 0.0 8.33% 0.04, 0.0 6.25% 0.02, 0.0 0.02 (0.70-4.10) (0.18-0.68) (0.30-0.42) ? Cyhalothrin 10% 0.22, 0.0 16.67% 0.37, 0.0 12.S% 0.50, 0.0 0.005 (1.39-3.39) (0.16-5.69) (0.103-6.13) DEET, N,N-Diethyl-meta-toluamide; LOD, limit of detection; ND, not detected. Colonies were placed in a non-agricultural area, adjacent to a maize field grown from untreated seed and adjacent to a maize field grown from seed treated with neonicotinoids and fungicides. - 17:116291 DOI: 10.1038/ncomms11629 I www.nature.com/naturecommunications 3 Harmon, MA, MF Boehm, RA Harmon and DJ Mangelsdorf. 1995. Activation of mammalian retinoid X receptors by the insect growth regulator methoprene. Proceedings of the National Academy of Sciences USA. 92:6157-6160 Harmon et al. report that methoprene and its metabolic derivatives interact with the mammalian retinoid X receptors and thereby stimulate gene transcription in vertebrates. Methoprene, an insect growth regulator, is used in agriculture and domestic settings as a pesticide because of its ability to prevent insect metamorphosis from larval to adult life stages. "Thus a pesticide that mimics the action of juvenile hormone in insects can also activate a mammalian retinoid- responsive pathway." Methoprene is now applied, among domestic and agricultural settings, to household carpets for flea control. Activation of marrunalian retinoid X receptors by the insect growth hor... https://www.researchgate.net/publication/15602237_Activation of n-L or Discover by : Join for free Log in 00000 QiAGEEN See all > See all > Access fuliext QIAGIEN RNA Technologies Activation of mammalian retinoid X receptors by the insect growth hormone methoprene Article in Proceedings of the National Academy of Sciences 92(13):6157-60 June 1995 with 13 Reads Impact Factor. 9.67 • D01: 10.1073/pnas.92.13.6157 -Source: PubMed - 5 p t_ Ins ht 1 st 2nd 3rd 4th Abstract We report that methoprene and its derivatives can stimulate gene transcription in vertebrates by acting through the retinoic acid-responsive transcription factors, the retinoid X receptors (RXRs). Methoprene is an insect growth regulator in domestic and agricultural use as a pesticide. At least one metabolite of methoprene, methoprene acid, directly binds to RXR and is a transcriptional activator in both insect and mammalian cells. Unlike the endogenous RXR ligand, 9-cis-retinoic acid, this activity is RXR-specific; the methoprene derivatives do not activate the retinoic acid receptor pathway. Methoprene is a juvenile hormone analog that acts to retain juvenile characteristics during insect growth, preventing metamorphosis into an adult, and it has been shown to have ovicidal properties in some insects. Thus, a pesticide that mimics the action of juvenile hormone in insects can also activate a mammalian retinoid-responsive pathway. This finding provides a basis through which the potential bioactivity of substances exposed to the environment may be reexamined and points the way for discovery of new receptor ligands in both insects and vertebrates. Do you want to read the rest of this publication? Access full-text Full-text (PDF) preview Available from: 1 of 4 6/20/2016 5:21 PM Activation of mammalian retinoid X receptors by the insect growth hor... https://www.researchgate.net/publication/15602237-Activation-oC n,,. Proc. Nail Acad Sri. USA Vol. 91, pp. 6157_6160, June 1995 Biochemistry Activation of mammalian retinoid X receptors by the insect growth regulator methoprene (retinoic acid receptor/ retinoic acid/juvenile hortnone/isoprevoids/pesticide) MARGARET A. HARMON', MARCus F. BOEHMt, RICHARD A. HEYMANt. AND DAVID J. MANGELSDORF*§ 'Howard Hughes Medical Institute and Department of Pharmacologv. Unis•ersac of Texas Southwestern Medical Center. Dallas. TX 75135.9054), and Departments of °Medicrnal Chemistry and %Cell Brology, ILgand Pharmaceuticals. Inc.. 9393 Towne Centre Drive, San Diego. Ca 9_121 Communicated In Ronald M. Evans. Tire Salk Institute, San Diego. G4. March 23. 1095 ABSTRACT we report that methoprene and its deriva- do not appear to have a retinoid requirement (except for tives can stimulate gene transcription in vertebrates by acting vision) to maintain viability. In insects. besides ecd}sone, there through the retinoic acid-responsive transcription factors, the is found another lipophilic hormone, juvenile hormone (JH), retinoid X receptors (RX"Rs). Methoprene is an insect growth that is chemically similar to the retinoids (9, 10). Like the regulator in domestic and agricultural use as a pesticide. At retinoid and steroid hormones, JH is synthesized from the least one metabolite of methoprene, methoprene acid, directly common isoprenoid precursor farnesol pyrophosphate via the binds to RXR and is a transcriptional activator in both insect mevalonate biosmthetic pathway. Given the shared portions of and mammalian cells. Unlike the endogenous RXR ligand, the biosynthetic pathways of the known insect and vertebrate 9-ris-retinoic acid, this activity is RXR-specific, the metho- hormones and the similarity between the insect and mamma- prene derivatives do not activate the retinoic acid receptor lian receptors, we investigated the possibility that JH-like pathway. Methoprene is a juvenile hormone analog that acts ligands may have homologs in mammalian systems. To exam- to retain juvenile characteristics daring insect growth, pre- ine the prospect of alternative RXR ligands, we screened venting metamorphosis into an adult, and it has been shown several natural and s3mthetic isoprcnoid compounds for their to have oAcidal properties in some insects. Thus, a pesticide ability to activate transcription from an RXR response ele- that mimics the action of juvenile hormone in insects can also ment. This screen identified several RXR-selective agonists activate a mammalian retinoid-responsive pathway. This find- that are metabolites of the noncvclic svmthetic terpenoid ing provides a basis through which the potential bioactivity of methoprene. substances exposed to the ensiroament may be reexamined and points the way for discovery of new receptor ligands in MATERIALS AND METHODS - - ebrates ppQQ{{ Schneider and CV-I Cell Cotransfection Assays. Construc- Citations 192 thett'rok Qtti, it, 32 nner in which tion of receptor expression and reporter plasmids for expres- .ir biological effects resides in their abil- sion in Drosophila and mammalian cells has been described (4. ity to regulate gene expression. Vitamin A metabolites-i.e., 6. 11, 12). Schneider cells in 6-well culture plates were co- retinoids-play essential roles in many aspects of development, transfected with OS µg of the luciferase reporter plasmid metabolism, and reproduction in vertebrates (1). Some of the ADH-CRBPII-LUC, 0.5 µg of the 0-calactosidaw expression rnd nrrvinMC of vitamin A mrtahnikm have hPen iclentif-ti ac .,t--mint -rid I µg of receptor expression plasmid mRXRP, A5C-mRXRy, or A5C- um phosphate precipitation method (4, - - = = _ late ligands or solvent control was added wing the transfected cells. The cells were " ind extracts were prepared and assayed - = - 11). Luciferase values were normalized arvesting efficiency b% measuring )3-ga- ` A the results reported as average relative A Possible Link Between Pyriproxyfen and Microcephaly Preview Article - Apr 2016 Dan Evans Fred Niihout Raphael Parens +1 more author... Alfredo J. Morales 2 of 4 6/20/2016 5:21 PM 4. Retinoic acid signaling pathways in development and diseases. T t'?.~r.- 1, 11 try=- ,r t^ -IC I? e -1 5. The Truth About Mosquitoes and West Nile Virus 'Oi:: II CI `.t~I LS/t;?t 0 /ClOCILI EEIII c/?Ia.~cC IILo, u https://en.wikipedia.org/wiki/Deltamethrin deltamethrin Br 0 CB 4 0 I! N . l r~ ° r'. 'e a e~ a.org/-\,,-H `/Del~a ~ eL t4 I Deltamethrin products are among the most popular and widely used insecticides in the worldt-,,V: )!r "f,610 ] and have become very popular with pest control operators and individuals in the United States.= This material is a member of one of the safest classes of pesticides: synthetic This pesticide is highly toxic to aquatic life, particularly fish, and therefore must be used with extreme caution around water. Although generally considered safe to use around humans, it is still ne rc[ xic to humans. Deltamethrin is able to pass from a woman's skin through her blood and into her breast milk.= Deltamethrin plays key role in controlling .G!ariv vectors, and is used in the manufacture of long-lasting insecticidal ~~c_.-- It is used as one of a battery of pyrethroid insecticides in control of malarial vectors, particularly hi e, and whilst being the most employed pyrethroid insecticide, can be used in conjunction with, or as an alternative to, n, cv;:) r , eL",- and other organophosphate-based insecticides, such as malathion and fenthion. Resistance to deltamethrin (and its counterparts) is now extremely widespread and threatens the success of worldwide vector control programmes. Since deltamethrin is a -it temporarily attacks (in medical terms, "insults") the nervous system of any animal with which it comes into contact. Skin contact can lead to tingling or reddening of the skin local to the application. If taken in through the eyes or mouth, a common symptom is facial which can feel like many different abnormal sensations, including burning, partial numbness, "pins and needles", skin crawling, etc. There are no reports indicating that chronic intoxication from pyrethroid insecticides causes motor neuron damage or Recently, residues of deltamethrin were found in together with in an area that used E) D treatment for ~ µs 'a_- u control, as well as pyrethroids in small- scale agriculture. There are no u and treatment must be symptomatic, as approved by a physician. Over time, deltamethrin is with a rapid loss of toxicity, and passed from the body. A should be contacted in the event of an accidental poisoning. Stephanie L. Johnson & James J. Klug 329 Grandview Drive Guardrail Concerns To be considered before the meeting on 6/2/2016 1. Mike said no easements or encroachments on our property. All work done on Grandview drive must be done without easements or encroachments upon our property. 2. Power poles in the area of the new work will not increase in height even if moved closer to the right-away. The two power poles located on the south side of Grandview won't be raised above their current height even if their move towards our property line. The two powerline poles will remain on the city right away. 3. This will be taken care for. Water and irrigation meter relocation. 4. Mike said there would be no parking along the proposed immediate work area, except for the small area across from the 340 driveway. This area should have designated parking spaces only. Parking, it is our belief and strong recommendation that all parking on Grandview drive in vicinity of the proposed work be eliminated. That would include the area just across the street from 340's driveway and any other places along Grandview drive. 5. Very important. During our meeting on the 261h you mentioned the possibility of rumble strips being employed. The noise that would result from these would be unacceptable. The chiller noise from the ACH hospital below caused by poor design had already diminished the ability to open our windows and sliding doors in the evening, additional noise above tire noise would result in decreased value of our property and enjoyment on it. Mike, thank you for all your concern and efforts to resolve and create the best options for the residents of Ashland. Jim and Steph Steph L. Johnson James J. Klug 329 Grandview Drive Ashland, Or. 97520 541-482-1.398