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Learning from West Nile
September 15, 2003

In mid-August, mosquitoes carrying West Nile Virus (WNV) were found in California’s Salton Sea, at the southern extension of an important bird migration route. As communities across the country choose different strategies to battle WNV, it’s important to take stock of what we have learned from West Nile’s four years on our shores, to reduce the possibility that our defense against West Nile may bring unexpected consequences.

While the West Nile Virus is common in mosquitoes in Africa and Europe, the first U.S. human case was reported in 1999 in New York State. The number of human cases has increased each year; so far in 2003 the U.S. Centers for Disease Control (CDC) reports 2,874 human cases and 53 deaths (as of September 9, 2003). In 2002 there were 4,156 human cases and 214 deaths.

Most people who contract West Nile virus do not experience symptoms. According to the CDC, about 13% of those infected develop West Nile fever, with headaches and flu-like symptoms from which they eventually recover. About one in 150 people bitten by an infected mosquito will develop meningitis, an infection of the spinal cord, or encephalitis, an infection of the brain. Either condition can cause death or permanent injury. Many of those who have succumbed to the virus have been older, chronically ill, or with weak immune systems.

In the years the since the first outbreak, the CDC and local vector control agencies have altered their public recommendations on dealing with West Nile. There is now much greater emphasis on public education, on the removal of standing water as mosquito breeding sites, and application of larvicides instead of widespread sprays targeting adult mosquitoes.

However the spraying of adulticides does continue, even though it is inefficient for controlling mosquitoes and may even increase mosquito populations by decimating the predators (such as dragonflies) that feed on mosquitoes and their larvae. In a new report on the risks of pesticide spraying for West Nile, Pesticide Watch lists two organophosphate pesticides, malathion and naled (sold as Dibrom) which are approved for use in California against mosquitoes. Organophosphates are a highly toxic class of pesticides affecting the central nervous, cardiovascular and respiratory systems. Malathion and naled have both been linked to cancer and malathion has been associated with blood, vision and reproductive disorders.

Synthetic pyrethroids, such as sumithrin (Anvil) and permethrin are also widely used on mosquitoes. Both can cause dermatitis and asthma-like reactions. When sumithrin was sprayed for West Nile carrying mosquitoes in New York in 2000, the health department reported 200 calls to the city’s hotline for pesticide poisoning. Permethrin is a possible human carcinogen, and studies have shown it mimics the hormone estrogen, which can cause breast cancer, lower sperm counts, and affect sexual traits as well as childhood development.

The efficacy of insecticide sprays in cities and towns is also a concern. Unlike an agricultural field where vegetation is relatively uniform and obstacles are few, a chemical mist on a city street encounters cars, buildings and other barriers and is unlikely to affect insects in backyards or protected by shrubbery. Even more problematic are the timeframes for spraying. West Nile carrying mosquitoes are most active, and spraying is most effective, at dawn or dusk, both times when people are going to or coming from work.

Several cities and towns have vowed not to spray adulticides for West Nile. Lyndhurst, Ohio, a suburb of Cleveland, passed a landmark ordinance in early July of 2003, and Ft. Worth, Texas and Washington, DC have both pledged not to spray.

It is not known why some cases of West Nile virus lead to the more serious complications of encephalitis or meningitis. One emerging concern is the impact of pesticides on the human body’s ability to resist encephalitis-like pathogens. In addition to the spraying of pesticides in residential areas for West Nile, officials are warning those outside at dawn or dusk to apply a mosquito repellent containing DEET, (N,N-diethyl-m-toluamide) and reapply as needed.

Yet some research in young rats has indicated that certain chemicals, including pyrethroid, organophosphate and organochlorine pesticides can weaken the blood-brain barrier that prevents the entry of microorganisms and toxic substances into brain tissue. Studies have also shown that certain chemicals can make the blood-brain barrier more permeable to viruses. Lab tests have indicated that mice injected with West Nile virus are asymptomatic until this barrier is breached, and that several chemicals including DEET and permethrin can increase the permeability of the blood-brain barrier.

Four years after West Nile Virus has made headlines across the nation, the U.S. EPA is still without information on the effectiveness of adulticide sprays in reducing populations of West Nile carrying mosquitoes, or the impacts of this spraying on public health and wildlife.

Sources: Overkill: Why Pesticide Spraying for West Nile Virus in California May Cause More Harm than Good, Pesticide Watch, August 2003, http://www.pesticidewatch.org; Steve Tvedten Web site, The Best Control, http://www.thebestcontrol.com; CNS Penetration by Noninvasive Viruses Following Inhalational Anesthetics, Ben-Nathan, Kobiler, Rzotkiewicz, Lustig, and Katz, Annals of the New York Academy of Sciences 2000, 917; Combined exposure to DEET (N,N-diethyl-m-toluamide) and permethrin: pharmacokinetics and toxicological effects, Abu-Qare and Abou-Donia, J Toxicol Environ Health, 2003, Jan-Feb.

Contact: PANNA

PANUPS is a weekly email news service providing resource guides and reporting on pesticide issues that don’t always get coverage by the mainstream media. It’s produced by Pesticide Action Network North America, a non-profit and non-governmental organization working to advance sustainable alternatives to pesticides worldwide.

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