A deadly kiss — Chagas disease, an exotic bug-borne infection that can kill, is spreading in Texas

 A joint investigation from:

Hidden Threat:  The Kissing Bug

Texas

Kissing bugs – so called because they bite us around our eyes and mouth – can be found in rats’ nests and wood piles but also inside our Texas homes.  (Smiley N. Pool/Staff Photographer)

By Seema Yasmin | Staff Writer; Scott Friedman and Eva Parks | NBC5

If she hadn’t gone to donate blood, Candace Stark wouldn’t have discovered that she harbored a dangerous parasite.

Although she hadn’t left Texas in 20 years, swimming in her blood was a tropical parasite that causes a disease called Chagas.

The parasite buries itself in heart muscle and the gut and can hide for two decades or more before causing symptoms, including sudden death.

Textbooks will tell you that Chagas disease, caused by the parasite Trypanosoma cruzi, is a problem for Central and South Americans living in poverty. Eight million to 11 million people are infected worldwide, according to the Pan American Health Organization.

But parasites care little about your bank balance, and although being poor is a risk factor for Chagas disease, the parasite is infecting Texans from all backgrounds.

Chagas is one of about 40 infections known as neglected tropical diseases, so-called because they are largely ignored by governments and drug companies. They infect 1.5 billion people in tropical and subtropical regions of the world.

But neglected tropical diseases are right at home in Texas. Rising temperatures, oblivious doctors and high poverty rates mean seven of these infections are already here or fighting to gain a foothold.

Experts warn that more cases of Chagas and other neglected tropical diseases are being reported in the U.S. An estimated 12 million Americans have one or more tropical infections, including an estimated 300,000 with Chagas disease.In Texas, one in every 6,500 blood donors are infected with Chagas disease, compared with one in every 27,500 donors across the country.

Chances are, if you have it, you don’t know it. That’s because the parasite stays dormant for years and because American doctors are uneducated about the infection.

Chagas disease isn’t new to Texas, and neither is the dime-size kissing bug that spreads the infection. The first case in the U.S. was reported in 1955, and kissing bugs have been spotted in Texas since the early 1800s.

Kissing bugs live in rats’ nests and wood piles or in the nooks of your furniture or cracks in your house. They earned their name by biting us around our eyes and mouth. They poop where they eat, and when you rub the irritated bite, you rub the poop — and the parasite — into your skin. The infection is also spread through blood transfusions, organ transplants and, during pregnancy, from mother to baby.

Penn_Medicine

Penn Study Shows Bed Bugs Can Transmit Parasite that Causes Chagas Disease

Like the “Kissing” Bug, Bed Bugs Can Transmit Deadly Parasite Via Feces

PHILADELPHIA — November 17, 2014 — The bed bug may be just as dangerous as its sinister cousin, the triatomine, or “kissing” bug. A new study from Penn Medicine researchers in the Center for Clinical Epidemiology and Biostatistics demonstrated that bed bugs, like the triatomines, can transmit Trypanosoma cruzi, the parasite that causes Chagas disease, one of the most prevalent and deadly diseases in the Americas.

In a study published online this week in the American Journal of Tropical Medicine and Hygiene, senior author Michael Z. Levy, PhD, assistant professor in the department of Biostatistics and Epidemiology at the University of Pennsylvania’s Perelman School of Medicine, and researchers at the Universidad Peruana Cayetano Heredia in Peru conducted a series of laboratory experiments that demonstrated bi-directional transmission of T. cruzi between mice and bed bugs.

In the first experiment run at the Zoonotic Disease Research Center in Arequipa, Peru, the researchers exposed 10 mice infected with the parasite to 20 uninfected bed bugs every three days for a month. Of about 2,000 bed bugs used in the experiment, the majority acquired T. cruzi after feeding on the mice.  In a separate experiment to test transmission from bug to mouse, they found that 9 out of 12 (75 percent) uninfected mice acquired the parasite after each one lived for 30 days with 20 infected bed bugs.

In a third experiment, investigators succeeded in infecting mice by placing feces of infected bed bugs on the animal’s skin that had either been inflamed by bed bug bites, or scraped with a needle. Four out of 10 mice (40 percent) acquired the parasite by this manner; 1 out of 5 (20 percent) were infected when the skin was broken by the insect’s bites only. A final experiment performed at the Penn bed bug lab in Philadelphia demonstrated that bed bugs, like triatomines, defecate when they feed.

“We’ve shown that the bed bug can acquire and transmit the parasite. Our next step is to determine whether they are, or will become, an important player in the epidemiology of Chagas disease,” Levy said. “There are some reasons to worry—bed bugs have more frequent contact with people than kissing bugs, and there are more of them in infested houses, giving them ample opportunity to transmit the parasite. But perhaps there is something important we don’t yet understand about them that mitigates the threat.”

T. cruzi is also especially at home in the guts of bed bugs.  “I’ve never seen so many parasites in an insect,” said Renzo Salazar, a biologist at the Universidad Peruana Cayetano Heredia and co-author on the study. “I expected a scenario with very low infection, but we found many parasites—they really replicate well in the gut of the bed bugs.”

Wicked Cousins

Bed bugs and kissing bugs are distant cousins but share many striking similarities. Both insects hide in household cracks and crevices waiting for nightfall and the opportunity to feed on sleeping hosts. They are from the same order of insects (Hemiptera) and both only feed on blood.  (One main difference is their size: kissing bugs are five times as big as a bed bug). With so much in common, it seemed logical to the authors that the kissing bug’s most infamous trait, the transmission of T. cruzi, is also shared by the bed bug.

Other investigators have shared this suspicion. In 1912, just three years after Carlos Chagas described the transmission of the disease by kissing bugs, French parasitologist Émile Brumpt recounted that he had infected almost 100 bed bugs exposed to an infectious mouse, and then used them to infect two healthy mice. Decades later an Argentine group replicated his work.  These experiments, largely ignored during the recent bed bug resurgence, missed one key point.

“Mice can hunt and eat bed bugs,” said Ricardo Castillo-Neyra, DVM, PhD, coauthor and postdoctoral fellow at the Universidad Peruana Cayetano Heredia and Penn. “The older studies were almost certainly only documenting oral transmission of the parasite. Our work shows for the first time that bed bugs can transmit the parasite when their feces are in contact with broken skin, the route by which humans are usually infected.”

Emerging Problem

More people in the U.S. are infected with T. cruzi now than ever before. The Centers for Disease Control and Prevention estimates that the number of Chagas disease cases in the U.S. today could be as high as 300,000.

“There have always been triatomine bugs and cases of Chagas disease in the U.S., but the kissing bugs we have here don’t come into homes frequently like the more dangerous species in South and Central America do,” Levy said. “I am much more concerned about the role of bed bugs. They are already here—in our homes, in our beds and in high numbers. What we found has thrown a wrench in the way I think about transmission, and where Chagas disease could emerge next.”

Equally worrying is the invasion of bed bugs into areas where Chagas disease is prevalent, especially in countries where traditional insect vectors of the parasite have been nearly eliminated, Levy said.  In these areas, bed bugs will be repeatedly exposed to T. cruzi, and could re-spark transmission where it had been extinguished.

“Bed bugs are harder to kill than triatomines due to their resistance to common insecticides.” Levy said. “No one is prepared for large scale bed bug control. If the parasite starts to spread through bed bugs, decades of progress on Chagas disease control in the Americas could be erased, and we would have no means at our disposal to repeat what had been accomplished.”

Often referred to as a silent killer, Chagas disease is hard to diagnose in its early stages because the symptoms are mild or absent. The parasites are hidden mainly in the heart and digestive muscle and over time can cause cardiac disorders and sometimes digestive or neurological problems. In later years, the infection can lead to sudden death or heart failure caused by progressive destruction of the heart muscle. Although there are some drugs to treat Chagas disease, they become less effective the longer a person is infected.

The long asymptomatic period of Chagas disease complicates surveillance for new outbreaks of transmission. In Arequipa, Peru, thousands became infected with the parasite before a case appeared in the hospital. The same could happen in cities in the United States if the parasite were to emerge in the bed bug populations, the authors say.

“Carlos Chagas discovered T. cruzi in triatomine insects before he saw a single case of the disease,” Levy said. “We need to learn from his intuition—check the bugs for the parasite.”

Other co-authors of the study include Aaron W. Tustin, Katty Borrini-Mayorí and César Náquira.

###

Memphis_Channel_3

‘Kissing bugs’ may be kiss of death for babies & small children

MEMPHIS, Tenn. — The ‘kissing bug’ can cause Chagas disease, which can lead to heart problems and, in some cases, death.

The bugs often emerge at night and attack while you are sleeping.

“They’re called kissing bugs because they may bite around the lips,” Daniel Sprenger, manager of Vector Control in Shelby County, said.

The Centers for Disease Control (CDC) explained people who live in the South need to be on the lookout.

The ‘kissing bug’ is most commonly found in South America, but a CDC map reveals there have been reported cases in the Mid-South.

triatomine_map_sm

“They’ll maybe get in the garage,” Sprenger said. “I heard of behind peg board.”

The CDC said the bugs can also be found under porches, stones, animal structures, and rodent nests.

“It actually can lead to death, unfortunately,” Sprenger said.

Death is most common in babies or small children, according to Sprenger. Most people who contract the disease end up breaking out into a severe allergic reaction.

Sprenger said there is a moderate amount of ‘kissing bugs’ in Tennessee and doesn’t believe people need to be extremely concerned.

“Worrying is excessive,” Sprenger said. “Being aware of something like this is good.”

November 13, 2014 | Michael Quander

This Isn’t Syria – It’s NYC!

Stop NYC’s New Round of Pesticide Spraying, Now

August 11, 2015 — The NYC Department of Health and Mental Hygiene (NYC DOH) renews its annual pesticide-spraying assault on the people of New York City tonight in Staten Island and Queens.

Areas of New Jersey are also being widely sprayed.

All mass spraying of pyrethroid and organophosphate pesticides are dangerous to human health (especially to children, the elderly, and those with weakened immune systems), as well as to pets, fish, and other animals. The spraying must be halted immediately.

Every year, the NYC DOH grants itself waivers from New York City Local Law 37, a law passed in 2005 in response to growing concerns over the health and environmental consequences of mass-spraying of Malathion (and other organophosphates) and Anvil 10+10 (and other pyrethroids, especially those containing the carcinogen Piperonyl Butoxide).

Only through application and granting of such waivers is the Department of Health enabled to legally conduct the pesticides spraying.

But the NYC DOH is circumventing the law. It applies for a waiver to itself, and then it grants itself pro forma the right and authority to spray deadly pesticides in NYC. No other agency reviews its application. The checks and balances envisioned in Local Law 37 are thus thwarted.

See, especially, a powerful review in City Limits of the waivers to Local Law 37, here.

The No Spray Coalition, which won its lawsuit against the City government in federal court in 2005 and achieved a settlement agreement two years later, is outraged by the spraying. The City’s Department of Health has failed to seriously consider:

a) the admissions it made concerning the dangers of pesticides in the 2007 stipulated Settlement Agreement with the No Spray Coalition, et al. in federal court; and

b) the 4 pillars for waivers in Local Law 37 (referenced also as a separate point in the Settlement Agreement).

These amount to a violation of the terms of the Settlement Agreement as well as key provisions of Local Law 37.

This year’s spray of choice is, once again, Anvil 10+10. It is listed in Local Law 37 as containing piperonyl butoxide and MGK-284. These are both “synergists” in Anvil 10+10, and they are both classified as possible human carcinogens by the EPA’s Office of Pesticide Programs.

Local Law 37 prohibits the use of pesticides by NYC in public places if they contain PBO and/or MGK-264. Why are they violating their own law?

“After years of litigation to stop this reckless spraying of pesticides which has contributed to skyrocketing increases in cancer and asthma, and now the collapse of bee colonies in the New York area, I am outraged that the New York City government is renewing its mindless criminal poisoning of the people and environment of our City,”

said Howard Brandstein, coordinator of SOS-FOOD, NY State Against Genetic Engineering, and a plaintiff in the federal lawsuit brought in 2000 by the No Spray Coalition and other organizations against the New York City government’s pesticide-spraying campaign. That lawsuit ended in April 2007 when NYC signed a settlement agreement acknowledging, among other stipulations, that pesticides:

  • may remain in the environment beyond their intended purpose
  • cause adverse health effects
  • kill mosquitoes’ natural predators (such as dragonflies, bats, frogs and birds)
  • increase mosquitoes’ resistance to the sprays, and
  • are not presently approved for direct application to waterways.

The Department of Health contravenes that settlement by now stating that there are “no significant risks” of adverse impact to human health associated with the proper use of this product. Levi Fishman, deputy press secretary at the Dept. of Health, explained to City Limits reporter Elah Feder:

“When properly used, this product poses no significant risks to human health. It degrades rapidly in sunlight, provides little or no residual activity, and does not accumulate in the environment.”

Feder immediately pointed out that “nevertheless, the city advises residents to bring children’s toys, outdoor equipment, and clothing indoors before spraying takes place, and to wash anything that has come in contact with Anvil.” If there are no significant risks, why all that advice?

The fact is, the spraying puts many New York City residents and visitors at grave risk.

“These ignorant and lying politicians and bureaucrats apparently have no problem destroying our health in order to ‘save’ us from the so-called West Nile virus,”

said Howard Brandstein, adding:

“Clearly, the spraying jeopardizes a thousand times more people than the disease.”

The pesticide the City is spraying — “Anvil 10 + 10 — belongs to a class of adulticides known as pyrethroids, which are endocrine disruptors. They mimic hormones such as estrogen, and may cause breast cancer in women and drastically lower sperm counts in men. Pyrethroids have also been associated with prostate cancer, miscarriages and preterm delivery, asthma, toxicity to many vital organs including the nervous system, liver, kidneys and the gastro-intestinal tract, skin rashes, itching and blisters, and nausea and vomiting.

Anvil contains the cancer-causing chemical piperonyl butoxide, which the Environmental Protection Agency lists as a suspected carcinogen. It also contains Sumithrin — a synthetic toxin (not a naturally occurring pyrethrin), made in the laboratory — as well as dangerous benzene-related chemicals (which the label calls “inert ingredients.”)

Thousands of New Yorkers are severely sickened by the spraying every year, but they go unrecorded and unreported. Several members of the No Spray Coalition, including two of the plaintiffs in the lawsuit, died from pesticide-related illnesses. Many suffer from Multiple Chemical Sensitivities (MCS) or Asthma caused or exacerbated by the spraying.

The City administration must be made to understand that pesticides are extremely dangerous to human health as well as to the natural environment, and have long-term consequences.

The No Spray Coalition details the reasons for vacating NYC DOH’s waivers as follows:

  1. The Department of Health has illegally circumvented Local Law 37’s attempt to protect against health and environmental dangers;
  2. The City has entered into a multi-year pattern that misinterprets and misuses blindspots in the law, which in general forbids spraying of toxic pesticides on City lands;
  3. The City has failed to abide by its own admissions in the Settlement Agreement with the No Spray Coalition et al. in 2007, review the latest scientific research, and participate in discussions with the No Spray Coalition in good faith;
  4. The City has failed to evaluate the “public health threat” from pesticide spraying as well as West Nile virus. There has been no Environmental Impact Statement in the last 15 years on which to examine the effects of the spraying;
  5. There have been no public hearings in contradiction to the requirements in Local Law 37 and other regulations;
  6. The City has repeatedly failed to adequately notify the public before spraying pesticides, in violation of Local Law 37 and other regulations, and in violation of the Settlement Agreement;
  7. The City has failed to seriously utilize safer alternatives to pesticide spraying;
  8. The City has failed to respond in a timely fashion to important questions and concerns from NY Assembly member William Colton, and others;
  9. The City is illegally spraying toxic pesticides on the people and environment of New York.

The No Spray Coalition strongly urges the City to stop pesticide spraying immediately, reconsider its entire approach, and seek alternative, safe means to control mosquitoes. There are natural, safe ways for each person to ward off mosquitoes. The City should not be poisoning the entire population.

We call on the Mayor and City Council to hold the DOH in violation of the intent of Local Law 37 and other laws, and of the Court-mandated “Settlement Agreement” with the No Spray Coalition, et al., and urge City officials to stop the spraying NOW. Please protect the residents and visitors to New York and the natural environment from the extremely dangerous, unnecessary, ineffective and illegal mass spraying of toxic pesticides.

Stop spraying now. Stop poisoning people, animals and the environment.

Visit NoSpray.org for more information.

Bedbugs may play role in spread of drug-resistant bacteria MRSA, study finds

WP

Smith_2
In a study released Wednesday, Canadian scientists detected drug-resistant MRSA bacteria in bedbugs from three hospital patients from a Vancouver neighborhood.

Anyone who has ever had a bedbug infestation knows full well what a nuisance the pests can be. Unlike ticks and mosquitoes, however, bedbugs, which feed on human blood, are not known to spread disease and are generally not viewed as a major public health threat.

But a peer-reviewed study published online Wednesday in a journal of the U.S. Centers for Disease Control and Prevention suggests the pests could play a role in transmitting disease. In a tiny sample of bedbugs, collected from a small number of residents living in crowded conditions in a poor neighborhood in Canada, researchers found the drug-resistant bacterium known as MRSA.

The researchers at a Vancouver, B.C., hospital tested three patients from the neighborhood who were infested with bedbugs. Researchers collected five bedbugs and determined that the insects carried two types of drug-resistant bacteria. Three bedbugs from one patient contained methicillin-resistant Staphylococcus aureus (MRSA), and the two from the other patients each contained vancomycin-resistant Enterococcus faecium (VRE).

MRSA has increasingly turned up in hospitals and in outbreaks outside of health-care settings, such as among athletes, prison inmates and children. MRSA, which is spread by casual contact, can cause serious health problems, including disfiguring “necrotizing” abscesses that eat tissue and life-threatening infections if the microbe gets into vital organs.

“Even though this is a small study, it suggests that bedbugs may be playing a role in the transmission of MRSA in inner-city populations where bedbug infestations are a problem,” said Marc Romney, one of the study’s authors. Romney is medical director of infection prevention and control at St. Paul’s Hospital.

Other experts said the new information was interesting but inconclusive.

“It emphasizes the need for some further studies to determine the potential bedbugs have for transmitting these agents,” said Robert Wirtz, chief of entomology at the CDC’s Center for Global Health. “While the work was well done and it shows an association, it doesn’t establish that bedbugs are capable of transmitting the bacteria.”

The study leaves many key questions unanswered. It did not determine whether the bacteria were transmitted from bugs to patients or the other way around. Nor did it determine whether the bacteria were on the outside of each bug or living and growing inside it, which would be more significant, researchers said.

But even if the bugs were carrying the bacteria on their exteriors, the finding is still significant, Romney said. Bedbugs could spread the germ from person to person, especially in crowded places, such as the homeless shelters where many patients were living in downtown Vancouver. The bacteria typically survive for hours, and possibly days, under the right conditions, he said.

Residents in that Vancouver community tend to be more susceptible to infection because their immune systems are compromised by chronic illness, drug use, crowding and poor nutrition.

Vancouver, like New York, Washington and other cities, has had a disturbing increase in bedbugs in recent years. Experts suspect the resurgence is related to greater domestic and international travel, to the bugs’ resistance to available pesticides, and to lack of knowledge about pests that were virtually eradicated in the 1940s and ’50s by widespread used of DDT. The insecticide was banned in the 1970s.

Bedbugs can live for months without a meal, hidden deep in mattress seams, baseboard cracks and clutter near beds. They travel easily, hitchhiking from person to person, city to city. They have turned up in college dorms, government buildings, Google’s offices and even luxury hotels such as the Waldorf-Astoria, which has been sued by guests who say they were bitten at the New York landmark.

Researchers in Canada wanted to know whether bedbugs may spread the bacteria in poor, overcrowded communities, such as the downtown area where the patients lived.

The CDC’s Wirtz said the next step should be to determine whether a colony of bedbugs fed with blood infected with MRSA or VRE could transmit the bacterium to a clean, sterile system, he said.

Bedbug research has focused more on insecticide resistance and less on public-health effects, scientists said, because they are not known to spread disease.

The study was published online in Emerging Infectious Diseases, a journal published by the CDC that analyzes and tracks disease trends.

By Lena H. Sun | May 11, 2011

Penn Study Shows Bed Bugs Can Transmit Parasite that Causes Chagas Disease

Penn_Medicine

Like the “Kissing” Bug, Bed Bugs Can Transmit Deadly Parasite Via Feces

PHILADELPHIA — The bed bug may be just as dangerous as its sinister cousin, the triatomine, or “kissing” bug. A new study from Penn Medicine researchers in the Center for Clinical Epidemiology and Biostatistics demonstrated that bed bugs, like the triatomines, can transmit Trypanosoma cruzi, the parasite that causes Chagas disease, one of the most prevalent and deadly diseases in the Americas.

In a study published online this week in the American Journal of Tropical Medicine and Hygiene, senior author Michael Z. Levy, PhD, assistant professor in the department of Biostatistics and Epidemiology at the University of Pennsylvania’s Perelman School of Medicine, and researchers at the Universidad Peruana Cayetano Heredia in Peru conducted a series of laboratory experiments that demonstrated bi-directional transmission of T. cruzi between mice and bed bugs.

In the first experiment run at the Zoonotic Disease Research Center in Arequipa, Peru, the researchers exposed 10 mice infected with the parasite to 20 uninfected bed bugs every three days for a month. Of about 2,000 bed bugs used in the experiment, the majority acquired T. cruzi after feeding on the mice.  In a separate experiment to test transmission from bug to mouse, they found that 9 out of 12 (75 percent) uninfected mice acquired the parasite after each one lived for 30 days with 20 infected bed bugs.

In a third experiment, investigators succeeded in infecting mice by placing feces of infected bed bugs on the animal’s skin that had either been inflamed by bed bug bites, or scraped with a needle. Four out of 10 mice (40 percent) acquired the parasite by this manner; 1 out of 5 (20 percent) were infected when the skin was broken by the insect’s bites only. A final experiment performed at the Penn bed bug lab in Philadelphia demonstrated that bed bugs, like triatomines, defecate when they feed.

“We’ve shown that the bed bug can acquire and transmit the parasite. Our next step is to determine whether they are, or will become, an important player in the epidemiology of Chagas disease,” Levy said. “There are some reasons to worry—bed bugs have more frequent contact with people than kissing bugs, and there are more of them in infested houses, giving them ample opportunity to transmit the parasite. But perhaps there is something important we don’t yet understand about them that mitigates the threat.”

T. cruzi is also especially at home in the guts of bed bugs.  “I’ve never seen so many parasites in an insect,” said Renzo Salazar, a biologist at the Universidad Peruana Cayetano Heredia and co-author on the study. “I expected a scenario with very low infection, but we found many parasites—they really replicate well in the gut of the bed bugs.”

Wicked Cousins

Bed bugs and kissing bugs are distant cousins but share many striking similarities. Both insects hide in household cracks and crevices waiting for nightfall and the opportunity to feed on sleeping hosts. They are from the same order of insects (Hemiptera) and both only feed on blood.  (One main difference is their size: kissing bugs are five times as big as a bed bug). With so much in common, it seemed logical to the authors that the kissing bug’s most infamous trait, the transmission of T. cruzi, is also shared by the bed bug.

Other investigators have shared this suspicion. In 1912, just three years after Carlos Chagas described the transmission of the disease by kissing bugs, French parasitologist Émile Brumpt recounted that he had infected almost 100 bed bugs exposed to an infectious mouse, and then used them to infect two healthy mice. Decades later an Argentine group replicated his work.  These experiments, largely ignored during the recent bed bug resurgence, missed one key point.

“Mice can hunt and eat bed bugs,” said Ricardo Castillo-Neyra, DVM, PhD, coauthor and postdoctoral fellow at the Universidad Peruana Cayetano Heredia and Penn. “The older studies were almost certainly only documenting oral transmission of the parasite. Our work shows for the first time that bed bugs can transmit the parasite when their feces are in contact with broken skin, the route by which humans are usually infected.”

Emerging Problem

More people in the U.S. are infected with T. cruzi now than ever before. The Centers for Disease Control and Prevention estimates that the number of Chagas disease cases in the U.S. today could be as high as 300,000.

“There have always been triatomine bugs and cases of Chagas disease in the U.S., but the kissing bugs we have here don’t come into homes frequently like the more dangerous species in South and Central America do,” Levy said. “I am much more concerned about the role of bed bugs. They are already here—in our homes, in our beds and in high numbers. What we found has thrown a wrench in the way I think about transmission, and where Chagas disease could emerge next.”

Equally worrying is the invasion of bed bugs into areas where Chagas disease is prevalent, especially in countries where traditional insect vectors of the parasite have been nearly eliminated, Levy said.  In these areas, bed bugs will be repeatedly exposed to T. cruzi, and could re-spark transmission where it had been extinguished.

“Bed bugs are harder to kill than triatomines due to their resistance to common insecticides.” Levy said. “No one is prepared for large scale bed bug control. If the parasite starts to spread through bed bugs, decades of progress on Chagas disease control in the Americas could be erased, and we would have no means at our disposal to repeat what had been accomplished.”

Often referred to as a silent killer, Chagas disease is hard to diagnose in its early stages because the symptoms are mild or absent. The parasites are hidden mainly in the heart and digestive muscle and over time can cause cardiac disorders and sometimes digestive or neurological problems. In later years, the infection can lead to sudden death or heart failure caused by progressive destruction of the heart muscle. Although there are some drugs to treat Chagas disease, they become less effective the longer a person is infected.

The long asymptomatic period of Chagas disease complicates surveillance for new outbreaks of transmission. In Arequipa, Peru, thousands became infected with the parasite before a case appeared in the hospital. The same could happen in cities in the United States if the parasite were to emerge in the bed bug populations, the authors say.

“Carlos Chagas discovered T. cruzi in triatomine insects before he saw a single case of the disease,” Levy said. “We need to learn from his intuition—check the bugs for the parasite.”

Other co-authors of the study include Aaron W. Tustin, Katty Borrini-Mayorí and César Náquira.

November 14, 2014

###

Bed Bugs Transmit Deadly Chagas Disease into U.S. Population

40,000 Pregnant Women and 300,167 People Infected in U.S.

forbes

Chagas: An Emerging Infectious Disease Threat In U.S.

October 1, 2015 | By:  Judy Stone

Chagas, a parasitic disease, is the latest invisible killer infection to be recognized as a growing threat here. The infection is transmitted by the Triatomine bug, known as the “kissing” bug. The bugs infect people through bites—often near the eyes or mouth—or when their infected feces are accidentally rubbed into eyes or mucous membranes. Some transmission occurs from mother to child during pregnancy. Occasionally, transmission is through contaminated food or drink.

Triatoma sanguisuga - CDC/James Gathany

Most people in the U.S. with Chagas disease probably became infected as children, living in Latin America. The infection often has few symptoms early on, but after several decades, strikes fatally, often with sudden death from heart disease. I suspect that, similar to Lyme disease, the magnitude of disease and deaths from the protozoan parasite, Trypanosoma cruzi, which causes Chagas disease, is unrecognized in the U.S.

In Latin America, however, up to 12 million people might be infected, with a third going on to develop life-threatening heart complications. Chagas is a major cause of congestive heart failure and cardiac deaths, with an estimated 11,000 people dying annually, according to the WHO.

There are an estimated 300,167 people with Trypanosoma cruzi infection the U.S., including 40,000 pregnant women in North America. There are 30,000-45,000 cardiomyopathy cases and 63-315 congenital infections each year. Most of the people come from Mexico, El Salvador, Guatemala, Honduras, or Argentina; Bolivia has the highest rate of Chagas in the world.

But in the U.S., we don’t often think of Chagas. Even as an infectious disease physician, I’ve never treated anyone with it, and it is not on my radar. So when a physician sees a patient who may have come to the U.S. as a child, and now has diabetes and hypertension, he or she is likely to attribute the heart disease to that and not look for infection. In fact, though, there are large pockets of undiagnosed disease. For example, a survey in Los Angeles of patients with a new diagnosis of cardiomyopathy who had lived in Latin America for at least a year, found 19% had Chagas disease, and they had a worse prognosis than those without the infection.

There are other reasons Chagas is overlooked. One is that Chagas is not a reportable disease except in four states, and Texas only began reporting in 2010. Most cases here have been detected by screening of blood donations, which has found about 1 in every 27,500 donors to be infected, according to CDC. However, a 2014 survey showed “one in every 6,500 blood donors tested positive for exposure to the parasite that causes Chagas disease.” A map of positive donations is here. While the triatome bugs are most common in the southern half of the U.S., they are actually quite widespread, as shown here.

Much bigger barriers to diagnosis are social and cultural. Many patients lack health insurance. Others are undocumented immigrants fearing deportation. Health literacy and language barriers are huge. There is a stigma associated with the diagnosis, as there is for many patients with TB, as Chagas is associated with poverty and poor living conditions. As Daisy Hernández noted in her excellent story in the Atlantic, “it’s hard, if not impossible, for moms with Chagas and no health insurance to see the doctors who would connect them to the CDC” and “patients don’t necessarily have savings in case they have adverse reactions to the medication and can’t work.”

There are pockets of Chagas in the states, including Los Angeles, the Washington metropolitan area, and the Texas border, where there are large immigrant communities from endemic areas. But I suspect that with climate change, we’ll see more Chagas in the southwest U.S., as more triatomine bugs are found further north. One recent study found more than 60% of the collected bugs carried the Trypanosome parasite, up from 40-50% in two similar studies. There are also now seven reports of Chagas infection that are clearly autochthonous, or locally acquired. University of Pennsylvania researcher Michael Levy has shown that bedbugs might be capable of transmitting Chagas, but no one has shown that they actually do. Entomologist and Wired author Gwen Pearson nicely explains why bedbugs are an unlikely vector and notes that you “far more likely to be injured by misusing pesticides to try to exterminate” them.

There’s more bad news. Treatment for Chagas is effective if given early in infection, although with significant side effects. There is no effective treatment for late stages of gastrointestinal or cardiac disease. A newly released study showed that benznidazole was no more effective than placebo in reducing cardiac complications, even though it reduced levels of parasites in the blood.

Trypanasoma cruzi parasite in heart tissue - CDC

The two drugs available to treat Chagas, benznidazole and nifurtimox, are not yet FDA approved and are only available through the CDC under investigational protocols. Both carry significant side effects. Treatment of children with early Chagas is generally effective but, as with many drugs, treatment is hampered by lack of data on pediatric dosing and limited formulations. There is little research funding for new drug development, with less than US $1 million (0.04% of R&D funding dedicated to neglected diseases) focused on new drugs for Chagas disease, according to the Drugs for Neglected Diseases Initiative (DNDi).

Where do we go from here? The most immediate and cost-effective proposals are to increase surveillance for disease and screening of high-risk populations. Since the most effective treatment is given early in the course of infection, screening of pregnant women and children is a priority, as is education for these women and Ob-Gyn physicians.

While there is no effective treatment for advanced disease, efforts are underway to develop a vaccine against Chagas. The National School of Tropical Medicine at Baylor College of Medicine just received a boost from a $2.6 million grant from the Carlos Slim Foundation for their initiative.

Chagas, like sickle cell, highlights disparities in access to screening and early treatment for serious illnesses disproportionately affecting the poor and people of color. While a moral and ethical issue, the choices made to gut public health programs for “cost saving” will also be unnecessarily costly in the end.

About:  Judy Stone

I cover infectious diseases, medicine, drug development, and ethics.

I am an Infectious Disease specialist, experienced in conducting clinical research and the author of Conducting Clinical Research, the essential guide to the topic. I survived 25 years in solo practice in rural Cumberland, Maryland, and now work part time as an Infectious Diseases locum tenens physician. I especially love writing about ethical issues, and tilting at windmills as I advocate for social justice. As part of my overall desire to save the world when I grow up, I have become particularly interested in neglected tropical diseases. In my next life, I would love to teach overseas. When not slaving over hot patients, I can be found playing with photography, friends’ dogs, or in my garden. Follow on Twitter @drjudystone

Wikipedia: “Say no To Pesticides” – they Cause Cancer in Our Children #bedbugfree

Health effects of pesticides

Pesticide toxicty
Warning2Pesticides.jpg

A sign warning about potential pesticide exposure.
Classification and external resources
Specialty emergency medicine
ICD10 T60
ICD9-CM 989.4
MedlinePlus 002430
eMedicine article/815051

Health effects of pesticides may be acute or delayed in those who are exposed.[1] A 2007 systematic review found that “most studies on non-Hodgkin lymphoma and leukemia showed positive associations with pesticide exposure” and thus concluded that cosmetic use of pesticides should be decreased.[2] Strong evidence also exists for other negative outcomes from pesticide exposure including neurological problems, birth defects, fetal death,[3] and neurodevelopmental disorder.[4]

According to The Stockholm Convention on Persistent Organic Pollutants, 9 of the 12 most dangerous and persistent chemicals are pesticides.[5][6]

Acute effects

Main article: Pesticide poisoning

Acute health problems may occur in workers that handle pesticides, such as abdominal pain, dizziness, headaches, nausea, vomiting, as well as skin and eye problems.[7] In China, an estimated half million people are poisoned by pesticides each year, 500 of whom die.[8] Pyrethrins, insecticides commonly used in common bug killers, can cause a potentially deadly condition if breathed in.[9]

Long-term effects

Cancer

Many studies have examined the effects of pesticide exposure on the risk of cancer. Associations have been found with: leukemia, lymphoma, brain, kidney, breast, prostate, pancreas, liver, lung, and skin cancers.[6] This increased risk occurs with both residential and occupational exposures.[6] Increased rates of cancer have been found among farm workers who apply these chemicals.[10] A mother’s occupational exposure to pesticides during pregnancy is associated with an increases in her child’s risk of leukemia, Wilms’ tumor, and brain cancer.[6][11]

Neurological

Evidence links pesticide exposure to worsened neurological outcomes.[3] The risk of developing Parkinson’s disease is 70% greater in those exposed to even low levels of pesticides.[12] People with Parkinson’s were 61% more likely to report direct pesticide application than were healthy relatives. Both insecticides and herbicides significantly increased the risk of Parkinson’s disease.[13] There are also concerns that long-term exposures may increase the risk of dementia.[14]

The United States Environmental Protection Agency finished a 10-year review of the organophosphate pesticides following the 1996 Food Quality Protection Act, but did little to account for developmental neurotoxic effects, drawing strong criticism from within the agency and from outside researchers.[15][16] Comparable studies have not been done with newer pesticides that are replacing organophosphates.[17]

Reproductive effects

Strong evidence links pesticide exposure to birth defects, fetal death and altered fetal growth.[3] In the United States, increase in birth defects is associated with conceiving in the same period of the year when agrochemicals are in elevated concentrations in surface water.[18] Agent Orange, a 50:50 mixture of 2,4,5-T and 2,4-D, has been associated with bad health and genetic effects in Malaya and Vietnam.[19][20] It was also found that offspring that were at some point exposed to pesticides had a low birth weight and had developmental defects.[21]

Fertility

A number of pesticides including dibromochlorophane and 2,4-D has been associated with impaired fertility in males.[22] Pesticide exposure resulted in reduced fertility in males, genetic alterations in sperm, a reduced number of sperm, damage to germinal epithelium and altered hormone function.[23]

Other

Some studies have found increased risks of dermatitis in those exposed.[3]

Additionally, studies have indicated that pesticide exposure is associated with long-term health problems such as respiratory problems, including asthma,[24][25] memory disorders and depression.[26] Summaries of peer-reviewed research have examined the link between pesticide exposure and neurologic outcomes and cancer, perhaps the two most significant things resulting in organophosphate-exposed workers.[27][28]

According to researchers from the National Institutes of Health (NIH), licensed pesticide applicators who used chlorinated pesticides on more than 100 days in their lifetime were at greater risk of diabetes. One study found that associations between specific pesticides and incident diabetes ranged from a 20 percent to a 200 percent increase in risk. New cases of diabetes were reported by 3.4 percent of those in the lowest pesticide use category compared with 4.6 percent of those in the highest category. Risks were greater when users of specific pesticides were compared with applicators who never applied that chemical.[29][30]

Route of exposure

People can be exposed to pesticides by a number of different routes including: occupation, in the home, at school and in their food.

There are concerns that pesticides used to control pests on food crops are dangerous to people who consume those foods. These concerns are one reason for the organic food movement. Many food crops, including fruits and vegetables, contain pesticide residues after being washed or peeled. Chemicals that are no longer used but that are resistant to breakdown for long periods may remain in soil and water and thus in food.[31]

The United Nations Codex Alimentarius Commission has recommended international standards for maximum residue limits (MRLs), for individual pesticides in food.[32]

In the EU, MRLs are set by DG-SANCO.

In the United States, levels of residues that remain on foods are limited to tolerance levels that are established by the U.S. Environmental Protection Agency and are considered safe.[33] The EPA sets the tolerances based on the toxicity of the pesticide and its breakdown products, the amount and frequency of pesticide application, and how much of the pesticide (i.e., the residue) remains in or on food by the time it is marketed and prepared.[34] Tolerance levels are obtained using scientific risk assessments that pesticide manufacturers are required to produce by conducting toxicological studies, exposure modeling and residue studies before a particular pesticide can be registered, however, the effects are tested for single pesticides, and there is little information on possible synergistic effects of exposure to multiple pesticide traces in the air, food and water.[35]

Strawberries and tomatoes are the two crops with the most intensive use of soil fumigants. They are particularly vulnerable to several type of diseases, insects, mites, and parasitic worms. In 2003, in California alone, 3.7 million pounds (1,700 metric tons) of metham sodium were used on tomatoes. In recent years other farmers have demonstrated that it is possible to produce strawberries and tomatoes without the use of harmful chemicals and in a cost-effective way.[36]

Exposure routes other than consuming food that contains residues, in particular pesticide drift, are potentially significant to the general public.[37]

Some pesticides can remain in the environment for prolonged periods of time. For example, most people in the United States still have detectable levels of DDT in their bodies even though it was banned in the US in 1972.[6]

Prevention

Pesticides exposure cannot be studied in placebo controlled trials as this would be unethical.[3] A definitive cause effect relationship therefore cannot be established.[3] Consistent evidence can and has been gathered through other study designs.[3] The precautionary principle is thus frequently used in environmental law such that absolute proof is not required before efforts to decrease exposure to potential toxins are enacted.[38]

The American Medical Association recommend limiting exposure to pesticides.[39] They came to this conclusion due to the fact that surveillance systems currently in place are inadequate to determine problems related to exposure.[39] The utility of applicator certification and public notification programs are also of unknown value in their ability to prevent adverse outcomes.[39]

Epidemiology

The World Health Organization and the UN Environment Programme estimate that each year, 3 million workers in agriculture in the developing world experience severe poisoning from pesticides, about 18,000 of whom die.[40] According to one study, as many as 25 million workers in developing countries may suffer mild pesticide poisoning yearly.[41] Detectable levels of 50 different pesticides were found in the blood of a representative sample of the U.S. population.[42]

Society and culture

Concerns regarding conflict of interests regarding the research base have been raised. A number of researchers involved with pesticides have been found to have undisclosed ties to industry including: Richard Doll or the Imperial Cancer Research Fund in England and Hans-Olov Adami of the Karolinska Institute in Sweden.[43]

Other animals

A number of pesticides including clothianidin, dinotefuran, imidacloprid are toxic to bees.[44] Exposure to pesticides may be one of the contributory factors to colony collapse disorder.[45] A study in North Carolina indicated that more than 30 percent of the quail tested were made sick by one aerial insecticide application. Once sick, wild birds may neglect their young, abandon their nests, and become more susceptible to predators or disease.[46]

See also

References

  1. ^ U.S. Environmental Protection Agency (August 30, 2007), Pesticides: Health and Safety. National Assessment of the Worker Protection Workshop #3.
  2. ^ >Bassil KL, Vakil C, Sanborn M, Cole DC, Kaur JS, Kerr KJ (October 2007). “Cancer health effects of pesticides: systematic review”. Can Fam Physician 53 (10): 1704–11. PMC 2231435. PMID 17934034.
  3. ^ a b c d e f g Sanborn M, Kerr KJ, Sanin LH, Cole DC, Bassil KL, Vakil C (October 2007). “Non-cancer health effects of pesticides: systematic review and implications for family doctors”. Can Fam Physician 53 (10): 1712–20. PMC 2231436. PMID 17934035.
  4. ^ Jurewicz J, Hanke W (2008). “Prenatal and childhood exposure to pesticides and neurobehavioral development: review of epidemiological studies”. Int J Occup Med Environ Health 21 (2): 121–32. doi:10.2478/v10001-008-0014-z. PMID 18614459.
  5. ^ “What are POPs?”. Pops.int. Retrieved 2014-02-04.
  6. ^ a b c d e Gilden RC, Huffling K, Sattler B (January 2010). “Pesticides and health risks”. J Obstet Gynecol Neonatal Nurs 39 (1): 103–10. doi:10.1111/j.1552-6909.2009.01092.x. PMID 20409108.
  7. ^ Ecobichon DJ. 1996. Toxic effects of pesticides. In: Casarett and Doull’s Toxicology: The Basic Science of Poisons (Klaassen CD, Doull J, eds). 5th ed. New York:MacMillan, 643–689.
  8. ^ Lawrence, Dune (February 13, 2007), Chinese develop taste for organic food: Higher cost no barrier to safer eating. Bloomberg News, International Herald Tribune Retrieved on 2007-10-25.
  9. ^ Medline Plus (May 17, 2006), Medical Encyclopedia: Insecticide. Retrieved on September 15, 2007.
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  13. ^ “Study confirms Parkinson’s-pesticides link”. Reuters. April 18, 2008.
  14. ^ Baldi I, Gruber A, Rondeau V, Lebailly P, Brochard P, Fabrigoule C (November 2010). “Neurobehavioral effects of long-term exposure to pesticides: results from the 4-year follow-up of the PHYTONER Study”. Occup Environ Med 68 (2): 108–115. doi:10.1136/oem.2009.047811. PMID 21097948.
  15. ^ Phillips ML (2006). “Registering skepticism: does the EPA’s pesticide review protect children?”. ENVIRONMENTAL HEALTH PERSPECTIVES 114 (10): A592–A595. doi:10.1289/ehp.114-a592. PMC 1626397. PMID 17035127.
  16. ^ Pulaski A (May 26, 2006), EPA workers blast agency’s rulings on deadly pesticides: Letter sent to EPA administrator Stephen L. Johnson by unions representing 9,000 EPA scientists. The Oregonian, Mindfully.org Retrieved on 2007-10-10.
  17. ^ Mascarelli, A. (2013). “Growing Up with Pesticides”. Science 341 (6147): 740. doi:10.1126/science.341.6147.740.
  18. ^ Winchester, D.; Huskins, J.; Ying, J. (Apr 2009). “Agrichemicals in surface water and birth defects in the United States”. Acta paediatrica (Oslo, Norway : 1992) 98 (4): 664–669. doi:10.1111/j.1651-2227.2008.01207.x. ISSN 0803-5253. PMC 2667895. PMID 19183116.
  19. ^ Ngo AD, Taylor R, Roberts CL, Nguyen TV (October 2006). “Association between Agent Orange and birth defects: systematic review and meta-analysis”. Int J Epidemiol 35 (5): 1220–30. doi:10.1093/ije/dyl038. PMID 16543362.
  20. ^ Ngo AD, Taylor R, Roberts CL (2010). “Paternal exposure to Agent Orange and spina bifida: a meta-analysis”. Eur. J. Epidemiol. 25 (1): 37–44. doi:10.1007/s10654-009-9401-4. PMID 19894129.
  21. ^ http://link.springer.com/article/10.1186%2F1477-7827-4-30/fulltext.html
  22. ^ Sheiner EK, Sheiner E, Hammel RD, Potashnik G, Carel R (April 2003). “Effect of occupational exposures on male fertility: literature review”. Ind Health 41 (2): 55–62. doi:10.2486/indhealth.41.55. PMID 12725464.
  23. ^ http://www.arhp.org/publications-and-resources/clinical-proceedings/RHE/Pesticides
  24. ^ Amaral, André F. S. (2014). “Pesticides and Asthma: Challenges for Epidemiology”. Frontiers in Public Health 2. doi:10.3389/fpubh.2014.00006.
  25. ^ Doust, E; Ayres, JG; Devereux, G; Dick, F; Crawford, JO; Cowie, H; Dixon, K (June 2014). “Is pesticide exposure a cause of obstructive airways disease?”. European respiratory review : an official journal of the European Respiratory Society 23 (132): 180–92. PMID 24881073.
  26. ^ Beseler CL, Stallones L, Hoppin JA, et al. (December 2008). “Depression and pesticide exposures among private pesticide applicators enrolled in the Agricultural Health Study”. Environ. Health Perspect. 116 (12): 1713–9. doi:10.1289/ehp.11091. PMC 2599768. PMID 19079725.
  27. ^ Alavanja MC, Hoppin JA, Kamel F (2004). “Health effects of chronic pesticide exposure: cancer and neurotoxicity”. Annu Rev Public Health 25: 155–97. doi:10.1146/annurev.publhealth.25.101802.123020. PMID 15015917.
  28. ^ Kamel F, Hoppin JA (June 2004). “Association of pesticide exposure with neurologic dysfunction and disease”. Environ. Health Perspect. 112 (9): 950–8. doi:10.1289/ehp.7135. PMC 1247187. PMID 15198914.
  29. ^ Montgomery MP, Kamel F, Saldana TM, Alavanja MC, Sandler DP (May 2008). “Incident diabetes and pesticide exposure among licensed pesticide applicators: Agricultural Health Study, 1993–2003”. Am J Epidemiol. 167 (10): 235–46. doi:10.1093/aje/kwn028. PMC 2832308. PMID 18343878.
  30. ^ Newswise: Long-term Pesticide Exposure May Increase Risk of Diabetes Retrieved on June 4, 2008.
  31. ^ Cornell University, College of Veterinary Medicine (March 1999), Consumer concerns about pesticides in food. Fact Sheet #24. Retrieved on 2007-10-25.
  32. ^ Codex Alimentarius Commission Code of Ethics for International Trade in Food. CAC/RCP 20-1979 (Rev. 1-1985). Retrieved on 2007-10-25.
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  34. ^ U.S. Environmental Protection Agency (July 24, 2007), Setting tolerances for pesticide residues in foods. epa.gov. Retrieved on September 15, 2007.
  35. ^ Rabideau, Christine L. Multiple pesticide exposure: Immunotoxicty and oxidative tress 2001
  36. ^ Levine, Marvin J. (2007). Pesticides: A Toxic Time Bomb in our Midst. Praeger Publishers. pp. 213–214. ISBN 978-0-275-99127-2.
  37. ^ U.S. Environmental Protection Agency (December 1999), Spray drift of pesticides. Retrieved on September 15, 2007.
  38. ^ Lockwood AH (December 2000). “Pesticides and parkinsonism: is there an etiological link?”. Curr. Opin. Neurol. 13 (6): 687–90. doi:10.1097/00019052-200012000-00013. PMID 11148671.
  39. ^ a b c “Educational and informational strategies to reduce pesticide risks. Council on Scientific Affairs”. Prev Med 26 (2): 191–200. 1997. doi:10.1006/pmed.1996.0122. PMID 9085387.
  40. ^ Miller GT (2004), Sustaining the Earth, 6th edition. Thompson Learning, Inc. Pacific Grove, California. Chapter 9, Pages 211-216.
  41. ^ Jeyaratnam J (1990). “Acute pesticide poisoning: a major global health problem”. World Health Stat Q 43 (3): 139–44. PMID 2238694.
  42. ^ Gilden RC, Huffling K, Sattler B (January 2010). “Pesticides and health risks”. J Obstet Gynecol Neonatal Nurs 39 (1): 103–10. doi:10.1111/j.1552-6909.2009.01092.x. PMID 20409108. Biomonitoring results of the Centers for Disease Control and Prevention’s (CDC) National Health and Nutrition Examination Survey (2005–2006) are published in a report titled Third Exposure to Environmental Chemicals Report (2005). This report stated that detectable body levels of about 50 pesticides have been found in a representative sample of the U.S. population.
  43. ^ Hardell L, Walker MJ, Walhjalt B, Friedman LS, Richter ED (March 2007). “Secret ties to industry and conflicting interests in cancer research”. Am. J. Ind. Med. 50 (3): 227–33. doi:10.1002/ajim.20357. PMID 17086516.
  44. ^ Decourtye A, Devillers J (2010). “Ecotoxicity of neonicotinoid insecticides to bees”. Adv. Exp. Med. Biol. 683: 85–95. doi:10.1007/978-1-4419-6445-8_8. PMID 20737791.
  45. ^ Myrna E. Watanabe‌ (May 2008). “Colony Collapse Disorder: Many Suspects, No Smoking Gun”. BioScience 58 (5): 384–388. doi:10.1641/B580503.
  46. ^ http://ipm.ncsu.edu/wildlife/corn_wildlife.html

Indoor Pesticide Exposure Tied to Childhood Cancers. Childhood Exposure to Indoor Insecticides Linked to 47% Increased Risk of Childhood Leukemia and 43% Increased Risk of Childhood Lymphomas

A new analysis of existing research finds that kids exposed to pesticides indoors are at higher risk for childhood cancers.

Reuters Health – POSTED: 16 Sep 2015

(Reuters Health) – A new analysis of existing research finds that kids exposed to pesticides indoors are at higher risk for childhood cancers.

The study, based on data mainly from North America, Europe and Australia, suggests that policies should be developed to limit children’s exposures at home and school to insect killers, researchers say.

“When you apply pesticides so close to where kids are and they spend so much time in the household, I’d really be concerned about their exposure,” said Chensheng Lu, the senior author of the analysis from the Harvard T.H. Chan School of Public Health in Boston.

The researchers write in Pediatrics that children can be exposed to pesticides when they play on treated surfaces and then put their fingers in their mouths.

Unlike adults, children may not be able to break down or excrete some of the chemicals used in pesticides. Reports show children had respiratory, stomach, nerve and hormone problems tied to pesticides, Lu and colleagues add.

In the same issue of the journal, researchers from Italy published a report of a seven-month-old child dying after repeated exposure to massive amounts of a household insecticide.

“I think that case highlights the acute effects of insecticides,” Lu told Reuters Health. “The blood cancers highlight the risks of chronic exposure.”

For the new study, Lu’s team looked at published research on childhood exposures to pesticides both indoors and out, and any associated cancers. Sixteen studies were included in the final analysis, each looking at samples of a few hundred to a few thousand children.

The studies looked at exposure both to professionally-applied pesticides and to household bug sprays and weed killers.

Overall, childhood exposure to indoor insecticides was linked to a 47 percent increased risk of childhood leukemia and a 43 percent increased risk of childhood lymphomas, which are cancers of the lymphatic system.

The researchers also found a slightly increased risk of childhood cancers with the use of outdoor herbicides, or weed killers, but the association was only significant for leukemia.

The link between outdoor exposure and childhood cancers was not as strong as for indoor exposure, because people tend to spray more pesticides indoors, Lu said.

More research is needed to determine how exposure to pesticides may be linked to childhood cancers, the researchers write. Lu cautions, however, that parents should keep in mind that many pesticides are meant to be deadly to insects and pests.

“Those chemicals have lethal potencies,” he said. “Why would people want to spray so close to their kids?”

Eliminating the possibility of increased risk for childhood cancers comes down to parents and caregivers not spraying pesticides in their homes, Lu said.