The cause of death for Knut, the polar bear

Were pesticides to blame for the death of Knut, the polar bear?

Many thousands of people mourn the sudden death of Knut, the polar bear. He was the darling at a German zoo. Why did Knut die? Initial autopsy results showed that Knut, the polar bear, suffered from a brain disease. A former animal keeper at a zoo reported the death of gorilla babies dying from pesticide use. The keeper herself fell ill and nearly died. Were pesticides the cause of death of the polar bear, Knut? Recent scientific research has shown that pesticides cause different brain diseases. What caused Knut’s brain disease will require further investigation. It is possible, because pesticides are used regularly in zoos to keep the zoo animals free of vermin.

All mourn the loss of Knut, the polar bear

In the media, on Twitter and Facebook, the death of Knut, the polar bear , remains the main topic for days now. The sweet polar bear was raised by a nurse with a bottle in the German zoo after his mother abandoned him. The little polar bear in no time, won the hearts of all the visitors. Now the sadness is great, and the cause of Knut’s brain disease is still under investigation. Zoo visitors witnessed the polar bear turning itself around several times and falling into the pond. Over 500 people observed the death of this polar bear and reported that he had an epileptic-like seizure before he sank into the water in his polar bear enclosure. Knut’s keeper also died suddenly at the age of 44 from a heart attack in 2008.

Dream job, but health went downhill

The young woman worked in one of the biggest zoos in Germany. She loved her job as a veterinary nurse above everything. She was responsible for the gorillas. With the bottle, she helped gorilla babies grow when needed. Most of all, she never wanted to go home after work because she loved her job so much. During her training, her health was deteriorating. The reason for her health decline was first discovered years later. Several radiological studies including SPECT, CT, and MRT scans of her brain showed severe brain damage and atrophy. Pesticides were the reason the keeper’s health went downhill.

Gorilla babies dead due to the use of pesticides

During training, the young keeper had to deal with pesticides during the spraying of the gorilla’s sleeping quarters. The pesticide nerve agents, pyrethroids and organophosphates were used. The young woman had to spray the sleeping caves. As she kneeled in front of the caves, she couldn’t avoid breathing in the poison. “The gorilla babies died, and now I know it was because they were exposed to the pesticides,” she told me several years ago when we met at a special clinic. Her immune and nervous system were severely damaged, and she had problems with her muscles and her heart was weakening. Her hair was falling out and she had the typical nerve agent seizures. She stated, “I initiated a workers’ compensation lawsuit and won.” There was no question that the health of the animal keeper was destroyed by pesticides.

Knut died from pesticide exposure?

We do not know exactly which brain disease Knut, the public’s favorite animal in the Berlin Zoo, suffered from, but further studies will hopefully determine the nature and cause of his brain disease. Pesticides may well be on the short list, because they are regularly used in zoos to keep the zoo animals free of fleas and other parasites. Certain herbicides, which are often used on pavements and along roadsides in zoos in order to be kept free of weeds, are quite capable of causing life-threatening seizures.

Author: Silvia K. Müller, CSN – Chemical Sensitivity Network, March 21, 2011

Translation: Thanks to Christi Howarth.

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Chemicals can make you fat

If it hadn’t been for the Big Macs that Joannie ate pretty much three times a week, she wouldn’t have gotten fat.  If she hadn’t been exposed while in her mother’s womb to chemicals x, y and z, Joannie wouldn’t have had the propensity to get fat.  And if Joannie’s mom had eaten more sensibly, both waistlines would be slimmer.

Fat people most likely are programmed to become fat before taking their first sip of milk.

Today’s news is, that pesticides are among the chemicals responsible for this reprogramming.

Two of three U.S. adults are now classified as overweight.  Type II diabetes has increased in like measure over the same decades, and so has heart disease.  This is not a coincidence.  These illnesses share common characteristics: they are triggered while in the womb by exposure to the same kinds of chemicals and the outcomes show up in adulthood.  Scientists now call this pattern “the fetal origins of adult diseases”.

The most likely culprits are chemicals now grouped together under the rubric “endocrine disrupters.” It’s been known for about two decades, though disputed by the manufacturers, that these chemicals alter the normal signaling pathways of hormones.  Think of Bisphenol A (BPA), right now the nation’s most celebrated endocrine disruptor.

Pesticides, though not specifically thought of as endocrine disruptors nor regulated as such, can similarly knock normal development off track.  Research has just found that a family of pesticides among the most widely used in the world is connected to these three adult illnesses.  This is the family of organophosphates, concocted from petroleum with an addition of phosphoric acid.

When lab rats are exposed to these pesticides through the mother’s diet, at a time in their development equivalent to a human baby’s second trimester in the womb, their metabolism changes in two ways: their cholesterol and triglycerides rise.  These abnormal and lasting changes resemble the major factors that predict and lead, later in life, to obesity, diabetes and cardiovascular heart disease (specifically, atherosclerosis, a condition in which fatty material collects along the arteries and hardens artery walls).

These changes in metabolism happen at low levels, within the levels we are uniformly exposed to, which the Environmental Protection Agency declares as “safe” but are evidently not.  The changes are the strongest when the mother rats are fed a high-fat diet.  Human babies may even be underweight at birth (and there’s an epidemic of underweight babies in the U.S.), but quickly become overweight

Humans run into these pesticides in our food and water.  Of course, children continue to be exposed once they are born and are in fact exposed more than adults because they eat and drink more in relation to their body weight and have a higher ratio of skin.

The other groups of people exposed most to organophosphates and other pesticides are the same groups with the highest rates of obesity – people who live in run-down inner-city neighborhoods, the poor, and farmworkers.  Again, not a coincidence but a connection, a trigger.

Dr. Ted Slotkin of Duke University, the researcher responsible for these discoveries, found another compelling clue: exposure caused harm to the rodent’s brain, as well as its metabolism.  Once the exposed lab animal was born and started to eat at will, its consumption of a high-fat diet reduced the adverse symptoms in its brain functioning.  As Dr. Slotkin muses, “If you’ve got neurofunctional deficits, and they can be offset by continually eating Big Macs, then you will naturally (but unconsciously) select that kind of food because it will make you feel better.”  Unfortunately, increased fat will further harm the animal’s, or human’s, metabolism.

What this means for you:

Particularly while trying to conceive, during pregnancy, while nursing, and for your children, avoid pesticides; eat organic foods.

For information about endocrine disruptors, read the new booklet published by the nonprofit Learning and Developmental Disabilities Initiative.

Author: Alice Shabecoff for CSN – Chemical Sensitivity Network, November 5, 2009

Alice Shabecoff is the co-author with her husband Philip of Poisoned Profits: The Toxic Assault on our Children, published by Random House last year.  See their website,

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Pesticides exposure linked to suicidal thoughts

Pesticides exposure linked to suicidal thoughts

A new study in China has found that people with higher levels of pesticide exposure are more likely to have suicidal thoughts. The study was carried out by Dr Robert Stewart from the Institute of Psychiatry at King’s College London together with scientists from Tongde Hospital Zhejiang Province. 

The agricultural pesticides commonly used in China are organophosphates which are in wide use in many lower income countries but have been banned in many Western nations. It is well known that they are very dangerous if ingested as an overdose but there is also biological evidence that chronic low-grade exposure to these chemicals, which are very easily absorbed into the body through the skin and lungs, may have adverse effects on mental health. This study is the first epidemiological evidence to suggest possible effects on suicidal thoughts. 

The study was carried out in central/coastal China, a relatively wealthy area with a rapidly developing economy. In a very large survey of mental health in rural community residents, participants were also asked about how they stored pesticides. The study found that people who stored pesticides at home, i.e. those with more exposure, were more likely to report recent suicidal thoughts. Supporting this, the survey also found suicidal thoughts to be associated with how easily accessible these pesticides were in the home and that the geographic areas with highest home storage of pesticides also had highest levels of suicidal thoughts in their populations. 

Given the high level of pesticide exposure and the high suicide risk in rural China, clarification of the causal mechanisms underlying this association and the development of appropriate interventions should be priorities for public health and health policy. 

Dr Robert Stewart comments: ‘Organophosphate pesticides are widely used around the world although are banned in many countries because of their risk to health. They are particularly lethal chemicals when taken in overdose and are a cause of many suicides worldwide. Our research findings that suggest that higher exposure to these chemicals might actually increase the risk of suicidal thoughts provides further support for calls for tighter international restrictions on agricultural pesticide availability and use.’

Dr Jianmin Zhang, Associate Chief Psychiatrist, Tongde Hospital of Zhejiang Province, and Vice Director, Zhejiang Office of Mental Health, China added: “The findings of this study suggested potential causal links and might partially account for the much higher incidence of suicide in rural than urban areas of China. However, further studies particularly with more precisely defined and assessed exposure are critically needed, as awareness of safer access to pesticides is important both to policy-makers and pesticide users.”


Reference: King’s College London, Pesticides exposure linked to suicidal thoughts, October 22, 2009  


Pesticide exposure and suicidal ideation in rural communities in Zhejiang province, China by Jianmin Zhang, Robert Stewart, Michael Phillips, Qichang Shi & Martin Prince was published in the October issue of the WHO Bulletin. The full article can be accessed on 

The analysis involved data from a survey of a representative sample of 9,811 rural residents in Zhejiang province who had been asked about the storage of pesticides at home and about whether or not they had considered suicide within the two years before the interview. The Chinese version of the 12-item General Health Questionnaire (GHQ) was administered to screen for mental disorder.

Children susceptible to pesticides longer than expected, Berkeley study finds

Although it is known that infants are more susceptible than adults to the toxic effects of pesticides, this increased vulnerability may extend much longer into childhood than expected, according to a new study by researchers at the University of California, Berkeley.

Among newborns, levels of paraoxonase 1 (PON1), an enzyme critical to the detoxification of organophosphate pesticides, average one-third or less than those of the babies’ mothers. It was thought that PON1 enzyme activity in children approached adult levels by age 2, but instead, the UC Berkeley researchers found that the enzyme level remained low in some individuals through age 7.

Based upon the findings, reported this month in the journal Environmental Health Perspectives, the study authors recommend that the U.S. Environmental Protection Agency (EPA) re-evaluate the current standards for acceptable levels of pesticide exposure.

“Current EPA standards of exposure for some pesticides assume children are 3 to 5 times more susceptible than adults, and for other pesticides the standards assume no difference,” said Nina Holland, UC Berkeley adjunct professor of environmental health sciences and senior author of the paper. “Our study is the first to show quantitatively that young children may be more susceptible to certain organophosphate pesticides up to age 7. Our results suggest that the EPA standards need to be re-examined to determine if they are adequately protecting the most vulnerable members of the population.”

In 2001, the EPA began restricting organophosphate pesticides in products sold for use in homes, mainly because of risks to children. However, organophosphate pesticides, such as chlorpyrifos and diazinon, are still used in agriculture in the United States and elsewhere.

The study, conducted by UC Berkeley’s Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS), involves 458 children from an agricultural region who were followed from birth through age 7. Cord blood samples were collected from all children to determine their PON1 genotype and to obtain baseline measures of the enzyme’s activity level.

For more than 100 of the children in the study, researchers were able to obtain at least four additional measurements – at ages 1, 2, 5 and 7 – of PON1 activity. Almost all the children in the study had 2 to 3 time points assessed, for a total of 1,143 measurements of three types of PON1 enzyme activity.

One’s PON1 genotypic profile determines how effectively the enzyme can metabolize toxins. For example, people with two copies of the Q form of the gene – known as a QQ genotype – produce a PON1 enzyme that is less efficient at detoxifying chlorpyrifos oxon, a metabolite of chlorpyrifos, than the enzyme produced by people with two R forms of the gene. Similarly, individuals with two T forms of the PON1 gene on a different part of the chromosome generally have a lower quantity of the enzyme than do those with two C forms of the gene.

Previous research led by Holland found that some of the QQ newborns may be 50 times more susceptible to chlorpyrifos and chlorpyrifos oxon than RR newborns with high PON1 levels, and 130 to 164 times more susceptible than some of the RR adults.

Of the children in this latest study, 24 percent had the QQ genotype, and 18 percent had the TT genotype, both of which are associated with lower activity of the PON1 enzyme. Moreover, 7.5 percent of the children had both QQ and TT genotypes, which is considered an even more vulnerable profile.

On average, the quantity of enzyme quadrupled between birth and age 7. The greatest rise in enzyme activity was among children with the RR and CC variants of the PON1 gene, which quickly outpaced the increase in children with the QQ and TT genotypes.

The fact that enzyme activity remained low for certain kids with vulnerable genotypes well past age 2 was surprising for the study authors. The researchers are continuing to collect data for these children as they grow older to see if the pesticide susceptibility continues.

“In addition to its involvement in the metabolism of pesticides, many studies are now finding that PON1 may play an important role in protecting against oxidative stress, which is linked to diseases from asthma to obesity and cardiovascular disease,” said study lead author Karen Huen, a UC Berkeley Ph.D. student in environmental health sciences. “The children in our study whose genotypes are related to lower PON1 activity may not only be more susceptible to pesticides throughout much of their childhood, they may also be more vulnerable to other common diseases related to oxidative stress.”

Notably, other studies have found that PON1 genotypes vary by race and ethnicity, with the Q variants more common among Caucasians, less common among Latinos, and least common among African Americans. The majority of the subjects in this study were Mexican-American.

“What’s important about this study is that it shows that young children are potentially susceptible to certain organophosphates for a longer period of time than previously thought,” said Brenda Eskenazi, UC Berkeley professor of epidemiology and director of CHAMACOS and the Center for Children’s Environmental Health Research. “Policymakers need to consider these vulnerable populations when establishing acceptable levels of exposure to different pesticides.”

Funding from the National Institute of Environmental Health Sciences and the EPA helped support this research.

Reference: UC Berkeley, Children susceptible to pesticides longer than expected, study finds, June 22, 2009

Reducing the incidence of acute pesticide poisoning by educating farmers on integrated pest management

farmer in India

Sixty-five farmers reported on pesticide use and the signs and symptoms of acute pesticide poisoning when using two different plant protection strategies: in 2003 using chemical controls and in 2004 using an approach to Integrated Pest Management (IPM) based on an ecological analysis of the field conditions.

Exposure to organophosphates was confirmed as a serious risk factor for occupational poisoning. The adoption of IPM reduced the use of pesticides and halved the incidence of acute pesticide poisoning. Overall, the pesticide use spectrum shifted towards lower WHO Hazard Classes. A reduction of adverse health effects was attained through a reduction in exposure to toxic pesticides and behavioural changes. Given that other strategies to reduce the rate of acute poisoning have proven ineffective, interventions aiming to minimize pesticide poisoning in India and in other developing countries with similar rural conditions should focus on restricting the use of highly toxic compounds and educating farmers on IPM.

Reference: Mancini F, Jiggins JL, O’Malley M., Reducing the incidence of acute pesticide poisoning by educating farmers on integrated pest management in South India, Wageningen University, Int J Occup Environ Health. 2009 Apr-Jun;15(2):143-51