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How concerned should I be about pesticides?


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#1 InquilineKea

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Posted 19 August 2011 - 11:28 PM


And do pesticide "washes" even work at all?

http://www.reddit.co...ing_fruits_and/ says that you don't get rid of them by washing them with water.

http://www.reddit.co...ts_and_veggies/ suggests some long-term risk. The thing is, that risk here is more than just mortality data. It's also about brain damage (which is rarely reflected in mortality data)

Also, since many of us don't accumulate fat, does it mean that we'll flush out more of the pesticides, or does it mean that more of them will accumulate in our brains?

If you look at http://pubs.cas.psu..../pdfs/uo198.pdf, it says this...

Organophosphate and carbamate
insecticides inhibit the activity of
cholinesterase, resulting in a buildup
of acetylcholine in the body. An
increase in acetylcholine results in the
uncontrolled flow of nerve transmissions between nerve cells. The nervous system becomes “poisoned”; the
accumulation of acetylcholine causes


But do organophosphates do *more* damage than just that? More acetylcholine is generally a "good" thing, at least to some extent.

Edited by InquilineKea, 19 August 2011 - 11:34 PM.


#2 niner

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Posted 20 August 2011 - 03:13 AM

My biggest concern would be estrogen mimetics. Minute quantities of acetylcholinesterase inhibitors aren't going to do jack. Sometimes I wash fruit with dishwashing detergent, but usually I just rinse it. Water isn't likely to get much pesticide off. It washes off dirt and bugs, I suppose. I eat a mix of organic and non-organic food. I think that most of the time, the dangers of pesticides are overblown, but every once in a while they're real. The problem is you don't know when that's the case. You can either say "F it" and not worry about it, or worry about all of it. I lean toward the former. I think not eating fruits and vegetables would be a bigger danger than the pesticide residues they might harbor.
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#3 InquilineKea

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Posted 20 August 2011 - 07:18 AM

Oh - good reply! I'll look up more into this issue.

Unfortunately, research published this year suggests that an agricultural pesticide *does* destroy dopaminergic neurons. And it's quite potent too.

http://www.latimes.c...0,4772737.story


California researchers who first established a link between two commonly used pesticides and Parkinson's disease have found a third crop-enhancing chemical -- ziram -- that appears to raise the risk of developing the movement disorder. And they have found that people whose workplaces were close to fields sprayed with these chemicals -- not just those who live nearby -- are at higher risk of developing Parkinson's.

In animal studies conducted as part of the research on agricultural chemicals and Parkinson's disease, the researchers found that ziram was powerfully destructive to neurons that use the transmitter chemical dopamine to send messages. These brain cells are the ones that die off in regions of the brain that govern motor function, causing the tremors, unsteady gait and difficulty initiating movement that are the hallmarks of Parkinson's.


Two other pesticides too (http://www.safelawns...insons-disease/):

IN 2009, researchers at UCLA linked Parkinson’s Disease (PD) to two chemicals commonly sprayed on crops to fight pests. The study didn’t examine farmers, but rather focused on people living near the farm fields where the chemicals maneb and paraquat were sprayed. They found that, for those residents, the risk for PD increased 75%.
A follow-up study adds two new twists. Funded by the National Institutes of Environmental Health Sciences and Neurological Disorders and Stroke, the U.S. Department of Defense Prostate Cancer Research Program, and the American Parkinson’s Disease Association, researchers have now implicated a third pesticide, ziram.
This time, the population tested also included people who worked near sprayed fields- including firefighters, teachers, and clerks. They found that the combined exposure to ziram, maneb and paraquat near any workplace increased the risk of PD threefold, while combined exposure to ziram and paraquat alone was associated with an 80 percent increase in risk. The results appear in the current online edition of the European Journal of Epidemiology.


Then another 2011 study (though rotenone is thankfully not sprayed on crops)

http://www.nih.gov/n...11/niehs-11.htm

"Rotenone directly inhibits the function of the mitochondria, the structure responsible for making energy in the cell," said Freya Kamel, Ph.D., a researcher in the intramural program at NIEHS and co-author of the paper appearing online in the journal Environmental Health Perspectives. "Paraquat increases production of certain oxygen derivatives that may harm cellular structures. People who used these pesticides or others with a similar mechanism of action were more likely to develop Parkinson's disease.


In 2010, a study was published detailing the progression of Parkinson's-like symptoms in mice following chronic intragastric ingestion of low doses of rotenone. The concentrations in the central nervous system were below detectable limits, yet still induced PD pathology.[23]

The main thing is that I'm concerned that they'll build up in brain tissue. =/

And for the record - none of the 3 pesticides above are organophosphates. Looking at the individual articles for http://en.wikipedia....Organophosphate, it seems that their effects aren't even that bad at all (at least to people who aren't children anymore - their effects seem to be more acute than chronic, although one cannot rule out effects we do not know about). So I guess I should look for fruit that has more of the organophosphates and less of the "evil 3" above, for any given level of pesticide exposure.
EDIT: Sorry, my initial conclusion was wrong - I just found that organophosphates damage the brain in ways different from their cholinergic effects

Edit: Carbamates are even milder than organophosphates (reversible acetylcholinesterase inhibition). So maybe safer? (though there can be unknown effects).

Then there are organochlorides, fungicides, and fumigants. Not sure about organochlorides - DDT is not *that* bad for humans. But http://www.thelancet...IIS0140-6736(00)04249-5/fulltext suggests otherwise (deteriorating cognitive function with increased years of exposure - though effect different from that of organophosphates)

The latter two seem more worrisome.

Fumigants: http://en.wikipedia....ation#Chemicals . Example fumigants seem to be more known for acute than for chronic effects, so maybe not as worrisome? (here is where my vocabulary ALWAYS confuses people - I always worry FAR more about chronic effects than acute ones, so I have surprisingly lax attitudes towards cyanide and carbon monoxide, and freak out about nanoparticles and chemicals people consider more benign).

But they might have missed out on many

Then there's this: http://en.wikipedia....yrethroid#Types .

==

But paraquat is a herbicide. Maneb is a fungicide. And people are less inclined to (prima facie) suspect herbicides and fungicides of neurotoxicity. And that's where the research might be REALLY lacking.

More on Maneb: http://www.mitochond...p?pmid=16889834

So for fungicides, well, there are the triazoles. Surprisingly, many of them are actually prescribed as antifungals (to humans), so we can at least be sure that their effects probably aren't THAT horrible. Triadimefon http://www.sciencedi...892036289900718 is another interesting antifungal that acts a lot like amphetamine (with similar neurotoxicity potential - probably not TOO much to worry about). http://www.ncbi.nlm..../pubmed/8600615 also suggests little to worry about for triazoles. But again, I don't know what maneb is. Maneb is FRIGHTENING. And http://en.wikipedia....LinksHere/Maneb doesn't show anything significant linking to it

Edited by niner, 21 August 2011 - 01:41 AM.

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#4 InquilineKea

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Posted 20 August 2011 - 07:25 AM

Ugh, this is motivating enough for me to make another post


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 metam 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.[32]


Ok, sometime I will try to dissect the types of pesticides used most often for each crop. There is very little information on http://en.wikipedia....i/Metham_sodium - this could be bad

One thing I wonder: are vegetarians exposed to less? Because pesticides often do accumulate on the food chain, and people don't really care about the quality of food that animals eat.

Edited by InquilineKea, 20 August 2011 - 07:28 AM.


#5 InquilineKea

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Posted 20 August 2011 - 07:39 AM

Two lit reviews (keep in mind that they were done before the 2011 studies above):

http://www.ncbi.nlm....pubmed/17981626

Pesticides are substances widely used to control unwanted pests such as insects, weeds, fungi and rodents. Most pesticides are not highly selective, and are also toxic to nontarget species, including humans. A number of pesticides can cause neurotoxicity. Insecticides, which kill insects by targeting their nervous system, have neurotoxic effect in mammals as well. This family of chemicals comprises the organophosphates, the carbamates, the pyrethroids, the organochlorines, and other compounds. Insecticides interfere with chemical neurotransmission or ion channels, and usually cause reversible neurotoxic effects, that could nevertheless be lethal. Some herbicides and fungicides have also been shown to possess neurotoxic properties. The effects of pesticides on the nervous system may be involved in their acute toxicity, as in case of most insecticides, or may contribute to chronic neurodegenerative disorders, most notably Parkinson's disease. This brief review highlights some of the main neurotoxic pesticides, their effects, and mechanisms of action.


http://www.ncbi.nlm....pubmed/17615113

There is a wealth of literature on neurotoxicological outcomes of acute and short-term exposure to pesticides in laboratory animals, but there are relatively few studies of- long-term exposure. Many reports in the literature describing ;chronic' exposures to pesticides are, in fact, as short as five days and rarely longer than three months. Furthermore, routes of administration range from subcutaneous to dietary. Doses used in many of the studies produce signs of acute or overt toxicity. In contrast, human symptoms have been reported following exposures that are prolonged and often without obvious toxic effects. A survey of the literature was conducted to identify rodent studies with neurobehavioral and neurophysiological endpoints of pesticide exposures lasting 30 days or longer. This survey indicated that the majority of studies concentrate on cholinesterase inhibitors (organophosphorus and carbamate insecticides). Various neuromotor, cholinergic, physiological, affective and cognitive disorders were reported at doses producing cholinesterase inhibition; however, there were a fewer effects at non-inhibiting doses. Other classes of pesticides produced similar effects, with the exception of cholinergic signs. In many studies, the changes were subtle, which may correspond to the nonspecific changes in psychomotor and cognitive function reported in humans. It appears, then, that the data from animal and human pesticide exposures are generally comparable, but the specific outcomes are influenced by many experimental differences. Future research should concentrate on analogous exposures and outcomes to facilitate interpretation.


Will try to analyze until I fall asleep. Even through my university proxy, I can't get past the paywall for the first article. If someone could get the first article for me (my email is simfish A T gmail), that would be great.

Just read 2nd article. I wasn't satisfied with it since it reported behavioral changes, but completely confused (possibly temporary) effects with neurotoxicity. But it did report that organophosphate pesticides *could* sometimes improve memory (of course, some negative effects could also be reported).

Edited by InquilineKea, 20 August 2011 - 07:53 AM.


#6 InquilineKea

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Posted 20 August 2011 - 12:53 PM

http://www.neurology...5/1346.abstract

Herbicides are NASTY

When adjusted for these variables and smoking status, there was a significant association of occupational exposure to herbicides (odds ratio [OR], 4.10; 95% CI, 1.37, 12.24) and insecticides (OR, 3.55; 95% CI, 1.75, 7.18) with PD, but no relation was found with fungicide exposure. Farming as an occupation was significantly associated with PD (OR, 2.79; 95% CI, 1.03, 7.55), but there was no increased risk of the disease with rural or farm residence or well water use


Both insecticides and herbicides -- most notably organochlorines, organophosphorus compounds, chlorophenoxy acids/esters, and botanicals -- significantly increased the risk of Parkinson's disease, the researchers report in the online journal BioMedCentral (BMC) Neurology.



==

On the other hand, regarding insecticides: http://en.wikipedia....iki/Insecticide

The organochlorines are nasty. I'm trying to read more into organophosphates right now. The others not so bad in very small doses (one category is even a nicotine analog)

==

wtf, why does my university NOT have a subscription to Neurology. If any one of you could send the pdf of that to me, I'd be immensely grateful. Thanks!

Edited by InquilineKea, 20 August 2011 - 01:11 PM.


#7 InquilineKea

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Posted 20 August 2011 - 01:15 PM

Quotes from organophosphate paper at
http://dx.doi.org/10...6/S0300-483X(02)00447-X

Knew it - organophosphate neurotoxicity is UNRELATED to its cholinergic effects

Exposure to organophosphorus (OP) esters can
cause several syndromes including acute choliner-
gic clinical episodes, the so-called Intermediate
syndrome, organophosphate induced delayed neu-
ropathy (OPIDN) and chronic neurological ef-
fects. Acute toxicity is produced by irreversible
inactivation of the enzyme cholinesterases, the
exact mechanism of the intermediate syndrome is
not understood while the OPIDN is claimed to be
‘marked’ by the inhibition and subsequent ageing
(dealkylation) of a protein enzyme in nerve cells
called neuropathy target esterase (NTE). The
ability to produce OPIDN is not even related to
the degree of inhibition of AchE and there is no
indication that the intermediate syndrome is
related to the cholinergic effect of OP compounds
.
It took the medical and scientific body more than
50 years to recognise OPIDN despite its dramatic
nature of clinical presentation.


This is not an argument as such against the
existence of chronic neurotoxicity. We do agree on
the necessity of such studies. We have done some
work in this regard and our early results indicate
that some patients show clear improvement after
cessation of exposure and peripheral neurophysio-
logical parameters may even normalise, while
other patients do not. This is typically seen in
other chronic toxic neuropathies such as those
caused by lead and thallium.


So, I'll try to make a list of further literature to explore (after throwing out all the acute toxicity studies, and all studies before 1980)

NEGATIVE statistical significance (does not indicate absence of effect yet though - must see the odds ratios before firmly concluding)

Maizlish, N., Schenker, M., Weisskopf, C., Seiber, J., Samuels,
S., 1987. A behavioural evaluation of pest control workers
with short-term, low-level exposure to the organophosphate
diazinon. Am. J. Indust. Med. 12, 153  / 172.

Fiedler, N., Kipen, H., Kelly-McNeil, K., Fenske, R., 1997.
Long term use of organophosphates and neuropsychologi-
cal performance. Am. J. Indust. Med 32, 487  / 496.

Ames, R., Steenland, K., Jenkins, B., Chrislop, D., Russo, J.,
1995. Chronic neurologic sequelae to cholinesterase inhibi-
tion among agricultural pesticide applicators. Arch. En-
viron. Health 50, 440  / 443.

==

POSITIVE statistical significance

Misra, U.K., Prasad, M., Pandey, C.M., 1994. A study of
cognitive functions and event related potentials following
organophosphate exposure. Electromyogr. Clin. Neurophy-
siol. 34, 197  / 203.

Stokes, L., Stark, A., Marshall, E., Narang, A., 1995. Neuro-
toxicity among pesticide applicators exposed to organopho-
sphates. Occup. Environ. Med. 52, 648  / 653.

Or actually, just read Table 6.

BAD PESTICIDES:

sarin
pyridostig-mine bromide, DEET, and chlorpyrifos.

NEED MORE INFORMATION pesticides:

diazinon

===

THIS quote possibly related to those who down huperzine A or other nootropics:

What was
also unique among OP exposed patients was that
certain cholinergic functions were selectively pre-
served; for example, the sudomotor function in the
skin and respiratory modulation of cardiac vagal
tone in the bulbar reticular formation in the
brainstem were often not affected and yet other
functions that do not require cholinergic nerves in
the same anatomical sites were abnormal. It is well
known that chronic low level of anticholinesterase
activity protects cholinergic synapses from episo-
dic large anticholinesterase poisoning, but could it
at the same time damage non-cholinergic synapses
in the same area? This is a strong possibility given
the evidence from our patients chronically exposed
to LTLL of OP


Edited by InquilineKea, 20 August 2011 - 01:54 PM.


#8 InquilineKea

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Posted 20 August 2011 - 01:35 PM

organochlorines = bad

http://aje.oxfordjou...ent/167/10/1235

Using logistic regression, the authors considered two primary measures of pesticide exposure: ever use and cumulative lifetime days of use. They found seven specific pesticides (aldrin, chlordane, heptachlor, dichlorvos, trichlorfon, alachlor, and cyanazine) for which the odds of diabetes incidence increased with both ever use and cumulative days of use. Applicators who had used the organochlorine insecticides aldrin, chlordane, and heptachlor more than 100 lifetime days had 51%, 63%, and 94% increased odds of diabetes, respectively



http://newswise.com/...es/view/541427/

Risks were greater when users of specific pesticides were compared with applicators who never applied that chemical. For example, the strongest relationship was found for a chemical called trichlorfon, with an 85 percent increase in risk for frequent and infrequent users and nearly a 250 percent increase for those who used it more than 10 times. In this group, 8.5 percent reported a new diagnosis of diabetes compared with 3.4 percent of those who never used this chemical. Trichlorfon is an organophosphate insecticide classified as a general-use pesticide that is moderately toxic. Previously used to control cockroaches, crickets, bedbugs, fleas, flies and ticks, it is currently used mostly in turf applications, such as maintaining golf courses.


Edited by InquilineKea, 20 August 2011 - 01:36 PM.


#9 InquilineKea

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Posted 20 August 2011 - 01:44 PM

Study showing that pesticide exposure DECREASES reasoning ability: http://dx.doi.org/10...oem.2009.047811

Considering that the oldest farmers started their occupational exposure in the 1970s and that latency is important, pesticides used in vineyards during the 1970s and 1980s are of primary concern for the effects we observed. During that period, the most probable fungicides used were dithiocarbamates, phtalimides, dicarboximides, triazoles and inorganic substances (copper, sulphate, arsenic) with, to a lesser extent, insecticides (organophosphates, organochlorines and carbamates) and some herbicides (triazines or sulfamides)



Follow-up of the PHYTONER cohort showed lower cognitive performances in pesticide-exposed subjects. Among the seven cognitive tests significantly associated with pesticide exposure, three have a cognitive speed component: (i) the TMT, also implying a selective attention component, (ii) the FTT, a very simple motor speed test with a strategic component and (iii) the IST, a semantic verbal fluency test which implies integrity of semantic memory, as well as strategic search, working memory and a speed component. Performance on two of these tests with a speed component have already been found to be associated with chronic pesticide exposure (the TMT22–24) as has often been found with other cognitive speed tests, such as the TMT part B22 25 26 and the Digit Symbol Substitution Test.22 24 25 27 28 The most strongly associated test, the BVRT, is a visual working memory test, which also implies selective attention and inhibition, and this test and other quite similar ones have already been shown to be associated with chronic pesticide exposure.22 29–32 The second most associated measure is the number of good answers on the Stroop interference test, implying selective attention and inhibition of an automatic response. Finally, performances on two episodic memory tests were also associated with pesticide exposure, as was the case with the Rey Auditory Verbal Learning Test in another study.32 Associations between pesticide exposure and test results were very strong with ORs for having a performance in the lower quarter of the distribution exceeding 5 for the visual working memory test (the BVRT) and 1 for the cognitive speed test (the TMT) and being even stronger for some cognitive measures if one considers the risk to be in the lower 10% of performances, with a risk multiplied by more than eight for the BVRT and more than 10 for the ST. No clear dose–effect relationship was observed between the directly and indirectly exposed. The evolution of performances over a 4–5-year period demonstrated that exposed subjects generally had the greatest decrease: on the MMSE they had a 1.97 risk of lowering their score by two points between baseline and follow-up compared to non-exposed subjects, and a 1.64 risk of lowering their score by three points. This result is particularly striking in view of the short duration of follow-up and the relatively young age of the participants.


A longitudinal study of performances in a French population aged 65 and over without dementia showed a slight decline over 5 years only in tests with a speed component, but not on the MMSE or the BVRT.33 The observed decline in pesticide-exposed subjects on the MMSE, a composite measure reflecting global cognitive deterioration, cannot therefore be considered a sole effect of ageing, especially as the subjects were relatively young.



It can even strip away the protective effect of education

We also observed a stronger impact of pesticide exposure in groups who had protective characteristics at baseline with regard to cognitive performances (highly educated, no alcohol consumption, women) even if these groups had and continued to have a higher performance than others. Several studies have demonstrated that highly educated people have a lower risk of Alzheimer's disease and dementia, which is often explained by a hypothetic ‘reserve capacity’.34 35 This ‘reserve’ might explain why their performances were better than those of the less educated subjects at baseline. They may initially resist pesticide exposure better, but their accelerated decline showed that prolonged exposure combined with ageing may considerably reduce their protective factors.



relevant quote only for experimental design

It should be underlined that some subjects, mostly those who were non-exposed, also had better results at follow-up than at baseline, which might be attributable to the well-known effect of practice when tests are repeated.


Edited by InquilineKea, 20 August 2011 - 01:46 PM.


#10 InquilineKea

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Posted 20 August 2011 - 01:51 PM

ONE CAVEAT: many occupational exposure studies were done on BANNED pesticides. So in all actuality, many aren't that relevant for today's world. Still, the "horrid 3" I've originally identified are still relevant today

==

looking at the pesticide databases for one particular molecule - unfortunately - all of them don't report chronic effects of pesticides (as general practice, I always post what doesn't work - it's necessary for responsible science)

http://www.pesticide...?Rec_Id=PC35079
http://www.beyondpes...de/diazinon.htm
http://www.atsdr.cdc...p?id=512&tid=90
http://toxipedia.org...ipedia/Diazinon
http://scorecard.goo...nce_id=333-41-5
http://www.atsdr.cdc...files/tp86.html

Edited by InquilineKea, 20 August 2011 - 02:01 PM.


#11 InquilineKea

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Posted 20 August 2011 - 02:13 PM

Effects of vegetarianism (http://www.ncbi.nlm....pubmed/19707917)

This study aims to compare the pesticide residue dietary intake of the French general population and the vegetarian population, separated into five specific diets: omnivorous (OMN), lacto-vegetarian (LV), ovo-lacto-vegetarian (OLV), pesco-lacto-vegetarian (PLV) and vegan (VG). Theoretical Maximum Daily Intakes (TMDIs) based on Maximum Residue Levels (MRLs) were calculated as a percentage of the Acceptable Daily Intake (ADI). Among the 421 pesticides studied, only 48 had TMDI above ADI for at least one population subgroup. An excessive exposure was noticed for 44, 43, 42, 41 and 30 pesticides in the OLV, VG, OMN, LV and PLV groups, respectively, versus 29 in the general population. Meat and egg products consumption was responsible for higher intakes of organochlorine pesticides in the general population than in the vegetarian population (TMDI = 348% versus 146-183% ADI for aldrin). However, as the limited consumption of animal-origin commodities was largely offset by a higher fruit, vegetable and cereal intake in the vegetarian diets, vegetarians appear to be preferentially exposed to pesticides, for which fruit, vegetables and cereals are the main contributors, such as tri-allate, chlorpyrifos-methyl and diazinon. This study illustrates that consumption habits have a real impact on pesticide exposure in terms of intake levels, number and type of pesticides, representing a potential risk of dietary exposure. Except for organochlorine compounds, the vegetarian population may be more exposed to pesticide residues than the general population due to specific dietary habits. Thus, this population should be considered for risk assessment of pesticide residues.


From preliminary Google Scholar searches, tri-allate does not seem to be that bad (http://pmep.cce.corn...allate-ext.html). chlorpyrifos-methyl, though, is nasty (see http://en.wikipedia....#Health_effects). diazinon significantly increases one's chances of lung cancer - http://aghealth.nci....gCancer2006.pdf - but few other studies have been done

Also,

When compared to applicators who had never used these chemicals, those who had used
metolachlor over 457 lifetime days had a four-fold risk of lung cancer. For those who had used
pendimethalin more than 225 days, their risk was 3.5 times greater for developing lung cancer.


Wikipedia templates

http://en.wikipedia....te:Insecticides

http://en.wikipedia....late:Herbicides

Edited by InquilineKea, 20 August 2011 - 02:36 PM.


#12 InquilineKea

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Posted 20 August 2011 - 02:17 PM

Wow, canning and freezing foods destroys pesticides?

http://www.vegetaria.../pesticides.php

I guess I had a LEGITIMATE reason to fight with my parents over that. Especially given that last study showing that humans don't really absorb bisphenol A.


The washing and treatment process to prepare fruits and vegetables for canning or freezing removes or destroys most of the pesticide residues. For example, 80-90% of the benomyl residue (the fungicide suspected of causing birth defects) is removed when apples are made into applesauce and when tomatoes are converted into tomato juice.


In other words, contrary to popular wisdom, fresh food is NOT better for you. In fact, it may be FAR WORSE

Edited by InquilineKea, 20 August 2011 - 02:18 PM.


#13 InquilineKea

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Posted 20 August 2011 - 03:11 PM

http://peer.ccsd.cnr...30903031171.pdf shows that meat-eaters have higher exposures to organochlorides; vegetarians have higher exposures to everything else (including ziram and maneb). Paper is a bit flawed since it didn't even categorize ziram and maneb as potentially dangerous.

also Chlorpyrifos-methyl is highest in cereal; Diazinon is highest in fruit

===

From Exposure of several Belgian consumer groups to pesticide residues through fresh
fruit and vegetable consumption
...

Pesticide residues that were detected most frequently in fresh
fruit and vegetables on the Belgian market in 2008, are the fungi-
cides iprodione, boscalid, dithiocarbamates, imazalil, difenocona-
zole, propamocarb, cyprodinil and thiabendazole. Residues were
detected (i.e. result >LOQ) in approximately 72% of the samples and
approximately 94% of the samples were compliant (i.e. result <LOQ
or no violation of the MRL).
The main fruit groups for which residue levels exceeded the
MRL, are exotic fruits (passion fruit), citrus fruit (oranges) and
berries and small fruits (currants and strawberries). The main
groups of vegetables showing MRL exceeding measures are fruiting
vegetables (Chili peppers, eggplants, melons and lauki), bulb
vegetables (garlic) and legume vegetables (beans).
Fruit and vegetables imported from outside the European
Community showed relatively more MRL exceeding measures than
fruit and vegetables originating from Member States (10.5%
compared to 3.7% for Belgium and 3.1% for other Member States).


For the record - I think we should give little credence to MRLs, since they're more useful for acute toxicity than for chronic toxicity. There weren't even MRLs for ziram and maneb. But it's still important to learn more about this

Edited by InquilineKea, 20 August 2011 - 03:15 PM.


#14 InquilineKea

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Posted 20 August 2011 - 03:27 PM

As for the databases...

http://www.fda.gov/F...s/ucm229204.htm

More readable form

http://www.fda.gov/F...s/ucm228867.htm

i'm gonna spend much of today poring over the data for some of my favorite fruits.

#15 InquilineKea

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Posted 20 August 2011 - 03:31 PM

). I n addition, Fleming
e t a1.21 found a significant association between PD,
diagnosed postmortem, and the presence of the or-
ganochlorine insecticide dieldrin in these brains.
The biologic mechanisms contributing t o the risk
of PD associated with exposure to herbicides and
insecticides are unknown. However, many pesticides
a r e known t o induce oxidative stress, a prominent
biochemical defect in the PD nigra,22 by inhibiting
mitochondria1 oxidative p h o ~ p h o r y l a t i o n , ~ ~ including
complex I activityz4; releasing iron from f e r ~ i t i n , ~ ~
potentially increasing Fenton-promoted generation
of cytotoxic hydroxyl radicals; and depleting cells of
reduced glutathione,26 diminishing t h e ability to
scavenge toxic free radicals



#16 niner

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Posted 21 August 2011 - 02:20 AM

Wow, that's quite a bit of research you've done. I was struck by the case-control study where they looked at people living within 500 m of sites where ziram, maneb, or paraquat had been sprayed. Those people were found to have significantly higher rates of Parkinson's. My question is how does our exposure from eating food compare to the people who were near spraying? One possibility is that they inhaled tiny droplets of the compounds, which is essentially the same as an IV dose. This allows the compound to skip first-pass metabolism. OTOH, if we eat residual amounts of these compounds, they see the stomach and gut environment first, including a number of xenobiotic metabolism enzymes. Then, to the extent they get in, they hit the liver before the brain. This could alter toxicity substantially.

Since you've done all this work, it would be really cool if eventually you could distill it down to some simple guidelines regarding specific pesticides or foods that should be avoided. Right now it's kind of a scary mountain o' danger, but like you said, some of it is based on pesticides that are now banned. Ultimately, we want to know about what's on store shelves today.

When I was a little kid, you could buy chlordane (now banned) for home use. We even had some. I wonder how many suburban yards are toxic waste dumps?
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#17 InquilineKea

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Posted 21 August 2011 - 04:26 AM

My question is how does our exposure from eating food compare to the people who were near spraying? One possibility is that they inhaled tiny droplets of the compounds, which is essentially the same as an IV dose. This allows the compound to skip first-pass metabolism. OTOH, if we eat residual amounts of these compounds, they see the stomach and gut environment first, including a number of xenobiotic metabolism enzymes. Then, to the extent they get in, they hit the liver before the brain. This could alter toxicity substantially.

Since you've done all this work, it would be really cool if eventually you could distill it down to some simple guidelines regarding specific pesticides or foods that should be avoided. Right now it's kind of a scary mountain o' danger, but like you said, some of it is based on pesticides that are now banned. Ultimately, we want to know about what's on store shelves today.


Yup definitely - that's now what I'm concerned about too. I'll try to see what I can get at tomorrow. Reddit Scholar is actually surprisingly helpful for journal articles

#18 InquilineKea

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Posted 21 August 2011 - 05:15 AM

Rotenone/Paraquet study: http://ehp03.niehs.n...289/ehp.1002839

Ziram + other 2 study: https://docs.google....4/edit?hl=en_US

#19 InquilineKea

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Posted 21 August 2011 - 05:19 AM

Ugh - turns out that they both have flaws. Neither of them report exposure dose - they just report whether or not someone was exposed

but wow


Rotenone is a plausible cause of PD because of its mechanism of action. Like 1-methyl-4-phenyl-1,2,3,6-tetrahydropyri​dine (MPTP), a toxicant known to cause parkinsonism in humans, rotenone directly inhibits mitochondrial complex I (Langston et al. 1983; Sherer et al. 2007). In experimental models, both MPTP and rotenone cause selective injury of dopaminergic neurons in the substantia nigra, a key pathological feature of PD (Greenamyre et al. 1999; Langston et al. 1984). Because rotenone is believed to have a relatively short environmental half-life and limited bioavailability, a relationship to human disease has been questioned (Hatcher et al. 2008; Li et al. 2005). However, recent work in rodent models indicated that a temporally limited exposure to rotenone later caused progressive functional and pathologic changes in the enteric nervous system of rodents, mimicking changes found in human PD; as in PD, these enteric nervous system changes preceded central nervous system pathology (Abbott et al. 2001; Braak et al. 2006; Drolet et al. 2009; Greene et al. 2009; Pan-Montojo et al. 2010). Chronic rotenone exposure in the laboratory has been reported to have additional effects associated with PD pathogenesis, including ones similar to changes observed in monogenic forms of PD (Henchcliffe and Beal 2008). Rotenone toxicity, therefore, provides a conceptual bridge, suggesting shared mechanisms for both sporadic and inherited forms of PD.

Although we report here findings for agricultural use of rotenone, the ubiquitous use of rotenone in both work and home settings that occurred until recently suggests that many people may have been exposed. Humans have used rotenone-containing plants as pesticides for centuries (Cabras et al. 2002). Because rotenone is plant derived, it has been considered an organic pesticide and was commonly used as a household insecticide in home gardening and agriculture, and to kill fish. For example, the California Department of Pesticide Regulation (2007) reported that almost 15,000 pounds of rotenone were used in 2007, not including home use. Rotenone was withdrawn from use in the European Union in 2007 (Schapira 2010), after which time most uses were voluntarily cancelled in the United States (U.S. EPA 2007). Other agents associated with mitochondrial complex I inhibition remain in common use. For example, permethrin is used in nonagricultural settings as an insect repellant, including use of permethrin-impregnated fabric for military uniforms and recreational clothing (Armed Forces Pest Management Board 2010).


Edited by InquilineKea, 21 August 2011 - 05:24 AM.


#20 e Volution

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Posted 21 August 2011 - 05:44 AM

Hans Wu a member of this forum has some blog posts on washing fruit and vegetables. He recommends a certain vegetable wash for this purpose. hanswuhealth.blogspot.com

edit:
post: http://hanswuhealth....ts-on-diet.html
one he recommends: http://www.naturecle...ash_concentrate

I think he covers it more in you search around

Edited by e Volution, 21 August 2011 - 05:47 AM.


#21 frederickson

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Posted 21 August 2011 - 02:06 PM

excellent review of the literature!

frightening, especially considering that these are only the published studies. many in the field suspect a type of "reverse publication bias" in that it is difficult to get work that finds health risks associated with pesticides published. the reason, of course, is money and journal advertising.

nevertheless, you have uncovered a wealth of evidence that suggests avoiding conventional products in favor of organic, or better yet, home-grown produce.
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#22 InquilineKea

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Posted 21 August 2011 - 06:27 PM

Hans Wu a member of this forum has some blog posts on washing fruit and vegetables. He recommends a certain vegetable wash for this purpose. hanswuhealth.blogspot.com

edit:
post: http://hanswuhealth....ts-on-diet.html
one he recommends: http://www.naturecle...ash_concentrate

I think he covers it more in you search around


Wow - thanks very much! Does anyone know if the fruit/veggie washes actually work though? That's something we'd also need research for.

#23 InquilineKea

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Posted 21 August 2011 - 06:37 PM

excellent review of the literature!

frightening, especially considering that these are only the published studies. many in the field suspect a type of "reverse publication bias" in that it is difficult to get work that finds health risks associated with pesticides published. the reason, of course, is money and journal advertising.

nevertheless, you have uncovered a wealth of evidence that suggests avoiding conventional products in favor of organic, or better yet, home-grown produce.


Ah - I appreciated that reply. Do you know which figures in the field suspect a type of "reverse publication bias?" I'd be interested to know (and then I could link to that in my Quora posts - I'm really trying to spread awareness about this)

#24 InquilineKea

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Posted 21 August 2011 - 07:11 PM

Just found some really good databases (better than any I mentioned):

http://www.ams.usda.gov/AMSv1.0/pdp

http://www.ams.usda....STELPRDC5091055

#25 InquilineKea

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Posted 25 August 2011 - 03:34 AM

Okay, here is my final preliminary answer:

In general, fruits from the Rosaceae family (apples, peaches, nectarines, and strawberries), are full of neurotoxic pesticide contamination. However, most non-organic vegetables do not contain such dangerous pesticides, so they aren't that much more dangerous.

The Rosaceae trees are also sprayed with neurotoxic herbicides that the USDA doesn't even measure - like paraquat and ziram - see What crops are most likely to be contaminated with ziram? Or paraquat?

As for what pesticides are inside...

[1] Note that the EWG site should only be seen as a rough source, and is somewhat misleading, as it counts the total number of pesticides inside. In reality, many of the "most contaminated" vegetables actually contain a lot of the more benign pesticides like the neonicotinoids. Also, note that the neurotoxic organophosphate Azinphos methyl will be banned by the EPA in mid-2012.
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#26 InquilineKea

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Posted 25 August 2011 - 03:49 AM

One small mess-up: I forgot celery, sweet bell peppers, and almonds - those also have substantial amounts of neurotoxic pesticides on them

Edited by InquilineKea, 25 August 2011 - 03:54 AM.


#27 tuckeverlasting

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Posted 23 September 2011 - 11:14 PM

Thank you InquilineKea. :cool:

#28 Florent Berthet

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Posted 05 February 2012 - 06:29 PM

Could someone do a summary of recommendations? InquilineKea has made a short one but what about washing fruits and veggies? Peeling? In the end, what should we avoid and what seems fairly safe?

#29 niner

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Posted 05 February 2012 - 10:55 PM


frightening, especially considering that these are only the published studies. many in the field suspect a type of "reverse publication bias" in that it is difficult to get work that finds health risks associated with pesticides published. the reason, of course, is money and journal advertising.


Ah - I appreciated that reply. Do you know which figures in the field suspect a type of "reverse publication bias?" I'd be interested to know (and then I could link to that in my Quora posts - I'm really trying to spread awareness about this)


I don't buy the 'reverse publication bias' argument, at least not if it's based on money. It's rare to find primary research journals that have advertising.

#30 sam7777

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Posted 18 February 2012 - 07:13 AM

http://www.epa.gov/comptox/

http://www.epa.gov/opprd001/section18/

http://iaspub.epa.go...vel=1&pItem=118




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