Does anyone have info or opinion on genetic AF?

AF runs in my family. I think I was probably genetically predisposed to Afib.
Was just wondering if others may have multiple family members with this arrhythmia?

To date:
1) My mom. She began having arrhythmias in her late 30's. I have no idea what the technical diagnosis was at that time, but in her 50's, she began to refer to this as AF. I can remember, when I was still young, watching the veins in her neck throb to the point you could actually see them protruding with each beat. Unfortunately, she (in spite of my objections) continued to stick with her long time cardiologist, who did not have her on coumadin, and she suffered a debilitating stroke 5 years ago, secondary to the AF.
My mother is a slender woman who loved to garden. Most of the vegetables my parents ate, they raised & processed themselves. My dad was also an avid sportsman & much of their meat, fish and fowl consumption was as a result of his hunting and fishing skills.

2) My mom's sister. She developed AF in her early 70's and had "an ablation" (that's all she knows) in Atlanta last fall with only mediocre results. She has spent her entire life in N. GA and is also an avid gardener.
She and mom grew up on a farm & both spent most of their lives eating home grown and home processed food. Mom, however, left GA when she married and spent the rest of her life, to this date, in middle TN.

3) My brother. He was diagnosed with AF 6 years ago when he was 50.
Fortunately for him, his HR is SLOW and irregular. He takes a mild med, but at this time, I'm having a "senior moment" and can't remember the name of it. He and I grew up in TN, but he's resided in FL for 20 years.

4) My Son. He is 35, and in Feb was taking a routine stress test for his flight physical (he's a C-130 navigator) & developed Afib on cool down (and has had a few episodes since). This young man is as health conscious and physically fit at they come. He grew up in TN but has spent his post college years bouncing around all over the world.

5) ME. I'm 58 and have been treated for AF for 12 years, although, in retrospect, I was having brief flutters and tachycardias in my 30's. I've spent most of my life in TN and AZ. Other than the AF (and a bout with breast cancer 6 yrs. ago....I'm fine...early detection!!) I'm pretty healthy.
As with my relatives, all of my echos, stress tests etc. have shown no "heart disease"....just my crazy electrical system.

This family is scattered about the US & I just can't see any specific environmental, geographical, or other factor that would include each and every one of us.....other than genetics. Your thoughts and info, please?

I have a lot of family member who have had AF. My mother has it and my grandmother had it and two of my father's sisters had it. My mother is still alive but my dad's sisters are deceased and so is my dad. None of them died from Afib though. One of them had a stroke but developed the Afib after the stroke. I got Af when I was 65 and have had it 3 times in the past 2 years. The last episode lasted longer and put me in the hospital and I was in Afib for 24 hours. The other two times I had it for about 13 hours and it coverted on its own without any medical intervention. I didn't know what it was. Both times it happened in the middle of the night and I went to the doctor the next morning but it had converted before I got there. He thought I was probably having PVCs but after having it for 24 hours last month I know it was Afib. I now know what it feels like.
Jan

Jan,

I'm certain, in my own mind, that genetics can be a factor. I wonder if anyone has ever done a study in this area? It would be interesting to know.

If your episodes become worrisome, you might consider having your cardiologist order an event monitor for you. It's a small monitor that you keep for 30 days. When you have an "event" you press a button and record your heart beat (like a mini EKG). Then you call an 800 #, press another button and send the recording to an office who prints out a telemetry strip & then sends that to your cardiologist. He/she can then determine the identity of you arrhythmia. Since you know you have had at least one documented episode of AF, the others are probably the same, but not necessarily so. My EP ordered another event monitor for me last fall & I discovered that some of my "fainty spells" were actually premature ventricular beats, not AF. A medication change has apparently cured that problem because I haven't had any since then....that I know of, and I do believe I would know because they were rather frightening.

Hello, Cilla. If you use the search function here and type in the word genetics, it will turn up the discussions we have had here on that subject. Someplace here, not too long ago, somebody quoted a chinese [i think] study where the researchers found one or more genes for afib.

It runs in my family, for sure. My mother had it, and i do, and my daughter is getting PVC's, her doctor says.

PeggyM

Cilla,
Last August when I went to the Cleveland Clinic Foundation to get my Pulmonary Vein Ablation, I noticed there was a sign at one of the desk where you got "prepped" advertising a study about genetic afib. They were looking for participants. I don't remember the exact name of doc in charge, but it sounded Spanish or Latin.

I only know of one relative in my family who was diagnosed with lone afib besides myself. However, my son, siblings. nieces and nephews have all had fainting spells as children which I suspect could be related.

Thanks PeggyM and njb,

I'll try the "search" that Peggy recommended and I plan to call CCF about an appt. on Monday (just in case I don't like what the UAB EP has to say) & I'll inquire about a familial study.

My best to you both!

Hans' Book P65-66 discusses genetic connection. 43% of 100 AFers who responded to his survey had a close relative with AF.

Anton,

I'm relatively new to this site, so I don't have the book. I was pretty sure that a study would confim my suspisions. Thanks for the info!

Carol If you do a search on google - and this board, there are a few studies on genetic AF. The most notible one I can remember was on a Chinese family. They isolated the gene that was mutant.

Also, just wondering about the avid gardeners in your family. Did they use pesticides? OP's are a know cause of AF. It could be that you were all exposed to the pesticides through what you ate. Just a thought.

Fran

Genetic defects in nutrient absorption as in magnesium, potassium or other critical enzymes to allow for normal cardiac functioning are a distinct possibility.

Polymorphisms are definitely passed along through generations.

polymorphism
1. The regular and simultaneous occurrence in a single interbreeding population of two or more alleles of a gene, where the frequency of the rarer alleles is greater than can be explained by recurrent mutation alone (typically greater than 1%). The concept includes chromosome polymorphism.

Bringing forward a previous post (3/1/04) for consideration:


Food Sensitivities, Nutritional Genomics, Gene Expression, and Diet

I’ve been known here as a self-appointed queen of supplements and in defense of that, I must add that they have been directed by functional medicine MD who is now into genomics and the relevant testing. I’ve been tested and the supplements I take are called targeted nutrients and medical foods.

My research on this topic is ongoing; I’ve attended a few seminars on the topic. The genomics concept makes sense and also makes yet another possible connection to the origins of AF. We all have the common problem, but how we get there is varied. That said, I want to emphasize that the solution to AF is more than just taking a shotgun approach to supplementation and taking handfuls of capsules daily without knowing what your target truly is. I’m not suggesting everyone run out and do genomic testing.

What I am suggesting is to read this post and understand that many diseases and conditions such as AF manifest as a result of gene expression… and this expression can be the result of nutritional deficiencies and other influences pointed out.

In light of the recent posts on food sensitivities, it seems appropriate once again to bring up the topic of nutritional genomics and gene expression. I’ve paraphrased, excerpted directly, text from two sources on the gene expression topic. The references are at the end. All is paraphrased. Nothing is my own “brain storm.”

I truly believe that afibbers need to understand why there seems to be such a variation amongst us with regard to solutions, symptoms, reactions, tolerances to medications, etc. Give this post some thought. Note especially, the comments toward the end about why some people tolerate minerals like magnesium and calcium and some don’t.

Also keep in mind that these genetic inheritances are not from your immediate ancestors… these are long-standing alterations compounded by current deficiencies and other influences. The good news is that 75% are changeable – modifyable to regain health or prevent disease. These are exciting times and genomics on is the cutting edge of future diagnostic tools. (Hey – they even mentioned it at the recent Cleveland Clinic seminar I attended ….so you know if they want in on it, it must have merit.)

Jackie


Food sensitivities are now identified as altered gene expression. Only 25% of our genetic makeup is fixed or unalterable, but clearly 75% are modifyable either in a positive or negative way through lifestyle.

Each element of nutrition is responsible for the way the genetic message is translated and utilized by the cell. These messages from gene expression signal the body and tell it how to perform. If a diet is poor and nutrients are lacking or are not available due to impaired intestinal absorption, gene expression is altered. Genetic characteristics can be induced by exposure to specific foods and nutrients as well as toxins and other characteristics may be suppressed.

The communication between the food you eat and your genotype contributes to your health by modifying your phenotype or function. Specific genetic inheritance factors (genetic sensitivities) predispose a person to food sensitivities. Inflammation from the intestinal tract and impaired intestinal function from continuous exposure to foods to which the genes respond adversely can result in poor absorption of nutrients. In extreme cases, genetic sensitivity can result in life-threatening anaphalactic response (shock).

The body protects itself against potentially injurious toxic substances through a complex process called metabolic detoxification. Nearly every organ in the body contains specific enzymes that participate in the detoxification process and the message for the process is buried in the genes.

Individuals vary greatly in detoxification abilities because of inheritance factors. One person could have a mild reaction to toxic exposure and another, due to genes, can have a 3- to 5-fold increase in toxic reaction which ultimately develops into a disease condition. The liver is the major organ of detoxification. If your liver is impaired from alcohol, there will be altered detoxification and other complications with food and drug tolerance.

If a person who carries a specific detoxification-altering genetic sensitivity also has a poor diet inadequate in essential nutrients, the person can be at greatly increased risk of adverse reactions to these substances. So, then, the question becomes – how your body will detoxify substances before they cause injury and depends on the complex array of protective detoxification enzymes (buried in the genes.) Manufacture of those enzymes is determined not only by your genetic hardwiring, but also as a consequence of foods you eat and the nutrients they contain. As an example, people who are poor detoxifiers have increased risk of developing Parkinson’s or Alzheimer disease.

A few nutrients that play a role in promoting proper detoxification function are the amino acid glycine, the B-complex vitamin pantothenic acid, the sulfur-containing amino acids, taurine and cysteine, and the minerals magnesium, selenium and zinc as well as the substance glutathione.

Some genetic characteristics are “constitutional,” which means the expression of the genes that encode for these characteristics is not easily modified by changes in diet, lifestyle or environment. Other genetic characteristics, however, are “inducible”: their expression can be activated or suppressed by dietary, environmental or lifestyle exposures.

Some scientists say different individuals have receptors that react differently – genetic variations explain why two people can eat exactly the same diet and respond very differently to it—one maintaining his weight, for example, and the other ballooning.
This same analogy can be made with regard to foods, vitamins, minerals and toxins. Everyone is going to react differently.
At the heart of philosophical nutrigenomics is the controversy of biological relevance of race – even it’s very existence – is hotly debated.

Consider this familiar example:
If you're of Northern European ancestry, you can probably digest milk, and if you're Southeast Asian, you probably can't. In most mammals, the gene for lactose tolerance switches off once an animal matures beyond the weaning years. Humans shared that fate as well—until a mutation in the DNA of an isolated population of Northern Europeans around 10,000 years ago introduced an adaptive tolerance for nutrient-rich milk. The likelihood that you tolerate milk depends on the degree to which you have Northern European blood.

''That, essentially, is the model—a very dramatic one,'' says Jim Kaput, the founder of NutraGenomics, a biotechnology company. ''As humans evolved, and as our bodies interacted with foods on each of the continents, we sort of self-selected for these naturally occurring variants. And certain populations have variants that, when presented with Western-type food—which is usually fatty and overprocessed and high in calories—pushes them toward disease rather than health.''

Plenty of examples bear out this ill fit between certain cultures and certain diets -- suggesting, if not quite proving, some interplay of genes and nutrition: the Japanese who relocated to the United States after World War II soon saw their cholesterol levels soar.

The Alaskan Inuit, whose metabolism was perfectly suited to moving around all day, looking for high-fat food, were suddenly saddled with an evolutionary disadvantage when they began living in heated homes and traveling on snowmobiles, and they now show high levels of obesity, diabetes and cardiovascular disease. The Masai of East Africa have developed new health problems since they abandoned their traditional cattle-meat-and-blood-and-milk diet for corn and beans.


The cradle of nutrigenomics is the cradle of humankind itself: the original migration out of Africa created widely separated subpopulations with distinct collections of gene variants.

The members of each subpopulation tend to respond similarly to diet and environmental conditions. But the genetics of race is an inexact science. And since many people have ancestors from different continents—making them a genetic admixture—the data are rarely clean-cut. In other words, ethnicity is relevant to nutritional genomics, but only as a starting point. Which is why the idea of sorting ourselves by race and pursuing a diet consistent with the original continental diet isn't going to be very helpful. And why, in fact, the customized diets of most people's perfect genomic future will probably not be all that different from one another.


Mainstream scientific researchers are finally turning their attention to what Metabolic Typing researchers have been piecing together over the last 100 years—namely, that the key to a healthy diet is not what some "diet expert" says, or what works for your friend, or what you read about in the " latest and greatest" column of your favorite health and fitness magazine.

Rather, the secret to good health and what constitutes a good diet lies in discovering and defining your own genetically-based biochemical and metabolic individuality and eating accordingly. Let's take a look at what the article's author called his "blue-skying" and compare it to what's available here and now today through Metabolic Typing.


"Nobody is eating exactly what you are. Your diet is uniquely tailored. It is determined by the specific demands of your genetic signature, and it perfectly balances your micronutrient and macronutrient needs." Metabolic Typing researchers couldn't agree more. Your nutritional requirements are indeed dictated by your genes, not whim, fancy, theory, belief, wishful thinking, arm-chair nutritionists, popular writers or even so-called expert opinion.

Human beings have inhabited almost every corner of our planet. Except for very recent times, people were born, lived their lives and died in the same locality. Over countless generations, forces of natural selection, genetic mutation, and survival of the fittest assured that inhabitants of a region became perfectly adapted to the foods naturally available in their locality. The kinds of foods available in turn were dictated by geography and climate.
Notably, although the natural diets of indigenous cultures from all over the world varied tremendously, each local population was perfectly healthy. Of greater significance, when people left their indigenous diet and adopted foods from another culture, their natural good health eroded.


Thus, the adage of one man's food being another's poison is literally true. In this sense, there are no good foods, and there are no bad foods, except relative to each person's Metabolic Type. The notion that there is one diet that is right for everyone has neither a logical nor, as the Genome Project is revealing, a scientific basis. Whether it is the Atkins Diet, McDougall Diet, Ornish Diet, Zone Diet or any other diet you can think of, the days of the one-size-fits-all diet are numbered.

Every nutrient has specific stimulatory and inhibitory effects on the body's regulatory control systems. If nutrition has the power to heal, it also has the power to do harm if used improperly. A nutrient that can rid one person of a health problem can actually cause it in another person of a different Metabolic Type.


"…diet is a big factor in chronic disease, responsible, some say, for a third of most types of cancer. Dietary chemicals change the expression of one's genes and even the genome itself. And -- here's the key—the influence of diet on health depends on an individual's genetic makeup. … A diet that's particularly out of balance, nutritional-genomics scientists say, will cause gene expressions that nudge us toward chronic illness—unless a precisely tailored ''intelligent diet'' is employed to restore the equilibrium.


Current Metabolic Typing research has revealed a lot more to this story than is suggested here. Through Metabolic Typing, we have learned that any given nutrient actually behaves differently in different Metabolic Types. This means that ultimately the effect of a nutrient on someone has more to do with the type of metabolism a person has than with the inherent qualities of the nutrient itself.


For example, in one Metabolic Type, calcium will have a stimulatory, acidifying effect, while in a different Metabolic Type, the same calcium will have a sedating, alkalinizing effect. We now know that fruits and vegetables, long believed to have an alkaline impact on the body, will actually acidify certain Metabolic Types, and that meat will alkalinize instead of acidify certain Metabolic Types. This discovery changes everything and shatters many of the traditional, allopathic ways of practicing nutritional science.

In order to be successful, you must treat the person who has the disease, the Metabolic Type, before you treat the disease that has the person. More importantly, you must know your Metabolic Type before you can know how nutrients behave in your metabolism as compared to someone else's.
"…since many people have ancestors from different continents—making them a genetic admixture—the data are rarely clean-cut.

In other words, ethnicity is relevant to nutritional genomics, but only as a starting point. Which is why the idea of sorting ourselves by race and pursuing a diet consistent with the original continental diet isn't going to be very helpful. And why, in fact, the customized diets of most people's perfect genomic future will probably not be all that different from one another. Kaput estimates that the middle 60 percent of the bell curve are probably not going to need to deviate too much from the basic fruit-and-vegetable-heavy diet recommended by the Department of Agriculture."

Knowing your family tree is not that helpful. Each of us carries genetic influences from countless ancestors from time immemorial. What genes come to the fore in an individual is really a matter of a kind of genetic roulette.

We see routinely that even within the same family, there can be dramatic variations of the Metabolic Type requirements between siblings. If one child tends to be lean, energetic and thriving while the other child tends to be overweight, slow and failing, the chances are very high that the diet is right for the first child's Metabolic Type but very wrong for the second child's Metabolic Type.

As a workable concept, ''eat right for your genotype'' may be a decade or two —or more—down the road.

If that's a definition of the future, then the future is now! Metabolic Typing analyses are currently available that can precisely determine the proper diet and supplementation for each person's Metabolic Type. There is no need to wait 10 years to obtain that kind of information.

Bottom line: you can eat the best organic foods, drink plenty of purified water, get sufficient rest, exercise until you're "blue in the face," and take the finest supplements money can buy, but if you don't eat right for your Metabolic Type and take supplements accordingly, you're only wasting your time and money. And as the genome research is revealing, you might even be doing yourself some harm.
End of excerpts.

Resources:
Genetic Nutritioneering
Jeffrey S. Bland, PhD
Keats Publishing - 1999
ISBN 0-87983-921-X

Weston Price Foundation
May 14, 2003
What your Genes Want You to Eat
Bruce Grierson

Reply Quote

Cilla,

Below is one of the articles detailing the results of the Chinese study on this. This mutation concerned chromosome 11. This is followed by another describing a mutation on chromosome 10. And finally is an abrstract of an article by David Van Wagoner of the Cleveland Clinic that addresses how this fits in with AF in general.

Study of four generations of a Chinese family with autosomal dominant
hereditary atrial fibrillation (AF) has revealed a single missense
mutation on chromosome 11 as a cause of this disorder.
Based on this finding, the authors of the study, which is published
in the January 10th issue of Science, suggest that potassium channel
blockers may be of use in the treatment of some patients with AF.
Drs. Yi-Han Chen of Tongji University and Shi-Jie Xu of the Chinese
National Human Genome Center, both in Shanghai, and their colleagues
performed microsatellite whole-genome screening on samples from 44
living members of the family, 16 of whom were affected by familial AF.
They identified a missense mutation at nucleotide 418 of the KCNQ1
gene, which encodes a potassium channel subunit, in all 16 affected
family members and 1 as-yet-unaffected family member. The mutation
was absent in 188 healthy control subjects, the report indicates.
By expressing the mutant gene in COS-7 cells and performing whole-
cell patch-clamping, the research team identified the resulting
alteration as a gain of potassium channel function, which "is likely
to initiate and maintain AF by reducing action potential duration and
effective refractory period in atrial myocytes," they write.
"The mutation in KCNQ1 causes a marked enhancement of its function,
tips the normal balance of the process, and renders the cardiac
myocytes more susceptible to atrial fibrillation," Drs. Chen and Xu
commented in a press statement.
The researchers note that this mutation was absent from 6 other
hereditary AF families and 19 sporadic idiopathic AF patients, and
that a 1997 report had identified an abnormality on chromosome 10 in
other affected individuals. Thus, "familial AF is likely to be
genetically heterogeneous," they conclude.
Science 2003;299:251-254


Genetics of cardiovascular disease with emphasis on atrial fibrillation.

Brugada R, Brugada J, Roberts R.

Department of Cardiology, Baylor College of Medicine, Houston, Texas 77030, USA.

Cardiology has embraced the techniques of molecular genetics later than other medical disciplines but is now completely submerged in the genetic mapping of cardiac diseases. The techniques of molecular biology, and in particular, their application to the genetics of inherited diseases, have brought the clinician and the scientist together in an unparalleled dependence. The chromosomal mapping of genes responsible for disease requires the identification of families with inherited diseases. This step involves the cooperation of the clinician. In order to continue improving our understanding of the molecular basis, it is imperative to raise the clinician awareness of the role of genetics in cardiac diseases. Arrhythmias can also have a familial origin and it is not generally appreciated that atrial fibrillation could be inherited. In the last two years, we have identified more than 100 families all over the world with individuals affected by the familial form of the disease. With the techniques of genetic mapping we have identified an area on chromosome 10 that carries a gene causing the disease in some of the families and there is ongoing research to identify the specific mutation. The clinician/scientist relationship has just started and the application of the discoveries in molecular genetics will probably have a direct role on how to approach medicine in the future, from prevention of diseases in patients carrying the susceptibility genes to gene therapy in those individuals with the disease.
Science 2003;299:251-254


Molecular basis of atrial fibrillation: a dream or a reality?

Van Wagoner DR.
Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA. vanwagd@ccf.org

AF is a difficult disease to treat because of the numerous (ischemic, metabolic, inflammatory, structural) mechanisms contributing to its etiology. AF persistence requires both an adequate tissue substrate for reentrant activity and triggers to initiate the arrhythmia. In a few interesting instances, AF may have a monogenic cause. Although there are common electrophysiologic characteristics of myocytes from a variety of AF models and clinical presentations, it is unrealistic to expect that all patients will respond equally to the same interventions. Thus, patients with AF of an inflammatory etiology may respond better to anti-inflammatory therapies, whereas those with enlarged atria secondary to valvular disease may require surgery. Some may respond better to ablation than others. However, the heterogeneity of the substrate does not negate the value of searching for the underlying molecular mechanisms. As we begin to comprehend these mechanisms in greater detail, the dream of using individualized rational therapies will come closer to reality.
J Cardiovasc Electrophysiol. 2003 Jun;14(6):667-9

PC

Thanks, Fran and Jackie, I appreciate your input.

Fran, I doubt that my mom's family used pesticides, but don't know for sure.
I do know that my dad used "Seven" a white powery pesiticide on his garden. I don't know, however, what or if anything, my mom's sister used/uses on hers.

Jackie, I appreciate all the info & plan to study what you have written & will attempt to make some lifestyle adjustments. My hope is to get off all this medication and if I can do that without having an ablation, that is certainly a pleasant thought.

Have either of you had a PVI?

Thanks, PC, I'm going to pass this bit of information on to all my family members and my EP. I haven't discussed the family issue with my current EP, but plan to do so. Perhaps, this clan can be included in a study. I'm game to be anyone's guinea pig if it will advance knowledge and/or treatment of this frustrating condition.

Cilla, the 'seven' that you remember was probably 'Sevin', a tradename for carbaryl, if i remember correctly. Nasty stuff. Organic gardening is a real good idea for this and other reasons. Personally, i never put anything on garden vegetables that i would not want for a salad dressing. Otherwise, what's the point of raising your own?
PeggyM

Cillia - Yes - I had PVI in 11/03. Seem to be fine now. You can go to the Search box at the top of this page and do an Author Search for Jackie.... I've posted prolifically on my experiences leading up to and after PVI.

Happy researching! Jackie

SEVIN (Carbaryl)

TRADE OR OTHER NAMES

Product names include Carbamine, Denapon, Dicarbam, Hexavin, Karbaspray, Nac, Ravyon, Septene, Sevin, Tercyl, Tricarnam, and Union Carbide 7744.

INTRODUCTION

Carbaryl is a wide-spectrum carbamate insecticide which controls over 100 species of insects on citrus, fruit, cotton, forests, lawns, nuts, ornamentals, shade trees, and other crops, as well as on poultry, livestock and pets. It is also used as a molluscicide and an acaricide. Carbaryl works whether it is ingested into the stomach of the pest or absorbed through direct contact. The chemical name for carbaryl is 1- naphthol N-methylcarbamate.

Carbaryl is formulated as a solid which varies from colorless to white to gray, depending on the purity of the compound. The crystals are odorless. This chemical is stable to heat, light and acids under storage conditions. It is non-corrosive to metals, packaging materials, or application equipment. It is found in all types of formulations including baits, dusts, wettable powder, granules, oil, molassas, aqueous dispersions and suspensions (13).

Carbaryl is a general use pesticide.

TOXICOLOGICAL EFFECTS

ACUTE TOXICITY

Carbaryl is moderately to very toxic, and is labeled with a WARNING signal word. It can produce adverse effects in humans by skin contact, inhalation or ingestion. The symptoms of acute toxicity are typical of the other carbamates. Direct contact of the skin or eyes with moderate levels of this pesticide can cause burns. Inhalation or ingestion of very large amounts can be toxic to the nervous and respiratory systems resulting in nausea, stomach cramps, diarrhea and excessive salivation. Other symptoms at high doses include sweating, blurring of vision, incoordination, and convulsions. About fifty cases of occupational or accidental illnesses due to exposure to carbaryl have been reported, but no fatalities have been documented. The only documented fatality from carbaryl was through intentional ingestion.

The oral LD50 of carbaryl ranges from 250 mg/kg to 850 mg/kg for rats, and from 100 mg/kg to 650 mg/kg for mice (12, 13). The inhalation LC50 for rats is 0,005 to 0.023 mg/kg (13). Low doses can cause minor skin and eye irritation in rabbits, whose dermal LD50 has been measured at greater than 2,000 mg/kg (12). Technical carbaryl has little potential for skin or eye irritation.

Occupational workers have the greatest potential for exposure through inhalation or through the skin. The general public's highest risk of exposure is through ingestion of contaminated food (14).

CHRONIC TOXICITY

Athough it may cause minor skin and eye irritation, carbaryl does not appear to be a significant chronic health risk at or below occupational levels. Male volunteers who consumed low doses of carbaryl for six weeks did not show symptoms, but tests indicated slight changes in their body chemistry (12).

Reproductive and Teratogenic Effects

No reproductive or fetal effects were observed during a long-term study of rats which were fed high doses of carbaryl (12). The evidence for teratogenic effects due to chronic exposure are minimal in test amimals. Birth defects in rabbit and guinea pig offspring occurred only at dosage levels which were highly toxic to the mother. A 1980 New Jersey epidemiological study found no evidence of excess birth defects in a town sprayed with carbaryl for gypsy moth control. There is only limited evidence that carbaryl causes birth defects in humans. The EPA has concluded that carbaryl does not pose a teratogenic risk to humans if used properly (16). [Reality Check: No pesticide is safe even when used according to the label - FIFRA]

Mutagenic Effects

Numerous studies indicate that carbaryl poses only a slight mutagenic risk (8, 12). However, carbaryl can react with nitrite under certain conditions to give rise to N-nitrosocarbaryl. Nitrosocarbaryl has been shown to be highly mutagenic at low levels in laboratory test systems. This may be a concern to humans because there is a possibility that carbaryl, a pesticide, and nitrite, a substance found in food additives and in human saliva, may react in the human stomach to form nitrosocarbaryl (2, 8). Carbaryl has been shown to affect cell mitosis (cell division) and chromosomes in rats (13).

Carcinogenic Effects

Carbaryl has not caused tumors in ten longterm and lifetime studies of mice and rats. Rats were administered high daily doses of the pesticide for two years, and mice for eighteen months, with no signs of carcinogenicity (3). However, N-nitrosocarbaryl, formed by the reaction of carbaryl and nitrite, has been shown to be carcinogenic in rats at high doses (7). Also, mice exposed to carbaryl in the product, tricaprylin, for four weeks each, developed lung tumors (12).

Organ Toxicity

Ingestion of carbaryl affects the lungs, kidneys and liver. Inhalation will also affect the lungs (14, 17). Nerve damage can occur after administration of high doses for 50 days in rats and pigs (12). Several studies indicate that carbaryl can affect the immune system in animals and insects. These effects however have not been documented in humans.

Fate in Humans and Animals

Most animals, including humans, readily break down carbaryl and rapidly excrete it in the urine and feces. Workers occupationally exposed by inhalation to carbaryl dust excreted 74% of the inhaled dose in the urine in the form of a breakdown product (13). This is consistent with information on other species which excreted nearly three quarters of a dose in their urine within 24 hours of administration (14). The metabolism of up to 85% of carbaryl occurs within 24 hours after administration (13).

ECOLOGICAL EFFECTS

Carbaryl is lethal to many nontarget insects. The pesticide is more active in insects than in mammals. The destruction of honeybee populations in sprayed areas is sometimes a problem. Carbaryl is moderately toxic to aquatic organisms, such as rainbow and lake trout, bluegill, and cutthroat. It is also moderately toxic to wild bird species, with low toxicity to Canada geese (12).

Accumulation of carbaryl can occur in catfish, crawfish, and snails, as well as in algae and duckweed. Residue levels in fish were 140 fold greater than the concentration of carbaryl in water. In general, due to its rapid metabolism and rapid degradation, carbaryl should not pose a significant bioaccumulation risk in alkaline waters. However, under conditions below neutrality it may be significant (14). [Reality Check: Why is the word "should" used. This is not a guessing game.]

ENVIRONMENTAL FATE

Carbaryl has a short residual life on treated crops. The insecticide remains at the application site, where it is slowly taken into the plant and metabolized. Insecticidal properties are retained for 3-10 days. Loss of carbaryl is due to evaporation and uptake into plants. Breakdown by sunlight does not appear to be significant.

Degradation of carbaryl in the soil is mostly due to sunlight and bacterial action. It is bound by organic matter and can be transported in soil runoff. Carbaryl has a half-life of 7 days in aerobic soil and 28 days in anaerobic soil (9). Degradation of carbaryl in crops occurs by hydrolysis inside the plants. It has a short residual life of less than two weeks. The metabolites of carbaryl have lower toxicity to humans than carbaryl itself. The breakdown of this substance is strongly dependant on acidity and temperature.

In pond water, carbaryl is broken down by bacteria through chemical processes. Evaporation does not occur. Carbaryl has a half-life of from 1 to 32 days in pond water. In a stream, carbaryl that had washed in from forest spraying, decayed to 50% within a 24 hour period. It has been shown to degrade more slowly in the presence of mud in aquatic habitats. Carbaryl has been detected in groundwater in three separate cases in California.

Carbaryl has a half-life in the air of one to four months. Crops, shade trees, shrubs and other vegetation in bloom should not be sprayed with carbaryl as bee kills are possible.

PHYSICAL PROPERTIES AND GUIDELINES

Carbaryl is a solid which varies from colorless to white or gray, depending on the purity of the compound. The crystals are odorless. Carbaryl is stable to heat, light and acids. It is not stable under alkaline conditions. It is non-corrosive to metals, packaging materials or application equipment.

Gee Whiz, Fran & PeggyM, that is scarey!

Sevin...I'm sure that is what I remembered, not seven. I know my dad was very particular when he used this insecticide...seems he and mom wouldn't pick the vegetables for some time afterwards. Gardening was never "my thing", so I didn't pay a lot of attention...just ate the food once it was cooked.

Everytime I'd get in the garden, I'd start itching and scratching...allergic to everything...so I was made to do the housework, which was fine with me!
I'd rather wax a floor any day (on my hands and knees back then) than sweat and itch and scratch. :-) That was miserable.

Jackie,

Thanks, I'll check out your posts on the PVI.