Nov 22 2012

Banned Additives

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The food and chemical industries have said for decades that all food additives are well tested and safe. And most additives are safe. However, the history of food additives is riddled with additives that, after many years of use, were found to pose health risks. Those listed below have been banned. The moral of the story is that when someone says that all food additives are well tested and safe you should take their assurances with a grain of salt.


Glossary

ANTIOXIDANTS retard the oxidation of unsaturated fats and oils, colorings, and flavorings. Oxidation leads to rancidity, flavor changes, and loss of color. Most of those effects are caused by reaction of oxygen in the air with fats.
CARCINOGEN is a chemical or other agent that causes cancer in animals or humans.
CHELATING AGENTS trap trace amounts of metal atoms that would otherwise cause food to discolor or go rancid.
EMULSIFIERS keep oil and water mixed together.
FLAVOR ENHANCERS have little or no flavor of their own, but accentuate the natural flavor of foods. They are often used when very little of a natural ingredient is present.

THICKENING AGENTS are natural or chemically modified carbohydrates that absorb some of the water that is present in food, thereby making the food thicker. Thickening agents “stabilize” factory-made foods by keeping the complex mixtures of oils, water, acids, and solids well mixed.

Cancer Testing

Chemicals usually are tested for an ability to cause cancer by feeding large dosages to small numbers of rats and mice. Large dosages are used to compensate for the small number of animals that can be used (a few hundred is considered a big study, though it is tiny compared to the U.S. population of more than 300 million). Also, the large dosages can compensate for the possibility that rodents may be less sensitive than people to a particular chemical (as happened with thalidomide). Some people claim that such tests are improper and that large amounts of any chemical would cause cancer. That is not true. Huge amounts of most chemicals do not cause cancer. When a large dosage causes cancer, most scientists believe that a smaller amount would also cause cancer, but less frequently.
It would be nice if lower, more realistic dosages could be used, but a test using low dosages and a small number of animals would be extraordinarily insensitive. It would also be nice if test-tube tests not using any animals were developed that could cheaply and accurately identify cancer-causing chemicals. While some progress has been made in that direction, those tests have not proven reliable. Thus, the standard high-dosage cancer test on small numbers of animals is currently the only practical, reasonably reliable way to identify food additives (and other chemicals) that might cause cancer.
The Delaney Clause is an important part of the federal Food, Drug, and Cosmetic Act. That important consumer-protection clause specifically bans any additive that “is found to induce cancer when ingested by man or animal.” The food and chemical industries are seeking toweaken or repeal that law.
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Research.

1. Brain Damage Detected in Children with Attention Deficit Disorder
and Learning Disabilities
  (
Information Compiled byRichard W. Pressinger, M.Ed.)

University of South Florida

Graduate Student Research Project – Special Education Department

Environmental Causes of Learning Disabilities and Attention Deficit Disorder

There has been a growing amount of medical research identifying various types of brain damage in children with attention deficit disorder, hyperactivity and learning disabilities. The nationwide increases being observed in these child disorders is being explained by many scientists as resulting from environmental and chemical exposures during pregnancy.  These include the obvious culprits such as alcohol and cigarette use, but serious new concerns are being raised by government and university research showing many common household chemicals are also being found to damage brain development during pregnancy. These include cleaning chemicals, home pesticide use, cosmetic chemicals (such as nail polish and perfume), prescription medications, artificial food additives, chemicals in plastics, synthetic perfume and cologne ingredients, job chemicals, and the pesticide chlordane (found as a contaminant in the air of most U.S. homes built before 1988) .

In a summary report entitled the Principles of Developmental Neurotoxicity, from the National Centerfor Toxicological Research (7), it was stated:

“According to the Congressional Office of Technology Assessment’s recent report on neurotoxicity, among the known or suspected causes of brain-related disorders are exposure to chemicals including pesticides, therapeutic drugs, food additives, foods, cosmetic ingredients and naturally occurring substances

If we are to agree with this research that repeated exposure to certain consumer chemicals can weaken or damage brain growth and result in increases in mental retardation, learning disabilities or behavior disorders, then it is quite plausible to expect a corresponding subtle decrease in mental function of our above average students, but detecting such effects will be extremely difficult. Also, it is important to realize that a decrease in mental capacity is not strictly limited to academic function. The human brain is also responsible for all other mental functions including talent, personality, sense of humor, articulation skills and even conscience oriented behavior. Therefore, it is quite realistic to suspect the potential for these areas of the human brain to be compromised by the same compounds being found to cause learning disabilities and attention deficit disorder.

Many researchers now agree, as will be addressed in this paper, that subtle brain disorders can be the cause of learning disabilities, hyperactivity, attention deficits and even propensity toward behavior problems such as aggression and behavior “void of conscience.” In fact, it has been only recently that abnormalities in brain structure have been found in people with learning disabilities and attention deficit disorders.

Examples of visually detected brain damage in learning disability and attention deficit individuals are discussed in three different research projects below. One incident reported by Dr. Albert Galaburda at Harvard  Medica  School (9), investigated the unfortunate accidental death of an individual with known serious reading learning disabilities in school. At age 18 he had a reading level of fourth grade despite a 105 intelligence score on the Stanford- Binet test. Because of this discrepancy in intelligence and reading level, he was given the diagnosis of Developmental Dyslexia. He also had moderate math difficulties and mild difficulties with right-left orientation and finger recognition.

At age 20, six days after beginning his first paying job, the patient died suddenly as the result of an accidental fall from a great height. The cause of death was multiple internal injuries producing massive bleeding. An autopsy of the brain showed no evidence of trauma or other gross abnormalities according to the researchers. After receiving permission from the man’s parents, the physicians conducted a thorough examination of the man’s brain structure. The results are seen in the picture at left. The top picture shows a normal brain with good column organization and larger cells. The bottom (learning disabilities) brain shows poor organization, smaller cells.

The researchers stated the area of the learning disability brain shows abnormalities also to a location in the brain called the “Wernicke’s Speech Area,” and appears to play a particularly important role in language function. 

The researchers concluded by saying,

“The findings reported here lend support to the notion that language-relevant areas in the brains of patients with developmental dyslexia (a type of learning disability) may be small in the two cerebral hemispheres, a possibility which is also supported by findings of curtailed linguistic processing by both hemispheres in dyslexic patients.”

 

2. Learning Disability & Attention Deficit Children Have

Lower Blood Flow in Some Brain Areas

A method for determining abnormalities in the brains of living learning disability (LD) and attention deficit disorder (ADD) children was used in a study of 13 LD and ADD children at the Department of Neurology, Kennedy Institute in Denmark(13). The study was conducted using a method called emission computed tomography which takes a picture of a “slice” of the brain after the child inhales a very small amount of a radioactive substance called xenon 133. The picture then allows the scientists to visually see how much blood is being used by different parts of the brain (a greater illumination in the picture represents increased blood flow). This also represents the level of metabolic activity in the brain areas. After comparing the photographs taken of all children the investigators stated,
“The cerebral blood flow distribution was abnormal in both hemispheres (both sides of the brains) in all patients, as compared with the mean cerebral blood flow distribution of nine normal children…. All 11 patients with attention deficit disorder (ADD) have hypoperfusion (low blood flow) in the mesial frontal lobes, in particular in the white matter…. Methylphenidate hydrochloride (Ritalin)increased perfusion (blood flow) in the central region, including the mesencephalon and the basal ganglia, and decreased perfusion of motor and primary sensory cortical areas…. Hypoperfusion and low metabolic activity may be due to subtle morphologic abnormalities not detectable with computed tomography but with important pathogenetic implications.”
To bring this into perspective and without the multi-syllable medical terms, the investigators found lower levels of blood in Attention Deficit Disorder children in the area of the brain that is just behind the central forehead going in about an inch or two. When ritalin was given and measurements taken again, normal blood flow was created, thereby providing a biological explanation of why children improve after taking Ritalin.

3. Glucose Metabolism Defective in Attention Deficit Hyperactive Disorder Syndrome

In a study of hyperactive students conducted at the National Institute of Mental Health, reported in the November 15, 1990 New England Journal of Medicine, researchers found the brain cells of these individuals were using lower levels of glucose than other non-hyperactive people (glucose is the primary fuel used by the brain cells which enables them to function).
In a study of hyperactive students conducted at the National Institute of Mental Health, reported in the November 15, 1990 New England Journal of Medicine, researchers found the brain cells of these individuals were using lower levels of glucose than other non-hyperactive people (glucose is the primary fuel used by the brain cells which enables them to function).
In conclusion, the investigators stated:
“Glucose metabolism, both global and regional, was reduced in adults who had been hyperactive since childhood. The largest reductions were in the pre-motor cortex and the superior prefrontal cortex – areas earlier shown to be involved in the control of attention and motor activity.”
Since there is common agreement among researchers and medical professionals that learning disabilities and attention deficits can, in fact, result from subtle brain damage caused by a variety of common environmental chemical exposures in today’s “modern” society, it is imperative to organize this information into an easy to read format.  This will give couples who desire to have children a far better chance of having a child that is neurologically healthy  without the complications accompanied by attention deficit disorder or learning disabilities.  This has been the goal of this research project.
4. An Interesting Observation from an Older Medical Journal
In the 1975 Canadian Psychiatric Association Journal, Dr. R. Denson discusses the increase societyhas observed in children with hyperactive disorders.
“The hyperkinetic syndrome is often encountered at the present time, although the textbooks of thirty years ago make scant reference to it. Henderson and Gillespie characterized hyperkinetic disease as one of the “very rare” psychoses of childhood (1), and Kanner, who devoted only five sentences to “the restless, fidgety, hyperkinetic child”, omitted hyperactivity altogether when discussing the causes of scholastic problems (2). Recent estimates imply that persistent, disruptive hyperactivity occurs in from five to ten percent of North American elementary school children and Wender (5) who depicts hyperactivity as “the single most common behavioral disorder seen by child psychiatrists”, has calculated that there are approximately five million hyperactive children in the United States, where more than 150,000 youngsters are receiving treatment with stimulant drugs for hyperkinesis and similar disorders.”

 

5. Fathers’ Drinking Lowers Birth Weight of Babies
    SOURCE: Miami Herald, June 19, 1986, pg. 24a
Fathers who were considered “regular” drinkers had babies that weighed over one-third of a pound less than babies whose fathers were only “occasional” drinkers. The study was outlined in the June 19, 1986 Miami Herald and reported in the New England Journal of Medicine. The study was conducted by epidemiologist Ruth Little and Charles Sing at the University of Michigan. As part of the study, the researchers questioned 377 mothers about their drinking and smoking habits before and during pregnancy, and about the drinking habits of their husbands in the month before they conceived. To their surprise, the researchers found that the fathers who drank an average of two drinks a day per month had the lower weight babies.
 
Dr. Little stated,“The father’s drinking was significantly related to the infant’s birth weight independently of the mother’s alcohol, tobacco and marijuana use. There are lots of theories. If you expose the reproductive material to enough of anything, you’ll damage it and the offspring will be damaged.”The research did not investigate whether this loss of weight occurred in the child’s body mass or brain weight.Dr. Ruth Little and Dr. Charles SingUniversity of MichiganMiami Herald, page 24A, Thursday, June 19, 1986

 


6. MSG & Aspartame During Pregnancy 
Two Common Food Additives Show Potential for Causing Brain Damage at Normal Human Exposure Levels.  Environmental Neurotoxicology Research Project
University of South Florida, Tampa – 1997 Richard Pressinger (M.Ed.)

 

INTRODUCTION
There has been considerable media attention given to the harmful health effects of MSG over the past several years. The Food and Drug Administration (FDA) has also come out with its recent report that MSG is “safe” for most people except for those with serious asthma difficulties.
MSG is a flavor enhancer used by the food industry for several reasons. The primary reason for its use is that it increases the “perceived” taste of any item that contains MSG. For instance, when Campbell’s soup makes chicken soup, they found they would only have to add only about one-half as much chicken to their product while using MSG to achieve the same taste profile as as if they added no MSG but added twice the amount of chicken. As you can see the addition of MSG to consumer products increases the profit margin of companies that use it. Unfortunately, the use of MSG is not without consequence.
World production in 1976 was 262,000 metric tons per year. Studies by Reif-Lehrer (67 in Special Article) reported that 25% of a population sample who have been exposed to Chinese restaurant food exhibit at least some adverse symptoms.
Prior to the 1970’s, MSG was routinely added to baby food before the practice was stopped following government suggestions. Commenting on this issue, Dr. Olney, at the Department of Psychiatry, Washington University states,

According to an NAS ( National Academyof Science) Subcommittee, in considering the safety of added MSG in baby foods, one must remember that the levels added are small – not higher than 0.6 g%…. This means that one small jar of baby food (130 g) would provide about 0.78 g of MSG or 0.13 g/kg of body weight for a human infant weighing 6 kg. Based on our finding that an oral dose of 1 g/kg in the primate or 0.5 g/kg in the mouse is sufficient to destroy hypothalamic neurons, this leaves a 4 to 8 fold margin of safety for a human infant eating one jar, a 2 to 4 fold margin if two jars are eaten and so forth. This is substantially less than the 100-fold margin generally recommended to accommodate contingencies such as species or individual differences in susceptibility to the mechanism of a toxic compound.

In support of their assumption that human infants are invulnerable to MSG-induced brain damage, the NAS Subcommittee pointed to absence of behavioral manifestations in human infants given intravenous infusions of protein hydrolysates providing 0.3 g/kg/day of free glutamic acid. Our demonstration that MSG destroys hypothalamic neurons in monkeys as well as mice at intake doses lower than those required to produce acute behavioral manifestations points to a serious flaw in this line of reasoning. The subcutaneous injection of protein hydrolysate (0.2 cc) produces, in 10 day old infant mice, a hypothalamic lesion unaccompanied by behavior disturbances (22).”

There have been at least two other MSG studies using infant primates which found no significant brain lesions after MSG exposure (Abraham et al. (10). However, in criticism of these reports, Dr. Olney states that because of the “remarkable efficiency” with which degenerate elements are removed from the scene of MSG-induced lesion (minimal lesions are cleared from mouse brain within 12 to 18 hours), it is essential to examine the brain earlier than 24 hours (Dr. Olney’s studies examined at 3 and 5 hours). This is particularly true if, due to vomiting, the infant retained very little MSG, and therefore, sustained only a minimal lesion.
Infant Seizures Improve After MSG Removal
A child experiencing “innumerable seizures” at 6 months of age showed dramatic improvements after removal of MSG from the child’s diet. The case history, reported by Dr. L. Reif-Lehrer of Harvard Medical School in the journal Federal Proceedings, showed the child did not respond to dilantin treatment but had symptoms “completely alleviated by a diet that excluded exogenously added glutamate.”
The child’s first seizures began at 6 months of age on October 14, 1971. For the next four months the child’s seizures continued even with treatment using dilantin, mysoline and pyridoxine. At 9 months of age the child was experiencing 100 or more seizures per day.
The following medical bibliography lists chronologically the events observed from removal of MSG from the child’s diet:

 

February 15, 1972

 

Physicians removed all MSG containing foods from the child’s diet

 

 

February 20, 1972

 

 

(Age 10.5 mo.)

 

 

No seizures for past 3 days, first free period since onset.
Reduction of anticonvulsants begun

 

 

March 20, 1972

 

 

(Age 11.5 mo.)

 

 

Off all anticonvulsants.
No seizures.

 

 

May 10, 1972

 

 

(Age 13 mo.)

 

 

Attacks 2-3 hr after surreptitious ingestion of pizza
(“Snitched” from the refrigerator with the help of an older brother).

 

 

August, 1972

 

 

(Age 17 mo.)

 

 

Several attacks after ingestion of family hog, locally prepared sausage later found to contain MSG.

 

 

February, 1973

 

 

(Age 2.0 years)

 

 

No attacks for 7 months.

 

 

August, 1973

 

 

(Age 2.5 years)

 

 

Deliberate trial of a spaghetti dinner with
commercially prepared sauce containing MSG.
Seizures within 3 hours, the first one in 1 year.

 

 

February, 1974

 

 

(Age 3.0 years)

 

 

Diet-watch continues.
No attacks since spaghetti trial in August 1973.

 

The child’s physician, Dr. M. G. Stemmermann, M.D., noted there were still no attacks as of September, 1975, except after annual test trials with an “MSG meal.” Commenting on this case, Dr. Reif-Lehrer states,
“The case of the child with shudders (seizures), as well as some of the symptoms reported in a questionnaire study in our laboratory indicates a very wide spectrum of sensitivity toward MSG and suggests that perhaps some individuals should avoid exogenously added MSG. In some individuals, glutamate (or some other chemical that results from glutamate ingestion) may be getting through the blood-brain barrier, or, e.g., to certain areas of the hypothalamus, and may result in undesirable effects….. One wonders, particularly in countries where the per capita consumption of MSG is high, if there is any possibility that any subtle nervous disorders or unexplained retinal pathology could be due to cumulative effects of MSG in individuals with pre-existing abnormalities that may make them more susceptible.”

Dr. Liane Reif-Lehrer,

Department of Ophthalmology, Harvard Medical School; Department of Connective Tissue Research, Boston Biomedical Research Institute

Federation Proceedings 1(11);2205-2212 (1976)

Obesity – Shorter Growth – and Reproduction Problems

From MSG Intake

To investigate the possibility of long term effects from MSG ingestion, Dr. Olney followed five litters of Swiss albino mice, consisting of 38 healthy animals, from birth to nine months of age. Twenty animals received injections of MSG daily from 1 to 10 days after birth, 18 control animals received no treatment.

The results showed MSG treated animals appeared stunted in growth and still remained shorter than controls on day 30. Of significant interest, animals treated with MSG continued to gain weight on unrestricted diets beyond the age of 5 months. Average weights of the 5 month old animals were 37 grams for the non-MSG treated and 57 grams for the MSG treated animals (see picture at right). It is important to point out that contrary to expectation, the “obese” MSG treated animals actually consumed less food than their thinner control counterparts, implying damage to the brain area responsible for controlling body weight. Mean per capita food consumption over the daily 4 hour measuring period was 2.5 grams for the controls and 1.7 grams for the MSG treated animals.

Also noted at 5 months, the MSG animals were quite lethargic as adults, and they lacked the sleekness of body coat seen in the controls. The reproductive capacity of the MSG females was also modified in that they repeatedly failed to conceive in spite of adequate exposure from 5 to 9 months of age.

In summary, Dr. Olney writes,

“These observations, linking MSG treatment of the neonatal mouse with a syndrome of manifestations, including skeletal stunting, marked adiposity, and sterility of the female, coupled with histopathological findings in several organs associated with endocrine function, suggest a complex endocrine disturbance. In view of the additional finding of lesions in regions of the brain thought to function as neuroendocrine regulatory centers, a unitary hypothesis might be constructed relating all or most of the findings to the neonatal disruptions of neuronal development in these centers…. The assumption that MSG is an entirely innocuous substance for human consumption has been questioned recently in view of its role in the Chines Restaurant syndrome. The finding that neuronal necrosis can be induced in the immature mouse brain by 0.5 mg/kg of MSG raises the more specific question whether there is any risk to the developing human nervous system by maternal use of MSG during pregnancy. The primate placenta maintains amino acids in consistently higher concentrations in the fetal circulation than those found in the maternal circulation, the ratio of glutamic acid being grater than 2:1. In fact, when high doses of phenylalanine were given to a pregnant rhesus monkey, the ratio of mother to fetus for this amino acid remained unchanged so that exceedingly high fetal blood levels resulted. The possibility that brain lesions could occur in the developing primate embryo in response to increased glutamic acid concentrations in the maternal circulation, therefore, warrants investigation.”

 

Dr. John W. Olney

Department of Psychiatry, Washington University SchoolMedicine, St. Louis, Missouri SCIENCE 164:719-721 (1969)

——————

Cigarette Smoking During PregnancyLinks to Learning Disabilities

–Attention Deficit Disorder – A.D.D. -Hyperactivity and Behavior Disorders

By Richard W. Pressinger, M.Ed.

Graduate Research Project – June 1998 – Special Education Department

University of South Florida, Tampa, Florida. email:

INTRODUCTION

Although the percentage of smoking in the general population is declining, the rate of this is slowest among women of childbearing age. The recent National Household Survey on Drug Abuse reported that among women of reproductive age, approximately one-third smoke cigarettes on a regular basis. These figures for the United States are within one or two percentages of those noted in Canadaand Sweden. In five surveys throughout the U.S., the extent of cigarette use by women during pregnancy in non-ghetto, urban regions has been reported to be between 22% and 30%. An additional recent statistic that bears upon the issue of smoking habits and pregnancy is that the proportion of heavy smokers has increased in the past decade, particularly among women. In Sweden, the proportion of heavy smokers has almost doubled while in Canada, the increase of heavy smokers was 57% among females versus 31% among males. This has important implications because the relationship between the consequences of maternal smoking and effects on the offspring appears to be dose related. Also of concern is that it is estimated by the Office of Smoking and Health that one-third to one-half of nonsmoking pregnant women are exposed to significant levels of involuntary or second hand smoke. Demonstrating the increased toxic insults today’s developing child has from cigarette smoke, figures show smoking has increased 3 to 4-fold from 1940 to the beginning of the 1980’s, although it has since then decreased somewhat (6).

It’s of interest to point out that textbooks written in the 1940’s and 50’s make very little reference to the hyperkinetic syndrome in school age children. In fact, Henderson and Gillespie (1) characterized “hyperkinetic disease”as one of the “very rare” psychoses of childhood. In other early textbooks, Kanner (2) gave only five sentences to “the restless, fidgety, hyperkinetic child”, and did not even discuss hyperactivity as a possible cause for scholastic problems. In contrast, textbooks beginning in the 1970’s give estimates that persistent, disruptive hyperactivity occurs in from five to 10 percent of North American elementary school children (3,4) and Wender (5), describes hyperactivity as “the single most common behavioral disorder seen by child psychiatrists.” Regarding these observations, the current authors stated:

“This apparent increase in prevalence (of hyperactivity) during the past thirty years has coincided with a wide expansion of cigarette smoking, particularly cigarette smoking by women. The child of smoking parents is continually exposed to the products of tobacco combustion and some of these are able to disrupt the normal activity of the central nervous system. Therefore, it seemed appropriate to investigate the prenatal and postnatal exposure of hyperkinetic children to tobacco smoke, and to compare it with the exposure of non-hyperkinetic control groups.”  

The results of their study are explained in the lead article summary below.


Smoking Mothers More Likely To Have

Hyperactive (ADHD) Children

SOURCE: Canadian Psychiatric Association Journal, Vol. 20:183-187, 1975

Mothers of “hyperkinetic” children were found to smoke an average of 14 cigarettes during pregnancy compared to only 6 cigarettes smoked on average for mothers of “normal” children. The study, conducted by the Department of Psychology at the University of Saskatoon, Canada, studied 20 children (18 boys, 2 girls) who were currently being treated with Ritalin for their hyperactivity. Although cigarette smoke contains many highly poisonous compounds, the researchers speculate that the accumulation of carbon monoxide in the fetal blood stream could lead to serious reductions in oxygen to the developing infant. It was found that the carboxyhemo-globin levels (hemoglobin that is carrying carbon monoxide instead of oxygen) was concentrating in the developing fetus reaching twice the levels of that in the mother. The potential for second hand smoke effects could also be a problem as it was found that after birth, mothers of hyperactive children consumed an average of 23 cigarettes per day compared to 8 cigarettes daily for the normal control mothers.

In summary the researchers stated,                                                                                                    

“The hyperkinetic syndrome is the result of several causes and the effect of any single agent is difficult to discern. Although the apparent association with heavy maternal smoking, in methylphenidate (Ritalin)-sensitive cases, does not predicate a causal connection, it does justify a careful assessment of the possible role of tobacco addiction in the etiology of this common disorder.”

R. Denson, M.D.,  J.L. Nanson, M.A.,   M. A. McWatters, R.N.

University of Saskatchewan, Canada


Child Test Scores Lower When Mothers Smoke

A Study of 2nd and 5th Grade Students

SOURCE: British Medical Journal, 4:573-575, 1973

This study of a very large sample of children gives insights into the real dangers of smoking during pregnancy. Known as the National Child Development Study, in Britain, there were over 9,000 children measured to determine the effects of their mother’s smoking either 0, 10, or more than 10 cigarettes per day during pregnancy. When each child reached 7 and 11 years, there were a number of tests given to evaluate math ability, reading ability and general physical measurements. Results showed children of mothers who smoked 10 or more cigarettes a day are on average 1.0 centimeters shorter and between three and five months behind in reading, mathematics, and general ability when compared to the offspring of non-smokers, after allowing for associated social and biological factors (see fig.1 & 2).

Below are the charts used by Dr. Butler and Dr. Goldstein to represent the damage to the child’s reading and math ability from the mother’s cigarette smoking.    

     Reading Ability & Smoking        Math Ability & Smoking

 

Dr. R. Butler, H. Goldstein, Bristol Royal Hospitalfor Sick Children
Smoking in Pregnancy and Subsequent Child Development

Auditory Processing Reduced in School Age Children Exposed to Cigarette Smoke

SOURCE: Neurotoxicology and Teratology, Vol. 16(3), 1994

The ability to process auditory information in a child relates to his ability to listen to what a teacher is saying, to follow directions or to remember what the teacher has said. Obviously, all of these skills are important for effective academic performance in school. This present study, carried out by Dr. Joel S. McCartney, Department of Psychology, CarletonUniversity, Ottawa, Canada, found overall poorer performance on central auditory processing tasks (SCAN) among 110, six to eleven year old children exposed to prenatal cigarette smoke. Maternal smoking during pregnancy was linearly associated with the poorer performance on the overall SCAN tests which assessed listening skills in a noisy background and the dichotic task, which required the child to attend to simultaneous information in both ears and is thought to be a measure of the child’s auditory maturation or developmental level. This task involves a greater degree of auditory processing, aspects of memory, and word discrimination. Also of interest, it was found that children exposed to passive cigarette smoke performed more poorly than children of non-smokers and equal to that found in children exposed to “light” prenatal smoking.

 

Drs. Joel S. McCartney, Peter A. Fried
Department of Psychology, Carleton University, Ontario. Canada
Central Auditory Processing in School-Age Children Prenatally Exposed to Cigarette Smoke

Math, Language, & Behavior Problems Elevated in Children of Smoking Parents

SOURCE: Neurotoxicology and Teratology, Vol. 13, 1991

Ninety-one children between the ages of six and nine years were tested for a wide range of developmental, academic and behavioral skills by researchers at the Department of Psychology, CarletonUniversity, Ottawa, Canada. This is one of the most thorough studies to date looking for harmful effects from cigarette smoke.

Children of nonsmoking mothers generally were found to perform better than the two smoking groups (active and passive) on tests of math ability, speech and language skills, intelligence, visual/spatial abilities and on the mother’s rating of behavior. The performance of children of passive smokers was found, in most areas, to be between that of the active smoking and nonsmoking groups. Some of the tests given included the Wechsler Intelligence Scale for Children-Revised (WISC-R), the Wide Range Achievement Test -Revised (WRAT-R) for measuring general reading, spelling and math ability and the Test of Language Development-Primary (TOLD), which measures grammatical understanding, the ability to imitate sentences and correctly produce speech sounds. The behavioral assessment was done by the Conners Parent Questionnaire, a behavioral symptom checklist, completed by the child’s mother. On the academic achievement tests, the mathematics score was the most lowered by active and passive cigarette smoking. The three main areas appearing more often in the Connors behavior rating scale were Hyperactivity, Conduct Problems and Impulsivity. Of significant interest, twice as many children in the active smoking group compared to the nonsmoking group were perceived by the mother as having problems in school. This is in agreement with five other studies showing children of active smokers have a higher incidence of misbehavior, poorer adjustment at school and increased activity levels. The nonsmoking group was rated as showing the best attention and cooperation.

 

Drs. Judy Makin, Peter A. Fried
Department of Psychology, Carleton University, Ottawa, Canada
A Comparison of Active and Passive Smoking During Pregnancy: Long Term Effects

Nicotine Damages Brain Cell Quality

SOURCE: Neurotoxicology and Teratology, 16(4) 1994

Human reports as well as animal studies have recorded accelerated motor activity, learning and memory deficits in offsprings of mothers exposed to nicotine during pregnancy. This study, conducted by Dr. T. S. Roy, Department of Anatomy, All India Institute of Medical Sciences, New Delhi, India, is the first to investigate actual physiological changes of the cerebral cortex of rats after prenatal nicotine exposure. Several groups of experimental rats were exposed to varying levels of nicotine reaching up to that experienced by a heavy smoker. Animals were examined at different periods after birth. Observable effects included significantly reduced thickness of the cerebral cortex, smaller cerebral cortex neurons, and reduced brain weight. Also noted was an overall decrease in “dendritic branching” (connections to other brain cells), as seen in the camera lucida drawings at right. The present study also shows that the greater the dose of nicotine, the greater the biological effects upon the offspring. This research provides an excellent biological model to support the many other studies linking increased hyperactivity, attention deficits, lower IQ, and learning disabilities in children with parents who smoked during pregnancy.

Dr. T. S. Roy

Department of Anatomy, All India Institute of Medical Sciences New Delhi, India

Effects of Prenatal Nicotine Exposure on the Morphogenesis of Somatosensory Cortex


 Severe Child Behavior Problems 
Linked to Mother’s Smoking
Linked to Mother’s Smoking

SOURCE: Associated Press –  Florida Today Newspaper, September 4, 1992

The more cigarettes a mother smoked during pregnancy, the greater the likelihood her child would demonstrate severe behavior problems as the child became older. Women who smoked at least a pack a day had children with twice the rate of extreme behavior problems – such as anxiety, conflict with others, or disobedience, when compared with children of non-smokers.

Smoking less than a pack a day also was shown to increase behavior problems, but the rates were not as high as for heavier smokers, the researchers found. The study was conducted by the Labor Department in which parents of 2,256 youngsters ages 4 to 11 were interviewed. The fathers smoking was not assessed in this study.

In a following September 4, 1992 Associated Press article describing the study, Dr. Michael Weitzman, the lead author stated, 

 

“We are aware of no other study to date that has investigated the relationship between maternal smoking and behavior problems in children.”
Associated Press – Reported in Florida Today, September 4, 1992

Smoking During Pregnancy Increases Conduct Disorders

SOURCE: Archives General Psychiatry, 54:670-676, July, 1997

More evidence on the connection between a mother’s smoking during pregnancy and increased risk of having a child with behavior disorders. Below is a direct quote of the summary of the 1997 journal article report in the Archives of General Psychiatry, 54:670, 1997.

Background: Previous animal and human studies have indicated that prenatal exposure to nicotine isassociated with adverse reproductive outcomes, including altered neural structure and functioning,cognitive deficits, and behavior problems in the offspring. Our study extends previous research onhumans by controlling a broad range of correlates of maternal smoking during pregnancy todetermine if smoking is associated with behavior problems in the offspring severe enough to qualifyfor DSM-III-R diagnoses. 

Method: Subjects were 177 clinic-referred boys, ages 7 to 12 years at the time of the first assessment, who underwent longitudinal assessment for 6 years using annual structured diagnostic interviews. Correlates of maternal smoking during pregnancy and previously identified demographic, parental, perinatal, and family risk factors for the disruptive behavior disorders were controlled in logistic regression analyses. 

Results: Mothers who smoked more than half a pack of cigarettes daily during pregnancy were significantly more likely to have a child with conduct disorder (odds ratio, 4.4; P=.001) than mothers who did not smoke during pregnancy. This association was statistically significant when controlling for socioeconomic status, maternal age, parental antisocial personality, substance abuse during pregnancy, and maladaptive parenting.

Conclusions: Maternal smoking during pregnancy appears to be a robust independent risk factor for conduct disorder in male offspring. Maternal smoking during pregnancy may have direct adverse effects on the developing fetus or be a marker for a heretofore unmeasured characteristic of mothers that is of etiologic significance for conduct disorder.

 

Lauren S. Wakschlag PHD; Benjamin B. Lahey PHD; Rolf Loeber PHD;
Stephanie M. GreenMS; Rachel A. Gordon MA; Bennett L. Leventhal MD
====================================================
Children Age 14 Still Show Harmful Effects

if Mothers Smoked During Pregnancy

SOURCE: Department of Public Health, University of Oulu, Oulu, Finland

Several thousand 14 year old children were included in a follow up study which found more health and academic problems among the children whose mothers smoked during pregnancy. This large study was conducted by the Department of Public Health, University of Oulu, Finland.

The study began with an assessment of 12,068 pregnant mothers in two northern provinces in Finland. A questionnaire given to the 12,000+ women showed 19.7% of the mothers smoked at the beginning of pregnancy. However, by the second month of pregnancy, 15.5% of the mothers were smoking for a total of 1,819 women. It was of these 1,819 women that the study of health and academic performance was conducted.

At the end of 1980 and early 1981, 11,780 of the original children (now age 14) were located for the follow up study. The questionnaire inquired on the children’s health, growth, school performance, various habits (smoking, drinking, participation in sports) and family conditions including father’s smoking history.

RESULTS

On the positive side, there were no significant differences between the groups in respect to “severe” mental retardation, diabetes, rheumatic diseases or other long term diseases, according to the questionnaire sent to the families or from information received from the school or national registers.

Asthma proportion was similar in both groups, about 2.1% of cases, however, the children of smokers did have over a 50% higher chance of being administered to the hospital for severe asthma reactions, 1.30% compared to .80% for the non-smokers.

In conclusion the researchers stated, 

“School performance of the smokers’ children was poorer than that of their controls when measured in terms of their mean ability on theoretical subjects and scored from 4 to 10 on the child’s school report, this trend being seen among both the boys and the girls and in all social classes The children of the smokers were more prone to respiratory diseases than the others. They were also shorter in length by nearly 1 centimeter (a little less than a half an inch) and their mean ability at school was poorer than among the controls for mothers who smoked 10 cigarettes and 20 cigarettes per day. The differences remained significant after adjusting for the mother’s height and age, social class as determined by the father’s occupation, number of older and younger children in the family and the sex of the child.”

Department of Public Health, University of Oulu, Oulu, Finland

1,819 Mothers Who Smoked During Pregnancy

 

Additional References
  • Henderson, D. K., Gillespie, R. D.: A Textbook of Psychiatry for Students and Practitioners; 6th edition. London, Oxford UniversityPress, p. 647, 1944
  • Kanner, L.: Child Psychiatry; 2nd Edition. Sprinfield, Charles C. Thomas, pp.418,541, 1948.
  • Vermont. Acta paedopsychiatr., ( Basel), 34:130-135, 1967, Huessy, H. R.:
  • Journal of Pediatrics, 78:985-990, 1971, Serotonin Concentrations In Whole Blood Of Hyperactive Children, Coleman, M.
  • Wender, P. H.: The Hyperactive Child. New York. Crown Publishers, pp. 3- 31, 1973
  • Population Dev. Reviews, 16:213-240, 1990,Tobacco’s Global Death March, Ravenhkolt, R. T. 
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