Environmental Influences: Whether it is through active behaviors or passive activity, humans are exposed to environmental risks affecting health and safety through a variety of interactions with their environment in everyday situations. A. Physical influences include toxins, nutrition, sick buildings, noise pollution, second-hand smoke, and lead. B. Social influences include violence, substance abuse, child-rearing practices, and poverty. A prevention activity to decrease aggression or violent behavior is teaching school-age children how to use appropriate social or pragmatic communication skills. C. Nutrition and Health. Nutrition’s contributions to primary conditions leading to communication disorders among adults are numerous. Diet accounts for one third of cancer risk. Prenatally, nutrition greatly effects the fetus. Transition Point: It is very important to consider the role that an individual’s culture plays in their involvement in any prevention efforts...
<number> The connection between toxic environmental exposures and neurodevelopment is an emerging area of concern. Exposures to environmental toxicants such as the heavy metals lead, mercury, hormone disrupters, PCBs, perchlorate and solvents such as alcohol, toulene and tobacco have all been proven to cause permanent DD. Other toxic exposures from the organophosphate and organochlorine pesticides, flame retardants, and plastics similarly disrupt brain development and while some research has been conducted of the 80,000 chemicals in our environment about 12 have been thoroughly tested for neurotoxicity.
<number> The effects of methylmercury on the developing brain were first recognized in the tragic poisoning epidemic in Minimata Bay, Japan during the 1950s. In this episode, residents regularly consumed fish highly contaminated with methylmercury resulting from industrial discharges into the bay. Infants born to mothers who consumed the fish had a variety of neurological findings, including mental retardation and disturbances of gait, speech, sucking, swallowing, and reflexes,(1) while their mothers often showed no signs of mercury poisoning. Because methylmercury was not identified as the cause until very late in the course of the epidemic, mercury exposures were never quantified, and a toxic threshold for the effects seen at Minimata was never established. The quantitative study of methylmercury neurotoxicity began with a second major poisoning epidemic in Iraq in 1972. In this tragic incident, infants were born with severe disabilities, including mental retardation, cerebral palsy, seizures, blindness, and deafness, after their mothers consumed bread contaminated with a methylmercury fungicide. As in Minimata, many mothers of affected infants suffered minimal if any symptoms themselves. The first case reports of these severely retarded infants provided an apparent toxic threshold for mercury of greater than 34 micrograms/kilogram/day.(2,3) (This appeared to be a “no observed effect level,” or NOEL, for severe retardation at birth.) 1. Harada H. Congenital Minimata Disease: intrauterine methylmercury poisoning. Teratology 18:285- 288, 1978. 2. Amin-Zaki L, Elhassani S, Majeed MA, et al. Perinatal methylmercury poisoning in Iraq. Am J Dis Child 130, 1070-1078, 1976. 3. Amin-Zaki L, Elhassani S, Majeed MA, et al. Intra-uterine methylmercury poisoning in Iraq. Pediatrics 54(5) pp 587-595, 1974.
<number> Are a family of chlorinated hydrocarbons The available data support the hypothesis that PCB levels typically observed in individuals in industrialized countries may result in neurotoxicity in the offspring. Several studies of children exposed to elevated levels of polychlorinated biphenyls (PCBs) have linked these contaminants to neurodevelopmental effects, including lowered intelligence and behavioral deficits such as as inattention and excessive reaction to stimulation. Most of these studies find that the effects are associated with exposure in the womb. EPA America’s Children and the Environment. As exposure assessment has improved over the past several decades, persistent and pervasive adverse neurodevelopmental effects of prenatal PCB exposure have emerged at exposure levels typical of the general population. These effects have been demonstrated in large prospective cohort studies in the Netherlands, North Carolina, and Germany in addition to the Michigan study. In each of these studies, PCB effects were seen after controlling for large numbers of potentially confounding variables. In the newborn, the effects of low-level prenatal PCB exposure include decreased birth weight, head circumference, and gestational age, as well as motor immaturity, poor lability, and increased startle and decreased reflexes on the Brazelton Neonatal Behavioral Assessment.(1,2) 1. Fein GG, Jacobson JL, Jacobson SW, et al. Prenatal exposure to polychlorinated biphenyls: effects on birth size and gestational age. J Pediatr Aug;105(2):315-20, 1984. 2. Patandin S, Koopman-Esseboom C, de Ridder MA et al. Effects of environmental exposure to polychlorinated biphenyls and dioxins on birth size and growth in Dutch children. Pediatr Res Oct;44(4):538-45, 1998.
Pollution and the nervous system
Environmental POLLUTION and
By Dr. Shewikar El Bakry
Lecturer of Neuropsychiatry
The Developing Brain
Brain development begins very early in human
gestation and continues well after birth through
adolescence. It depends on a tightly orchestrated
cascade of sequential and concurrent events.
The abnormalities observed after exposure to a single
toxic agent may vary with the timing of the exposure.1
The nature of the neurotoxicant, the extent of
exposure, and the timing of exposure are, therefore,
each important determinants of outcome.
Although genetic inheritance plays a
prominent role in fetal brain
development, environmental factors
also significantly contribute to final
outcomes through their direct impact on
developing tissues, by alteration of
signaling chemicals that are essential
mediators of brain development
(neurotrophins), or by modifying gene
Attributable to DD
25% of developmental and
neurological deficits in children are
due to the interplay between
chemicals and genetic factors
3% of DD can be attributed to
chemical exposure alone
Known Causes of
DSM4 (Diagnostic and Statistical Manual for Psychiatric
Disorders, American Psychiatric Association)
1. Score of 70 or below on a standard IQ (intelligence
3. Adaptive functioning: how well the individual meets
age and culture specific standards
Age of onset before 18
Degrees of severity:
Profound: below 20
The cause of approximately 80 percent
of developmental disorders of
childhood is not known; and in the
absence of knowledge about causal
factors, environmental exposures
should be considered prime suspects
for causing such problems or
interacting with other factors (e.g.
physical, genetic or psychosocial
factors) to cause or exacerbate these
Seafood: larger fish have most mercury, due to eating
Vaccines: many childhood vaccines used to contain 12.5-25
ug of thimerosal, so that a fully-vaccinated child could
receive up to 237.5 ug of thimerosal injected into them
Dental amalgams: usually emit 1-10 ug/day; amount of
mercury in brain strongly correlated with number of dental
fillings; could release much more when first placed or
US Centers for Disease Control
and Prevention (CDC)
“Mercury occurs naturally and is found
everywhere in the environment.”
“The level of mercury exposure from vaccines is
“Evidence is accumulating of lack of harm
resulting from exposure to thimerosal in
KNOW YOUR MERCURY (Hg)
Elemental Hg Thermometers
Inorganic Hg Coal power plants Air pollutants
Organic Methyl Hg
Organic Ethyl Hg Thimerosal
The LDA is convinced that there
is a direct relationship between
human exposure to mercury
pollution-especially for women
of child-bearing years- and the
rising incidence of cognitive
Mercur y Toxicity
“Mercury is considered to be a developmental toxicant.
… The symptoms observed in offspring of exposed
mothers are primarily neurological in origin and have
ranged from delays in motor and verbal development to
severe brain damage.”
“The infant may be born apparently normal, but later
show effects that may range from the infant being
slower to reach developmental milestones, such as the
age of first walking and talking, to more severe effects
including brain damage with mental retardation,
incoordination, and inability to move.”
“Other severe effects observed in
children whose mothers were exposed
to very toxic levels of mercury during
pregnancy include eventual blindness,
involuntary muscle contractions and
seizures, muscle weakness, and
inability to speak.”
“It is important to remember, however,
that the severity of these effects
depends upon the level of mercury
exposure and the time of dose.”
Maximum Hg exposure in 1st year of life US Childhood Schedule - 1992-200?
8lb infant (3.6kg)– EPA Hg limit: 0.36mcg = 35 times over
4lb infant (1.8kg) – EPA Hg limit: 0.18mcg = 70 times over
(subtotal for visit):
Avg. weight: 10lbs/4.5kg EPA limit: 0.45mcg = 138 times over
(subtotal for visit):
Avg weight: 14lbs/6.5kg EPA limit: 0.65mcg = 72 times over
ETHYL VS METHYL
Main chemical difference: Ethyl form contains extra carbon compound on molecule,
making it larger.
Some scientists contend extra carbon compound makes ethylmercury less likely to
cross the blood-brain barrier.
Methylmercury shown to remain in blood longer than ethyl (1/2 life of 50 days vs. 7 days
for ethyl); it accumulates more readily in the body. But ethyl converts more readily to
inorganic Hg, which appears to remain in brain longer.
Despite these differences, FDA researchers assumed that the two forms of mercury
were equal in toxicity.
Arsenic is “less toxic” than cyanide.
Bolus vs. Chronic Exposure
FDA totaled 4 large “bolus” doses at birth, 2, 4, & 6 months
(162.5mcg) and divided by 180 days.
162.5mcg divided by 180 = 0.9mcg per day.
This “average” daily exposure was just above the EPA limit, but
below FDA and CDC limits.
Analogy: You can take 2 tylenol a day for 60 days and be fine.
But 120 tylenol in one day is a lethal dose.
CHILD WITH ACRODYNIA CHILD WITH AUTISM
Impact of Pb on human health
Pb is a highly toxic, heavy metal and remain stable
over time (entering into ecological systems, water
supply, plants, …)
Pb accumulates in the body over time causing health
Pb has been confirmed to hamper neurological and
physical development (harmful for children below 6
Low level of exposur e to lead can
physical r etar dation
High level of exposur e (blood contains
> 25 mg Pb/dl) can cause
Anemia, hypertension, mental
r etar dation, convulsions, coma
Performance on Brazelton Neonatal Behavioral Assessment
(BNBA) - motor immaturity, inc. startle
Memory, attention, verbal ability, information processing
Delayed psychomotor development; changes in play behavior
Word and reading comprehension
Full scale and verbal IQ
Memory and attention
non-auditor y ef fects on health
auditor y ef fects
Hearing is essential for well-being and safety.
Hearing impairment is typically defined as an
increase in the threshold of hearing as
clinically assessed by audiometry.
Studies suggest that children seem to be
more vulnerable than adults to noise induced
non-auditor y effects on
1-Interference with the spoken
2- Sleep Disturbances.
3- Cardiovascular Diseases.
4- Disturbances in Mental Health.
5- Impaired Task Performance.
6- Negative social Behaviour and Annoyance
Missing the Dark: Health
Effects of Light Pollution
Electric lighting has become an integral part of
modern society. When such light is inefficient,
annoying, or unnecessary, it is known as light
pollution. Many environmentalists, naturalists, and
medical researchers consider light pollution to be one
of the fastest growing and most pervasive forms of
environmental pollution. Moreover, a growing body
of scientific research suggests light pollution can
impair biologic functions in both