Pollution and the nervous system

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  • 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...
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    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.
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    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.
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    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.
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Transcript

  • 1. Relation between Environmental POLLUTION and mental disability By Dr. Shewikar El Bakry Lecturer of Neuropsychiatry Benha University.
  • 2. 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.
  • 3. 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 expression
  • 4. Environmental Influences  Physical  Toxins  Nutrition  Sick buildings  Noise pollution  Second-hand smoke  Lead  Social  Violence  Substance abuse  Child rearing practices  Poverty
  • 5. Environmental Factors 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
  • 6. Known Causes of Developmental Disabilities  Lead  Alcohol  Nicotine  Mercury  PCBs
  • 7. MENTAL RETARDATION DSM4 (Diagnostic and Statistical Manual for Psychiatric Disorders, American Psychiatric Association) 1. Score of 70 or below on a standard IQ (intelligence quotient) test 3. Adaptive functioning: how well the individual meets age and culture specific standards 3. Age of onset before 18 Degrees of severity: Mild: 55-70 Moderate: 35-55 Severe: 20-35 Profound: below 20
  • 8. 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 conditions.
  • 9. Mercury Exposure: Sources Major  Seafood: larger fish have most mercury, due to eating smaller fish  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 removed
  • 10. OFFICIAL STATEMENT: 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 low.”  “Evidence is accumulating of lack of harm resulting from exposure to thimerosal in vaccines.”
  • 11. KNOW YOUR MERCURY (Hg) TYPE SOURCE EXPOSURE Elemental Hg Thermometers Vapor Amalgams Lights/batteries Inorganic Hg Coal power plants Air pollutants (hydrophilic) Volcanoes Organic Methyl Hg Fish Ingestion (lypophilic) Organic Ethyl Hg Thimerosal (lypophilic) Fish(?) Vaccines OTC Topicals
  • 12. 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 disabilities.
  • 13. Mercury Exposure Low Dose Prenatal  Impairments of:  motor skills  attention  visual spatial skills  language  memory  Blood pressure, heart rate variability
  • 14. Mercury Exposure Prenatal High-Dose Effects  Mental retardation  Seizures  Cerebral palsy  Disturbances of vision, hearing, sensation  Abnormal gait  Abnormal speech  Disturbances of swallowing and sucking  Abnormal reflexes
  • 15. 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.”
  • 16. “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.”
  • 17. Maximum Hg exposure in 1st year of life US Childhood Schedule - 1992-200? AGE SHOTS BIRTH Hep B HG CONTENT 12.5mcg 8lb infant (3.6kg)– EPA Hg limit: 0.36mcg = 35 times over 4lb infant (1.8kg) – EPA Hg limit: 0.18mcg = 70 times over 2 MONTHS Hep B 12.5mcg HIb 25.0mcg DTaP 25.0mcg (subtotal for visit): 62.5mcg Avg. weight: 10lbs/4.5kg EPA limit: 0.45mcg = 138 times over 4 MONTHS DTaP HIb 25.0mcg 25.0 mcg (subtotal for visit): 50.0 mcg Avg weight: 14lbs/6.5kg EPA limit: 0.65mcg = 72 times over
  • 18. 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.
  • 19. Bolus vs. Chronic Exposure FDA’s “Interpretation”  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.
  • 20. CHILD WITH ACRODYNIA CHILD WITH AUTISM (Mercury poisoning) (Will Redwood)
  • 21. 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 problems. Pb has been confirmed to hamper neurological and physical development (harmful for children below 6 years)
  • 22. Low level of exposur e to lead can result in physical r etar dation low IQ hyperactivity hearing loss behavioural changes insomnia High level of exposur e (blood contains > 25 mg Pb/dl) can cause lead poisoning Anemia, hypertension, mental r etar dation, convulsions, coma
  • 23. PCB Exposure Developmental Effects Infant  Birth weight  Head circumference  Performance on Brazelton Neonatal Behavioral Assessment (BNBA) - motor immaturity, inc. startle Early Childhood  Memory, attention, verbal ability, information processing  Delayed psychomotor development; changes in play behavior  Hyperactivity Preteen  Word and reading comprehension  Full scale and verbal IQ  Memory and attention
  • 24. Nicotine  Reduced IQ  Learning disabilities  Attention deficits
  • 25. Noise pollution:  non-auditor y ef fects on health  auditor y ef fects
  • 26. Hearing Impairment  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 hearing impairment
  • 27. non-auditor y effects on health  1-Interference with the spoken communication.  2- Sleep Disturbances.  3- Cardiovascular Diseases.  4- Disturbances in Mental Health.  5- Impaired Task Performance.  6- Negative social Behaviour and Annoyance Reaction.
  • 28. 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