危険な道:第5章:障害の複数の原因6 | 化学物質過敏症 runのブログ

化学物質過敏症 runのブログ

化学物質過敏症 電磁波過敏症 シックスクール問題を中心としたブログです

・例3:鉛代謝に影響する遺伝・環境相互作
用また、遺伝・環境相互作用は、体が鉛を処理する様式に影響することが突きとめられている。
これらの相互作用には、鉛代謝と骨貯蔵・血液鉛レベルに影響することが知られている、デルタ ALA 酵素(デルタアミノレブリン酸脱水素酵素)をコードしている遺伝子が関与する。
体が鉛を処理する様式にどのように遺伝子が影響するかを理解し始めているが、鉛の神経毒性に関する遺伝子の影響はまだ解明されていない。52,53,54,55,56,57,58,59,60


社会環境の役割
毒物と遺伝は、過去 20 年から 30 年に渡って学習と発達で重要な影響として現れてきた。
しかし、人間の発達で社会環境の重要な役割は、20 世紀のほとんどの間認識されてきている。61
大量の研究が、社会環境要因と発達の結果との間の関連を証明している。62
例えば、良い親の精神衛生と社会的支援・教育・相互関係によって特徴づけられる親としての接し方は、改善された発達結果と全て関連している。
大規模な介入研究も、社会的支援と親として接する技術訓練・質の高い食の小児教育がリスクの高い子供で発達閣下を改善することを示している。63,64
実際上のこととして、社会環境の重要性は、発達障害の評価と治療介入の両方が社会環境の分野で主に起こっているという事実によって、強調されている。
大部分の学習と発達障害のある子供を取り扱う、心理学者と教育者は社会環境に焦点を当てた行動流儀で一般に訓練を受けている。
反対に、毒物学と遺伝学は、鉛や PKU・甲状腺機能低下と遺伝子欠陥により起こる様々な稀な代謝病を検査する医学スクリーニング計画の重要な例外があるが、臨床的領域にまだ日常的に説明されていない。

そのため、私たちは学習と発達障害で原因要因と治療様式の両方としての重大さを認めることを除いて、この報告でさらに社会環境を考察しないだろう。


1 Mash EJ, Terdal LG. Assessment of child and family
disturbance:a behavioral-system approach. In: Assessment of
Childhood Disorders.Third Edition. Eds. Mash EM, Terdal LG.
New York: Guilford Press, 1997, p. 21-22.
2 Plomin R, Craig I. Human behavioral genetics of cognitive
abilities and disabilities. BioEssays 19(12):1117-1124, 1997.
3 Taylor HG. Critical issues and future directions in the
development of theories, models, and measurements for
attention, memory, and executive function. In:Attention, Memory
and Executive Function. Eds. Lyon GR, Krasnegor NA.
Baltimore: Paul H. Brookes Publishing Co., 1996,p.401.
4 Bouchard TJ. Genes, environment, and personality. Science Vol.
264: 1700-1701, 1994.
5 Plomin R, Owen MJ, McGuffin P. The genetic basis of complex
human behaviors. Science Vol. 264: 1733-1739, 1994.
6 Mann CC. Behavioral genetics in transition. Science
264:1686-1689, 1994.
7 Plomin R, DeFries JC. The genetics of cognitive abilities and
disabilities. Scientific American, May, 1998:62-69.
8 Plomin R, Owen MJ, McGuffin P. The genetic basis of complex
human behaviors. Science Vol. 264: 1733-1739, 1994.
9 Bailey RC. Hereditarian scientific fallacies. Genetica
99(2-1):125-133, 1997.
10 Mann CC. Ibid. 11 McClearn GE, Vogler GP, Plomin R.
Genetics and behavioral medicine. Behavioral Medicine
22:93-102, fall, 1996.
12 Lilly, LS. Ischemic heart disease in Textbook of Primary Care
Medicine, Second Edition, Ed. Noble J. St. Louis: Mosby, 1996,
p.218.
13 Goldberg RJ, Yarzebski J, Lessard D et al. A two-decades
(1975-1995) long experience in the incidence, in-hospital and
long-term case-fatality rates of acute myocardial infaction: a
community-wide perspective. Journal American College of
Cardiology 33(6):1533-9, 1999.
14 Wilhelmsen L. ESC population studies lecture 1996.
Cardiovascular monitoring of a city over 30 years. European
Heart Journal 18(8):1220-30, 1997.
15 Pell S. Trends in the incidence of myocardial infaction and in
associated mortality and morbidity in a large employed
population, 1957-1983. New England Journal of Medicine
312(16):1005-11, 1985.
16 Plomin R, Owen MJ, McGuffin P. The genetic basis of complex
human behaviors. Science Vol. 264: 1733-1739, 1994.
17 Plomin R, Owen MJ, McGuffin P. 1994. Ibid. 18 Plomin R,
EdFries JC, McClearn GE et al. Behavioral Genetics, Third
Edition. New York: WH Freeman and Company, 1997, p. 111.
19 McClearn GE, Vogler GP, Plomin R. Genetics and behavioral
medicine. Behavioral Medicine 22:93-102, fall, 1996.
20 Mutch E, Blain PG, Williams FM. Interindividual variations in
enzymes controlling organophosphate toxicity in man. Human
and Experimental Toxicology 11(2):109-116, 1992.
21 Costa LG, Li WF, Richter RJ, Shih DM et al. The role of
paraoxonase (PON1) in the detoxification of organophosphates
and its human polymorphism. Chemico-Biological Interactions
119-120:429-38, 1999.
22 Clendenning JB, Humbert R, Green ED, et al. Structural
organization of the human PON1 gene. Genomics 35(3):586-9,
1996.
23 Shih DM, Gu L, Xia YR, et al. Mice lacking serum paraoxonase
are susceptible to organophosphate toxicity and atherosclerosis.
Nature 394(6690):284-7, 1998.
24 Genc S, Gurdol F, Guvene S, Kargi Y. Variations in serum
cholinesterase activity in different age and sex groups.
European Journal of Clinical Chemistry and Clinical
Biochemistry 35(3):239- 40, 1997.
25 Trundle D, Marcial G. Detection of chilinesterase inhibition. The
significance of cholinesterase measurements. Annals of Clinical
and Laboratory Science 18(5):345-2, 1988.
26 Brock A, Brock V. Plasma cholinesterase activity in a healthy
population group with no occupational exposure to known
cholinesterase inhibitors: relative influence of some factors
related to normal inter-and intra-individual variationsScandinavian Journal of Clinical and Laboratory Investigation
50(4):401-8,1990.
27 Trundle D, 1988. Ibid.
28 Rosenman KD, Guss PS. Prevalence of congenital deficiency in
serum cholinesterase. Archives of Environmental Health
52(1):42-4, 1997.
29 Pinto Pereira LM, Clement Y, Telang BV. Distribution of
cholinesterase activity in the population of Trinidad. Canadian
Journal of Physiology and Pharmacology 74(3):286-9, 1996.
30 Reiner E, Simeon-Rudolf V, Skrinjaric-Spoljar M. Toxicology
Letters 82-83:447-52, 1995.
31 Trundle D, 1988. Ibid. 32 Brock A, Brock V, 1990. Ibid.
33 Costa LG, Li WF, Richter RJ, Shih DM et al, 1999. Ibid.
34 Furlong CE, Li WF, Costa LG et al. Genetically determined
susceptibility to organophosphorus insecticides and nerve
agents: developing a mouse model for the human PON1
Polymorphism. Neurotoxicology 19(4-5):645-50, 1998.
35 Furlong CE, 1998. Ibid.
36 Furlong CE, Richter RJ, Seidel SL, et al. Role of genetic
polymorphism of human plasma paraoxonase/arylesterase in
hydrolysis of the the insecticide metabolites chlorpyrifos oxon
and paraoxon. American Journal of Human Genetics
43(3):230-8,
1988.
37 Furlong CE, Richter RJ, Seidel SL, 1988. Ibid.
38 Padungtod C, Niu T, Wang Z, Savitz DA, Christiani DC, et al.
American Journal of Industrial Medicine 36(3):379-87, 1999.
39 Trifiletti RR, Packard AM. Immune mechanisms in pediatric
neuropsychiatric disorders. Tourette’s syndrome, OCD, and
PANDAS. Child and Adolescent Psychiatric Clinics of North
America 8(4):767-75, 1999.
40 Swedo SE, Leonard HL, Garvey M. Pediatric autoimmune
neuropsychiatric disorders associated with streptococcal
infections: clinical description of the first 50 cases. American
Journal of Psychiatry 155(2):264-71, 1998.
41 Hollander E, DelGiudice-Asch G, Simon L, et al. B lymphocyte
antigen D8/17 and repetitive behaviors in autism. American
Journal of Psychiatry 156(2):317-20, 1999.
42 Trifiletti RR, Packard AM, 1999. Ibid.
43 Asbahr FR, Negrao AB, Gentil V et al. Obsessive-compulsive
and related symptoms in children and adolescents with
rheumatic fever with and without chorea: a prospective 6-month
study. American Journal of Psychiatry 155(8):1122-4, 1998.
44 Asbahr FR, Ramos RT, Negrao AB et al. Journal of the
American Academy of Child and Adolescent Psychiatry
38(12):1522-5, 1999.
45 Giedd JN, Rapoport JL, Leonard HL, et al. Case study: acute
basal ganglia enlargement and obsessive-compulsive
symptoms in an adolescent boy. Journal of the American
Academy of Child and Adolescent Psychiatry 35(7):913-5, 1996.
46 Perlmutter SJ, Leitman SF, Garvey MA, et al. Therapeutic
plasma exchange and intravenous immunoglobulin for
obsessive-compulsive disorder and tic disorders in childhood.
Lancet 354(9185):1153-8, 1999.
47 Hollander E, DelGiudice-Asch G, Simon L, et al, 1999. Ibid.
48 Swedo SE, Leonard HL, Mittleman BB, et al. Identification of
children with pediatric autoimmune neuropsychiatric disorders
associated with streptococcal infections by a marker associated
with rheumatic fever. American Journal of Psychiatry
154(1):110-2, 1997.
49 Garvey MA, Giedd J, Swedo SE. Journal of Child Neurology 13
(9):413-23, 1998.
50 Asbahr FR, Negrao AB, Gentil V et al, 1998. Ibid.
51 Kurlan R. Neurology 50(6):1530-4, 1998.
52 Smith CM, Wang X, Hu H et al. A polymorphism in the
delta-aminolevulinic acid dehydratase gene may modify the
pharmacokinetics and toxicity of lead. Environmental Health
Perspectives 103(3):248-53, 1995.
53 Bergdahl IA, Grubb A, Schutz A et al. Lead binding to
delta-aminolevulinic acid dehydratase in human erythrocytes.
Pharmacology and Toxicology 81(4):153-8, 1997.
54 Wetmur JG. Influence of the common human
delta-aminolevulinate dehydratase polymorphism on lead body
burden. Environmental Health Perspectives 102 Suppl 3:215-9,
1994.
55 Wetmur JG, Lehnert G, Desnick RJ. The delta-aminolevulinate
dehydratase polymorphism: higher blood lead levels in lead
workers and environmentally exposed children with the 1-2 and
2-2 isozymes. Environmental Research 56(2):109-19, 1991.
56 Claudio L, Lee T, Wolff MS, et al. A murine model of genetic
susceptibility to lead bioaccumulation. Fundam Appl Toxicol 35
(1):84-90, 1997.
57 Tomokuni K, Ichiba M, Fujisiro K. Interrelation between urinary
delta-aminolevulinic acid, serum ALA, and blood lead in workers
exposed to lead. Industrial Health 31(2):51-7,1993.
58 Schwartz BS, Lee BK, Stewart W et al. Delta-Aminolevulinic
acid dehydratase genotype modifies four hour urinary lead
excretion after oral administration of dimercaptosuccinic acid.
Occupational and Environmental Medicine 54(4):241-6, 1997.
59 Sithisarankul P, Cadorette M, Davoli CT et al. Plasma
5-aminolevulinic acid concentration and lead exposure in
children. Environmental Research 80(1):41-9, 1999.
60 Sithisarankul P, Schwartz BS, Lee BK et al. Aminolevulinic acid
dehydratase genotype mediates plasma levels of the
neurotoxin, 5-aminolevulinic acid, in lead-exposed workers.
American Journal of Industrial Medicine 32(1):15-20, 1997.
61 Plomin R, DeFries JC. The genetics of cognitive abilities and
disabilities. Scientific American, May, 1998:62-69.
62 Taylor HG. Critical issues and future directions in the
development of theories, models, and measurements for
attention, memory, and executive function. In:Attention, Memory
and Executive Function. Eds. Lyon GR, Krasnegor NA.
Baltimore: Paul H. Brookes Publishing Co., 1996, p. 400-1.
63 Ramey CT, Bryant DM, Wasik BH et al. The infant health and
development program for low birthweight, premature infants:
program elements, family participation, and child intelligence.
Pediatrics 89(454-65),1992.
64 Ramey CT, Ramey SL. Which children benefit the most from
early intervention? Pediatrics 94(6 Pt 2):1064-6, 1994.
65 Ecobichon DJ. Toxic effects of pesticides. In: Casarett and
Doull’s Toxicology, Fifth Edition. Ed Klaasses CD. New York:
McGraw-Hill, 1996.
訳 渡部和男