Document xjOOdwMMNnOrjeR3goVepBJQ1

,j; / AU - ALFANQ BP A.U - PETIT TL TI - Behavioral effects of postnatal lead .exposure! Passible relationship to hiPPOcem.p-31 dysfunction * * SI - HEEP/82/06522 BO - BEHAV NEURAL BIOL? 32 -(3). 1981. 319-333. . A8 -- HEEP COPYRIGHT! BIOL ABB. A review of p'rev iaus evidence suggested the possibility of hippocampal involveinertt in the behavioral chsnaes observed following postnatal Pb exposure. To further assess this possibility? Long-Evens hooded rat p u p s were exposed' to inorganic Pb from Postnatal days _.l-25 via maternal milk. Mothers were fed diets containing 4.0% PbCQ3? 0.45% PhC:Q3 or a 2*2% Na2CD3 control diet* Animals 'were tested at maturity- in 4 situations considered sensitive to hippocampal dysfunction* Exposure to Pb resulted in delayed acquisition of the radial 8 arm s>lftTsT mass but" produced no" changes in "'the susceptibil its" to' 'au'cTiLoSenie seniUT-eS'- or-the acouisition and performance of a 2-way active avoidance response* Pb--exposed animals also performed deficiently on a'DRL-20 schedule of operant reinforcements although significant variation "was observed between litters in the control group on this task* Results were discussed in terms of a relationship between postnatal Pb exposure and hippocampal dysfunction* Other forms of CMS alterations resulted from early Pb exposure and alternative explanations for these behavioral changes were also suggested* Mi/iman B* po&ujju- 'iU LUPAKI 8 MF YU - PHONE wM U ~ Qccupetio.rt.9l lead exposure? scute intoxication and chronic nephropath.y; A esse and review of the literature* F! HEEP/B4/0B321 ?Q -- J AN OSTEOPATH ASSOC? 83 (5), 1984, 361-366, :iB - HEEP CGPYRIG-HT ** BIOL ABS, The longest known esse of toxic Pb nephropathy resulting from chronic? symptomatic occupational Pb exposure was reported. The patient hsd been exposed continuously to Pb from the age of 19-29 yr? with probable absorption through lungs? -gastrointestinal tract and skin. Clinical evaluation at' b W~6T' ar reveal ed symmetrieariy steal 1 kidnews snd a markedly 'di.min'rs-he"8~gTbffl-eruiar f i Itf a'tion `rate , '' SubseguentlV?~a" enaTHij 1-o p sy' demonstrated interstitial fibrosis ;and.fe.w dlmaeruli, A discussion of the signs and symptoms'bf Pb intoxication and the"'deVeTopment of chronic Pb nephropathy in the -USA snd other countries ensued. The paper emphasised the probable pathogenesis? diagnosis and treatment of this rare and Potentially reversible cause of chronic renal fai 1ure * DUP040011201 fills OeriVi Je T F X - Le3d neu ropatha * 21 - TQXBIB/84/157841 30 - CEO Cr.it Rev Toxicol? UPS. 12? ISS 2? 1984.? P149-213 <REF? 214.) VE The still unexplained nature of the neurotropie set ion of lead has prompted this chronological survey of the .course of development of the medics! attitude towards the problems of lead neuropathy all along the centuries.... from ancient times u p to the present* Once e conspicuous? severe? and even f reouent clinics.], type of piumbisro? peripheral lead neuropathy has r-eceiy'e'd''^due'''atlvervtibn in the esrla classics (Tgnauerel diTT lances? Duchenne? Aran? Remak? Romberg? Erb? etc*:) and of the pioneers in industrial medicine (Ladds? Aub? Tglefcy-? Hamilton)* Even the modern era? however? has not come further than to state that lead produces different neurolodicsl effects in different animal species and even in humans--different patterns of neuromuscular involvement* With the advent of eleetraphysiaiady? conflicting and inconsistent findings have also appeared? particularly in regard to overt and latent lead neuropathies * Theories regarding the mode and site of thenourptoxic action of lead are reviewed and data which -might be used as arguments both in favor and against are presented* DUP040011202 'I Til Jan in V VU -- Couinsud C MS -- Stone A Hi - Wise !... ri The " lead-induced colic* syndrome in lead intoxication-* H T OX BIB / 8 5 / .1.4 27 02 0 Surd Annul VOL 17? 1985? P287--307 (REF * 169) Lead -has a mul tipi ieity of biologic effects* The universal occurrence qf lead accounts for the continuous appearance of new instances of human lead FDisoninsJ* The most common and one pf the earliest manifestations of lead intoxication in the adult is so-celled leadTMinduced colic? which is a syndrome with a multiplicity of clinical' patterns and at least three possible different pathogenic mechanisms* It may be caused by changes in the visceral smooth muscle tone secondary tq'_:i~hVaction of lead on' the visceral autonomic nervous system? lead-induced alterations in sodium" transport in thi'e small-intestinal mucosa? and lead-induced interstitial pancreatitis * It should be considered in the differential diagnosis of abdominal pain of obscure etiology and whenever a disparity is observed between the symptoms and the abdominal findings in a patient with abdominal pain? especially in the presence of a history of occupational exposure to lead. DUP040011203 PARKINSON DK Exposure to lead-- Psychological and behavioral seauelae (.human) C RIS P / 8 S/M H 3 6:2 21-04 U6 DEPT, OF HEALTH AND HUMAN SERVICES ? PUBLIC HEALTH SERVICE ? NATIONAL INST, OF HEALTH? NATIONAL INSTITUTE OF MENTAL HEALTH Crisp Bata Ossa National Institutes Of Health RPROJ/CR1SP The purpose of this renewal application is to extend our comprehensive assessment of the mental health? social functioning and neuropsychological .performance of workers occupationally exposed to lead. In the fall of 1981 we initiated an epidemiologic study into the effects of cumulative and current lead exposure using a 'cross-sectional design in which lead Workers and na.n--exposed controls were assessed with a neuropswcholodic3.1 test battery? sections of the Diagnostic Interview Behedule? a detailed social functioning inventory? and an occupational history Questionnaire* Biological measures of past and current lead exposure and recent alcohol and drug use are also obtained, A maJor goal of the renewal application is to complete the analysis of these data. The ultimate aim of our research is to provide data that may be useful in the prevention of mental health problems resulting from lead exposure. In the course of conducting our Pilot studs? a striking association was observed between elevated current blood lead levels and deficits 'in"'~''" r:,e rf drm-ance oh" the n iur b'ps aclh'oT osf i c a i tests'. In this app.l i cat ion .?' "we Fropbse to liiystematacalTy "ascertain `"the" acute effects of high lead exposure and the recovery of functioning following the decline in blood lead levels associated with removal from exposure. Development of a comprehensive prevention program also reauires knowledge of the natural history of a disorder. The time course for the development of neuropsychological deficits and deteri.orat-ion in psychosocial functioning in relation to duration and intensity .of lead exposure is not known. Therefore? we wish to initiate a prospective study of the natural history of neuropsychological and psychosocial changes in lead workers. We also propose to verify psychosocial information by interviewing a significant other adult. 0 W S 1031405 DUPQ40011204 Shwkla 6.8 ....... ........ 8 ingha 1 Rl, / The present status of biological effects of toxic metals in the environment! lead* cadmium? and manganese* T0XB1B/.85/O2437 4 Can J Phs-siol Pharmacol? VOL 62f ISS 8? 1984.? P1015-31 (REF? 187) The number of reports concerning the chemical toxicology of metals which ere released in the environment by natural as well as anthropogenic sources? have been increasing constantly. Lead? cadmium? and manganese have found a variety of uses in industry? craft? and agriculture owing to their physical and chemical properties. The environmental burden of heavy metals has been rising substantially by smelter emission in air and waste sewssie in water. Further? organic' compounds of lead and manganese used as; antiknock substances in gasoline are emitted into the atmosphere bs automobile exhaustion. Such environmental contamination of air? water? soil? and food is a serious threat to all living kinds. Although these metals fere known to produce their; toxic effects on a variety of body systems? much amphasis has been placed on their effects on the nervous system .owing to' apparent association of relatively low or " subcl inical i levels o'? ic exFSsure witTi LTeHavToraI""s'n3" 'psychological disorders Clinical and animal data on environmental exposure show that while lead and^nra/Tg'ITtlfse are most "toxic to tfte nervous system? cadmium exerts profound .adverse effects on kidney and the male reproductive system. it appears that the consequences of exposure to lead in adults are less severe f-han the types of exposure associated with hyperactivity in neonates','''Except' for a few reports? hyperactivity has indeed been oosefveLl' in animals exposed to aiji.hff of these three metals. Experimental work hag also shown that these medals produce behavioral changes by altering the metabolism of brain, neurotransmitters? especially catecholamines. Recently? it is hypothesised that these metals exert their tOxie effect by damaging biological defences which exist in the body to serve as protective mechanisms against exogenous toxins. A voluminous publication list with diverse opinions on the biological effects of metals is available and there is an urgent need to compile assessment of the existing 'literature to identify the future theme of research work. The problem of metal toxicity becomes even more complex owing to simultaneous or successive exposure of the general population to different' Physical? chemical? biological? and psychological factors in the environment. The net toxic manifestations produced by multiple exposure should? therefore? be different from those produced by a single factor as the result of their additive? synergistic or antagonistic action. Even though a metal may not exist in sufficient amounts to cause any disability? the toxicity coulijj result when a second factor is also p resent , < ABSTRACT TRUNCATED AT WORDS) J W &.0314C6 DUP040011205 AU - HEATHERY MW ) AU -- MILLER WJ TI -- Metabolism end toxicity of cadmium? mercury end lead in animals* A review* 61 " HEEP/76/06903 80 -- J DAIRY SCI I 58 <12 ), 1975 (RECD 1976) 1767-1781 AD - KEEP COPYRIGHT* BIOL ABS, Cd? He and Pb are toxic to humans and_ smijne 1 s, Although Cd and inorganic He -toxicities occur in humans, they ha've" not been observed in domestic livestock under practical conditions. Cattle? especially young calves? are extremely susceptible to Pb t^oxici tif * Apparent is? cattle are more tolerant of Cd than are other animal species* Due partially to higher absorption and longer retention times in the bods? the alkyl mercuries? especially methyl mercury? are more toxic than inorganic Hg compounds* inorganic forms of Cd? Kg and Pb are poorly absorbed from the intestine* However? duef~to lack of effectfve' HomebsTaifs ? 'iffteF absorption retention time is long* Injected Cd? Hg and Pb are .metabolized differently from that naturally absorbed* Most Cd and Hd are in kidney and liver (50 and 23,% of total body in goats) 7 but highest total load of methyl mercury is in muscle <7:2% in cows)* With low to moderate body burden? most Pb is retained in the sk.eleton, However? be y ond ...a cartain p o irit ? the ki dnay aecu in u 1 ates"Targe a^uanTrtttffeOnly minute amounts of Cd and'Hg are secreted 'irit'd 'm'i IkV but milk is only inode rate la well protected from dietary Pb* Likewise? little Cd and inorganic Hg pass the placental barrier? Pb and methyl mercury i; < s m a r e r e a d i 1 y * DUP040011206 fiU " Pounds JG TI Effect .of lead intoxication o.n calcium homeostasis and calcium-mediated cell f u nct i an * a r evi Su S T T 0'{BIB./ 88 /11175.2 GO Neu-ro toxicology (.Park Forest II)? VOL 5j IBS 3? 1984? P295-331 (REF l 118) AD The interaction between lead and essential metals is a complex? well recognized? but poorly understood phenomenon* Dietary deficiencies or excesses of certain essential metals may Biter the absorption? elimination? or dose response of lead* Lead:? in turn? may alter the homeostasis and function of essential meTaTs *~ 'This review will be'Timited to the effect of lead on calcium? an essential metal with elaborate systemic and cellular .homeostatic mechanisms and innumerable second messenger and couPlins-factpr functions* Lead may ultimately perturb calcium-regulated or calcium-mediated functions <a> directly by ........ :i. htffrre ring with ' calcium ' CFanspo'rt 6T""s tor ad e"> r aeesse s ? e .* d .* ? Ca.2-t transport proteins? calcium dates? etc*? (b) indirectly ,bu altering cell functions required.for calcium homeostasis? a*d*? enerdy production? plasma membrane .permeability? etc*? (c) by substitution of Pb2+ for Ca2+ at functionally important calcium '.binding sites? e.d*? calmodulin* While any individual study may not Provide adeeuate experimental verification of the causal role of perturbations of calcium metabolism and function as the primary toxic lesion of lead intoxication? the collective observations of many studies do strongly .support load-calcium interactio.n as an important Functional lesion in load intoxicated n rssnsl 1 as ? cells? tissues? and or dan systems:* DUP040011207 She I l.enbe rge r MK TI Effects of early lead exposure on .neuratrshsmitter systems in the brain, A review wi th commentary. h 'iS - The mechanism by which early lead exposure alters the functional development of the brain remains an open Question* One primary avenue of approach has been to study the effects of neonatal lead exposure on to the interact ion of lead with each of those systems. Further? each dosing paradigm has been evaluated with a view to experimental error and interact!ve variables. It was concluded that factors such as the time at which p rednant animals were shipped and mode of dosing may have been uncontrolled variables causing variability in reported results between and within laboratories. The majority of publications deal with the interaction of lead with catecholamine systems and with dopamine in particular. Reports of effects are highly variable and many observations lack confirmation by other laboratories or have not been replicated. However? the bulk.of observations leads to the tentative conclusion that 1 e a d d o e s re s u 3. Jtn,,,j.n' altered fuiTctronal "state of ...the a tech o.l a in i n e s?sterns~i T'h 1 s is true for cho 1 inerdic: func~tion as well, Some perturbation of ' "a c efy 1 c hoTl n e^Tfiet a b cl i s m probably exists but the specificity and significance of the effect are suspect. Reports that lead alters the functional state of GABA pathways are interesting but reauire confirmation. The generality arid variability of effects on neuro-transmitter systems Questions the degree of specificity that mas be expected* It is suggested that lead may effect a variable change in the functional state of all these systems by limiting glucose metabolism during periods of vulnerability, ,/nn > DUP040011208 : i11 - Triebig B ji li - B t J4t1 n e r J 'I I ~ ENsurotoxic occupational substancesf .L Metals ..and their compounds 'A literature review of the years 1970 to 19823 31 - "f D.XB X B / 8 4 /149317 SO - Zentralbl Bakteriol Hikrobiol Hyg .C.B3? VOL 177> IS-S 1-2j 1983? PI l-36 (REFt 129) AB - The knowledge of the neurotoxicity to the peripheral nervous system of arsenic* lead* thallium and mercury as well as their compounds is reviewed according to the literature of the Period 1'970-1-9-82 - First acute and chronic intoxications are described with special reference of the neurological symptoms * Then we review the results of electromyographic? neurophysiological and histological investigations* Field studies in occupationally exposed groups and evaluation of dose"re-oponse-relationships are specified in detail* Further the presented results are discussed according to aspects in occupational medicine* The following conclusions can be drawn! Neuropathies after arsenic into;;ications are characterized by symmetric sensory symptoms as usually numbness and psresthesias of the distal extremities? but the neurophysiological and 'histological studies showed a great variety of results* In a former study a significant dose-response-relationship between arsenic load and evidence of neuropathy in workers was demonstrated* The onset of impairments of the peripheral nervous system caused by ohroriic"Tr@"ad~ex~aosure .is discussed controversially* Some r;Tpor`ts showed a dose-response-relationship between a slowering of nerve c.ondup't'Tjcm velocities and an'ihcreas"'df"""the lead body burden* Proposals o~f threshold values^ ranged between 50 to GO micragrams lead/dl blood* Other aTrthTrrs'did not confirm these results* ''.Longitudinal studies are? with one exception? not available at present* Thus a relevant evaluation? particularly regarding relevance and prognosis of a mild glowering of nerve conduction velocity? can not be given now. The neurotoxicity of mercury and its compounds is well demonstrated* In case of the metal and the inorganic compounds a direct damage of the peripheral nerve is possible? whereas for organic compounds the pathophysiological mechanism is unclear* Studies concerning dose--response--relationships as well as evaluation of threshold values in chronically exposed workers are limited* It seems at present not possible to define a threshold value for the neurotoxic effects of mercury according to peripheral nervous system* Thallium caused .peripheral neuropathy is described in many casuisties But to our knowledge there are no reports of neurophysiological studies in occupationally exposed groups* ] j | | | JI | | | j f j I i \ DWS DUP040011209