Document N2zeLeY90NaB0gNerEV1G6KGw

- . ' * r Pig, g Fig. 9 Fig. 10 Fig* H 0 the intestines following ingestion, or through the skin following physical contact. A fish can absorb them through its gills. Once inside the body, they gradually distribute them selves equally among all fat deposits p resen t, and tend to stay, th e re . A fish sw im m ing in polluted w ater may a c c u m u la te them u n til its tissues contain up to 300,000 tim es as much PCB as was in the w a ter. The body's m ethods of g e ttin g rid of PCB's are slow and in e ffic ie n t. PCB's aren't volatile enough to be breathed out through the lungs, and they ex it only slowly through the action of th e liver, bile and in testin es. A nother way the body tries to get rid of lipid-soluble foreign ch em icals is by c o n v ertin g them into water-soluble substances by chem ical processes. These processes are cataly zed by enzym es c alled m icrosom al oxidases. The w ater-so lu b le products of these reactions can be e x c re te d in th e u rin e. U n fo rtu n ately , this ro u te is also inefficient. The enzym es apparently a tta ck PCB m olecules too slowly, p articularly if th ere are m ore than four chlorines p re sen t. In ad d itio n , th e PCB species present may not be capable of inducing the form ation of the particular kinds of enzymes needed. The enzym e-inducing a c tiv itie s of su b stan ces such as those found in PCB m ixtures can result in a num ber of biological e ffe c ts , which are m ost stro n g ly expressed in the liver. The e ffe c ts on liver tissue occur in m ore or less of a progression., First, the liver produces quantities of those m icrosom al enzym es I mentioned that carry out chem ical reactions to get rid of foreign substances. This is rapidly followed by p ro life ra tio n of m icrosom es -- bits of pro to p lasm inside the liver cells th a t provide site s for the re a c tio n s - and by new ceil grow th, to provide room for all this a c tiv ity . All of th ese changes a re mild and reversible as far as the liver is co n cern ed . But the high load of m icrosom al enzymes can a lte r 'th e levels of fa ts and stero id s in the c irc u la tio n . With m ore toxicant, some liver cells may die, and eventually fatal collapse of liver function may resu lt. A lte rn a tiv e ly , p a rtic u la rly in ro d en ts, th e re may ap p ea r benign or even m alignant tu m o rs. This brings up the issue of the possible role of PCB's in causing c a n c e r. I should point out th a t chem icals are known to be able to co n trib u te to can cer developm ent in several w ays. Som e, like c h lo ro m e th y le th e r, are d ire c t a c tin g carcinogens. They can a tta c k and m u tate DNA,m olecules. Some, like vinyl chloride, are so-called procarcinogens, which means they can be converted to d irect-actin g carcinogens in the body and then cause m u tatio n s. Som e, like cigarette tar, can be eith er prom oters, which make m utant cells turn m a lignant, or enzyme inducers or activ ato rs, which activ ate other procarcinogens. Many people are p articu larly concerned over d ire c t-a ctin g carcinogens and procarcinogens since DNA m u tatio n is an irrev e rsib le e v e n t. H ence, th ey arg u e th a t no additions to th e n a tu ra l burdens of such species should be to le ra te d . Conversely, promotion and enzym e induction are regulatory events. They are parts of the body's regular system of biochem ical checks and balances and do not occur unless the control lim its are exceeded. At present, I believe most scientists would regard it as highly unlikely th a t PCB's are e ith er d ire c t a ctin g or procarcinogens. However, we cannot rule out the possibility th a t they could play a role as prom oters or a c tiv a to rs in som e c irc u m sta n c e s. The next generic e f f e c t I'd like to m ention is c h lo racn e. This syndrom e comprises a slowly developing skin condition resem bling severe adolescent acn e. In addition, the victim feels g en erally sick, and may ex h ib it o th er signs such as g astrointestinal and neu ro lo g ical d istru b a n ce s. In ch ick en s, which a re very 783149 - 2- GENP010338 r t . Fig. 12 sensitive to the agents that produce chloracne in man, other effects can include edema disease and birth defects, Chloracne has been known for more than SO years. It is now known to be induced by chlorinated coal tar; chlorinated napthalcne, or Halowax; some bad batches of PCB; and many bad batches of polychlorinated phenol fungicides, 2, 4, 5-T herbicide, and Agent Orange. A good deal of scientific work has been aimed at relating the molecular structures of individual PCB and contaminant species to their biological effects. From this work, three interesting correlations have emerged. First, various molecules having a propeller-like shape have been found to induce the P^5G cytochromes, which are the less active oxidases. Many individual PCB species, especially those of the more highly chlorinated Aroclors, have this shape and show P450 activity. Second, molecules shaped like flat rectangles with chlorines at the corners are active at inducing P448 cytochromes. Three minor PCB isomers, which constitute less than one percent of the higher Aroclors, and virtually none of the lower Aroclors, can assume this shape and do show some P448 activity. The really active P ^ 8 inducers, however, are the PCDPs, sometimes present as PCB impurities, and the dioxins, which were the actively toxic impurities in 2, 4, 5-T and Agent Orange. Third, although it is known that P448 itself is not toxic in the body, it has been found that all species active in causing chloracne possess comparable activity in inducing PW8. Fig- 13 What all this shape-specificity means is that ail three types of biological response -- P448, P450, and chloracne -- must be initiated by binding to shape- specific recognition sites on receptor proteins inside the cell. Such proteins have indeed been identified. It is believed that the agent-receptor complex then induces expression of normally silent gene sequences. These result in the production of several new proteins, some of which are known and some aren't. It is presumed that some of the latter interfere with normal cell growth and function. Pig- M The practical implications of this theory are both encouraging and cautionary. The bad news is that even apart from dibenzofuran impurities, the PCB's themselves may not be totally devoid of some forms of regulatory activity. The good news is that if the biological effects are basically regulatory --enzyme induction, cell growth stimulation, and so on -- then there should be definite threshold doses below which no effects occur. 1-5' Let's move now -from basic biological properties to the actual health effects on humans. What have they been? Pig* 16 First, chloracne. Chloracne is a very easily observed condition. The American occupational health literature relating to Halowaxes, herbicides, and tetrachloroazobenzenes repeatedly describes chloracne outbreaks. However, there are only three reports of unambiguous chloracne outbreaks associated with PCB's. The first, in 1933, involved workers at Swann Chemical in Alabama, who ran into one bad batch of the stuff, that had been made from off-spec benzene. It was recognized at the time that an impurity must have been responsible; however, attempts to identify it were fruitless and the effort *7n n - < r n , V ENP 010339 ^ *. Fig. 17 Fig. 18 Fig. 19 was forgotten. The other two episodes both involved strongly heated PCB. Neither was as thoroughly investigated at the time as was the first episode, but the occurrence of chloracne was noted as being unusual. Second, occupational liver disease. Early test at the Harvard School of Public Health showed that heavy doses of various Aroclors, whether admin istered orally or by inhalation, would cause liver'injury in rats. However, they also established no-effect doses, upon which the long accepted threshold limit values or TLV's were based. During the 40 years between 1937 and 1977, U.S. manufacturing industry handled over one billion pounds of PCB's under these guidelines, with no reported incidents of liver disease, none of unambiguous chloracne except for the episodes I just mentioned, and no other indications of significant health problems. This was an impressive accomplishment. Un fortunately, it produced not one single bit of medical or scientific documentation to prove that it actually had been the occupational health experience. Then in 1968 came Yusho. In southwestern Japan, 1300 people came down with some of the worst and most persistent cases of chloracne syndrome ever seen. Even newborn babies had it. Simultaneously, an epidemic of chick edema disease killed 400,000 chickens in western Japan. Patient investigations by a group at Kyushu University tracked the human disease down to use of a particular brand of rice oil, and to lots produced on two days in February 1968. The chickens, it turned out, had got the inedible by-products of these lots in their feed. Both lots had been produced in one leaky heat exchanger, and in that heat exchanger was the Japanese PCB, Kanechlor 400. The average amount of heat exchanger fluid consumed by the victims was estimated at two grams. As this news trickled out of Japan from 1969 to 1972, many people became concerned over PCB hazards, and many new toxicological studies were initiated. PCB's were fed to everything: Bacteria, algae, water-fleas, oysters, lobsters, minnows, bluegills, trout, quail, chickens, rats, mice, rabbits, guinea pigs, cows, pigs, mink, dogs, and monkeys. In ail cases, it was found that PCB's, like ail other known substances, could sicken and kill the creatures if the dose were made high enough. Three of the species tested, chickens, mink, and monkeys appeared relatively susceptible; however, the magnitudes of the effects produced in them varied considerably from one experiment to the next. The first clue to the source of the variation was provided by a Dutch scientist, J.G. Vos, who showed that the ability of PCB's to cause birth defects in chickens or chloracne in guinea pits depended upon the PCDF content of the PCB used. It was the impurity, polychlorinated dibenzofuran, PCDF, not PCB, that was the major source of the problem. It gradually developed that the European and Japanese PCB's contained 5-20 ppm of PCDPs, while the American Aroclors had only 0-2 ppm, even before purification for electrical use. The Japanese picked up this observation, and rechecked their specimens. The Yusho heat exchanger fluid was found to have been thermally decomposed, mostly to polychlorinated quarterphenyls, or PCQ's. Only 40% of the original PCB remained. In addition, it contained 2000 to 5000 ppm PCDF's, which can be formed from PCB's by thermal oxidation above 500F. The Yusho victims were found to have rather thoroughly eliminated their body burdens of PCB; however, the PCDPs lingered, particularly in the liver, and the people remained sick with chloracne. . a . 783151 GENP 010340 ' " ' ' Fig- 20 Fig. 21 Fig. 22 r Fig. 23 Fig.'2 Meanwhile, PCB's were tested for carcinogenicity, with quite variable results. American tests, made with commercial Aroclors as received, gave, uniformly negative findings for the lower, capacitor-type Aroclors such as 1221, 1016, and 1242. However, both positive and negative findings were reported for 1254 and 1260. Japanese tests with Kanechlors in mice also gave positive findings of tumors, but showed that the PCB's could reduce the incidence of tumors induced by other common carcinogens. The official FDA assessment of this situation in 1979 was that the evidence for the carcinogenicity of PCB's themselves was inconclusive. At the present time, it is our impression that the more knowledgeable public health officials are well aware that the PCB's found in our equipment, service shops, landfills and neighboring waterways are chemically different from that at Yusho, and almost certainly toxicologically different. However, they face a public that has become very alarmed over the earlier parts of the Yusho story, and the subsequent PCB testing frenzy. What they really need, and what they've repeatedly asked for, is good epidemiological data on whatever it is that ordinary electrical grade PCB's do to people. Which leads to may final question: What do our PCB's do to people? Can we supply the data that the authorities are asking for? Remarkably enough, it appears that a definitive human exposure event actually did occur. This exposure event involved a statistically-large human population, heavy exposure to electrical PCB's alone, and sufficient elapsed time for the development of some delayed health effects. This population consists of present and past GE employees at the Capacitor Department in Hudson Falls. About 1000 people worked there in jobs providing significant exposure betweeh 1946 and 1977. The exposure, in fact, is still in progress, since the people involved are retaining the accumulated PCB's in their bodies, and hence must be continuing to experience whatever effects they producel As a result, these people are beginning to attract medical attention, both by ourselves and others. In 1976, Dr. Irving Selikoff o$/Mt. Sinai Medical School was called in by the union to check on their health status. He examined 326 volunteers (onethird of whom had jobs providing medium to high PCB exposure), and eventually reported that they were mainly normal; however, he also indicated some evidences of decreased pulmonary function, which did not correlate with PCB body buden, and some1evidences for increased incidence of dermatological symptoms, such as rash, burning sensation, and acne, which did correlate, somewhat. Meanwhile, in 1976 the plant physician, Dr. Joseph Feingold, initiated a study of his own on 195 heavily-exposed employees and 20 Fairfield controls. Blood samples were taken, clinical examinations made, and the absence of obvious health problems noted. However, no detailed analysis of the data was attempted until the fall of 1979, when CRD got permission from the Corporate Environmental Quality Council to undertake a research study of the health effects issue. This stimulated a repeat examination of the people involved by Dr. Feingold and an ongoing statistical analysis of each individual clinical parameter by CRD. Current objectives are to determine, first, whether there are any significant departures from normal within this group; second, whether they correlate with PCB body burdens; and third, how both body burdens and health parameters are changing with time. 783152 010341 Fig. 25 Fig. 26 Fig- 27 ' Shortly after Dr. Feingold's repeat examination, Dr. Selikoff's associates arrived to repeat their 1976 tests. They have stated privately that one of their concerns is to confirm the reality of their alleged findings of respiratory impairment and significant dermatology. What they actually did was to draw more blood samples for PCB analyses and subject the members of their volunteer panel to an extraordinarily extensive medical examination. Dr. Selikoff's lab people are currently quite badly backlogged with other work, however, and it may be many months before any data emerge. In parallel with these efforts, in 1977, the National Institute of Occu pational Safety and Health -- NIOSH -- initiated a mortality data analysis on both the GE capacitor population at Hudson Falls and the Aerovox capacitor population at New Bedford, Mass., using information supplied by the companies in both cases. In the fall of 1979 the NIOSH investigator issued a draft report on his findings, and turned further investigation of the Hudson Falls population over to Dr. Phil Taylor of the NYS Health Dept. Dr. Taylor secured our cooperation for the identification of individuals who had been missed in the . earlier study and initiated a more rigorous analysis of the mortality data than had been done by NIOSH, and also an appraisal of the available records on births. Finally, in late 1979, a small effort was begun by Mt. Sinai and American 1 Cancer Society investigators to track down other evidences of unusual health effects or birth defects in the area. This is being done primarily by telephone survey. From the data now available, we know, first, that people who had moderate to heavy work exposure to capacitor PCB's now have an average of 1.5 grams of PCB in their bodies. Individuals in the top one percent are carrying about 10 grams. By way of comparison, normal Americans carry a little less than one-tenth of a gram as a background level, and the average Yusho victims ingested eight-tenths of a gram of actual PCB. We have no evidence yet of any significant decline in PCB levels in the people's bodies between 1976 to 1979. This is in marked contrast to the findings of Yusho, where the extra PCB load was 99% gone after a year. Obviously, whatever PCB excretion process got induced by the PCB/PCDF/PCQ mixture at Yusho is not operative at Hudson Falls; the PCB's are persisting. Third, our own clinical findings to date, and the preliminary NIOSH mortality data, both indicate a lack of serious health effects in our population. The death rates for cancer, cardiovascular disease, neurological disease, accidents, and for all causes are all slightly below normal. Fourth, there are indications of subclinical abnormalities in the exposed population. In addition to the presence of PCB's themselves, we see some elevations of serum triglycerides in males though not in females, and some elevations of serum enzymes, both of which suggest slight alteration in liver function. Other parameters may also be slightly abnormal; our analyses of the available data aren't yet complete. In addition, we have no inkling as to the other examples of physiological alterations or statisticaily-marginal health effects that may be revealed by Dr. Selikoff's colleagues at Mt. Sinai and the ' Cancer Society. GENP 010342 783153 r Fig. 28 Fig. 29 ^8* 30 So, w hat are we now doing about th is, w hat are our plans, and w hat do we hope to accomplish? First of all, we are helping the New York S tate H ealth D epartm ent obtain the personnel and exposure data needed for their studies of m ortality and birth abnorm alities. Conceivably, they may need financial encouragem ent later on. We consider it very im portan t th a t th is study be co m p le ted and published in th e open literature. Second, we are continuing to m onitor the M t. Sinai/C ancer Society investigations as best we can. Third, we are attem p tin g to resolve anom alies and establish the reliability of the PCB analyses run on the Hudson Falls popu latio n . It is im p o rtan t for us to have solid d a ta on PCB body burdens if our sto ry is to be c re d ib le. Fourth, we are continuing th e analysis of Dr. Feingold's 1976 and 1979 d ata to identify any clinical abnorm alities and establish co rrelatio n s with the levels of both higher and lower PCB's. F ifth, we are working on an unam biguous a n a ly tic a l m ethod for defining th e level of PCDF im purities in PCB sp ecim en s. When we have it, we will be applying it to PCB's from many old cap acito rs to estab lish the levels of PC D Ps in th e PCB's th a t produced the o ccu p atio n al exposure during th e 1946-77 period. Our im m ediate o b jectiv es, in sh o rt, a re to be able to show, f ir s t, th a t our PCB was actually virtually free of PCDF, second, th a t heavy human uptake of this P C D F -free PCB did occur, and th ird , th a t this u p tak e had no serious h ealth consequences. This is not all th a t we are doing ab o u t PCB problem s, of co u rse. Until last fall, all of our effo rts a t CRD w ere focused on the environm ental fate of PCB's; environm ental clean-up procedures involving m icrobial degradation or other techniques, and procedures for g ettin g PCB's out of contam inated tran sfo rm er oil. We are still heavily involved in all of th e se a re as; how ever, they don't bear on the health e ffe c ts issues, so I will pass over them for the present. Some p ro je c ted futu re a c tiv itie s th a t do bear d ire c tly on em erging h ealth e ffe c ts issues are listed h ere. One issue is th a t both we and Dr. Seiikoff will soon know th a t we have a GE em ployee population th a t will carry PCB's with them for the rest of their lives. They aren't clearly sick, but they aren't en tirely norm al e ith e r. The first thing th a t we will have to do is to m ain tain m edical surveillance of them to ensure th a t the a lte ratio n s seen are physi ological rather than pathological, and to be able to answer their inevitable questions. Second, we should endeavor to learn how to m easu re P448 c y to ch ro m es in these peoples' blood cells and to c o rrelate these m easurem ents with other data on subclinical h ealth e ffe c ts . Animal d a ta show th a t th ese cy to ch ro m es represent the most sensitive, specific, and q uantifiable indicators of PCB b io e ffe c ts. We need to know w hat they can tell us ab o u t our em ployees' physiological status. GB^P 010343 783154 - 7- Fig. 31 Third, we need to determine PGDF levels in both new and used trans- ; former fluids, in order to ensure that the transformer PCB's are as low as i capacitor PCB in toxic contaminants. Fourth, we need to ensure the.development of analytical capabilities for i determining the PCDF levels in environmental specimens, such as fish and ! sludge. If the agencies are ever to regulate environmental PCB hazards on the ! basis of the toxic irppurity present, rather than the total PCB, they will have to have access to some analytical method that can be used on field specimens by ! their enforcement agents. ! Where will all this lead? ! Looking into the future, we anticipate that ongoing academic medical I research will gradually reveal the detailed chemical and biological mechanisms ' involved in toxic responses to PCB's. Concurrently, we would hope to see the ' sort of health status documentation effort that's now shaping up at Hudson Fails extended to other locations. As the results of such findings become available, | we anticipate some easing of regulatory controls, particularly those over fishing and low level waste management. Such relaxation could be most easily instituted by changing the basic criterion for human protection from the level, of PCB to that of PCDF. With such regulatory reform, deescalation of the PCB' supertoxicity myth, which has so bemused the media in recent year, could begin. i i 783155 \ i. i t ! Ii H s tOdHar, HEALTH EFFECTS OF PCB's What are PCB's? What are their Biological Properties? How Toxic are they? What do Electrical PCB's do to People? 783156 SKOIOdNao 1 TYPICAL PCB STRUCTURES 0+7CATA ,T M U r> 783157 Average No . of Cl 's 1.5 3 5 6 POLYCHLORINATED BIPHENYLS "Aroclor" Designation 1221 12*12 125A 1260 Electrical .Use CAPACITORS CAPACITORS TRANSFORMERS TRANSFORMERS 783158 in OIOdNSO 783159 I .0 01 Cl oz / j f T ^ n v' ^ n / v r .09 9Z Z 0T AT It GENP 010348 ,0il -ST " i s* Q * ll * CONTAMINANTS IN PCB's POLYCHLORINATED DIBENZOFURAN PCDF jh c O -- 0 - CH3 POLYCHLORINATED METHYL BIPHENYL 783160 POLYCHLORINATED NAPHTHALENE 6K0I0 JNJRO o-6-o POLYCHLORINATED TERPHENYL HEALTH EFFECTS OF PCB's What are PCB's ? What are their Biological Properties? 783161 ArcATA JfKTvir 6 BIOLOGICAL PROPERTIES Easy tissue penetration a Lungs Intestines Skin Gills Bioaccumulation and retention 783162 783163 z c fo io d siao EXCRETION ROUTES Volatilization through lungs Liver ----Bile ------ - Intestines Feces o Oxidation--- - Kidneys--- - Urine 6 -o ^ OXIDASE * o 2 -------------- (cytochrome P M 8 or P450) {^0H 8 EFFECTS OF CHLORINATED ORGANICS ON LIVER Physiological Responses Microsomal Enzymes formed Proliferation of Microsomes Cell growth Toxic Effects Cell death Collapse of liver function Tumors eseorodMao 783164 783165 CANCER-CAUSIN6 AGENTS Direct-acting Carcinogens Mutate cell's DNA Procarcinogens Metabolizable to direct-acting carcinogens Promoters Make mutant cells malignant Activators Induce enzymes that activate procarcinogens weoioaNao 10 CHLORACNE SYNDROME Man Skin: blackheads, pustules, pigmentation Sometimes gastrointestinal, neurological disorders Chickens Edema disease; birth defects (Teratogenesis) 783166 sseoro JN?rr> II RELATION OF STRUCTURE AND BIOLOGICAL EFFECTS Propeller-shaped molecules induce P450 Cytochromes - Many individual PCB species Flat rectangular molecules induce P448 Cytochromes - Three minor forms of PCB - PCDF IMPURITIES - Dioxins Species active in causing Chloracne also induce P*!^ 9O rO /TK Tqm .9V^ THEORY OF BIOLOGICAL RESPONSE Active agent binds to shape-specific recognition site on receptor protein Agent-receptor complex induces expression of normally silent gene sequences New proteins produced: - P M 8 or.PA50 Cytochromes - Other intracellular enzymes - Stimulators/suppressors of cell growth? - Stimulators/suppressors of cell function? 010 cfkftfr} 89t8^ IMPLICATIONS Biological effects are basically regulatory; SHOULD EXHIBIT DEFINITE THRESHOLDS FOR OCCURRENCE Even pure PCB's may not be devoid of some forms of REGULATORY ACTIVITY RfOTO 783169 HEALTH EFFECTS OF PCB's What are PCB's ?. What are their Biological Properties? How Toxic are they? < --------- 783170 6S010 dbldn 15 \ REPORTED U.S. EPISODES OF PCB-RELATED CHLORACNE Episode 1 2 3 Date 1933 1950-2 ~1963 Affected/ Exposed 23/24 7/14 13/15 Comment BAD BATCH PCB FROM EARLY PRODUCTION VAPORS FROM LEAKY HEAT EXCHANGER VAPOR FROM BAKING PCB- PLASTICIZED ENAMEL 783171 fato dwao 16 OCCUPATIONAL HEALTH STANDARDS AND EXPERIENCE Heavy doses of Aroclors caused liver disease in rats No-effect doses TLV's established 40 YEARS OCCUPATIONAL HEALTH EXPERIENCE - NO LIVER DISEASE - NO FURTHER CHLORACNE EPISODES - No OTHER HEALTH PROBLEMS Lack of scientific documentation &lB l O ff) rT M tm 17 YUSHQ EPISODE - SOUTHWEST JAPAN 1968 1300 CASES OF SEVERE CHLORACNE 400,000 DEAD CHICKENS Traced to rice oil contaminated with Kanechlor 400 FROM HEAT EXCHANGER ^ Z9OlOdM3Q ANALYSIS OF YUSHO INCIDENT Findings of J,G. Vos * - Birth defects and Chloracne in animals CORRELATE WITH PCDF CONTENT OF PCB's t PCDF CONTENT OF PCB's VARIES - European and Japanese: 5-20 ppm - American: 0-2 ppm Yusho heat exchanger contained 2000-5000 ppm PCDF's PCB's eliminated; PCDF's lingered & moiodMao 783174 FDA FINDS CARCINOGENICITY TESTS INCONCLUSIVE (44 FR 38330 - Ju n e 29, 1979) Evidence: Aroclor 1221 1016 1242 1242 1254 1254 1254 1260 1260 Species rabbit RAT RAT RAT RAT RAf RAT RAT RAT Result NEG. NEG. NEG, NEG. NEG. POS. NEG. NEG. POS, Author Keller Burse Monsanto Burse Monsanto Kimbrough NCI Monsanto Kimbrough Date 1973 1974 1969 1974 1969 1972 1977 1969 1972 783175 rodmo CONCLUSIONS FROM YUSHO AND RELATED ANIMAL TESTS American PCB's chemically and toxicologically DIFFERENT FROM THOSE CAUSING YuSHO EPISODE Bui Public has become alarmed . 783176 S9OIO<TNtaO HEALTH EFFECTS OF PCB's What are PCB's ? What are their Biological Properties? How Toxic/ are they? What do Electrical PCB's do to People? <^0T0<TN3O 783177 HEALTH INVESTIGATIONS AT HUDSON FALLS Dr . I. Selikoff - Mt . Sinai Medical School - 1976 Examined 326 volunteers Reported them mainly normal Some evidence of decreased pulmonary functions Some evidence of increased dermatological symptoms <g> ^ 9010 dKftfn 783178 HEALTH INVESTIGATIONS AT HUDSON FALLS Dr . J. Feingold - General Electric - 1976 / 195 HEAVILY EXPOSED EMPLOYEES AND 20 FAIRFIELD CONTROLS Blood samples, clinical examinations No obvious health problems seen Detailed data analysis begun fall 1979 Repeat examination 1979 890l0JM 3O 783179 HEALTH INVESTIGATIONS AT HUDSON FALLS Dr . I. Selikoff's Associates - Mt . Sinai Medical School - 1979 Repeat of 1976 tests Many new tests performed Results still unknown 783180 9 e69010 25 HEALTH INVESTIGATIONS AT HUDSON FALLS NIOSH - 1977 Mortality data analysis of Hudson Falls and Aerovox POPULATIONS Draft report issued 1979 Investigation turned over to NYS Health Department 1979 m< * *i U r Ci / f OJO JKTTTn 783181 FINDINGS TO DATE 1. PCB LEVELS MUCH ABOVE NORMAL Exposed capacitor workers Fairfield controls 1.5 grams 0.1 grams 2. PCB l e v e l s r e m a i n i n g h i g h 3. No SERIOUS HEALTH EFFECTS Examination results normal Mortality rates all below normal 4. Possible subclinical abnormalities Triglycerides, Serum Enzymes 783182 0 T/rOTOrTKmo 27 ONGOING ACTIVITIES \ Assisting NIOSH/NYSDH in completing their mortality studies Monitoring Mt . Sinai/American Cancer Society studies Qualifying reliability of PCB analyses Working on analysis of Dr . Feingold's clinical data Devising reliable method for PCDF analysis Determing PCDF levels in 19A6-77 capacitors 783183 77,010 aw ao 28 OTHER ONGOING PCB-RELATED ACTIVITIES Environmental fate - Microbiological studies - Adsorption - Volatilization Destruction of PCB's in contaminated transformer oil - Laboratory investigations - Field test at ASBD Philadelphia site - Advanced methods 783184 *' 010 rTKRr 29 FUTURE ACTIONS t Maintain surveillance of exposed Hudson Falls population Correlate levels of P450 and P448 Cytochromes with OTHER SUBCLINICAL DATA Determine PCDF levels in transformers Determine PCDF levels in fish, river bottom sludge, dump sites 783185 & TA TkTrTf^ 30 OUTLOOK Research results on detailed toxicity mechanisms Extension of health status documentation Easing of regulatory controls 'yeO 10 dNHf) 783186