Document MG07YMXb271zjvEovb42GJpO7

I. I I C OO-jJU /.S/H * f C - f Y4 7 7 - Edited by llchard E. Ulster Dynamac Carp Enviro Control Division Rockville. Maryland JUfla L Young U .S. Veterans Administration Wasflington. D .C . and Alan r. Gray Dynamac Corp Enviro Control Division Rockville, Maryland ! PLENUM PRESS NEW YORK AND LONDON > 1 k I ! I 000214 Library of Congress Cataloging in Publication Oata Main entry under title: Human and environmental risks of chlorinated dioxins and related compounds. (Environmental science research: v. 26) Proceedings of an international symposium on Chlonnated Dioxins and Related Com* pounds, held October 2 5 -2 9 , 1981 in Arlington, Va. Includes bibliographical references and index. 1 TetrachJorodibenzodioxin--Environmental aspects--Congresses. 2. Tetrachloro- dlbenzodioxin--Toxicology--Congresses. I. Tucker, Richard E. II. Young, Alvin L III Gray, Allan P. IV. Series. QHS45.P4H8S 1982 6 6 V .8 9 1 5 82-18121 ISBN 0306*41170-9 Proceedings of an international symposium on Chlorinated Oioxins and Related Compounds, held October 25--29. 1981, in Arlington, Virginia 1983 Plenum Press, New York A Division of Plenum Publishing Corporation 233 Spring Street, New York. N .Y. 10013 All rights reserved No part of this book may be reoroduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, microfilming, recording, or otherwise, without written permission from the Publisher Pnnted in the United States of America 000215 ENVIRONMENTAL SCIENCE RESEARCH Editorial Board Alexander Hollaender Associated Universities. Inc. Washington, D .C . Ronald F. Probstein Massachusetts Institute o f Technology Cambridge. Massachusetts Bruce L. Welch Environmental Biomedicine Research. Inc. and The Johns Hopkins University School o f M ediane Baltimore. Maryland Recent Volumes in this Series Volume 17 P O L L U T E D RAIN Edited by Taft Y . Toribara. Morton W . Miller, and Paul E . Morrow Volume 18 E N V IR O N M E N T A L E D U C A T IO N : Principles. Methods, and Applications Edited by Trilochan S . Bakshi and Zev Naveh Volume 19 P R IM A R Y P R O D U C T IV IT Y IN T H E SE A Edited by Paul G . Falkowski Volume 20 T H E W A TER E N V IR O N M E N T : Algal Toxins and Health Edited by Wayne W . Carmichael Volume 21 M E A S U R E M E N T O F R ISK S Edited by George G . Berg and H . David Maillie Volume 22 SHORT-TERM BIOASSAYS IN TH E A N A LYSIS OF CO M P LEX EN V IR O N M EN TA L M IX T U R E S II Edited by Michael D . Waters. Shahbeg S. Sandhu. Joellen Lewtas Huisingh,' Larry Claxton. and Stephen Nesnow Volume 23 B IO SA L IN E R E S E A R C H : A Look to the Future Edited by Anthony San Pietro Volume 24 C O M P A R A T IV E C H E M IC A L M U T A G E N E SIS Edited by Frederick J . de Serres and Michael D . Shelby Volume 25 G E N O T O X IC E FFE CT S O F A IR B O R N E A G E N T S Edited by Raymond R. Tice, Daniel L. Costa, and Karen Schaich Volume 26 H U M A N A N D E N V IR O N M E N T A L RISKS O F C H L O R IN A T E D DIOXINS AND RELATED COMPOUNDS Edited by Richard E. Tucker. Alvin L . Young, and Allan P, Gray A Continuation Order Plan is available for this senes. A continuation order will bring delivery o f each new volume immediately upon publication. Volumes are billed only upon actual shipment. For further information please contact the publisher. G0023.S A MORTALITY STUDY OF WORKERS EMPLOYED AT THE MONSANTO COMPANY PLANT IN NITRO, WEST VIRGINIA Judith A. Zack, and William R. Gaffe Monsanto Company St. Louis, Missouri USA BACKGROUND The compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a highly toxic impurity that is formed in trace quantities during the production of 2,4,5-trichlorophenoxyacetic acid (2,4,5-T). Exposure to TCDD can cause chloracne, a skin disorder characterized by comedones, cysts, and abscesses.1 Outbreaks of chloracne have been reported among workers associated with the production of 2,4,5-T and 2,4,5-T based products. Such Incidents resulting from both accidental and routine occupational exposures have been reported from several countries.2 f The first reported industrial accident Involving exposure to TCDD occurred in 1949 at the Monsanto Company plant in Nitro, West Virginia. A total of 122 employees developed symptoms of chloracne following a trichiorophenol (TCP) process accident. An undetermined number of other employees developed symptoms of chloracne resulting from exposure to the regular operations concerned with 2,4,5-T pro duction over the period 1948-1969. Between 1949 and 1953, Ashe and Suskind5,if examined thirtyeight Nitro plant employees with chloracne. Twelve of these had developed symptoms of chloracne directly following the 1949 TCP acci dent; twenty-six other chloracne cases had resulted from exposure to the regular 2,4,5-T production operations. In addition to chloracne, other signs and symptoms were observed in this group. These included severe aches in the lower extremities, fatigue, nervousness and irritability, loss or decrease of libido, dyspnia, and vertigo. These findings are consistent with those that have been reported in ocher industrial incidents.5 575 I .t il y F Si ;i 000217 5 7 6 J. A . Z A C K A N D W. R. G AFFEY To examine the chronic health effects of exposure to TCDD, a .mortality study of Che Nitro plant employees who had developed symptoms of chloracne following the 1949 TCP accident was conducted.* The study cohort was comprised of 121 of the 122 chloracne cases; one female who was living as of the endpoint of the study was exclude from analysis. Ac the time of the incident, it was assumed that the symptoms were caused by exposure to unknown products of decompositior Prom today's vantage point, these symptoms suggest exposure to TCDD. The 121-member study cohort, with a presumptive high-peak exposure to TCDD, was followed for mortality through 1978. The entire cohort was traced: thirty-two. deaths were observed and eighty-nine persons were confirmed as living. Analysis indicated no excess in total mortality or in deaths from malignant neoplasms. The study presented here examines the mortality of Nitro plant workers who were assigned to an area of TCP or 2,4,5-T production, with potential for exposure to TCDD. The mortality of these workers Is examined in the context of the mortality experience of the total Nitro plant worker population. The Monsanto Nitro plant began operations in 1922, when the Rubber Service Laboratories purchased the plant as war surplus and began production of chemicals and additives for the growing rubber industry. In 1929, Monsanto Company purchased the Nitro plant from the Rubber Service Laboratories and entered the rubber chemicals business. Over the years, the Nitro plant has diversified to where it now produces agricultural chemicals, paper chemicals, plasticizers, fine chemicals, and intermediates, in addition to rubber chemicals. The plant is situated In the Kanawha River Valley, an area containing one of the largest concentrations of chemical production facilities in the United States. Of the many chemicals used over the years at the Nitro plant, one has an established association with the occurrence of cancer in man. Para-aminobiphenyl (PAB), used from 1941 through 1952 for use as a rubber antioxidant and dye intermediate, was shown in 1954 by Walpole et a-1.7 to Induce bladder cancer in dogs. In 1955, Melick et al. confirmed the carcinogenicity of para-aminobiphenyl to man with the reporting of bladder tumors among workers exposed to thi3 chemical at two Monsanto plants. Para-aminobiphenyl was produced at one plant and then transferred by tank car to the Nitro plant where additional processing was carried out. The minimum duration of exposure reported to have produced a bladder tumor is 133 days; the latent period has ranged from 15 to 35 years.9 An intensive screen ing program was instituted at Monsanto Company about 1955 to examine, on a continuing basis, all workers exposed to this chemical. Seven deaths from bladder cancer have occurred among Nitro plant employees enrolled in this program. These seven deaths are included in the present study. 000218 MORTALITY STUDY OF WORKERS 577 Other chemicals with known health effects produced at the Nitro plant include methylparathion and carbon disulfide. The acute effects of exposure to each of these chemicals have been described* while the chronic effects are less well understood. Besides p-aminobiphenyl, several other rubber chemicals are of potential health concern. For all of these, there is insufficient evidence to evaluate their carcin ogenicity to man. Tetramethyl thiuram disulfide is considered an animal carcinogen** and there is some evidence, although not suffi cient. that N-methyl-N,4-dinitrosaniline is also an animal carcin ogen.*2 For several other rubber chemicalsr there is insufficient evidence to evaluate the carcinogenicity to animals. However, these chemicals have the potential for forming nitrosamines, certain of which are known animal carcinogens.* Zinc dimethyl dithiocarbamate, tetramethyl thiuram disulfide and tetramethyl thiuram monosulfide have the potential to form N-nitrosodimethylamine. N-Nitrosomorpholine has been found in product samples of 2-(morphollnothio) benzothiazole and 4,4'-dithiodimorpholine.(Frisone, G.J., The General Tire and Rubber Company, unpublished data). Although several of the chemical compounds produced or used at 'the Nitro plant over the years have been associated with adverse health effects, no attempt has been made to relate chemical exposure to mortality with the exception of decedents exposed to the TCP or 2,4,5-T operations and potentially exposed to TCDD. As a result, the only specific hypothesis that can be tested is whether a relation ship, exists between potential TCDD exposure and proportional mortal ity, especially for malignant neoplasms. The mortality for this group is examined in addition to that of the total Nitro plant worker population. POPULATION AND METHODS A study cohort was developed from the Nitro plant consisting of employees active on or after January 1, 1955 with one or more years of employment on the hourly roll prior to December 31, 1977. Salaried personnel who had never worked on the hourly roll were excluded from study because many of these employees had no appreciable exposure to the plant environment and, for the most part, their exposure cannot be determined from plant records. Females and non-white males were also excluded because of their small numbers. The cohort was assembled using government earnings reports, independent of the plant work history records. Annual earnings reports were available on a computer file* from 1951 through 1977. Names and social security numbers were identified from this source. Work history records were used to supplement the earnings records. Information on race, sex, date of birth, date of hire, date of sepa ration, and, if deceased, 2,4,5-T exposure was abstracted from these records. Ascertainment of 2,4,5-T exposure was confined to decedents only because it was too tedious to do for the entire cohort. The 578 J. A. ZACK AND W. R. GAFFEY information from the work history records was used to determine whicl names identified from the annual earnings records met the cohort entrance criteria. Employees identified from the earnings records who terminated prior to 1955 were not included in this study because work history records for all such employees were not retained prior to this date. Exposure to 2,4,5-Twas determined by assignment to a 2,4,5-T operation based on the work history records. 2,4,5-T exposure was determined for all but one decedent. Employees holding a job having plant-wide responsibilities with the potential for expos'ure to 2,4,5-T were, for the purposes of this study, considered to be nonexposed. The vital status of each member of the-study cohort was deter mined using standard follow-up techniques and ascertained as of December 31, 1977. Death certificates were coded by an Independent nosologist for the underlying cause of death, according to the rules of the Eighth Revision of the International Classification of Diseases, Adapted. Data for the total Nitro plant study population were analyzed by the modified life-table method using the U.S. population as the standard. Vith this method of analysis, the age-, race-, time-, and cause-specific mortality rates for the U.S. general population are applied to the person-years lived classified by age, race, and time. A standardized mortality ratio (SMR) was calculated for. 23 selected cause of death categories. Cause-specific SHR's for 15 selected cancer sites were calculated for subgroups of the total Hltro plant study population defined by date of death, age at death, and year of hire. 'The statistical' significance of the deviation in a SMR from 100 was tested using the formula: - 1 standard error of SMR = 100 Vho. observed deaths no. expected deaths If the observed SMR differed from 100 by 1.96 standard errors, it was regarded as significant at the 57. level. A SMR was tested for significance only when the observed number of deaths was five or greater. Data for those deceased were also analyzed according to 2,4,5-T exposure using the proportional mortality method. In this case, the expected number of deaths is calculated on the basis of proportions of deaths observed in the U.S. general population.- A proportional mortality ratio (PMR) was calculated for 23 selected cause-of-death categories. ?MR's were calculated separately for those exposed to 2,4,5-T and for those not exposed. The statistical significance of the deviation of a PMR from 100 was tested by calculating the 95Z C00220 MORTALITY STUDY OF WORKERS 579 confidence interval for the PMR for a given cause k according to the formula: confidence interval N(confidence limits for Z of observed deaths) for PMR^ exp^ where N * number of observed deaths for all causes Both the standardized and proportional mortality analyses were conducted using the computer program developed by Monson. 5 The observed mortality was compared to that of the United States white male population for the time period of study. RESULTS .A total of 884 men were identified for study and traced for deaths through 1977. The entire cohort was successfully traced. Death certificates were obtained for all deaths. Seven hundred twenty-one (82Z) were verified as living and 163 (18Z) were confirmed dead by death certificates. Tables 1-3 characterize the total Nitro plant study population by age at hire, year of hire, and length of employment. The dis tribution of the study population by age at hire indicates that the workers were fairly young at first hire (Table 1). Seventy-two percent of the study cohort were hired by age 30. Hone were hired at age 50 or above. Table 2 shows the distribution of the study population by year of hire. The majority of workers (75.3Z) were hired during the period 1940-1959, while smaller percentages of workers were hired prior-to 1940 (10.8Z) and after 1960 (13.9Z). An examination of the study population by length of employment indicates a fairly even distribution over the intervals less than 10 years, 10-19 years, 20-29 years, and greater than 30 years (Table 3). Observed and expected deaths occurring during 1955-1977 among the total Nitro plant study population are shown by cause in Table 4. The SMR for all causes of death was 103 with 163 deaths observed and 158.10 expected. There were 35 deaths from malignant neoplasms with 30.92 expected, yielding a SMR of 113. (Singlficantly elevated SMR's were seen for the categories of malignanfneoplasms of the genitourinary organs and of the bladder. The SMR for bladder cancer was 989 with 9 deaths observed and 0.91 expected. This excess in bladder cancer deaths is reflected in the elevated SMR for malignant Qiio^lasms of the genitourinary organs. A significantly elevated SMR is also seen for arteriosclerotic heart disease. There were 79 deaths from this cause with 59.40 expected (SMR - 133). The SMR for \ i*i * \ 000221 r 582 J. A. ZACK AND W. R. GAFFEY ocher circulatory diseases was significantly low at 56. A significant deficit was also seen for the category of all other diseases where Chi SMR was 48 with 5 deaths observed and 10.46 expected. Trends for malignant neoplasm deaths with calendar time are showi in Table 5. SMR's which increased consistently over the period 1955-- 1977 are seen for the categories of all malignant neoplasms and malig nant neoplasms of the respiratory system. The SMR for all malignant neoplasms rose from 32 to 131. The SMR for malignant neoplasms of ch< respiratory system rose from 0 to 172 reflecting a SMR for lung cance which increased from 0 to 181. Although based on very small numbers, Che SMR for malignant neoplasms of the digestive organs and peritonea consistently decreased over time from 99 to 24. The SMR for malignan neoplasms of the genitourinary organs peaked during the period 19601969. This is reflected in Che SMR for bladder cancer which increase' from 0 in 1955-1959 to a peak of 1471 in 1960-1969 and decreased to 833 in 1970-1977. The analysis of observed and expected deaths from malignant neo plasms by age at death revealed little in terms of consistent trends with age (Table 6). For most of the cause-of-death categories, the SMR peaked at age 45-64 rather than continuing to rise with lncreasin age. Bladder cancer is one category where the SMR remained high at age 65 and over. The distribution of deaths from malignant neoplasms by year of hire is shown in Table 7. No deaths from malignant neop_lasms were observed among workers hired after 1960. The SMR for all malignant neoplasms was similar for those hired prior to 1945 and for those hired in the period 1945-1959. The greatest difference in SMR's be tween chose hired prior to 1945 and those hired from 1945-1959 occurs with bladder cancer. The SMR for bladder cancer is highest for chose hired prior to 1945 with a SMR of 1111. A subset of deaths identified from the total Nitro plant study population was studied separately. Table 8 characterises the deced ents according to 2,4,5-T exposure. Of the 163 decedents, 58 (35.6Z) were considered to be exposed to 2,4,5-T based on their work history records, while 104 (63.82) were considered to be non-exposed. The exposure of one decedent was unkown. The results of the proportional mortality analysis by 2,4,5-T exposure classification are presented in Table 9. The proportion of cancer deaths among 2,4,5-T workers is lower than in the non-exposed group (PMR: 82 vs. 122). The PMR for lung cancer deaths is slightly higher in the exposed group (PMR: 159 vs. 117). The proportion of deaths due to bladder cancer is higher among the decedents not ex posed to 2,4,5-T. There were 7 deaths from bladder cancer among thes workers with 0.65 expected (PMR * 1077). The PMR for bladder cancer among decedents exposed to 2,4,5-T was 909 with 2 deaths observed and 000222 MORTALITY STUDY OF WORKERS , 587 0.22 expected. PMR's for both exposure groups are quite similar for diseases of circulatory and respiratory system. Slight differences appear in Che PMR's between the two groups for diseases of the diges tive system and all other diseases. However, the PMR's for both groups are quite low. The PMR for external causes of death is slightly higher in the exposed group (PMR: 129 vs. 86). A listing of the cancer deaths among the 2,4,5-T exposed is given in Table 10. Table 11 listed the cancer deaths among the non-exposed group. DISCUSSION The observation made many years ago of an apparent excess in Sladder cancer among Nitro plant workers was confirmed and quantified in the mortality analysis of the total Nitro plant population presented here. The SMR for bladder cancer was 989 and was the only statisti cally significant SMR among those for malignant neoplasms. The excess in mortality is not seen until 1960. The SMR peaked in the 1960's and declined somewhat in the 1970's. The excess also appeared to be clustered in those decedents aged 65 years and older at death and in chose hired prior to 1945. This would suggest that we should see a further decline in the SMR for bladder cancer over time. Although not statistically significant, the SMR for lung cancer appears to be elevated. The SMR increased with calendar time and was highest in those hired prior to 1945. The elevation appears to be clustered in those aged 45-64 years of age at death (SMR * 184) and does not show a gradient with age. Further analyses to evaluate trends in lung cancer deaths as they relate to occupation cannoc be carried out due to limitations in the data collected in this study. The SMR for diseases of the circulatory system was elevated at 111. This is most likely a reflection of the higher mortality from heart disease which has been observed for Charleston, West Virginia and Kanawha County, Vest Virginia (unpublished data, Neas LM, 1979 and Edterline PE, 1979). For the total Nitro plant study population, there was a statistically significant excess in deaths from arterio sclerotic heart disease and a deficit In deaths from other circulatory diseases. This variation in the distribution of deaths from that of the U.S. may be due to risk factor or medical care differences in the slant population and the local area. These may include differences in smoking habits, the availability and use of medical services and :he specificity of diagnoses. The proportional mortality analysis of decedents by 2,4,5-T exposure classification indicated no unusual patterns of mortality .n the 2,4,5-T exposed. The proportional mortality ratio (PMR for lalignanc neoplasms was low (PMR 82) in the exposed group. Lung .ancer was the only site among the malignant neoplasms which was omewhat higher in the exposed group. i J f s A ;i ti 000223 590 J. A. ZACK ANO W. R. GAFFEY The PHR analysis is limited in that an assessment of the total force of mortality cannot be made. The cause-specific FMR's only approximate what an SMR analysis would have produced.*6 The PMR analysis presented here estimates the cause-specific risks associated with 2,4,5-T exposure and potential TCDD exposure. It is interesting to compare the results of this study of Nitro plant workers potentially exposed to TCDD with the results of the study of Nitro workers involved in the 1949 TCP accident. The workers Involved in that incident had'presumed TCDD exposure as evidenced by chloracne. The results of the two studies are similar in that neither shows an excess in deaths' from any site among malignant neoplasms. A recent study of Ott et al.*7 found no excess in total mortality or in deaths from malignant neoplasms among.workers exposed to 2,3,5-1 These workers were probably exposed to very low levels of TCDD since no cases of chloracne were observed. Other studies of workers who developed chloracne resulting from TCDD exposure have been conducted and have been reviewed.6 At the present time, data from these various studies do not constitute corroborative evidence of a cancer risk to man for any particular cancer site. REFERENCES 1. Greig, J.B.: The toxicology of 2,3,7,8-tetrachlorodibenzo-pdioxin and its structural analogues. Ann. Occup. Hyg. 22: 411-420, 1979. 2. International Agency for Research on Cancer: Long-term hazards of polychlorinated dibenzodioxins and polychlorinated dibenzofurans. IARC Internal Technical Report No. 78/001. Lyon: IARC, 1978. 3. Ashe, W.F. and Suskind, R.R.: Reports on chloracne cases, Monsanto Chemical Company, Nitro, West Virginia. Reports of the Kettering Laboratory, December 1949 and April 1950. 4. Suskind, R.R.: A clinical and environmental survey, Monsanto Chemical Company, Nitro, West Virginia. Report Of the Kettering Laboratory, July 1953. 5. International Agency for Research on Cancer. IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Vol. 15. Some Fumigants, the Herbicides 2,4-D and 2,4,5-T, Chlorinated Dibenzodioxlns and Miscellaneous Industrial Chemicals. Lyon: IARC, 1977. 6. Zack, J.A. and Suskind, R.R.: The mortality experience of workers exposed to tetrachlorodlbenzodioxin in trlchlorophenol process accident. J. Occup. Med, 22:11-14, 1980. 7. Walpole, A.L., Williams, M.H.,. and Roberts, D.C.: Tumours of urinary bladder in dogs after ingestion of 4-aminodiphenyl. Brit. J. Industr. Med. 11:105-109, 1954. 000224 MORTALITY STUDY OF WORKERS 591 8. Melick, W.F.: First reported cases of human bladder tumors due to a new carcinogen - xenylamine. J. Urol. 74:760-766, 1955. 9. Melick, U.F., Naryka, J.J., and Delly, R.E.: Bladder cancer.due to exposure to para-aminobiphenyl: a 17-year followup. J. Urol. 106:220-226, 1974. 10. Key, M.M.: Ocuppational Diseases: A Guide to Their Recognition. U. S. Department of Health, Education and Welfare, Public Health Service, Center for Disease Control, National Institute for Occupational Safety and Health. DHEW (NIOSH) Publication No. 77-181. Washington: U.S. Government Printing Office, 1977. 11. International Agency for Research on Cancer. IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Man. Vol. 12. Some Carbamates, Thiocarbamates, and Carbazides. Lyon: IARC, 1971. 12. International Agency for Research on Cancer. IARC Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Man. Vol. 1. Lyon: IARC, 1971. 13. Magee, P.N.,: N-nitroso compounds and related carcinogens. In: Searle, C.E.(ed): Chemical Carcinogens. Monograph 176. Washington: American Chemical Society, 1976. 14. Eighth Revision, International Classification of Diseases, Adapted for Use in the United States. U.S. Department of Health, Ed ucation, and Welfare, Public HealthService, PHS Publication No. 1693. Washington: U.S. Government Printing Office, 1977. 15. Monson, R.R.,: Analysis of relative survival and proportional mortality. Comput. Biomed. Res. 7:325:332, 1974. 16. Decoufle, P., Thomas, T.H., and Pickle, L.W.: Comparison of the proportionate mortality ratio and standardization mortality ratio risk measures. Am. J. Epidemiol. 111:263-269, 1980. 17. Ott., G., Holder, B.B., and Olson, R . : A mortality analysis of .employees engaged in the manufacture of 2,4,5-crichlorophenoxyacetic acid. J, Occup. Med. 22:47-50, 1980. < 000225 5 8 8 J. A . Z A C K A N D W. R. 000226 Table 10. Deaths Due to Malignant Neoplasms Among Nltro Plant Workers Exposed to 2,4,5-T Year pf Birth Year of Hire Year of 1st Year of Year of Smoking Cause of Death as Given on Exposure Terra. Death History* Death Certificate 1917 1946 1951 1972 1972 Cigarettes Carcinoma left lung with metastases (162.1) 1911 1948 1955 1972 1972 * Cigarettes Metastatic carcinoma of the lung (162.1) 1916 1946 1959 196B 1968 Cigarettes Bronchlogenlc carcinoma of right upper lobe (162.1) 1901 1944 1956 1963 1973 Cigarettes Carcinoma lung with metastases (162.1) 1911 1941 1948 1971 1975 Cigarettes Bronchlogenlc carcinoma with cerebral metastases (162.1) 1922 1945 1948 1972 1973 Non-smoker Bronchlogenlc carcinoma iwith metastases (162.1) 1923 1946 1950 1972 1972 Cigarettes Generalized llposarcoma (171.9) 1902 1922 1948 1966 1966 Non-smoker Metastatic carcinoma urinary bladder (188.0)** 1910 1944 1948 1968 ` 1968 Non-smoker * Obtained by interview with former coworkers of decedents. ** Included on the Nltro plant PAB roster. 1 Carcinoma of the urinary bladder (188.0)** a > m*-nn 5 86 J. A . Z A C K A N D W . R. G AFFEY Table 9. Observed and Expected Number of Deaths During 1955-1977 by Cause and 2,4,5-T Exposure Category Showing Proportional Mortality Ratios (PMR'S) Cause of Death 2,4,5-T Exposure Category Exposed Non-exposed <Observed Expected PMR Observed Expected PMR All malignant neoplasms Buccal cavity and pharynx Digestive organa and peritoneum Stomach Liver All other digestive organs Respiratory system Lung All other respiratory organs Skin Genitourinary organs Bladder Ail other genitourinary organs Lymphatic and hematopoietic tissue Other sites Diseases of the nervous system and sense organs Diseases of the circulatory system Arteriosclerotic heart disease, including CHD All other diseases of the circulatory system Diseases of the respiratory system Diseases of the digestive system All other diseases External causes of death Total number of deaths: *p < .05 9 0 0 0 0 0 6 6 0 0 2 2 0 0 1 0 31 27 4 2 1 3 12 58 10.94 0.38 2.80 0.52 0.19 2.09 3.78 3.57 0.21 0.29 0.96 0.22 0.74 1.35 1.38 0.61 26.48 19.72 6.76 2.67 3.70 4.31 9.29 58.00 82 0 0 0 0 0 159 168 0 0 208 909 0 0 . 72 >0 117 137 59 75 27 70 129 25 0 3 0 0 3 8 6 0 0 10 7 3 1 3 0 61 52 9 4 4 2 8 104 20.43 122 0.64 0 5.74 52 1.06 0 0.39 0 4.29 70 6.81 117 6.42 125 0.39 0 0.35 0 2.70 370* 0.65 1077* 2.05 146 2.07 48 2.12 142 0.83 0 55.34 110 39.68 131* 15.66 57 6.49 62 4.93 81 6.70 30 9.28 86 104.00 Table 4. Observed and'Expected Humber of Deaths Standardized Mortality Ratios (SMR'S) I Cause of Death All causes of death All malignant neoplasms Buccal cavity and pharynx Digestive organa and peritoneum Stomach Liver All other digestive organs Respiratory system Lung All other respiratory organs Skin Genitourinary organs Bladder All other genitourinary organs Lymphatic and hematopoietic tissue Other sites Diseases of the nervous system and sense organs Diseases of the circulatory system Arteriosclerotic heart disease, including CHD All other diseases of the circulatory system Diseases of the respiratory dystem Diseases of the digestive system All other diseases* External causes of death_______________________ Number at risk: 684 Person-years at risk: 13968,7 *p < ,05 000228 During 1955--1977 by Cause Showing for Total Nitro Plant Study Population 1GDA Codes 8th Rev. Observed Expected 1A0-209 140-149 150-159 151 155-156 -- 160-163 162-163 --- 172-173 185-1B9 188 -- 200-209 320-389 390-458 410-413 -- 460-519 520-577 :-- 800-998 163 158.10 35 30.92 0 1.03 4 8.65 1 1.63 0 0.60 3 6.42 14 10.51 14 9.91 0 0.60 0 0.58 12 3.75 9 0.91 3 2.84 1 3.15 4 3.25 0 1.28 92 82.59 79 59.40 13 23.19 6 9.13 5 8.03 5 10.46 20 15.69 SMR 103 113 0 46 61 0 47 133 141 0 0 320* 989* 106 32 123 0 111 133* 56* 66 62 48* 127 nS 30 H r>; H -< (/> H C o -< o -n s 37^0 m 3) CO VI --CDt MORTALITY STUDY OF WORKERS Table 5. Observed and Expected Deaths from Malignant Neoplasms During 1955-1977 by Calendar Time Showing Standardized Mortality Ratios (SMR'S) for Total Nltro Plant Study Population Cause of Death Calendar Time 1955-1959 1960-1969 1970-1977 Observed Expected SMR Observed Expected SMR Observed Expected SMR All malignant neoplasms 1 Buccal cavity and pharynx 0 Digestive organs and peritoneum 1 Stomach 0 Liver 0 All other digestive organs 1 Respiratory system Lung 0 0 All othet respiratory organs 0 Skin 0 Genitourinary organs 0 Bladder 0 All other genitourinary organa 0 Lymphatic and hematopoietic 0 tissue Other sites 0 *p < .05 3.13 32 13 0.11 00 1.01 99 2 0.25 00 0.09 00 0.67 149 2 0.87 04 0.60 04 0.07 00 0.07 00 0.33 05 0.09 05 0.24 00 0.40 00 0.34 02 11.81 110 0.41 0 3.48 57 0.70 0 0.28 0 2.50 80 3.83 104 3.59 111 0.24 0 0.23 0 1.37 365 0.34 1471* 1.03 0 1.24 0 1.25 160 21 0 1 1 0 0 10 10 0 0 7 4 3 1 2 15.98 131 0.50 0 4.16 24 0.69 145 0.23 0 3.24 0 5.81 , 172 5.52 181 0.29 0 0.28 0 2.05 341 0.48 833 1.57 191 1.50 67 1.68 119 ' 583 **7;r 000229 5 8 4 J. a . Z A C K AN D W . R. GAFFEY 000230 Table 6. Observed and Expected Deaths' from Malignant Neoplasms During 1955-1977 by Age at Death Showing Standardized Mortality Ratios (SMR'S) for Total Nltro Plant Study Population Cause of Death Age at Death <45 45-64 65+ Observed Expected SMR Observed Expected SMR Observed Expected SMR All malignant neoplasms 2 Buccal cavity and pharynx 0 Digestive organa and peritoneum 0 Stomach 0 Liver 0 All other digestive organs 0 Respiratory system 0 Lung 0 All other respiratory organs 0 Skin 0 Genitourinary organs 1 Bladder 1 All other genitourinary organs 0 Lymphatic and hematopoietic 0 tissue Other sites 1 *p < .05 2.39 0.06 0.51 0.10 0.03 0.38 0.54 0.51 0.03 0.13 0.20 0.02 0.18 0.55 0.40 84 0 0 0 0 0 0 0 0 0 500 15000 0 0 250 21 0 4 1 0 3 11 11 0 0 3 2 1 1 2 16.85 125 0.67 0 4.58- 87 0.85 118 0.32 0 3.41 88 6.36 173 5.99 184 0.37 0 0.3 0 1.43 210 0.39 513 1.04 96 1.60 .63 1.90 105 12 0 0 0 0 0 3 3 0 0 8 6 2 0 .1 11.69 0.31 3.57 0.68 0.24 2.65 3.61 3.42 0.19 0.14 2.12 0.50 1.62 1.00 103 0 0 0 0 0 83 88 0 0 377* 1200* 123 0 0.94 106 MORTALITY STUDY OF WORKERS Table 7. Observed and Expected Deaths from Malignant Neoplasms During 1955-1977 by Year of Hire Shoving Standardized Mortality Ratios (SMR'S) for Total Nltro Plant Study Population Cause of Death Observed Expected SMR Observed Expected SMR Observed Expected SMR All malignant neoplasms 25 Buccal cavity and pharynx 0 Digestive organs and peritoneum 2 Stomach 0 Liver o All other digestive organs 2 Respiratory system 10 Lung 10 All other respiratory organs 0 Skin 0 Genitourinary organs 9 Bladder 8 All other genitourinary organs 1 Lymphatic and hematopoietic 1 tissue Other sites 3 *p < .05 21.30 0.70 6.27 1.21 0.45 4.61 7.14 6.73 0.41 0.31 2.90 0.72 2.18 1.95 117 0 32 0 0 43 140 149 0 0 310* 1111* 46 . 51 10 0 2 1 0 1 4 4 0 0 3 1 2 0 2.03 148 1 8.63 0.31 2.19 0.39 0.14 1.66 3.09 2.93 0.16 0.22 0.76 0.18 0.58 1.00 116 0 91 256 0 60 129 137 0 0 395 556 345 0 1.06 94 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0.99 0.03 0.19 0.03 0.01 0.15 0.27 0.26 0.01 0.05 0.09 0.01 0.08 0.20 0.16 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 Table B. 2,4,5-T Exposure Classification for Decendents During 1955-1977 Among Total Nltro Plant Study Population 2,4,5-T Exposure Classification Number of Deaths Percent Exposed 58 - 35.6 Non-exposed 104 63.8 __________ Unknown_______ ______________________________________1___________________________ 0.6 Total 163 100.0 , 585 000231 580 J. A. ZAC K AND W. R. GAFFEY Table 1. Discribution of Total Nitro Plant Study Population by Age at Hire Age at Hire Number Percent <20 20-29 30-39 40-49 50+ Total 122 518 191 53 0 884 13.8 58.6 21.6 6.0 0.0 100.0 Table 2. Distribution of Total Nitro Plant Study Population by Year of Hire Year of Hire Number Percent Prior to 1930 1930-1939 1940-1949 1950-1959 1960-1976 Total 21 74 361 305 123 884 2.4 8.4 40.8 34.5 13.9 100.0 Table 3. Distribution of Total Nitro Plant Study Population by Length of Employment Length of Employment (yrs.) Number Percent <10 10-19 20-29 30+ Total 225 213 204 242884 25.5 24.1 . 23.1 27.4 100.1 i 000232 MORTALITY STUDY OF WORKERS Table 11. Deaths Due to Malignant Neoplasms Among Nitro Plant Workers Not Exposed to 2,4,5-T Year of .Year of Year of Year of Smoking Birth Hire Termin. Death History* Cause of neath as Given on Death Certificate 1911 1945 1966 1968 Cigarettes Carcinoma of colon (153.8) 1904 1935 1957 1957 Cigarettes Carcinoma of liver (157.9) 1899 1929 1959 1960 Pipe Tntraperltoneal carcinoma (158.9) 1905 1944 1970 1972 Cigarettes Carcinoma of lung (162.1) 1909 1943 1962 1962 Cigarettes Carcinoma of left lung (162.1) 1910 1927 1966 1970 Cigarettes Pulmonary carcinoma (162.1) 1912 1944 1965 1965 Cigarettes Carcinoma of apex of right lung (162.1) 1915 1937 1977 1977 Cigarettes Carcinoma of lung (162.1) 1915 1939 1969 1970 Cigarettes Carcinoma of lungs (162.1) 1894 1944 1960 1964 Non-smoker Carcinoma of lung (162.1) 1912 1937 1973 1974 Cigarettes Carcinoma of lung (162.1) 1919 1946 1963 1964 Cigarettes Carcinoma of urinary bladder (188.0)** 1901 1933 1962 1977 Cigarettes Carcinoma of bladder (188.0)** 1897 1941 1962 1965 Cigarettes Carcinoma of urinary bladder (188.0)** 1898 1933 1962 1965 Smoked years ago Carcinoma of urinary bladder (188.0)** 1905 1943 1971 1975 Cigarettes Carcinoma of bladder (1B8.0) 1898 1943 1963 1970 Cigarettes Bladder tumor (188.0)** 1888 1944 1956 1970 Unknown Carcinoma of bladder (188.0) 1905 1933 1969 1977 Cigars Prostatlc carcinoma (185.0) 1906 1946 1968 1977 Cigarettes Carcinoma of prostate (185.0) 1925 1945 1973 1974 Smoked years ago Carcinoma of prostate (185.0) 1919 1943 1972 1973 Cigarettes Hodgkin's Disease (201.0) 1901 1941 1964 1965 Cigars Osteosarcoma arising from left arm (170.4) 1901 1943 1966 1977 Cigarettes Carcinoma of liver & pancreas (197.8) 1922 1944 1964 1964 Cigarettes Adenocarcinoma (199.0) * Obtained by Interview with former coworkers of decedents. ** Included on the Nitro plant FAB roster. 589 000233