Document B5NqYaeGm6eVbr8Nb4bDrvkRm

DEPARTMENT OF HEALTH. EDUCATION. AND WELFARE PUBLIC HEALTH SERVICE CENTER FOR OISEASE CONTROL NATIONAL INSTITUTE FOR OCCUPATIONAL SaPETY AND HEALTH ROBERT A. TAFT LABORATORIES 4676 COLUMBIA PARKWAY. CINCINNATI. OHIO 4S226 October 3, 197/ Mr. Paul Bureau Personnel Manager Monsanto Plastics and Resins Co. 730 Worcester Street Indian Orchard, Ma. 01151 Dear Mr. Bureau: Enclosed please find a copy of the NIOSH preliminary report of the epidemiologic study done on decedents from the Indian Orchard Plant during the period 1950 - 1976. We ask that you review these results and send us your criticism as soon as possible. We will make every effort to consider your criticisms in preparing our final report. Sincerely yours Enclosure cc: Dr. Nessell Mr. Schriver Robert Spirtas, Dr. P.H. Chief, Illness Effects Section Surveillance Branch Division of Surveillance, Hazard Evaluations, and Field Studies RSV 0020131 <L J draft A PROPORTIONAL MORTALITY ANALYSIS OF A CHEMICAL PLANT IN MASSACHUSETTS c * PREPARED BY THE NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH KAREN STANISLAWCZYK ROSE KAMINSKI ROBERT SPIRTAS RSV 0020132 r,^-=vn - - -n y^U_ *vu U uV^liU SUMMARY A mortality analysis of 465 deaths among males formerly employed at a chemical-producing plant demonstrated significantly elevated proportions for cancer of the digestive organs and peritoneum and cancer of the genito urinary tract. The deaths represented those employees who were eligible for death benefits during the period 1950-1976. Mortality excesses remained elevated when specific digestive sites were examined individually. Prostatic cancer was significantly elevated in addition to the general genito-urinary categ6ry. Occupational factors are suspected in association with the observed exces'S of digestive cancers, since the effects of foreign birth do not seem to account for all the excess observed. Moreover, when U.S. born workers are examined separately, digestive cancers remain elevated in proportion to total deaths. RSV 0020133 ni' *= "= ~ r=^ u iJ rn -- - j U _ 'i BACKGROUND In 1975, the National Institute for Occupational Safety and Health (NIOSH) was informed of the occurrence of 86 deaths among former workers of a chemical-producing plant. Analysis of the 86 deaths indicated an excess of cancer, particularly of the pancreas. Among the 86 deaths, 21 (24.4%) were attributed to cancer, four of which were due to cancer of the pancreas. In comparing the mortality experience of the plant with that observed for United States males in 1972, 15 deaths due to all cancers and less than one death due to cancer of the pancreas could have been expected among the 86 observed deaths. Upon reviewing this information, NIOSH initiated further study of the mortality experience among plant employees. The plant, located in Massachusetts, has been operating since 1901. It currently employs about 1500 workers. The majority of active employees at the plant have been working over 10 years and therefore comprise a rela tively stable working population. In 1901, the plant started the production of cellulose nitrate and cellulose acetate which ended in the late fifties and sixties. In 1938, the plant began the production of polyvinyl butyral and phenol-formaldehyde. A few years later, the plant began the production of formalin, formaldehydes, amino plastics, and polystyrene. Production of polystyrene was expanded in the mid-fifties and early sixties and included processes such as polymerization and compounding. Between 1948 and 1955, various polyvinyl chloride products were handled and manufactured. In 1968, styrene alcohol products were introduced, and in 1972, barrier resin production RSV 0020134 ja began at the plant. In addition, various other chemicals have been manufactured at both the pilot and main plant. Review of the recent literature for health effects related to the manufacture of these chemicals has revealed no established association with cancer excesses 1-18 with the exception of vinyl chloride products. Production of vinyl chloride and its polymers has been most frequently associated with the increased occurr ence of angiosarcoma of the liver. However, increased risk for other cancers of the digestive system, cancers of the respiratory system, brain, and lymphomas has also been observed for workers exposed to these compounds.-* It should be recognized that a large number of chemicals are used in the M H manufacture of the major products made at the plant under study. Although some specific chemicals have already been associated with health effects, it is very difficult to pinpoint etiologic agents because workers frequently have exposures to numerous substances over their working lifetime.16-18 RSV 0020135 METHODS The plant was asked to identify all deaths among former male employees for the interval 1950 to April, 1976. Women were excluded since such a small number of female deaths occurred. The plant was able to identify 484 deaths which occurred during the designated interval. Death certificates were acquired for 465 (96%) of the identified deaths. The majority of the deaths occurred either among active employees (who were currently working at the time of their deaths) or among retirees (who were eligible for pension or death benefits). Only deaths of employees for which plant records were main tained were identified. Deaths occurring among employees who terminated employment or who retired and were ineligible for death benefits were, essen- * tially not identified. Therefore, the 465 deaths studied are probably raore^ representative of long-term employees than of those who left after a short period of employment. Additional data was collected on deaths identified by the union and other sources. Since these deaths were not identified by any one method, we excluded them from the PMR analysis but utilized them to verify company-identified deaths. No unusual mortality patterns were observed among the additional deaths that would substantially change the results of the PMR analysis. In addition, the plant classified each decedent as wage (hourly) or salary, according to the decedent's last held job at the plant. This information, along with demographic data such as race, age at death, place of birth, and RSV 0020136 L A'" w _ J J - &* -t J date of death were considered as independent variables in the analysis. In the statistical analysis, emphasis was placed on disease etiologies which may be associated with chemical manufacturing processes. Death certificates were coded by a trained nosologist for underlying cause of death, according to the rules of the Seventh Revision of the International Classification of Diseases, Adapted.^ Mortality data from 1967 United Stntes Vital Statistics were used for comparing the plant*s mortality experience with that of U.S. males.^ The data was analyzed by using the proportional mortality method (PMR), in which the number of observed deaths is compared to the number of expected deaths, based on a standard population. x The following formula was used to calculate the PMR for 21 selected causes of death. Adjustments were made for age by using age-specific values for the expected, number of deaths in the total PMR calculation. PMR^ = Observed^ Expected^ ^ jk j Z Tj Sj^ Where tjj. " number of observed deaths from cause k in the jth age group of the test population. Tj = number of observed deaths from all causes in the jth age group of the test population. Sjk number of deaths from cause k in the jth age group of the standard population. Sj = number of deaths from all causes in the jth age group of the standard population. RSV 0020137 J U'u^lJ jj ,, ^ /j y~j Ja - -as J~~ u - Vi'1 U " The Chi-Square test for significance was applied to all PMR's which have five or more observed cases. Two tailed tests of significance were made on PMRs based on fewer than five cases, assuming the ratios had a Poisson distribu tion. All tests of significance were made at the .05 level. RSV 0020138 RESULTS ii- *. - . . . ^u\J The 465 deaths were grouped by race and classification of jobs held at the plant, resulting in the distribution of deaths as shown in Table 1*. The majority of the deaths were among whites (441), 358 of which occurred among wage workers. Due to the relatively small number of black deaths (24) observed, the greatest emphasis in statistical analysis was placed on the mortality patterns of the white workers. In grouping the total deaths by.age, it was observed that the greatest number of deaths occurred in the 55-64 age group (Table 2). The frequency of deaths increased with age up to age 65 and then decreased with advancing age. Black wage workers, however, tended to die at earlier ages than their white counter parts. While both white wage and salary workers died most frequently at ages 55-64, most black wage workers died between ages 45-54. The concentration of deaths at earlier than expected ages may indicate the effects of occupational hazards or may simply reflect biases in the reporting system. Active workers were more likely identified through the plant's death benefit program. If a retrospective cohort study had been conducted, relatively more deaths in the older age groups would have been expected. Proportional mortality ratios were calculated for 21 causes of death for ages 20-75+, using the following age groupings: 20-34, 35-44, 45-54, 55-64, 65-74, and 75+ for 441 white and 24 black deaths separately (Tables 3 and 3.1). RSV 0020139 J y <1 u wj _ u Among whites, a significant excess (PMR " 1.49, " 5.81, p <0.025) of deaths (36) were attributed to cancers of the digestive organs and peritoneum. Cancer of the genito-urinary tract was responsible for 16 deaths and resulted in an elevated PMR of 1.64 (X^ " 4.02, p <0.05). Each specific cancer site within digestive cancers displayed elevated PMRs, although they were not individually statistically significant values (Table 3.1). The largest proportion of the 36 digestive cancers were due to cancer of the large intes tine and rectum. Cancer of the liver, however, while based on 4 cases, demonstrated tl.* most elevated PMR of 2.77 (n.s.). Nine of the genito-urinary cancers were attributed to prostatic cancer. The calculated PMR of 1.94 (X^ 4.06, p <0.05) is a significantly elevated value. White workers did not demonstrate an overall increased risk for any of th non-Dalignant causes of death, although significant excesses in mortality occurred in individual age groups for both heart and digestive diseases. Heart disease occurred more than four times greater than expected in the 20-34 age group but less than expected in workers aged 65 or older. Digestive diseases were most elevated in workers aged 75 or older. Age Trend Because of the inherent bias of the study design, it is difficult to interpret relative differences in PMR's across age. Additional deaths may have occurred among persons aged 65 or older or among former workers who quit before retire ment but remained unidentified due to pension ineligibility. On the other RSV 0020140 ,J , b\J^ii U Vto-J u -- w Si' -- " d U^U{J hand, since deaths are being examined in a proportional manner, the deficiency may be due to the effects of competing causes of-death* The unusual number of deaths in the 20-34 age group, however, does not seem to be explained by study design. The excess might have resulted simply by chance, since multiple comparisons have been made. Individual age groups also displayed elevated PMRs for digestive cancers, although in most instances statistical significance was not attained, possibly due to small numbers. In general, however, the greatest relative excess occurred in the age group 33-44 and steadily decreased over age (Table 3.1), Time Trend Deaths from all causes among white males occurred with increasing frequency when grouped in five year intervals between 1950 and 1974 (Table 4). Totalcancer deaths followed a similar pattern with the largest number of deaths occurring in the five year interval between 1970 and 1974. When black deaths are included in this distribution, the pattern of an increasing frequency of deaths over time is maintained. The total 441 white deaths were divided into two approximately equivalent intervals so that any changes in mortality trends could be observed. In com paring the deaths which occurred between 1950-1964 and 1965-1976, several notable differences in mortality can be seen (Table 5). A greater proportion of deaths (268) fell into the latter interval and proportional mortality for RSV 0020141 nn.^TT* fp^rrTi li'-j =. :i ii cr^n^nf] ,JJ . j. -'/j U -jvUJIjM selected causes differed. While deaths due to all cancers increased by 2% with time, deaths due to heart disease and cerebrovascular lesions decreased. Cancers of the digestive organs and peritoneum increased from 6.9% to 8.9%. This increase was also reflected by the significantly elevated PMR of 1.62 (X2 * 5.67, p <0.025) for digestive cancers in the latter interval. Several specific digestive sites also demonstrated increased PMRs which however, were not significantely elevated, possibly due to small numbers. In addition, diseases of the respiratory system became more prevalent, while cancer of the respiratory system declined with time. Socio-Economic Effects The mortality experience of white workers was further examined by class of * worker and by birth place, because they are recognized factors in disease, etiology. Increased risks for particular cancers have been associated with* socio-economic class and ethnicity. 22--27 Increased disease risks among wage employees also may suggest occupational exposure to hazardous substances.*w>8-30 Proportional mortality ratios were calculated separately for white wage and salary workers. A significant excess (PMR * 1.52, x2 ** 5.36, p <0.025) of diges tive cancer was observed among wage employees. Thirty of the total 36 digestive cancers observed among all white workers occurred in the wage group. The distribution of these 30 cases by specific cause and age group resulted in excesses of deaths for several younger age categories. A significantly elevated proportion (PMR 1.74, X2 4.45, p<0.05) of genito-urinary cancers RSV 0020142 was seen among wage workers. The heart disease excess previously observed in the 20-34 age group in all white workers became more apparent when wage workers were examined separately. Salary workers, on the other hand, demonstrated an elevated proportion of non-malignant digestive diseases in the 75 and older age group. In order to control for the effects of birth place, PMRs were calculated separately for U.S. and foreign born. The foreign born were found to have a greater risk (PMR 1.93, * 5.37, p <0.024) for digestive cancers, while the U.S. born demonstrated increased risk (P 1.81, * 4.30, p <0.05) for genito-urinary cancer. Cancer of the large intestine and rectum was also proportionately elevated (P * 2.26, x * 4.19, p <0.05) among the foreign * born. U.S. born, likewise, demonstrated proportional elevations in cancers of specific digestive sites, but none demonstrated statistical significance. In many instances, because of small numbers, tests for significance are not reliable. Further examination of the 109 foreign born decedents was made by separating them into Eastern European and other foreign born, since previous studies have shown that Eastern Europeans tend to have increased risks for digestive cancers.22-25 Approximately the same proportion of digestive cancers were found to occur in each group. Six cases occurred among 56 decedents of Eastern European birth. The same number of cases occurred among 53 decedents born in other foreign countries. RSV 0020143 ' Although country of birth may explain part of the excess of digestive cancer in the study population, there still appears to be some other factor affect ing the observed excess of digestive cancer deaths. Racial Effects Twenty-four of the 465 identified deaths were among black wage employees. Although no unusual mortality excesses were noted among blacks, it is interest ing that several proportions of deaths from selected causes were essentially the same as in whites. While 5 (20.8%) of the black deaths were attributed to cancer, 92 (20.9%) deaths were attributed to cancer in whites. Comparable proportions were observed also for deaths due to cerebrovascular lesions. One of 24 (4.2%) black deaths were due to cerebrovascular lesions, and 18 (4.1%) % occurred among white deaths. Heart disease, however, varied slightly between the two races. Thirty-three percent of black deaths were due to heart disease, whereas forty-seven percent of white deaths were attributed to heart disease. The PMRs calculated for black deaths for selected causes did not reveal any unusual mortality excesses. DISCUSSION The apparent excess of each of the digestive cancer sites seems to indicate some common relationship in etiologic agents. The excess of digestive cancers may suggest the ingestion of hazardous substances. In an least one previous study of a chemical factory, workers in dusty jobs experienced an excess of stomach and colo-rectal cancer.^ Particles which are too large to be deposited RSV 0020144 in the alveoli of the lungs are cleared by ciliary action and deposited in the mouth and nose. The particles may then be transported into the pharynx and passed through the rest of the digestive tract. Particles which are small enough to be deposited in the alveoli are partially cleared by another mechanism, the alveolar transport system.32-33 The iacfc Qf can cer excesses of the respiratory organs may indicate an etiologic agent consisting of particles too large to be deposited in the alveoli. The increased risk for genito-urinary cancers does not seem related to the excess of digestive cancers. Rather, it may suggest that another independent etiologic agent is at work. H The methods used here have several limitations which should be recognized H in interpreting the results. The data collected in this study represents only a portion of the total deaths which actually occurred during the interval 1950-1976. Therefore, study design may have influenced mortality patterns observed in the plant population. As previously discussed, the distribution of deaths by age and year of death might have been affected. No differential effect, however, on cause-specific mortality should have resulted, since there seems to be no explainable bias toward particular causes of death. Only the 1967 U.S. male population was used for comparison with the plant population, and only the Seventh revision of the International Classification of Disease was used for coding causes of death. These methods were selected. RSV 0020145 loT u fusliit::! although the study interval covers a 26 year period because of the small number of identified deaths. Moreover, use of one revision of the ICDA maximized consistency in death coding, since variations in coding o'ccurred between the Seventh and Eighth revisions of the ICDA. The paucity of deaths occurring in an analysis of one plant resulted in small numbers when sub-dividing the deaths into categories by age, race, class of worker, place of birth, and year of death. Frequently, excesses or deficits were observed but lacked statistical significance due to the small number of observed deaths in a given category. Consideration of geographic variations in cancer rates has also been made^ While cancer rates for most sites are higher in Massachusetts than for the United States, county rates should not be overlooked.^ The county where the plant is located demonstrated higher rates of cancer than the state for many of the digestive organs, although they are not significantely different. The largest difference in rates was observed for cancer of the stomach as the state rate is 17.7 and the county rate is 18.8 per 100,000 white males. Although the mortality patterns of the plant may be reflecting those of the local area, the local area might in turn be reflecting trends influenced by the industrial population. The proportional mortality method compares the proportion of deaths from specific causes to the total deaths observed. It cannot provide information such as the rate of mortality in a population nor measure the incidence or RSV 0020146 prevalence of a disease. The PMR, however, does provide information describ ing the general pattern of cause-specific mortality in a population. Results of the PMR analysis should be used in planning follow-up studies for which more definitive methods are employed. Information on work history and occupational exposures should be acquired for all the decedents, particularly for those whose deaths were attributed to digestive cancers. A case control method of study, utilizing deaths from all sources, would allow the comparison of disease frequencies between those exposed and not exposed to suspected occupational hazards. f RSV 0020147 ij u '.v j if - . J Table 1. Total Observed Deaths Classified by Race and Type of Job WHITE BLACK ROW TOTAL WAGE 358 24 382 SALARY 83 0 83 COT.TJMN TOTAL 441 24 465 RSV 0020148 n VWbu n ^ n e-P ** ^ n ^ j"J ll u ii\i jJJ La Table 2. Frequency of Deaths by Age, Race, And Type of Job AGE 20-34 35-44 45-54 55-64 65-74 75-99 Column Total WAGE WHITE 9 (2.5) 27 (7.5) 62 (17.3) 127 (35.5) 92 (25.7) 41 (11-5) 358 WAGE BLACK 3 (12.5) 3 (12.5) 10 (41.7) 5 (20.8) 2 (8.3) 1 (4.2) 24 SALARY WHITE 2 (2.4) 9 (10.8) 22 (26.5) 24 (28.9) 21 (25.3) 5 (6.0) 83 TOTAL 14 (17.4) 39 (30.8) 94 (85.5) 156 (85.2) 115 (59.3) 47 (21.7) 465 RSV 0020149 Table 3, PROPORTIONAL MORTALITY RATIOS AMONG WHITE MALES FOR SELECTED CAUSES OF DEATH Cause Death ICDA Code Seventh Revision PMR All Causes 001-999 1.00 Malignant Neoplasms 140-205 1.09 Buccal Cavity & Pharynx 140-148 0.36 Digestive Organs & Peritoneum 150-156A, 157-159 ' 1.49 * Respiratory System 160-164 0.71 Genito-urinary Tract 171-179, 180, 181 1.64 * Prostate 177 1.94 * Bladder & Other. Urinary Organs 181 1.60 Neoplasms of Lymphatic & Hematopoietic Tissues 200-203, 204, 205 0.95 Diabetes 260 0.31 Cerebrovascular Lesions 330-334 1.02 Heart Disease Diseases of Respiratory System Diseases of Digestive System 400-402, 410-443 VIII IX 1.07 1.20 0.91 Cirrhosis of Liver. Other+ 581 0.56 0.82 +"0therM ICDA Codes are all those not mentioned above * p * 3.84, a= 5% N^Number of Deaths 441 92 1 36 20 16 9* 4. 8 2 30 206 28 21 7 62 RSV 0020150  T3 f o* r* U ft) b> ft 3 < JO *1 o 1 W n * it It BO n n it 96> A rt ft 4Ob * U w C hH 3ft S' w ID Q (0 rt 1 f* 3 H It *3 S3 --oV o o* -- ^o --' o N> N5 Vo O O' N os w CO K> SO P o S 3 3 **v 0) > 0 & I--* a fto sr "O >-- oo- 0 00 3 Ui PI 00 it It CJ O c (1) 3 n CD rt ft it O 3 <Z It it it C o a *3 *- o Pi > H X BUO <to0 33 CO (A "IJ OI H- Ni_n w sO Os > Crt t-H pj n <o s> HO xo o 37 pj m < i-t C/1 -I o z O o o J w> *J fo N9 U> wO H U o* --> O it tl Ul m M en n >5Zr _o 3 w o cn z Z *3 H E> o m r- 58 < pj o t-H a > S m HI--I i S3 zZ c/i > po"0i c- o PI 58 (A H 5* to -C M "3 PsoI Z to > H-< l-H PJ 3) *-} o 3 H Z m 58 O to <--s M /-i w * -- o . O UJ oo o f-v w O wo w t-of to O' ui w s^O W O' Xw VO &pp >I--i i--i CD RSV 0020151 Table 4. Number of White Deaths Per Five-Year Intervals by Cause of Death 1950 - 1976 Cause of Death Number of White Deaths 1950-54 1955-59 1960-64 1965-69 1970-74 1975-77 All Causes 39 55 79 98 124 46 All Cancers 7 15 12 21 25 12 Cancers of 3 5 4 8 11 5 Digestive Organs and Peritoneum 1950-1976 4>4l 9236 RSV 0020152 CAUSE :>F..<TH ICDA CO!)E SSVE! .TH REVISION .*.11 Ciuses TLiliitnant Seoplasas 001-999 140-205 E-jccal Cavity 6 Pharynx 15,0-146 Dig-stive Organ* 6 Perltcncuc 1S0-1S6A. 157-159 Esc-r-hatu* ISO StL-JCh 151 Ur.'e Inttstine 6 RijCtur. 153. 154 Li/rr 153. 156 Pancreas 157 Respiratory Syatea 160-164 C-nl to-urinary Tr^a 171-179, 160. 181 Pr^r.tace Bladder 6 Other Urinary OrRins 177 161 * ? -3.8. a- ST PrfR 1.00 1.01 T.iUlt 5. PROPORTIONAL FREQUENCIES OF MUTE DEATHS FOR THE INTERVALS: 1950 - 1964 AND 1965 - 1976 t 1950 - 1964 X of DEATHS NO. IN INTERVAL 173 100 34 19.6 PMR 1.00 1.14 1965 - 1976 X of DEATHS NO. IN INTERVAL 268 100 58 21.6 0.0 1.29 0 12 0.0 6.9 0.60 1.62* 1 24 0.3 8.9 0.0 2.42 1.05 0 0.0 4 2.3 4 . 2.3 2.48 1.10 1.77 3 3 11 1.1 1.1 4.1 1.76 1.S1 0.94 1.79 1 3 11 6 0.5 1.7 6.3 3.4 3.43 0.99 0.S4 1.57 3 3 9 10 1.1 1.1 3.3 3.7 2.20 2.26 ,3 2 1.7 1.1 1.83 1.24 6 2 2.2 0.7 r^nn^n n,?^ ^cTf3n ii . .... il RSV 0020153 Table 5. (Continued) CAL Sc OF DEATH Ncoplasns of . I.y-phatlc 4 Hes-ttopoletlc Tissue* ICDA CODE seve;'.i> revision 200-20), 204. 205 Diabetes 260 Cerebrovascular Lesions 330-334 Heart Disease Olseases of Respiratory Systea 400-402, 410-443 VIII Disuses of Digestive Systta IX Cirrhosis of Liver 581 Other* PMR 0.57 1950 - 1964 NO. X of DEATHS IN INTERVAL 2 1.1 0.0 1.26 1.13 0.82 0 12 83 7 0.92 0.36 0.92 9 2 28 0.0 6.9 47.9 4.0 5.2 1.1 16.1 "Other" ICDA codes are all those not sientioned above p - ).84. a- 51 ,5^n ^/i\ lii/' Lta li li PMR 1.22 196S - 1976 X of DEATHS NO. IN INTERVAL 6 2.2 0.51 0.91 1.04 1.42 2 18 123 21 0.89 0.72 0.86 12 5 34 0.7 6.7 45.8 7.8 4.4 1.8 12.6 in o CM oo > 10 a: Table 6. np/Sx.crp F\|, ,, ,f^rt r ^ ;; i I'j :j if.--'!] -yi .-u u ~fc/u\J PROPORTIONAL MORTALITY RATIOS FOR CANCERS OF THE DIGESTIVE ORGANS AND PERITONEUM BY COUNTRY OF BIRTH AMONG 441 WHITE DECEDENTS Birthplace Total White Decedents U.S. Born Foreign Born Number 441 332 109 Digestive Cancers No. Cases Observed PMR 36 1.49* 24 1.34 12 1.93* * p = 3.84, a = 5% RSV 0020155 REFERENCES n ' ^ sr <-3- u 1 Eckardt, R.E. and Hindin, R.: The health hazards of plastics. Journal Occupational Medicine, 15, 10: 808-819, October 1973. 2. Wilson, R. M. and McCormick, W.E.: Plastics. The toxicology of synthetic resins. AMA Archives Industrial Health, 21: 536-548, 1960. 3. Harris, D. K.: Some hazards in the manufacture and use of plastics. British Journal of Industrial Medicine. 16, 221-229, 1959. 4, Zapp, J.A., Jr.: Toxic and health effects of plastics and resins. Archives of Environmental Health, 4: 335-346, 1962. 5. Tabershaw, I.R. and Gaffey, W.R.: Mortality study of workers in the manufacture of vinyl chloride and its polymers Journal of Occupational Medicine, 16, 8: 509-518, August 1974. 6. Pimentel, J.C., Avila, R. and Lourenco, G.: Respiratory disease caused by synthetic fibers a new occupational disease. Thorax, 30, 204-219, April 1975. 7. Vandervort, R. and Brooks, S.M.: Polyvinyl Chloride film thermal '/ decomposition products as an occupational illness. Journal of Occupational Medicinr-, 19, 3: 188-191, March 1977. 8. Brooks, S.M. and Vandervort, R.: Polyvinyl Chloride film thermal decomposition products as an occupational illness. Journal of Occupational Medicine, 19, 3: 192-196, March 1977. 9. _______ .; Criteria for a Recommended Standard: Occupational exposure to phenol, HEW Publication No. (NIOSH) 76-196, July 1976. 10. _______ . : Criteria for a Recommended Standard: Occupational exposure to formaldehyde, HEW Publication No. (NIOSH) 77-126, December 1976. 11. _______.: Criteria for a Recommended Standard: Occupational exposure to acrylamide, HEW Publication No. (NIOSH) 77-112, October 1976. 12. Nicholson, W.J. et al.: Mortality experience of a cohort of vinyl chloride polyvinyl chloride workers. Annals of the New York Academy of Sciences, 246: 225-230, January 31, 1975. 13. Van Duuren, B.L.: On the possible mechanism of carcinogenic action of vinyl chloride. Annals of the New York Academy of Sciences, 246: 258-265, January 31, 1975. 14. Decoufle, P., et al: A Retrospective survey of cancer in relation to occupation, DHEW (NIOSH) Publication No. 77-178. RSV 0020156 15. Couzens, E. G. and Yarsley, V.E.: Elastics, Penquin Books Inc. Baltimore, Md., 1968. 16. Spirtas, R.: A Statistical analysis of work history data as a retrospective occupational mortality study of the association of solvents with'leukemia in rubber workers. The Institute of Statistics Mimeo Series No. 1049, January 1976. 17. Gamble, J.F. et al.: Respiratory function and symptoms: an environmental epidemiological study of rubber workers exposed to a phenol-formaldehyde type resin. American Industrial Hygiene Association Journal 37 (9): 499-513, September 1976. 18. _______.: Proceedings of NIOSH styrene - butadiene briefing. HEW Publication No. (NIOSH) 77-129, December, 1976. 19. _______ .: International Classification of Diseases, Adapted. 1955 revision. World Health Organization, Geneva, 1957, Volume 1. 20. _______ .: Vital Statistics of the United States, 1967 Volume II - Mortality, Part A, HEW Public Health Service, Washington, 1969. 21. Guralnick, L.: Mortality by industry and cause of death among men 20 to.64 years of age: United States; 1950, Vital Statistics - Special Reports * Vol. 53, No. 4, September 1963. * 22. Haenszel, W.: Cancer mortality among the foreign-born in the United States. Journal of the National Cancer Institute,26,l: 37-132, January 1961. 23. Dublin, L.I.: Factors in American mortality. A study of death rates in the race stocks in New York State, 1910. American Economic Review, 6: 523-548, 1916. 24. Dublin, L.I.: The mortality of foreign race stocks. Scientific Monthly 14: 94 - 104, 1922. 25. Lombard, H.L., and Doering, C.R.: Cancer studies in Massachusetts. Cancer mortality in nativity groups. Journal of Preventive Medicine. 3: 343-361, 1929. 26. Mancuso, T.F.: Cancer mortality among native white, foreign-bom white, and nonwhite male residents of Ohio: Cancer of the lung, larynx, bladder and central nervous system. Journal of the National Cancer Institute, 20, 1: 79-105, January 1958. 27. Blot, W.J., et al.: Geographic patterns of large bowel cancer in the United States. Journal of the National Cancer Institute, 57,6: 1225-1231, December 1976. RSV 0020157 ? rp^.rg Ihi .T. j if .-/j *,i] ^ *-- - * * -J 28 . Selikoff, I., J.et al.: Asbestos exposure and neoplasia. Journal of the American Medical Association, 188: 22-26, 1964. 29. Berg, J.W. and Howell, M.A.: Occupation and bowel cancer. J. Toxicology and Environmental Health 1: 75-89, 1975. 30. Deichmann, W.B. and MacDonald, W.E.: Liver cancer deaths in the continental USA from 1930 to 1972. American Industrial Hygiene Association Journal, 37 (9): 495-8, September 1976, 31. McMichael, A.J., et al-: Mortality among rubber workers; relationship to specific jobs. Journal of Occupational Medicine, 18; No. 3, 178-185, March, 1976. 32. Parkes, W.R.; Occupational Lung Disorders, London, Butterworths, 1974. 33. Morgan, W.K, ai.l Seaton, A.; Occupational Lung Disorders. Philadelphia, London, Toronto, W.B, Saunders-, 1975. 34. Mason, T.J. et al.: U.S. Cancer Mortality by County; 1950-1969, DHEW Publication No. (NIH) 74-615. i t RSV 0020158 ANNOUNCEMENT TO: MONSANTO-SPRINGFIELD EMPLOYEES: About a year ago, we Informed you of the results of a mortality study on Springfield plant employees conducted by the University of Pittsburgh, Graduate School of Public Health. Those results showed no new evidence of worker health problems at the Springfield plant. As a second phase In the study, the University of Pittsburgh was to examine the work histories of former employees who died of digestive system and genito-urlnary tract cancers. While we had expected this second phase of the study to be completed in 1980, it is only now nearing completion. However, very preliminary results have been reported to us by Dr. Marsh of the University of Pittsburgh who indicated that no correlation of work place and Incidences of cancer has been determined. Final study results should be avail able early in the second quarter. In addition, you should know that we recently became aware of the death of a former Monsanto-Springfield employee who had an angiosarcoma of the liver. As you know this form of cancer has been associated with exposure to vinyl chloride. Dr. Marsh has been advised of this case and will make a special effort to determine whether there is any additional evidence in the study data relating to this type of cancer. We are currently unaware of any such cases in the study. Final results of the second phase of the mortality study will-be communicated to you as soon as received. /SBN 3-20-81 J. L. Shriver RSV 0020159 ANNOUNCEMENT On Wednesday, January 20, the "Valley Advocate" published what it stated was the second in a three-part series on the "Monsanto Company's Springfield Operation." Predictably its authors Bush and Michak have cleverly woven together a rehash of past news, questions out of context, misrepresentations, innuendos and informa tional errors purporting to demonstrate Monsanto is conducting a conspiracy of silence to keep important information from its employees concerning worker health and cancer. It specifically attempted to link vinyl chloride exposure to alleged employee health problems ignoring a comprehensive study by the University of Pittsburgh which showed no such connection. As you know, Monsanto has consistently and in a timely manner, advised its employees, local union officials, and appropriate government agencies of the results of any health studies it conducted or had conducted by outside impartial professional organizations. None of these studies has conclusively shown a causal relationship between cancer and a particular workplace exposure. For your reference, the attached prior bulletin board notices openly summarize previous studies, checkpoints and results which indicate the facts of the matter and refutes the alleged cover-up claim. Our actions in handling employee health studies have been as follows: 1. Monsanto has always cooperated with governmental agencies requesting data on worker health evidenced by a joint Monsanto-NIOSH health study completed in 1976. 2. Monsanto has communicated frequently and truthfully on the status of its health study results to all employees and to other concerned parties (see attached notices). 3. The health studies either conducted by Monsanto or by the University of Pittsburgh School of Public Health have been designed with the best statisti cal approaches and historical Information. 4. Monsanto has always been and will continue to be concerned with worker health and safety. Our continuing environmental and industrial health programs are evidence of this concern. It's obviously Impossible for me, in this communication, to answer every issue raised in the "Valley Advocate" article. However, if anyone has any additional concerns or questions, please feel free to contact me or Paul Bureau. 1-22-82 Att. J. L. Shriver, Plant Manager RSV 0020161 1. INTERPRETATION. STATUS-. PROCEDURES RSV 0020162 * K .7. V ** **** dOliSaiitO 7ROM ('_ A. P. Torrenzano - Springfield March 21, 1974 co |R. L. Bourget SyJKCT RErHENU Interpretation of Health S:ar.dard Reco-- rr.er.ded By NOI5H. 3-ll-74(Relative to Springfield Plant; TO Pile ,1. 3 A SIS Angiosarcoma of liver Detected in deceased Detected in living 5 at BFG, Louisville 1 at CC, South Charleston 1 at Goodyear, Niagara 2 at BFG, Louisville IL GENERAL APPROACH A. Define "Regulated Area" 1. Where there is a potential for measurable concentration of VCM... VCM handling, polymerization, drying, packaging, whse. 2, Implicit - - any area where there is a measurable amount of VCM, such as locker rooms, smoking rooms, offices, etc. B. In "Regulated Area11 1. Monitor VCM concentration frequently 2. If VCM concentration is detectable: a. wear full face air respirators b. ~ decontaminate all exhaust ventillation air before emitting to environment (action on dryer air exhaust is vague) c. develop control plan to reduce VCM concentration and report results to 05HA 3. If VCM concentration is not detectable: a. Full face air respirator ncr required, however other safeguards still necessary -- as listed belovr. b. Coveralls and gloves RSV 0020163 c. No eating,, drinking, smcking (or possession of tobacco) or chewing r 2- - 3. d. Specific procedures and clothing for specific jobs such as kettle entry, VCM transfer, maintenance of equipment e. Records of personnel f. Posting of specific warning labels g. Decontamination procedures for clothes, equipment, waste resin and people. XU. TIMING A Within 60 days report to OSHA 1. Brief description of in-plant location of "Regulated Areas", including number of employees normally in the area. 2. Control Plan a. Initial VCM cone, survey b. Program and timing to reduce VCM concentration B. Every 6 months report to OSHA performance versus goals established in the Control Plan. IV. EFFECT ON FUTURE PLANTS A. Outside plant B. Remote operation, closed kettle plant C. Complete degassing of slurry before drying and packaging, and possibly in some cases, extraction of hydrocarbons before drying and packaging. D. Complete accounting for all VCM with closed loops; approach 100% VCM yield. V. EFFECT ON EXISTING PLANT A. If dryer exhaust gases must be decontaminated--then shutdown of existing plant would be required until process is defined and equipment installed. B. If building ventillation gases must be decontaminated, as specified-then shutdown of existing plant would be required until process and equipment installed. RSV 0020164 -3- V. EFFECT ON EXISTING PLANT (cont.) C. All other practices specified could be implemented, pending purchase of monitoring equipment and protective equipment. VI. clarification required A. Dryer exhaust gases to be decontaminated. B* Available process to meet decontamination of building ventillation air. /dh A. P. Torrenzano RSV 0020165 Q a i in m RSV 0020166 6*f a /3/*j ** An*r tm ^Fc***TMv* *j*n?> </r--*n/Ln^j iryfr Jf>*# * /Jf# C00 Cfcj /*, rt ^ir J *,*# -- e^7 , c^7 r*rc*'J /-$* *fo Xm *4ct /c Otf#crT> - ,/***, r*v C Ay ... t0 - ** 2* ftn 4% ^ 4 ^4*<) 2 *# ^*,t*t /! . /^c^ <2 A * A* /V JfO * i ^ *X1. L*m CV^*^f 7*r/fc *>/*, /(j< ................. V fr*U*+f * (A wfcJ tft-jpJ/a*-*,rrl CA*J * * m 4f*7 4? J#0 />^#y 4 t/tIJ /i^-T ; *. it*rtTH u/mnrK -. /*& J re**rry RSV 0020167