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D.
The volume of air sampled as converted to standard conditions of 25 C and 760 mm Hg.
v
s
v
x
Px 298 760 x (T + 273)
where
V
g
V P T
NOTE:
volume of air at STP volume of air as measured
barometric pressure in mm Hg
Temperature of air in *C
start
In cases where temperature and B.P. changed from sample Co end, an average figure was used.
of
E.
Calculate ppb vapor phase from above data.
ppb volume
where
ng x 24.45 M^
^
s
^
ng V
M.W.
corrected ng (C) corrected air volume (D) molecular weight
The total amount of chlordane in the denim patch was determined from the expression.
Q
when
A x Vc
ul
Q, A and ul are as above Vt total volume of hexane extract in milliliters (100 ml) or final volume of extract requires dilution or concentration.
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D.
The volume of air sampled as converted to standard conditions of 25'C and 760 mm Hg.
V x
's
where
Px 298 760 x (T + 273)
V V P T
NOTE:
volume of air at STP volume of air as measured
barometric pressure in mm Hg Temperature of air in *C
sample
E.
In cases where temperature and B.P. changed from start of to end, an average figure was used.
Calculate ppb vapor phase from above data.
ppb volume
where
ng x 24.45 y x M W s
ng V M.W.
corrected ng (C) corrected air volume (D)
molecular weight
The total amount of chlordane in the denim patch was determined from the expression.
Q
when
A x Vc ul
Q, A and ul are as above Vt total volume of hexane extract in milliliters (100 ml) or final volume of extract requires dilution or concentration.
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OiLCRHWE IN
MILITARY HOUSING
prepared for the
U^S. Air Force
by the
^
^;
^
%
SUBCOMITTEE CN fflLCRnANE IN MILITARY HOUSING
of the
^
OCM^JTIEE CN TCOaCOLOGy
-^
^
Board on Toxicology and fiwironmental Health Hazards Assesnbly of Life Sciences National Research Council
National Academy of Sciences Washington, D.C.
August 1979
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NOTICE
The project that is the subject of this report vas approved by the Governing Board of the National Pjesearch Council, ttose sobers are drawn frcan the Councils of the National Academy of Sciences, the National Academy of Engineering, and the Institute of Medicine. The aenabers of the Coroittee responsible for the report were chosen for their special cc=?etences and with regard for appropriate balance.
This report has been reviewed by a group other then the authors according to procedures approved by a Report Review Comnittee consisting of ncnibers of the National Academy of Sciences, the National Academy of Engineering, and the Institute of Medicine.
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3) It is reccnanended that chlordane exposure in contaminated housing be reduced by cleaning or sealing floors, walls, and other surfaces in the houses and by modifying heating
systems to eliminate the possibility of continued or future exposure to chlordane from subslab treatment for termite control.
'^s '^^^^\ J.
^ap
4) The Subconiaittee examined Table 2 in the Wherry Itousing Report from Scott AFB in Illinois fAppendiy T^ ar^---^ t,^, w pragmatically deteminsd^lhal. STi the interim airborne Air Force nous ing should not j ^^\ \^ chlordane l exceed 5 iig/'pt5: this maxijttjn concentration woul^ pprmit ^p^s.
e^estires^n
^'
^^^ ^Y^ -\. ^ ^^ v^
j
\*
^J^ t^''
'^^^ '^S, ^\<^
\
occupahcv^gf most housij^ units. 1pat compares with_a giaxijnum permissible household residue of chlordane of _4.112 yg/m^ reccyrgnended by the USAF Health Laboratory report on the Webb AFB incident in
Environmentar
-
^
S^Saxijnum allowable daily intake (ADI) of 1.0 ug/kg.^-^^ assuming that half the ADI is obtained fron the food s^ply> that a nornal adult inspires 9,201 L of air HI-^y' that 90t of the inspired chiordane is-ib*sorted, and that the average adult weighs ISO Ib.
^970;
this latter concentration vas determined from
lro<
^0 /"'
.^
^
.',
\^
<>
^
Y
^^ ^^^A^ ^
<\-
y
^?
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Chlordane Contamination in Wherry Housing
Scott AFB IL
In October 1978, residents of a base housing unit (5543B) at Scott AP5 IL detected a strong, objectionable odor when they activated the central heating unit for the first time during the heating season. A short time
later, civil engineering personnel working in a then unoccupied unit (5020E ) Bl so noticed an odor. It was noted that both
'^^^tf'^^^
^
^ESvfrbnr.entaTHe^Tth ^S^^
units and submitted them to USAF OEHL for chlordane analysis.
Analysis of the two samples showed high airborne concentrations of chlordane in Quarters 5543B (490 ug/M3) and in 5020E (70 UP/M^Y. Sampling the sane units a second time indicated 630 UQ/MJ In 55438 and 260 u?/fj3 in 5020E. Subsequent sampling} of 11 houses treated in 1978 revealed
rnnrpn-^rm. frnm. IP^ th^n th^
^^l^EgH^^^^^^I--------in
in
severe
units to a hioh of 51 uo/MJ
Quarters
5232A.
At the recjest of AFMSC/SGPA, USAF OEHL conducted a survey during 14-19 Jan 75 t: further define the concentrations of chlordane in t^e 1978 treats; houses. Additionally, sampling was performed to statistically estimcts background levels of chlordane for the Wherry housing complex at Scott. AFB IL.
rteteri&ls and Methods
those treated Houses chosen for s&mpling were divided into two groups and those treated prior to 1978. Eleven available for termites in 1978 houses that had been treated in 1978 were sampled while 43 randomly were ^o selected houses from the P^^o1" ^-0 ^78 treated no.^Mfftgr^gf^^5,1S^^^apgi^l^^ .^P^* houses that had to serve as and 502GE (5020G) were sampled to determine if chlordane was being introduced into those quarters.
9^^
contro'fr^^l^^
'KfffW^
The basic sampling train consisted of an electric Millipore vacuum pump with & sampling tube containing Chromosorb^ 102 as the collecting medium. Chromosorb tubes consisted of 200 mg of Chrbmosorb 102 capped with anhydrous sodium sulfate in a 7" Pasteur pipette plugged with glass wool. The Chromosorb tubes were connected to the pump by a sm&ll piece of Tygor^ tubing. Flow rates were measured using a precision rotometer after the pump was turned on and again imnediately prior to completion of the'sample. In instances when there was a drop ih'flow rate. the beginning and ending flow rates were averaged to give a mean flow. The range pf flow rates in this survey was 2.7-4.5 liters per minute.
In the unoccupied units (5543B and 5020E). the pumps were located in the approximate center of the living room on the floor. Qji all other units, the pump was located on> the floor within 2 ft of one of the living room or dining room heating vents depending on which was more feasible considering the occupants' furniture location^} The sampling-tube inlet
*$ee
Attachment 1
3
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Appendix I
&
was always located approximately 6" above the floor. Normel room temperature of about 70-75F wss maintained during the sampling period. Outside air temperatures ranged from -80F to 41oF during the week sampling was accomplished.
All 1S78 houses were sampled utilizing two consecutive 4 hr samples except 5543B which had a total of five samples taken, 5020E which had four and 50195 which had only a single 2 hr sample taken. Those houses treated prior to 1978 and the untreated controls were sampled with e single 2 hr sample. The time of day that the sample was taken was dependent on the availability of the occupant to provide entry authorization.
/
'Sampling precision was measured in quarters 5543B and 5020E. In 5543B, two sets of matched samples and one high volume sample were taken. The sets of matched samples were run for four hours. The single Ms^1 volume sample was run for approximately five hours. )n 5020L\ two seU of matched samples were taken with a duration of approximately 5 hr for one set and 4 hr for the second.
Results
Verification of sampling precision in the unoccupied quarters (5543B and 5020E) using different flow rates indicated the sampling technique was relatively precise (Table 1). The mean concentration determined by 5 samples in 5543B was 263.48 t 34.88 pg/M3 with a range-of 208.59 to 292.02. In 5020E, the mean of four samples was 25.6 i 6.87 with a range of 16.35 to 31..87. These results Indicate that variability due to sampling technique and analysis was approximately 13-27S. Duplicate 4 hr samples in ,1978 treated houses often showed temporal differences in. concentration but those differences were not consistent.
Of all housing units sampled^ S3 put of 60 had^^r^orne^cMgy^anp shown in CQncen^r^nrig ^h^vc t^fe f^gTggE^^Ife^ Table 2. The untreated controTs^nad' ncrrtefectable level of chlordane. The range of chlordane concentrations above trace was 0.42 ug^MS-to
263.46
ps/T.3.
'.
When housing units were categonzed by year of treatinent, statistical a significant difference analysis using ^ ggiff^^^y^^ff^ between 1978 treated units and those treated prior to. 3978. Tti (P=.05) four highest concentrations were found in the ^978 treated units with only twojfnitr having rofK^"^ations less than 1.0 po/M-3. This contrasts with other single year groups where adequate samples were taken to make comparisons. For example the 1973 treated houses that .were sampled had chlord&ne concentrations ranging from a hioh of 5.22 pg/H3 to a low of 0.69 ps/M3. In 1970 treated houses, the high concentration wss 4.56 pg/M3 and three houses had less than the quantitative detection licit
^
(0.02 pg/M3).
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Table 1.
Sampling precision as measured In unoccupied quarters 5543B and 5020E.
Time
Sample Number
o
Flow Rate (/cnn)
(nnn)
240 240 292 222 222
Concentration
(ps/M3)
1 (5543B) 2 (5543B)
3 (5543B)
(5543B) .5 (5543B)
4
2.9 2.6 4.3 2.8 2-9 4.0 4.0 4.0 3.5
292.01 208.59
268.62 293.96 254.24 29.60 31.87 16.35 24.68
6 (5020E) 7 (5020E)
(5020E)
9 (5020E)
300 300 260 260
5
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Table 2.
Concentration of airborne chlordane in Wherry housing at Scott AF5 1L arranged by year of treatment.
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Year
1978
Quarters
5543B 5020E 5445A 5534F 5220B 5019B
Concentration
(pg/M3)
Year
1972 1971
Quarters
50335 5142A 5519A 5033E 53115
5462A 5470A 5546A 5425A 5426B 5346B 5466B 5113A 5109B 5414B 5474A 5473B 5436A 51255 5544A 5476E
Concentration (vs/H
0<97
1,61
.5.232A
-51125 5301B 5521B 5026A
1977 1976
5112E 5114E 5126B 5211E 5317A 116A
5033A 5110A 5517B 5136A 5226A 5322A 5n7A 5456A 5239A 50Z6E
1975
1974 1973
263.48 25.63 22.44 22.30 4.81 4.58 4.53 3.97 3.32 0.55 0.42 2.27 1.45 4.02 0.99 0.95 0.56 3.37 0.86 1.25 0.76
0.49 5.22a 3.69
I.SB
1.17 1.25
0.42 1.76 1.31 1.02 0.72 0.61
1970
Te
1969
1968
3.0Bb
1.90 0.94
T T 7.41
0'.55
'HD<
1966 1955
52165
5033B 5009B 5247A
2.99
1.73 1.69
1964
Untreated
Upstairs
5476F
500SA
7 1.16 0.72 0.62 4.K 0.67 ND
5126E
5444B 5553B
1.62 1.31 0.69
5117B
5543D 5020G
T
O^
3.58=
a Unit family Is now living In that had previously lived In 5543B. b Unit family Is now living In that had previously lived In 5020E. c Unit above 5543B.
d Unit above 5020E.
e T
f ND
trace
none detected at a quantitative detection limit
o<
0.02
vg/M3.
6
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By using statistical tolerance limits, the maximum expected chlordane concentrations in the units treated prior to 1978 having concenfrfctions above trace can be estimated with 95t confidence. For example 95L of aft units treated prior to 1978 should have chlordane concentrations eousl to or less than 5.68 ug/H^ and 9 should have concentrations equal to or less than 6.91 vg/M^.
^
Tic'^tfferT^n concentrations in other ground level ur. i fs. TorTxan^Te, tn untreated unit (5117B) had less than the quantitative detection limit white the adjacent unit (5117A) had 3.69 ug/M3. On the other ha.ng.
id^t^t^taTe
Quarters 50206 nsd 0.57 vg/M-3 anc* 5543D had 3.5S pg/M3 indicating that airborne chtordane in a ground unit car. influence the concentration of chtordane in an upper unit.
tevetS of
chlorbane.
Discussion
From these data, ^^^a^^aS^^2S5ggeCtn^
^j^^i^t^m>re^^^ ^ogimg^xg^nmon^Ts^ ^S^^'^^W^--tf^^n
(jhe
results of random sampling of the units treated prior to 1S76
suggest..& 1% probability of any chlorda'ne con^entratinn^ ^p excess of b.yi ,jg/r-iT However, the results of 1978 treated units indicate there _Drobabi"h'tv that the two 1978 treated quarters not sampled may is c
exhibit high chlordane concentrations."^ Recomendations
h^h
Quarters 55435, 5020E, 5445A and 5534F should have the present theatins ducts sealed, the quarters painted and the heat reducted through /above ground ducts.. :' '- '."."...-. '
1.
The airborne concentrations of chlordane in these units are significantly higher than concentrations in all other units. 'The source of the chlordane is apparently the heatino ducts. By seating the present flucts and reducting through above ground ducts, the source of contamination will be isolated from the living area.
Rationale:
'-' ''
-'
2.
Quarters 553SB and 55518 should be sampled for airborne chlordane.
Rationale: Since 4/31 of the 1978 quarters sampled had unusually high concentrations of chlordane. there is a high probability thet these two quarters will also have hioh chlordane concentrations.
7
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3.
Ho more routine sampling of units treated prior to 1978 should be tccomplished.
Rationale: Statistical evaluation of the sample data indicates that 9^ of the units should have airborne concentrations of chlordane at trations less than or equal to 6.91 pg/K3.
concert
<.
The Civil Engineering Entomology Shop should closely evaluate their technique for ^h^Pr^Sm^^liS^^FS^^^Ea^^ ^^^^TM.rf.i>igii-Wii
nfSll.a'fi'K.aitfiai.ii^'1'11'1
^--Ti--i^l-glr''"tifTit-r.-i^3Ci;-*3
Rationale: The clustering of high chlordane concentrations in 3978 indicates something was consistently wrong with the procedure used to treat those units.
8
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Appendix I
Analytical Detection Limits Analytical detection limits are not fixed but vary depending on many factors. Instrument sensitivity is one of the most critical
deterninants of a detection limit. Priority of the sample is notner factor that is involved. If several compounds re eluted in the sample extraction process, interference may occur that decreases the sensitivity of the oas chromatograph. Other factors are related to the samplino scheme/ Larger volumes of air enable the gas chromatograph to detect smaller quantities of chlordane per cubic meter due to a greater mass of chlordane adsorbed to the sampling medium.
As a result of the different methods of calculating a detection limit, i.e., mass basis vs concentration basis, several different detecfon limits are referred to.
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References
1.
National Research Council, Pesticide Information Review amd Evaluation Comittee. 1977. An Bvaluation of the Carcinogenicity of Chlordane and Heptachlor. Kashinston, D.C.: National Academy of Sciences. National Cancer Institute.
2.
1977. Bioa-ssay of chlordane for possible carcijiogenicity. CAS No. 57-74-9. Carcinogenes.ls Technical Report Series No. 8. NCI-CG-TR-8. rHSW Pub. No. (NIH) 77-808. "Washington, D.C.
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2.
Gas Chromatograph:
Varian 3700 with
f.t
Ni electron capture detector.
Column:
6 ft. x 2 mm ID glass column. 102 SP 2100 on 100/120 Supelcoport. or
42 OV101 on 100/120 GCQ.
Carrier Gas:
Nitrogen a^ 30 ml/min.
oven,
Temperatures;
200*
injector, 230' detector, 250'
Attenuation:
16
3.
Standard Curve
The standard curve will be constructed by plotting the sum of the peak heights of the 7 components characteristic of technical chlordane
(Compound C, Heptachlor, Compound E, Compound F, Trans chlordane, Cis chlordane. Compound K) versus the nanograms of technical chlordane
injected into the gas chromatograph (References 4 and 5). The total amount of technical chlordane in the impinger is determined from the expression.
Q
A x V
IL
x 1000
ul/ml
^
where
Q
A
ul
amount of technical chlordane in the amount of technical chlordane in the
sample (in micrograms). injected aliquot in
V
nanograms. volume of extract injected into GC in roicroliters. volume of ethylene glycol from impxnger + rinses (50 ml).
The total number of nanograms present in the ethylene glycol sample The program Cook into account flow rate was then put into a computer. of pump, length of time pump ran, temperature of air at beginning and end of sampling, and barometric pressure. Results were printed out in and mg/cubic meter. The program involved the followparts per billion
ing calculations.
A.
-Determine weight of chlordane present in ethylene glycol sample from gas chromatographic analysis in nanograms.
B.
Correct this total weight of chlordane by subtracting any weight value from the blank ethylene glycol sample.
Corrected weight is divided by the recovery factor (corresponds to desorption coefficient for air tubes) to obtain the final corrected weight of chlordane present.
C.
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^
Table 5. Observed*/Expected Deaths frcm Lung Cancer According to Age at Entry into Occupation and Age at Death.
Table 6.
Observed'/Expected Deaths from Lung Cancer According to Duration ol Employment and Years Since Employment Began.
0-4
Years Since Employment Began Total 10 + 5-9
6/4.4 2/2.3 8/6.7 0/0.0 0/3.3 0/3.3
19/15.6
Age at
Observation
<50 <45
12/5.4
Age
at
Entry
into Occupation
Duration ol
45-49
0/0.8
5/8.4
60 +
1/0,4
Total
12/ 6.2
Employment
50-64
65 +
Tola!
0/2.6 0/0.1 12/8.1
6/11-5
3/ 3-5
0/0.6 5/9.8
3/2.8 4/3.2
0-4 5+ Total
13/11.1 13/11.1
11 5.6
21/21.1
21/21.2
Observed deaths nol adjusted lor deaths ol unknown cause Observed numbers no! adjusted loi deatns of unknown cause
clustered among workers who were first employed prior and who died before age 50 (Table 5). In fact, in this sub-group the excess is formally significant (p < 0.05), if one disregards the facts that this was not an a priori hypothesis and that many comparisons have been made in the data. No explanation for this observation has been found yet. Table 6 examines the question of "latency" the interval between the time the individual's employment began and the years during which he was observed in the study- The table shows that relatively few of the study subjects so far were followed for 10 years or more after first employment None of those with lung cancer fell into this category If the excess of lung cancers had been of occupational origin, one would have expected to see
to age 45 most of the excess in this category.
seen in the applicators were not reflected in the manufacturing workers- Similarly the unexpected excess of deaths from cerebrovascular disease.seen in the manufacturing workers is not seen in the applicators, either in the group as a whole or in the termite control applicators. The principal limitation of the present study, particularly as it relates to cancer experience, is that there were relatively few workers who had substantial work experience and who were followed for long periods after first employment. Thus, only about 15% of the personyears were contributed by workers who had more than five years of employment and who were observed more than 10 years after first employment. It is hoped that the establishment of the cohort at this point in time will permit more decisive analyses in the future.
Conner and making daia Management and staff of rangements wilh the companies for provision Rollins. Ini. TermineiL International. Inc and Truly Nolt-n Iniernational providing other information The helpful supervising data abstraction and that Social Security Administration arranned fof the data
The authors
indebted
Cuneo. Washington. DC. tor
Mi )ohn D Conner. |r. of Setleri. suggesting thi study and lor
Discussion
Borkers
Although there have been several clinical studies of occupationally exposed to pesticides, these generally have been based on small numbers and have involved clinical and laboratory examination at a single point in time,4"1-' Essentially no data could be found on the long-term mortality of occupationally exposed workers other than a study of workers employed in the manufacture of chlordane and heptachlor' There is no consistent pattern of excess mortality seen in either of these two studies. The overall SMRs were 72 in the manufacturing workers and 84 in the applicators both figures expressing the reduced mortality generally found in occupational cohorts. SMRs for deaths from cancer were 82 and 83. respectively. In both groups there was z slight excess of deaths from lung cancer but in neither is it significant, and even if the two series are coma difbined, there are 36 3 observed and 30,2 expected ference that is neither significant nor remarkable in the absence of data on cigarette smoking in the two cohorts. Moreover, the manufacturing workers were exposed predominantly to chlordane and heptachlor Among the applicators, the excess lung cancer mortality occurred not among the group most likely to be exposed to chlordane and heptachlor the termite control operators but among the general pesticide applicators. Nevertheless. special attention should be paid to this cause of death in the future follow-up of these cohorts, The excesses of cancer of the skin and of the bladder
References
1 Wang HH and MacMahon B: Mortality of workers employed in Occup Med the manufacture of chlordane and heptachlor 21 745-748. 1979 2 Monson RR Analysis of relative survival and proportional mortality Comput Biomed Res 7:325-332. 1974 3 Wang HH and Miettinen 0. Evaluation of three asymptotic preparation methods of interval estimation for the odds ratio 4 Pnnci F and Spurbeck CH A study of workers exposed to ihf insecticides chlordane. aldnn. dieldnn Arch Ind Hyg Occup Med
364-72.1951;
5 Alvarez WC and Hyman S, Absence of toxic manifestations in workers exposed to chlordane Arch Snd Hyg Occup Med 8 480-483. 1953 6 Ortelee MF Study of men with prolonged intensive occupational exposure 10 DDT Arch tnd Health 18433-440. 1956 7 Fishbetn Wl. White V. and Isaac?. H) Survey of workers exposed 10 chlordane tnd Med Surs 33 726-727. 1964 8 Stem Wj and Hayes W| Health survey of pest control operators tnd Med Surs 33.549-555. 1964 9 laws ER. Curley A. and Biros F). Men with intensive occupational exposure to DOT Arch Environ Health IS 766-775. 1967 10 Sandifer SH. Keil II. Finklea |F. and Cadsden RH Pesticide effects on occupationally exposed worker". A summary of four years South Carolina Ind observation of industry and farm volunteer*,
Med 41 9-12.1972 11 Warmck Sl and Carter |E Some finding", in study of workers occupationally exposed to pesticide*. Arch Environ Health 25 26^-270.
1972 12 Morion Wi,. Crawford ED. Maude RA. et at Hypertension Oregon pesticide-formDialing worker-. Occup Med 17 182-185.1975
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Table 3.
Observed and Expected Deaths from Selected Causes in Termite Control
Termil e Control Operator
Operators and Other Applicators.
Others Expected
220.9
Cause of Death All causes
Malignant neoplasms
Observed"
Expected
SMR
Observed*
SMR
78
138
Cancer of digestive organs
and peritoneum
21.6 1.2 7.2
1.2
150.1 25.9 5.9 8.3
0.8 0.5
92 83 20 87 148 245 90 39 120
173 32.6 5.6 16.9 2.2 2.2 61.8 5.6
44.9
39.3
9.1
83 62
131
Cancer of lung
Cancer o) skin Cancer of bladder
Iscnemic heart disease Cerebrovascular disease External causes
1.2 37.2 2.4
50.4
41.2 6.1 41.8
12.9 1.2 0.8 63.2 9.2 56.9
187 296 98 61
79
23; others -19
Deaths with m.ssing certificates distributed according to the distribution of actual observed numbers for each cause: TCOs
intensity of exposure was desired. Each company was supplied with a list of all the Job titles found among the cohort members and a knowledgeable person or persons was asked to classify each title into one of three groups according to relative intensity of exposure. In an attempt to evaluate the effect of exposure to chlordane and heptachlor. separate analyses have been conducted for persons ever holding jobs as "termite control operators" (TCOs) Chlordane and heptachlor are particularly effective in the control of termites and, since 1975. their use
has been legally restricted to the subterranean control of them and to a very few other applications. It is recognized that TCOs are'also exposed to a variety of other pesticides and that general pest control operators may well have had exposure to chlordane and heptachlor, particularly prior to 1975, Nevertheless, it is almost certainly |true that, as a group. TCOs have heavier exposure to chlordane and_ heptachlor than those in other job categories. The distribution of the study population as to TCO or non-TCO status and by estimated relative intensity of exposure is shown in Table 1. The 243 applicators who had held job titles under more than one level of intensity of exposure arc classified according to the one
held for the longest period of time.
Results
Observed and expected deaths by cause are shown in Table 2. The overall SMR has a point estimate of 84 and a 95% confidence interval of 75-94, Underascertainment of deaths, as well as the selective factors involved in the "healthy worker effect." no doubt contributes to the fact
Table 4.
that the SMR is less than 100, although the value of 84 is not atypical for an occupational cohort. SMRs are over cancer of the lung 100 for only three causes of death (115), cancer of the skin (173) and cancer of the bladder (277). The confidence intervals of two of these ratios (for lung and for skin) include 100 and so the excess is not formally significant (p > 0.05). For bladder cancer the excess is on the borderline of statistical significance. The very low SMRs for cancers of the digestive organs and for other diseases of the digestive and respiratory systems are notable. The extent to which occupational selection is responsible for these low ratios can only be conjectured, but it is probably considerable. There was one death from cancer of the common bile duct but none attributed to cancer of the liver. Table 3 gives observed and expected deaths separately for the TCOs and for other applicators. The only significant differences between expected and observed values (p < 0.05) are those for cancer of digestive organs and for cerebrovascular disease, both in TCOs and both in the direction of lower observed values than expected. None of the differences between SMRs in TCOs and non-TCOs is significant but the slight excess of lung cancer is restricted to the non-TCO groupTable 4 shows observed and expected deaths by estimated relative intensity of exposure. For lung cancer there is no evidence that risk increased with intensity.of exposure as Judged from job title; in fact, there is a slight, though not significant, trend in the opposite direction. Further analysis of the lung cancer data showed only one curjous feature. The lung cancer deaths were
Observed and Ex peeled Deal tis from Selected Cau ses Accordi ng to Intensity of Expinsure.
Minimal Expected
Cause of Death
-Ail
Observed"
SMR
81
causes
Malignant neoplasms Cancer o1 digeslive
91 19.8 2-3
9.3
111.9 20.6
4.9
97
48
Intens Ity of Exposun Intermediate SMR Expected Observed" 63 102.0 64 69 18.4 12.8 76 4.2 3.2
7.5
1.1
Highest
Observed*
156 21.4 1.2 7.1
Expected
SMR
157.2
26.3
5.9
99 82 20 87
138 243 108
organs & peritoneum Cancer of lung Cancer of skin
Cance^ of bladder Iscnemic neart
1.2
2,3
6.8 0.6 0.4
34.4
138 198 530
92
0
23.5
31.5
6.2 0.6 0.3 29.4
3.8
120 187
0 80 56
1.2
1.2
44.1
8.2 0.9 0.5 40.7
6.2
L
1
disease Cerebrovasculai disease
External causes Deaths with
moderale
1-2 23.3
5.3 24.6
22 95
2.1 22.4
26.3
65
4.8 48.8
47.9
77 102
missing certificates distributed according
to the dislribulion of actual observed numbers for each cause: minimal exposure
13-
4. heavy
25
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Table 1, Distribution of Study Population by Genera! Level of Exposure to Pesticides and by Whether or Not Employed in Termite Control.
Exposure
Level
Minimal
Termite Control
Yes
2713 (40.3) 664 (9.9) 3357 (49.9) 6734 (100.1)
No
1426 (15.2) 4320 (46.0) 3642
Total
Moderate
Heavy
Total
(38.8) 9392(100.0)
4139 (25.7) 4984 (30.9) 6999 (43.4) 16126(100-0)
from the states or registration areas were obtained. There was no reason to believe that the 42 deaths for which death certificates could not be obtained are distributed by cause differently from those for which certificates were obtained. For some estimates, therefore, as the total number of "observed" deaths by cause, the actual number observed, plus the 42 deaths with missing certificates distributed by cause according to the distribution of causes noted in the death certificates obtained, were
Figures in parentheses are percentages
Includes foul subjects with unknown level ol general exposure
on what grounds each of the 27,957 excluded subjects was declared ineligible. However, a sample of 4,000 of these was examined and in this sample Tl % had been ex-
cluded because they were female, 71% because they were employed for less than three months and 18% because of missing information. Information on race was not available on personnel records and could not be used as an eligibility criterion. However, the majority of the workers were white. In the course of the study death certificates which did specify race were obtained for 269 of the subjects; 253 of these subjects were white. 15 were black and the race
of one was unrecorded. Individual follow-up was not attempted Identifying information on the 16,126 eligible subjects was submitted to the Social Security Administration which provided, for those known to be dead, information on date of death and the state in which the death certificate might be found In another set of records submitted together with those from this study, the SSA search identified 104 of 109 deaths which had been ascertained through individual follow-up.' Among the 16,126 subjects in this cohort, SSA identified 311 deaths, for 269 of which death certificates
Table 2.
Cause of Death
All
used. Expected numbers of deaths by cause have been estimated by means of a computer program described by Monson.2 The program applied national mortality rates of white males specific for five-year categories of age and for calendar year to the person-years accumulated during the period of observation. The beginning of this period was January 1, 1967. or January 1, 1968 [as described earlier). For employees entering after these beginning dates the beginning date was taken to be the end of the third month of employment. There were also two termination dates since records were submitted to SSA in two batches. For individuals whose record was submitted in the first batch the termination date was |une 30.1976. For the second group it was December 31. 1976- In the computations, persons who were known to have died did not contribute person-years after the year of death but, otherwise, subjects were assumed to be alive until the end of the follow-up period. Standardized mortality ratios (SMR) were estimated by dividing the numbers of observed deaths (with the 42 of unknown cause distributed as previously described) by the expected values and multiplying by 100. An extension of the Cornfield method^ was used to compute 95% asymptotic confidence intervals of the SMRs. The applicators had been exposed to a broad spectrum of pesticides including fumigants, botanicals, carbamates, chlorinated hydrocarbons and organophosphates- Particular interest was focused on applicators exposed to chlordane and heptachlor. In addition, some measure of
Observed and Expected Deaths from Selected Causes.
Observe6
A'
311
causes
Inleclive and parasitic diseases Malignant neoplasms Digestive organs and
peritoneum
2
47 6
311.0 2.3 54.3 6.9 24.3
^
Expected
370.9
SMR}
2.8 65.2 15.1 21.2 2.0 1.3 8-8 16.9 139.9
104.4
84 83
83 46
C.I. of SHR 75- 94
25-281
64-109 22- 95 77-170 63-473 101-761 30-146 34-112
Lung
Skin
21 3
3
3.5
3.5
Bladder
Lymphatic and hematopoielic
115 173 277
66
5
9
111
5.8
10.4
Other
Diseases of circulatory system ischemic heart disease Cerebfovascular disease
61
92
128.3
99.4 8.1
86 7
18 4 10
95
53
77-109 78-116
27-104
15.3
20.2 16.0
Other Diseases of respiratory system Diseases of digestive system External causes
All other causes
20.8
4.6
103
29 55
11.6
20.9
98,7
82
94.8
15.0
551
27.4
96 55
67-158 12- 70 31- 98 79-117
33- 90
Actual numbers lor which causes of death known
1-Wilh 42 deaths with missing certilicates distributed according to the distribution in Column A 1SMR Observed (Bl/Expecled 100 (computed from values expressed to two decimal places)
95%
^including 42
asymptotic confidence intervals' with missing death certilicales
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Mortality of Pesticide Applicators
Helen H. Wang. M.D., and Brian MacMahon, M.D.
Information has been obtained on a cohort of professional pesticide applicators which will be followed prospectively. The cohort consists of 76,726 mates employed for three months or more between 7967 and 7976 by any of three nationwide pest control companies. Deaths which occurred between 7967 and 7976 were reported by the Social Security Administration as a result of a search of its records. Overall, 311 deaths were ascertained, giving a standardized mortality ratio (5MR) of 84. SMRs were over cancer of the lung (115). 700 for three causes of death cancer of the skin (173) and cancer of the bladder f277/. The confidence intervals of two of these ratios include 100. and the observed numbers therefore do not differ significantly from those expected. For bladder cancer the excess is on the border of statistical significance (p < 0.05). The excess of deaths from lung cancer was not seen for applicators classified as termite control operators, a group more likely to be exposed to chlordane and heptachlor. There were significantly low SMRs for cancer of the digestive organs (46) and for other diseases of the digestive (55) and respiratory (29) systems. Deaths from cerebrovascular disease were also less than expected, though not significantly so.
that do not produce acute symptoms is still not known. In particular, there is concern, deriving from experimental work on laboratory animals, that chronic exposure may be associated with increased risk of malignancy. There has been little published epidemiologic work addressing this problem in humans. The cancer experience of professional pesticide applicators would seem to be relevant. Although, from any presently available information, it is not possible to assess the doses to which professional applicators are, or in the past have been, exposed, it is unquestionable that as a group their exposures exceed many-fold those of the general population. It is reasonable, therefore, to look among this group for the first signs of a carcinogenic effect of pesticides in man. This paper reports on the establishment of a cohort of professional pesticide applicators which will be followed prospectively. It also reports the results of such observations as can be made retrospectively on the same cohort.
L-hemical control of insect pests essentially began in the middle of the nineteenth century with the introduction of arsenical pesticides. However, pesticide use was confined to fruit and high value crops, or to instances of severe infestation, until the development of the chlorinated hydrocarbons a little over 30 years ago. The high potency and residual action of these compounds reduced the cost of pest control and led to a rapid increase in the levels of chemical pesticides in the environment generally, Acute health effects of heavy exposure to chemical pesticides are reasonably well known. They can be serious and sometime? fatal Whether there are long-term health effects of chronic exposure of humans'to levels
IpittrTiioloyv. Harvard School of Publn Health. 677 from the Drpririrnt-ni Huniinijion Avc Bo'.ion. MA 021T* Supporifd b\ K'-"""' i'om Vel'.iiol Chf-miral Corpoianon and the National Can< Insiiiulr. U S Publi< Health Sefvi(f(S-P01-CA()b373) ihc Comprfhcnstvc Camel Cfnifr. Duke University Dr Wann prcsrnilv Medical (fftHT. Durham. NC 27710
Materials and Methods Employees of three nationwide pest control companies form the study cohort. The three companies have headquarters in Atlanta, Ca.. Memphis. Tenn.. and Tucson, Ariz.. respectively. but .their branch offices cover more than 40 states. At the time this study was begun, centralized personnel records had been maintained only for approximately 10 years in all three companies because of the record storage problems associated with rapid turnover and a large number of employees. In two companies January 1, 1967, was identified as the earliest date for those inactive as well as which a roster of all personnel could be assembled, and in those still active in 1976 the third, and largest, company this date was January 1, 1968- Personnel records of all persons in job categories potentially involving exposure to pesticides and employed on those dates or hired between those dates and June 30.1976. were reviewed. From a total of 44,083 records, 16,126 subjects were identified who satisfied the criteria of (1) being male. (2) being employed for three months or more, and (3) having name. Social Security number, date of birth and dates of employment recordedThe assembly of the cohort involved a combination of computer and manual procedures and, without considerable clerical labor, it is not possible to say precisely
Rtprintri from Jounrl of Occupational MtSctn* Nov*mbf. 1B78. Volum* 21, No. 11 pp. 741-744
(C)JOH 187B
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Table 8.
Cause ol
Death
Observed/Expected Deaths from Selected Causes According to Duration of Follow-up.
Duration of
Follow-up
20 +
47/54.7 7/11.6 17/21.8
<10
21/44.4
3/ 6-6
10.19
45/58.4 14/11.0 16/21.3
Total
113/157.5
24/ 29.2 37/ 53.8
All causes
Malignant neoplasms
Ischemic heart disease
4/10.8
'deaths from cancer compared to the number expected, even among persons followed 20 and more years after first employment. There was only one death from liver cancer the tumor associated with chlordane exposure
in mice.*
to blood pressure and to cerebrovascular disease deserves more investigation.
The authors indebted to Sidney Shindelt. M D.. of the Medical College of supplementing the information deaths in the study group The Social Security Administration carried the matching of individuals the cohort with Social Security records.
Wisconsin lor
The only tumor in excess in these data is cancer of the lung. For this tumor the excess is not statistically significant and does not follow any pattern of association with duration of exposure or latency that suggests an etiologic relationship between occupational exposure and lung cancer. The fact that there are no data on cigarette smoking in this study group is further reason for caution in interpreting the observations on lung cancer. A surprising observation is the statistically significant excess of deaths from cerebrovascular disease. This appears not to have been observed or suspected previously and should be confirmed in other data or further followup of these workers before it is accepted as evidence of a consequence of exposure to chlordane or heptachlor. There is, however, some equivocal evidence of increased blood pressure among pesticide workers. Thus, no increase in blood pressure was reported in three surveys of ^k'orkers specifically exposed to chlordane.6 In one of ^^hese surveys two cases of hypertension were found among 24 workers but there was no control group and the finding was considered incidental.7 increased systolic and diastofic pressures have been reported among workers with mixed pesticide exposures' but lack of increase has also been reported." Hypertension was reported in two studies of workers exposed to DOT, another chlorinated hydrocarbon, but in the absence of a comparison group in either study the findings are difficult to interpret.^ Obviously, research in this area is in an Onsatisfactory state. The relationship of pesticide exposure
References
1. U.S Department of Health, Education and Welfare: Eighth Revision International Classification of Diseases Adapted for Use in the United States Public Health Service Publ. No. '1693 Superintendent
of Documents. U.S. Government
Printine Office. Washington, D.C-,
1967. 2. Monson RR: Analysis of relative survival and proportional mortality, Cbmput Biomed Res 7:325-332, 1974. 3. Wang HH and Miettinen 0: Evaluation of three asymptotic methods of interval-estimation for the odds ratio In preparation. 4- Data provided by Velsicol Chemical Corporation.
5,
Epstein SS: Carcinogenicity of heptachlor and chlordane. Set
Tora/ cnv/ron 6:103-154, 1976. 6- Ptinci F and Spurbecic CH: A study of workers exposed to the in-
secticides chlordane. aldrin. dieldrin Arch Ind Hyg Occup Med
3:64-72,1951 7. Alvarez WC and Hyman S" Absence of toxic manifestations in
workers exposed to chlordane. Arch Ind Hyg Occup Med 8 480-483.
1953. 6. Fishbein Wl, White IV. and Isaacs H): Survey of workers exposed to chlordane, Ind Med Surg 33:726-727, 1964. 9- Sandifer SH, Keil )E. Finklea IF, and Cadsden RH: Pesticide effects occupationalty exposed workers: A summary of four years observation of industry and farm volunteers in South Carolina, Ind
Med41.9-12.1972.
10. Warnick SL and Carter )E: Some findings in study of workers occupationally exposed to pesticides Arch Environ Health 25:265-270.
1972.
11. Morion WE, Crawford ED. Maricle RA, et al,. Hypertension in Oregon pesticide-formulating workers Occup Med 17:162-185.1975, 12. Ortelee MF: Study of with prolonged intensive occupational exposure to DDT. Arch Ind Health 18433-440. 1958. 13. Laws ER. Curley A, and Biros FI- Men with intensive occupational exposure to DDT. Arch Environ Health 15:766-775,1967.
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Table 4.
Observed/Expected Dealhs from Lung Cancer According to Age at Observation and Age at Entry into
Occupation.
Tab le6.- Observed/ Expected Deaths from Cerebrova scular Disease Acco rding to Age at Obsep vation and / at Entry nto Occ upation. \ge
Age at
Observation
Age al Entry
<35
5/1.2 2/1.4
into Occupation
Age at
Total
6/1.7
Age at Entry into Occupation
<35 2/1.1
0/0.7 2/1.8
35.49
1/0.5 1/2.8
50+
0/0.4 3/1.0
Observation
35-49
1/0.4
50+
2/0.5
6/2.7 8/3.2
Total
3/1-5 5/3.3
9/4.5 17/9.3
<50
<50
50-64 65 +
Total
50-64
65 + Tolal
3/4.7
3/2-0
3/1.8
7/4.3
7/2.6
0/1.6 2/4.9
3/1.4
3/2.6 12/9.0
and significantly so. since its confidence interval does not include 100. However, the value (72) is typical of that observed in an employed population. This deficit of observed deaths relative to expected seen in working populations is generally attributed to the selective factors associated with employment. Observed deaths from cancer are also fewer than expected, but not significantly so. Only one type of cancer shows more observed deaths cancer of the lung than expected, but again the difference is not statistically significant. There was one death attributed to carcinoma of the liver. This occurred in a man who worked for the company for five years, beginning in 1944 when he was 68 years old, and who died in 1958, at the age of 81, of "carcinoma of the liver." The carcinoma was not specified as primary but was so coded by us. The expected number of deaths from cancer of the liver and biliary tract (ICD8 #155. 156) was 0.59, There was one death each from cancer of the bladder, the prostate and the central nervous system, and one with primary site unspecified. ^k While diseases of the circulatory system as a whole acfor fewer deaths than expected, there is a substantial and statistically significant excess of deaths due to cerebrovascular disease. No other causes of death are in
^Bbunt
excess.
Table 3 gives similar data separately for the two plants. The features outlined above are present in both sets of data.
Table 4 shows observed and expected lung cancer deaths according to age at entry into occupation and age at observation. Almost the entire lung cancer excess occurs among workers who were aged less than 35 at entry into occupation and less than 50 at observation. In this particular category the difference between observed and expected is statistically significant (p < 0.01). Because of small numbers in the individual cells of this table it is not possible to tell whether the excess is a function of young age at entry, young age at observation, or both. Relationships to duration of follow-up ("latency") and duration of employment are explored in Table 5, Again numbers are small but there is no pattern suggesting a real relationship with either variable- For both variables the excess appears
Table 5. Observed/Expected Deaths from Lung Cancer According to Duration of Employment and Duration of
in the subgroup with intermediate durations. It is noteworthy that in the person-years with 20 or more years of latency there is a statistically significant deficiency of lung cancer deaths. The lack of any clear pattern in this table casts doubt on the meaningfulness of the relationship seen in Table 4. Similar analyses of deaths from cerebrovascular disease are given in Tables 6 and 7. Within the variability inherent in the small numbers in these tables the excess appears to be distributed more or less evenly throughout and there is no clear relationship with any of the four variables. Although 3.2 deaths from cerebrovascular disease would have been expected among currently employed workers, there were none. Six deaths from this cause occurred within five years after termination; four occurred 5-9 years after termination; and seven, 10 or more years after termination. The expected values for the latter three periods were 1.7,1.5 and 2.9. The effects of worker selection are explored for deaths from two principal causes and from all causes in Table 8. All three categories show substantial deficits of observed deaths in the first 10 years of the follow-up period. For deaths from malignant disease, the effects of the selective factors which are presumed to be responsible for these deficits seem to have disappeared by 10 years after the beginning of the follow-up. For deaths from ischemic heart disease and for all deaths, the deficits persist throughout all three categories of duration of follow-up, though not so markedly as in the first ten years.
Discussion To the authors' knowledge this is the only published study of cause-specific mortality among workers occupationally exposed to chlordane or heptachlor and there are. therefore, no other data with which these can be compared directly. The impetus to the study was a search for evidence of carcinogenicity of these compounds to man- None has been found, although the study population is too small and the period of follow-up too short to translate this into a statement that there is no excess risk of cancer associated with exposure in man. There was no excess of
Table 7. Observed/Expected Deaths from Cerebrovascular Disease According to Duration of Employment and Duration of Follow-up.
Duration of Employment
<10 <10
3/2.0
Follow-up.
Duration of Employment
Ouration of Foltow-up
<10
3/1.5
10-19
2/1.3 6/2.1 8/34
20+
0/1.4 0/0.8 1/1.8
1/4.0
Total
5/4.3 6/2.9
1/1.8
Duration of Follow-up 20+ 10-19
3/1.4
Total
9/4.7 8/34 0/1.3 17/9.3
B<10
r
10-19
3/1.3
10-19
20+
Total
3/2.0
2/2.1 5/3.5
6/1.3
0/1.3 9/3.9
20+
Tolal
3/1.5
12/9.0
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Table 1.
Duration of
Distribution of Study Subjects by Duration of Foliow-up and by Plant.
Total Marshall
Follow-up <10 10-19 20-29 30 + Total
Memphis
No.
481
%
129 99 193
149
352
324 159 835
422*
35T 149 1403
34.3 3D.1 25.0
10.6
570
100.0
'Includes one subject who worked in bolh plants
the state in which the beneficiary filed a claim for benefits. A Social Security Administration search of its records identified 104 deaths in the study cohort through the end of 1975, for which death certificates were sought from the states and registration areas. Contemporaneously, Dr. Sidney Shindell of the Medical College of Wisconsin had been conducting individual follow-up of terminated workers in these plants. He informed us of nine deaths in our cohort which had not been identified by SSA, four of which occurred in 1976 after the termination of the SSA search. These have been added to the known deaths and the closing dates of Dr. Shindell's foliow-up June 30, 1976, for Marshall employees and December 31.1976, for Memphis employees were used as the termination dates for computing person-years of observation. Dr. Shindell also provided copies of some death certificates which had not been obtained by the authors. There remain two deaths for which certificates could not be found. The distribution of deaths by cause was based on death trtificate causes coded by one of the authors (HHW) to
Table 2.
Cause of Death causes
Malignant neoplasms Digestive organs and peritoneum
the 8th Revision of the International Classification of Diseases Adapted.' Expected numbers of deaths by cause were estimated using a computer program developed by Monson.2 The program applies national mortality rates specific for sex, race and age and calendar time in fiveyear groups to the comparable person-years accumulated during the period of observation. Since the publication of the reference cited, the program has been updated to use national mortality rates through 1975. The rates for white males were used for this analysis- For the computation of person-years, the beginning date was taken to be January 1,1946, for Marshall and January 1,1952, for Memphis if the employee was eligible on those dates, or at the end of three months employment if he was first employed later. Standardized mortality ratios (SMR) were estimated by dividing the observed deaths by the expected and multiplying by 100. An iterative method based on mid-p values* was used to compute 95% confidence intervals. An attempt was made to examine the relationship between the intensity of exposure and mortality experience among these workers- However, a complete occupational history was not available for each individual. Moreover, serum pesticide levels of workers actively employed in the plants in 1975 and 1976* did not correlate with a classification of presumed exposure level based on Job category. Therefore, analyses according to presumed level of exposure are not presented. Results
The distribution of the study group by plant and by duration of follow-up is given in Table 1. Table 2 gives observed and expected numbers of deaths by cause and estimates of the SMRs. The overall SMR is lower than 100
Observed and Expected Deaths from Selected Causes.
Observed
Expected
SMR*
All
Lung
Lymphatic and hemalopoietic Other Diseases o( circulalory system
Ischemic heart disease Cerebrovascutar disease
113 24 7 12
4 63 37 17 9 3
4 14
157.4
29.3
8.2
9.0 3.3 8.8 75.8
53.9
9.3 12.6
,8.1
72 82 86 134 30 45 83 69
183 71
C. .01 SMRf 59- 86
54- 120
387321464170
228
151 109
106
Other Diseases of respiratory system Diseases of digestive system External causes All other causes
37
47
8.5
49- 94 110- 287 35- 131 9- 101 15- 114
22.8
13.1
5t
61 38
35- 101
14- 85
Observed/Expected x 100 (computed from values expressed 10 two decimal places) computed by iteration based on mid-p values' ^Including two with missing, death certificates
SMR
f95% exact confidence intervals
Tabfe 3.
Observed and Expected Deaths from Selected Causes According to Plant.
Marshall
Cause of Death
All causes Malignant neoplasms Cancer of digestive organs and peritoneum Cancer of tung tschemic heart disease Cerebrovascular disease External causes
Observed
76 13 5
7
Expected "107.1 20 5.9
6.1 38.1 7.0 12.3
SMR
71 65 85
115
Observed
37 11 2
Memphis Expected
SMR
74
50.1 9.1 2.3 2.9 15.6 2.3
10.4
121 88
174 70 260 48
5
11
26
11
68 158
73
9
6 5
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Mortal ity of Workers Employed in the Manufacture of Chlordane and Heptachlor
Helen H. Wang, M.D., and Brian MacMahon, M.D.
A retrospective mortality study has been carried out on workers employed in the manufacture of chlordane and heptachlor between 7946 and 7976. The study group was comprised of 1403 white males who worked for more than three months at either of the two plants in the United States now producing these compounds. Information on deaths among terminated employees was obtained from the Social Security Administration and supplemented by collected by another investigator by individual ^^bllow-up. There were 773 deaths observed in the group, compared to 757 expected, giving a standardized mortality ratio (SMR) of 72. There was no overall excess of deaths from cancer, even among workers followed Twenty or more years after entry into the occupation. There was one death from liver cancer. An excess of deaths from lung cancer (12 observed, 9.0 expected) was not statistically significant and was not distributed by duration of exposure or of latency in any pattern suggesting an etiologic role for chtordane-hepta chlor exposure. Although diseases of -the circulatory sysfem as a whole showed fewer deaths than expected (SMR 83), there was a statistically significant excess of deaths from cerebrovascular disease (17 observed. 9.3 expected). This excess was not related to duration of exposure or latency and occurred exclusively after termination of employment.
Central to the suspension proceedings and to the ban subsequently negotiated was concern that these compounds might be carcinogenic to man. The evidence is controversial and derives entirely from long-term feeding studies in laboratory animals. There are a few crosssectional clinical studies of heavily exposed humans but essentially no data on long-term mortality associated with chronic or heavy exposure in man. A study of the mortality of workers engaged in the manufacture of these pesticides at the only two plants currently engaged in their production in the United States is reported here. While current levels of exposure are reasonably well characterized, the total exposure experienced by workers in these plants in the past cannot be reconstructed. However, it is very likely that a substantial proportion of workers has been exposed to levels well above those prevailing in the general population. The study was undertaken at the invitation of the Velsicol Chemical Corporation which owns and operates the two plants.
Materials and Methods Velsicot Chemical Corporation began producing chlordane in its plant at Marshall. Illinois, in 1946 and heptachlor and endrin in the plant at Memphis, Tennessee, in 1952. Personnel records are available for all of the 951 employees at Marshall and the 1425 employees at Mem-. phis who had ever worked in these plants before the spring of 1976, when this study was initiated. After exclusion of females, males who worked for three months or less. and persons with inadequate identifying information, there remained 1403 eligible subjects. No information on race was available but all the deaths identified in the course of the study were of whites. Among the 973 employees excluded, approximately 7% were excluded because they were female, 64% because they worked for three months or less and 29% because of missing information.
^Information
\-/hlordanc and heptachlor are chlorinated hydrocarbons which were widely used as agricultural and domestic pesticides until 1975, when the Environmental Protection Agency suspended their use for all but subterranean termite control and certain other limited applications. A complete ban for agricultural use is now being phased in.
MK------------------------------------------the Department of pidemiolom Harvard Schoot of Publit Health. b77 ^Bnnngton AK- Bo^ion. MA 02115 Supported by granc, fiom the Velsicol Chemical Corporation and the National Cam in-.niutr. U S Public Health Service (5-P01-CAOi>3731 D' Wdrit; prfscnilv thr Corn pro hen Cancer Cenler. Duke-UniverMtv Mt-diial ("enit-r Durham, NC 27710
^rom
Identifying information was submitted to the Social Security Administration (SSA) which provided, for those workers known dead, information on date of death and
fttprinit! from Journal of Occupational Mwdlctif Nownt-f, IBTt, Volum* 21, No. 11 pp. 74S-741
Case 1:05-cv-01020-MMS
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Case 1:05-cv-01020-MMS
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Summary and Conclusions
A study was conducted of
a cohort of
783 current and former em-
ployees who worked three months or more at the Marshall, Illinois plant
of the Velsicol Chemical Corporation from 1 January 1946 through 31 December 1979.
Of the study cohort, 97.37, of the males and 98.87o of the
females were located and data on morbidity and mortality obtained.
The data indicate that overall mortality was significantly lower
in the male employees than that expected in the comparable segment of
the U.S. population as a whole, probably as a result of the life style
of the community in which the plant is located.
Deaths from heart dis-
ease are not significantly different from the U.S. population and are
consistent with overall mortality patterns.
There were minor differto
ences among specific classes -of workers due
chance variations en-
countered when subclasses are analyzed containing small numbers of
study subjects, but none of the variables is statistically signifi-
cant, nor can they be related to-any specific job classes or products
handled.
No variations related to length of employment were evidenced
by the data obtained.
Morbidity data are likewise comparable to expectations in a work
force of the age composition present in the Marshall facility and
among those no longer employed and surviving at the time of the termination of the study.
There is, thus, no evidence of any long-term latent effect on
health related in any way
Co
employment
at the
Velsicol plant in Mar-
shall, Illinois, for the thirty-four year period in which it has been
engaged in the production of chlorinated hydrocarbon insecticides.
Case 1:05-cv-01020-MMS
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Case 1:05-cv-01020-MMS
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APPENDIX II OMITTED
^f
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Case 1:05-cv-01020-MMS
;?
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3
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