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PCBs and Dioxin May Cause
Pancreatic Cancer
| The pancreas is a yellowish organ which secretes digestive
enzymes and hormones. It lies beneath the stomach and is connected to the
small intestine.
Twelve of the fourteen studies listed below show a link
between PCBs and/or dioxin exposure and pancreatic cancer.
(Not all studies are the same size or quality.)
For additional information about PCBs and dioxin impacts
on the pancreas, see the Diabetes
section. |
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Study #1
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PCBs caused a significant increase in mortality from pancreatic
cancer in exposed workers
This study examined mortality to December 31, 1989 in a cohort
of 2,222 males employed between 1947 and 1975 at a transformer manufacturing
plant in Canada, where there had been extensive use of transformer fluid,
some containing polychlorinated biphenyls (PCBs). A combined cohort list
of 2,222 names was independently obtained from plant management and union
officials. Mortality of 1,939 workers with known birthdates was ascertained
by record linkage with the Canadian Mortality Database. Standardized mortality
ratios (SMRs) for different criteria for acceptance of the death certificate
link and for cohort membership (based on work history) ranged from .71-1.05.
There was no significant increase in overall cancer deaths. The only significant
site-specific increased mortality was pancreatic cancer (11
deaths), with SMRs ranging from 2.92-7.64 and higher mortality risk in
those who entered the cohort prior to 1960. All but one of these deaths
had a latency period of at least 10 years. Results of earlier studies which
found an excess of pancreatic cancer in association with oil exposure and
electrical equipment manufacturing are summarized. (Yassi et al, 1994)
Study #2
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PCBs are significantly correlated with pancreatic cancer,
on a dose-response basis
Occupational exposure to p,p'-dichlorodiphenyltrichloroethane
(DDT) has been associated with increased pancreatic cancer risk. We measured
organochlorine levels in serum obtained at the study enrollment from 108
pancreatic cancer cases and 82 control subjects aged 32-85 years in the
San Francisco Bay Area between 1996 and 1998. Cases were identified using
rapid case-ascertainment methods; controls were frequency-matched to cases
on age and sex via random digit dial and random sampling of Health Care
Financing Administration lists. Serum organochlorine levels were adjusted
for lipid content to account for variation in the lipid concentration in
serum between subjects. Median concentrations of p,p'-dichlorodiphenyldichloroethylene
(DDE, 1290 versus 1030 ng/g lipid; P = 0.05), polychlorinated biphenyls
(PCBs; 330 versus 220 ng/g lipid; P<0.001), and transnonachlor (54 versus
28 ng/g lipid; P = 0.03) were significantly greater among cases than controls.
A significant dose-response relationship was observed for total PCBs
(P for trend <0.001). Subjects in the highest tertile of PCBs (> or
=360 ng/g lipid) had an odds ratio (OR) of 4.2 [95% confidence interval
(CI) = 1.8-9.4] compared to the lowest tertile. The OR of 2.1 for the highest
level of p,p'-DDE (95% CI = 0.9-4.7) diminished (OR = 1.1; 95% CI = 0.4-2.8)
when PCBs were included in the model. Because pancreatic cancer is characterized
by cachexia, the impact of this on the serum organochlorine levels in cases
is difficult to predict. One plausible effect of cachexia is bioconcentration
of organochlorines in the diminished lipid pool, which would lead to a
bias away from the null. To explore this, a sensitivity analysis was performed
assuming a 10-40% bioconcentration of organochlorines in case samples.
The OR associated with PCBs remained elevated under conditions of up to
25% bioconcentration. (Hoppin et al, 2000)
Study #3
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workers heavily exposed to PCBs experience excess pancreas
neoplasias (pancreatic cancer)
Health hazards associated with the production and industrial
use of polychlorinated biphenyls (PCB) are reviewed. Production techniques
used in the preparation of PCB mixtures and the sources of production are
described. Main properties of PCB that account for its widespread industrial
use are identified. PCBs are absorbed into worker metabolism primarily
through cutaneous, respiratory, or digestive exposures. PCB carcinogenicity
is demonstrated in animal experiments. Excess incidence of malignant tumors
in Japanese accidently exposed during consumption of rice oil contaminated
with PCB during manufacture is discussed. Workers heavily exposed to PCBs
experience an excess of malignant melanomas and pancreas neoplasias.
Exposed workers have relatively high PCB residue concentrations ranging
from several tens to several hundred parts per billion (ppb). Workers involved
with the assembly of capacitors and transformers have PCB plasma concentrations
ranging from 10 to 2,500ppb with concentration increasing with longer duration
of exposure. Plasma PCB concentrations decrease relatively fast in workers
exposed to short periods and very slowly in workers exposed 10 years or
longer and in those exposed to highly chlorinated PCB mixtures. Digestive,
upper respiratory, neurological, and other symptoms of exposed workers
are described. Safety and health protection methods are discussed and inspection
and monitoring techniques available to maintain PCB concentrations within
approved concentrations are described. A need for periodic clinical examination
of workers is stressed and specific medical tests and treatments are discussed.
(Wasserman et al, 1983)
Study #4
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some PCBs may increase pancreatic cancer risks through modulation
of K-ras gene activation
Organochlorine compounds such as 1,1,1-trichloro-2,2-bis(p-chlorophenyl)-ethane
(p,p'-DDT), 1,1-dichloro-2,2-bis(p-chlorophenyl) ethylene (p,p'-DDE), and
some polychlorinated biphenyls (PCBs) are carcinogenic to animals and possibly
also to human beings. Occupational exposure to DDT may increase the risk
of pancreas cancer. The high frequency of K-ras mutations in pancreatic
cancer remains unexplained. We analysed the relation between serum concentrations
of selected organochlorine compounds and mutations in codon 12 of the K-ras
gene in patients with exocrine pancreatic cancer. METHODS: Cases were prospectively
identified in five hospitals. Mutations in K-ras were analysed by PCR and
artificial restriction fragment length polymorphism. Cases of pancreatic
cancer with wild-type K-ras (n=17) were frequency matched for age and sex
to cases of pancreatic cancer with a K-ras mutation (n=34, case-case study).
These 51 cases were further compared with 26 hospital controls (case-control
comparison). Serum organochlorine concentrations were measured by high-resolution
gas chromatography with electron-capture detection and negative ion chemical
ionisation mass spectrometry. FINDINGS: Serum concentrations of p,p'-DDT
were significantly higher in pancreatic cancer cases with a K-ras mutation
than in cases without a mutation (odds ratio for upper tertile 8.7 [95%
CI 1.6-48.5], p for trend=0.005). For p,p'-DDE the corresponding figures
were 5.3 (1.1-25.2, p for trend=0.031). These estimates held after adjusting
for total lipids, other covariates, and total PCBs. A specific association
was observed between a glycine to valine substitution at codon 12 and both
p,p'-DDT and p,p'-DDE concentrations (odds ratio 15.9, p=0.044 and odds
ratio 24.1, p=0.028; respectively). A similar pattern was shown for the
major di-ortho-chlorinated PCBs (congeners 138, 153, and 180), even after
adjustment for p,p'-DDE, but without a specific association with spectrum.
Concentrations of p,p'-DDT and p,p'-DDE were similar among wild-type cases
and controls, but significantly higher for K-ras mutated cases than for
controls (p<0.01). INTERPRETATION: Organochlorine compounds such as
p,p'-DDT, p,p'-DDE, and some PCBs could play a part in the pathogenesis
of exocrine pancreatic cancer through modulation of K-ras activation.
The results require replication, but they suggest new roles for organochlorines
in the development of several cancers in human beings. (Porta et al, 1999)
Study #5
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pancreatic cancer is a toxic effect of PCBs
The general hygienic and toxicological aspects of PCBs and
the results of PCB residue analyses in food products in Mexico are described.
Aroclor 1254 is used illegally as a diluent for pesticide preparations.
The toxic effects of PCBs in humans include atrophy and fatty degeneration
of the liver, chloracne, fatigue, emesis, and cancer of the pancreas
and skin. Residue levels of 0.61-3.37 mug/g were found in cereal products,
including 1.68 mug/g in baby food. Levels of 10.4-33.15 mug/g were found
in cardboard and plastic packaging materials used for cereal products
[…
from paper recycling?]. (Albert et al, 1979)
Study #6
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PCBs may help other chemicals cause pancreatic cancer
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PCBs may act synergistically to support tumor induction by
other chemicals, through enzyme induction
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PCBs increased the impact of tobacco nitrosamine by 2.5 fold
The tobacco-specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone
(NNK) induces tumor formation in the liver, lung, nasal cavity, and pancreas
of rats. Metabolic activation is required for the tumorigenicity of
this compound. The involvement of cytochrome P450 enzymes in NNK bioactivation
was investigated in rats by studies with chemical inducers and antibodies
against P450s. Liver microsomal enzymes catalyzed the formation of 4-oxo-1-(3-pyridyl)-1-butanone
(keto aldehyde), 4-hydroxy-1-(3-pyridyl)-1-butanone (keto alcohol), 4-(methylnitrosamino)-1-(3-pyridyl-N-oxide)-1-butanone
(NNK-N-oxide), and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL)
from NNK. When the activity was expressed on a per nanomole P450 basis,
treatments of rats with 3-methylcholanthrene (MC), phenobarbital (PB),
pregnenolone 16-alpha-carbonitrile (PCN), Aroclor 1254 (AR), safrole
(SA), and isosafrole (ISA) increased the keto aldehyde formation in liver
microsomes 2.0-, 2.4-, 3.8-, 2.5-, 2.1-, and 1.8-fold, re (incomplete
abstract) (Guo et al, 1992)
Study #7
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electrical workers show increased rates of pancreatic cancer,
which may be linked in part to PCB exposures
Calculated cumulative exposures to electromagnetic (EM) fields
during the production and distribution of hydroelectric power and the incidence
of cancer were compared. The study cohort included 5,088 men employed in
eight large Norwegian hydroelectric power companies. They had been employed
for at least 1 year between 1920 and 1985. During the follow up period
from 1951 through 1991, 486 new cases of cancer were observed. Stomach
cancer showed an excess risk among workers with more than 30 years on the
job. An increase in the standardized incidence ratio was detected for malignant
melanoma as well. An analysis by duration of employment indicated an increased
incidence ratio for all cancers combined, cancer of the pancreas,
lung, and kidney, malignant melanoma, nonmelanoma, and lymphoma. Of the
three cases of leukemia, two were among workers who had been employed for
less than 20 years. An excess risk was noted for malignant melanoma at
cumulative exposures above 35 microtesla years. The evaluation of risk
for malignant melanoma and combined exposures to magnetic fields and possible
exposure to electric discharges or to oils contaminated with polychlorinated
biphenyls showed a tendency toward an effect. The authors conclude
that no association was observed between the occurrence of leukemia or
brain tumors and exposure to electric or magnetic fields in hydroelectric
power companies. (Tynes et al, 1994)
Study #8
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it’s difficult to study the role of organochlorines in pancreatic
cancer, due to many complicating factors
Studies on the possible role of organochlorine compounds
in the etiology of pancreatic and other cancers face a set of methodologic
and logistic issues that stem from the lipophilic nature of most organochlorines,
and from the fact that tumor-induced lipid mobilization, weight loss, and
metabolic changes can be profound before diagnosis. The question thus arises:
do the xenobiotic concentrations in blood and adipose tissue result, in
part, from such pathophysiologic changes? To assess and control potential
selection and information biases, a flexible framework is warranted. It
could be based on indicators such as time elapsed between the first symptom
of cancer and blood or fat sample extraction; signs, symptoms and clinical
status at the time of extraction; cholesterol and triglycerides levels;
other laboratory findings; tumor stage at diagnosis; diagnostic procedures;
treatment type and timing; clinical complications; and survival. Before
adopting qualitative criteria and quantitative standards, their impact
upon causal estimators should be assessed empirically. (Porta, 2001)
Study #9
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no increase or decrease in pancreatic cancer
In 1968, a mass food poisoning (yusho) occurred in western
Japan involving more than 1,850 people, the majority of whom were residents
of Fukuoka and Nagasaki prefectures. The poisoning is now understood to
have been caused by ingestion of a commercial brand of rice oil contaminated
with polychlorinated derivatives of biphenyls, dibenzofurans, quaterphenyls,
and some other related compounds. The number of deaths seen among 1,761
victims (887 males and 874 females) from the date of official registration
as yusho up to the end of 1983 was compared with the expected number of
deaths which was calculated on the basis of the national age, sex, and
cause-specific death rates. Neither significantly increased nor significantly
decreased mortality was seen among overall causes of death in males and
females. A significant excess mortality was seen for malignant neoplasms
at all sites in males but not in females. Neither significantly increased
nor decreased mortality was seen for cancer of the esophagus, stomach,
rectum and colon, pancreas, breast, and uterus. For cancer of the
liver, however, a considerably increased mortality was seen in both males
and females but the excess was statistically significant only in males.
It was also notable that such increased mortality due to liver cancer was
seen mainly among the patients living in Fukuoka prefecture but not at
all among those in Nagasaki prefecture which approximate the yusho patients
in Fukuoka prefecture in number. Deaths from chronic liver diseases and
liver cirrhosis were also found to be increased in both sexes but the increase
was not statistically significant. (Kuratsune et al, 1987)
Study #10
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PCBs induce growth of pancreatic tissue inside the liver
Pancreatic-type tissue induced in the livers of rats
treated with polychlorinated biphenyls was characterized by transmission
electron microscopy and high-resolution immunocytochemistry. The cells
of pancreatic-type tissue were arranged as acini and in small groups. By
electron microscopy the pancreatic-type tissue showed features very similar
to normal pancreatic acinar tissue, such as well developed rough endoplasmic
reticulum (RER), large numbers of mature zymogen granules, and a basally
located nucleus. Protein A-gold immunocytochemical technique showed localization
of amylase and trypsinogen over the zymogen granules and RER. These findings
confirm that this tissue in the liver is morphologically and functionally
identical to pancreatic acinar tissue. (Rao et al, 1986)
Study #11
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slight increases in pancreatic cancer in pulp and paper mill
workers exposed to chlorinated compounds such as PCBs and dioxin
Case/control and cohort studies of dioxin exposed populations
were reviewed. In Swedish case/control studies, exposure to phenoxyacetic
acids, chlorophenols or dioxins was related to increased risks of soft
tissue sarcoma (STS) and nonHodgkin's lymphoma (NHL). Other case/control
studies from Kansas, Nebraska, Iowa, and Minnesota on the risks of herbicide
exposure among farmers found an association between 2,4-dichlorophenoxyacetic-acid
(94757) use and NHL. Exposure to 4-chloro-2-methylphenoxyacetic-acid (94746)
(MCPA) was associated with an increased risk of leukemia. In a Washington
State study, elevated risks of NHL were found for farmers, forestry herbicide
applicators, and others potentially exposed to phenoxy herbicides for 15
years or more. Increased risks for STS and NHL were also found by studies
in New Zealand, and increased risk of STS was found in a study in Italy.
In a NIOSH cohort study, standardized mortality ratios (SMRs) were determined
for 2,3,7,8-tetrachlorodibenzo-p-dioxin (1746016) (TCDD) exposed workers.
In a subgroup with a latency of at least 20 years, the SMRs were 146 for
all cancers, 922 for STS, and 142 for respiratory system cancers. Similar
increased risks were reported in cohort studies in Germany, Italy, Japan,
and on Vietnam veterans. Cohort studies on pulp and paper mill workers
exposed to a number of chlorinated organic compounds, including polychlorinated
dibenzodioxins, found increased mortality from tumors of the liver and
lung, as well as slight increases in malignant lymphomas, leukemias
and pancreatic and stomach cancers. Odds risks were also
determined for populations environmentally exposed through drinking water,
fish consumption, and proximity to contaminated areas. Reports of increased
risks to sheep and dogs were mentioned. The authors conclude that STS and
NHL are associated with exposure to phenoxy herbicides and related chlorinated
phenols, and that TCDD exposure is related to various other cancers. (Hardell
et al, 1994)
Study #12
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one case of pancreatic cancer following dioxin exposure (out
of 4 people examined)
A study of polychlorinated dioxins and furans was made using
autopsy tissue samples taken from four persons who had been exposed to
dioxins during an uncontrolled decomposition reaction in November 1953
at the BASF facility in Ludwigshafen, Germany. All four subjects died of
cancer. The first individual, a mechanic who performed cleanup work for
1 week after the accident, developed severe chloracne and subsequently
died in May of 1989 of acute myelogenous leukemia. The second individual
was an assistant supervisor at a neighboring facility who was assigned
shift work in the accident building for a few days in December 1953. He
developed mild chloracne and died from bronchogenic carcinoma in 1990 at
age 66. Five months prior to death the 2,3,7,8-tetrachlorodibenzo-p-dioxin
(1746016) (TCDD) level in his blood was 17 parts per trillion (ppt). The
third case was a fireman who entered the autoclave room for a brief cleanup
within hours of the accident and helped in the general cleanup for several
weeks. He died at age 80 in December 1989 of pancreatic carcinoma.
His TCDD level was 518ppt. The last case was a mechanic who took part in
cleanup for several weeks starting immediately after the accident. He developed
mild chloracne and was diagnosed in 1988 with carcinoma of the liver. His
blood TCDD level was 553ppt in 1989 and 590ppt in 1990. He died of hepatic
coma in April 1992. Blood concentrations of TCDD correlated well with other
tissue concentrations on a lipid weight bases. Liver tissues were more
likely to contain higher chlorinated dioxins and furans than brain tissues.
Concentrations of TCDD increased by more than an order of magnitude during
cancer cachexia. (Zober et al, 1993)
Study #13
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elevated rates of pancreatic cancer in men exposed to dioxin
The risk of cancer mortality among the individuals exposed
to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the Seveso, Italy, accident
of 1976 was examined in this study. The subjects consisted of 45,373 exposed
individuals and 232,747 controls. Of the 45,373 exposed subjects, 805 resided
in the most contaminated area, Zone-A, 5,943 resided in the intermediately
contaminated area, Zone-B, and 38,625 resided in the least contaminated
area, Zone-R. Cancer mortality information covering the years 1976 to 1991
was obtained from the Italian National Statistics Institute. The relative
risks (RRs) for mortality from all causes did not differ significantly
from the expected value in any zone. Among males, the RRs for cancer mortality
were reduced in Zone-A and Zone-R and unchanged in Zone-B. Among females,
the RRs for cancer mortality were slightly lower or slightly higher than
expected in the contaminated zones. The RRs for pancreas and bladder
cancer
were elevated among the males in Zone-A. The females in Zone-A exhibited
increased RRs for digestive and ovarian cancers and melanoma. Among the
males in Zone-B, the risks of rectal, pleura, and lymphohemopoietic cancers
and leukemia were significantly elevated, with RRs of 2.9, 5.3, 2.4, and
3.1, respectively. Among the females of Zone-B, the risk of myeloma was
significantly elevated, with an RR of 6.6. The risk of Hodgkin's disease
was increased in both sexes in Zone-B, although not significantly. The
RR for esophagus cancer was increased among the males of Zone-R. The RR
for bone cancer was increased among the women of Zone-R. The authors conclude
that the increased risks of cancers of specific sites in the Seveso population
may be related to TCDD exposure. (Bertazzi et al, 1997)
Study #14
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significantly more pancreatic cancer
In a June 24, 1976 letter, Mobil Oil Corporation reported
to the National Institute for Occupational Safety and Health (NIOSH) preliminary
results of an epidemiological analysis based on medical records of employees
exposed to PCBs at their Paulsboro, New Jersey plant. The study included
Mobil employees reported to have had varying exposure to PCB Aroclor 1254.
The research and development employees were exposed to PCBs between 1949
and 1957 and refinery plant employees between 1953 and 1958. The extent
of exposure to other chemicals is not known. The cancer incidence among
these workers for the period 1957 through 1975 was determined using Mobil
medical records. Because medical records for 37 employees were incomplete,
these workers were excluded from this analysis. Among the 92 workers in
these two groups for whom adequate medical records were available, eight
cancers (in seven workers) were observed between 1957 and 1975. Of these
eight cancers, three were malignant melanoma and two were cancer of the
pancreas. This is significantly more skin cancer (melanoma) and
pancreatic
cancer than would be expected in a population of this size. The remaining
cancers were found at three other sites in two employees; sarcoma of the
right thigh and multiple myeloma in one employee, and recto-sigmoid cancer
in the other. (DHHS, 1998)
Links to More Information
Pancreatic
Cancer: An Agenda for Action --- Report of the Pancreatic Cancer Progress
Review Group
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