IMPACT OF DIETARY EXPOSURE TO FOOD CONTAMINANTS ON THE
RISK OF PARKINSON’S DISEASE
Maria Skaalum Petersena, Jónrit Hallingb, Sára Bechc, Lene Wermuth,d Pál Weihea,c,
Flemming Nielsena, Poul J. Jørgensene, Esben Budtz-Jørgensenf and Philippe
Grandjeana,g
a
Institute of Public Health, Environmental Medicine, University of Southern Denmark,
Winslowparken 17, 5000 Odense C, Denmark.
b
Institute of Public Health, Clinical Pharmacology, University of Southern Denmark,
Winslowparken 17, 5000 Odense C, Denmark.
c
The Faroese Hospital System, Department of Occupational and Public Health,
Sigmundargota 5, 100 Tórshavn, Faroe Islands.
d
e
Department of Neurology, Odense University Hospital, 5000 Odense C, Denmark
Institute of Clinical Research, Odense University Hospital, Odense, Denmark
f
Department of Biostatistics, Institute of Public Health, University of Copenhagen,
Copenhagen, Denmark
g
Department of Environmental Health, Harvard School of Public Health, Boston, MA
02215, USA
Corresponding author
Maria Skaalum Petersen, MSc
Institute of Public Health,
Environmental Medicine,
University of Southern Denmark,
Winslowparken 17, 5000 Odense C, Denmark.
Phone: (+45) 65503037, Fax (+45) 65911458
E-mail: mskaalum@health.sdu.dk
1
Abstract
This study aimed to investigate the association of Parkinson’s disease (PD) with dietary
exposure to polychlorinated biphenyls (PCBs) and methylmercury (MeHg) in a
community with increased exposure levels. A total of 79 clinically verified idiopathic PD
cases and 154 controls matched by sex and age were examined in this case-control study
in the Faroe Islands. Blood and hair samples were collected and a questionnaire recorded
lifetime information on residence, dietary habits, smoking history, and occupational
exposure to solvents, pesticides, and metals. Both unconditional and conditional logistic
regression analyses were used to estimate the odds ratio (OR) and 95% confidence
interval (CI) in regard to relevant exposure variables. Increased ORs for dietary intakes of
whale meat and blubber during adult life were statistically significant. The ORs for
occupational exposure to solvents, pesticides and metals also suggested an increased risk
for PD. Current serum concentrations of PCB and related contaminants suggested
slightly increased ORs, although only -hexachlorocyclohexane (-HCH) was
statistically significant. Increased intake of whale meat and blubber in adult life was
significantly associated with PD, thus suggesting a positive association between previous
exposure to marine food contaminants and development of PD.
Key words: Diet; Environmental exposure; Methylmercury compounds; Polychlorinated
biphenyls; Faroe Islands; Parkinson’s disease.
2
1. Introduction
Parkinson’s disease (PD) occurs in the Faroes at a prevalence about twice as high as
expected [Wermuth et al., 1997, 2000, 2006]. This high prevalence is unexplained, but
could conceivably be linked to the increased exposure to methylmercury (MeHg) and
polychlorinated biphenyls (PCBs) associated with the tradition of eating meat and
blubber from pilot whales that bioaccumulate these neurotoxicants [Bloch et al., 1990;
Deutch and Hansen, 2003; Longnecker et al., 2003]. A register-based, retrospective study
showed that prenatal MeHg exposure alone is unlikely to explain the doubling of the PD
prevalence in the Faroes [Petersen et al., 2007]. However, the study indicated a tendency
of higher risk of PD in subjects born in the Faroes, perhaps suggesting a greater risk
associated with life-time reliance on traditional foods among locally-born Faroese
[Petersen et al., 2007]. Further, no association was found between PD and genetic
variations in the CYP2D6 and HFE genes, which both occur in excess in the Faroes
[Halling et al., 2007]. The present study explores whether postnatal, dietary exposure to
neurotoxic marine contaminants may be a possible explanation for the high prevalence of
PD in this population.
Degenerative diseases of the nervous system, such as PD, are hypothesized to be due
to an environmental insult, either prenatally or postnatally, to specific regions of the
central nervous system; a state of “silent toxicity” may be induced that can remain
subclinical for up to several decades but makes those affected more susceptible to
degeneration of the neurons with subsequent environmental insults or with aging alone
[Barlow et al., 2007; Calne et al., 1986]. The cause of PD is likely multi-factorial with a
3
number of environmental and genetic factors being involved in the etiology [DiMonte et
al., 2002].
The same brain functions that are affected in patients with PD are also known to be
sensitive to environmental neurotoxicants [Feldman, 1999; White, 1992], such as MeHg
or PCB, and exposure to these substances may therefore cause exacerbation of PDassociated deficits. Long-term exposure to mercury has been reported as a risk factor for
PD, but the epidemiological evidence in support of a relation between MeHg and PD
remains equivocal [Gorell et al., 1999; DiMonte, 2003; Ohlson and Hogstedt, 1981;
Semchuk, 1993]. Occupational PCB exposure may cause a slightly increased risk for PD
[Steenland et al., 2006], and laboratory studies indicate that the exposure to PCB
decreases brain dopamine levels [Caudle et al., 2006; Seegal et al., 1989, 1990, 1991,
1994, 1998, 2002]. The dopaminergic toxicity especially relates to the persistent
congeners with di-ortho substitution [Mariussen et al., 2001], and a synergistic effect
may occur in co-exposure to MeHg [Bemis and Seegal, 1999]. Furthermore, chemical
analysis of brain tissue from deceased PD patients and controls suggests that di-ortho
substituted PCB congeners and certain persistent organochlorine pesticides may reach
higher accumulated concentrations in affected brain tissue of PD patients than in agematched controls [Corrigan et al., 1998, 2000].
Thus, in light of the increased exposure to PCBs and MeHg through traditional food
and the high prevalence of PD in the Faroes, we carried out a case-control study of the
association of PD with postnatal, dietary exposures to PCBs and MeHg.
4
2. Methods
2.1 Cases
The recruitment of the PD cases has been previously described [Wermuth et al, 2006].
Briefly, a total of 102 potential cases was recruited and clinically examined by a
neurologist in 2005. The diagnostic assessment of the idiopathic PD cases was based on
clinical information, development of the disease, response to levodopa treatment and
used internationally accepted criteria. Cases with parkinsonism but with additional
atypical features were diagnosed as having other neurodegenerative diseases. The cases
with atypical parkinsonism were subclassified as progressive supranuclear palsy (PSP),
multiple system atrophy (MSA), corticobasal degeneration (CBD), and dementia with
Lewy bodies (DLB) [Wermuth et al, 2006]. Of the 102 cases, 79 cases had idiopathic PD,
9 cases had atypical parkinsonism and the remaining 14 subjects were excluded for
various reasons, e.g., parkinsonism due to multi-infarct syndrome and long-term use of
narcoleptics. The cause of the different neurodegenerative diseases could be different.
Therefore, we only included the 79 cases with idiopathic PD in this study, i.e., 43 males
and 36 females.
2.2 Controls
The recruitment of controls has been previously described [Halling et al., 2007]. Briefly,
six controls for each case were retrieved from the Faroese Population Registry, using
vital status, sex and age as matching parameters. Potential controls were contacted first
by letter and then, one week later, by telephone and invited to participate in the study.
5
Examinations were carried out at the Department of Occupational Medicine and Public
Health; consenting subjects unable to come to the department were visited at home.
The potential control subject with a date of birth closest to the case was contacted first.
If he/she declined to participate, the person with the next closest date of birth was
contacted and so forth. From the six potential controls, two were included for each PD
case, except for four cases where only one control of the six subjects retrieved agreed to
participate.
The 154 controls included 85 men and 69 women. In the course of recruiting the
control group, 77 subjects (49 women and 28 men) declined to participate, and efforts to
obtain response from six invited subjects (4 women and 2 men) were unsuccessful.
2.3 Measurement of exposure
Blood and hair samples were collected from all cases and controls. Further, all subjects
completed a questionnaire by face-to-face interview in order to record lifetime
information on residence, dietary habits, smoking history, and occupational exposure to
solvents, pesticides, and metals.
The questions regarding dietary habits focused on the frequency of food items with
known increased content of MeHg and PCB, i.e.,whale meat, whale blubber, fish and
seabirds. Information was sought for three lifetime periods: average in childhood,
average in adulthood and during the last year and seven categories of average intake
were available: never (1), 1-2 times per year (2), 3-6 times per year (3), 7-12 times
per year (4), 2-3 times per month (5), 1-3 time per week (6) and more than 3 times
per week (7).
6
Occupational exposures were assessed ever/never exposure to solvents, pesticides, and
metals. In regard to smoking history, the subject’s cigarette smoking status (never, past or
current smoker) was supplemented by the age at starting smoking, number of years as a
smoker, number of cigarettes smoked per day, and number of years since quitting
smoking.
For logistic reasons, cases were interviewed by one interviewer (MSP) and controls by
another (JH). In order to minimize the influence of interviewer bias, ten training
interviews were conducted; the first two with both interviewers present in order to obtain
an agreement on the exact procedures and specific wordings. The remaining interviews
were conducted separately by both interviewers and subsequently compared. Comparison
of the ten interviews conducted showed complete agreement. Results were not exchanged
between the two interviewers until all subjects had been interviewed.
The study was approved by the Ethical Review Committee covering the Faroe Islands
and the institutional review board at Harvard School of Public Health. Informed written
and verbal consent was obtained.
2.4 Analysis of serum-PCB
The serum samples were analyzed for major PCB congeners (PCB-101, PCB-105, PCB118, PCB-138, PCB-153, PCB-156, PCB-180) and four other persistent organohalogen
pollutants (POPs) ((1,1,1,-trichloro-2-(o-chlorophenyl), 2-(p’-chlorophenyl) ethane (o,p’DDT), hexachlorobenzene (HCB), -hexachlorocyclohexane (-HCH) and 1,1,-dichloro2,2-bis (p-chlorophenyl)ethene (p,p’-DDE)) by gas chromatography with electroncapture detection as previously described [Petersen et al., 2006]. These substances are
7
persistent in the marine environment and occur at greatly increased concentrations in the
Faroese traditional food, especially in whale blubber [Bloch et al., 1990; Deutch and
Hansen, 2003]. Current serum concentrations would therefore be expected to reflect
cumulated life-time exposure.
The results were adjusted for the total serum lipid content and reported as μg per gram
lipid. The median limit of detection was 0.03 μg/L for all substances, which, at a mean
lipid concentration of 10 g/L, corresponds to 0.003 μg/g lipid [Petersen et al., 2006].
2.5 Analysis of blood and hair mercury
Both blood and hair samples (the latter as the proximal 2-cm segment) were analyzed for
total mercury by flow-injection cold-vapor atomic absorption spectrometry after
digestion in a microwave oven as previously described [Grandjean et al., 1992, 1997].
For the blood analysis, the analytical imprecision using the control materials Seronorm
Trace Elements lot OK0336, MR9067, OK0337 (SERO A/S, Oslo, Norway) was
estimated (n=33) to be 14.6, 3.6 and 3.1% at mercury concentrations 2.1, 8.2 and 13.8
µg/L respectively. The assigned values are 2.3, 8.4 and 13.1 µg/L. For the hair analysis,
the analytical imprecision was estimated to be 2.4 and 3.7% at mercury concentrations
4.61 and 11.51 µg/g respectively. The accuracy of the mercury determination in human
hair was ensured by using the certified reference material CRM 397 (IRMM, Geel,
Belgium) as quality control material; the mercury concentration averaged 11.51µg/g
compared to the assigned value of 11.93µg/g+0.77µg/g. Because of the shorter half-time
of MeHg in the body, these analyses reflect exposure during the past several months.
8
2.6 Statistics
Odds ratios (OR) with 95% confidence intervals (CI) were first estimated using
unconditional logistic regression analysis. In addition, conditional logistic regression
analysis was conducted to take into account that the data were matched on sex and
age. A potential effect of smoking was considered by including this variable as a
covariate. Rather similar results were obtained in the two analyses, hence only the
results from the conditional logistic regression analysis are provided in this paper.
Further, potential gender differences were examined using stratified analysis techniques.
Because PCB is a mixture of several congeners, the PCB was calculated as the sum
of PCB-138, PCB-153 and PCB-180 multiplied by 2, because the sum of these three
major congeners represents close to 50% of the total PCB concentration in Faroese
human milk and serum [Grandjean et al., 1995]. In addition, the estimated dioxin-like
activity of the major mono-ortho PCBs, expressed as TCDD equivalents (TEQs), was
computed as the total for the three congeners PCB-105, PCB-118 and PCB-156
according to international guidelines [Ahlborg et al., 1994]. Because of skewed
distributions, all POP results were log-transformed; non-detectable concentrations were
assumed to equal 0.001 μg/g lipid, which corresponds to about one-third of the detection
limit. The log-transformed serum concentrations of POPs and mercury in men and
women were compared by t-test and correlations examined by Pearson’s correlation
coefficient. Conditional logistic regression analysis was performed to examine the
association between risk of PD and current log-transformed serum concentrations of
PCB, PCB-TEQ, other POPs, blood mercury and hair mercury with adjustment for the
9
effect of smoking. All two-sided p-values below 0.05 were considered statistically
significant.
3. Results
The mean ages of cases and controls were 74.49.5 years and 75.29.6. The mean age at
onset of PD was 65.410.7 years.
Subjects were asked about their average intake of whale meat and blubber, fish and
seabirds in childhood, during adult life, and during the past year (seven frequency
categories). Frequencies were classified in two groups: high and low exposure. Due
to differences in distribution, each food item was classified to achieve two frequency
groups of approximately the same size (rarely/often). ORs for intake of whale meat
and blubber during adult life were significantly associated with PD risk (table 1). The OR
for intake of whale meat in childhood as well as during the most recent year was also
above unity, although not significant. Because of collinearity between blubber and whale
meat consumption (r=0.85, p<0.001), it was impossible to separate possible effects of
these two parameters. Gender-stratified analysis revealed higher risks for men caused by
higher life-time intake of whale blubber and meat compared with the women, but this
difference was not significant. In addition, no interaction was found between
consumption and residence.
As shown in table 2, the adjusted ORs suggested an increased risk for PD with
occupational exposure to solvents (OR=1.68), pesticides (OR=6.00) and metals
(OR=1.25), but these ORs were far from statistically significant due to small numbers.
For pesticides and metals, the OR is based on the risk in males only, as no female case or
10
control stated exposure to pesticides and only two female controls had experienced
exposure to metals. The gender-stratified analysis for solvents showed similar OR in
women and men.
The current serum concentration of POPs and the mercury biomarkers are shown in
table 3. Both among cases and controls, women had significantly lower serum
concentrations than men for all substances analyzed, except for the highly persistent HCH that was significantly higher in women. All log-transformed PCB congeners and
other POPs were significantly correlated (p<0.01), with Pearson’s correlation coefficients
ranging from 0.18 to 0.99. There was a clear effect of age on the current concentrations
of PCB, PCB-TEQ, HCB, p,p-DDE, o,p-DDT and -HCH that also differed between
women and men. For -HCH, sex by itself was not significant (data not shown). In
contrast, age was unrelated to the mercury concentrations, but males had higher levels
than females.
The current serum concentration of -HCH was significantly associated with an
increased PD risk (table 4). Gender-stratified analysis showed a higher adjusted OR
among women for -HCH and hair Hg (OR=2.59, 95%CI=1.03-6.51 and OR=1.96,
95%CI=1.10-3.48, respectively) than men (OR=1.21, 95%CI=0.73-2.00 and 0.79 (0.541.16) respectively). Single PCB congeners showed similar trends with slightly elevated,
mostly non-significant adjusted ORs, although PCB-101 was significantly associated
with PD risk (OR=1.36, 95%CI=1. 10-1.68). Stratification by sex did not reveal any
tendencies that differed between women and men.
The smoking history variable suggested that smoking is associated with lower risk of
PD, but the association was not statistically significant. Compared with never smokers,
11
adjusted ORs of PD was 0.92 (95% CI= 0.53-1.61) for ever smokers; 0.63 (95% CI =
0.26-1.55) for current smokers; and 1.06 (95% CI = 0.58-1.95) for past smokers. The
duration of smoking appeared to be associated with a lower PD risk; a borderline
significant association was seen with smoking for 30 years or more (adjusted OR=0.53,
95% CI=0.26-1.08). The effect of sex on the OR did not show a uniform, significant
tendency (data not shown).
4. Discussion
This study examines the increased prevalence of PD in the Faroe Islands in regard
to the possible significance of traditional diets that include locally harvested pilot
whale. Due to the position of pilot whale at the top of marine food chains, this toothed
whale accumulates marine contaminants, in particular MeHg, PCBs [Bloch et al., 1990]
and other POPs, such as -HCB [Deutch and Hansen, 2003].
PD cases had a much higher past consumption of whale blubber and whale meat
during adult life than did the controls. The same tendency was seen for whale meat
consumption also in childhood and during the most recent year but not for the other
traditional food items. While childhood and adult exposures may both be relevant in
regard to PD development, the marine pollution with PCBs and related substances may
have been substantial only during adult life of the subjects examined. Thus, the increased
OR for intake of whale blubber during adult life – during the second half of the 20th
century - when PCBs and related substances may have caused increased exposure levels,
appears meaningful. This conclusion is supported by the OR for childhood blubber intake
– that occurred before the advent of environmental exposure to these substances – was
12
close to one. In regard to whale meat, the elevated ORs for childhood, adult and recent
intakes, appear plausible, because whale meat has been contaminated with MeHg
throughout the 20th century, in part from natural sources. The use of a dietary
questionnaire is the only feasible way to assess past exposures, but the likely
imprecision and the risk of recall bias constitute an important limitation in our
study, although traditional food was addressed in only a few questions out of many.
In the absence of any publicly known linkage between traditional food habits and
PD, any bias would be small, and the main problem would be exposure
misclassification that could cause a bias toward null
The possible significance of POPs and MeHg as risk factors for PD is poorly
documented at present. The first study of occupational PCB exposure in relation to
increased neurodegenerative disease risk was only recently published [Steenland et al.,
2006]. Further, the Inuit population in Greenland has a PD prevalence as high as in the
Faroes, and they are exposed to the same food contaminants from their traditional
seafood diets [Wermuth et al., 2002]. Moreover, several experimental studies indicate
that exposure to PCBs decrease brain dopamine levels in rats, monkeys and mice [Caudle
et al., 2006; Seegal et al., 1991,, 1994, 2002], thus linking it to PD. A few studies on past
mercury exposure and risk of PD have been published, though with equivocal results. In a
case-control study of 54 cases and 95 controls, an increased blood-mercury concentration
was associated with an increased risk of PD [Ngim and Devathasan, 1989]. However, this
was not the case in other studies [Gorell et al., 1999; Ohlson and Hogstedt, 1981;
Semchuk et al., 1993]. A synergistic effect may occur in co-exposure to MeHg and PCB
[Bemis and Seegal, 1999], thus supporting the plausibility of a high risk of PD associated
13
with consumption of whale meat and blubber, i.e., foods that contain high levels of MeHg
and POPs. Further, oxidative cell damage seems to be an important mechanism in the
destruction of neurons [Gutteridge, 1995; Knight, 1997; Recchia, 2004] in
neurodegenerative diseases, and both PCBs [Dogra et al., 1988] and mercury [Gorell et
al., 1999] may induce or increase peroxidation damage.
Current serum POP concentration levels mainly reflect cumulated body burdens,
although decreases will happen with time after cessation of exposure. The POP results
were fairly similar, with only -HCH being associated with a significantly higher risk for
PD. In addition, hair mercury was significantly associated with higher PD risk,
although only for women. The fact that most current levels were quite similar in cases
and controls is in accordance with the anticipation that the cases would have eaten less
whale meat and blubber after the onset of the disease, thereby possibly neutralizing a
difference in consumption during premorbid adulthood. This assumption is supported by
the similar mercury concentrations in cases and controls.
Men had significantly higher current serum concentrations of PCBs and other POPs,
both among cases and controls, with the exception of -HCH where women had higher
concentrations. Gender-stratified analysis showed that the higher risk associated with HCH was only significant in women, although a chance finding cannot be ruled out. HCH could conceivably originate mainly from sources that release more -HCH than
PCBs, perhaps along with other neurotoxicants, although it is highly correlated with the
PCB congeners and other POPs. The -HCH half-life is considered to be similar to the
most persistent chlorinated PCBs, the median half-life being 7-8 years [Jung et al., 1997].
14
Elevated ORs were present for occupational exposure for solvents, pesticides and
metals. Although plausible as neurotoxic exposures, statistical significance was not
reached. However, only 22%, 2% and 7 % were exposed to solvents, pesticides and
metals respectively, thus reducing the power of the study to detect significant differences.
Further, we obtained only questionnaire information on whether the subjects had been
occupationally exposed or not, not the duration or likely intensity. However, the elevated
ORs are generally supported by literature, where most studies find positive association
between pesticide exposure and risk of PD [DiMonte et al., 2002; DiMonte, 2003;
Priyadarshi et al., 2001]. Some, but not all, case-control studies find a moderately
increased risk of Parkinson's disease in association with organic solvent exposure
[Priyadarshi et al., 2001], while evidence regarding association between metals and PD
remains inconclusive [Gorell et al., 1999a,b; Lai et al., 2002; DiMonte, 2003]. As only a
small portion of the Faroese population is exposed to those substances, occupation is not
likely to explain their high frequency of PD. The protective effect of smoking reported in
numerous studies [Allam et al., 2004; Thacker et al., 2007] was seen here as well,
although not statistically significant. In general, these findings on other risk factors tend
to support the validity of the present study. However, the absence of a clear protective
effect of smoking is a likely result of the small sample size, which constitutes a limitation
in our study. This issue can be overcome by the use of larger population samples and
meta-analyses [McCann et al., 1997], but the Faroese population itself can contribute
only small sample sizes. Still, the homogeneous Faroese population and the elevated
exposure to POPs and MeHg provide a unique opportunity to detect possible influences
15
of these exposures on the PD risk, while taking into account the limited sensitivity due
to the small sample size within this island population.
In conclusion, ORs for intake of whale meat and blubber in adult life were
significantly associated with PD, thus suggesting a positive association between lifetime
POP and MeHg exposure and development of PD. Current blood concentration levels
were fairly similar in cases and controls, but -HCH was significantly higher in the cases.
Acknowledgments
This work was supported by the European Commission through its Sixth Framework
Programme for RTD (contract no FOOD-CT-2006-016253, PHIME). The paper reflects
only the authors' views. The Community is not liable for any use that may be made of the
information contained therein. This work was further supported by the Danish Parkinson
Foundation and the Faroese Parkinson Foundation.
16
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22
Table 1 Odds ratios (ORs) for increased intakes of whale meat and blubber, fish and sea
birds as predictors of Parkinson’s disease
Lifetime period
Cases
Adjusted ORb
Controls
(95% CI)
N
N
high/low
high/low
exposurea
exposurea
64/8
132/21
All
Women
Men
1.30
0.71
2.61
(0.53-3.22)
(0.17-2.98)
(0.26-25.91)
0.94
0.95
1.22
(0.42-2.09)
(0.20-4.49)
(0.27-5.56)
0.33
0.26
0.50
(0.18 - 0.62)
(0.07-0.9 )
(0.18-1.38)
0.85
0.69
1.07
(0.47-1.53)
(0.18-2.70)
(0.36-3.17)
6.53
7.04
10.57
(3.02-14.14)*
(1.51-32.88)*
(2.42-46.16)*
5.61
4.24
7.63
(2.46-12.81)*
(1.06-16.97)*
(1.67-34.74)*
0.88
1.21
1.26
(0.46-1.67)
(0.27-5.36)
(0.50-3.15)
0.98
1.66
0.54
(0.55-1.78)
(0.52-5.36)
(0.18-1.62)
Average in childhood
Whale meat
consumptionc
Blubber
61/11
131/22
consumptionc
Fish consumptiond
Seabird consumptione
22/53
38/29
85/69
92/62
Average in adulthood
Whale meatf
66/12
74/79
consumption
Blubber consumptionf
Fish consumptiond
Seabird consumptiong
67/11
21/57
43/31
86/67
43/109
90/63
Average during the
23
last year
Whale meat
43/36
74/78
1.28
3.04
0.71
(0.72-2.27)
(0.90-10.18)
(0.27-1.85)
1.12
2.24
0.55
(0.62-2.01)
(0.67-7.41)
(0.20-1.50)
0.38
0.29
0.56
(0.17 - 0.85)
(0.08-1.07)i
(0.19-1.69)
0.48
0.19
0.62
(0.25-0.89)
(0.04-0.95)
(0.22-1.72)
consumptione
Blubber
45/34
83/69
consumptione
Fish consumptiond
Seabird consumptionh
9/70
26/53
37/116
72/80
Abbreviations: OR, odds ratio; CI, confidence interval
a
the food frequency categories are grouped in high and low exposure to achieve a distribution so close to 50/50 as
possible
b adjusted
for smoking
c
grouping: at least once per week/less than once per month
d
grouping: at least four times per week/less than four times per week
e
grouping: at least seven times per year/less than seven times per year
f
grouping: at least twice per month/less than twice per month
g
grouping: at least three times per year/less than three times per year
h
grouping: at least once per year/never
i
Data too sparse to allow OR estimate in conditional logistics regression analysis. Instead the OR of a unconditional
logistics regression analysis is presented.
* statistical significant (p0.05)
24
Table 2 Odds ratios (ORs) for occupational exposures to solvents, pesticides and metals
as predictors of Parkinson’s disease.
Exposed
Not exposed
Adjusted ORa
(95 % CI)
N (women/men) N (women/men)
Solvents
Case
19(4/15)
48(30/18)
1.68
Control
32(5/27)
121(64/57)
(0.80-3.50)
Case
3(0/3)
72(35/37)
6.00
Control
1(0/1)
152(69/83)
(0.62-57.68)
Case
6(0/6)
59(34/25)
1.25
Control
10(2/8)
143(67/76)
(0.40-3.90)
Pesticides
Metals
Abbreviations: OR, odds ratio; CI, confidence interval
a Adjusted
for smoking.
25
Table 3 Current serum concentration (μg/g lipid) of polychlorinated biphenyls (PCBs),
persistent organohalogen pollutants (POPs) and mercury (Hg) in 79 Faroese Parkinson
cases and 154 controls.
Geometric mean (total range)
PD
PCB-101
Controls
All subjects
Women
Men
All subjects
Women
Men
N=79
N=36
N =43
N =154
N =69
N =85
0.02 (0.002-0.10)
0.02***
0.03
0.014 (0.0001-
0.01***
0.02
0.23)
PCB-118
0.34 (0.03-2.72)
0.25**
0.44
0.34 (0.03-1.83)
0.27***
0.42
PCB-138
1.28 (0.12-9.22)
0.87***
1.77
1.26 (0.08-6.53)
0.92***
1.63
PCB-153
1.78 (0.20-11.88)
1.21***
2.47
1.66 (0.10-8.84)
1.19***
2.16
PCB-105
0.07 (0.004-0.66)
0.05*
0.09
0.07 (0.001-
0.05***
0.09
0.58)
PCB-156
0.20 (0.02-1.37)
0.14***
0.28
0.19 (0.01-1.05)
0.14***
0.25
PCB-180
1.49 (0.17-13.56)
0.93***
2.20
1.31 (0.09-9.45)
0.91***
1.77
PCBa
9.18 (0.98-62.56)
6.05***
13.00 8.50 (0.54-
6.10***
11.21
47.66)
PCB-TEQb 14.58 (1.44-91.20) 10.02*** 19.96 13.96 (0.99-
10.35*** 17.80
72.49)
p,p-DDE
3.62 (0.17-28.11)
2.64*
4.72
3.55 (0.03-
2.67***
4.47
25.20)
HCB
0.21 (0.04-1.32)
0.17*
0.25
0.21 (0.03-0.97)
0.18*
0.24
-HCH
0.06 (0.01-0.22)
0.08***
0.04
0.04 (0.01-0.22)
0.05***
0.04
o,p-DDT
0.37 (0.01-2.73)
0.23***
0.57
0.41 (0.04-3.03)
0.27***
0.58
26
B-Hg
9.36 (1.04-61.25)
6.51***
12.69 8.80 (0.91-
6.05***
11.99
1.72***
3.16
108.33)
H-Hg
2.29 (0.22-16.01)
1.48***
3.30
2.40 (0.00124.57)
Abbreviations: OR, odds ratio; CI, confidence interval; p,p-DDE, 1,1,-dichloro-2,2-bis (p-chlorophenyl)ethane; HCB,
hexachlorobenzene; β-HCH, beta-hexachlorocyclohexane; o,p-DDT, 1,1,1,-trichloro-2-(o-chlorophenyl), 2-(p’chlorophenyl)ethane; B-Hg, blood-mercury (µg/l); H-Hg, hair-mercury (µg/g)
aPCB
is calculated as 2.0 x PCB (138+153+180)
bPCB-TEQ
*t-test;
is calculated as ((PCB105 + PCB118 + 5*PCB156) *10). Unit: pg TEQ/g lipid
women compared with men: p0.05; **t-test; women compared with men: p0.01; ***t-test; women compared
with men: p0.001
27
Table 4 Association between Parkinson’s disease and log transformed current serum
concentration
(μg/g
lipid)
of
polychlorinated
biphenyles
(PCBs),
persistent
organohalogen pollutants (POPs) and mercury (Hg) in 79 PD cases and 154 controls.
Adjusted ORa (95% CI)
All
Women
Men
PCBb
1.08 (0.86-1.37)
1.21 (0.72-2.03 )
0.98 (0.62-1.55 )
PCB-TEQc
1.05 (0.83-1.32 )
1.16 (0.70-1.93)
0.95 (0.60-1.49)
p,p-DDE
1.01 (0.83-1.22)
1.06 (0.76-1.49)
0.98 (0.68-1.41)
HCB
1.02 (0.77-1.34)
1.09 (0.57-2.08)
0.95 (0.60-1.50)
-HCH
1.44 (1.05-1.97)* 2.59 (1.03-6.51)*
1.21 (0.73-2.00)
o,p-DDT
0.93 (0.75-1.14)
1.00 (0.62-1.61)
0.80 (0.51-1.25)
B-Hg
1.08 (0.87-1.34)
1.96 (1.10-3.48)*
0.79 (0.54-1.16)
H-Hg d
1.01 (0.83-1.23)
1.47 (0.85-2.55)
0.74 (0.50-1.11)
Abbreviations: OR, odds ratio; CI, confidence interval; p,p-DDE, 1,1,-dichloro-2,2-bis (p-chlorophenyl)ethane; HCB,
hexachlorobenzene; β-HCH, beta-hexachlorocyclohexane; o,p-DDT, 1,1,1,-trichloro-2-(o-chlorophenyl), 2-(p’chlorophenyl)ethane; B-Hg, blood-mercury; H-Hg, hair-mercury
a adjusted
bPCB
for smoking.
is calculated as 2.0 x PCB (138+153+180)
cPCB-TEQ
d
is calculated as ((PCB105 + PCB118 + 5*PCB156) *10
hair samples were not available from two controls, thus data is from 152 controls
* statistical significant (p0.05)
28