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PCB-containing wood floor finish is a likely source of elevated PCBs in residents' blood, household air and dust: A case study of exposure


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Polychlorinated biphenyls (PCBs) are persistent pollutants identified worldwide as human blood and breast milk contaminants. Because they bioaccumulate, consumption of meat, fish, and dairy products predicts human blood concentrations. PCBs were also used widely in building materials, including caulks and paints, but few studies have evaluated the contribution of these exposures to body burden. In an earlier study, we detected PCBs in indoor air in 31% of 120 homes on Cape Cod, MA. Two of the homes had much higher concentrations than the rest, so we retested to verify the initial finding, evaluate blood PCB concentrations of residents, and identify the PCB source. Air and dust concentrations remained elevated over 5 years between initial and follow-up sampling. Blood serum concentrations of PCBs in residents of the homes were generally elevated above the 95th percentile of a representative sample of the US population. Serum concentrations in residents and air and dust concentrations were especially high in a home where a resident reported use of PCB-containing floor finish in the past, and where the floor of one room was sanded and refinished just prior to sample collection. This case-study suggests that PCB residues in homes may be more significant contributors to overall exposure than diet for some people, and that use of a commercially-available PCB-containing wood floor finish in residences during the 1950s and 1960s is an overlooked but potentially important source of current PCB exposure in the general population.
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BioMed Central
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Environmental Health
Open Access
PCB-containing wood floor finish is a likely source of elevated PCBs
in residents' blood, household air and dust: a case study of exposure
Ruthann A Rudel*
, Liesel M Seryak
and Julia G Brody
Silent Spring Institute, 29 Crafts Street, Newton, MA 02458, USA and
Division of Environmental Health Sciences, College of Public
Health, The Ohio State University, 320 West 10th Ave., Columbus, OH 43210, USA
Email: Ruthann A Rudel* -; Liesel M Seryak -; Julia G Brody -
* Corresponding author
Background: Polychlorinated biphenyls (PCBs) are persistent pollutants identified worldwide as
human blood and breast milk contaminants. Because they bioaccumulate, consumption of meat,
fish, and dairy products predicts human blood concentrations. PCBs were also used widely in
building materials, including caulks and paints, but few studies have evaluated the contribution of
these exposures to body burden.
Methods: In an earlier study, we detected PCBs in indoor air in 31% of 120 homes on Cape Cod,
MA. Two of the homes had much higher concentrations than the rest, so we retested to verify the
initial finding, evaluate blood PCB concentrations of residents, and identify the PCB source.
Results: Air and dust concentrations remained elevated over 5 years between initial and follow-
up sampling. Blood serum concentrations of PCBs in residents of the homes were generally
elevated above the 95
percentile of a representative sample of the US population. Serum
concentrations in residents and air and dust concentrations were especially high in a home where
a resident reported use of PCB-containing floor finish in the past, and where the floor of one room
was sanded and refinished just prior to sample collection.
Conclusion: This case-study suggests that PCB residues in homes may be more significant
contributors to overall exposure than diet for some people, and that use of a commercially-
available PCB-containing wood floor finish in residences during the 1950s and 1960s is an
overlooked but potentially important source of current PCB exposure in the general population.
Polychlorinated biphenyls (PCBs) are persistent organic
pollutants and have been identified worldwide as human
blood and breast milk contaminants. They are established
developmental neurotoxicants in humans [1,2], with ele-
vated prenatal PCB concentrations being associated with
cognitive deficits in children [1,3-5]. PCBs are also associ-
ated with thyroid toxicity, effects on immune, reproduc-
tive, nervous, and endocrine systems, and cancer effects
including breast cancer [6-10].
PCBs were primarily used in electrical equipment and flu-
orescent lighting fixtures prior to 1977, but can also be
found in other products manufactured before 1977 such
as plasticizers, surface coatings, inks, adhesives, flame
retardants, pesticide extenders, carbonless duplicating
Published: 17 January 2008
Environmental Health 2008, 7:2 doi:10.1186/1476-069X-7-2
Received: 17 September 2007
Accepted: 17 January 2008
This article is available from:
© 2008 Rudel et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Environmental Health 2008, 7:2
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paper, paints, wire insulators, caulking materials, elastic
sealants, and heat insulation [6]. Because of the tendency
of PCBs to bioaccumulate, several studies have concluded
that consumption of meat and dairy products, as well as
processed foods and fish, contributes significantly to over-
all intake of PCBs [11-15].
It is likely that major contributors to PCB exposure vary
across the population depending on proximity to specific
sources. For example, studies of Great Lakes fish eaters
have shown that fish consumption is a significant predic-
tor of blood PCB concentrations [16,17]. Use of PCB-con-
taminated caulk in commercial buildings and schools,
which appears to be common in pre-1980 construction
[18,19], has been shown to increase blood PCB concen-
trations, especially for lower-chlorinated congeners
[20,21]. A few studies have proposed that multiple path-
ways contribute significantly to total human PCB expo-
sure. Currado and Harrad determined that inhalation
could account for 6 to 64% (mean 25%) of overall human
PCB exposure [22].
In 2003 we reported results from a household exposure
study of 120 homes on Cape Cod [23]. We tested for 89
target chemicals, mostly endocrine disrupting com-
pounds (EDCs), and detected 52 chemicals in air and 66
in dust. Three PCB congeners were among the target
chemicals: PCB 52, PCB 105, and PCB 153. We detected
PCBs in air (>1 ng/m
) from 38 homes (32%) and dust
(>0.2 µg/g) from 22 homes (18%) [23]. PCBs were
detected in air in 76% of homes where it was detected in
dust. Two homes had much higher air and dust PCB con-
centrations (sum of PCB 52, 105, 153 in air 23 and 35 ng/
; dust 21 and 68 µg/g) than the rest of the study sample
(max of sum PCB 52, 105, 153 in air 14 ng/m
; median <
3 ng/m
; max in dust 8 µg/g, median < 0.6 µg/g). These
two homes were retested in an attempt to verify the initial
finding, evaluate blood PCB concentrations of residents,
and identify the source of PCBs with an ultimate goal of
recommending potential exposure reduction techniques
to the homeowners.
Human research review committees at Brown University,
Providence, RI, and at the Shattuck Hospital, Boston, MA,
approved study protocols and all participants provided
informed consent prior to sampling.
The 120 participants of the Cape Cod household exposure
study were female breast cancer cases or age-matched con-
trols who had participated in the case-control portion of
the Cape Cod Breast Cancer and Environment Study [24]
and had lived in their home at least 10 years at the time of
original sampling (1999–2001). The average age of the
women in the exposure study was 75 (median 77). In
2004–2005, new air and dust samples were collected from
the 2 homes with high PCBs, and a visual survey of each
house and the general area around the 2 homes was con-
ducted to identify any potential sources of PCBs (e.g., elec-
trical or industrial equipment, fluorescent lights,
industrial window sealant, etc.). Residents were also asked
about electrical and mechanical hobbies, businesses, his-
torical land use, flooring, lighting, and older electrical
Sampling took place in single-family owner-occupied
homes on Cape Cod, Massachusetts. Cape Cod is a coastal
peninsula consisting of 15 towns in Southeastern Massa-
chusetts. The area has very little industry and is considered
a summer vacation destination. Follow-up air and dust
samples were collected in winter 2004–2005, 4–6 years
after the initial samples were taken from these homes, and
analyzed using the same methods reported previously
[23,25]. Briefly, air samples were collected over 24 hours
by drawing air at 8–9 L/min through a personal pesticide
sampling cartridge (University Research Glassware, URG).
URG cartridges were fitted with a quartz fiber filter fol-
lowed by XAD-2 resin sandwiched between two poly-
urethane foam (PUF) plugs. The total volume of air
sampled ranged from 10–14 cubic meters.
Dust samples were collected using a Eureka Mighty-Mite
vacuum cleaner, modified to collect dust through a Teflon
crevice tool into a cellulose extraction thimble (Whatman
Inc., Clifton, NJ). Dust sample collection did not begin
until the air sample collection was complete. Sample col-
lection was accomplished by slowly and lightly drawing
the crevice tool just above the surface of rugs, upholstery,
wood floors, windowsills, ceiling fans and furniture in
each room. Sampling was conducted in the most fre-
quently-used rooms of the house, usually 4–5 rooms and
including hallways. Cellulose thimbles containing dust
were placed in cleaned glass sample jars with Teflon lined
lids (Environmental Sampling Supply, Oakland, CA).
URGs and dust samples were stored at -4°C until they
were shipped overnight on dry ice to Southwest Research
Institute (SWRI) for analysis. Prior to extraction, dust was
tapped out of the thimbles, weighed, and sieved to < 150
Chemical analysis of air and dust samples was conducted
at SWRI, San Antonio, TX as described in [23,25]. Each
XAD-2/PUF/filter was soxhlet extracted in 6% ether in
hexane. Each sieved (< 150 um) dust sample was spiked
with surrogate, equilibrated, then soxhlet extracted using
6% ether in hexane. The extracts were concentrated and
cleaned by running through a florisil column. Analysis
was performed using an Agilent 6890/5973 GC/MS in
selected ion monitoring (SIM) mode. The GC/MS instru-
ment was scanned to monitor the following ions: PCB 52
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(290,294), PCB 105 (324,328), PCB 153 (362,358). The
base peak ion was used as the quantification ion for each
compound. Quantification was performed using d12-
labeled PAHs as internal standards. PCBs were not
detected in air matrix blanks or dust extraction blanks.
Congener sums assumed a value of 0 for values below the
detection limit.
Within one month of air and dust re-sampling, blood
samples were collected from residents of the two homes
with elevated PCBs to better describe personal exposure.
Serum samples were analyzed for 33 PCB congeners along
with several other organochlorines (e.g., p,p'-dichlo-
rodiphenyl dichloroethylene, or 4,4'-DDE) at the Envi-
ronmental Chemistry Laboratory, Division of Analytical
Chemistry, Massachusetts Department of Public Health
State Laboratory Institute in Jamaica Plain, MA. The anal-
ysis followed the AOAC standard method for polychlorin-
ated biphenyls in serum [26] and involved extraction with
hexane/ethyl ether, silica column cleanup with hexane
elution, and analysis by dual column gas chromatography
with electron capture detection as described in Brock et al.
[27]. Standard operating procedures for all analyses are
available from the authors. Results were reported as ng/g
lipid and detection limits were about 15 ng/g lipid. Any
detects in a reagent blank prepared and analyzed with the
samples were subtracted from sample results. Congener
sums assumed a value of 0 for below detection limit val-
ues. These sums underestimate total PCB concentrations
in serum because 1) zero very likely underestimates the
concentrations of some congeners that may be present
below detection limits, and 2) only 33 of 209 PCB conge-
ners were analyzed.
PCBs in Indoor Air
PCBs in indoor air remained elevated on re-testing in both
homes with high PCB concentrations in the initial study
(Table 1). Measurements were taken in the living area of
the homes initially, and in the living area and bedroom at
retest. In home #1, living area concentrations remained
high. PCBs were not detected in the bedroom, which was
on the second floor of the home, but the limit of detection
was elevated because of the small sample volume (see
Table 1). Home #2 was small and the living area and bed-
room were close together – concentrations were similar in
both rooms. Both retest samples were collected during the
winter, while initial samples from home 1 were collected
in winter and home 2 in summer.
Concentrations of PCBs in air were high compared with
another Massachusetts study and well above EPA health-
based guidelines (Table 2). In our study, the sum of PCBs
52, 105, and 153 ranged from 8 to 35 ng/m
in the living
areas of the two homes. Vorhees et al. found a maximum
of 7.3 ng/m
for the sum of those 3 congeners in 15 homes
intended to represent "background" PCB concentrations
in Southeastern Massachusetts, close to Cape Cod [28].
Congeners 52, 105, and 153 represent 9% of the sum of
all 65 congeners measured in air in the Vorhees study, and
this proportion is stable across many homes (standard
deviation of 3% for 70 measurements in 34 homes)
(unpublished observation). Therefore, it is likely that total
PCB concentrations in the two Cape Cod homes are con-
siderably higher (>10X) than the sum of the 3 measured
congeners. The EPA health-based screening value of 3.4
for total PCBs is intended to be protective for
health effects following long-term exposure [29]. The sum
of 3 PCB congeners in indoor air in the Cape Cod samples
Table 1: PCB concentrations in indoor air, house dust, and residents' serum in two Cape Cod homes
Indoor air(ng/m
House dust (micrograms/
Serum (ng/g lipid)
Home Participant Initial PCBs,
Initial PCBs
[52, 105, 153]
PCBs [52,
105, 153]
Total PCBs (#
Sum 10 PCB
1 1-A 23 [19, 4, <2] 21 (<68) [10,
2.9, 7.7]
21 [1.1, 14,
190 [15, 53,
1630 (13) 1520 848
993 (11) 967 208
2 2-A 35 [25, 6.7,
8.0 (13) [8,
<2.8, <2.8]
68 [16, 35,
140 [37, 34,
760 (16) 652 292
2-B 179 (5) 179 96
Abbreviations: PCB, polychlorinated biphenyl; LR, living room; BR, bedroom; ND, not detected; DL, detection limit
PCB concentrations reported as sum of PCB 52, 105, 153 in air or dust (<DL values set to 0), followed by results for the 3 individual congeners
(PCB 52, 105, 153)
Sum of the concentrations of all PCB congeners detected in serum (of 33 tested). Values < DL set to 0. Individual congeners reported in Additional
File 1
Limited to the 10 PCB congeners also measured in NHANES. Values < DL set to 0
Included as an alternate bioaccumulative, persistent organochlorine
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exceeds this health-based screening value for ambient air
by about a factor of 10, and total PCBs are likely substan-
tially above the guideline.
PCBs in Dust
PCBs in house dust remained elevated or increased on re-
testing in both homes with high PCB concentrations in
the initial study (Table 1). Concentrations of PCBs in
house dust samples were high compared with the Vorhees
study in Massachusetts [30] and a large study with over
1000 samples collected across the US [31]; and were well
above EPA health-based guidelines (Table 2) [29]. In our
study, the sum of PCBs 52, 105, and 153 ranged from 21
to 190 µg/g dust in the two homes. In house dust samples
in a set of 15 homes intended to represent background
PCB concentrations in Southeastern Massachusetts, Vor-
hees et al. found a maximum concentration of 0.6 µg/g for
the sum of PCB 52, 105, and 153, and these 3 congeners
made up 12% of the sum of 65 congeners reported ([30];
unpublished observation). In 1000 vacuum cleaner bag
samples collected from homes in Iowa, Seattle, Detroit,
and Los Angeles as part of a case-control study of organo-
chlorines and non-Hodgkin lymphoma, Colt et al.
reported a maximum concentration of the sum of PCBs
105 and 153 in dust of 10 µg/g [31] compared with our
190 µg/g. Although no health-based screening values have
been developed for PCBs in house dust, the EPA screening
values for residential soil may be a reasonable compari-
son, since exposure assumptions for house dust and resi-
dential soil are generally similar in EPA risk assessments.
The EPA Region 9 soil screening value may be slightly
higher (less protective) than a screening value for dust
exposure would be, because infants are assumed not to be
exposed to soil, while they are expected to have high expo-
sures to house dust. PCB concentrations in house dust in
this study exceed health-based screening values for resi-
dential soil developed by EPA by a factor of 860 without
adjustment for the expected total PCB represented by the
three congeners we measured. The EPA health-based
screening value of 0.22 µg/g for total PCBs is intended to
be protective for health effects following long-term expo-
sure [29].
PCBs in Blood Serum
The concentrations of PCBs in the participants' blood
serum were elevated compared with those reported in the
US Centers for Disease Control and Prevention's 3
National Report on Human Exposure to Environmental Chem-
icals [32] – a survey of exposure in US residents conducted
as part of the National Health and Nutrition Examination
Survey (NHANES) (Tables 1 and 2). We measured the
PCB concentrations in two residents from each home, a
total of three women (participants 1A, 2A, and 2B) and
one man (1B). It has been established that age, sex, and
race are predictors of human PCB concentrations [15,33].
Therefore, we also compared our blood data with a subset
of the NHANES 1999–2002 reference data similar to our
demographic group of white women (or men) over the
age of 59 (Table 2). Comparing results for the sum of 10
PCB congeners measured in both NHANES data and the
Cape Cod samples shows that 3 of the 4 Cape Cod resi-
dents are above the 95
percentile of the NHANES study
sample. In fact participant #1A has total PCBs above the
maximum reported in NHANES 1999–2002 for the set of
Table 2: Comparison values and context for Cape Cod PCB levels.
Indoor air (ng/m
) House dust (µg/g) Serum (ng/g lipid)
EPA health-based guideline
3.4 0.22
Maximum for 16 MA homes
b (PCB 52+105+153 only)
7.3 0.6
Maximum for 16 MA homes
b (sum of 65 PCB congeners)
51 3.6
Maximum for 1046 U.S. homes
c (sum of PCB 105+153)
median 267
75th percentile 394
95th percentile 715
maximum 1466
median 692
75th percentile 1314
95th percentile 2569
maximum 6510
abbreviations: PCBs, polychlorinated biphenyls; NHANES, National Health and Nutrition Examination Survey
EPA Health-based guidance value for total PCBs – EPA Region 9 Preliminary Remediation Goals for ambient air and residential soil (2004).
Maximum concentration of the sum of PCB congeners tested in a study of 16 homes (15 homes for dust) intended to represent background PCB
levels in Southeastern, MA (Vorhees et al. 1997 and 1999). On average PCBs 52+105+153 represent 9% of the 65 congeners in air samples from
this study and 12% of the congeners in dust.
Sum of the maximum concentrations of PCBs 105 and 153 in a non-hodgkin lymphoma case-control study of 1046 homes in the U.S. (Colt 2005).
NHANES 1999–2002 data for white women over age 59 (n = 319) – sum of 10 PCBs measured on Cape Cod; non-detects set to 0. The 95th
percentile for white men over age 59 (n = 295) is 679 ng/g lipid.
NHANES 1999–2002 data for white women over age 59 (n = 319) – 4,4'-DDE included as an alternate bioaccumulative, persistent organochlorine
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319 white women over the age of 59 (Table 2). Participant
2B, who has blood PCB concentrations below the
NHANES median, had been living in the home less than
6 months at the time of the sampling (other participants
had lived in homes > 10 years). Individual congener
results for serum samples are included in Additional File
4,4'-DDE measured in these blood samples serves as an
indicator of body burden of persistent, bioaccumulative
organochlorine contaminants which, like PCBs, tend to
be higher in older persons and those with high intake of
animal fats. DDE concentrations were not elevated in
these four participants – three tested below the 50
centile of the older white women (or men) subset of
NHANES, and participant #1A was between the 50
percentiles (Tables 1 and 2).
Interviews about likely PCB sources
In the Cape Cod Breast Cancer and Environment Case-
Control Study, participants were asked about their past
and present fish-eating habits. No data are available for
participant #1A. Participant #2A, who had elevated PCBs
in her home and her blood, reported eating saltwater fish
from Cape Cod waters less than once per month but more
than 6 times per year. She reported not eating Cape Cod
freshwater fish, seafood, or lobster on a regular basis
(more than 6 times per year).
During participant interviews and household surveys to
identify potential sources of PCBs, one resident in home
#1 recalled having used a floor finish called Fabulon on
hardwood floors throughout the 1950s and 1960s. We
consulted an out-of-print set of reference books designed
for poison control centers and medical professionals,
Clinical Toxicology of Commercial Products, which reported
that in 1957 Fabulon's formula contained chlorinated
biphenyl, hexachlor bi-phenyl, and quadraclor bi-phenyl,
as shown in Figure 1[34]. By 1969, PCBs were no longer
listed as part of the Fabulon formula, according to a later
edition of the same resource book [35]. The resident of
home #2 did not recall what particular floor finish was
used in the 1950s and 1960s, but the home had wood
floors that had not been refinished in many years. No
other likely sources of PCBs were identified in our home
surveys and questionnaires.
The resident in house #1 also informed us that some of
the floors in the house had been sanded and refinished
since the 1960s, while the Fabulon finish remained on
other floors in the home. Interestingly, the floor in one of
the rooms in home #1, the home with the very high dust
concentrations on retest and the resident with the serum
PCBs above the maximum reported in NHANES 1999–
2002, had been sanded and refinished immediately prior
to the 2005 blood sampling and air and dust re-sampling.
Because sanding of wood floors liberates a large amount
of dust, the sanding of a Fabulon-coated wood floor may
account for the unusually high concentrations we meas-
ured in dust (more than 8 times higher than first dust
sample) and blood observed in the female resident of
home #1. Blood PCB concentrations in a male resident of
home #1 were also quite elevated (above the 95
tile) relative to the comparison group of older white men
In this study we have identified 2 Cape Cod homes with
air and dust PCB concentrations much higher than in 118
other homes in the same region of the US and much
higher than reported in homes in other parts of the US
[23,28,30,31]. Elevated air and dust concentrations per-
sisted over 5 years between initial and follow-up sam-
pling. Follow-up samples of blood serum showed that
Entry for Fabulon floor finish from 1957 edition of Gleason et alFigure 1
Entry for Fabulon floor finish from 1957 edition of Gleason
et al. Clinical Toxicology of Commercial Products lists PCBs
among the ingredients
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concentrations of PCBs in residents of these homes were
also generally elevated above the 95th percentile of
NHANES, except in one resident who had moved into the
home during the 6 months prior to sampling. Serum and
dust concentrations were especially high in residents of
home 1, where a PCB-containing floor finish was report-
edly used in the past, and where the floor of one room was
sanded and refinished within a week prior to the sample
collection. No other likely sources of PCBs were identified
in either home by inspection, and wood floors in home 2
had not been refinished in many years. Based on these
observations, we hypothesize that the source of PCBs in
these two homes, and in the residents of those homes, is
PCB-containing wood floor finish such as the Fabulon
product reported to have been used in home #1. In addi-
tion to the listing of Fabulon in Gleason et al. [34] as con-
taining chlorinated biphenyls, other sources indicate that
PCBs were used in varnishes and paints in the 1950s and
1960s [36,37]. We have not confirmed that the wood
floors are a source of PCBs in these homes. Such a confir-
mation could create regulatory and disclosure obligations
that pose significant challenges to individual home own-
ers. We are working to develop helpful and appropriate
follow up in this context.
Earlier studies of PCBs in humans have often focused on
diet as the primary source of PCB exposure. Several of
these studies found that people who ate greater amounts
of Great Lakes fish – known to contain large amounts of
PCBs – had higher PCB serum loads than people who ate
minimal amounts of contaminated fish [12,16,17]. How-
ever, these studies never examined exposure to PCBs from
alternate sources like household products contributing
PCBs to the air and dust.
It is unlikely that the body burdens of PCBs we observed
would be coming from the participants' diets. First, PCBs
were found at very high concentrations in the blood of
participants who had high concentrations in their air and
dust. Second, these participants do not have similarly
high concentrations of other fat-soluble persistent organ-
ochlorines in their blood, although the same constituents
of diet that contribute PCBs are presumed to be the major
source of exposure to banned organochlorine pesticides.
Participant #1A's blood concentration of 4,4'-DDE is
between the 50
and 75
percentile for older white
women in NHANES. All other participants are well below
the 50
percentile for the older white women (or men)
subset of NHANES (Tables 1 and 2).
Analysis of the specific congeners in the serum (given in
Additional File 1) also indicates that the 3 participants
who have been long time residents in these homes have
congener profiles that are more similar to workers
exposed to commercial mixtures of PCBs while the partic-
ipant who recently moved into the home has a serum con-
gener profile more consistent with general population
exposure through dietary sources. Due to the transforma-
tion of PCBs as they move through the environment, a dif-
ferent distribution of congeners is observed in individuals
exposed to PCBs through fish consumption compared
with individuals exposed in an occupational setting.
Freels et al. [38] compared congener profiles in capacitor
plant workers occupationally exposed to PCBs and Great
Lakes sport-fish consumers, with about 200 individuals in
each group. They found that the ratio of congeners
(74+153+201)/(74+153+201+138+180) correctly classi-
fied more than 99% of the individuals in the study, with
fish-eaters having a ratio in the range 0.26–0.49 (mean
0.39) and capacitor workers having a ratio in the range
0.42–0.95 (mean 0.68). For our participants, the ratios
were 0.54, 0.50, 0.47, and 0.43; so 2 of our participants
were outside the range observed in the fish eaters and 2
were in the area of overlap between the two groups, with
the lowest ratio being observed in the participant who
moved to the home recently.
Wingfors et al. [39], compared serum congener profiles
between Swedish workers removing PCB-containing
caulk and the general population in Sweden. The ratio of
certain congeners to congener 153 was shown to differen-
tiate occupationally exposed individuals from the general
population whose exposure is primarily through diet. In
our set of 4 participants, the three longer-term residents
had ratios more like the occupationally exposed individu-
als compared to the one who moved in more recently.
Our exposed participants' serum was particularly enriched
with congeners 74, 99, 118, and 105 (relative to 153); and
diminished in congener 180 (relative to 153). However,
the actual ratios were quite different between our partici-
pants and the Swedish cohort, suggesting the exposure
source is a different PCB mixture. A limitation of our study
is that only 3 PCB congeners were analyzed in the air and
dust samples, limiting our ability to compare congener
profiles in the environmental media with serum.
Although background concentrations of PCBs in human
blood may be closely correlated with diet, the case-study
data presented here suggest that some people may be
exposed to PCB residues in their homes that are more sig-
nificant contributors to their overall exposure than diet.
The use of a commercially-available PCB-containing
wood floor finish in residences in the 1950s and 1960s is
an overlooked but potentially important source of PCB
exposure in the general population. In addition, potential
exposure to floor sanders may be significant and studies to
evaluate blood PCB concentrations among this group are
needed. Taken together with the prevalence of PCB-con-
taining caulk in commercial buildings and schools
Environmental Health 2008, 7:2
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[18,19], and the observation by Jamshidi et al. that PCBs
in outdoor air originate from indoor sources [40], these
findings suggest that the exposure potential posed by his-
toric use of PCBs in building materials may be signifi-
cantly underestimated.
p,p'-dichlorodiphenyl dichloroethylene, 4,4'-DDE; endo-
crine disrupting compounds, EDCs; Environmental Pro-
tection Agency, EPA; Massachusetts, MA; National Health
and Nutrition Examination Survey, NHANES; not
detected, ND; polychlorinated biphenyl, PCB; poly-
urethane foam, PUF; United States, US; University
Research Glassware, URG; Southwest Research Institute,
Competing interests
The author(s) declare that they have no competing inter-
Authors' contributions
RR and JB conceived the idea for the follow-up study and
directed it. RR carried out some follow-up sampling with
technical support, interviewed the participants about
potential sources of PCBs in their homes, and made the
discovery that PCBs had been a major component of the
wood finish described by the study participant. LS drafted
the manuscript, and RR revised it. All three authors con-
tributed to deliberations about ethical and policy implica-
tions of this finding.
Additional material
This work was supported by the National Institute of Environmental Health
Sciences (grant # 1 R25 ES013258-01), the National Science Foundation
(grant # SES-0450837), the Hurricane Voices Breast Cancer Foundation,
and an appropriation of the Massachusetts Legislature administered by the
Massachusetts Department of Public Health.
We acknowledge Massachusetts Department of Public Health for collec-
tion and analysis of blood samples and inspection of homes for PCB
sources; Southwest Research Institute for analysis of air and dust samples;
David Long, Kathleen Attfield, and Cheryl Osimo for sample collection; and
Phil Brown, Rachel Morello-Frosch, and the late M. Robert Dushman who
helped us consider regulatory and ethical issues. We are grateful to the res-
idents of homes we sampled. Finally, we wish to acknowledge Robert Gos-
selin, Roger Smith, Harold Hodge, and Marion Gleason for their Herculean
effort to compile and publish chemical ingredients lists for many commer-
cial products in the series "Clinical Toxicology of Commercial Products,"
published between 1957 and 1985. These reference books were the key to
our identifying wood floor finish as a likely source of elevated PCBs in these
homes – it is troublesome that no equivalent reference continues to pro-
vide this valuable information.
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Additional file 1
Concentrations of PCB congeners measured in residents' serum. The data
provided represent individual PCB congener measurements for each of the
four blood samples discussed in the paper.
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Supplementary resource (1)

... These products are commonly used as coolants, insulating fluids for transformers and capacitors, stabilizing additives, electronic components, and so on. (Rudel et al., 2008). PCBs are now a global health concern due to their negative impact on human health and the ecosystem (Gupta et al., 2018). ...
Phenolic compounds have been enlisted by the United States Environmental Protection Agency (USEPA) and the European Union (EU) as pollutants of priority concern. The biphenyl degradation pathway plays an essential role in prokaryote polychlorinated biphenyls degradation. Our understanding of prokaryotic pathways and their evolution has dramatically increased in recent years with the advancements in prokaryotic genome sequencing and analysis tools. In this work, we applied bioinformatics tools to study the evolution of the biphenyl degradation pathway focusing on the phylogeny and initiation of four representative species (Burkholderia xenovorans LB400, Polaromonas naphthalenivorans CJ2, Pseudomonas putida F1 and Rhodococcus jostii RHA1). These species contained partial or full concatenated genes from bph gene cluster (i.e. bphRbphA1A2A3A4BCKHJID). The aim was to establish this pathway's origin and development mode in the prokaryotic world. Genomic screening revealed that many bacterial species possess genes for the biphenyl degradation pathway. However, the micro‐synteny conservation analysis indicated that massive gene recruitment events might have occurred during the evolution of the biphenyl degradation pathway. Combining with the phylogenetic positions, this work points to the evolutionary process of acquiring the biphenyl degradation pathway by different fragments through horizontal gene transfer in these bacterial groups. This study reports the first‐ever evidence of the birth of this pathway in the represented species.
... These products are commonly used as coolants, insulating fluids for transformers and capacitors, stabilizing additives, electronic components, and so on. (Rudel et al., 2008). PCBs are now a global health concern due to their negative impact on human health and the ecosystem (Gupta et al., 2018). ...
Dementia is a complex syndrome of neurological disorders which is associated with cognitive functions of the body. The present review focuses on the role and application of natural products in the treatment of dementia and related diseases. The studies highlight that there exist some potent synthetic/semisynthetic drugs that can effectively target dementia and related diseases. In contrast, despite the existence of a large library of natural products, only a few of them (galantamin, huperzine A etc.) have been approved as drugs against dementia. This fact is not discouraging because a large number of natural products including classes of polyphenols, alkaloids, isothiocyanates, phytocannabinoids, and terpenoids, are in the process of drug development stages against dementia and related diseases. It is because they display some promising and diverse biological activities including antioxidant, acetylcholinesterase inhibitory activity, and anti-amyloidogenic properties which are significantly associated with prevention of dementia syndrome. The studies reported in the literature reveal that bioactive natural products particularly target Alzheimer’s and Parkinson’s diseases by suppressing the risks which are responsible for dementia. Huperzine A has been identified as a potent natural product against Alzheimer’s. Despite an efficient role of natural products in dementia prevention, their direct application as drugs are still limited due to some controversial results obtained from their clinical trials however bioassay guided drug development studies can prove them potential drugs against dementia and related diseases. This review provides useful information for a researcher working in the field, pharmacologists, medical doctors, and for the pharmaceutical industry.
... As carcinogenic and teratogenic chemicals, PCBs represent a considerable threat to humans and wildlife. Despite bans and restrictions, PCB sources affecting wildlife are highly varied (Huang et al., 2007) and likely include use in the electricity generation sector (Ministry of Water and Environmental Affairs, 2012; Gioia et al., 2014), but also in many other household products and fixtures (Rudel et al., 2008). While caracals generally avoid the urban matrix, they do select for areas closer to the urban edge (Leighton et al., 2021), where density of humans and electrical transformers is higher. ...
Wildlife around cities bioaccumulate multiple harmful environmental pollutants associated with human activities. Exposure severity can vary based on foraging behaviour and habitat use, which can be examined to elucidate exposure pathways. Carnivores can play vital roles in ecosystem stability but are particularly vulnerable to bioaccumulation of pollutants. Understanding the spatial and dietary predictors of these contaminants can inform pollutant control, and carnivores, at the top of food webs, can act as useful indicator species. We test for exposure to toxic organochlorines (OCs), including dichloro-diphenyl-trichloroethane (DDT) and polychlorinated biphenyls (PCBs), in a medium-sized felid, the caracal (Caracal caracal), across the peri-urban and agricultural landscapes of the city of Cape Town, South Africa. Concentrations in both blood (n = 69) and adipose tissue (n = 25) were analysed along with detailed spatial, dietary, demographic, and physiological data to assess OC sources and exposure risk. The analysis revealed widespread exposure of Cape Town's caracals to organochlorines: detection rate was 100% for PCBs and 83% for DDTs in blood, and 100% for both compounds in adipose. Caracals using human-transformed areas, such as vineyards and areas with higher human population and electrical transformer density, as well as wetland areas, had higher organochlorine burdens. These landscapes were also highly selected foraging areas, suggesting caracals are drawn into areas that co-incidentally increase their risk of exposure to these pollutants. Further, biomagnification potential was higher in individuals feeding on higher trophic level prey and on exotic prey. These findings point to bioaccumulation of OC toxicants and widespread exposure across local food webs. Additionally, we report possible physiological effects of exposure, including elevated white blood cell and platelet count, suggesting a degree of immunological response that may increase disease susceptibility. Cape Town's urban fringes likely represent a source of toxic chemicals for wildlife and require focused attention and action to ensure persistence of this adaptable mesocarnivore.
... Silent Spring Institute's household exposure study on Cape Cod, mentioned above, provides an example of a CBPR study that tested for household exposure to environmental contaminants. The study focused on exposure to EDCs, including the first indoor measures for 30 compounds, and identified a wood floor finish as a widespread ongoing source of PCBs (Rudel et al. 2003(Rudel et al. , 2008. In subsequent exposure monitoring, Silent Spring expanded the household exposure study to Richmond, California to measure exposure to similar chemicals in a poor, minority community (Brody et al. 2009). ...
This book examines the relationship between environmental justice and citizen science, focusing on enduring issues and new challenges in a post-truth age. Debates over science, facts, and values have always been pivotal within environmental justice struggles. For decades, environmental justice activists have campaigned against the misuses of science, while at the same time engaging in community-led citizen science. However, post-truth politics has threatened science itself. This book makes the case for the importance of science, knowledge, and data that are produced by and for ordinary people living with environmental risks and hazards. The international, interdisciplinary contributions range from grassroots environmental justice struggles in American hog country and contaminated indigenous communities, to local environmental controversies in Spain and China, to questions about “knowledge justice,” citizenship, participation, and data in citizen science surrounding toxicity. The book features inspiring studies of community-based participatory environmental health and justice research; different ways of sensing, witnessing, and interpreting environmental injustice; political strategies for seeking environmental justice; and ways of expanding the concepts and forms of engagement of citizen science around the world. While the book will be of critical interest to specialists in social and environmental sciences, it will also be accessible to graduate and postgraduate audiences. More broadly, the book will appeal to members of the public interested in social justice issues, as well as community members who are thinking about participating in citizen science and activism. Toxic Truths includes distinguished contributing authors in the field of environmental justice, alongside cutting-edge research from emerging scholars and community activists.
... Per-and polyfluoroalkyl substances (PFAS), polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), and organochlorine pesticides (OCPs) are examples of chemical classes with these properties, each of which has been used widely in industry and consumer products (Glüge et al., 2020;California Environmental Protection Agency, 2019;Fernandez et al., 2021;U.S. Environmental Protection Agency, 2017a;U.S. Environmental Protection Agency, 2021a). Human exposure to these chemical classes is common in the U.S. (U.S. Centers for Disease Control and Prevention, 2019;U.S. Environmental Protection Agency, 2013), and previous research has identified a wide range of correlates of biomarker (Caspersen et al., 2016;Bradman et al., 2007;Sagiv et al., 2015;Horton et al., 2013) and dust concentrations for these compounds (Whitehead et al., 2014a;Rudel et al., 2008;Allen et al., 2008;Bradman et al., 2014;Rodgers et al., 2020). Indoor environments remain an important microenvironment for exposure to each of these persistent classes. ...
Full-text available
Indoor spaces contain several classes of persistent organic chemicals, including per- and polyfluoroalkyl substances (PFAS), polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), and organochlorine pesticides (OCPs). However, concentrations of PFAS and persistent chemical mixtures and their associations with building characteristics on college campuses are understudied. We collected dust from 43 nonresidential spaces on four U.S. college campuses in 2016 and evaluated associations of room characteristics (carpeting, upholstered furniture, and years since last furnished) with dust concentrations of PFAS, PBDEs, PCBs, and OCPs. Nine PFAS, twelve PBDEs, two PCBs, and four OCPs were each detected in at least 75% of the spaces, including several chemicals (e.g., DDT) that have been banned for decades. Concentrations were correlated within and, in some cases, between chemical classes. Wall-to-wall carpeting (compared to rooms without wall-to-wall carpeting) was associated with higher concentrations of six individual PFAS and a mixture of PFAS, and the number of pieces of upholstered furniture was associated with increased concentrations of a mixture of PBDEs. These findings indicate that carpeting and furniture are current sources of PFAS and PBDEs, respectively. Building and finish materials should be carefully selected to avoid exposure to persistent chemicals.
... Thus, the PCB concentrations in the floodplain soils were compared with those stipulated by some international regulatory bodies. The Canadian Soil Quality Guideline (CSQG) value for PCBs in agricultural soils is 500 ng g −1 (CCME, 1999), and the Australian and New Zealand Ecological Investigation Level (ANZEIL) and Dutch action value for PCBs is 1000 ng g −1 (ANZECC, 1992;VROM, 1994), while a value of 220 ng g −1 total PCBs was stipulated by the US EPA as the health-based screening level designed to avert adverse health effects relating to long-term exposure (Rudel et al., 2008). The PCB concentrations in 46% of the soil samples were above the CSQG value for PCBs in agricultural soils, while 21% of samples had Ʃ28 PCB concentrations above the Dutch action value and that of ANZEIL, and 64% of the soil samples had Ʃ28 PCB concentrations above the health-based screening level of the US EPA. ...
Full-text available
The concentrations of 28 polychlorinated biphenyls (PCBs) were determined in soils collected at three depths from thirteen different sites along the floodplain of the lower reaches of the River Niger (LRRN) in Nigeria. The aim of the study was to provide data on the levels of contamination, sources of the contaminants, and risks to the ecosystem and humans. Soil samples were Soxhlet extracted with a solvent mixture of dichloromethane (DCM)/n-hexane and cleaned up on a column packed with Florisil and silica gel. The PCBs in the samples were quantified by gas chromatography-mass spectrometry. The Ʃ28 PCB concentrations in the floodplain soils varied between not detected (nd) and 11,151 ng g−1 for different sampling sites and depths. The PCB concentrations and homologue distribution patterns in soil profiles of the floodplain of the LRRN showed remarkable differences with respect to sites and depths. The results obtained were used to evaluate the ecological and human health risks, which indicated that there is a potential risk to organisms and humans from exposure to PCBs in these soil profiles. The source evaluation as determined by principal component analysis suggested that PCBs in these soil profiles came from burnt circuit boards, cable wires, use of paints, discharges from transformers, long-range migration, and deposition.
... Colt et al. (2005), showed an association between the increased risk of non-Hodgkin lymphoma and exposure to PCBs in carpet dust. Although no longer in use (PCBs were strictly banned in 2001), it has been suggested that their evaporation and abrasion from old building materials and consumer products, manufactured before 1977, can result in considerable house dust contamination (Rudel et al., 2008). The majority of studies concentrated on a subset of PCB congeners, especially seven indicator congeners (i.e., and twelve dioxin-like PCBs (Anh et al., 2021). ...
Organic contaminants often documented in house dust include mainly chemicals released from construction materials and consumer products and compounds emitted from indoor combustion activities. The occurrence of major chemical classes of toxic organic pollutants, included polybrominated diphenyl ethers (PBDEs), polychlorinated biphenyls (PCBs), polycyclic aromatic hydrocarbons (PAHs) and nitrated polycyclic aromatic hydrocarbons (NPAHs), was for the first time investigated in house dust in Greece. The mean concentrations of ∑16PAHs, ∑20PBDEs, ∑7NPAHs and∑15PCBs in house dust were 4650 ng g-1, 564 ng g-1, 7.52 ng g-1, and 6.29 ng g-1, respectively. Exposure to dust organic contaminants via ingestion, inhalation and dermal absorption was estimated for two age classes (adults and children) and carcinogenic and non-carcinogenic risks were assessed. The hazard index (HI) for adults and children for PBDEs, PCBs, PAHs and NPAHs in all samples was less than 1 suggesting a very low level of concern for all human age group due to exposure to those chemicals. Total carcinogenic risk via the three exposure pathways (ingestion, inhalation and dermal contact) was within the safe range of 10-6 to 10-4. Keywords: PBDEs; PCBs; PAHs; NPAHs; Human Exposure; House dust; Risk assessment
Polychlorinated biphenyls (PCBs), "famous" as persistent organic pollutants (POPs), have been managed nationally since the 1970s and globally under the Stockholm Convention on POPs since 2004, requiring environmentally sound management (ESM) of PCBs by 2028. At most, 30% of countries are on track to achieve ESM by 2028. Globally over 10 million tonnes of PCB-containing materials remain, mostly in countries lacking the ability to manage PCB waste. Canada (Ontario) and Czechia, both parties to the Stockholm Convention, are close to achieving the 2028 goal, having reduced their stocks of pure PCBs by 99% in the past 10 years. In contrast, the USA, not a party to the Stockholm Convention, continues to have a substantial but poorly inventoried stock of PCBs and only ∼3% decrease in mass of PCBs since 2006. PCB management, which depends on Stockholm Convention support and national compliance, portends major challenges for POP management. The failure to manage global PCB stocks >30 years after the end of production highlights the urgent need to prioritize reducing production and use of newer, more widely distributed POPs such as chlorinated paraffins and per- and polyfluorinated alkyl substances, as these management challenges are unlikely to be resolved in the coming decades.
Hormone-active substances are those compounds which behave like hormone activity, irrespective of mechanism. Hormone system is controlled by endocrine system in organism's body; therefore, they are also called as endocrine-active substances (EASs). Endocrine system, important communication system, comprises of endocrine glands that secrete “hormones” in blood stream (in response to stimulus) to regulate body function. Endocrine-disrupting chemicals disturb inadvertently the complex communication system and interfere with synthesis and secretion of bodily hormones. Endocrine substance influences the regular activity hormones. If these substances cause negative change in body, then they are also called endocrine disrupters. Endocrine disruptors are exogenous substances or mixture of substances that alter functions of endocrine system that eventually cause adverse impact on health of intact organism, its progeny, and subpopulations. Endocrine disrupters/EASs affect the health of exposed human and animals by entering into ecosystem via different sources. EAS could be naturally occurring (like phytoestrogen in soya) or synthetic. The artificially or synthetic EASs are man-made such as pesticides, dioxins, PCBs, Biphenyl A, and other environmental pollutants. Endocrine disrupters are also considered as environmental micropollutants or toxins that could harm the organism's health. These disrupting toxins (chemicals) could affect the endocrine system and cause diseases and dysfunctions across the whole life span of organisms. They are omnipresent, so they enter into body via different sources and pathways. Some environmental toxins are heavy metals, dioxins, pesticides, and polychlorinated biphenyl and other atmospheric pollutants (ozone, smog). The severity of effects on exposed organisms depends on dose-response relationship. The amount or concentration of dose is proportional to effect. These EASs induce toxic impacts on animals and plant's health by entering into food chain. In this chapter, different toxic impacts of hormone-active substances on animals, plants, and human health are mentioned in detail.
This study determined the concentrations, origin, and associated ecological and human health risks of Ʃ28PCBs in soil profiles from selected telecom-masts in the Niger Delta, Nigeria. A total of 18 soil samples were quantified for Ʃ28PCBs with gas chromatography-mass spectrometry after soxhlet extraction with n-hexane/dichloromethane and purified with florisil and silica gel column. The occurrence of the ∑28PCBs varied widely, and ranged from 88.0 to 293 mg kg⁻¹, with pollution load in the order of subsoil > topsoil, and SS 3 > SS 2 > SS 1 > SS 6 > SS 7 > SS 9 > SS 4 > SS 8 > SS 5. The compositional pattern of the ∑28PCBs were in the order of deca-PCB > tetra-PCBs > di-PCBs > penta-PCBs > hexa-PCBs > hepta-PCBs > tri-PCBs > octa-PCBs > nona-PCBs. Also, the LC-PCBs are the dominant PCBs with a composition of 50 to 91.8%, while the HC-PCBs accounted for 34.8 to 78.8%. The levels of the ∑28PCBs from the telecom-masts were significantly higher than the recommended standards for urban and agricultural soils. The ecological risk index, toxic equivalence, hazard index, and total cancer risk suggest ecological risk to soil-dwelling organisms and on-site human occupational risk to soils around the telecom-masts. The source identification depicts that PCBs originated from the use of Aroclor1254 mixtures, cable and wire insulators, lubricants, paints, transformer oils, pesticides, and power capacitors in the telecom masts. Standard guidelines for the operations of telecom-masts should be carried out to mitigate the potential ecological and on-site human occupational risks in soil profiles around the telecom-masts, and similar land use somewhere else around the world.
Polychlorinated biphenyls (PCBs) were measured in house dust and yard soil at 34 homes surrounding New Bedford Harbor during dredging of highly contaminated harbor sediments. PCBs can volatilize from sediments and seawater and subsequently deposit on surrounding soil, resulting in potential exposures for nearby residents. House dust was collected from carpet, while yard soil was collected from the main entryway to evaluate whether PCBs might be tracked indoors. All samples were analyzed for 65 PCB congeners to evaluate the relative importance of the harbor and indoor sources for human exposure. PCB concentrations (260−23 000 ng/g) in house dust were about 10 times higher than yard soil concentrations (15−1800 ng/g), although similar congener patterns were detected in these two media. Yard soil concentrations in neighbor hoods closest to the harbor were significantly higher than those in comparison neighborhoods (23−1800 ng/g and 15−290 ng/g, respectively), while house dust concentrations did not differ significantly between these two locales (320−23 000 ng/g and 260−3600 ng/g, respectively). PCB concentrations in house dust were correlated with those in indoor air, but house dust and yard soil concentrations were not correlated, suggesting that track-in may not be the only source of PCBs in house dust.
Polychlorinated biphenyl (PCB) concentrations were measured in air from a total of 14 different indoor environments in Birmingham and the West Midlands area of the United Kingdom and compared to ambient outdoor levels. In four instances, spatially and temporally consistent indoor and outdoor samples were taken for comparison. Other indoor samples were compared to 25 outdoor samples from the Birmingham area taken at regular intervals between February 1997 and February 1998. Higher levels were present in indoor air (1.1−69 ng of ∑PCB m-3, mean = 9.0 ng of ∑PCB m-3) than in outdoor air (0.08−1.5 ng of ∑PCB m-3, mean = 0.31 ng of ∑PCB m-3). This limited data set indicates daily mean background U.K. PCB intake via inhalation to be 110 ng of ∑PCB person-1 (0.7 pg of ∑i-TE person-1), with a range of 23−590 ng of ∑PCB person-1 (0.03−2 pg of ∑i-TE person-1). Inhalation may thus represent a significant exposure pathway to ∑PCB but not ∑i-TE for some individuals, given that 1992 daily U.K. intake of PCB via diet has been estimated elsewhere to be 340 ng of ∑PCB person-1 (54 pg of ∑i-TE person-1).
Polychlorinated biphenyl (PCB) concentrations were measured in indoor and outdoor air at 34 homes surrounding New Bedford Harbor during dredging of highly contaminated harbor sediments. PCB volatilization from harbor sediments and water leads to inhalation exposure for nearby residents. On each sampling day, 24 h indoor and outdoor air samples were collected simultaneously and analyzed for 65 PCB congeners to evaluate the relative importance of the harbor and indoor sources for human inhalation exposure. Outdoor air concentrations were higher in neighborhoods closest to the harbor (0.4−53 ng/m3) relative to comparison neighborhoods (0.1−8.2 ng/m3) and contained slightly greater proportions of volatile PCB congeners. Outdoor air concentrations near the harbor are some of the highest measured in recent years. Indoor air concentrations in homes near the most contaminated part of the harbor (7.9−61 ng/m3) were slightly higher than concentrations in homes distant from this area (5.2−51 ng/m3). In all neighborhoods, indoor concentrations exceed corresponding outdoor concentrations (mean ratio = 32), suggesting the importance of indoor PCB sources even near a highly contaminated waste site.
The sources and speciation of trace elements in street and house dusts are reviewed. Soil is a major component of both dusts, but a number of elements are enriched in both materials. These include Pb, Zn, Cu, Cd, As, Sb, Cr, Ca, Na, Au, Cl and Br. They arise from a number of contributing and polluting sources. In the case of house dust, some elements, such as Cu, Co, As, Sb, Zn, Cd, Au, Cl, C and Pb, are produced in the house. There are a number of problems associated with the determination of the speciation of trace elements in dusts. These include the low concentrations of many of the elements, and the interpretation of the results from selective sequential extractions. The mobility and potential availability of the trace elements from dust lies in the order Cd greater than Zn, Pb greater than Mn, Cu greater Fe.
We identified 24 modern studies of childhood exposures to lead in relation to IQ. From this population, 12 that employed multiple regression analysis with IQ as the dependent variable and lead as the main effect and that controlled for nonlead covariates were selected for a quantitative, integrated review or meta-analysis. The studies were grouped according to type of tissue analyzed for lead. There were 7 blood and 5 tooth lead studies. Within each group, we obtained joint P values by two different methods and average effect sizes as measured by the partial correlation coefficients. We also investigated the sensitivity of the results to any single study. The sample sizes ranged from 75 to 724. The sign of the regression coefficient for lead was negative in 11 of 12 studies. The negative partial r's for lead ranged from -.27 to -.003. The power to find an effect was limited, below 0.6 in 7 of 12 studies. The joint P values for the blood lead studies were less than .0001 for both methods of analysis (95% confidence interval for group partial r, -.15 +/- .05), while for the tooth lead studies they were .0005 and .004, respectively (95% confidence interval for group partial r, -.08 +/- .05). The hypothesis that lead impairs children's IQ at low dose is strongly supported by this quantitative review. The effect is robust to the impact of any single study.
Developmental hypothyroidism causes growth deficits, motor dysfunction, and hearing disorders in humans and animals. Therefore, environmental toxicants, such as polychlorinated biphenyls (PCBs), may secondarily affect these endpoints via thyrotoxicity. In this study, Long-Evans rats were given Aroclor 1254 (po), at 0, 1, 4, or 8 mg/kg from Gestation Day 6 through Postnatal Day (PND) 21. We evaluated the offspring at various age intervals for circulating thyroid hormone concentrations [thyroid-stimulating hormone, and free and total triiodothyronine (T3) and thyroxin (T4)], body weight, eye opening, survival, motor activity development, auditory startle response, and auditory thresholds. Circulating T4 concentrations were sharply reduced in a dose-dependent fashion in PCB-exposed groups at PND 1, 7, 14, 21, and 30 but recovered to control levels by PND 45. Moderate reductions in T3 concentrations were apparent in the 4 and 8 mg/kg groups on PND 21 and 30. Deficits in body weight gain and early eye opening were apparent in the treated pups; by weaning, pup mortality was 20% in the 4 mg/kg group and 50% at the highest dose. Motor activity was also transiently reduced in 15 day old offspring from the 8 mg/kg group. At this dose, animals showed reduced auditory startle amplitudes at PND 24, but not when tested as adults. Importantly, Aroclor 1254 caused permanent auditory deficits (20-30 dB threshold shift) at the lowest frequency tested (1 kHz) in both the 4 and 8 mg/kg groups, whereas auditory thresholds were not significantly affected at higher frequencies (4, 16, 32, or 40 kHz). These data indicate that while some effects of Aroclor 1254 exposure are dissimilar to drug-induced hypothyroidism (e.g., age of eye opening), effects on hormone levels and body weight are comparable. Detection of auditory deficits in PCB-treated animals is a novel finding and may reflect the effects of thyroid hormone disruption on the development of the cochlea.