The Toxicologist - Society of Toxicology
The Toxicologist - Society of Toxicology
The Toxicologist - Society of Toxicology
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a limited subset <strong>of</strong> PAHs (16 US-EPA PAHs). <strong>The</strong>refore, additional potential toxicity<br />
assessment via in vitro assays as well as mechanistic studies e.g., assessing PAH<br />
availability to the cells and understanding the activation and/or suppression <strong>of</strong> signal<br />
transduction, appears warranted. <strong>The</strong> aim <strong>of</strong> this study was to assess PAH toxicity<br />
via chemical PAH analysis, a specific in vitro PAH transactivation assay and<br />
metabolism studies. Two different PM samples were analyzed (TD-GC-MS/MS)<br />
for the presence <strong>of</strong> 16 PAHs. PAH-induced toxic potency was determined with the<br />
PAH CALUX transactivation assay. <strong>The</strong> PAH CALUX system suggested the presence<br />
<strong>of</strong> a toxic potency several fold above that indicated by chemical analysis. In addition,<br />
human type II alveolar epithelial cells (A-549) were exposed to different PM<br />
concentrations and Benzo(a)pyrene (B[a]P) as a positive control. PM as well as<br />
B[a]P exposure resulted in a higher CYP1A1 mRNA expression than in controls.<br />
CYP1A1 enzyme activity was confirmed via a luminogenic assay. CYP1A1 enzyme<br />
activity was inhibited at high PM and B[a]P concentrations and assumed to result<br />
from increased expression <strong>of</strong> AhRR, a repressor <strong>of</strong> the AhR signaling cascade.<br />
Consequently understanding the status <strong>of</strong> both the AhR and AhRR appear important<br />
in order to interpret the potential toxicity <strong>of</strong> PMs and B[a]P in human alveolar<br />
cell systems.<br />
1214 SULFUR EMISSIONS FROM CHINESE DRYWALL IN<br />
CHAMBERS AND HOMES.<br />
J. Matheson 1 , M. Babich 1 , T. Thomas 1 , K. Hatlelid 1 , J. Recht 1 , R. Maddalena 2 ,<br />
M. Apte 2 , J. McCarthy 3 , B. Baker 3 , J. Allen 3 , D. MacIntosh 3 and L. Saltzman 1 .<br />
1 U.S. Consumer Product Safety Commission, Bethesda, MD, 2 LBNL, Berkeley, CA<br />
and 3 EH&E, Needham, MA.<br />
<strong>The</strong> CPSC has received 3600 consumer complaints reporting health effects and<br />
metal corrosion in homes built/renovated in 2001-2008. Reported health effects<br />
include: migraines, nosebleeds, irritated eyes, dyspnea, cough, and sinus problems.<br />
Affected homeowners <strong>of</strong>ten note the homes have an <strong>of</strong>fensive odor. Certain drywall<br />
imported from China (CDW) was implicated as the probable cause <strong>of</strong> reported corrosion;<br />
but other home materials have not been ruled out as contributory factors.<br />
Chamber testing <strong>of</strong> domestic and imported drywall emissions and in-home air sampling<br />
are part <strong>of</strong> a multi-track test program to evaluate the relationship between<br />
drywall emissions, material degradation, and reported symptoms. Chamber testing<br />
on 30 drywall samples was performed at LBNL. Emissions from preconditioned<br />
samples were measured in 10.5 L chambers at a ventilation rate <strong>of</strong> 0.5 L/min at<br />
25°C and 50% relative humidity. Four methods were used for emission sampling<br />
and analysis depending on the target chemical class. A new method, solid phase<br />
micro extraction, was developed to measure reactive volatile sulfur gases. <strong>The</strong> majority<br />
<strong>of</strong> emissions consisted <strong>of</strong> H 2 S and SO 2 ; total sulfur emission factors ranged<br />
from 0.3 to 209 μg/m 2 /h. Higher sulfur gas emissions were observed from CDW<br />
made in 2005-2006. EH&E’s investigation in 51 homes included source characterization<br />
using FTIR and XRF; measurements <strong>of</strong> indoor environment including<br />
gases, ventilation rate, temperature and relative humidity; and copper and silver<br />
corrosion rates. Compared to control homes, complaint homes had significantly<br />
higher H 2 S levels (0.82 μg/m 3 vs 〈LOD) and rates <strong>of</strong> copper sulfide (476 vs 〈LOD<br />
A/30d) and silver sulfide corrosion (1472 vs 389 A/30d). A consistent finding <strong>of</strong> elevated<br />
sulfur emissions associated with CDW was observed in the chamber and inhome<br />
testing. <strong>The</strong> home sulfur gas levels were below known irritant levels; however,<br />
it is possible that additive or synergistic effects <strong>of</strong> these and other compounds could<br />
potentially cause irritant effects to consumers.<br />
1215 EXPOSURE MODEL FOR INDIVIDUALS (EMI) IN<br />
HUMAN HEALTH STUDIES: PREDICTING<br />
RESIDENTIAL INDOOR EXPOSURES TO FINE<br />
AIRBORNE PARTICLES.<br />
M. Breen 1 , M. Breen 1, 2 , B. Schultz 1 , T. Long 1 , R. Williams 1 , A. Vette 1 and R.<br />
Devlin 1 . 1 U.S. EPA, Research Triangle Park, NC and 2 North Carolina State<br />
University, Raleigh, NC.<br />
In many epidemiological studies, particulate matter (PM) is associated with increased<br />
risk for adverse cardiopulmonary events. Due to cost and participant burden<br />
<strong>of</strong> indoor and personal measurements, health studies <strong>of</strong>ten estimate exposures<br />
using ambient measurements. However, ambient levels do not necessarily reflect<br />
personal exposures since indoor levels can differ from ambient levels, and people<br />
spend considerable time indoors. To reduce this exposure error, which adds uncertainty<br />
to risk estimates, we are developing an exposure model for individuals (EMI)<br />
in cohort health studies. A critical aspect <strong>of</strong> EMI is estimation <strong>of</strong> the ambient contribution<br />
to concentrations within individual homes, where people spend most <strong>of</strong><br />
their time. A mass-balance indoor air quality (IAQ) model was linked to an air exchange<br />
rate (AER) model to predict ambient-generated indoor PM 2.5 mass from<br />
260 SOT 2011 ANNUAL MEETING<br />
ambient concentrations, meteorology, and questionnaire data on housing characteristics<br />
and operation. First, AER model predictions were compared to 642 daily AER<br />
measurements across 31 detached homes in central North Carolina. For individual<br />
model predicted and measured AER, median absolute difference was 40% (0.17 hr -<br />
1 ). Second, IAQ model was evaluated with concurrent daily measurements <strong>of</strong> ambient<br />
and residential indoor-outdoor PM 2.5 mass. Using cross validation, model predictions<br />
were compared to measurements <strong>of</strong> ambient-generated indoor PM 2.5 ,<br />
which were derived from sulfate (outdoor tracer <strong>of</strong> PM 2.5 ). For individual model<br />
predictions and measurements, median absolute difference was 24% (2.2 μg/m 3 ).<br />
This study demonstrates the ability <strong>of</strong> EMI to predict residential indoor PM 2.5 <strong>of</strong><br />
ambient origin in support <strong>of</strong> developing exposure metrics for health studies.<br />
1216 EXPOSURE TO PHTHALATES AMONG<br />
PREMENSTRUAL GIRLS FROM RURAL AND URBAN,<br />
GHARBIAH, EGYPT.<br />
J. Colacino 1, 2 , A. Soliman 2, 3 , M. Nahar 1 , A. Hablas 4 , I. Seifeldin 4 , A. Van<br />
Zomeren-Dohm 1 , L. S. Rozek 1 and D. C. Dolinoy 1 . 1 Environmental Health<br />
Sciences, University <strong>of</strong> Michigan School <strong>of</strong> Public Health, Ann Arbor, MI, 2 Center for<br />
Global Health, University <strong>of</strong> Michigan, Ann Arbor, MI, 3 Epidemiology, University <strong>of</strong><br />
Michigan, Ann Arbor, MI and 4 Tanta Cancer Center, Gharbiah, Egypt.<br />
Phthalates have been identified as endocrine active compounds associated with developmental<br />
and reproductive toxicity. Phthalate exposure in premenstrual<br />
Egyptian females, a potentially vulnerable population, remains unknown. <strong>The</strong> objective<br />
<strong>of</strong> this study was to quantify phthalate exposure in premenstrual females<br />
from rural and urban areas <strong>of</strong> the Gharbiah province <strong>of</strong> Egypt as well as describe<br />
potential routes <strong>of</strong> exposure. We collected one spot urine sample from 60 premenstrual<br />
females, 30 each from urban and rural areas, as well as anthropometrics and<br />
questionnaire data regarding cooking, cosmetic use, and food storage behaviors.<br />
Urinary concentrations <strong>of</strong> 11 phthalate metabolites were quantified by isotope dilution<br />
tandem mass spectrometry at the National Center for Environmental Health<br />
<strong>of</strong> the Centers for Disease Control and Prevention. Urinary concentrations <strong>of</strong> diethyl<br />
phthalate and di(2-ethylhexyl) phthalate metabolites measured in this study<br />
were similar to those measured in age-matched US girls in the National Health and<br />
Nutrition Examination Survey 2003-2006. Median mono-benzyl phthalate concentrations<br />
were higher in US girls (31.1 ng/mL) compared to Egyptians (1.6<br />
ng/mL). In contrast, median levels <strong>of</strong> mono-isobutyl phthalate were higher in<br />
Egyptians (21.1 ng/mL) compared to US girls (7.5 ng/mL). We found no significant<br />
difference in concentrations <strong>of</strong> phthalate metabolites based on the urban or<br />
rural status <strong>of</strong> the Egyptian girls. In principle components analysis, storage <strong>of</strong> food<br />
in plastic was found to be associated with phthalate body burden (p=0.036), suggesting<br />
that dietary intake is likely an important route <strong>of</strong> phthalate exposure in<br />
both urban and rural Egyptians. <strong>The</strong>se findings suggest that phthalate exposure in<br />
developing countries may be <strong>of</strong> equal concern as in the US.<br />
1217 BLOOD ANALYSIS OF SWEDISH FIRE VICTIMS 1992-<br />
2009 SUGGEST HYDROGEN CYANIDE AS AN<br />
IMPORTANT CAUSE OF DEATH.<br />
K. Stamyr 1 , G. <strong>The</strong>lander 2 , L. Ernstgård 1 and G. Johanson 1 . 1 Work Environment<br />
<strong>Toxicology</strong>, Institute <strong>of</strong> Environmental Medicine, Karolinska Institutet, Stockholm,<br />
Sweden and 2 Department <strong>of</strong> Forensic Genetics and Forensic <strong>Toxicology</strong>, National<br />
Board <strong>of</strong> Forensic Medicine, Linköping, Sweden.<br />
BACKGROUND For people caught in fires, or fire fighters entering fires, a major<br />
threat is posed by toxic fumes. 60-80% <strong>of</strong> all deaths related to fire have been attributed<br />
to such fumes. Carbon monoxide (CO) is a major component and is commonly<br />
thought to be the major cause <strong>of</strong> most fire-related fatalities. However, hydrogen<br />
cyanide (HCN) is also formed, especially during combustion <strong>of</strong><br />
nitrogen-containing materials such as polyurethane foam, a material increasingly<br />
encountered in indoor environments. <strong>The</strong> exact contribution <strong>of</strong> HCN to fire-related<br />
fatalities is unknown (Stamyr et al. Toxicol. Lett. 2008). AIM <strong>The</strong> study was<br />
undertaken to investigate the impact <strong>of</strong> HCN in relation to CO as a cause <strong>of</strong> intoxication<br />
and death in fire victims. METHOD Swedish data on all fire victims in the<br />
period 1992-2009 were collected from two nationwide forensic databases (ToxBase<br />
and RättsBase). Among the 1300 victims, 500 had been analyzed for both carboxyhemoglobin<br />
(COHb) and HCN in blood. Nearly half <strong>of</strong> the victims had lethal<br />
COHb levels (>50% COHb). Further, 7% had HCN levels above 2 μg/g (an indication<br />
<strong>of</strong> lethal or life-threatening intoxication), 30% had levels above 1 μg/g and<br />
over 50% had levels above 0.5 μg/g (an indication <strong>of</strong> significant HCN exposure).<br />
HCN continues to be eliminated from blood also after death (McAllister et al. J.<br />
Anal. Toxicol. 2008) and the exact time lapse from death to sampling and analysis<br />
is unknown for these blood samples. Thus, measured HCN is probably a serious<br />
underestimate <strong>of</strong> true blood levels at the time <strong>of</strong> death. CONCLUSION Overall,<br />
these Swedish forensic data suggest that HCN may be an equally or even more im-