1) The study assessed exposure to VOCs and oxidative stress in populations exposed to different air pollution sources including environmental tobacco smoke (ETS). 2) Urinary biomarkers of BTEX VOCs and 8-oxo-dG, a marker of DNA damage, were measured and correlated with ETS exposure as measured by urinary cotinine levels. 3) A strong relationship was found between urinary BTEX and cotinine, indicating ETS is a major source of BTEX exposure even at low levels, and a threshold of 550ng/L total urinary VOCs was identified above which VOC exposure contributes significantly to oxidative stress.

1. Biomonitoring of Exposure to Air Pollutants: Contribution of Different Air Pollution Sources Towards Oxidative Stress
Massimiliano Mascelloni*1, Barbara Macias-Hernandez1, Silvia Fustinoni2, Elisa Polledri2, Laura Campo2, Mu-Rong Chao3, Chiung-Wen Hu4, Marcus S. Cooke5, Roy M. Harrison1, Juana Maria Delgado-Saborit1
1School of Geography, Earth and Environmental Sciences, University of Birmingham, B15 2TT, United Kingdom
2Department of Clinical and Community Sciences, Universitá degli studi di Milano, Italy
3Department of Occupational Health and Safety, Chung Shan Medical University, Taiwan
4Department of Public Health, Chung Shan Medical University, Taiwan
5 Department of Environmental and Occupational Health, Florida International University, Florida, USA
*Now at Department of Environmental Health Sciences, University of Massachusetts, Amherst, MA 01003, USA
E-mail: mmascelloni@umass.edu
Introduction
Exposure to air pollutants is a well known issue both indoors and outdoors.
People spend a large portion of the day in indoor microenvironments, and
although the exposure levels found indoors are often lower than outdoors,
indoor exposure makes a relevant contribution towards the total exposure.
The goal of this study (FIXAT) was to assess the exposure to VOCs and the early
effects in general population. Different subgroups were compared to identify
sources and tasks related to different levels of exposure arising from building
materials and consumer products in new or recently refurbished buildings.
Methods
FIXAT results were compared with previous studies (MATCH1) that included
environmental tobacco smoke (ETS) and high levels of exposure.
For each subject, after a 24h personal exposure sampling, a first morning
urine sample was collected and analysed for unmetabolized BTEX (benzene,
toluene, ethylbenzene, o- m- p-xylene) and naphthalene to assess VOC
exposure, and 8-oxo-dG (8-oxo-2’deoxyguanosine) to assess DNA damage.
The data was compared between the main groups and between subgroups
created ad-hoc using different variables (e.g. smoking habits, ETS exposure).
Correlation analyses were performed between the different biomarkers, and
subgroups were compared using different statistical approaches.
Relationship between urinary BTEX, ETS
and 8-oxo-dG
• The single VOCs showed statistically significant correlation with the DNA
damage biomarker 8-oxo-dG for ethylbenzene (p=0.045) and xylenes
(p=0.019 and p=0.035).
• The sum of urinary BTEX + naphthalene showed statistically significant
correlation with urinary cotinine (p<0.001) and a marginally significant
correlation with 8-oxo-dG (p=0.041).
• The observed correlations evidenced a strong relationship between urinary
BTEX and ETS. Interestingly, a similar relationship was observed in the non-
ETS exposed subjects with urinary cotinine >1µg/L (p=0.004), suggesting a
major role of ETS as a source of BTEX even at extremely low
concentrations.
Acknowledgements
The authors would like to thank CEFIC and Wellcome Trust fund for financial support, authors would also like to thank all the volunteers that participated in the study.
References:
Saborit, J. M. D. et al. Measurement of personal exposure to volatile organic compounds and particle associated PAH in three UK regions. Environ. Sci.
Technol. 43, 4582–4588 (2009).
Exposure at
home/workplace
Living in buildings built
or refurbished in less
than 1 year
(n= 15)
Occupational
exposure
Working in traffic or
operating petrol engine
powered tools
(n= 14)
Control
Not living in buildings
built or refurbished in
less than 1 year
(n= 15)
MATCH study
(n= 41)
Midstream
urine
sample
Personal sampler: one VOC
sorbent tube and quartz filter
connected to a pump and one
Microaethalometer
Thermal desorption GC-
MS for VOCs in personal
exposure samples
8-oxo-DG in urine using
LC-MS, cotinine using LC-
MS/MS
Unmetabolized BTEX
(benzene, toluene,
ethylbenzene, o- m- p-
xylene) and naphthalene
in urine using Headspace
SPME-GC-MS Non-ETS
exposed
ETS exposed +
Smokers
2.74
Total urinary VOCs >550ng/L
Threshold of effect
• ETS contribution towards the concentration of total urinary VOCs is
showed by the strong relationship between urinary cotinine and urinary
BTEX in both ETS exposed (p=0.010) and non-ETS exposed subjects
(p=0.004).
• The relationship is not conserved between urinary BTEX and 8-oxo-dG
(p=0.826) and urinary cotinine and 8-oxo-dG (p=0.840) for non-ETS
exposed subjects.
• In ETS exposed subjects urinary cotinine and total urinary VOCs showed
statistically significant correlation with 8-oxo-dG (p=0.007 and p=0.036
respectively).
• The observed differences in the correlation between urinary VOCs,
cotinine and 8-oxo-dG suggested a “threshold of effect”, which was
identified as 550ng/L of total urinary VOCs. The value was identified with
the intercept of the trend line for the cotinine/total VOCs.
• Under the threshold of effect, no relationship is observed between 8-oxo-
dG and urinary BTEX, suggesting that the measured oxidative stress
damage has other sources, while past the threshold, VOC exposure (from
ETS and other sources) is a significant contributor of oxidative stress.
Conclusions
• No significant difference was observed between subjects living or working in
a new or recently refurbished building and the control groups for both
urinary BTEX concentration and oxidative stress.
• One of the main sources of VOC exposure was identified as cigarette smoke,
even under the threshold of ETS exposure of 1µg/L of urinary cotinine.
• Large majority of the time was spent indoors by the subjects, suggesting that
ETS could have been carried indoors by either air diffusion or from off-
gassing of the pollutants from cloths and surfaces that came in contact with
cigarette smoke (third-hand smoke).
• ETS represents one of the main confounding factors for BTEX measurement,
even under the typically used threshold for ETS exposure of 1µg/L of urinary
cotinine.
• While this biomonitoring approach has been proven to be effective in high
exposure populations and occupational exposures, it is not possible to
observe any relationship with oxidative stress at the levels of exposure of
this study.
• Threshold of effect is a good example of a “limit of detection” of this
approach, together with suggesting that at these low levels of exposure, the
sources of oxidative stress are to be identified elsewhere.
Figure 2: Scatter plot representing the full
data set for MATCH and FIXAT project
showing the relationship between the
sum of urinary BTEX + naphthalene and 8-
oxo-dG. The vertical reference line
identifies the intercept of the regression
line of Figure 1, representing the
threshold of effect.
Figure 1: scatter plot representing the
full data set for MATCH and FIXAT project
showing the relationship between the
sum of urinary BTEX + naphthalene and
cotinine. The vertical line represents the
threshold of discrimination between ETS
exposed and non ETS exposed subjects
(urinary cotinine=1µg/L).