Abstract
BackgroundThere is accumulating epidemiologic evidence that exposure to traffic-related air pollutants, including particulate matter (PM) and polyaromatic hydro carbons (PAHs), plays a role in etiology and prognosis of a large scale of illnesses, although the role of specific causal agents and underlying mechanisms for different health outcomes remains unknown.ObjectiveOur general objective was to assess the relations between personal exposure to traffic exhausts, in particular ambient PM2.5 and PAHs, and the occurrence of DNA strand breaks by applying personal monitoring of PM and biomarkers of exposure (urinary 1-hydroxypyrene-glucuronide, 1-OHPG) and effect (urinary 8-hydroxydeoxyguanosine, 8-OHdG and DNA strand breaks).MethodsWe recruited 91 traffic conductors and 53 indoor office workers between May 2009 and June 2011 in Taipei City, Taiwan. We used PM2.5 personal samplers to collect breathing-zone particulate PAHs samples. Spot urine and blood samples after work shift of 2 consecutive days were analyzed for 1-OHPG, 8-OHdG and DNA strand breaks, respectively. Statistical methods included linear regression and mixed models.ResultsUrinary 8-OHdG levels and the occurrence of DNA strand breaks in traffic conductors significantly exceeded those in indoor office workers in mixed models. Particulate PAHs levels showed a positive association with urinary 1-OHPG in the regression model (β = 0.056, p = 0.01). Urinary 1-OHPG levels were significantly associated with urinary 8-OHdG levels in the mixed model (β = 0.101, p = 0.023). Our results provide evidence that exposure to fine particulates causes DNA damage. Further, particulate PAHs could be biologically active constituents of PM2.5 with reference to the induction of oxidative DNA damages.
Highlights
Traffic emissions include large quantities of carbon dioxide (CO2), carbon monoxide (CO), hydrocarbons (HC), nitrogen oxides (NOx), particulate matter (PM), and mobile source air toxics (MSATs), such as benzene, formaldehyde, acetaldehyde, 1,3-butadiene, and lead
There is accumulating epidemiologic evidence that exposure to traffic-related air pollutants plays a role in etiology and prognosis of a large scale of illnesses, including asthma, impaired lung function, allergy, adverse birth outcomes, cardiovascular disease and cancer, the role of specific causal agents and underlying mechanisms for different health outcomes remains unknown [1]
Our results provide evidence that exposure to particulate polyaromatic hydro carbons (PAHs) in PM2.5 is a determinant of urinary 1-OHPG levels; urinary 1OHPG could serve as a biomarker of ambient exposure to PAHs
Summary
Traffic emissions include large quantities of carbon dioxide (CO2), carbon monoxide (CO), hydrocarbons (HC), nitrogen oxides (NOx), particulate matter (PM), and mobile source air toxics (MSATs), such as benzene, formaldehyde, acetaldehyde, 1,3-butadiene, and lead (where leaded gasoline is still in use). There is accumulating epidemiologic evidence that exposure to traffic-related air pollutants plays a role in etiology and prognosis of a large scale of illnesses, including asthma, impaired lung function, allergy, adverse birth outcomes, cardiovascular disease and cancer, the role of specific causal agents and underlying mechanisms for different health outcomes remains unknown [1]. There is accumulating epidemiologic evidence that exposure to traffic-related air pollutants, including particulate matter (PM) and polyaromatic hydro carbons (PAHs), plays a role in etiology and prognosis of a large scale of illnesses, the role of specific causal agents and underlying mechanisms for different health outcomes remains unknown
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