Traffic-Related Air Pollution and DNA Damage: A Longitudinal Study in Taiwanese Traffic Conductors

BACKGROUND: 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, although the role of specific causal agents and underlying mechanisms for different health outcomes remains unknown. OBJECTIVE: Our general objective was to assess the relations between personal exposure to traffic exhausts, in particular ambient PM(2.5) 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). METHODS: We recruited 91 traffic conductors and 53 indoor office workers between May 2009 and June 2011 in Taipei City, Taiwan. We used PM(2.5) 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. RESULTS: Urinary 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 PM(2.5) with reference to the induction of oxidative DNA damages

Biomonitoring of complex occupational exposures to carcinogens: The case of sewage workers in Paris

<p>Abstract</p> <p>Background</p> <p>Sewage workers provide an essential service in the protection of public and environmental health. However, they are exposed to varied mixtures of chemicals; some are known or suspected to be genotoxics or carcinogens. Thus, trying to relate adverse outcomes to single toxicant is inappropriate. We aim to investigate if sewage workers are at increased carcinogenic risk as evaluated by biomarkers of exposure and early biological effects.</p> <p>Methods/design</p> <p>This cross sectional study will compare exposed sewage workers to non-exposed office workers. Both are voluntaries from Paris municipality, males, aged (20–60) years, non-smokers since at least six months, with no history of chronic or recent illness, and have similar socioeconomic status. After at least 3 days of consecutive work, blood sample and a 24-hour urine will be collected. A caffeine test will be performed, by administering coffee and collecting urines three hours after. Subjects will fill in self-administered questionnaires; one covering the professional and lifestyle habits while the a second one is alimentary. The blood sample will be used to assess DNA adducts in peripheral lymphocytes. The 24-hour urine to assess urinary 8-oxo-7, 8-dihydro-2'-deoxy-Guanosine (8-oxo-dG), and the in vitro genotoxicity tests (comet and micronucleus) using HeLa S3 or HepG2 cells. In parallel, occupational air sampling will be conducted for some Polycyclic Aromatic Hydrocarbons and Volatile Organic Compounds. A weekly sampling chronology at the offices of occupational medicine in Paris city during the regular medical visits will be followed. This protocol has been accepted by the French Est III Ethical Comitee with the number 2007-A00685-48.</p> <p>Discussion</p> <p>Biomarkers of exposure and of early biological effects may help overcome the limitations of environmental exposure assessment in very complex occupational or environmental settings.</p

Cardiovascular health and particulate vehicular emissions: a critical evaluation of the evidence

A major public health goal is to determine linkages between specific pollution sources and adverse health outcomes. This paper provides an integrative evaluation of the database examining effects of vehicular emissions, such as black carbon (BC), carbonaceous gasses, and ultrafine PM, on cardiovascular (CV) morbidity and mortality. Less than a decade ago, few epidemiological studies had examined effects of traffic emissions specifically on these health endpoints. In 2002, the first of many studies emerged finding significantly higher risks of CV morbidity and mortality for people living in close proximity to major roadways, vs. those living further away. Abundant epidemiological studies now link exposure to vehicular emissions, characterized in many different ways, with CV health endpoints such as cardiopulmonary and ischemic heart disease and circulatory-disease-associated mortality; incidence of coronary artery disease; acute myocardial infarction; survival after heart failure; emergency CV hospital admissions; and markers of atherosclerosis. We identify numerous in vitro, in vivo, and human panel studies elucidating mechanisms which could explain many of these cardiovascular morbidity and mortality associations. These include: oxidative stress, inflammation, lipoperoxidation and atherosclerosis, change in heart rate variability (HRV), arrhythmias, ST-segment depression, and changes in vascular function (such as brachial arterial caliber and blood pressure). Panel studies with accurate exposure information, examining effects of ambient components of vehicular emissions on susceptible human subjects, appear to confirm these mechanisms. Together, this body of evidence supports biological mechanisms which can explain the various CV epidemiological findings. Based upon these studies, the research base suggests that vehicular emissions are a major environmental cause of cardiovascular mortality and morbidity in the United States. As a means to reduce the public health consequences of such emissions, it may be desirable to promulgate a black carbon (BC) PM2.5 standard under the National Ambient Air Quality Standards, which would apply to both on and off-road diesels. Two specific critical research needs are identified. One is to continue research on health effects of vehicular emissions, gaseous as well as particulate. The second is to utilize identical or nearly identical research designs in studies using accurate exposure metrics to determine whether other major PM pollutant sources and types may also underlie the specific health effects found in this evaluation for vehicular emissions

Is a quantitative risk assessment of air quality in underground parking garages possible?

International audienceLittle information is available about the health risks associated with time spent in underground parking garages. The objective of this study was to determine whether it is possible to quantify the health risks associated with these garages without epidemiologic data on the subject. We followed the standard procedure for health risk assessment. We searched the literature for pollutant concentrations in the air samples of underground parking garages, the hazards associated with their inhalation, and their toxicological reference values. Conditions of occupational and user exposure were estimated by scenarios and taken into account to discuss toxicological reference values by modifying (with Haber's law) the adjustment factors for exposure frequency and duration. Risk quantification was possible for 39 pollutants. Acute exposures to CO and NO2 exceed toxicological reference values, as does chronic exposure to benzene for threshold effects. The risk of a carcinogenic effect associated with benzene may be greater than 10(-5). Excess exposure to air pollution indicators (PM and NO2) is also elevated, judging by the WHO Air Quality Guidelines, and also when comparing to levels with reported effects in epidemiologic studies. The risk associated with underground parking garages can be evaluated only in part. The information available is nonetheless sufficient to justify actions to reduce exposure. PRACTICAL IMPLICATIONS: The risks associated with exposure in underground parking garages cannot be thoroughly evaluated because of inadequate knowledge of exposures and of the toxicity of pollutants. The available knowledge is nonetheless sufficient to advise that risk management measures should be taken to reduce both acute and chronic exposures

Investigating the potential for interaction between the components of PM10

The adverse health effects of elevated exposures to PM10 (particulate matter collected through a size selective inlet with an efficiency of 50% for particles with an aerodynamic diameter of 10 μm) in relation to morbidity and mortality, especially in susceptible individuals, are now well recognised. PM10 consists of a variable cocktail of components differing in chemical composition and size. Epidemiological and toxicological data suggest that transition metals and ultrafine particles are both able to drive the cellular and molecular changes that underlie PM10-induced inflammation and so worsen disease status. Toxicological evidence also suggest roles for the biological components of PM10 including volatile organic compounds (VOC's), allergens and bacterial-derived endotoxin. Many of these components, in particular transition metals, ultrafine particles, endotoxin and VOC's induce a cellular oxidative stress which initiates an intracellular signaling cascade involving the activation of phosphatase and kinase enzymes as well as transcription factors such as nuclear factor kappa B. Activation of these signaling mechanisms results in an increase in the expression of proinflammatory mediators, and hence enhanced inflammation. Given that many of the components of PM10 stimulate similar or even identical intracellular signaling pathways, it is conceivable that this will result in synergistic or additive interactions so that the biological response induced by PM10 exposure is a response to the composition rather than the mass alone. A small number of studies suggest that synergistic interactions occur between ultrafine particles and transition metals, between particles and allergens, and between particles and VOC's. Elucidation of the consequences of interaction between the components of PM10 in relation to their biological activity implies huge consequences for the methods used to monitor and to legislate pollution exposure in the future, and may drive a move from mass based measurements to composition