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Because people tend to move from one place to another during the day, their exposure to air pollution will be determined by the concentration at each location combined with the exposure encountered in transport. In order to estimate the exposure of individuals in a population more accurately, the activity-based modeling framework for Black Carbon exposure assessment, AB(2)C, was developed. An activity-based traffic model was applied to model the whereabouts of individual agents. Exposure to black carbon (BC) in different microenvironments is assessed with a land use regression model, combined with a fixed indoor/outdoor factor for exposure in indoor environments. To estimate exposure in transport, a separate model was used taking into account transport mode, timing of the trip and degree of urbanization. The modeling framework is validated using weeklong time-activity diaries and BC exposure as revealed from a personal monitoring campaign with 62 participants. For each participant in the monitoring campaign, a synthetic population of 100 model-agents per day was made up with all agents meeting similar preconditions as each real-life agent. When these model-agents pass through every stage of the modeling framework, it results in a distribution of potential exposures for each individual. The AB(2)C model estimates average personal exposure slightly more accurately compared to ambient concentrations as predicted for the home subzone; however the added value of a dynamic model lies in the potential for detecting short term peak exposures rather than modeling average exposures. The latter may bring new opportunities to epidemiologists: studying the effect of frequently repeated but short exposure peaks on long term exposure and health., (© 2013.)

Travel demand management (TDM) consists of a variety of policy measures that affect the transportation system's effectiveness by changing travel behavior. The primary objective to implement such TDM strategies is not to improve traffic safety, although their impact on traffic safety should not be neglected. The main purpose of this study is to evaluate the traffic safety impact of conducting a fuel-cost increase scenario (i.e. increasing the fuel price by 20%) in Flanders, Belgium. Since TDM strategies are usually conducted at an aggregate level, crash prediction models (CPMs) should also be developed at a geographically aggregated level. Therefore zonal crash prediction models (ZCPMs) are considered to present the association between observed crashes in each zone and a set of predictor variables. To this end, an activity-based transportation model framework is applied to produce exposure metrics which will be used in prediction models. This allows us to conduct a more detailed and reliable assessment while TDM strategies are inherently modeled in the activity-based models unlike traditional models in which the impact of TDM strategies are assumed. The crash data used in this study consist of fatal and injury crashes observed between 2004 and 2007. The network and socio-demographic variables are also collected from other sources. In this study, different ZCPMs are developed to predict the number of injury crashes (NOCs) (disaggregated by different severity levels and crash types) for both the null and the fuel-cost increase scenario. The results show a considerable traffic safety benefit of conducting the fuel-cost increase scenario apart from its impact on the reduction of the total vehicle kilometers traveled (VKT). A 20% increase in fuel price is predicted to reduce the annual VKT by 5.02 billion (11.57% of the total annual VKT in Flanders), which causes the total NOCs to decline by 2.83%., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Transportation policy measures often aim to change travel behaviour towards more efficient transport. While these policy measures do not necessarily target health, these could have an indirect health effect. We evaluate the health impact of a policy resulting in an increase of car fuel prices by 20% on active travel, outdoor air pollution and risk of road traffic injury. An integrated modelling chain is proposed to evaluate the health impact of this policy measure. An activity-based transport model estimated movements of people, providing whereabouts and travelled kilometres. An emission- and dispersion model provided air quality levels (elemental carbon) and a road safety model provided the number of fatal and non-fatal traffic victims. We used kilometres travelled while walking or cycling to estimate the time in active travel. Differences in health effects between the current and fuel price scenario were expressed in Disability Adjusted Life Years (DALY). A 20% fuel price increase leads to an overall gain of 1650 (1010-2330) DALY. Prevented deaths lead to a total of 1450 (890-2040) Years Life Gained (YLG), with better air quality accounting for 530 (180-880) YLG, fewer road traffic injuries for 750 (590-910) YLG and active travel for 170 (120-250) YLG. Concerning morbidity, mostly road safety led to 200 (120-290) fewer Years Lived with Disability (YLD), while air quality improvement only had a minor effect on cardiovascular hospital admissions. Air quality improvement and increased active travel mainly had an impact at older age, while traffic safety mainly affected younger and middle-aged people. This modelling approach illustrates the feasibility of a comprehensive health impact assessment of changes in travel behaviour. Our results suggest that more is needed than a policy rising car fuel prices by 20% to achieve substantial health gains. While the activity-based model gives an answer on what the effect of a proposed policy is, the focus on health may make policy integration more tangible. The model can therefore add to identifying win-win situations for both transport and health., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Persistent antigenic stimulation during chronic hepatitis C may alter the T-cell receptor variable chain beta (TCR BV) repertoire as well as the cytokine responses of hepatitis C virus (HCV)-specific T lymphocytes. We analysed the distribution of the TCR BV subsets 2.1, 3.1, 5.1, 6.1, 8, 13.1, 13.6, 14.1, 17.1, 21.3 in relation to intracytoplasmic expression of interleukin-2, interferon-gamma, interleukin-4 and interleukin-10. Using flow cytometry, CD45RO+ memory T cells of 27 patients with chronic hepatitis C, eight patients with resolved HCV infection and 16 non-HCV-related controls were studied with and without stimulation by the HCV core, NS3, NS4, NS5a and NS5b proteins. Patients with chronic and resolved hepatitis C differed by larger basal TCR BV2.1+, BV6.1+, BV17.1+ and BV21.3+ subsets in chronic hepatitis C, which were correlated to the numbers of T cells with spontaneous interleukin-2 and interferon-gamma production (r=0.51-0.73, P<0.05). Upon HCV-specific stimulation these subsets did not expand, whereas a marked in vitro expansion of TCR BV8+ T cells in response to all HCV proteins was selectively noted in chronic hepatitis C (P<0.05). This expansion of TCR BV8+ memory T cells was significantly correlated to HCV-induced interleukin-10 expression (r=0.58-0.98, P<0.01). Thus, differential involvement of selected TCR BV subsets may be related to the outcome of HCV infection.

Parenteral transmission of HCV is well established but other possible routes such as heterosexual transmission are still questioned. The Central African region is characterised by a high HCV endemicity without any evidence on the route of transmission. The information on HCV genotypes that circulate in this area is also limited and controversial. HIV infection is very frequent in this region and mostly acquired via the heterosexual route. The aim of this work was to investigate the trend of HCV infection and genotypes among HIV high-risk groups from Cameroon. Four hundred eighty-two patients including 229 tuberculosis clinic attendants, 184 sexually transmitted disease clinic attendants, and 69 HIV clinical suspects from another clinic were enrolled. All plasma samples were screened for antibodies to HCV and HCV RNA. Genotypes were assigned by sequencing a 5'UTR amplified fragment. The overall prevalence of HCV markers was 11.6% and a significant increasing trend with respect to age was observed. A proportion of 64.1% (34/53) of HCV antibody positive samples was viraemic. HCV RNA was found in 3 samples that were indeterminate in RIBA 3.0. One was negative in the antibody screening test and the two others were weakly positive. The data on HCV genotypes revealed that genotype 1 was involved in 57% of viraemias, genotype 2 in 24%, while genotypes 4 and 5a accounted for 16 and 3%, respectively. In contrary to the predominance of genotype 4 reported in some African countries and even the neighbouring countries, these data demonstrate clearly that HCV infection in Cameroon is dominated by genotypes 1 and 2. No association was found between the HCV markers and the presence of HIV infection. It is concluded, therefore, that the heterosexual route plays a minor role in HCV transmission in this country., (Copyright 2002 Wiley-Liss, Inc.)

Objective: Epidemiological data indicate that hepatitis C virus (HCV) infection runs a more rapid and severe course of disease in HIV-coinfected patients, probably because of an altered immune response., Design: We investigated whether HCV-specific cytokine responses are affected by HIV coinfection., Methods: Using triple colour flow cytometry on peripheral blood lymphocytes after stimulation with the four major immunodominant HCV core T cell epitopes, CT1-CT4, we determined intracytoplasmic production of IFN-gamma, IL-2, IL-4, IL-10 and CD30 expression, a putative surrogate marker of type 2 cells. Fifteen patients with asymptomatic HIV/HCV coinfection (group A), 15 patients with chronic HCV infection (group B) and 10 HIV-infected patients without hepatitis C (group C) were included in the study., Results: In group A, HCV antigens induced significantly higher IL-2 and IFN-gamma production than groups B and C (P < 0.05). Groups A and B showed a similar induction of CD30, which was significantly higher than in group C (P < 0.001). Remarkably, in group A HCV antigens induced IL-4 production in addition to IL-10 and IFN-gamma in the CD30 subset, whereas in groups B and C no IL-4 induction was observed in this T cell subset (P < 0.002)., Conclusion: Our data suggest that asymptomatic HIV coinfection importantly alters the HCV-specific cytokine response towards a greater production of proinflammatory type 1 cytokines. Moreover, the antiviral activity of type 1 cytokines may be modified by an increased production of type 2 cytokines in the CD30 subset. The altered cytokine pattern may contribute to the adverse natural course of hepatitis C in HIV coinfection.