Characterising professional drivers’ exposure to traffic-related air pollution: Evidence for reduction strategies from in-vehicle personal exposure monitoring

Professional drivers working in congested urban areas are required to work near harmful traffic related pollutants for extended periods, representing a significant, but understudied occupational risk. This study collected personal black carbon (BC) exposures for 141 drivers across seven sectors in London. The aim of the study was to assess the magnitude and the primary determinants of their exposure, leading to the formulation of targeted exposure reduction strategies for the occupation. Each participant’s personal BC exposures were continuously measured using real-time monitors for 96 h, incorporating four shifts per participant. ‘At work’ BC exposures (3.1 ± 3.5 µg/m3) were 2.6 times higher compared to when ‘not at work’ (1.2 ± 0.7 µg/m3). Workers spent 19% of their time ‘at work driving’, however this activity contributed 36% of total BC exposure, highlighting the disproportionate effect driving had on their daily exposure. Taxi drivers experienced the highest BC exposures due to the time they spent working in congested central London, while emergency services had the lowest. Spikes in exposure were observed while driving and were at times greater than 100 µg/m3. The most significant determinants of drivers’ exposures were driving in tunnels, congestion, location, day of week and time of shift. Driving with closed windows significantly reduced exposures and is a simple behaviour change drivers could implement. Our results highlight strategies by which employers and local policy makers can reduce professional drivers’ exposure to traffic-related air pollution

Combustion of dried animal dung as biofuel results in the generation of highly redox active fine particulates.

BACKGROUND: The burning of biomass in the developing world for heating and cooking results in high indoor particle concentrations. Long-term exposure to airborne particulate matter (PM) has been associated with increased rates of acute respiratory infections, chronic obstructive lung disease and cancer. In this study we determined the oxidative activity of combustion particles derived from the biomass fuel dung cake by examining their capacity to deplete antioxidants from a model human respiratory tract lining fluid (RTLF). For comparison, the observed oxidative activity was compared with that of particles derived from industrial and vehicular sources. RESULTS: Incubation of the dung cake particle suspensions in the RTLF for 4 h resulted in a mean loss of ascorbate of 72.1 +/- 0.7 and 89.7 +/- 2.5% at 50 and 100 microg/ml, respectively. Reduced glutathione was depleted by 49.6 +/- 4.3 and 63.5 +/- 22.4% under the same conditions. The capacity of these samples to deplete ascorbate was in excess of that observed with diesel or gasoline particles, but comparable to that seen with residual oil fly ash and considerably in excess of all three control particles in terms of glutathione depletion. Co-incubation with the metal chelator diethylenetriaminepentaacetate inhibited these losses, whilst minimal inhibition was seen with superoxide dismutase and catalase treatment. The majority of the activity observed appeared to be contained within aqueous particle extracts. CONCLUSION: These data demonstrate that biomass derived particles have considerable oxidative activity, largely attributable to their transition metal content

HIPTox—Hazard Identification Platform to Assess the Health Impacts from Indoor and Outdoor Air Pollutant Exposures, through Mechanistic Toxicology:A Single-Centre Double-Blind Human Exposure Trial Protocol

Over the past decade, our understanding of the impact of air pollution on short- and long-term population health has advanced considerably, focusing on adverse effects on cardiovascular and respiratory systems. There is, however, increasing evidence that air pollution exposures affect cognitive function, particularly in susceptible groups. Our study seeks to assess and hazard rank the cognitive effects of prevalent indoor and outdoor pollutants through a single-centre investigation on the cognitive functioning of healthy human volunteers aged 50 and above with a familial predisposition to dementia. Participants will all undertake five sequential controlled exposures. The sources of the air pollution exposures are wood smoke, diesel exhaust, cleaning products, and cooking emissions, with clean air serving as the control. Pre- and post-exposure spirometry, nasal lavage, blood sampling, and cognitive assessments will be performed. Repeated testing pre and post exposure to controlled levels of pollutants will allow for the identification of acute changes in functioning as well as the detection of peripheral markers of neuroinflammation and neuronal toxicity. This comprehensive approach enables the identification of the most hazardous components in indoor and outdoor air pollutants and further understanding of the pathways contributing to neurodegenerative diseases. The results of this project have the potential to facilitate greater refinement in policy, emphasizing health-relevant pollutants and providing details to aid mitigation against pollutant-associated health risks

The potential of omics approaches to elucidate mechanisms of biodiesel-induced pulmonary toxicity.

BACKGROUND: Combustion of biodiesels in place of fossil diesel (FD) has been proposed as a method of reducing transport-related toxic emissions in Europe. While biodiesel exhaust (BDE) contains fewer hydrocarbons, total particulates and carbon monoxide than FD exhaust (FDE), its high nitrogen oxide and ultrafine particle content may still promote pulmonary pathophysiologies. MAIN BODY: Using a complement of in vitro and in vivo studies, this review documents progress in our understanding of pulmonary responses to BDE exposure. Focusing initially on hypothesis-driven, targeted analyses, the merits and limitations of comparing BDE-induced responses to those caused by FDE exposure are discussed within the contexts of policy making and exploration of toxicity mechanisms. The introduction and progression of omics-led workflows are also discussed, summarising the novel insights into mechanisms of BDE-induced toxicity that they have uncovered. Finally, options for the expansion of BDE-related omics screens are explored, focusing on the mechanistic relevance of metabolomic profiling and offering rationale for expansion beyond classical models of pulmonary exposure. CONCLUSION: Together, these discussions suggest that molecular profiling methods have identified mechanistically informative, novel and fuel-specific signatures of pulmonary responses to biodiesel exhaust exposure that would have been difficult to detect using traditional, hypothesis driven approaches alone

Urban particulate matter stimulation of human dendritic cells enhances priming of naive CD8 T lymphocytes

Wellcome Trust. Grant Number: 098882/Z/12/Z National Institute for Health Research (NIHR

Assessing the exposure and hazard of diesel exhaust in professional drivers: a review of the current state of knowledge

It is well-established that traffic-related air pollution has a detrimental impact on health. Much of the focus has been on diesel exhaust emissions due to a rapid increase in vehicle numbers and studies finding that this pollutant is carcinogenic. Unsurprisingly, the highest diesel exposures that the general population experiences are during urban daily commutes; however, few studies have considered professional drivers who are chronically exposed to the pollutant due to their work in transport microenvironments. In this narrative review, we address the literature on professional drivers’ exposure to diesel exhaust and advocate that a modern exposure science approach utilised in commuter personal exposure studies is needed. This type of evaluation will provide a more detailed understanding of the time-activity of professional drivers’ exposures which is required to identify specific interventions to reduce their risk to diesel exhaust emissions

Putting fine particulate matter and dementia in the wider context of noncommunicable disease : where are we now and what should we do next : a systematic review

Introduction: A significant proportion of the global population regularly experience air quality poorer than that recommended by the World Health Organization. Air pollution, especially fine particulate matter (PM2.5), is a risk factor for various noncommunicable diseases (NCDs) and is emerging as a risk factor for dementia. To begin to understand the full impact of PM2.5, we review the longitudinal epidemiological evidence linking PM2.5 to both dementia and to other leading NCDs and highlight the evidence gaps. Our objective was to systematically review the current epidemiological evidence for PM2.5 as a risk factor for cognitive decline and incident dementia and to put this in context with a systematic overview of PM2.5 as a potential risk factor in other leading NCDs. Methods: We performed 2 systematic reviews. A high-level review of reviews examining the relationship between PM2.5 and leading NCDs and an in-depth review of the longitudinal epidemiological data examining relationships between PM2.5 incident dementia and cognitive decline. Results: There were robust associations between PM2.5 and NCDs although in some cases the evidence was concentrated on short rather than longer term exposure. For those articles reporting on incident dementia, all reported on longer term exposure and 5 of the 7 eligible articles found PM2.5 to be associated with increased risk. Conclusion: The evidence base for PM2.5 as a risk factor for dementia is growing. It is not yet as strong as that for other NCDs. However, varied measurement/methodology hampers clarity across the field. We propose next steps

Air pollution and dementia: A systematic review

BACKGROUND: Both air pollution and dementia are current and growing global issues. There are plausible links between exposure to specific air pollutants and dementia. OBJECTIVE: To systematically review the evidence base with respect to the relationship between air pollution and later cognitive decline and dementia. METHODS: Medline, Embase, and PsychINFO® were searched from their inception to September 2018, for publications reporting on longitudinal studies of exposure to air pollution and incident dementia or cognitive decline in adults. Studies reporting on exposure to tobacco smoke including passive smoking or on occupational exposure to pollutants were excluded. Using standard Cochrane methodology, two readers identified relevant abstracts, read full text publications, and extracted data into structured tables from relevant papers, as defined by inclusion and exclusion criteria. Papers were also assessed for validity. CRD42018094299Results:From 3,720 records, 13 papers were found to be relevant, with studies from the USA, Canada, Taiwan, Sweden, and the UK. Study follow-up ranged from one to 15 years. Pollutants examined included particulate matter ≤2.5 μ (PM2.5), nitrogen dioxide (NO2), nitrous oxides (NOx), carbon monoxide (CO), and ozone. Studies varied in their methodology, population selection, assessment of exposure to pollution, and method of cognitive testing. Greater exposure to PM2.5, NO2/NOx, and CO were all associated with increased risk of dementia. The evidence for air pollutant exposure and cognitive decline was more equivocal. CONCLUSION: Evidence is emerging that greater exposure to airborne pollutants is associated with increased risk of dementia