Health Impact Assessment of Volcanic Ash Inhalation: A Comparison With Outdoor Air Pollution Methods.

This paper critically appraises the extrapolation of concentration-response functions (CRFs) for fine and coarse particulate matter, PM2.5 and PM10, respectively, used in outdoor air pollution health impact assessment (HIA) studies to assess the extent of health impacts in communities exposed to volcanic emissions. Treating volcanic ash as PM, we (1) consider existing models for HIA for general outdoor PM, (2) identify documented health effects from exposure to ash in volcanic eruptions, (3) discuss potential issues of applying CRFs based on the composition and concentration of ash-related PM, and (4) critically review available case studies of volcanic exposure scenarios utilizing HIA for outdoor air pollution. We identify a number of small-scale studies focusing on populations exposed to volcanic ash; exposure is rarely quantified, and there is limited evidence concerning the health effects of PM from volcanic eruptions. That limited evidence is, however, consistent with the CRFs typically used for outdoor air pollution HIA. Two health assessments of exposure to volcanic emissions have been published using population- and occupational-based CRFs, though each application entails distinct assumptions and limitations. We conclude that the best available strategy, at present, is to apply outdoor air pollution risk estimates to scenarios involving volcanic ash emissions for the purposes of HIA. However, due to the knowledge gaps on, for example, the health effects from exposure to volcanic ash and differences in ash composition, there is inherent uncertainty in this application. To conclude, we suggest actions to enable better prediction and assessment of health impacts of volcanic emissions.

Health impact assessment of transport policies in Rotterdam: Decrease of total traffic and increase of electric car use.

BACKGROUND: Green house gas (GHG) mitigation policies can be evaluated by showing their co-benefits to health. METHOD: Health Impact Assessment (HIA) was used to quantify co-benefits of GHG mitigation policies in Rotterdam. The effects of two separate interventions (10% reduction of private vehicle kilometers and a share of 50% electric-powered private vehicle kilometers) on particulate matter (PM2.5), elemental carbon (EC) and noise (engine noise and tyre noise) were assessed using Years of Life Lost (YLL) and Years Lived with Disability (YLD). The baseline was 2010 and the end of the assessment 2020. RESULTS: The intervention aimed at reducing traffic is associated with a decreased exposure to noise resulting in a reduction of 21 (confidence interval (CI): 11-129) YLDs due to annoyance and 35 (CI: 20-51) YLDs due to sleep disturbance for the population per year. The effects of 50% electric-powered car use are slightly higher with a reduction of 26 (CI: 13-116) and 41 (CI: 24-60) YLDs, respectively. The two interventions have marginal effects on air pollution, because already implemented traffic policies will reduce PM2.5 and EC by around 40% and 60% respectively, from 2010 to 2020. DISCUSSION: The evaluation of planned interventions, related to climate change policies, targeting only the transport sector can result in small co-benefits for health, if the analysis is limited to air pollution and noise. This urges to expand the analysis by including other impacts, e.g. physical activity and well-being, as a necessary step to better understanding consequences of interventions and carefully orienting resources useful to build knowledge to improve public health.

Suitability of human and mammalian cells of different origin for the assessment of genotoxicity of metal and polymeric engineered nanoparticles.

Nanogenotoxicity is a crucial endpoint in safety testing of nanomaterials as it addresses potential mutagenicity, which has implications for risks of both genetic disease and carcinogenesis. Within the NanoTEST project, we investigated the genotoxic potential of well-characterised nanoparticles (NPs): titanium dioxide (TiO2) NPs of nominal size 20 nm, iron oxide (8 nm) both uncoated (U-Fe3O4) and oleic acid coated (OC-Fe3O4), rhodamine-labelled amorphous silica 25 (Fl-25 SiO2) and 50 nm (Fl-50 SiO) and polylactic glycolic acid polyethylene oxide polymeric NPs - as well as Endorem® as a negative control for detection of strand breaks and oxidised DNA lesions with the alkaline comet assay. Using primary cells and cell lines derived from blood (human lymphocytes and lymphoblastoid TK6 cells), vascular/central nervous system (human endothelial human cerebral endothelial cells), liver (rat hepatocytes and Kupffer cells), kidney (monkey Cos-1 and human HEK293 cells), lung (human bronchial 16HBE14o cells) and placenta (human BeWo b30), we were interested in which in vitro cell model is sufficient to detect positive (genotoxic) and negative (non-genotoxic) responses. All in vitro studies were harmonized, i.e. NPs from the same batch, and identical dispersion protocols (for TiO2 NPs, two dispersions were used), exposure time, concentration range, culture conditions and time-courses were used. The results from the statistical evaluation show that OC-Fe3O4 and TiO2 NPs are genotoxic in the experimental conditions used. When all NPs were included in the analysis, no differences were seen among cell lines - demonstrating the usefulness of the assay in all cells to identify genotoxic and non-genotoxic NPs. The TK6 cells, human lymphocytes, BeWo b30 and kidney cells seem to be the most reliable for detecting a dose-response.

Using PM2.5 concentrations to estimate the health burden from solid fuel combustion, with application to Irish and Scottish homes.

BACKGROUND: This study estimates the potential population health burden from exposure to combustion-derived particulate air pollution in domestic settings in Ireland and Scotland. METHODS: The study focused on solid fuel combustion used for heating and the use of gas for cooking. PM2.5 (particulate matter with an aerodynamic diameter < 2.5 µm) was used as the pollutant mixture indicator. Measured PM2.5 concentrations in homes using solid fuels were adjusted for other sources of PM2.5 by subtracting PM2.5 concentrations in homes using gas for cooking but not solid fuel heating. Health burden was estimated for exposure indoors 6 pm - midnight, or all day (24-hour), by combining estimated attributable annual PM2.5 exposures with (i) selected epidemiological functions linking PM2.5 with mortality and morbidity (involving some re-scaling from PM10 to PM2.5, and adjustments 'translating' from concentrations to exposures) and (ii) on the current population exposed and background rates of morbidity and mortality. RESULTS: PM2.5 concentrations in coal and wood burning homes were similar to homes using gas for cooking, used here as a baseline (mean 24-hr PM2.5 concentrations 8.6 µg/m3) and so health impacts were not calculated. Concentrations of PM2.5 in homes using peat were higher (24-hr mean 15.6 µg/m3); however, health impacts were calculated for the exposed population in Ireland only; the proportion exposed in Scotland was very small. The assessment for winter evening exposure (estimated annual average increase of 2.11 µg/m3 over baseline) estimated 21 additional annual cases of all-cause mortality, 55 of chronic bronchitis, and 30,100 and 38,000 annual lower respiratory symptom days (including cough) and restricted activity days respectively. CONCLUSION: New methods for estimating the potential health burden of combustion-generated pollution from solid fuels in Irish and Scottish homes are provided. The methodology involves several approximations and uncertainties but is consistent with a wider movement towards quantifying risks in PM2.5 irrespective of source. Results show an effect of indoor smoke from using peat (but not wood or coal) for heating and cooking; but they do not suggest that this is a major public health issue.

Costs of occupational asthma in the UK.

OBJECTIVES: To estimate the social costs of occupational asthma in the UK. METHODS: A desk-top approach using cost-of-illness methodology was employed, defining direct and indirect lifetime costs for six scenarios: a male and a female worker each exposed to isocyanates, latex and biocides (eg, glutaraldehyde) or flour. The numbers of new cases annually in each industry were estimated from Survey of Work-related and Occupational Respiratory Disease (SWORD) data. The main outcome measure was the current value total working lifetime costs of new cases annually for each scenario. RESULTS: Assuming 209 new cases of occupational asthma in the six scenarios in the year 2003, the present value total lifetime costs were estimated to be £25.3-27.3 million (2004 prices). Grossing up for all estimated cases of occupational asthma in the UK in 2003, this came to £70-100 million. About 49% of these costs were borne by the individual, 48% by the state and 3% by the employer. CONCLUSIONS: The cost to society of occupational asthma in the UK is high. Given that the number of newly diagnosed cases is likely to be underestimated by at least one-third, these costs may be as large as £95-135 million. Each year a new stream of lifetime costs will be added as a newly diagnosed cohort is identified. Approaches to reduce the burden of occupational asthma have a strong economic justification. However, the economic burden falls on the state and the individual, not on the employer. The incentive for employers to act is thus weak.