Air pollution mortality benefits of sustained COVID-19 mobility restrictions in Australian cities.

OBJECTIVES: Emissions from road traffic, power generation and industry were substantially reduced during pandemic lockdown periods globally. Thus, we analysed reductions in traffic-related air pollution in Australian capital cities during March-April 2020 and then modelled the mortality benefits that could be realised if similar reductions were sustained by structural policy interventions. STUDY DESIGN: Satellite, air pollution monitor and land use observations were used to estimate ground-level nitrogen dioxide (NO2) concentrations in all Australian capital cities during: (a) a typical year with no prolonged air pollution events; (b) a hypothetical sustained reduction in NO2 equivalent to the COVID-19 lockdowns. METHODS: We use the WHO recommended NO2 exposure-response coefficient for mortality (1.023, 95 % CI: 1.008-1.037, per 10 µg/m3 annual average) to assess gains in life expectancy and population-wide years of life from reduced exposure to traffic-related air pollution. RESULTS: We attribute 1.1 % of deaths to anthropogenic NO2 exposures in Australian cities, corresponding to a total of 13,340 years of life lost annually. Although COVID-19-related reductions in NO2 varied widely between Australian cities during April 2020, equivalent and sustained reductions in NO2 emissions could reduce NO2-attributable deaths by 27 %, resulting in 3348 years of life gained annually. CONCLUSIONS: COVID-19 mobility restrictions reduced NO2 emissions and population-wide exposures in Australian cities. When sustained to the same extent by policy interventions that reduce fossil fuel consumption by favouring the uptake of electric vehicles, active travel and public transport, the health, mortality and economic benefits will be measurable in Australian cities.

The role of seasonal grass pollen on childhood asthma emergency department presentations.

BACKGROUND: Few studies have focused on the role of grass pollen on asthma emergency department (ED) presentations among children. None have examined whether a dose-response effect exists between grass pollen levels and these asthma exacerbations. OBJECTIVES: To examine the association between increasing ambient levels of grass pollen and asthma ED presentations in children. To determine whether these associations are seen only after a thunderstorm, or whether grass pollen levels have a consistent influence on childhood asthma ED visits during the season. METHODS: A short time series ecological study was conducted for asthma presentations to ED among children in Melbourne, Victoria, and grass pollen, meteorological and air quality measurements recorded during the selected 2003 period. A semi-parametric Poisson regression model was used to examine dose-response associations between daily grass pollen levels and mean daily ED attendance for asthma. RESULTS: A smoothed plot suggested a dose-response association. As ambient grass pollen increased to about 19 grains/m(3) , the same day risk of childhood ED presentations also increased linearly (P < 0.001). Grass pollen levels were also associated with an increased risk in asthma ED presentations on the following day (lag 1, P < 0.001). CONCLUSION: This is the first study to establish a clear relationship between increased risk of childhood asthma ED attendance and levels of ambient grass pollen below 20 grains/m(3) , independent of any impact of thunderstorm-associated asthma. These findings have important implications for patient care, such as asthma management programs that notify the general public regarding periods of high grass pollen exposure, as well as defining the timing of initiation of pollen immunotherapy.

Relationships between alumina and bauxite dust exposure and cancer, respiratory and circulatory disease.

OBJECTIVES: To examine the associations between alumina and bauxite dust exposure and cancer incidence and circulatory and respiratory disease mortality among bauxite miners and alumina refinery workers. METHODS: This cohort of 5770 males has previously been linked to national mortality and national and state cancer incidence registries (1983-2002). In this paper, Poisson regression was used to undertake internal comparisons within the cohort based on subgroups of cumulative exposure to inhalable bauxite and alumina dust. Exposure was estimated using job histories and historical air monitoring data. RESULTS: There was no association between ever bauxite exposure and any of the outcomes. There was a borderline significant association between ever alumina exposure and cerebrovascular disease mortality (10 deaths, RR 3.8, 95% CI 1.1 to 13). There was some evidence of an exposure-response relationship between cumulative bauxite exposure and non-malignant respiratory disease mortality (seven deaths, trend p value: 0.01) and between cumulative alumina exposure and cerebrovascular disease mortality (trend p value: 0.04). These associations were based on very few cases and for non-malignant respiratory disease the deaths represented a heterogeneous mixture of causes. There was no evidence of an excess risk for any cancer type with bauxite or alumina exposure. CONCLUSIONS: These preliminary findings, based on very few cases, suggest that cumulative inhalable bauxite exposure may be associated with an excess risk of death from non-malignant respiratory disease and that cumulative inhalable alumina dust exposure may be associated with an excess risk of death from cerebrovascular disease. Neither exposure appears to increase the risk of incident cancers.

A panel study of air pollution in subjects with heart failure: negative results in treated patients.

OBJECTIVES: To investigate preclinical adverse effects of ambient particulate air pollution and nitrogen oxides in patients with heart failure. METHODS: A cohort of 132 non-smoking patients living in Aberdeen, Scotland, with stable chronic heart failure were enrolled in a repeated-measures panel study. Patients with atrial fibrillation or pacemakers were excluded. Participants were studied for 3 days every 2 months for up to 1 year with monitoring of pollutant exposure and concurrent measurements of pathophysiological responses. Measurements included daily area concentration of particulate matter with a median aerodynamic diameter of <10 micrometres (PM(10)), particle number concentration (PNC) and nitrogen oxides; daily estimated personal concentration of particulate matter with a median aerodynamic diameter of <2.5 micrometres (PM(2.5)) and PNC exposures; and 3-day cumulative personal nitrogen dioxide (NO(2)). Concurrent meteorological data were recorded. Blood was taken at the end of each 3-day block for assays of markers of endothelial activation, inflammation and coagulation. Cardiac rhythm was monitored by ambulatory Holter monitor during the final 24 h of each block. RESULTS: The average 24 h background ambient PM(10) ranged from 7.4 to 68 microg.m(-3) and PNC from 454 to 11 283 particles.cm(-3). No associations were demonstrated between the incidence of arrhythmias, heart rate variability or haematological/biochemical measures and any variations in pollutant exposures at any lags. CONCLUSION: Assuming that low-level pollution affects the parameters measured, these findings may suggest a beneficial effect of modern cardioprotective therapy, which may modify responses to external risk factors. Widespread use of such drugs in susceptible populations may in future reduce the adverse effects of air pollution on the heart.

The London Underground: dust and hazards to health.

AIMS: To assess hazards associated with exposure to dust in the London Underground railway and to provide an informed opinion on the risks to workers and the travelling public of exposure to tunnel dust. METHODS: Concentrations of dust, as mass (PM2.5) and particle number, were measured at different underground stations and in train cabs; its size and composition were analysed; likely maximal exposures of staff and passengers were estimated; and in vitro toxicological testing of sample dusts in comparison with other dusts was performed. RESULTS: Concentrations on station platforms were 270-480 microg/m3 PM2.5 and 14,000-29,000 particles/cm3. Cab concentrations over a shift averaged 130-200 microg/m3 and 17,000-23,000 particles/cm3. The dust comprised by mass approximately 67% iron oxide, 1-2% quartz, and traces of other metals, the residue being volatile matter. The finest particles are drawn underground from the surface while the coarser dust is generated by interaction of brakes, wheels, and rails. Taking account of durations of exposure, drivers and station staff would have maximum exposures of about 200 microg/m3 over eight hours; the occupational exposure standard for welding fume, as iron oxide, is 5 mg/m3 over an eight hour shift. Toxicology showed the dust to have cytotoxic and inflammatory potential at high doses, consistent with its composition largely of iron oxide. DISCUSSION: It is unjustifiable to compare PM2.5 exposure underground with that on the surface, since the adverse effects of iron oxide and combustion generated particles differ. Concentrations of ultrafine particles are lower and of coarser (PM2.5) particles higher underground than on the surface. The concentrations underground are well below allowable workplace concentrations for iron oxide and unlikely to represent a significant cumulative risk to the health of workers or commuters.

Ultrafine particles and nitrogen oxides generated by gas and electric cooking.

OBJECTIVES: To measure the concentrations of particles less than 100 nm diameter and of oxides of nitrogen generated by cooking with gas and electricity, to comment on possible hazards to health in poorly ventilated kitchens. METHODS: Experiments with gas and electric rings, grills, and ovens were used to compare different cooking procedures. Nitrogen oxides (NO(x)) were measured by a chemiluminescent ML9841A NO(x) analyser. A TSI 3934 scanning mobility particle sizer was used to measure average number concentration and size distribution of aerosols in the size range 10-500 nm. RESULTS: High concentrations of particles are generated by gas combustion, by frying, and by cooking of fatty foods. Electric rings and grills may also generate particles from their surfaces. In experiments where gas burning was the most important source of particles, most particles were in the size range 15-40 nm. When bacon was fried on the gas or electric rings the particles were of larger diameter, in the size range 50-100 nm. The smaller particles generated during experiments grew in size with time because of coagulation. Substantial concentrations of NO(X) were generated during cooking on gas; four rings for 15 minutes produced 5 minute peaks of about 1000 ppb nitrogen dioxide and about 2000 ppb nitric oxide. CONCLUSIONS: Cooking in a poorly ventilated kitchen may give rise to potentially toxic concentrations of numbers of particles. Very high concentrations of oxides of nitrogen may also be generated by gas cooking, and with no extraction and poor ventilation, may reach concentrations at which adverse health effects may be expected. Although respiratory effects of exposure to NO(x) might be anticipated, recent epidemiology suggests that cardiac effects cannot be excluded, and further investigation of this is desirable.

Stimulation of IL-8 release from epithelial cells by gas cooker PM(10): a pilot study.

OBJECTIVE: To measure the effect of matter collected by a method that has a 50% efficiency for particles with an aerodynamic diameter of 10 microm (PM10), generated by gas and electric cooking, on A549 epithelial cells with and without nitrogen dioxide (NO2). METHOD: Multiple indoor PM10 samples were collected on Teflon filters during the use of gas or electric cookers. Interleukin-8 (IL-8) concentrations were measured with a sandwich enzyme linked immunosorbent assay (ELISA) system. RESULTS: Treatment of A549 cells with PM10 generated from gas cooking resulted in increased concentrations of IL-8 compared with untreated cells; particles from the electric cooker had no effect. NO2 did not alter the concentration of IL-8. CONCLUSION: PM10 generated by gas cooking has the potential to cause proinflammatory effects in lung cells. This may have implications for susceptible people.

Endotoxin exposure among softwood lumber mill workers in the Canadian province of British Columbia.

An increased prevalence of respiratory problems among softwood lumber mill workers has been observed in a number of studies. These workers are potentially exposed to a variety of respiratory hazards including wood dust, abietic or other resin acids, monoterpenes, and fungi, as well as endotoxins. The objectives of this study were to determine if lumber mill workers were exposed to hazardous levels of airborne endotoxin and to identify the factors contributing to high exposures. Personal endotoxin samples (n = 216) were collected in four lumber mills in the Canadian province of British Columbia. The mean personal exposure concentration was 2.09 ng/m.(3) and 9% of the samples were above 5 ng/m.(3). Factors related to the personal endotoxin exposure were type of job, use of compressed air, the percentage of time spent in a booth or cab during a shift, and dust concentration. Log storage practices were also suspected of playing a role. The levels of exposure observed in this study were low compared to the levels reported for populations with respiratory problems attributed to endotoxins.