Cardiac Autonomic Impacts of Bushfire Smoke-A Prospective Panel Study.

BACKGROUND: Air pollution is associated with cardiovascular disease and mortality. Most studies have focussed on urban or traffic-related pollution, and less is known about the impacts from bushfire smoke on cardiovascular autonomic function, although it is associated with increased sudden cardiac death and mortality. We sought to investigate its instantaneous and short-term impacts on heart rate variability (HRV). METHODS: Twenty-four (24)-hour Holter electrocardiography (ECG) was repeated twice (during bushfire [Phase 1] and then clean air [Phase 2]) in 32 participants from two Australian towns (Warburton and Traralgon, Victoria) surrounding planned burning areas. This was compared with 10 control participants in another town (Maffra, Victoria) with two clean air assessments during the same periods. The primary HRV parameters assessed were those assessing overall HRV (Standard Deviation of Normal-to-Normal intervals [SDNN]), long-term HRV (Standard Deviation of the Average of Normal Sinus-to-Normal Sinus intervals for each 5-minutes [SDANN]), low frequency [LF]) and short-term HRV (Root Mean Square of Successive Differences between N-N intervals [RMSSD], High Frequency [HF], LF:HF ratio). Average concentrations of particulate matter <2.5 µm in diameter (PM2.5) were measured at fixed site monitors in each location. RESULTS: Mean PM2.5 levels were significantly elevated during bushfire exposure in Warburton (96.5±57.7 µg/m3 vs 4.0±1.9 µg/m3, p<0.001) and Traralgon (12.6±4.9 µg/m3 vs 3.4±3.1 µg/m3, p<0.001), while it remained low in the control town, Maffra, in each phase (4.3±3.2 µg/m3 and 3.9±3.6 µg/m3, p=0.70). Although SDANN remained stable in controls, the exposed cohort showed significant worsening in SDANN during bushfire smoke exposure by 9.6±25.7ms (p=0.039). In univariable analysis, smoke exposure was significantly associated with higher ΔSDNN and ΔSDANN (p=0.03, p=0.01 exposed vs control). The association remained significant in ΔSDANN after adjusting for age, sex and cigarette smoking (p=0.02) and of borderline significance in ΔSDNN (p=0.06). CONCLUSIONS: Exposure to the bushfire smoke was independently associated with reduced overall and long-term HRV. Our findings suggest that imbalance in cardiac autonomic function is a key mechanism of adverse cardiovascular effects of bushfire smoke.

Predictive value of non-specific bronchial challenge testing for respiratory symptoms and lung function in aluminium smelter workers.

OBJECTIVE: To assess the predictive value of bronchial hyper-responsiveness (BHR) for the subsequent development of respiratory symptoms, airflow limitation and decline in lung function among aluminium smelter workers. METHODS: An inception cohort study of new employees at two Australian aluminium smelters was conducted. Participants completed a modified British Medical Research Council respiratory questionnaire, spirometry and a methacholine bronchial challenge test at baseline and at annual follow-up reviews. BHR was defined as PD20 ≤4000 µg. Poisson and mixed effects models were fitted to respiratory symptoms and lung function (forced expiratory volume in 1 s (FEV1) and FEV1/forced vital capacity (FVC)). RESULTS: Baseline interview and lung function testing were completed by 278 workers, who were followed for a median of 4 years. BHR at baseline, present in 82 workers, was not associated with incident wheeze risk ratio (RR)=1.07 (95% CI 0.74 to 1.55) and cough RR=0.78 (95% CI 0.45, 1.35), but there was some increased risk of chest tightness RR=1.40 (95% CI 0.99, 1.98) after adjustment for age, sex, smoking and atopy. BHR at baseline was associated with lower FEV1 and FVC, although the rate of annual decline in FEV1 or FVC was similar between those with or without BHR. The specificity of BHR was 77% for wheeze, 70% for cough and 77% for chest tightness, but the sensitivity was poor, at 33%, 24% and 39%, respectively. CONCLUSION: Methacholine challenge testing at entry to employment was not sufficiently predictive of later adverse respiratory outcomes, and notwithstanding the study limitations is unlikely to be a useful pre-employment or preplacement screening test in the aluminium smelting industry.

Respiratory outcomes among refinery workers exposed to inspirable alumina dust: A longitudinal study in Western Australia.

BACKGROUND: Information is scarce about the occupational health effects of exposure to alumina dust. This study examines the respiratory effects of inspirable alumina dust exposure in alumina refineries. METHODS: An inception cohort study at three alumina refineries in Western Australia recruited 416 participants (351 males, 65 females) between 1995 and 2000 who were followed up annually until 2008 or until exit from study. At each health interview a respiratory questionnaire and lung function test was undertaken, measuring forced expiratory volume in one second (FEV1 ) and forced vital capacity (FVC). Participants provided job histories which were combined with air monitoring data to calculate cumulative exposure to inspirable alumina dust (mg/m3 -years). Generalized estimating equations with Poisson distribution and mixed effects models were used to examine the effects of alumina exposure. RESULTS: The number of exposed participants was relatively small (n = 82, 19.7%). There was no association between alumina dust exposure and prevalence of cough, wheeze or rhinitis. No associations were found between measures of lung function and tertiles of alumina exposure in the first two follow-ups, or the whole follow-up period, though there was a suggestive dose-response trend across exposed groups for decline in absolute FEV1 (p for trend = .06). For mean annual change in FEV1 and FVC based on the first three follow-ups it was not possible to rule out an effect above a threshold level of exposure. CONCLUSION: There is no evidence of an association between exposure to alumina and the reporting of respiratory symptoms but some evidence for an effect on lung function.

Occupational exposure to solvents and lung function decline: A population based study.

RATIONALE: While cross-sectional studies have shown associations between certain occupational exposures and lower levels of lung function, there was little evidence from population-based studies with repeated lung function measurements. OBJECTIVES: We aimed to investigate the associations between occupational exposures and longitudinal lung function decline in the population-based Tasmanian Longitudinal Health Study. METHODS: Lung function decline between ages 45 years and 50 years was assessed using data from 767 participants. Using lifetime work history calendars completed at age 45 years, exposures were assigned according to the ALOHA plus Job Exposure Matrix. Occupational exposures were defined as ever exposed and cumulative exposure -unit- years. We investigated effect modification by sex, smoking and asthma status. RESULTS: Compared with those without exposure, ever exposures to aromatic solvents and metals were associated with a greater decline in FEV1 (aromatic solvents 15.5 mL/year (95% CI -24.8 to 6.3); metals 11.3 mL/year (95% CI -21.9 to - 0.7)) and FVC (aromatic solvents 14.1 mL/year 95% CI -28.8 to - 0.7; metals 17.5 mL/year (95% CI -34.3 to - 0.8)). Cumulative exposure (unit years) to aromatic solvents was also associated with greater decline in FEV1 and FVC. Women had lower cumulative exposure years to aromatic solvents than men (mean (SD) 9.6 (15.5) vs 16.6 (14.6)), but greater lung function decline than men. We also found association between ever exposures to gases/fumes or mineral dust and greater decline in lung function. CONCLUSIONS: Exposures to aromatic solvents and metals were associated with greater lung function decline. The effect of aromatic solvents was strongest in women. Preventive strategies should be implemented to reduce these exposures in the workplace.

Ambient Particulate Matter and Paramedic Assessments of Acute Diabetic, Cardiovascular, and Respiratory Conditions.

BACKGROUND: Ambulance data provide a useful source of population-based and spatiotemporally resolved information for assessing health impacts of air pollution in nonhospital settings. We used the clinical records of paramedics to quantify associations between particulate matter (PM2.5) and diabetic, cardiovascular, and respiratory conditions commonly managed by those responding to calls for emergency ambulance services. METHODS: We evaluated 394,217 paramedic assessments from three states in Southeastern Australia (population 13.2 million) and daily PM2.5 concentrations modeled at 5 km resolution from 2009 to 2014. We used a time-stratified, case-crossover analysis adjusted for daily meteorology to estimate the odds ratios (ORs) and 95% confidence intervals (CIs) for each clinical outcome per 10 µg/m increase in daily PM2.5 at lags from 0 to 2 days. RESULTS: Increased PM2.5 was associated with increased odds of paramedic assessments of hypoglycemia (OR = 1.07; 95% CI = 1.02, 1.12, lag 0), arrhythmia (OR = 1.05; 95% CI = 1.02, 1.09, lag 0), heart failure (OR = 1.07; 95% CI = 1.02, 1.12, lag 1), faint (OR = 1.09; 95% CI = 1.04-1.13, lag 0), asthma (OR = 1.06; 95% CI = 1.01, 1.11, lag 1), chronic obstructive pulmonary disease (OR = 1.07; 95% CI = 1.01, 1.13, lag 1), and croup (OR = 1.09; 95% CI = 1.02, 1.17). We did not identify associations with cerebrovascular outcomes. CONCLUSIONS: Ambulance data enable the evaluation of important clinical syndromes that are often initially managed in nonhospital settings. Daily PM2.5 was associated with hypoglycemia, faint, and croup in addition to the respiratory and cardiovascular outcomes that are better established.

A statistical downscaling approach for generating high spatial resolution health risk maps: a case study of road noise and ischemic heart disease mortality in Melbourne, Australia.

INTRODUCTION: Road traffic noise increases the risk of mortality from ischemic heart disease (IHD). Because noise is highly localized, high resolution maps of exposures and health outcomes are key to urban planning interventions that are informed by health risks. In Australia, publicly accessible IHD deaths data are only available at the coarse spatial aggregation level of local government area (LGA), in which about 130,000 people reside. Herein, we addressed this limitation of health data using statistical downscaling and generated environmental health risk maps for noise at the meshblock level (MB; ~ 90 people). METHODS: We estimated noise exposures at the MB level using a model of road traffic noise in Melbourne, Australia, from 2011. As recommended by the World Health Organization, a non-linear exposure-response function for traffic noise and IHD was used to calculate odds ratios for noise related IHD in all MBs. Noise attributable risks of IHD death were then estimated by statistically downscaling LGA-level IHD rates to the MB level. RESULTS: Noise levels of 80 dB were recorded in some MBs. From the given noise maps, approximately 5% of the population was exposed to traffic noise above the risk threshold of 55 dB. Maps of excess risk at the MB level identified areas in which noise levels and exposed populations are large. Attributable rates of IHD deaths due to noise were generally very low, but some were as high as 5-10 per 100,000, and in extremely noisy and populated MBs represented more than 8% excess risk of IHD death. We presented results as interactive maps of excess risk due to noise at the small neighbourhood scale. CONCLUSION: Our method accommodates low-resolution health data and could be used to inform urban planning and public health decision making for various environmental health concerns. Estimated noise related IHD deaths were relatively few in Melbourne in 2011, likely because road traffic is one of many noise sources and the current noise model underestimates exposures. Nonetheless, this novel computational framework could be used globally to generate maps of noise related health risks using scant health outcomes data.

Traffic-related air pollution exposure is associated with allergic sensitization, asthma, and poor lung function in middle age.

BACKGROUND: Traffic-related air pollution (TRAP) exposure is associated with allergic airway diseases and reduced lung function in children, but evidence concerning adults, especially in low-pollution settings, is scarce and inconsistent. OBJECTIVES: We sought to determine whether exposure to TRAP in middle age is associated with allergic sensitization, current asthma, and reduced lung function in adults, and whether these associations are modified by variants in Glutathione S-Transferase genes. METHODS: The study sample comprised the proband 2002 laboratory study of the Tasmanian Longitudinal Health Study. Mean annual residential nitrogen dioxide (NO2) exposure was estimated for current residential addresses using a validated land-use regression model. Associations between TRAP exposure and allergic sensitization, lung function, current wheeze, and asthma (n = 1405) were investigated using regression models. RESULTS: Increased mean annual NO2 exposure was associated with increased risk of atopy (adjusted odds ratio [aOR], 1.14; 95% CI, 1.02-1.28 per 1 interquartile range increase in NO2 [2.2 ppb]) and current wheeze (aOR, 1.14; 1.02-1.28). Similarly, living less than 200 m from a major road was associated with current wheeze (aOR, 1.38; 95% CI, 1.06-1.80) and atopy (aOR, 1.26; 95% CI, 0.99-1.62), and was also associated with having significantly lower prebronchodilator and postbronchodilator FEV1 and prebronchodilator forced expiratory flow at 25% to 75% of forced vital capacity. We found evidence of interactions between living less than 200 m from a major road and GSTT1 polymorphism for atopy, asthma, and atopic asthma. Overall, carriers of the GSTT1 null genotype had an increased risk of asthma and allergic outcomes if exposed to TRAP. CONCLUSIONS: Even relatively low TRAP exposures confer an increased risk of adverse respiratory and allergic outcomes in genetically susceptible individuals.

Occupational exposure to pesticides are associated with fixed airflow obstruction in middle-age.

RATIONALE: Population-based studies have found evidence of a relationship between occupational exposures and Chronic Obstructive Pulmonary Disease (COPD), but these studies are limited by the use of prebronchodilator spirometry. Establishing this link using postbronchodilator is critical, because occupational exposures are a modifiable risk factor for COPD. OBJECTIVES: To investigate the associations between occupational exposures and fixed airflow obstruction using postbronchodilator spirometry. METHODS: One thousand three hundred and thirty-five participants were included from 2002 to 2008 follow-up of the Tasmanian Longitudinal Health Study (TAHS). Spirometry was performed and lifetime work history calendars were used to collect occupational history. ALOHA plus Job Exposure Matrix was used to assign occupational exposure, and defined as ever exposed and cumulative exposure unit (EU)-years. Fixed airflow obstruction was defined by postbronchodilator FEV1/FVC <0.7 and the lower limit of normal (LLN). Multinomial logistic regressions were used to investigate potential associations while controlling for possible confounders. RESULTS: Ever exposure to biological dust (relative risk (RR)=1.58, 95% CI 1.01 to 2.48), pesticides (RR=1.74,95% CI 1.00 to 3.07) and herbicides (RR=2.09,95% CI 1.18 to 3.70) were associated with fixed airflow obstruction. Cumulative EU-years to all pesticides (RR=1.11,95% CI 1.00 to 1.25) and herbicides (RR=1.15,95% CI 1.00 to 1.32) were also associated with fixed airflow obstruction. In addition, all pesticides exposure was consistently associated with chronic bronchitis and symptoms that are consistent with airflow obstruction. Ever exposure to mineral dust, gases/fumes and vapours, gases, dust or fumes were only associated with fixed airflow obstruction in non-asthmatics only. CONCLUSIONS: Pesticides and herbicides exposures were associated with fixed airflow obstruction and chronic bronchitis. Biological dust exposure was also associated with fixed airflow obstruction in non-asthmatics. Minimising occupational exposure to these agents may help to reduce the burden of COPD.

Traffic-related air pollution exposure over a 5-year period is associated with increased risk of asthma and poor lung function in middle age.

Current evidence concerning the impact of exposure to traffic-related air pollution (TRAP) on adult respiratory morbidity mainly comes from cross-sectional studies. We sought to establish more robust measures of this association and potential gene-environment interactions using longitudinal data from an established cohort study.Associations between measures of TRAP (nitrogen dioxide (NO2) and distance to major roads) and wheeze, asthma prevalence and lung function were investigated in participants of the Tasmanian Longitudinal Health Study at 45- and 50-year follow-ups. Generalised estimating equations were used to quantify associations and the potential modifying effect of glutathione S-transferase gene variants.Living <200 m from a major road was associated with increased prevalence of current asthma and wheeze, and lower lung function. The association between living <200 m from a major road and current asthma and wheeze was more marked for carriers of the GSTT1 null and GSTP1 val/val or ile/val genotypes. Over the 5-year period, higher NO2 exposures were associated with increased current asthma prevalence. Higher NO2 exposure was associated with lower forced vital capacity for carriers of the GSTT1 null genotype.TRAP exposures were associated with increased risk of asthma, wheeze and lower lung function in middle-aged adults. The interaction with the GSTT1 genotype suggests that deficient antioxidant mechanisms may play a role in these adverse health effects.

Immunological effects among workers who handle engineered nanoparticles.

OBJECTIVE: To determine whether exposure of workers handling engineered nanoparticles (ENPs) may result in increased inflammation and changes in lung function. METHODS: A prospective panel study compared changes in several markers of inflammation for ENP handling and non-ENP handling control workers. Nanoparticle exposure was measured during ENP handling and for controls. Lung function, fraction of exhaled nitric oxide (FeNO), C-reactive protein (CRP), blood cell counts and several serum cytokines were measured at baseline, at the end of the shift and at the end of the working week. RESULTS: Nanoparticle exposure was not higher when ENPs were being handled; nanoparticle counts were higher in offices and in ambient air than in laboratories. There were no differences at baseline in lung function, FeNO, haemoglobin, platelet, white cell counts or CRP levels between those who handled nanoparticles and those who did not, with or without asthmatic participants. There were statistically significant increases in sCD40 and sTNFR2 over the working day for those who handled ENPs. The changes were larger and statistically significant over the working week and sCD62P also showed a statistically significant difference. The changes were slightly smaller and less likely to be statistically significant for atopic than for non-atopic participants. CONCLUSIONS: Even at low ENP exposure, increases in three cytokines were significant over the week for those who handled nanoparticles, compared with those who did not. However, exposure to low and transient levels of nanoparticles was insufficient, to trigger measurable changes in spirometry, FeNO, CRP or blood cell counts.

Exploring the influence of short-term temperature patterns on temperature-related mortality: a case-study of Melbourne, Australia.

BACKGROUND: Several studies have identified the association between ambient temperature and mortality; however, several features of temperature behavior and their impacts on health remain unresolved. We obtain daily counts of nonaccidental all-cause mortality data in the elderly (65 + years) and corresponding meteorological data for Melbourne, Australia during 1999 to 2006. We then characterize the temporal behavior of ambient temperature development by quantifying the rates of temperature change during periods designated by pre-specified windows ranging from 1 to 30 days. Finally, we evaluate if the association between same day temperature and mortality in the framework of a Poisson regression and include our temperature trajectory variables in order to assess if associations were modified by the nature of how the given daily temperature had evolved. RESULTS: We found a positive significant association between short-term mortality risk and daily average temperature as mortality risk increased 6 % on days when temperatures were above the 90th percentile as compared to days in the referent 25-75th. In addition, we found that mortality risk associated with daily temperature varied by the nature of the temperature trajectory over the preceding twelve days and that peaks in mortality occurred during periods of high temperatures and stable trajectories and during periods of increasing higher temperatures and increasing trajectories. CONCLUSION: Our method presents a promising tool for improving understanding of complex temperature health associations. These findings suggest that the nature of sub-monthly temperature variability plays a role in the acute impacts of temperature on mortality; however, further studies are suggested.

Fine particulate matter (PM2.5 ) exposure during a prolonged wildfire period and emergency department visits for asthma.

BACKGROUND AND OBJECTIVE: The 2006-2007 wildfire period was one of the most extensive and long lasting fires in Australian history with high levels of fine particulate matter (PM2.5 ). Large populations were exposed to smoke for over 2 months. The study aimed to investigate the association between wildfire-related PM2.5 exposure and emergency department (ED) visits for asthma. METHODS: A time-stratified case-crossover design was used to investigate associations between daily average PM2.5 and ED attendances for asthma from December 2006 to January 2007. ED data were obtained from the Victorian Emergency Minimum Dataset. Smoke dispersion during the wildfire event was modelled using a validated chemical transport model. Exposure data (daily average PM2.5 , temperature and relative humidity) were modelled for the study period. Various lag periods were investigated. RESULTS: There were 2047 ED attendances for asthma during the study period. After adjusting for temperature and relative humidity, an interquartile range increase in PM2.5 levels of 8.6 µg/m(3) was associated with an increase in ED attendances for asthma by 1.96% (95%CI: 0.02, 3.94) on the day of exposure. Lag periods up to 2 days prior did not show any association. A strong association was observed among women 20 years and older (5.08% 95%CI: 1.76, 8.51). CONCLUSIONS: Wildfire-related PM2.5 was associated with increased risk of ED attendance for asthma during the wildfire event. It is important to understand the role of wildfire PM2.5 as a trigger for asthma presentations.

Health effects of smoke from planned burns: a study protocol.

BACKGROUND: Large populations are exposed to smoke from bushfires and planned burns. Studies investigating the association between bushfire smoke and health have typically used hospital or ambulance data and been done retrospectively on large populations. The present study is designed to prospectively assess the association between individual level health outcomes and exposure to smoke from planned burns. METHODS/DESIGN: A prospective cohort study will be conducted during a planned burn season in three locations in Victoria (Australia) involving 50 adult participants who undergo three rounds of cardiorespiratory medical tests, including measurements for lung inflammation, endothelial function, heart rate variability and markers of inflammation. In addition daily symptoms and twice daily lung function are recorded. Outdoor particulate air pollution is continuously measured during the study period in these locations. The data will be analysed using mixed effect models adjusting for confounders. DISCUSSION: Planned burns depend on weather conditions and dryness of 'fuels' (i.e. forest). It is potentially possible that no favourable conditions occur during the study period. To reduce the risk of this occurring, three separate locations have been identified as having a high likelihood of planned burn smoke exposure during the study period, with the full study being rolled out in two of these three locations. A limitation of this study is exposure misclassification as outdoor measurements will be conducted as a measure for personal exposures. However this misclassification will be reduced as participants are only eligible if they live in close proximity to the monitors.

Do Variants in GSTs Modify the Association between Traffic Air Pollution and Asthma in Adolescence?

Polymorphisms in genes involved in the oxidative stress response may partially explain the documented heterogeneous associations between traffic-related air pollution (TRAP) exposure and asthma and allergies in children. We investigated whether the GSTT1, GSTM1 and GSTP1 gene polymorphisms modified the associations between TRAP exposure during the first year of life and asthma, wheeze and hay fever in adolescence. We used a birth cohort of 620 high risk infants from the Melbourne Atopy Cohort Study. TRAP exposure during the first year of life was defined as the cumulative length of major roads within 150 m of each participant's residence during the first year of life. Wheeze, asthma and hay fever were measured at ages 12 (n = 370) and 18 (n = 434) years. The associations and interactions with glutathione S-transferases (GST s) were investigated using regression models. Overall, there was no relationship between TRAP exposure during the first year of life and current asthma, wheeze and hay fever at ages 12 or 18 years. However, in GSTT1 null carriers, every 100 m increase in cumulative lengths of major road exposure during the first year of life was associated with a 2.31-fold increased risk of wheeze and a 2.15-fold increased risk of asthma at 12 years. TRAP is associated with some respiratory outcomes in carriers of genetic polymorphisms in oxidative stress metabolism genes.

Systematic Review of Guidelines for the Management of Asymptomatic and Symptomatic Carotid Stenosis.

BACKGROUND AND PURPOSE: We systematically compared and appraised contemporary guidelines on management of asymptomatic and symptomatic carotid artery stenosis. METHODS: We systematically searched for guideline recommendations on carotid endarterectomy (CEA) or carotid angioplasty/stenting (CAS) published in any language between January 1, 2008, and January 28, 2015. Only the latest guideline per writing group was selected. Each guideline was analyzed independently by 2 to 6 authors to determine clinical scenarios covered, recommendations given, and scientific evidence used. RESULTS: Thirty-four eligible guidelines were identified from 23 different regions/countries in 6 languages. Of 28 guidelines with asymptomatic carotid artery stenosis procedural recommendations, 24 (86%) endorsed CEA (recommended it should or may be provided) for ≈50% to 99% average-surgical-risk asymptomatic carotid artery stenosis, 17 (61%) endorsed CAS, 8 (29%) opposed CAS, and 1 (4%) endorsed medical treatment alone. For asymptomatic carotid artery stenosis patients considered high-CEA-risk because of comorbidities, vascular anatomy, or undefined reasons, CAS was endorsed in 13 guidelines (46%). Thirty-one of 33 guidelines (94%) with symptomatic carotid artery stenosis procedural recommendations endorsed CEA for patients with ≈50% to 99% average-CEA-risk symptomatic carotid artery stenosis, 19 (58%) endorsed CAS and 9 (27%) opposed CAS. For high-CEA-risk symptomatic carotid artery stenosis because of comorbidities, vascular anatomy, or undefined reasons, CAS was endorsed in 27 guidelines (82%). Guideline procedural recommendations were based only on results of trials in which patients were randomized 12 to 34 years ago, rarely reflected medical treatment improvements and often understated potential CAS hazards. Qualifying terminology summarizing recommendations or evidence lacked standardization, impeding guideline interpretation, and comparison. CONCLUSIONS: This systematic review has identified many opportunities to modernize and otherwise improve carotid stenosis management guidelines.

Longitudinal analysis of respiratory outcomes among bauxite exposed workers in Western Australia.

INTRODUCTION: Occupational exposure to bauxite is common in the aluminium industry but little is known about the associated health effects. This study investigates respiratory health in relation to respirable bauxite dust exposure longitudinally over a 13 year period. METHODS: An inception cohort study recruited 91 male bauxite miners and 363 male alumina refinery workers. Annual measurements of respiratory symptoms and lung function were made. Cumulative exposure to bauxite was derived from job histories and air monitoring data. Mixed-effects modeling was used. RESULTS: No associations were found between cumulative bauxite exposure and respiratory symptoms or lung function. However, when analysis was restricted to the first three rounds, FEV1 was significantly lower in all exposure groups than in those unexposed but with no significant trend. CONCLUSION: Increasing exposure to bauxite dust in the aluminum industry was not associated with respiratory symptoms or consistent decrements in lung function.

Impact of smoke from prescribed burning: Is it a public health concern?

UNLABELLED: Given the increase in wildfire intensity and frequency worldwide, prescribed burning is becoming a more common and widespread practice. Prescribed burning is a fire management tool used to reduce fuel loads for wildfire suppression purposes and occurs on an annual basis in many parts of the world. Smoke from prescribed burning can have a substantial impact on air quality and the environment. Prescribed burning is a significant source of fine particulate matter (PM2.5 aerodynamic diameter<2.5µm) and these particulates are found to be consistently elevated during smoke events. Due to their fine nature PM2.5 are particularly harmful to human health. Here we discuss the impact of prescribed burning on air quality particularly focussing on PM2.5. We have summarised available case studies from Australia including a recent study we conducted in regional Victoria, Australia during the prescribed burning season in 2013. The studies reported very high short-term (hourly) concentrations of PM2.5 during prescribed burning. Given the increase in PM2.5 concentrations during smoke events, there is a need to understand the influence of prescribed burning smoke exposure on human health. This is important especially since adverse health impacts have been observed during wildfire events when PM2.5 concentrations were similar to those observed during prescribed burning events. Robust research is required to quantify and determine health impacts from prescribed burning smoke exposure and derive evidence based interventions for managing the risk. IMPLICATIONS: Given the increase in PM2.5 concentrations during PB smoke events and its impact on the local air quality, the need to understand the influence of PB smoke exposure on human health is important. This knowledge will be important to inform policy and practice of the integrated, consistent, and adaptive approach to the appropriate planning and implementation of public health strategies during PB events. This will also have important implications for land management and public health organizations in developing evidence based objectives to minimize the risk of PB smoke exposure.

Evaluating portable air cleaner effectiveness in residential settings to reduce exposures to biomass smoke resulting from prescribed burns.

AIM: Prescribed burning is the most common method employed to reduce fuel loads in flammable landscapes. This practice is designed to reduce the hazard associated with uncontrolled bushfires. Prescribed burns are frequently conducted close to residential areas, and the associated smoke impacts can adversely affect community health. Particulate matter is the predominant pollutant within the smoke and is strongly and consistently linked with adverse health effects. Outdoor smoke readily infiltrates buildings and reduces the quality of indoor air. Portable air cleaners containing high-efficiency particulate air (HEPA) filters are a promising indoor air quality intervention for reducing outdoor smoke exposure. METHODS: We provided 10 homes from semirural regions of Victoria, Australia, with HEPA cleaners and conducted continuous monitoring of indoor and outdoor fine particulate matter (PM2.5) for 2-4 weeks during prescribed burning periods. We calculated the potential improvements to indoor air quality when operating a HEPA cleaner during a smoke episode. Ventilation measures were conducted to identify points of smoke ingress and housing characteristics that could lead to higher infiltration rates. RESULTS: Depending on the house, the use of HEPA cleaners resulted in a reduction in indoor PM2.5 concentrations of 30-74%. CONCLUSIONS: HEPA cleaners have the potential to substantially improve indoor air quality during episodic smoke episodes.

A Research Translation, Implementation and Impact Strategy for the Australian Healthy Environments and Lives (HEAL) Research Network.

Healthy Environments And Lives (HEAL) is the Australian national research network established to support improvements to health, the Australian health system, and the environment in response to the unfolding climate crisis. The HEAL Network comprises researchers, community members and organisations, policymakers, practitioners, service providers, and other stakeholders from diverse backgrounds and sectors. HEAL seeks to protect and improve public health, reduce health inequities and inequalities, and strengthen health system sustainability and resilience in the face of environmental and climate change, all with a commitment to building on the strengths, knowledge, wisdom, and experience of Aboriginal and Torres Strait Islander people, culture, and communities. Supporting applied research that can inform policy and practice, and effective research translation, implementation, and impact are important goals across the HEAL Network and essential to achieve its intended outcomes. To aid translation approaches, a research translation, implementation, and impact strategy for the HEAL Network was developed. The strategy has been created to inform and guide research translation across HEAL, emphasising communication, trust, partnerships, and co-design with communities and community organisations as well as the decision-makers responsible for public policies and programs. Development of the strategy was guided by research translation theory and practice and the Health in All Policies and Environment in All Policies frameworks. As described in this paper, the strategy is underpinned by a set of principles and outlines preliminary actions which will be further expanded over the course of the HEAL Network's activities. Through these actions, the HEAL Network is well-positioned to ensure successful research translation and implementation across its program of work.

Climate change, environmental extremes, and human health in Australia: challenges, adaptation strategies, and policy gaps.

Climate change presents a major public health concern in Australia, marked by unprecedented wildfires, heatwaves, floods, droughts, and the spread of climate-sensitive infectious diseases. Despite these challenges, Australia's response to the climate crisis has been inadequate and subject to change by politics, public sentiment, and global developments. This study illustrates the spatiotemporal patterns of selected climate-related environmental extremes (heatwaves, wildfires, floods, and droughts) across Australia during the past two decades, and summarizes climate adaptation measures and actions that have been taken by the national, state/territory, and local governments. Our findings reveal significant impacts of climate-related environmental extremes on the health and well-being of Australians. While governments have implemented various adaptation strategies, these plans must be further developed to yield concrete actions. Moreover, Indigenous Australians should not be left out in these adaptation efforts. A collaborative, comprehensive approach involving all levels of government is urgently needed to prevent, mitigate, and adapt to the health impacts of climate change.