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In epidemiologic studies, researchers often need to establish a nonlinear exposure-response relation between a continuous risk factor and a health outcome. Furthermore, periodic interviews are often conducted to take repeated measurements from an individual. The authors proposed to use fractional polynomial models to jointly analyze the effects of 2 continuous risk factors on a health outcome. This method was applied to an analysis of the effects of age and cumulative fluoride exposure on forced vital capacity in a longitudinal study of lung function carried out among aluminum workers in Australia (1995-2003). Generalized estimating equations and the quasi-likelihood under the independence model criterion were used. The authors found that the second-degree fractional polynomial models for age and fluoride fitted the data best. The best model for age was robust across different models for fluoride, and the best model for fluoride was also robust. No evidence was found to suggest that the effects of smoking and cumulative fluoride exposure on change in forced vital capacity over time were significant. The trend 1 model, which included the unexposed persons in the analysis of trend in forced vital capacity over tertiles of fluoride exposure, did not fit the data well, and caution should be exercised when this method is used. [ABSTRACT FROM AUTHOR]

Acute exposure to particles in urban air has been found to be associated with adverse health effects. It has been suggested that the particle number concentration of ultrafine particles (<0.1 µm in diameter) may be more relevant to the observed health effects than the particle mass concentration. In this study, (ultrafine) particle numbers and PM2.5 mass (<2.5 µm in diameter) concentrations were measured in different micro-environments and during different activities. There was a considerable variation of particle concentration depending on the location of the measurement and the nearby particle-generating activity. The highest concentrations of particle numbers were found to be due to traffic, but most importantly cooking. The highest concentration of PM2.5 mass was due to passive cigarette smoke. These data will be used to develop a model to estimate personal exposure to particle numbers and PM2.5 mass concentration. [ABSTRACT FROM AUTHOR]

Acute exposure to particles in urban air has been found to be associated with adverse health effects. It has been suggested that the particle number concentration of ultrafine particles (<0.1 μm in diameter) may be more relevant to the observed health effects than the particle mass concentration. In this study, (ultrafine) particle numbers and PM2.5 mass (<2.5 μm in diameter) concentrations were measured in different micro-environments and during different activities. There was a considerable variation of particle concentration depending on the location of the measurement and the nearby particle-generating activity. The highest concentrations of particle numbers were found to be due to traffic, but most importantly cooking. The highest concentration of PM2.5 mass was due to passive cigarette smoke. These data will be used to develop a model to estimate personal exposure to particle numbers and PM2.5 mass concentration. [ABSTRACT FROM AUTHOR]

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., Competing Interests: None declared.

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., Competing Interests: JA is a member of World Meteorological Organization Study Group on Integrated Health Services. OJ has contracts from the NSW Health and Victoria Government, Department of Health. OJ is a Management Committee Member of the Global Heat and Health Information Network. OJ has the patent of Environmental Measurement Unit (International Patent Application No: PCT/AU2021/051248)., (© 2023 The Author(s).)

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.

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 (PM 2.5 ) were measured at fixed site monitors in each location., Results: Mean PM 2.5 levels were significantly elevated during bushfire exposure in Warburton (96.5±57.7 μg/m 3 vs 4.0±1.9 μg/m 3 , p<0.001) and Traralgon (12.6±4.9 μg/m 3 vs 3.4±3.1 μg/m 3 , p<0.001), while it remained low in the control town, Maffra, in each phase (4.3±3.2 μg/m 3 and 3.9±3.6 μg/m 3 , 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., (Copyright © 2022 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.)

A common chemical exposure in alumina refining is caustic mist. Although recognized as a strong airways irritant, little is known of the chronic respiratory effects of caustic mist in alumina refining. A suitable metric for caustic mist exposure assessment in alumina refining for epidemiological purposes has not been identified. Peak exposure is likely to be important, but is difficult to assess in epidemiological studies. In this study, we investigate the respiratory effects of caustic mist in an inception cohort (n = 416) of alumina refinery workers and describe the development and use of a peak exposure metric for caustic mist. We then compare the results with a metric based on duration of exposure. Participants were interviewed annually about respiratory symptoms and had a lung function test. Job history data were collected from each interview and levels of caustic mist were measured periodically by air monitoring. We found a weak association between the caustic mist peak exposure metric and reported cough (P for linear trend = 0.079) with the highest peak exposure group odds ratio = 2.32 (95% confidence interval: 1.27, 4.22). For lung function, we found declines in the forced expiratory volume in 1 second and forced vital capacity for changes in annual and absolute lung function for both metrics of exposure, but only the ratio of absolute lung function was statistically associated with an increasing duration of caustic exposure (P for linear trend = 0.011). In this cohort, we did not observe an association with respiratory symptoms or consistent decrements in lung function. There was little difference between the exposure metrics used for investigation of the chronic effects from caustic mist., (© The Author(s) 2021. Published by Oxford University Press on behalf of the British Occupational Hygiene Society.)

Many Australians are intermittently exposed to landscape fire smoke from wildfires or planned (prescribed) burns. This study aimed to investigate effects of outdoor smoke from planned burns, wildfires and a coal mine fire by assessing biomarkers of inflammation in an exposed and predominantly older population. Participants were recruited from three communities in south-eastern Australia. Concentrations of fine particulate matter (PM 2.5 ) were continuously measured within these communities, with participants performing a range of health measures during and without a smoke event. Changes in biomarkers were examined in response to PM 2.5 concentrations from outdoor smoke. Increased levels of FeNO (fractional exhaled nitric oxide) (β = 0.500 [95%CI 0.192 to 0.808] p < 0.001) at a 4 h lag were associated with a 10 µg/m 3 increase in PM 2.5 levels from outdoor smoke, with effects also shown for wildfire smoke at 4, 12, 24 and 48-h lag periods and coal mine fire smoke at a 4 h lag. Total white cell (β = -0.088 [-0.171 to -0.006] p = 0.036) and neutrophil counts (β = -0.077 [-0.144 to -0.010] p = 0.024) declined in response to a 10 µg/m 3 increase in PM 2.5 . However, exposure to outdoor smoke resulting from wildfires, planned burns and a coal mine fire was not found to affect other blood biomarkers.

Ambient fine particulate matter <2.5 µm (PM 2.5 ) air pollution increases premature mortality globally. Some PM 2.5 is natural, but anthropogenic PM 2.5 is comparatively avoidable. We determined the impact of long-term exposures to the anthropogenic PM component on mortality in Australia. PM 2.5 -attributable deaths were calculated for all Australian Statistical Area 2 (SA2; n = 2310) regions. All-cause death rates from Australian mortality and population databases were combined with annual anthropogenic PM 2.5 exposures for the years 2006-2016. Relative risk estimates were derived from the literature. Population-weighted average PM 2.5 concentrations were estimated in each SA2 using a satellite and land use regression model for Australia. PM 2.5 -attributable mortality was calculated using a health-impact assessment methodology with life tables and all-cause death rates. The changes in life expectancy (LE) from birth, years of life lost (YLL), and economic cost of lost life years were calculated using the 2019 value of a statistical life. Nationally, long-term population-weighted average total and anthropogenic PM 2.5 concentrations were 6.5 µg/m 3 (min 1.2-max 14.2) and 3.2 µg/m 3 (min 0-max 9.5), respectively. Annually, anthropogenic PM 2.5 -pollution is associated with 2616 (95% confidence intervals 1712, 3455) deaths, corresponding to a 0.2-year (95% CI 0.14, 0.28) reduction in LE for children aged 0-4 years, 38,962 (95%CI 25,391, 51,669) YLL and an average annual economic burden of $6.2 billion (95%CI $4.0 billion, $8.1 billion). We conclude that the anthropogenic PM 2.5 -related costs of mortality in Australia are higher than community standards should allow, and reductions in emissions are recommended to achieve avoidable mortality.

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 (FEV 1 ) 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/m 3 -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 FEV 1 (p for trend = .06). For mean annual change in FEV 1 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., (© 2020 Wiley Periodicals LLC.)

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 PD 20 ≤4000 µg. Poisson and mixed effects models were fitted to respiratory symptoms and lung function (forced expiratory volume in 1 s (FEV 1 ) and FEV 1 /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 FEV 1 and FVC, although the rate of annual decline in FEV 1 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., Competing Interests: Competing interests: MJA holds investigator initiated grants from Pfizer and Boehringer-Ingelheim for unrelated research. He has undertaken an unrelated consultancy for and received assistance with conference attendance from Sanofi. He has received a speaker's fee from GSK. The other authors have no competing interests to declare., (© Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.)

Objectives: We aimed to examine the change in rates of hospital emergency presentations or hospital admissions during the coal mine fire, and their associations with the coal mine fire-related fine particles (PM 2.5 )., Methods: Daily data on hospital emergency presentations and admissions were collected from the Department of Health and Human Services for the period January 01, 2009 to June 30, 2015, at Statistical Area Level 2 (SA2). The coal mine fire-related PM 2.5 concentrations were modelled by the Chemical Transport Model coupled with the Cubic Conformal Atmospheric Model. A generalised additive mixed model was used to estimate the change in rates of hospital emergency presentations and hospital admissions during the coal mine fire period, and to examine their associations with PM 2.5 concentrations for smoke impacted areas, after controlling for potential confounders., Results: Compared with non-fire periods, we found increased risks of all-causes, respiratory diseases, and asthma related emergency presentations and hospital admissions as well as chronic obstructive pulmonary disease (COPD) related emergency presentations during the fire period. Associations between daily concentrations of coal mine fire-related PM 2.5 and emergency presentations for all-causes and respiratory diseases, including COPD and asthma, appeared after two days' exposure. Associations with hospital admissions for cerebrovascular and respiratory diseases appeared on the same day of exposure., Conclusions: Coal mine fire smoke created a substantial health burden. People with respiratory diseases should receive targeted messages, follow self-management plans and take preventive medication during future coal mine fires., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Background: This study assessed the association between coal-mine-fire-related fine particulate matter (PM2.5) and medical-service utilization, following a 6-week coal-mine fire in Australia, in 2014. Areas in the immediate vicinity of the mine experienced hourly mine-fire-related PM2.5 concentrations of up to 3700 μg/m3., Methods: Data on medical-service utilization were collected from the Medicare Benefits Schedule-a national database of payment for medical services. PM2.5 concentrations were modelled using atmospheric chemical transport modelling. Quasi-Poisson interrupted distributed lag time-series analysis examined the association between daily mine-fire-related PM2.5 concentrations and medical-service utilization, including General Practitioner (GP) consultations and respiratory, cardiovascular and mental health services. Confounders included seasonality, long-term trend, day of the week, maximum daily temperature and public holidays. Gender and age stratification were conducted., Results: A 10-μg/m3 increase in PM2.5 was associated with an increased relative risk of service usage for all long and short GP consultations [11% (95% confidence interval: 7 to 15%)] and respiratory services [22% (4 to 43%)] in both men and women. Sex stratification found an increased relative risk in mental health consultations in men [32% (2 to 72%)] but not women. No associations were found for cardiovascular services in men or women., Conclusions: Coal-mine-fire-related PM2.5 exposure was associated with increased use of medical services for GP consultations and respiratory services in men and women and mental health consultations in men. These findings can inform the development of future public-health-policy responses in the event of major air-pollution episodes., (© The Author(s) 2019; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.)

In 2014, wildfires ignited a fire in the Morwell open cut coal mine, Australia, which burned for six weeks. This study examined associations between self-reported respiratory outcomes in adults and mine fire-related PM 2.5 smoke exposure. Self-reported data were collected as part of the Hazelwood Health Study Adult Survey. Eligible participants were adult residents of Morwell. Mine fire-related PM 2.5 concentrations were provided by the Commonwealth Scientific and Industrial Research Organisation Oceans & Atmosphere Flagship. Personalised mean 24-h and peak 12-h mine fire-related PM 2.5 exposures were estimated for each participant. Data were analysed by multivariate logistic regression. There was some evidence of an association between respiratory outcomes and mine fire PM 2.5 exposure. Chronic cough was associated with an odds ratio (OR) of 1.13 (95% confidence interval 1.03 to 1.23) per 10 μg/m 3 increment in mean PM 2.5 and 1.07 (1.02 to 1.12) per 100 μg/m 3 increment in peak PM 2.5 . Current wheeze was associated with peak PM 2.5 , OR = 1.06 (1.02 to 1.11) and chronic phlegm with mean PM 2.5 OR = 1.10 (1.00 to 1.20). Coal mine PM 2.5 smoke exposure was associated with increased odds of experiencing cough, phlegm and wheeze. Males, participants 18-64 years, and those residing in homes constructed from non-brick/concrete materials or homes with tin/metal roofs had higher estimated ORs. These findings contribute to the formation of public health policy responses.

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.

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 FEV 1 (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 FEV 1 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., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.)

Victoria's (Australia) Environment Protection Authority (EPA), the state's environmental regulator, has recognized the need to develop an Environmental Health Tracking System (EHTS) to better understand environmental health relationships. To facilitate the process of developing an EHTS; a linkage-based conceptual framework was developed to link routinely collected environmental and health data to better understand environmental health relationships. This involved researching and drawing on knowledge from previous similar projects. While several conceptual frameworks have been used to organize data to support the development of an environmental health tracking system, Driving Force-Pressure-State-Exposure-Effect-Action (DPSEEA) was identified as the most broadly applied conceptual framework. Exposure and effects are two important components of DPSEEA, and currently, exposure data are not available for the EHTS. Therefore, DPSEEA was modified to the Driving Force-Pressure-Environmental Condition-Health Impact-Action (DPEHA) conceptual framework for the proposed Victorian EHTS as there is relevant data available for tracking. The potential application of DPEHA for environmental health tracking was demonstrated through case studies. DPEHA will be a useful tool to support the implementation of Victoria's environmental health tracking system for providing timely and scientific evidence for EPA and other decision makers in developing and evaluating policies for protecting public health and the environment in Victoria.

Bushfires, prescribed burns, and residential wood burning are significant sources of fine particles (aerodynamic diameter <2.5 μm; PM 2.5 ) affecting the health and well-being of many communities. Despite the lack of evidence, a common public health recommendation is to remain indoors, assuming that the home provides a protective barrier against ambient PM 2.5 . The study aimed to assess to what extent houses provide protection against peak concentrations of outdoor PM 2.5 and whether remaining indoors is an effective way of reducing exposure to PM 2.5 . The effectiveness of this strategy was evaluated by conducting simultaneous week-long indoor and outdoor measurements of PM 2.5 at 21 residences in regional areas of Victoria, Australia. During smoke plume events, remaining indoors protected residents from peak outdoor PM 2.5 concentrations, but the level of protection was highly variable, ranging from 12% to 76%. Housing stock (e.g., age of the house) and ventilation (e.g., having windows/doors open or closed) played a significant role in the infiltration of outdoor PM 2.5 indoors. The results also showed that leaving windows and doors closed once the smoke plume abates trapped PM 2.5 indoors and increased indoor exposure to PM 2.5 . Furthermore, for approximately 50% of households, indoor sources such as cooking activities, smoking, and burning candles or incense contributed significantly to indoor PM 2.5 . Implications: Smoke from biomass burning sources can significantly impact on communities. Remaining indoors with windows and doors closed is a common recommendation by health authorities to minimize exposures to peak concentrations of fine particles during smoke plume events. Findings from this study have shown that the protection from fine particles in biomass burning smoke is highly variable among houses, with information on housing age and ventilation status providing an approximate assessment on the protection of a house. Leaving windows closed once a smoke plume abates traps particles indoors and increases exposures.

Limited research has examined the impacts of coal mine fire smoke on human health. The aim of this study was to assess the association between prolonged smoke PM 2.5 exposure from a brown coal mine fire that burned over a seven week period in 2014 and medications dispensed across five localities in South-eastern Victoria, Australia. Spatially resolved PM 2.5 concentrations were retrospectively estimated using a dispersion model coupled with a chemical transport model. Data on medications dispensed were collected from the national Pharmaceutical Benefits Schedule database for 2013-2016. Poisson distributed lag time series analysis was used to examine associations between daily mine fire-related PM 2.5 concentrations and daily counts of medications dispensed for respiratory, cardiovascular or psychiatric conditions. Factors controlled for included: seasonality, long-term trend, day of the week, maximum ambient temperature and public holidays. Positive associations were found between mine fire-related PM 2.5 and increased risks of medications dispensed for respiratory, cardiovascular and psychiatric conditions, over a lag range of 3-7 days. A 10 μg/m 3 increase in coal mine fire-related PM 2.5 was associated with a 25% (95%CI 19-32%) increase in respiratory medications, a 10% (95%CI 7-13%) increase in cardiovascular medications and a 12% (95%CI 8-16%) increase in psychiatric medications dispensed. These findings have the potential to better prepare for and develop more appropriate public health responses in the event of future coal mine fires., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

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.

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., Competing Interests: Competing interests: None declared., (© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Objectives This study investigated the associations between occupational exposures to solvents and metals and fixed airflow obstruction (AO) using post-bronchodilator spirometry. Methods We included 1335 participants from the 2002-2008 follow-up of the Tasmanian Longitudinal Health Study. Ever-exposure and cumulative exposure-unit (EU) years were calculated using the ALOHA plus job exposure matrix (JEM). Fixed AO was defined as post-bronchodilator forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) <0.7 and FEV 1 /FVC1 /FVC<0.7 to define fixed AO plus low DLco. Multinomial regressions were used to estimate associations adjusting for possible confounders. Results Ever-exposure to metals was associated with fixed AO [relative risk (RR) 1.71, 95% CI 1.03-2.85] and fixed AO lower limit of normal (RR 1.67, 95% CI 1.00-2.78). Women had lower cumulative EU years to chlorinated solvents [mean 20.9, standard deviation (SD) 13.4] than men (mean 28.6, SD 36.9). However, the risk of developing fixed AO and fixed AO plus low DLCO associated with each cumulative EU year of chlorinated solvents were higher among women than men (RR 1.08 versus 0.99, P-value for effect measure modification=0.006; RR 1.08 versus 1.00, P-value for effect measure modification=0.02). Conclusions We have shown ever-exposure to metals and chlorinated solvents are important risk factors for fixed AO. The effects for solvents were strongest among women. Preventive strategies need to be followed to reduce these exposures at the workplace.

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 FEV 1 /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., Competing Interests: Competing interests: None declared., (© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

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 (NO 2 ) 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 NO 2 exposures were associated with increased current asthma prevalence. Higher NO 2 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., Competing Interests: Conflict of interest: Disclosures can be found alongside this article at erj.ersjournals.com, (Copyright ©ERS 2017.)

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 (NO 2 ) 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 NO 2 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 NO 2 [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 FEV 1 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., (Copyright © 2016 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

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.

Introduction: Due to contradictory literature we have performed a systematic review and meta-analyse of population-based studies that have used Job Exposure Matrices to assess occupational exposure and risk of Chronic Obstructive Pulmonary Disease (COPD)., Areas Covered: Two researchers independently searched databases for published articles using predefined inclusion criteria. Study quality was assessed, and results pooled for COPD and chronic bronchitis for exposure to biological dust, mineral dust, and gases/fumes using a fixed and random effect model. Five studies met predetermined inclusion criteria. The meta-analysis showed low exposure to mineral dust, and high exposure to gases/fumes were associated with an increased risk of COPD. We also found significantly increased the risk of chronic bronchitis for low and high exposure to biological dust and mineral dust. Expert commentary: The relationship between occupational exposure assessed by the JEM and the risk of COPD and chronic bronchitis shows significant association with occupational exposure. However, the heterogeneity of the meta-analyses suggests more wide population-based studies with older age groups and longitudinal phenotype assessment of COPD to clarify the role of occupational exposure to COPD risk.

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.