From Engineered Stone Slab to Silicosis: A Synthesis of Exposure Science and Medical Evidence.

Engineered stone (ES) is a popular building product, due to its architectural versatility and generally lower cost. However, the fabrication of organic resin-based ES kitchen benchtops from slabs has been associated with alarming rates of silicosis among workers. In 2024, fifteen years after the first reported ES-related cases in the world, Australia became the first country to ban the use and importation of ES. A range of interacting factors are relevant for ES-associated silicosis, including ES material composition, characteristics of dust exposure and lung cell-particle response. In turn, these are influenced by consumer demand, work practices, particle size and chemistry, dust control measures, industry regulation and worker-related characteristics. This literature review provides an evidence synthesis using a narrative approach, with the themes of product, exposure and host. Exposure pathways and pathogenesis are explored. Apart from crystalline silica content, consideration is given to non-siliceous ES components such as resins and metals that may modify chemical interactions and disease risk. Preventive effort can be aligned with each theme and associated evidence.

The aryl hydrocarbon receptor pathway is a marker of lung cell activation but does not play a central pathologic role in engineered stone-associated silicosis.

Engineered stone-associated silicosis is characterised by a rapid progression of fibrosis linked to a shorter duration of exposure. To date, there is lack of information about molecular pathways that regulates disease development and the aggressiveness of this form of silicosis. Therefore, we compared transcriptome responses to different engineered stone samples and standard silica. We then identified and further tested a stone dust specific pathway (aryl hydrocarbon receptor [AhR]) in relation to mitigation of adverse lung cell responses. Cells (epithelial cells, A549; macrophages, THP-1) were exposed to two different benchtop stone samples, standard silica and vehicle control, followed by RNA sequencing analysis. Bioinformatics analyses were conducted, and the expression of dysregulated AhR pathway genes resulting from engineered stone exposure was then correlated with cytokine responses. Finally, we inhibited AhR pathway in cells pretreated with AhR antagonist and observed how this impacted cell cytotoxicity and inflammation. Through transcriptome analysis, we identified the AhR pathway genes (CYP1A1, CYP1B1 and TIPARP) that showed differential expression that was unique to engineered stones and common between both cell types. The expression of these genes was positively correlated with interleukin-8 production in A549 and THP-1 cells. However, we only observed a mild effect of AhR pathway inhibition on engineered stone dust induced cytokine responses. Given the dual roles of AhR pathway in physiological and pathological processes, our data showed that expression of AhR target genes could be markers for assessing toxicity of engineered stones; however, AhR pathway might not play a significant pathologic role in engineered stone-associated silicosis.

Increased vascular stiffness in children exposed in utero but not children exposed postnatally to emissions from a coal mine fire.

Background: Chronic, low-intensity air pollution exposure has been consistently associated with increased atherosclerosis in adults. However, there was limited research regarding the implications of acute, high-intensity air pollution exposure during childhood. We aimed to determine whether there were any associations between early-life exposure to such an episode and early-life vascular function changes. Methods: We conducted a prospective cohort study of children (<9 years old) who lived in the vicinity of the Hazelwood coal mine fire (n = 206). Vascular function was measured using noninvasive diagnostic methods including carotid intima-media thickness and pulse wave velocity (PWV). Exposure estimates were calculated from prognostic models and location diaries during the exposure period completed by each participant's parent. Linear mixed-effects models were used to determine whether there were any associations between exposure and changes in vascular outcomes at the 3- and 7-year follow-ups and over time. Results: At the 7-year follow-up, each 10 µg/m3 increase in daily PM2.5 in utero was associated with increased PWV (ß = 0.13 m/s; 95% confidence interval [CI] = 0.02, 0.24; P = 0.02). The association between in utero exposure to daily PM2.5 was not altered by adjustment for covariates, body mass index, and maternal fire stress. Each 1 µg/m3 increase in background PM2.5 was associated with increased PWV (ß = 0.68 m/s; 95% CI = 0.10, 1.26; P = 0.025), in children from the in utero exposure group. There was a trend toward smaller PWV (ß = -0.17 m/s; 95% CI = -0.366, 0.02) from the 3- to 7-year follow-up clinic suggesting that the deficits observed previously in children exposed postnatally did not persist. Conclusion: There was a moderate improvement in vascular stiffness of children exposed to PM2.5 from a local coal mine fire in infancy. There was a mild increase in vascular stiffness in children exposed to PM2.5 from a local coal mine fire while their mothers were pregnant.

Landscape fire smoke airway exposure impairs respiratory and cardiac function and worsens experimental asthma.

BACKGROUND: Millions of people are exposed to landscape fire smoke (LFS) globally, and inhalation of LFS particulate matter (PM) is associated with poor respiratory and cardiovascular outcomes. However, how LFS affects respiratory and cardiovascular function is less well understood. OBJECTIVE: We aimed to characterize the pathophysiologic effects of representative LFS airway exposure on respiratory and cardiac function and on asthma outcomes. METHODS: LFS was generated using a customized combustion chamber. In 8-week-old female BALB/c mice, low (25 µg/m3, 24-hour equivalent) or moderate (100 µg/m3, 24-hour equivalent) concentrations of LFS PM (10 µm and below [PM10]) were administered daily for 3 (short-term) and 14 (long-term) days in the presence and absence of experimental asthma. Lung inflammation, gene expression, structural changes, and lung function were assessed. In 8-week-old male C57BL/6 mice, low concentrations of LFS PM10 were administered for 3 days. Cardiac function and gene expression were assessed. RESULTS: Short- and long-term LFS PM10 airway exposure increased airway hyperresponsiveness and induced steroid insensitivity in experimental asthma, independent of significant changes in airway inflammation. Long-term LFS PM10 airway exposure also decreased gas diffusion. Short-term LFS PM10 airway exposure decreased cardiac function and expression of gene changes relating to oxidative stress and cardiovascular pathologies. CONCLUSIONS: We characterized significant detrimental effects of physiologically relevant concentrations and durations of LFS PM10 airway exposure on lung and heart function. Our study provides a platform for assessment of mechanisms that underpin LFS PM10 airway exposure on respiratory and cardiovascular disease outcomes.

Lung function changes in children exposed to mine fire smoke in infancy.

BACKGROUND AND OBJECTIVE: Chronic, low-intensity air pollution exposure has been consistently associated with reduced lung function throughout childhood. However, there is limited research regarding the implications of acute, high-intensity air pollution exposure. We aimed to determine whether there were any associations between early life exposure to such an episode and lung growth trajectories. METHODS: We conducted a prospective cohort study of children who lived in the vicinity of the Hazelwood coalmine fire. Lung function was measured using respiratory oscillometry. Z-scores were calculated for resistance (R5 ) and reactance at 5 Hz (X5 ) and area under the reactance curve (AX). Two sets of analyses were conducted: (i) linear regression to assess the cross-sectional relationship between post-natal exposure to mine fire-related particulate matter with an aerodynamic diameter of less than 2.5 micrometres (PM2.5 ) and lung function at the 7-year follow-up and (ii) linear mixed-effects models to determine whether there was any association between exposure and changes in lung function between the 3- and 7-year follow-ups. RESULTS: There were no associations between mine fire-related PM2.5 and any of the lung function measures, 7-years later. There were moderate improvements in X5 (ß: -0.37 [-0.64, -0.10] p = 0.009) and AX (ß: -0.40 [-0.72, -0.08] p = 0.014), between the 3- and 7-year follow-ups that were associated with mean PM2.5 , in the unadjusted and covariance-adjusted models. Similar trends were observed with maximum PM2.5 . CONCLUSION: There was a moderate improvement in lung stiffness of children exposed to PM2.5 from a local coalmine fire in infancy, consistent with an early deficit in lung function at 3-years after the fire that had resolved by 7-years.

Understanding the pathogenesis of engineered stone-associated silicosis: The effect of particle chemistry on the lung cell response.

BACKGROUND AND OBJECTIVE: The resurgence of severe and progressive silicosis among engineered stone benchtop industry workers is a global health crisis. We investigated the link between the physico-chemical characteristics of engineered stone dust and lung cell responses to understand components that pose the greatest risk. METHODS: Respirable dust from 50 resin-based engineered stones, 3 natural stones and 2 non-resin-based materials was generated and analysed for mineralogy, morphology, metals, resin, particle size and charge. Human alveolar epithelial cells and macrophages were exposed in vitro to dust and assessed for cytotoxicity and inflammation. Principal component analysis and stepwise linear regression were used to explore the relationship between engineered stone components and the cellular response. RESULTS: Cutting engineered stone generated fine particles of <600 nm. Crystalline silica was the main component with metal elements such as Ti, Cu, Co and Fe also present. There was some evidence to suggest differences in cytotoxicity (p = 0.061) and IL-6 (p = 0.084) between dust samples. However, IL-8 (CXCL8) and TNF-α levels in macrophages were clearly variable (p < 0.05). Quartz explained 11% of the variance (p = 0.019) in macrophage inflammation while Co and Al accounted for 32% of the variance (p < 0.001) in macrophage toxicity, suggesting that crystalline silica only partly explains the cell response. Two of the reduced-silica, non-engineered stone products induced considerable inflammation in macrophages. CONCLUSION: These data suggest that silica is not the only component of concern in these products, highlighting the caution required as alternative materials are produced in an effort to reduce disease risk.

Exposure to air pollution concentrations of various intensities in early life and allergic sensitisation later in childhood.

BACKGROUND: Evidence on the relationship between air pollution and allergic sensitisation in childhood is inconsistent, and this relationship has not been investigated in the context of smoke events that are predicted to increase with climate change. Thus, we aimed to evaluate associations between exposure in two early life periods to severe levels of particulate matter with an aerodynamic diameter < 2.5 µm (PM2.5) from a mine fire, background PM2.5, and allergic sensitisation later in childhood. METHODS: We measured specific immunoglobulin E (IgE) levels for seven common aeroallergens as well as total IgE levels in a cohort of children who had been exposed to the Hazelwood coal mine fire, either in utero or during their first two years of life, in a regional area of Australia where ambient levels of PM2.5 are generally low. We estimated personal exposure to fire-specific emissions of PM2.5 based on a high-resolution meteorological and pollutant dispersion model and detailed reported movements of pregnant mothers and young children during the fire. We also estimated the usual background exposure to PM2.5 at the residential address at birth using a national satellite-based land-use regression model. Associations between both sources of PM2.5 and sensitisation to dust, cat, fungi, and grass seven years after the fire were estimated with logistic regression, while associations with total IgE levels were estimated with linear regression. RESULTS: No association was found between the levels of exposure at either developmental stage to fire-related PM2.5 and allergic sensitisation seven years after the event. However, levels of background exposure were positively associated with sensitisation to dust (OR = 1.90, 95%CI = 1.12,3.21 per 1 µg/m3). CONCLUSIONS: Chronic but low exposure to PM2.5 in early life could be more strongly associated with allergic sensitisation in childhood than time-limited high exposure levels, such as the ones experienced during landscape fires.

Contrasting Health Outcomes following a Severe Smoke Episode and Ambient Air Pollution in Early Life: Findings from an Australian Data Linkage Cohort Study of Hospital Utilization.

BACKGROUND: Episodic spikes in air pollution due to landscape fires are increasing, and their potential for longer term health impacts is uncertain. OBJECTIVE: Our objective is to evaluate associations between exposure in utero and in infancy to severe pollution from a mine fire, background ambient air pollution, and subsequent hospital care. METHODS: We linked health records of births, emergency department (ED) visits, and hospitalizations of children born in the Latrobe Valley, Australia, 2012-2015, which included a severe pollution episode from a mine fire (9 February 2014 to 25 March 2014). We assigned modeled exposure estimates for fire-related and ambient particulate matter with an aerodynamic diameter of 2.5µm (PM2.5) to residential address. We used logistic regression to estimate associations with hospital visits for any cause and groupings of infectious, allergic, and respiratory conditions. Outcomes were assessed for the first year of life in the in utero cohort and the year following the fire in the infant cohort. We estimated exposure-response for both fire-related and ambient PM2.5 and also employed inverse probability weighting using the propensity score to compare exposed and not/minimally exposed children. RESULTS: Prenatal exposure to fire-related PM2.5 was associated with ED presentations for allergies/skin rash [odds ratio (OR)=1.34, 95% confidence interval (CI): 1.01, 1.76 per 240 µg/m3 increase]. Exposure in utero to ambient PM2.5 was associated with overall presentations (OR=1.18, 95% CI: 1.05, 1.33 per 1.4 µg/m3) and visits for infections (ED: OR=1.13, 95% CI: 0.98, 1.29; hospitalizations: OR=1.23, 95% CI: 1.00, 1.52). Exposure in infancy to fire-related PM2.5 compared to no/minimal exposure, was associated with ED presentations for respiratory (OR=1.37, 95% CI: 1.05, 1.80) and infectious conditions (any: OR=1.21, 95% CI: 0.98, 1.49; respiratory-related: OR=1.39, 95% CI: 1.05, 1.83). Early life exposure to ambient PM2.5 was associated with overall ED visits (OR=1.17, 95% CI: 1.05, 1.30 per 1.4 µg/m3 increase). DISCUSSION: Higher episodic and lower ambient concentrations of PM2.5 in early life were associated with visits for allergic, respiratory, and infectious conditions. Our findings also indicated differences in associations at the two developmental stages. https://doi.org/10.1289/EHP12238.

Asthma and landscape fire smoke: A Thoracic Society of Australia and New Zealand position statement.

Landscape fires are increasing in frequency and severity globally. In Australia, extreme bushfires cause a large and increasing health and socioeconomic burden for communities and governments. People with asthma are particularly vulnerable to the effects of landscape fire smoke (LFS) exposure. Here, we present a position statement from the Thoracic Society of Australia and New Zealand. Within this statement we provide a review of the impact of LFS on adults and children with asthma, highlighting the greater impact of LFS on vulnerable groups, particularly older people, pregnant women and Aboriginal and Torres Strait Islander peoples. We also highlight the development of asthma on the background of risk factors (smoking, occupation and atopy). Within this document we present advice for asthma management, smoke mitigation strategies and access to air quality information, that should be implemented during periods of LFS. We promote clinician awareness, and the implementation of public health messaging and preparation, especially for people with asthma.

The understudied global experiment of pollution's impacts on wildlife and human health: The ethical imperative for interdisciplinary research.

The global impact of pollution on human and wildlife health is a growing concern. The health impacts of pollution are significant and far-reaching yet poorly understood as no one field of research has the practices and methodologies required to encapsulate the diversity of these consequences. This paper advocates that interdisciplinary research is essential to comprehend the full extent of the impact of pollution. Medical and ecological research play a key role in investigating the health consequences of the pollution crisis, yet the wildlife experience is often neglected. This paper outlines how applying advanced techniques and expertise adapted in medical research to wildlife exposed to pollutants offers a unique perspective to understanding the full diversity of impacts to health. The challenges that impede the progress of this research include the lack of support for interdisciplinary research among funding streams, limitations in field-specific techniques, and a lack of communication between researchers from different disciplines. Of awarded funding from major national research councils across Australia, Europe, and the United States of America, only 0.5% is dedicated to pollution focused research. This is inclusive of laboratory equipment, mitigation strategies, quantification of environmental samples and health consequences research. Of that, 0.03% of funding is awarded to explaining the wildlife experience and documenting the health consequences observed despite being model organisms to environmentally and biologically relevant models for pollution exposure. This calls for a coordinated effort to overcome these hurdles and to promote interdisciplinary research in order to fully comprehend the consequences of pollution exposure and protect the health of humans, wildlife, and the environment. An interdisciplinary approach to this problem is timely given the magnitude of negative health consequences associated with exposure, the number of pollutants already present within the environment and the continual development of new compounds.

Mechanical ventilation decreases tidal volume heterogeneity but increases heterogeneity in end-expiratory volumes.

How the heterogeneous distribution of lung volumes changes in response to different mechanical ventilation (MV) strategies is unclear. Using our well-developed four-dimensional computed tomography (4DCT) high-resolution imaging technique, we aimed to assess the effect of different MV strategies on the distribution and heterogeneity of regional lung volumes. Healthy adult female BALB/c mice received either 2 h of "injurious" MV [n = 6, mechanical ventilation at high PIP with zero PEEP (HPZP)] with a peak inspiratory pressure (PIP) of 20 cmH2O and zero positive end-expiratory pressure (PEEP), or 2 h of "protective" MV [n = 8, mechanical ventilation at low PIP with PEEP (LPP)] with PIP = 12 cmH2O and PEEP = 2 cmH2O. 4DCT images were obtained at baseline (0 h) and after 2 h of MV. Tidal volume (Vt) and end-expiratory lung volume (EEV) were measured throughout the whole lung on a voxel-by-voxel basis. Heterogeneity of ventilation was determined by the coefficient of variation (COV) of Vt and EEV. Our data showed that MV had minimal impact on global Vt but decreased EEV in the HPZP group (P < 0.05). Both ventilation modes decreased the COV of Vt (39.4% for HPZP and 9.7% for LPP) but increased the COV in EEV (36.4% for HPZP and 29.2% for LPP). This was consistent with the redistribution index, which was significantly higher in the HVZP group than in the LPP group (P < 0.001). We concluded that regional assessment of the change in EEV showed different patterns in progression between LPP and HPZP strategies. Both ventilation strategies decreased heterogeneity in Vt after 2 h of MV but increased heterogeneity in EEV. Further work is required to determine the link between these effects and ventilator-induced lung injury.NEW & NOTEWORTHY Tidal volume heterogeneity decreases over time in response to mechanical ventilation, in contrast to end-expiratory volume heterogeneity which increases.

Geogenic particles induce bronchial susceptibility to non-typeable Haemophilus influenzae.

Exposure to geogenic (earth-derived) particulate matter (PM) is linked to an increased prevalence of bronchiectasis and other respiratory infections in Australian Indigenous communities. Experimental studies have shown that the concentration of iron in geogenic PM is associated with the magnitude of respiratory health effects, however, the mechanism is unclear. We investigated the effect of geogenic PM and iron oxide on the invasiveness of non-typeable Haemophilus influenzae (NTHi). Peripheral blood mononuclear cell-derived macrophages or epithelial cell lines (A549 & BEAS-2B) were exposed to whole geogenic PM, their primary constituents (haematite, magnetite or silica) or diesel exhaust particles (DEP). The uptake of bacteria was quantified by flow cytometry and whole genome sequencing (WGS) was performed on NTHi strains. Geogenic PM increased the invasiveness of NTHi in bronchial epithelial cells. Of the primary constituents, haematite also increased NTHi invasion with magnetite and silica having significantly less impact. Furthermore, we observed varying levels of invasiveness amongst NTHi isolates. WGS analysis suggested isolates with more genes associated with heme acquisition were more virulent in BEAS-2B cells. The present study suggests that geogenic particles can increase the susceptibility of bronchial epithelial cells to select bacterial pathogens in vitro, a response primarily driven by haematite content in the dust. This demonstrates a potential mechanism linking exposure to iron-laden geogenic PM and high rates of chronic respiratory infections in remote communities in arid environments.

Impact of Landscape Fire Smoke Exposure on Patients With Asthma With or Without Laryngeal Hypersensitivity.

BACKGROUND: Individuals with asthma experienced severe and prolonged symptoms after the Australian 2019 to 2020 landscape fire. Many of these symptoms, such as throat irritation, occur in the upper airway. This suggests that laryngeal hypersensitivity contributes to persistent symptoms after smoke exposure. OBJECTIVE: This study examined the relationship between laryngeal hypersensitivity and symptoms, asthma control, and health impacts on individuals exposed to landscape fire smoke. METHOD: The study was a cross-sectional survey of 240 participants in asthma registries who were exposed to smoke during the 2019 to 2020 Australian fire. The survey, completed between March and May 2020, included questions about symptoms, asthma control, and health care use, as well as the Laryngeal Hypersensitivity Questionnaire. Daily concentration levels of particulate matter less than or equal to 2.5 µm in diameter were measured over the 152-day study period. RESULTS: The 49 participants with laryngeal hypersensitivity (20%) had significantly more asthma symptoms (96% vs 79%; P = .003), cough (78% vs 22%; P < .001), and throat irritation (71% vs 38%; P < .001) during the fire period compared with those without laryngeal hypersensitivity. Participants with laryngeal hypersensitivity had greater health care use (P ≤ .02), more time off work (P = .004), and a reduced capacity to participate in usual activities (P < .001) during the fire period, as well as poorer asthma control during the follow-up (P = .001). CONCLUSIONS: Laryngeal hypersensitivity is associated with persistent symptoms, reports of lower asthma control, and increased health care use in adults with asthma who were exposed to landscape fire smoke. Management of laryngeal hypersensitivity before, during, or immediately after landscape fire smoke exposure might reduce the symptom burden and health impact.

Primary and pharmaceutical care usage concurrent associations with a severe smoke episode and low ambient air pollution in early life.

BACKGROUND: Due to climate change, landscape fires account for an increasing proportion of air pollution emissions, and their impacts on primary and pharmaceutical care are little understood. OBJECTIVES: To evaluate associations between exposure in two early life periods to severe levels of PM2.5 from a mine fire, background PM2.5, and primary and pharmaceutical care. METHODS: We linked records of births, general practitioner (GP) presentations and prescription dispensing for children born in the Latrobe Valley, Australia, 2012-2014, where a severe mine fire occurred in February-March 2014 in an area with otherwise low levels of ambient PM2.5. We assigned modelled exposure estimates for fire-related (cumulative over the fire and peak 24-hour average) and annual ambient PM2.5 to residential address. Associations with GP presentations and dispensing of prescribed medications in the first two years of life (exposure in utero) and in the two years post-fire (exposure in infancy) were estimated using two-pollutant quasi-Poisson regression models. RESULTS: Exposure in utero to fire-related PM2.5 was associated with an increase in systemic steroid dispensing (Cumulative: IRR = 1.11, 95%CI = 1.00-1.24 per 240 µg/m3; Peak: IRR = 1.15, 95%CI = 1.00-1.32 per 45 µg/m3), while exposure in infancy was associated with antibiotic dispensing (Cumulative: IRR = 1.05, 95%CI = 1.00-1.09; Peak: IRR = 1.06, 95%CI = 1.00-1.12). Exposure in infancy to ambient PM2.5, despite relatively low levels from a global perspective (Median = 6.1 µg/m3), was associated with an increase in antibiotics (IRR = 1.10, 95%CI = 1.01-1.19 per 1.4 µg/m3) and in GP presentations (IRR = 1.05, 95%CI = 1.00-1.11), independently from exposure to the fire. We also observed differences in associations between sexes with GP presentations (stronger in girls) and steroid skin cream dispensing (stronger in boys). DISCUSSION: Severe medium-term concentrations of PM2.5 were linked with increased pharmaceutical treatment for infections, while chronic low levels were associated with increased prescriptions dispensed for infections and primary care usage. Our findings also indicated differences between sexes.

No association between in utero exposure to emissions from a coalmine fire and post-natal lung function.

BACKGROUND AND OBJECTIVE: Studies linking early life exposure to air pollution and subsequent impaired lung health have focused on chronic, low-level exposures in urban settings. We aimed to determine whether in utero exposure to an acute, high-intensity air pollution episode impaired lung function 7-years later. METHOD: We conducted a prospective cohort study of children who lived in the vicinity of a coalmine fire. Respiratory function was measured using the forced oscillation technique (FOT). Z-scores for resistance at 5 Hz (R5), reactance at 5 Hz (X5) and area under the reactance curve (AX) were calculated. Two sets of analyses were conducted to address two separate questions: (1) whether mine fire exposure (a binary indicator; conceived after the mine fire vs in utero exposed) was associated with the respiratory Z-scores; (2) whether there was any dose-response relationship between fire-related PM2.5 exposure and respiratory outcomes among those exposed. RESULTS: Acceptable lung function measurements were obtained from 79 children; 25 unexposed and 54 exposed in utero. Median (interquartile range) for daily average and peak PM2.5 for the exposed children were 4.2 (2.6 - 14.2) and 88 (52-225) µg/m3 respectively. There were no detectable differences in Z-scores between unexposed and exposed children. There were no associations between respiratory Z-scores and in utero exposure to PM2.5 (daily average or peak). CONCLUSION: There was no detectable effect of in utero exposure to PM2.5 from a local coalmine fire on post-natal lung function 7-years later. However, statistical power was limited.

The impact of the 2019/2020 Australian landscape fires on infant feeding and contaminants in breast milk in women with asthma.

BACKGROUND: The 2019/2020 Australian landscape fires (bushfires) resulted in prolonged extreme air pollution; little is known about the effects on breastfeeding women and their infants. This study aimed to examine the impact of prolonged landscape fires on infant feeding methods and assess the concentration of polycyclic aromatic hydrocarbons (PAHs) and elements in breast milk samples. METHODS: From May - December 2020, women with asthma, who were feeding their infants during the fires, were recruited from an existing cohort. Data on infant feeding and maternal concern during the fires were retrospectively collected. Breast milk samples were collected from a sample of women during the fire period and compared with samples collected outside of the fire period for levels of 16 PAHs (gas chromatography coupled with mass spectrometry), and 20 elements (inductively coupled plasma-mass spectrometry). RESULTS: One-hundred-and-two women who were feeding infants completed the survey, and 77 provided 92 breast milk samples. Two women reported concern about the impact of fire events on their infant feeding method, while four reported the events influenced their decision. PAHs were detected in 34% of samples collected during, versus no samples collected outside, the fire period (cross-sectional analysis); specifically, fluoranthene (median concentration 0.015 mg/kg) and pyrene (median concentration 0.008 mg/kg) were detected. Women whose samples contained fluoranthene and pyrene were exposed to higher levels of fire-related fine particulate matter and more fire days, versus women whose samples had no detectable fluoranthene and pyrene. Calcium, potassium, magnesium, sodium, sulphur, and copper were detected in all samples. No samples contained chromium, lead, nickel, barium, or aluminium. No statistically significant difference was observed in the concentration of elements between samples collected during the fire period versus outside the fire period. CONCLUSIONS: Few women had concerns about the impact of fire events on infant feeding. Detection of fluoranthene and pyrene in breast milk samples was more likely during the 2019/2020 Australian fire period; however, levels detected were much lower than levels expected to be related to adverse health outcomes.

Can Maternal Exposure to Air Pollution Affect Post-Natal Liver Development?

Emerging evidence suggests that inhalation of particulate matter (PM) can have direct adverse effects on liver function. Early life is a time of particular vulnerability to the effects of air pollution. On that basis, we tested whether in utero exposure to residential PM has an impact on the developing liver. Pregnant mice (C57BL/6J) were intranasally administered 100 µg of PM sampled from residential roof spaces (~5 mg/kg) on gestational days 13.5, 15.5, and 17.5. The pups were euthanized at two weeks of age, and liver tissue was collected to analyse hepatic metabolism (glycogen storage and lipid level), cellular responses (oxidative stress, inflammation, and fibrosis), and genotoxicity using a range of biochemical assays, histological staining, ELISA, and qPCR. We did not observe pronounced effects of environmentally sampled PM on the developing liver when examining hepatic metabolism and cellular response. However, we did find evidence of liver genomic DNA damage in response to in utero exposure to PM. This effect varied depending on the PM sample. These data suggest that in utero exposure to real-world PM during mid-late pregnancy has limited impacts on post-natal liver development.

Engineered Stone Fabrication Work Releases Volatile Organic Compounds Classified as Lung Irritants.

Engineered stones are often characterized for their crystalline silica content. Their organic composition, particularly that of the emissions generated during fabrication work using hand-held power tools, is relatively unexplored. We forensically screened the emissions from dry-cutting 12 engineered stone products in a test chamber for their organic composition by pyrolysis-gas chromatography-mass spectrometry (GC-MS) plus selected traditional capture and analysis techniques. Phthalic anhydride, which has a Respiratory Sensitization (RSEN) Notation by the American Conference of Governmental Industrial Hygienists (ACGIH), was the most common and abundant compound, at 26-85% of the total organic composition of engineered stone emissions. Benzaldehyde and styrene were also present in all twelve samples. During active cutting, the predominant volatile organic compound (VOC) emitted was styrene, with phthalic anhydride, benzene, ethylbenzene, and toluene also detected. These results have important health implications as styrene and phthalic anhydride are irritants to the respiratory tract. This study suggests a risk of concurrent exposure to high levels of respirable crystalline silica and organic lung irritants during engineered stone fabrication work.