Alcohol Consumption in the Australian Mining Industry: The Role of Workplace, Social, and Individual Factors.

BACKGROUND: Coal miners have been reported to have higher rates of risky/harmful alcohol misuse; however, it is not known if metalliferous mining employees whose working conditions differ in workplace practices, also have increased rates of risky/harmful alcohol misuse. This study aimed to examine alcohol consumption in a sample of Australian metalliferous mining workers and to examine the demographic and workplace factors associated with risky/harmful alcohol use. METHODS: All employees from a convenience sample of four Australian mine sites were invited to complete a paper-based cross-sectional survey between June 2015 and May 2017. The survey contained questions relating to social networks, health behaviors, psychological distress, demographic characteristics, and risky/harmful drinking. Current alcohol use was measured by the Alcohol Use Disorders Identification Test (AUDIT), a validated measure of risky and/or harmful drinking. Factors associated with risky/harmful drinking were investigated using univariate and multivariable logistic regression. FINDINGS: A total of 1,799 participants completed the survey (average site response rate 95%). Overall, 94.8% of males and 92.1% of females reported using alcohol in the preceding 12 months. The odds of risky/harmful alcohol use were significantly higher in those who were male, younger, and reported higher psychological distress. CONCLUSIONS/APPLICATION TO PRACTICE: This study identified that metalliferous mining employees engage in at-risk levels of alcohol consumption significantly higher than the national average despite workplace policies and practices that restrict alcohol use. Personal and workplace risk factors that may help target specific employee groups and inform the development of tailored, integrated multicomponent intervention strategies for the industry were identified.

Feasibility and acceptability of strategies to address mental health and mental ill-health in the Australian coal mining industry.

BACKGROUND: To evaluate the feasibility, acceptability and effectiveness of implementing a peer-based, multi-component mental health program in the Australian coal mining industry. METHODS: The multicomponent program included MATES in mining (a peer-based mental health and suicide prevention program) and supervisor training. Eight Australian coal mines participated in the research, with four mines receiving the mental health program. Primary outcome variables including mental health stigma, help-seeking behaviour and perception of the workplace commitment to mental health were measured prior to program implementation, and then again 10 months following using a paper based survey. Process evaluation of the mental health program was measured using a pre-test/post-test survey. RESULTS: MATES in mining 1275 miners participated in the MATES general awareness and connector training. Participants were more confident that they could identify a workmate experiencing mental ill-health; help a workmate, family member or themselves identify where to get support and were more willing to start a conversation with a workmate about their mental health. Supervisor training 117 supervisors completed the supervisor training and were subsequently more confident that they could: identify someone experiencing mental ill-health in the workplace; identify and recommend support services to a person experiencing mental ill-health; and have an effective conversation about performance issues that may be due to mental ill-health. CONCLUSIONS: Our findings show evidence to support the use of peer-based mental health programs in the mining industry, and for male-dominated industry more broadly.

Alcohol consumption in the Australian coal mining industry.

OBJECTIVES: To investigate patterns of alcohol use within the coal mining industry, and associations with the personal, social, workplace and employment characteristics. DESIGN: 8 mine sites across 3 eastern Australian states were surveyed, selected to encompass key geographic characteristics (accessibility and remoteness) and mine type (open cut and underground). Problematic alcohol use was measured using the Alcohol Use Disorders Identification Test (AUDIT) to determine: (1) overall risky or hazardous drinking behaviour; and (2) frequency of single-occasion drinking (6 or more drinks on 1 occasion). RESULTS: A total of 1457 employees completed the survey, of which 45.7% of male and 17.0% of female participants reported levels of alcohol use within the range considered as risky or hazardous, considerably higher than the national average. Hierarchical linear regression revealed a significant contribution of many individual level factors associated with AUDIT scores: younger age, male, current smoking status; illicit substance use; previous alcohol and other drug use (AOD) problems; and higher psychological distress. Workplace factors associated with alcohol use included working in mining primarily for the high remuneration, and the type of mining, with underground miners reporting higher alcohol use than open-cut miners. CONCLUSIONS: Our findings provide support for the need to address alcohol use in the coal mining industry over and above routine on-site testing for alcohol use.

Help-seeking for mental health problems by employees in the Australian Mining Industry.

BACKGROUND: The current study examined help-seeking behavior for mental health problems of employees in the mining industry. METHODS: The research involved a paper-based survey completed by a cross-section of employees from eight coalmine sites. The research aimed to investigate the frequency of contact with professional and non-professional sources of support, and to determine the socio-demographic and workplace factors associated. RESULTS: A total of 1,457 employees participated, of which, 46.6 % of participants reported contact with support to discuss their own mental health within the preceding 12 months. Hierarchical logistic regression revealed a significant contribution of workplace variables, with job security and satisfaction with work significantly associated with help-seeking behavior. CONCLUSIONS: The results provide an insight into the help-seeking behaviour of mining employees, providing useful information to guide mental health workplace program development for the mining industry, and male-dominated industry more broadly.

Chronic stress-induced disruption of the astrocyte network is driven by structural atrophy and not loss of astrocytes.

Chronic stress is well recognized to decrease the number of GFAP⁺ astrocytes within the prefrontal cortex (PFC). Recent research, however, has suggested that our understanding of how stress alters astrocytes may be incomplete. Specifically, chronic stress has been shown to induce a unique form of microglial remodelling, but it is not yet clear whether astrocytes also undergo similar structural modifications. Such alterations may be significant given the role of astrocytes in modulating synaptic function. Accordingly, in the current study we have examined changes in astrocyte morphology following exposure to chronic stress in adult rats, using three-dimensional digital reconstructions of astrocytes. Our analysis indicated that chronic stress produced profound atrophy of astrocyte process length, branching and volume. We additionally examined changes in astrocyte-specific S100ß, which are both a putative astrocyte marker and a protein whose expression is associated with astrocyte distress. While we found that S100ß levels were increased by stress, this increase was not correlated with atrophy. We further established that while chronic stress was associated with a decrease in astrocyte numbers when GFAP labelling was used as a marker, we could find no evidence of a decrease in the total number of cells, based on Nissl staining, or in the number of S100ß⁺ cells. This finding suggests that chronic stress may not actually reduce astrocyte numbers and may instead selectively decrease GFAP expression. The results of the current study are significant as they indicate stress-induced astrocyte-mediated disturbances may not be due to a loss of cells but rather due to significant remodeling of the astrocyte network.

Chronic stress induced remodeling of the prefrontal cortex: structural re-organization of microglia and the inhibitory effect of minocycline.

Recently, it has been discovered that the working memory deficits induced by exposure to chronic stress can be prevented by treating stressed animals with minocycline, a putative inhibitor of microglial activity. One of the pressing issues that now requires clarification is exactly how exposure to chronic stress modifies microglial morphology, this being a significant issue as microglial morphology is tightly coupled with their function. To examine how chronic stress alters microglial morphology, we digitally reconstructed microglia within the rat medial prefrontal cortex. Our analysis revealed that stress increased the internal complexity of microglia, enhancing ramification (i.e. branching) without altering the overall area occupied by the cell and that this effect was more pronounced in larger cells. We subsequently determined that minocycline treatment largely abolished the pro-ramifying effects of stress. With respect to mechanisms, we could not find any evidence of increased inflammation or neurodegeneration (interleukin-1ß, MHC-II, CD68, terminal deoxynucleotidyl transferase dUTP nick end labeling, and activated caspase-3). We did, however, find that chronic stress markedly increased the expression of ß1-integrin (CD29), a protein previously implicated in microglial ramification. Together, these findings highlight that increased ramification of microglia may represent an important neurobiological mechanism through which microglia mediate the behavioral effects of chronic psychological stress.

A comparative examination of the anti-inflammatory effects of SSRI and SNRI antidepressants on LPS stimulated microglia.

Selective serotonin and serotonin norepinephrine reuptake inhibitors (SSRI; SNRI) are the first choice pharmacological treatment options for major depression. It has long been assumed that the primary therapeutic mechanism of action of these drugs involves the modulation of monoaminergic systems. However, contemporary investigations have revealed that depression is linked with inflammation, and that SSRI/SNRIs possess significant anti-inflammatory actions. While these anti-inflammatory properties initially only related to work undertaken on cells of the peripheral immune system, it has recently become apparent that these drugs also exert anti-inflammatory effects on microglia, the principal cells within the CNS that regulate and respond to inflammatory factors. The aim of the current study was to compare SSRI/SNRIs in terms of their anti-inflammatory potency, and to determine the specific mechanisms through which these effects are mediated. Accordingly, the current study evaluated the ability of five different SSRIs (fluoxetine, sertraline, paroxetine, fluvoxamine and citalopram) and one SNRI (venlafaxine) to suppress microglial responses to an inflammatory stimulus. Specifically, we examined their ability to alter tumour necrosis factor-α (TNF-α) and nitric oxide (NO) production after 4 and 24 h stimulation with lipopolysaccharide. Our results indicated that the SSRIs potently inhibited microglial TNF-α and NO production. We then investigated whether these effects might involve either ß-adrenoceptor or cAMP signalling. Using the protein kinase A inhibitor Rp-CAMPs, we found evidence to suggest that cAMP signalling is involved in regulating the anti-inflammatory response. These findings suggest that antidepressants may owe at least some of their therapeutic effectiveness to their anti-inflammatory properties.

Repeated social defeat selectively increases δFosB expression and histone H3 acetylation in the infralimbic medial prefrontal cortex.

Exposure to social stress has been linked to the development and maintenance of mood-related psychopathology; however, the underlying neurobiological changes remain uncertain. In this study, we examined numbers of δFosB-immunoreactive cells in the forebrains of rats subjected to 12 episodes of social defeat. This was achieved using the social conflict model whereby animals are introduced into the home cage of older males ("residents") trained to attack and defeat all such "intruders"; importantly, controls were treated identically except that the resident was absent. Our results indicated that the only region in which δFosB-positive cells were found in significantly higher numbers in intruders than in controls was the infralimbic medial prefrontal cortex (mPFC). This same effect was not apparent using another psychological stressor, noise stress. Cells of the infralimbic mPFC also displayed evidence of chromatin remodeling. We found that exposure to repeated episodes of social defeat increased numbers of cells immunoreactive for histone H3 acetylation, but not for histone H3 phosphoacetylation, in the infralimbic mPFC. Collectively, these findings highlight the importance of the infralimbic mPFC in responding to social stress-a finding that provides insight into the possible neurobiological alterations associated with stress-induced psychiatric illness.

Chronic stress alters the density and morphology of microglia in a subset of stress-responsive brain regions.

The current study, in parallel experiments, evaluated the impact of chronic psychological stress on physiological and behavioural measures, and on the activation status of microglia in 15 stress-responsive brain regions. Rats were subjected, for 14 days, to two 30 min sessions of restraint per day, applied at random times each day. In one experiment the effects of stress on sucrose preference, weight gain, core body temperature, and struggling behaviour during restraint, were determined. In the second experiment we used immunohistochemistry to investigate stress-induced changes in ionized calcium-binding adaptor molecule-1 (Iba1), a marker constitutively expressed by microglia, and major histocompatibility complex-II (MHC-II), a marker often expressed on activated microglia, in a total of 15 stress-responsive nuclei. We also investigated cellular proliferation in these regions using Ki67 immunolabelling, to check for the possibility of microglial proliferation. Collectively, the results we obtained showed that chronic stress induced a significant increase in anhedonia, a decrease in weight gain across the entire observation period, a significant elevation in core body temperature during restraint, and a progressive decrease in struggling behaviour within and over sessions. With regard to microglial activation, chronic stress induced a significant increase in the density of Iba1 immunolabelling (nine of 15 regions) and the number of Iba1-positive cells (eight of 15 regions). Within the regions that exhibited an increased number of Iba1-positive cells after chronic stress, we found no evidence of a between group difference in the number of MHC-II or Ki67 positive cells. In summary, these results clearly demonstrate that chronic stress selectively increases the number of microglia in certain stress-sensitive brain regions, and also causes a marked transition of microglia from a ramified-resting state to a non-resting state. These findings are consistent with the view that microglial activation could play an important role in controlling and/or adapting to stress.

Neonatal lipopolysaccharide and adult stress exposure predisposes rats to anxiety-like behaviour and blunted corticosterone responses: implications for the double-hit hypothesis.

The double-hit hypothesis posits that an early life genetic or environmental insult sets up a neural predisposition to psychopathology, which may emerge in the presence of a subsequent insult, or 'second hit' in later life. The current study assessed the effect of neonatal lipopolysaccharide (LPS) exposure on anxiety-like behaviours in the adult Wistar rat. Rats were administered either LPS (Salmonella enterica, serotype enteritidis, 0.05 mg/kg, i.p.) or saline (equivolume) on days 3 and 5 of life (birth=day 1). In adulthood (85 days), subjects were allocated to either "stress" or "no stress" treatment groups. For the "stress" group, subjects were exposed to a three-day stress protocol consisting of a 30 min period of restraint and isolation. The "no stress" group was left unperturbed but were handled during this period to control for handling effects between adult "stress" and "no stress" conditions. All animals then underwent behavioural testing using standardised tests of anxiety-like behaviour, including either the Hide Box/Open Field, Elevated Plus Maze (EPM) or Acoustic Startle Response (ASR). Time and event measures for restraint and isolation, the Hide Box/Open Field and EPM were recorded using automated tracking software. Startle amplitude and habituation across time was measured in the ASR test. Prior to and following behavioural test sessions, peripheral blood was collected to assess serum corticosterone and ACTH levels. Data analysis indicated that LPS-treated animals exposed to stress in adulthood exhibited increased anxiety-like behaviour across all behavioural tests compared to controls. Sexually dimorphic effects were observed with males exhibiting increased anxiety-related behaviours compared to females (p<.05). Neonatal LPS exposure induced a significant increase in corticosterone compared to controls (p<.05), whereas corticosterone responses to stress in adulthood were associated with a significantly blunted HPA axis response (p<.05). No differences in ACTH were observed. These results lend support to the double-hit hypothesis of anxiety-related behaviour, demonstrating that neonatal immune activation produces an enhanced propensity toward anxiety-related behaviour following stress in adulthood, and that this susceptibility is associated with alterations to HPA axis ontogeny.