Review of ethics for occupational hygiene hazard monitoring surveys using sensors.

This review is about the ethical use of sensors to monitor occupational exposure to hazards. It considers whether the same or different, ethical measures apply to using sensors, compared to conventional hazard monitoring surveys. To undertake the review, subject experts developed a research question, identified suitable search terms, and set the scope of these searches. Candidate research papers dating from 2000 to mid-2022 that met inclusion criteria were identified and reviewed by each author. Ethical concerns were identified by the authors of studies in which sensors were used to monitor employee health and well-being, but most of the studies that used them to monitor employee exposure to hazards focused on the technical aspects of their deployment. These ethical concerns included questions about employee rights and privacy, the anonymity of the data collected with sensors, and how the security of this data is managed. The review considers ethical standards and codes of practice for occupational hygiene work and the ethical risks when sensors are used to gather data. Sensors may provide insight into occupational exposure to hazards, but their use is not always adequately explained to employees by those managing this monitoring work. The ethical concerns identified were relevant to many areas of industrial hygiene work, but more studies are required that consider the ethical use of sensors in workplaces. Studies that monitored employee health, well-being, and productivity, identified ethical risks in using sensors to monitor these endpoints. An ethical framework and checklist for hygienists are proposed including a set of questions that consider the risks of using sensors to monitor occupational hazards. Industrial hygiene professional bodies provide ethical codes of practice for their members but may also need to consider the implications of using sensors in workplaces. Ethical standards support the collection of industrial hygiene exposure data whilst maintaining the privacy rights of employees.

Occupational cancer burden in Great Britain.

A sound knowledge base is required to target resources to reduce workplace exposure to carcinogens. This project aimed to provide an objective estimate of the burden of cancer in Britain due to occupation. This volume presents extensive analyses for all carcinogens and occupational circumstances defined as definite or probable human occupational carcinogens by the International Agency for Research on Cancer. This article outlines the structure of the supplement - two methodological papers (statistical approach and exposure assessment), eight papers presenting the cancer-specific results grouped by broad anatomical site, a paper giving industry sector results and one discussing work-related cancer-prevention strategies. A brief summary of the methods and an overview of the updated overall results are given in this introductory paper. A general discussion of the overall strengths and limitations of the study is also presented. Overall, 8010 (5.3%) total cancer deaths in Britain and 13,598 cancer registrations were attributable to occupation in 2005 and 2004, respectively. The importance of cancer sites such as mesothelioma, sinonasal, lung, nasopharynx, breast, non-melanoma skin cancer, bladder, oesophagus, soft tissue sarcoma and stomach cancers are highlighted, as are carcinogens such as asbestos, mineral oils, solar radiation, silica, diesel engine exhaust, coal tars and pitches, dioxins, environmental tobacco smoke, radon, tetrachloroethylene, arsenic and strong inorganic mists, as well as occupational circumstances such as shift work and occupation as a painter or welder. The methods developed for this project are being adapted by other countries and extended to include social and economic impact evaluation.

Systematic review of respiratory outbreaks associated with exposure to water-based metalworking fluids.

INTRODUCTION: Potential demographic risk factors for outbreaks of respiratory disease due to water-based metalworking fluids (MWFs) were investigated through systematic review of published outbreak investigations. METHODS: Search terms were selected by a multidisciplinary team, assisted by an experienced library information service. Several computerized literature databases were searched for articles published between January 1990 and October 2011, relating to ill health outbreaks due to MWFs. Papers meeting the search criteria were reviewed in detail, and their references checked for additional articles. Study design and demographic details of the outbreak were extracted from the selected articles and entered into standardized evidence tables. RESULTS: Thirty-five articles relating to investigations of 27 outbreaks of respiratory ill health attributed to MWF exposure were identified. The majority of reports were case series of disease or observational cross-sectional studies of symptoms and hygiene measurements. Eight of the outbreak investigations included an element of case-control analysis. Most outbreaks were from the USA, had occurred in large car- or aeronautical-manufacturing plants, and were associated with the use of central shared sumps. Hygiene studies have not demonstrated consistent risk factors for respiratory outbreaks, in terms of the type of MWF utilized, degree of microbial contamination, or levels of personal exposure. Six studies were identified that found workers with MWF exposure during outbreaks were more likely to report respiratory or systemic symptoms than unexposed control workers. Six case-control analyses were also identified that found workers with extrinsic allergic alveolitis (EAA) were more likely to demonstrate certain immune responses to microbial contaminants and/or used MWFs than workers without EAA. CONCLUSION: Despite a number of detailed workplace and immunological studies of asthma and alveolitis outbreaks in MWF-exposed workforces, our understanding of their aetiology remains limited.

The effects of nickel and chromium on human keratinocytes: differences in viability, cell associated metal and IL-1alpha release.

This study was carried out to assess the effects of chromium and nickel upon isolated keratinocytes as an in vitro model of human skin. Keratinocytes were isolated from healthy volunteer skin samples of unknown metal sensitivity (n=10) and were compared with cells from patient biopsies of known metal sensitivity (n=7). Cells were dosed with a concentration range of nickel and chromium (0-10,000 microM) and cellular mitochondrial activity, viability, metal uptake and cytokine release were measured. Responses of primary versus passaged keratinocytes were also compared. Toxicity data from primary and passaged keratinocytes was statistically analysed by the non-linear Hill Plot model. Results showed that hexavalent chromium was significantly more cytotoxic, associated more with keratinocytes and induced a dose dependant release of IL-1alpha compared to nickel. Significant differences were observed between primary and passaged keratinocytes with regard to the toxicity of chromium and nickel and variation of response. No differences were observed in the cytotoxicity or cytokine release induced by chromium or nickel for the known sensitised biopsy patient samples (n=4) compared to patch test negative controls (n=3). The results from this study suggest human keratinocytes in vitro respond very differently to chromium and nickel.

The proteolytic profile of prelabour ruptured amnion at term: a case-control study.

OBJECTIVES: The aim of this study was to investigate whether prelabour ruptured membranes at term display increased proteolytic activity and to determine whether regional structural alterations within membranes are reflective of regional variations in proteolytic activity. STUDY DESIGN: Multiple amnion samples were collected from 37 women with prelabour membrane rupture and 37 women whose membranes ruptured spontaneously during labour. In all cases the gestation was greater than 37 weeks. Substrate zymography was used to qualitatively assess gelatinase and serine protease involvement. General protease activity (metallo, serine, acid and sulfhydryl) was measured quantitatively by fluorescent substrate cleavage. RESULTS: Substrate zymography revealed no active gelatinases or serine proteases. Fluorescent studies of general protease activity showed no significant difference between the groups and no significant regional variation. CONCLUSIONS: Gelatinase and serine protease activity do not play a major role in the formation of a membrane rupture initiation site or in prelabour membrane rupture at term.

Can the KG1 cell line be used as a model of dendritic cells and discriminate the sensitising potential of chemicals?

The KG1 myeloid leukaemia was used as source of dendritic cells (DC) to discriminate between respiratory and contact sensitising chemicals. A cocktail of cytokines was used to differentiate KG1 to dendritic like cells (termed dKG1) and the effects of nine chemicals (respiratory and contact sensitisers) and an irritant control on surface marker expression, 'antigen presenting' function and cytokine expression investigated. The stability of these chemicals when dissolved was characterised using MALDI ToF MS. A Hill plot model was used with the cellular viability data to quantify the lethal dose 50% (LD50) and a maximum sub toxic concentration of each chemical defined. Cytokine expression by the treated dKG1 was quantified using multiplex immunobead analysis. Whilst dKG1 cells were morphologically similar to DCs, expression of specific surface markers was not typical for DCs derived from healthy precursor cells. When the chemicals were applied at defined sub toxic doses no effects on dKG1 phenotype, function, or cytokine expression, attributable to the sensitisation properties were discriminated. However, dKG1 cells were much more sensitive to the toxic effects of these chemicals compared to the parent KG1 cells. Only 4 of the 9 chemicals tested were stable when dissolved indicating that the effect of sensitising chemicals on antigen presenting cells may be related to species other than the parent compound.

Chemical pollution, respiratory allergy and asthma: a perspective.

The European Centre for Ecotoxicology and Toxicology of Chemicals (ECETOC) convened a workshop in June 2005 to address the speculation that exposure to specific chemicals, and/or chemical pollutants in general, may play an important role in the increased prevalence of allergy and asthma in 'westernized' societies. This paper summarises one perspective arrived at during this workshop. It was acknowledged that certain chemicals and certain types of pollution might trigger or exacerbate asthmatic reactions in sensitised subjects. However, overall levels of pollution appear not to have had a major impact upon the prevalence of atopic allergy. Epidemiological studies suggest that pollution may in some circumstances protect from acquisition of sensitisation. Increasing exposure to household chemicals may enhance pre-existing allergies, but evidence for their causation of allergy is lacking. Other risk factors considered included societal dietary changes and exposure to endotoxins. Future research needs were identified which included epidemiological studies employing exposure and biomonitoring data, studies on domestic exposure to chemicals and their association with the incidence of allergy and asthma, and prospective birth cohort studies employing well-defined aspects of lifestyle, diet, chemical and endotoxin exposure as factors that may drive susceptibility to allergy and asthma.

Reduced collagen and ascorbic acid concentrations and increased proteolytic susceptibility with prelabor fetal membrane rupture in women.

Prelabor rupture of the fetal membranes affects approximately 10% of women at term, resulting in an increased risk of maternal and neonatal infection. Evidence suggests that membrane rupture is related to biochemical processes involving the extracellular matrix of the membranes. We tested the hypothesis that prelabor ruptured membranes are characterized by reduced collagen concentrations, altered collagen cross-link profiles, and increased concentrations of biomarkers of oxidative damage. We also set out to determine whether these effects are modulated by ascorbic acid status. In a case-control study, we explored the role that ascorbic acid, oxidative stress, collagen, and collagen cross-links play in determining membrane integrity and developed a functional assay to assess membrane proteolytic susceptibility. Prelabor ruptured membrane had a reduced ascorbic acid concentration in comparison with controls while protein carbonyl and malondialdehyde concentrations were increased. Collagen concentrations were also reduced in prelabor ruptured membrane, and while the concentration of collagen cross-links was not significantly different between prelabor and timely ruptured membrane, there was a regional variation in cross-link ratio within the amniotic sac. Proteolytic resistance in vitro was reduced in prelabor ruptured membrane and also exhibited regional variation within the amniotic sac. Our findings are strongly supportive of a role for the enhanced degradation of membrane collagen in the determination of prelabor rupture of fetal membranes. The formation of the rupture initiation site is a function of a regional variation in collagen cross-link ratio. Tissue ascorbic acid status may be an important mediator of these processes.